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Fano's Surgery
Fano's Surgery
Preface
Rotary is a global network of 1.2 million neighbors, friends, leaders, and problem-solvers that see a world
where people unite and take action to create lasting change across the globe, in our communities, and in
ourselves. Rotary’s 35,000+ clubs work together to promote peace, fight disease, provide clean water,
sanitation, and hygiene, save mothers and children, support education and grow local economies.
"Rotaract" stands for "Rotary in Action", and is a community service organization for young men and
women between the ages 18 and over.
Rotaract club of Fanos is a volunteer organization sponsored by Rotary club of Addis Ababa West. The
club’s main area of focus are maternal and child health, disease prevention and treatment, education and
literacy in addition to community development. The pass it on project, which aims to stir up the public
through books, happens to be one of the club’s promising projects. This medical guide book was prepared
by volunteers and members of the project who are medical students of Tikur Anbessa Specialized Hospital.
Medical students from all over the world go through rigorous training to be the doctors that have earned
the white coat. We wanted to lessen the loads of our fellow medical students by providing a guide book
with notes compiled from different reference books. Medical students will have gained quick review from
this book and will be inspired to edit and publish better medical books. Fanos’ surgery will allow
undergraduate students to prepare a well-crafted case report and it will equip them for bedsides, rounds,
long and short exams. The guidebook is focused on approach to cases and we have tried to include
frequently encountered surgical cases that will help students revise after a long read.
Nanati Jemal
Pass-it-on Project Manager
Acknowledgement
We would like to extend our deepest gratitude to the senior doctors of Tikur Anbessa Specialized
Hospital whose comments and suggestions have gone towards shaping this book to its present
form. We would also like to sincerely thank our Families who have put up with our late night zoom
meetings and readings in order to complete this book. In addition, our heartfelt appreciation goes
to authors of similar guide books who have inspired and motivated us.
This book wouldn’t come to light without our compilers and editors who have dedicated their time
to help the generation that will follow them. In spite of the constant bickering about the content of
the book, we have achieved something to be proud of. Last but not least, we would like to thank
our fellow classmates who have supported and appreciated the Fanos’ series and it is for this
reason we dedicate the book to 2009 undergraduate batch of Tikur Anbessa Specialized Hospital,
A.A.U, SoM.
Disclaimer
This book is prepared by medical students and is intended for educational purposes only. It is not a
substitute for professional medical advice, diagnosis or treatment. Never ignore professional
medical advice in seeking treatment because of something you have read on this book. The content
of this book are notes compiled from different standard textbooks mentioned on the reference
section at the end of the book.
Contributors and Reviewers
Compiled By:
Samuel Mesfin
Coordinator:
Nanati Jemal
Samuel Mesfin
Part 7: Neurosurgery
7.1. Head Injury………………………………….440 7.5. Neural Tube Defects (NTDs) ……………………485
7.2. Spinal Cord Injury…………………….….460 7.6. Hydrocephalus………………………………………...493
7.3. Peripheral Nerve Injury……………….472 7.7. Video QR Codes……………………………………….499
7.4. Brain Tumor……………………………..….475
Part 8: Orthopedics
8.1. Fracture……………………………………...501 8.2.4. Differential Diagnosis of Primary Lytic
8.2. Bone Tumor………………………………..510 Lesions…………………………………………………….519
8.2.1. Osteosarcoma……………….….518 8.3. Fracture Management…………………………….523
8.2.2. Chondrosarcoma……………….518 8.4. Talipes Equinovarus
8.2.3. Ewing’s Sarcoma……………….519 (Idiopathic Club-Foot) …………………………….529
8.5. Video QR Codes……………………………………….534
Index…………………………………………………………………………………………………………………………………………….…536
Reference…………………………………………………………………………………………………………………………………….….538
This Page Is Intentionally Left Blank
Part 1: Plastic Surgery
Content By:
Eyerusalem Nega
Nanati Jemal 1.1 . Wound …………………………………………………2
Edited By:
Samuel Mesfin 1.2 . Skin Tumor…………………………..……………...15
Reviewed By: 1.3 . Burn ………………..…………….....................24
Dr. Abiy Hailu
(Plastic and Reconstructive
Surgeon)
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1.1. Wound
History …………………………………………….2
Wound examination…………………………4
Discussion of the Case………………………7
History
Take proper information of the wound
When and where did the wound occur?
o Acute: surgical/ traumatic wound
o Chronic:
Leg ulcers Pressure ulcer
Pressure sores Malignancy associated
Ischemic ulcer Diabetic foot ulcer
Pressure sore frequency in descending order include:
o Ischium o Lateral malleolus
o Greater trochanter o Medial malleolus
o Scrum o Occiput
o Heel
Alcohol and drug consumption
What caused the wound?
o Mechanical
Puncture wounds
- X-ray exam to rule out retained foreign bodies
- Treat according to published protocols due to HIV and
hepatitis virus
Abraded wounds Cut
Incised
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Animal bite
- Was post rabies exposure prophylaxis given
- Ask provocation history
- Ask change in behavior of the dog
- Vaccination history of the dog
Torn wound Crush injury
Shot wound
o Chemical
Acid Base
o Thermal
Burning Freezing
o Radiation injury
o Special
Toxins
Venom
Skin necrosis
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Wound Examination
No inflammation
No breaks in aseptic technique
Elective procedure
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Hollow viscous entered but controlled 5-8%
Clean contaminated
No inflammation
Primary wound closure
Minor break in aseptic technique
Mechanical drain used
Bowel preparation preoperatively
Uncontrollable spillage from viscus 20-25%
Contaminated
Apparent inflammation
Open traumatic wound
Major break in aseptic technique
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2) Hematoma
A blood-filled localized collection under the skin or body tissue that
occurs due to internal blood vessel damage
3) Abrasion
They are made by a scraping injury to the skin surface, typically in an
irregular fashion.
Most are superficial and will heal by epithelialization.
Open wound: wounds in which skin has been compromised and underlying tissue
are exposed
1) An incised wound:
Is defined as a very regular cut made by a sharp object such as a
knife, glass or blade
Less contaminated
2) Lacerated wound:
Made when a surface is cut in an irregular fashion down to the
underlying tissue.
Deeper than abrasions and more irregular than incised wounds.
They are caused by blunt injuries like fall on a stone and RTA
3) Penetrating injuries
A wound in which the skin is broken and the agent causing the wound
entering subcutaneous tissue or deeply lying structure or cavity.
Eg. Stab injuries, bullet injuries
Internal organs may be involvoved.
P a g e 6 | 548
o Check depth of the wound
Superficial– epidermis
Partial thickness– Dermis
Full thickness – S/C tissue
Deep wound – Deeper [if the fascia is involved]
Introduction
Wound is a break in the skin which may result from physical, mechanical or
chemical damage, or develop as a result of the presence of an underlying medical or
physiological disorder.
Classification
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Tidy Untidy
o Duration of wound healing
Acute Chronic
o Integrity of the skin
Open Closed
o Degree of bacterial contamination
Clean Contaminated
Clean-contaminated Dirty
o Wound depth o Severity
Wound Healing
Phases of Wound healing: normal wound heals by 3 phases
1) The inflammatory phase
2) The proliferative phase
3) The remodeling phase (maturing phase)
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Types of wound healing
o Primary Intention - Skin edges opposed
o Secondary Intention - Wound left open
o Tertiary Intention – Wound closure or cover
Table 1.4: Primary intention vs Secondary intention
Features Primary intention Secondary intention
Cleanliness Clean Not clean
Topical agents
Ionizing radiation
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Abnormal wound healing:
o Deficient scar formation
o Excessive repair components
o Contracture
o Atrophic or Hypertrophic scar
o Pigment changes
Table 1.6: Features of Abnormal Wound Healing
Wound Management
The goals
1. Avoid further tissue damage
2. Achieve wound closure as rapidly as possible
3. Restore function to the injured tissue
4. Facilitate the patient’s expedient return to normal daily activities
5. Restore the patient’s quality of life.
Use of antibiotics
Tetanus prophylaxis
Wound dressings: no ideal wound
dressing exists.
Edema control: compression therapy
Rehabilitation and POD
Rabies post exposure prophylaxis
Improve systemic conditions:
o Fluid and hydro-electrolyte
o Nutrition
o Rx of coexisting diseases
P a g e 11 | 548
Management based on type of wound:
1) Abrasion:
Will heal on its own hence clean and prevent infections
2) Contusion:
Apply cold compressor for 24 hour then hot compressor to stimulate
vasculature and interstitial bleeding can be absorbed
3) Incised:
Clean and primary suturing
4) Lacerated:
Excise and primary suturing
5) Crushed or devitalized:
Wound debridement then allows for edema to subside for 2-3 days
followed by delayed primary suturing
6) Deep vitalized wound:
Allow complete granulation following debridement
If small wound, do secondary suturing
If large, use split skin graft to cover the defect
7) Wound with tension:
Fasciotomy to avoid compartment syndrome
8) Amputation:
Compressive gauze and elevate hand- to stop bleed (don’t ligate artery in
order to avoid nerve damage)
Wash then apply saline soaked gauze then put in ice bag
Re- implantation with microvascular surgery
9) Facial injury:
Worry about facial nerve and parotid duct injury
Wash aggressively then use tiniest suture
Remove the suture as soon as possible: eyelid on 3rd Post-op and the rest
of face on 5th post-op day
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1.2. Skin Tumor
Case Discussion.…………………………………..13
History…………………………..…………………….13
Physical Examination………..………………….14
Investigation…………………..……………………17
Management.………………...……………………17
Discussion of the Case………………………….18
Case Discussion
A 65-year- old male presents with a progressive skin lesion of 8 years duration. It began
on his forehead and proceeded to involve left half of his face including his outer ear.
Associated with that he complains of difficulty hearing on his left ear and loss of sensation
on the left side of his face. He has no bleeding or pain. He works as farmer for a living. On
physical examination, there is a destructive lesion with ulceration around the ear canal
with extension to the mastoid process of temporal bone. There is surrounding hypo and
hyperpigmentation around the lesion.
History
Duration
Progression
Check for symptoms of infection: fever, discharge
Is there associated symptom: hearing loss, loss of sensation, pain, ulceration,
bleeding
Is there any concerns about a particular lesion or if patients have noticed a new
mole or a change in a pre-existing mole?
Asses risk factors:
o Occupation history: to assess for sun and radiation exposure
P a g e 13 | 548
Patient’s tendency to sunburn and history of blistering sunburns
during childhood or teenage years
Degree of sun exposure in the past 5 to 10 years
Occupational exposure
Phenotypically: fair skin, light colored eyes, red hair, northern
European region
o Previous local (herbal) treatment
o Chemical carcinogen: arsenic
o Immunosuppressed patient: organ transplant patients, HIV patients
o Chronic inflammation: scars, burns, ulcers, sinus tracts Burn history:
Marjolijn’s ulcer is a risk factor for SCC
o Race
o Family history
o Smoking
o Blood type: mainly for BCC
In a cohort study, the risk of developing BCC was 4% lower among
patients with A, AB, or B blood types compared to those with type
O blood.
o HPV infection
o Inherited disorders
Xeroderma Epidermolysis bullosa
pigmentosa Albinism
Physical Examination
1. Check for lymphadenopathy on all accessible areas
2. Do total body skin examination (TBSE)
Examine the face and rest of the head and neck while the patient is sitting on
the examination table.
Examine the scalp.
Examine all surfaces of the arms and hands.
P a g e 14 | 548
Ask the patient to lie down on his/her back for viewing the chest, abdomen,
anterior thighs, anterior legs, dorsal feet, soles, and toe webs.
Ask the patient to turn over.
o Examine the calves, posterior thighs, buttocks, and back.
o The upper body could also be examined when the patient is sitting or
standing.
3. Describe the lesion:
Where is it?
What does it look like?
Is there a change in pigmentation? Diversity of colors?
Border regularity?
FOR Basal cell Carcinoma:
1. Nodular: 60% of the BCC
Pink or fresh colored papule with translucent quality
Telangiectasia vessel is seen within the papule
Ulceration is common
2. Morepheaform: 5-10%
Smooth, flesh colored papules or plaques that are frequently atrophic
Firm quality will ill-defined borders
3. superficial: 30%
On trunk
Slightly scaly papule that is light in color
Atrophic in center and rimmed with fine
translucent micro papules
For Squamous Cell Carcinoma:
SCC can develop on any cutaneous surface, including the head, neck, trunk,
extremities, oral mucosa, periungual skin, and anogenital areas
1. SCC in situ (bowen’s disease):
Well-demarcated, scaly patch or plaque
P a g e 15 | 548
Lesions are often erythematous, but can also be skin-colored or
pigmented.
Tends to grow slowly, enlarging over the course of years
2. Erythroplasia of Queyrat
Describe SCC in situ involving the pens
Presents as a well-defined, velvety, red plaque
Patients may experience pain, bleeding, or pruritus
3. Invasive SCC
Are often asymptomatic, but may be painful or pruritic.
Local neurologic symptoms (eg, numbness, stinging, burning, paresthesia,
paralysis, or visual changes) occur in approximately one-third of patients.
Well-differentiated lesions
o Usually appear as indurated or firm, hyperkeratotic papules,
plaques, or nodules.
o Lesions are usually 0.5 to 1.5 cm in diameter, although some are
much larger.
o Ulceration may or may not be present.
Poorly differentiated lesions
o Are usually fleshy, soft, granulomatous papules or nodules that
lack the hyperkeratosis
o May have ulceration, hemorrhage, or areas of necrosis.
For Melanoma:
Asymmetry (if a lesion is bisected, one half is not identical to the other half)
Border irregularities
Color variegation (brown, red, black or blue/gray, and white)
Diameter ≥6 mm
Evolving: a lesion that is changing in size, shape, or color, or a new lesion
The revised Glasgow seven-point checklist- Another set of criteria for referral or
biopsy was developed from a retrospective review of patients with melanoma, and
subsequently revised.
P a g e 16 | 548
o It includes three major and four minor features:
Major: Minor:
- Change in size/ - Diameter ≥7mm
new lesion - Inflammation
- Change in shape - Crusting or bleeding
- Change in color - Sensory change
Differential diagnosis
1. Skin tumour
2. Skin TB
3. Leishmaniosis
Investigation
FNA of skin Head CT
Wedge biopsy with normal skin FNA of lymph nodes
Organ function test: LFT, RFT
Chest x-ray, ultrasound/CT staging, and bone scans may be necessary
Principles of management
1) Surgical excision
2) Destructive therapy – cryosurgery, electrodessication & curettage
3) Topical 5-FU for premalignant lesions
4) Radiotherapy, chemotherapy
5) Block dissection of regional lymph nodes in melanoma is indicated if the nodes
are clearly involved and there are no other secondary
P a g e 17 | 548
Discussion of the Case
Introduction…………………………………………..18
Basal Cell Carcinoma………………………………18
Squamous Cell Carcinoma………………………20
Melanoma……………………………………………..22
Introduction
Table 1.7 TNM Staging of Basal Cell and Squamous Cell Carcinoma
Classification Definition
Primary tumor
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ
T1 Tumor ≤ 2cm in greatest dimension
T2 Tumor > 2cm in greatest dimension but ≤ 5cm in greatest
dimension
T3 Tumor > 5cm in greatest dimension
T4 Tumor invading deep extra dermal structures (e.g. cartilage,
skeletal muscle, or bone)
Regional lymph nodes
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Regional lymph node metastasis
Distant metastasis
MX Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
Histopathologic Grade
GX Grade cannot be assessed
G1 Well differentiated
G2 Moderately differentiated
G3 Poorly differentiated
G4 Undifferentiated
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1.2.3. Melanoma
Introduction:
• Is a cancer of melanocytes?
• Usually arises in skin
• Can arise anywhere that melanocytes exist:
o The bowel
o Mucosa
o The retina
Remember
o The leptomeninges
Tumors on hands, feet and
• Relatively less common
trunk especially the back
• The incidence in the black population is
have a poorer prognosis
much lower being 0.6 per 100,000
than those on the limbs.
• It is more common in young adults 20-39
Tumors that have
• Malignant Melanoma can occur at any site regressed or ulcerated
on the skin surface with a predilection for have a worse prognosis,
the legs of young women and the trunks of possibly because their true
men thickness is masked
• 90% of malignant melanomas arise from
otherwise normal skin
o Only 10% from an existing nevus
Types of melanoma
• Superficial spreading melanoma:
o The most common
• Nodular melanoma
o This is a raised, polypoid lesion
o It has the worst prognosis
• Lentigomaligna melanoma
o This arises in a background of lentigomaligna
• Amelanotic
o It has no dark color
P a g e 22 | 548
• Acral
o Lentiginous melanoma
o This is the least common occurring on hairless skin
o It is the commonest type in black races and south east Asia
Staging of Melanoma
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1.3. Burn
Introduction….………………..……...…….....24
Classification…………………..………..……….24
Pathophysiology…………..……..…...………28
Burn Wound Assessment……….....……..30
Investigation…………………..……...………..32
Admission Criteria…………………..…….....32
Management…………………..……..…….…..32
Other Etiologies of Burn….…..…….………35
Complications……………………...…….……..36
Introduction
Burn injury implies coagulative necrosis to the skin and underlying tissue due to
thermal, electrical, chemical, radiation,cold exposure.
It generally occurs in temperatures greater than 44° C.
Classification
Based on etiology:
Thermal (90%):
o Flame - Overheated rusty air
Majority in Adults, suicidal/Homicidal/Accidental
Most common cause of hospital admission
Have the highest mortality
o Scald – hot liquid
o Contact - Too hot or too cold object
P a g e 24 | 548
Too long contact
Chemical:
o Contact with harmful chemicals.
o It is potentially severe burn.
o Initial therapy:
Carefull removal of the toxic substance
Irrigation of the affected are with water for minimum of 30 minutes,
except in cases of concrete powder or powdered lye
o Certain chemicals can be systematically absorbed and cause metabolic
derangements.
Formic acid hemolysis and hemoglobinuria
Hydrofluoric acid -> hypocalcemia.
o The mainstay treatment is calcium based therapies.
o Topical calcium gluconate on the burn wound and IV calcium gluconate for
systemic symptom
o Alkalis burn more than acids
o Burn tends to be deep until the corrosive agent is completely removed
Electrical
o Special considerations are cardiac arrest and compartment syndrome with
rhabdomyolisis.
o Baseline ECG is recommended
o Can be:
High voltage
Low voltage
Radiation
Based on depth:
First degree burn
o Superficial and involve just the epidermis.
o Sunburn and inconsequential
o Painful, blanch with pressure, No edema, No blister
P a g e 25 | 548
o Heals with in 4-7 days
o For example – sun burn
Second degree burn (Partial thickness burn)
o Involves variable amounts of dermis.
o Exremely painful with weeping and blisters
o It is classified as superficial or deep by depth of the involved skin.
i. Superficial partial:
Goes no deeper than the papillary dermis.
Clinical features:
o Blistering
o Blanches with pressure
o Pinprick sensation is normal
o It appears as pink and moist
Superficial partial-thickness burns heal without residual scarring in 2
weeks.
The treatment is non-surgical.
ii. Deep partial thickness:
Involve damage to the deeper parts of the reticular dermis.
Clinically features:
o The epidermis is usually lost
o Abundant fixed capillary staining
o Non blanching
o Reduced sensation.
Deep dermal burns take 3 or more weeks to heal without surgery
Usually lead to hypertrophic scarring.
Third degree burn (Full Thickness Burn):
o Clinical features:
Leathery –Dry Non blanching
Discolored No blisters
No pain
Fourth degree burn:
P a g e 26 | 548
o Involving structures beneath the skin such as underlying fat, muscle, bones or
internal organs
Classification based on depth is dependent upon: Along with burn size and
o The burn sources patient age, burn depth is a
o The thickness of the skin primary determinant of
o The duration of contact and mortality.
o The heat dissipating capability of the skin Itis also a primary determinant
of healing, patient’s long term
Based on severity – which is related to: appearance and functional
The size (TBSA) outcome.
The depth
The age of the patient
Minor burn
o Partial thickness: <15% body surface area in adults and <10% of TBSA in
children
o <2% of TBSA full thickness burn
o Nothing involving the head, feet, hands or perineum.
o Can be treated as an outpatient
Moderate burn
o Partial thickness burn area of 15-25% body surface area in adults and 10-20%
of TBSA in children.
o 2-10% TBSA full thickness burn
o Superficial partial-thickness burns of the head, hands, feet or perineum.
o Suspect:
Child abuse.
Concomitant trauma
Significant pre-existing diseases
o Require hospitalization
Major burn
o Partial thickness burn surface involvement of 25% body surface area in adults
and >20% TBSA in children and elderly
P a g e 27 | 548
o Full-thickness burns 10% body surface area
o Deep burns of the head, hands, feet, joint, and perineum
o Inhalation injury
o Chemical or high-voltage electrical burn
o Comorbidities and associated injuries
o Require specialized care
Pathophysiology
Although most affected organ in burn injury is the skin, Burn injury has both local
and systemic effects
Local effect- The local changes that occur consist in the formation of three zones:
o Zone of coagulation:
Area that is in intimate contact with the causative agent.
Most severely injured area.
Typically in the center of the wound.
Coagulated and with frank necrosis occurs with irreversible tissue
damage
Need excision and graft
o Zone of stasis:
Moderate injury, peripheral to zone of coagulation
Decreased perfusion due to inflammation and impaired vasculature
Has a potential to recover or progress to coagulative necrosis
depending on the administration of optimum treatment
o Zone of hyperemia
Viable tissue, not at risk for further necrosis
o Burn wound edema
o Inflammation
o Increased capillary permeability
Systemic effects:
P a g e 28 | 548
o Significant burns cause release of inflammatory mediators which cause:
Vasoconstriction and vasodilatation
Capillary permeability and edema
o Fluid shift
Vasoactive mediators Vasoconstriction-dilatation capillary
permeability Protein loss tissue edema.
o Hypovolemia/burn shock /results from:
Fluid shift
Insensible fluid loss
Increase in BMR
May progress to hypovolumic shock
Cardiovascular effects
o Hypovolemia Decreased CO
Burn shock pathophysiology
o Increased capillary permeability
o Decreased plasma oncotic pressure
o Increased capillary hydrostatic pressure
o Reduced clearance of fluid and protein from interstitial space by lymphatic
ducts
o Intracellular fluid accumulation
o Increased evaporative water loss
o Depressed myocardial function and increased peripheral resistance.
Renal effects
o Hypovolemia
o Hemoconcentration
o Decreased renal blood flow
o Decreased GFR ->Tubular necrosis ->renal failure
Immune system effects
o Global depression of immune system in burns of >20 % TBSA
o Skin, cellular and humeral immunity
o Mainly cellular immunity is significantly reduced
P a g e 29 | 548
Predispose to infection (pseudomonas, fungal infection)
Prolonged allograft skin survival
Electrolyte disturbance
o Caused by changes in cellular permeability and fluid loss
Hyponatremia due to fluid loss
Hyperkalemia due to excessive tissue necrosis; serious
Cardiologic and neurologic consequences
GI effects
o Hypovolemia Hypoperfusion
Bacterial translocation -> as a cause to sepsis
Curling ulcer
Paralytic ileus
Hypermetabolism
o Tachycardia
o Increased CO due to energy expenditure:
o Proteolysis, lipolysis, nitrogen loss
o Weight loss and decreased strength until all the wounds are grafted
Variables with higher predictive value of mortality are
o Age
o %TBSA
o Inhalational injury
o coexistent injury
o Pneumonia
P a g e 30 | 548
o In adults, the anterior and posterior trunk each account for 18%, each lower
extremity is 18%, each upper extremity is 9%, and the head is 9
o tends to over/ underestimate burn area
Rule of seven – is in pediatrics
Palm rule:
o The palm including the fingers is estimated to be 1% of TBSA.
o It is used in estimating burnt area in relatively small burn(<15%), patchy burn
wounds and unburnt area in very large burns(>85%).
Lund and Browder chart:
o Is the most accurate method.
o Takes into account different proportional body surface area in children
according to age.
Burn wound depth
The history is important; temprature, time and burning material.
Three important elements in assessing burn depth are:
o Apperance
o Sensation
o Bleeding
Its difficult to assess depth of a burn initially because it’s a dynamic wound and
hence it’s depth will change depending on the success of resuscitation.
Obtain a medical history in detail:
o About the burning agent,
o Where the injury happened (closed versus open space)
o The possibility of smoke inhalation, exposure to noxious chemicals, and the
possibility of any related trauma
o History of chronic illnesses such as DM, HTN, and cardiac or renal disease
o Use of regular medications, alcohol, or drugs
o Allergies and history of tetanus immunizations
P a g e 31 | 548
Investigation
Admission criteria
P a g e 34 | 548
Other Etiologies of Burn Injury
Inhalational Injury
Electrical Burn
Extensive deep muscle damage
Fasciotomy instead of escharotomy
Myoglobinuria because of rhabdomyolysis
o Leading to ATN and ARF
Fluid requirement increased titrated to UO of 2mL/kg/hr
Sodium bicarbonate to alkalinize urine
Forced diuresis with manitol
P a g e 35 | 548
Cataracts, progressive demyelinating neurologic loss
Chemical Burn
Alkali Burns
o Liquefactive necrosis hence deeper injury
o Oven bleaches, fertilizers, cement
o Lavage area with copious amount of water
Acid Burns
o Coagulative necrosis
o Irrigate with water and sodium bicarbonate
Burn Complications
P a g e 36 | 548
Short Case Discussion
Content By:
Eyerusalem Nega 1.4 Hand Examination …...……………..…..…….…...38
Nanati Jemal
Edited By:
1.5 Cleft Lip and Palate ……………….…..….....…....43
Samuel Mesfin 1.6 Soft Tissue Tumor Examination………..…......48
Reviewed By: 1.7 Video QR Codes ……………………….…..…..……..55
Dr Abiy Hailu
(Plastic and Reconstructive
Surgeon)
P a g e 37 | 548
1.4. Hand Examination
Introduction……………………………..…….…….38
Prior steps in hand examination…….….…..38
Examination of the Hand……………..….…….39
Introduction
The hand is easily injured and the injuries can sometimes be easily missed which can
unfortunately lead to a permanent disability.
This is one of the reasons we need to know how to properly examine a hand so as
not to miss injuries.
P a g e 38 | 548
o Ask about: diabetes, cardiac, pulmonary, or renal disease
o Prior surgical history
Pulse oximetry: you can see the waves to see for blood flow
4) Range of motion
P a g e 40 | 548
Pulse
Color
Capillary refill (2 sec)
Temperature
1. Median nerve
Ok sign: flexion of thumb IP joint and index DIP (“A-OK
sign”) – FDP – FDS – FPL
o Flexor policus tendon: hold MP joint of the
thumb and ask the patient to flex
interphalangeal joint. In partial laceration, ask its
painful with resisted flexion.
o Flexor digitorum profundus: Isolate the proximal
and middle phalanges by holding them firmly
and then asking the patient to flex the distal
phalanx of that finger.
o Flexor digitorum superficialis: isolate the 3
fingers that are not being tested (simply hold
them in the natural anatomical position) and ask
the patient to flex the finger being tested (FDS)
Test opposition by touching the tip of the thumb to the tip of the little finger
Test thumb abduction by placing the hand palm up and raising the thumb to the
perpendicular while palpating the belly of the abductor pollicis muscle to insure it
is contraction.
Wrist flexor: Flex and palate tendons of flexor carpi radialis and ulnaris.
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2. Radial nerve
Extensor tendons are commonly injured
Extend the wrist against resistance (extensors)
Raise the thumb off of the pillow (Extensor policies longus)
Hold the wrist passively in extension and ask the patient to
extend their fingers (Extensor digitorum communis)
Flex 3 and 4 digit and ask the patient to extend the remaining finger- extensor
rd th
3. Ulnar nerve
Confirm finger abduction & adduction (tests palmar
and dorsal interossei)
Test the hypothenar muscle, extend the fingers and
then move the fifth finger away from the others
Froment's test; Technique:
o The patient is asked to make a strong pinch
between the thumb and index finger and grip a flat
object such as a piece of paper between the thumb
and index finger.
o The examiner then attempts to pull the object out
of the subject's hands.
o There is weakness of the adductor pollicus
innervated by the ulnar nerve which would keep
the Interphalangeal joint relatively straight;
instead, the Flexor policies longus muscle which is
innervated by the median nerve is substituted for
the abductor policies and will cause the
Interphalangeal joint to go into a hyper flexed
position.
Flex the fingers to 90oat the MCP joints and ask the patient
to extend their fingers again (lumbricals)
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Adduct fingers- interrosi muscle
1) Skeleton assessment
Swelling Tenderness
Deformity
Abnormal range of movement (decreased or increased)
2) Stability Testing
Ulnar collateral ligaments Radial collateral ligaments
Introduction
The most common craniofacial malformation identified in the new-born is the
orofacial cleft, which consists of cleft lip with or without cleft palate (CL/P) or
isolated cleft palate (CP).
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They can occur as part of a syndrome involving multiple other organs or as an
isolated malformation.
Prevalence
It varies by race/ethnicity: lowest in American blacks, highest in Native Americans
and Asians, and at an intermediate level in Caucasians.
The sex ratio among affected infants varies by type of defect:
o CL/P occurs more often in males while CP is more common in females.
Embryology
Cleft Lip
Complete closure of the lip is usually accomplished by 35 days post conception as the
lateral nasal, median nasal, and maxillary mesodermal processes merge.
Failure of closure of any one of the three normal sites of fusion can produce
unilateral, bilateral, or (rarely) median lip clefting.
o Unilateral CL on the left side is the most common presentation.
It can be mild, involving only the upper lip, or can extend into the palate or the
midface, thereby affecting the nose, forehead, eyes, and brain.
Cleft Palate
Isolated CP occurs when there is primary lack of fusion of the palatal shelves.
Isolated disruption of palate shelves can occur after closure of the lip because palatal
closure is not completed until 56 to 58 days post conception.
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Risk Factors
Genes
o Proliferation defects: eg, sonic hedgehog gene
o Extracellular matrix defects: eg, TGF-alpha variant
o Differentiation defects: eg, TGF-beta gene
o Interferon regulatory factors: eg, IRF-6
Maternal Medication
o Antiseizure agents o Methotrexate
Maternal Cigarette smoking Folate deficiency
Maternal alcohol consumption
Maternal obesity: small, but statistically significant risk
Associated Abnormalities
Fetuses found to have orofacial clefts should undergo careful assessment for
additional structural abnormalities as these defects are noted in:
o As many as 50 percent of newborns with isolated CP
o 20 percent of those with CL and CP
o 8 percent for those with isolated CL
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The anomalies typically involve the central nervous system/skeletal system (33
percent) and cardiovascular system (24 percent), all sites of tissues with neural
ectodermal origin.
Clinical Presentation
Cleft lip: no functional disability
Cleft palate
o Can’t suck o Speech impaired
o Middle ear infection: due to abnormally inserted Eustachian tube
o Middle face abnormalities
Prenatal Diagnosis
CL/P cannot be diagnosed reliably until the soft tissues of the fetal face can be
clearly visualized sonographically, which is at 13 to 14 weeks by transabdominal
ultrasound, but somewhat earlier by transvaginal ultrasound.
Three-dimensional ultrasound and magnetic resonance imaging can provide a clear
image of the malformation and may enhance detection of isolated cleft palate.
Management
Obstetrical Management:
Amniocentesis for karyotype should be offered to women with ultrasound findings
of fetal orofacial clefts and associated anomalies (due to high rate of chromosomal
defects)
Referral to a comprehensive management team
The neonatology service that will attend the delivery should be notified in advance
o Can counsel the parents about newborn management issues
o Plan surgical repair
Postnatal Management:
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During feeding
o Use large hole bottle for feeding
o Feed in erect position to avoid aerophagia
o Burp to remove ingested air
o Frequent small feedings
Surgery
o Cleft lip: at 10 weeks, 10 pounds, hemoglobin of 10 and <10,000 WBC
o Cleft palate: at 10 months, 10kgs, hemoglobin of 10 and <10,000 WBC
Dentist, ENT and speech therapist: for cleft palate patient.
Recurrence Risk
The presence of CL/P or CP in a parent, a prior child born to the couple, or in the family
history requires further investigation if appropriate risk assessment is to be provided.
Such assessment entails three important considerations
Delineation of CL/P from isolated CP
o Risk of recurrent isolated CP is higher than the risk of recurrent CL/P
Determination of a possible microform in the family
Presence of a possible syndrome
Table 1.10: Relative risk of cleft lip and Palate in a Family Pedigree
Relative Cleft lip (%) Cleft lip/Palate (%) Cleft palate (%)
Sibling 3.5 3.9 3.3
Half sibling 1.0 0.5 1.0
Parent 2.5 2.5 2.1
Offspring 3.5 4.1 4.2
Niece/nephew 0.9 0.8 1.1
Aunt /uncle 0.6 1.1 0.6
First cousin 0.3 0.5 0.4
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1. 6. Soft Tissue Tumor Examination
Introduction……………………...…...…...…48
Epidemiology…………………………...…....48
Clinical Manifestation…..…………...…..49
Differential Diagnosis……..…...…...…..52
Investigation………………………..…...……53
Introduction
Soft tissue is defined as the supportive tissue of various organs and the
nonepithelial, extra skeletal structures exclusive of lymph hematopoietic tissues.
It includes fibrous connective tissue, adipose tissue, skeletal muscle, blood/lymph
vessels, and the peripheral nervous system
Epidemiology
Benign soft-tissue tumors occur at least 10 times more frequently than malignant
ones.
Overall, the age-adjusted annual incidence of soft-tissue sarcomas ranges from 15 to
35 per 1 million populations.
The incidence increases steadily with age and is slightly higher in men than in women
Distribution:
o Approximately 45% of sarcomas occur in the lower extremities
o 15% in the upper extremities
o 10% in the head-and-neck region
o 15% in the retroperitoneum
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o The remaining 15% in the abdominal and chest wall
Clinical Manifestation
History:
Asses for risk factors
o Genetics/ family history
The NF1 gene in neurofibromatosis
o Possible generalized conditions
Neurofibromatosis is the best example of a generalized disease that
may be associated with one or more soft tissue masses
o Radiation
o Chronic lymphedema:
Predisposes to lymphangiosarcoma
o Carcinogens
Hepatic angiosarcoma has been linked to arsenic, thorium dioxide, and
vinyl chloride exposure.
o Trauma: probably draws medical attention to a preexisting lesion
o The patient's age
Infants and children may present with benign lesions that can
demonstrate local growth, disfigurement, overgrowth of the extremity
or loss of function (lipomas, hemangiomas, lymphangiomas,
neurofibromas, hamartomas, congenital or infantile fibromatosis).
Soft tissue sarcoma is extremely rare in children, but when it occurs, it
is most likely to be rhabdomyosarcoma.
In adults, rhabdomyosarcoma is rare in the extremities.
o Infections
Kaposi sarcoma resulting from human herpesvirus type 8 in patients
with human immunodeficiency virus (HIV).
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Epstein-Barr virus in an immunocompromised host also increases the
likelihood of soft-tissue tumor development.
A mass is the most common sign of a soft-tissue tumor.
o Ask for pain
Usually is painless and does not cause limb dysfunction.
It may cause pain or neurologic symptoms by compressing or
stretching nerves, by irritating overlying bursae, or by expanding
sensitive structures.
o Ask for progression rate
A rapid rate of increase in the size of a mass should arouse suspicion
that the lesion is malignant.
A mass that has been present for years and that begins to grow may be
transforming from a benign to a malignant lesion, or it may simply be
growth of a benign soft tissue tumor.
Physical Examination:
Aims:
To determine the location and size of a mass and to exclude other, more common
causes of pain.
To know whether the mass is deep or subcutaneous, transilluminates (cysts), and
adheres to underlying structures
Regional lymph nodes should be examined as well.
Neurovascular examination is useful for the detection of either primary or secondary
tumor involvement.
How to examine:
1) Lymphoglandular exam
Palpate the regional nodes, although soft tissue sarcomas rarely metastasize by
lymphangitic spread.
Rhabdomyosarcoma and synovial sarcoma are the most likely diagnoses if nodal
metastases are found
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N.B:
2) Integumentary system
Extremity masses larger than 5-7 Examine the skin should for evidence of:
cm and deeper than subcutaneous o Cafe au lait spots: fibrous dysplasia
tissue favors a diagnosis of a o Dermatofibromas
malignant soft-tissue tumor. o Axillary freckling, which may suggest
However, as many as 30% of soft- neurofibromatosis
tissue sarcomas occur in
subcutaneous tissue and exhibit 3) Musculoskeletal exam
relatively less aggressive behavior. Inspection
o Site
o Overlying skin change
N.B: Dermatofibrosarcoma Pro-
o Ulceration and disfigurement
tuberans
Palpation
This lesion is elevated above the o Depth of the mass: is the lesion superficial or
dermis, purplish in color, and it deep to fascia?
characteristically develops satellite o Most lesions developing superficial to fascia are
nodules as it grows. benign. Attempt to move the lesion over the
It behaves like a low-grade soft fascia, both before and after the patient tenses
tissue sarcoma and is generally the underlying muscle. If the lesion moves with
managed in a similar manner. the muscle, it is likely deep to fascia. If the
physical examination indicates that the lesion
arises in fascia, deep to fascia, or is uncertain,
N.B:
obtain imaging of the mass.
and trunk for soft tissue masses; o condition of the overlying tissues
Differential Diagnosis
Investigation
Imaging:
Useful for defining anatomic location, tumor extent, and involvement of vital
structures.
Useful to evaluate the relation of the tumor and surrounding normal structures to
the planned biopsy site and the functional status of the involved limb,
Check for signs of lymph node involvement
Plain radiography, CT, MRI, and bone scintigraphy is used to stage the disease.
PET is being used more frequently to assess the metabolic activity and, presumably,
the biologic aggressiveness of a lesion.
Angiography to evaluate any vascular involvement by soft tissue tumors has
essentially been replaced by MRI.
CT is useful in checking for the presence and number of pulmonary metastases
MRI best defines the relation between a tumor and adjacent anatomic structures,
such as compartment boundaries, nerves, vessels, and muscle.
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Biopsy:
Is indicated for
o Soft-tissue mass arising in a patient without a history of trauma
o For a mass that persists for more than 6 weeks after local trauma.
o All soft-tissue masses larger than 5 cm, as well as any enlarging or
symptomatic lesion.
Small, subcutaneous lesions that persist unchanged for years may be considered
for observation rather than biopsy.
o A high level of suspicion is necessary to ensure early treatment.
Several biopsy techniques are available and the choice of biopsy technique is based
on the size and location of the mass and the experience of the surgeon.
o The techniques including the following:
Fine-needle aspiration biopsy (FNAB)
Core needle biopsy
Incisional biopsy
Excisional biopsy
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1.7. Video QR Codes
Wound Examination
Burn Assessment
Skin Tumors
Hand Examination
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Part 2: Endocrine Surgery
Content By:
Fitsum Solomon
Nanati Jemal
Edited By: 2.1. Approach to Breast Pathologies…………………………57
Samuel Mesfin
Reviewed By: 2.2. Approach to Thyroid Disorders………………………….71
Dr. Endale Anberber
(General and Endocrine
Surgeon)
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2.1. Approach to Breast Pathologies
Case Discussion…………………………….…………………….57
History…………………………………………………….………….57
Physical Examination………………………………….……….59
Investigation…………………………………………….…………62
Differential Diagnosis……………………….………….……..62
Discussion of the Differential Diagnosis………….……63
Case Discussion
45 years old multiparous female patient came to regular OPD with right breast lump of 5-
month duration. The swelling increased in size gradually in the following months. It was
associated with intermittent aching pain of the lump. It showed gradual increment and was
associated with aching pain with no discharge. She also complains of easy fatigability,
anorexia, weight loss, global headache, tinnitus, vertigo and abdominal pain. On
examination there is an Upper outer quadrant mass, firm, tender, 6cm by 5cm in size, oval
shaped, irregular surface, well circumscribed, warm, mobile, not pulsatile and doesn’t
fluctuate. The nipples have no discharge or thickening and are elastic.
History
1) Describe the lump
Size: it can be expressed as a size of bean or lemon
Location (Right/Left)
How the patient felt the lump: it’s important to ask the activity the patient had
had before she felt the lump as most patients feel while they were taking shower
Duration
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Pain: if the lump is associated with pain its most likely periductal mastitis if not
malignant causes can be taken into consideration (advanced cancer with
ulceration or chest wall infiltration may cause pain)
2) Ask the risk factors
Age: 65+ vs. <65 years, although risk increases across all ages until age 80
Personal history of breast cancer is important for all age groups
Past history of benign breast disease should also be asked as some benign lesions
(proliferative lesions) increase risk of breast cancer.
Smoking history: because its predisposing factor for periductal mastitis
Family history: Two or more first-degree relatives with breast cancer diagnosed at
an early age
History of trauma to the breast: trauma can result in fat necrosis
History of radiation to the breast
Alcohol consumption
Early menarche (< 12 years)
Personal history of endometrium, ovary, or colon cancer
History of oral contraceptive usage
Recent and long-term use of menopausal hormone therapy containing estrogen
and progestin
Age at first full term pregnancy; parity affects risk of breast cancer
History of TB: TB mastitis
Diet history: vitamin A deficiency results in sloughing of the myoepithelial cells of
the duct. And also, evidence suggests that long-term consumption of foods with a
high fat content contributes to an increased risk of breast cancer by increasing
serum estrogen levels.
Breast feeding history: it’s important in preventing breast ca.
Socioeconomic status of the patient; there are a number of factors involved in
socioeconomic status
o Girls with good nutrition will have their menses at earlier age.
o In high socioeconomic status, girls delay age of first delivery
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o Delay of first delivery may need use of hormonal contraceptives
o With high socioeconomic status, there is a tendency for low parity.
o With high socioeconomic status, there is a tendency for not feeding breast
3) Associated symptoms
Discharge: Unilateral or bilateral? Does the discharge appear only after
compression of the nipple, or is it spontaneous?
Color of the discharge:
o Milky? (lactational, Non-lactational, hyperprolactinemia)
o Bloody? (Ductal papilloma, ductal carcinoma and duct ectasia)
o Watery? (duct ectasia and fibrocystic disease)
o Greenish? (duct ectasia) o Yellowish? (breast abscess)
Skin changes: local irritation of the nipple could be because of pagets disease,
breast cancer and eczema.
Cough, chest pain, fever, chills or night sweats (suspect TB Mastitis)
Yellowish discoloration of the eyes
Abdominal swelling: metastasizing breast cancer can cause ascites
Bone pain: some patients may come with joint or bone pain which reflects
metastasizing breast cancer
Weight loss Shoulder or back pain
Easy fatigability
Physical Examination
General appearance: acute or chronic sick looking
Vital signs
HEENT
o Eye: look for jaundice or anemia
Lympho-glandular system:
o Inspect all the peripherally accessible lymph nodes for the presence of
enlargement and associated pain; special attention should be given to
axillary and supra/infraclavicular lymph nodes
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o Breast examination
Inspection:
o Adequate inspection initially requires full exposure of the chest, but later
in the examination, cover one breast while you are palpating the other.
Inspect the breasts and nipples with the patient in the sitting position and
disrobed to the waist.
o In order to adequately inspect the breast, use four principal views which
are explained below
Arms at the sides:
o Skin color and thickening
o Size and symmetry of the breasts: Some differences in the size of the
breasts and areolae are common and usually normal.
o Breast contour
o Nipple and areola characteristics: inverted nipple can be suggestive of
breast cancer
Arms over the heads, hands pressing against hips and leaning
forward:
o Ask the patient to raise her arms over her head and press against the hips
which is crucial in inspecting the fixity of the mass.
o Also ask the patient to lean forward against a wall which helps in
inspecting the mobility of the mass.
Palpation:
o Palpation is best performed when the breast tissue is flattened.
o The patient should be supine.
o Palpate the rectangular area extending from the clavicle to the
inframammary fold and from the midsternal line to the posterior axillary
line and well into the axilla to ensure that you examine the tail of the
breast.
o A thorough examination takes at least 3 minutes for each breast.
Use the pads of the 2nd, 3rd, and 4th fingers, keeping the fingers
slightly flexed. It is important to be systematic.
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The vertical strip pattern is currently the best validated technique
for detecting breast masses.
Palpate in small, concentric circles applying light, medium, and
deep pressure at each examining point.
Press more firmly to reach the deeper tissues of a large breast.
Examine the entire breast, including the periphery, tail, and axilla.
Carefully examine the breast tissues for:
o Tenderness o Consistency
o Characterize the nodule in terms of:
Location: mention by quadrant or clock with the distance in
centimeters
Size: in centimeters
Shape: irregular or round shape with discreteness or matted
Boarders: well delineated or poorly circumscribed
Consistency: soft, hard or firm
Mobility: confirm the above inspected mobility.
Examine both the left and the right axilla:
o For the left axilla, ask the patient to relax with the left arm down and
warn the patient that the examination may be uncomfortable.
o Support the patient’s left wrist or hand with your left hand.
o Cup together the fingers of your right hand and reach as high as you can
toward the apex of the axilla Place your fingers directly behind the
pectoral muscles, pointing toward the midclavicular.
o Now press your fingers in toward the chest wall and slide them
downward, trying to palpate the central nodes against the chest wall.
o Of the axillary nodes, the central nodes are most likely to be palpable.
o One or more soft, small (<1 cm), nontender nodes are frequently felt.
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Investigation
Not all patients need both mammography and ultrasound of the breast.
o When age is above 35 years (lax breast), mammography is routine to
look for multifocal / multicentric mass and to screen the contralateral
breast.
o Ultrasound is the choice for a dense breast (age < 35 years).
Core biopsy is the standard for pathological diagnosis of breast mass or
abnormalities detected on imaging. In the absence of core biopsy, FNA is an
alternative with high specificity.
o Generally, core biopsy is superior to FNA.
MRI is very rarely indicated in special circumstances
Indications for bone scan should be mentioned as it is not a routine investigation.
In the absence of metastatic symptoms, our current metastatic work up is chest
x-ray and abdominal ultrasound.
o This can be replaced by chest and abdominal CT scan.
When patients present with early breast cancer, negative lymph node status,
favorable histology, avoidance of metastatic work up is a possibility.
Differential Diagnosis
Generally the list of differential diagnosis depends on age, history and physical findings,
Periductal mastitis
Subareolar abscess
Tuberculous mastitis
Fat necrosis
Fibrocystic disease
Fibroadenoma
Phyllodes tumor
Ductal papilloma
Breast cancer
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Discussion of the Differential Diagnosis
2.2.1. Periductal Mastitis/ Duct Ectasia
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2.1.2. Subareolar Abscess
2.1.6. Fibroadenoma
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2.1.9. Breast Cancer
It accounts for 29% of all newly diagnosed cancers in females and is responsible for
14% of the cancer-related deaths in women.
Etiology and Risk factors
o Age: it is very rare before 20 years but its incidence increases as age
increases. It is common in 35 to 75 years of age.
o Sex: women are 100 times to present with breast cancer than men.
o Ethnicity: more common in whites.
o Gene mutations: mutations in BRCA1 and BRCA2 and p53 mutations (li
Fraumeni syndrome) increase the chance of breast cancer.
o Family history: 3 to 4 times likely to develop in women who have first degree
relative with breast cancer.
o Diet: diet containing fatty foods increases the chance of breast cancer due
excess fat being converted to estrogen.
o Radiation exposure: patients who were previously treated with radiation
therapy for Hopkins disease are more likely to have their breast exposed to
the radiation.
Clinical features:
o Lump: it’s the most common symptom in which 60% involve the upper outer
quadrant.
o Changes in skin appearance: on examination, there will be typical peau de
orange appearance.
o Bleeding per nipple and nipple reaction.
o Lung and abdominal metastasis: history should include pulmonary and
abdominal symptoms.
o Bone pains and behavioral changes
Types
A. Carcinoma in situ (CIS)
o It consists of proliferating cells the absence of invasion of cells into the
surrounding stroma and their confinement within natural ductal and alveolar
boundaries.
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o LCIS originates from the terminal duct lobular units and develops only in the
female breast by which the average age at diagnosis is 45 years.
o It is characterized by distention and distortion of the terminal duct lobular
units by cells which are large but maintain a normal nuclear: cytoplasmic
ratio.
o DCIS is characterized by a proliferation of the epithelium that lines the minor
ducts, resulting in papillary growths within the duct lumina.
o Paget’s disease is associated with DCIS which presents with chronic,
eczematous eruption of the nipple which may ulcerate.
B. Medullary carcinoma
o Seen in around 15% of cases. It tends to occur in the reproductive age
group.
o Clinically the patient feels softer lump than hard lump. In addition to
undifferentiated cells,
o Occasionally well differentiated gland formation is present. Hence, the
name, medullary adenocarcinoma.
o Presence of lymphatic infiltration is thought to represent a good host
response, thus indicating a good prognosis.
C. Inflammatory carcinoma
o Constitutes less than 1% of breast cancer
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o More commonly seen in the reproductive age group and in pregnancy and
lactation.
o Clinical features include breast pain and redness which mimics mastitis.
o Usually it is ER positive.
o It has the worst prognosis.
D. Colloid carcinoma
o It is diagnosed because of production of mucin, intracellularly and
extracellularly.
o Prognosis of this variety of carcinoma breast is better than other infiltrating
duct carcinomas.
Mode of Spread
o It involves local spread, hematogenous spread and lymphatic spread
o Local spread is due to the growth of the tumor invading and obliterating
the adjacent structures such as the skin causing ulceration and retraction.
o Lymphatic spread involves the central, pectoral, supraclavicular and
subscapular nodes.
o Hematogenous it spreads to the flat bones and the brain.
Staging:
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Table 2.1: Breast carcinoma TNM anatomic stage group AJCC UICC 2017
T N M Stage Group
Tis N0 M0 0
T1 N0 M0 IA
T0 N1mi M0 IB
T1 N1mi M0 IB
T0 N1 M0 IIA
T1 N1 M0 IIA
T2 N0 M0 IIA
T2 N1 M0 IIB
T3 N0 M0 IIB
T0 N2 M0 IIIA
T1 N2 M0 IIIA
T2 N2 M0 IIIA
T3 N1 M0 IIIA
T3 N2 M0 IIIA
T4 N0 M0 IIIB
T4 N1 M0 IIIB
T4 N2 M0 IIIB
Any T N3 M0 IIIC
Any T Any N M1 IV
Treatment
o Treatment includes surgery depending on the cancer type and
chemotherapy.
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2.2. Approach to Thyroid Disorders
Case Discussion…………………………….………….………71
Clinical Manifestation………………………………….…..71
Investigation…………………………………………………….75
Differential Diagnosis………………………………….……76
Discussion of the Differential Diagnosis……….……76
Case Discussion
A 40-year-old patient, who was relatively well until 20 year ago, at which time she started
to develop swelling on the anterior neck. The swelling is small initially & not painful, and it
progressively increased in its size, to attain the current size. There is a relatively rapid
growth for four year. The patient also feels easy fatigability and shortness of breath, on
moderate activity like long distance walking for the last 4 years. She has history of
intolerance to cold. On examination she is Conscious and cooperative, over clothing, all
vital signs are stable, a firm 8x6cm anterior neck swelling, prominent on left, nodular and
non-tender, moves with swallowing and it is more prominent on the right side.
Clinical Manifestation
History
1. Describe the swelling
Onset: acute durations are more likely stem from inflammatory causes
whereas chronic duration results from endemic goiter or malignant conditions.
Pain: whether it is painful (thyroiditis) or painless (malignant)
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Duration: Long duration of thyroid swelling indicates benign condition, e.g.
multinodular goiter (MNG), colloid goiter. Short duration with rapid growth
indicates malignancy such as anaplastic carcinoma. Majority of thyroid
swellings do not produce pain.
Progression: rapid or slow progression
2. Associated symptoms
Fever Difficulty of swallowing
Shortness of breath Weight loss
Easy fatigability (better to include the types of activities the patient used to but
fails to perform)
Hoarseness of voice Loss of appetite
Sweating
3. Ask symptoms steaming from hyperthyroidism
Increased appetite Restlessness
Significant weight loss Palpitation
Diarrhea Shortness of breath
Irritability Lack of sleep
Anxiety Heat intolerance
4. Assess the symptoms of hypothyroidism
Weight gain despite Lack of motivation
decreased appetite Drowsiness
Constipation Lack of motor coordination
Body swelling Cold intolerance
5. Dig out the risk factors
Diet habit: this helps to assess the types of foods the patient regularly eats
that are prone to cause the swelling (for example Cabbage is a risk factor for
endemic goiter) the iodine content of the salt used in foods is also important
to ask about
Area where the patient came from: helps to figure out if there are other
people living in the same area having the illness and symptoms.
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Family history
History of neck radiation therapy: it’s one of the risk factors for malignancy.
History of drug intake
6. Rule out/ rule in the possible differential diagnoses
Slow growing lesion with shortness of breath and difficulty of swallowing=>
Endemic goiter.
Anterior neck swelling with increasing size, symptoms of hyperthyroidism with
predominating cardiovascular symptoms (palpitations) and skin manifestations
such as swelling of feet with positive family history=> Diffuse toxic Goiter
(graves’ disease)
A swelling with associated sleep disturbance and change in behavior Toxic
adenoma.
Anterior neck swelling with gradual size increment manifesting in old ages with
thyrotoxic symptoms Toxic multi nodular goiter.
Rapidly progressing anterior neck swelling with associated pain, fever and
hyperthyroid symptoms Inflammatory goiter (reidels thyroidits)
Slowly growing swelling with hoarseness of voice, positive history of neck
radiation therapy with old age and positive family history=> thyroid ca.
(medullary)
7. Ask if any treatment have been given
Physical Examination
General appearance: it is useful to assess the general appearance of the patient
as it depicts hyperthyroid symptoms such as restlessness, hypothyroid symptoms
such as drowsiness.
Vital signs
o Pulse rate: increased pulse rate is indicative of hyperthyroidism steming
from various causes such as Graves’ disease, toxic multinodular goiter etc.
Rhythm is also important.
o Blood pressure: raised blood pressure results from thyrotoxicosis. Wide
pulse pressure is also a feature of thyrotoxicosis.
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o Respiratory rate: tachypnea occurs in thyrotoxicosis, graves diseases
o Temperature: increased temperature occurs from hyperthyroidism and
inflammatory thyroiditis whereas decreased temperature results from
hypothyroidism
HEENT
o Eye: look for exophthalmos; also look for anemia and jaundice
Lymphoglandular: examination of the cervical and supraclavicular lymph nodes
for enlargement
Examination of the mass
Inspection
o Location
o Size and shape: mention the size in cm like 3*5cm
o Surface:
Smooth Adenoma, puberty goiter, Graves' disease
Nodular Multinodular thyroid
o Boarders
o Smooth adenoma, puberty goiter, Graves' disease
o Irregular carcinoma of the thyroid
o Nodular multinodular thyroid
o Swelling moving with deglutition:
This is because thyroid gland is enclosed to the pretracheal facia
which moves with swallowing.
It’s also because of the ligaments of berry with are attached
superiorly to the cricoid cartilage by which during swallowing the
thyroid gland moves together with cricoid cartilage.
o Movement of the swelling on protrusion of the tongue which most likely
indicates thyroglossal cyst.
Palpation
o Confirm the above inspected areas of the swelling such as size shape and
borders
o Consistency
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o Fixation: confirm the fixity or mobility of the thyroid gland by holding the
thyroid gland.
o Tracheal position
o Palpation of the lymph nodes
o Palpation of the carotid arteries
o Special testes
o Kocher test
o Berry sign
o Darymple sign
Percussion:
o Percussion over the sternum gives a resonant note in normal cases.
o In retrosternal goitres, it gives a dull note.
Auscultation:
o It should be done in the upper pole because of following reasons: Superior
thyroid artery is a direct branch of external carotid artery. It is more
superficial than inferior thyroid artery. Presence of thrill and bruit are the
features of toxic goiter.
o Features of hypervascularization (Grave's disease, malignancy)
Cardiovascular examination: examine the presence of palpitation
Integumentary: examine the skin for the presence swelling and associated skin
changes (myxedema in graves’ disease)
Neurologic examination: examine the deep tendon reflexes as they are brisk in
hyperthyroidism and absent in hypothyroidism
Investigation
CBC Ultrasonography
ESR, CRP FNAC
Thyroid function test Chest x-ray
CT-scan Core needle biopsy (rarely)
Radioactive iodine investigation MRI (rarely indicated)
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Differential Diagnosis
A) Physiologic Goiter
Puberty and Pregnancy goiter
B) Endemic Goiter
Iodine deficiency goiter
C) Toxic goiter
Diffuse toxic goiter Toxic adenoma
Toxic multinodular goiter
D) Inflammatory goiter
Acute suppurative thyroiditis Reidels thyroiditis
Subacute/dequervians thyroiditis Autoimmune thyroiditis
E) Neoplastic goiter
Follicular ca. Anaplastic ca.
Papillary ca. lymphoma
Medullary ca.
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2.2.2. Endemic Goiter
Calcium is also goitrogenic and goitre is common in low iodine areas. Although
iodides in food and water may be adequate, failure of intestinal absorption may
produce iodine deficiency.
Clinically, the patient is euthyroid.
The nodules are palpable and often visible; they are smooth, usually firm and not
hard, and the goitre is painless and moves freely on swallowing.
Complications include tracheal obstruction (due to enlargement of the thyroid
gland and compression of the trachea), secondary thyrotoxicosis which occurs in
30% of the patients and evolution to malignancy.
Iodine deficiency goitere can be prevented by including iodized salt to daily meal
and limiting the intake of goiterogenic foods suchas cabbage
Treatment involves surgical removal of the thyroid gland (thyroidectomy) which
may be subtotal or total depending on the status of the patient.
o Total thyroidectomy is the total removal of the thyroid gland with immediate
and lifelong replacement of thyroxine.
o Subtotal thyroidectomy involves partial resection of each lobe, removing the
bulk of the gland, leaving up to 8 g of relatively normal tissue in each remnant
lobes.
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2.2.3. Toxic Goiter
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overlying bruit or thrill over the thyroid gland and a loud venous hum in the
supraclavicular space.
• Graves’ disease may be treated by any of three treatment modalities:
antithyroid drugs, thyroid ablation with radioactive 131I, and thyroidectomy.
Both RAI and surgical resection may be used for treatment. When surgery is
performed, near-total or total thyroidectomy is recommended to avoid
recurrence and the consequent increased complication rates with repeat
surgery.
C) Toxic Adenoma
A
Arises from a single hyperfunctioning nodule which
typically occurs in younger patients who note recent
growth of a long-standing nodule along with the
symptoms of hyperthyroidism.
Physical examination usually reveals a solitary thyroid
nodule without palpable thyroid tissue on the
contralateral side.
o Treatment options range from antithyroid
medications to surgery (lobectomy or istmusectomy
depending on the size of the nodule.
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2.2.4. Inflammatory Goiter
C) Reidels Thyroidits:
It is a rare disease of the thyroid characterized by a marked dense, invasive
fibrosis that may extend beyond the thyroid capsule and involve surrounding
structures such as blood vessels, trachea and esophagus leading to
hypoparathyroidism.
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Although the exact etiology is not known, a more generalized condition known
as fibrosclerosis causing fibrosis in other parts of the body including the
retroperitoneum, mediastinum, lacrimal glands and bile ducts (sclerosing
cholangitis).
o The clinical presentations are symptoms of compression such as
stridor, hoarseness and dyspnea by which in more aggressive cases
dysphagia occurs.
o On physical examination, the thyroid gland is “woody” hard, and
nontender. Laboratory investigations are normal.
o Treatment involves istmusectomy to relieve the compressive
symptoms.
o Thyroxine replacement therapy is necessary in patients with
hypothyroidism.
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2.2.5. Neoplastic Goiter
A) Papillary Carcinoma
Papillary carcinoma accounts for 80% of all thyroid malignancies in iodine-
sufficient areas
It is the predominant thyroid cancer in children and individuals exposed to
external radiation.
Occurs more often in women, with a 2:1 female-to-male ratio
The mean age at presentation is 30 to 40 years.
Most patients are euthyroid and present with a slow-growing painless mass in
the neck.
Dysphagia, dyspnea, and dysphonia usually are associated with locally advanced
invasive disease.
Lymph node metastases are common
o Especially in children and young adults
o May be the presenting complaint.
The most common sites of metastasis are:
o Lungs
o Bone
o Liver
o Brain
Treatment involves surgical removal of the tumor which can be total or near total
thyroidectomy depending on the aggressiveness of the tumor.
It has an excellent prognosis with a >95% 10-year survival rate.
B) Follicular carcinoma
Accounts for 10% of thyroid cancers and occur more commonly in iodine-
deficient areas.
Women have a higher incidence of follicular cancer, with a female-to-male ratio
of 3:1, and a mean age at presentation of 50 years old.
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Longstanding endemic goitere could lead to follicular carcinoma which can be
hyperfunctioning, leading patients to present with signs and symptoms of
thyrotoxicosis.
Metastasizes by hematogenous spread.
FNAC is unable to distinguish benign from malignant follicular tumors
Treatment involves subtotal or total thyroidectomy.
In general, it has good prognosis with the cumulative mortality approximately
15% at 10 years and 30% at 20 years.
Poor long-term prognosis is due to:
o Age over 50 years old at presentation
o Tumor size >4 cm
o Higher tumor grade
o Marked vascular invasion
o Extrathyroidal invasion and
o Distant metastases at the time of diagnosis.
Hurtle cell carcinoma is a variant of follicular Ca which arises from oxyphilic cells
of the thyroid.
Hurtle cell tumors differ from follicular carcinomas in that they are:
o More often multifocal and bilateral (about 30%)
o Usually do not take up RAI (about 5%)
o More likely to metastasize to local nodes (25%) and distant sites
o Associated with a higher mortality rate (about 20% at 10 years)
C) Medullary carcinoma
Accounts for about 5% of thyroid malignancies and arises from the parafollicular or
C cells of the thyroid.
The female-to-male ratio is 1.5:1.
Present at a younger age; most patients present between 50 and 60 years old,
although patients with familial disease
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Medullary thyroid tumors secrete calcitonin and carcinoembryonic antigen (CEA)
which can be used as tumor markers.
o Spreads via lymph nodes.
o Total thyroidectomy + central lymph node dissection is the treatment
of choice.
o Prognosis depends on the stage of the disease.
The 10-year survival rate is approximately 80% but decreases to
45% with lymph node involvement.
D) Anaplastic carcinoma
Accounts for nearly 1% of thyroid malignancies.
Women are more commonly affected with age at presentation 70-80 years.
History of longstanding goiter can be presumed risk factor
A typical patient has a long-standing neck mass, which rapidly enlarges/may be
painful.
Associated symptoms such as dysphonia, dysphagia, and dyspnea are common.
Spreads via lymphatic route.
The treatment option includes:
o Total or near total thyroidectomy with therapeutic lymph node
dissection
o Radiotherapy and chemotherapy depending on the status of the patient
and tumor stage.
It has poor prognosis with few patients surviving 6 months after diagnosis.
E) Lymphoma
Accounts for <1% of thyroid malignancies.
Non-Hodgkin B-cell type is the most common variant.
The clinical presentations are similar to anaplastic carcinoma with the exception of
absence of pain.
Combined therapy of radiotherapy and chemotherapy is recommended.
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Short Case Discussion
Content By:
Fitsum Solomon
Nanati Jemal 2.3. Thyroid Examination………………..……………..86
Edited By:
Samuel Mesfin 2.4. Breast Examination………………..….……….……91
Reviewed By:
Dr. Endale Anberber 2.5. Video QR Codes………….…………..………….……96
(General and Endocrine
Surgeon)
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2.3. Thyroid Examination
Inspection…………………………….………….………….86
Palpation………………………………….………….………88
Percussion………………………………………………..….90
Auscultation………….………….………….………………91
Special Tests………….………….………….……………..91
Inspection
General appearance
Palpation
Examination of thyroid gland is usually done behind the patient to check for
similarity and accessible lymph nodes. But begin in front of the patient see comfort
of the patient.
A) The swelling for:
Size
Shape
Surface
o Smooth
Adenoma
Puberty Goiter
Grave’s disease
o Irregular o Nodular
Carcinoma Multi-Nodular Goiter
Border
o Round in thyroid disorders
Temperature
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Consistency
o Soft
Grave’s disease Colloid Goiter
o Firm
Adenoma Multi-nodular Goiter
o Hard
Thyroid carcinoma Calcification in multi-
nodular Goiter
Movement with swallowing
o Hold the thyroid gland and ask the patient to swallow
o To asses asymmetry of thyroid lobe elevation
o Differentials for a neck mass that moves with swallowing:
Thyroid disorders
Sub hyoid bursitis
Pre-tracheal and pre-laryngeal lymph nodes
Thyroglossal cysts
laryngocele
o Differentials for a fixed Thyroid mass
Malignancy
Retrosternal Goiter
Large Goiter
Previous Surgery
Intrinsic mobility test
Percussion
Over sternum
o Resonant- normal lobe
o Dull- Retrosternal Goiter
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Auscultation
Special Tests
Check for reflexes – hyporeflexia in hypothyroidism
Check for pre-tibial myxoedema in Graves
Assess for proximal Myopathy by asking the patient to stand up while crossing his
arms – hyperthyroidism
Inspection…………………………….…………………91
Palpation…………………………………………………93
Inspection
A) General appearance
Does the patient have weight loss? Are they in distress?
B) Arm- if there is edema due to lymphatic blockage
C) Breast
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Ask the patient to stand in 4 different positions while you are inspecting the
breast
o Hands by the side
o Hands on the hips
If a mass is visible, observe if
it moves when the pectoralis
muscle contracts which
suggests tethering to the
underlying tissue (e.g.
invasive breast malignancy).
The maneuver may
accentuate puckering
Hands raised above and behind head
o You can appreciate prominent peau d’orange
Leaning forward
o If there is malignancy in the chest wall, breast will not fall forward
While the patient is in “the hands by the side” position, inspect the following
o Asymmetry of the two breasts:
normal feature in most women.
o Incision scars: lumpectomy
(small scar) or mastectomy (large
diagonal scar).
o Lumps- if visible, characterize it
o Skin changes
Dimpling: due to malignancy
infiltrating to ligament of cooper
Peau d’orange- tumor in the areola
Erythema
Scaling: of the nipple and/or areola associated with erythema and
pruritis are typical features of Paget’s disease of the breast
o Nipple
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Is there a discharge?
Differential diagnosis for
Do you see a central retracted nipple?
Nipple retraction
If yes, is the retraction slit-like or circumferential?
1) Cancer of the breast Circumferential indicates malignancy
2) Chronic mastitis Slit-like can be due to duct ectasia or peri-ductal mastitis
3) Congential Level of the nipple; compare with the contralateral side
4) Chronic disease- TB To detect early malignancy
Destructed nipple in Paget disease
Palpation
A) Breast
How to examine?
o Ask the patient to place the hand on the side
being examined behind their head to fully
expose the breast.
o Start palpating the asymptomatic breast
o Ensure all 4 quadrants are palpated with
systematic palpation technique.
o Use the flats of your middle three fingers to compress the breast tissue
against the chest wall, as you feel for any masses.
o Use superficial, intermediate and deep pressure palpation.
o Complete palpation of entire breast before examining a mass in detail.
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Check local rise in temperature and tenderness
o In rapidly growing cancer and inflammatory cancer
Describe the lump if detected
o Location: breast cancer common in upper and outer quadrant of
breast
o Size
o Shape- breast cancer is usually irregular
o Consistency
Hard- common in breast cancer
Firm
Soft- mastitis carcinomatosis due to tumor necrosis
o Mobility
Does it move freely? - fibroadenoma
Does it move with the overlying skin?
Does it move with pectoral contraction?
o Fluctuance
o Overlying skin changes
Hold the mass by its sides and then apply pressure to the
center of the mass with another finger. If the mass is fluid-filled
(e.g. cyst) then you should feel the sides bulging outwards.
o With your palm facing towards you, palpate behind the lateral edge of the
pectoralis major (pectoral/anterior).
o Turn your palm medially and with your fingertips at the apex of the axilla
palpate against the wall of the thorax (central/medial) using the pulps of
your fingers.
o Facing your palm away from you now, feel inside the lateral edge of
latissimus dorsi (subscapular/posterior).
o Palpate the inner aspect of the arm in the axilla (humoral/lateral).
Reach upwards into the apex of the axilla with fingertips (warn the
patient this may be uncomfortable).
Breast Examination
Thyroid Examination
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Part 3: Cardiothoracic Surgery
Content By:
Samuel Mesfin
Zemichael Getu
Edited By: 3.1 . Approach to Dysphagia………………………………….98
Samuel Mesfin 3.2 . Chest Trauma………………………………………………..121
Reviewed By:
Dr. Ephraim Teffera 3.3 . Mediastinal Tumor………………………………………..134
(General and Cardiothoracic
Surgeon)
P a g e 97 | 548
3.1. Approach to Dysphagia
Introduction……………………….…………………….98
History ……………………………..……………………..100
Physical Examination………………………………..102
Investigation…………………………………………….103
Differential Diagnosis…………….…………………106
Discussion of the differentials…..………………107
Introduction
Dysphagia, difficulty with swallowing, refers to problems with the transit of food or
liquid from the mouth to the hypopharynx or through the esophagus.
Severe dysphagia can compromise nutrition, cause aspiration, and reduce quality of
life.
Solid Food Dysphagia becomes common when the lumen is narrowed to 60-70% but
can also occur with larger diameters in the setting of poorly masticated food or
motor dysfunction.
Additional terminology pertaining to swallowing dysfunction:
o Aphagia:
Denotes complete esophageal obstruction
Most commonly encountered in acute settings
For example: food bolus or foreign body impaction
o Odynophagia:
Refers to painful swallowing, typically resulting from mucosal ulceration
within the oropharynx or esophagus.
It commonly is accompanied by dysphagia, but the converse is not true.
o Globus Pharyngeus:
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It is a foreign body sensation localized in the neck that does not interfere
with swallowing and sometimes is relieved by swallowing.
o Transfer dysphagia:
It frequently results in nasal regurgitation and pulmonary aspiration
during swallowing and is characteristic of oropharyngeal dysphagia.
o Phagophobia:
Fear of swallowing and refusal to swallow may be psychogenic or related
to anticipatory anxiety about food bolus obstruction, odynophagia, or
aspiration.
Dysphagia can be classified as
i. With respect to location:
Oral
Oropharyngeal Dysphagia
Pharyngeal
Esophageal Dysphagia
ii. By the circumstances in which it occurs.
Structural Dysphagia: dysphagia caused by an oversized bolus
or a narrow lumen
Propulsive/Motor/Physiologic Dysphagia: dysphagia due to
abnormalities of peristalsis or impaired sphincter relaxation
after swallowing.
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History
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Dysphagia that is progressive over the course of weeks to months
raises concern for neoplasia.
Episodic dysphagia to solids that is unchanged over years indicates a
benign disease process.
Ask about the risk factors:
o For oropharyngeal dysphagia:
History of surgery and radiation therapy, often in the setting of head
and neck cancer.
Neurogenic causes resulting from cerebrovascular accidents,
Parkinson's Disease, and Amyotrophic Lateral Sclerosis
Myogenic causes: myasthenia gravis, polymyositis
Structural lesions causing dysphagia including: Zenker's diverticulum,
Cricopharyngeal Bar, and Neoplasia
o For Esophageal Dysphagia
Diseases that cause absent peristalsis and weakness of the LES like
scleroderma (it is almost always preceded by cutaneous
manifestations)
DES
Achalasia Cardia
o Ingestion of caustic agents or pills
o Prolonged nasogastric intubation
o those are associated with each differential diagnosis (mentioned below)
Ask for the presence of any associated symptoms like:
o Hoarseness:
Hoarseness preceding dysphagia Primary lesion is usually laryngeal
Hoarseness following dysphagia May result from compromise of
the recurrent laryngeal nerve by a malignancy (Indicates advancement
of malignancy and location of the tumor i.e upper thoracic tumor)
o Heart burn: related to a reflux disease with or without a stricture.
o Chest pain: frequently accompanies dysphagia whether it is related to Motor
Disorders, Structural Disorders, or Reflux Disease
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o Accompanying odynophagia: usually is indicative of ulceration
Infectious
Pill-induced Esophagitis
o Loss of appetite and significant/remarkable weight loss: red flags for
esophageal Ca
o Respiratory symptoms: can occur due to aspiration or compression.
o Regurgitation: common in achalasia.
o History of atopy: eosinophilic esophagitis
o In patients with AIDS or other immunocompromised states:
Esophagitis due to opportunistic infections such as Candida, Herpes
Simplex Virus, or Cytomegalovirus
Tumors such as Kaposi's Sarcoma and Lymphoma should be
considered
Physical Examination
General appearance:
o Emaciated in case of esophageal ca.
HEENT:
o A careful inspection of the mouth and pharynx could disclose lesions that may
interfere with passage of food
o Signs of Bulbar or Pseudobulbar Palsy, including Dysarthria, Dysphonia,
Ptosis, Tongue Atrophy, and Hyperactive Jaw Jerk should be elicited.
Lymphoglandular system:
o Palpable Virchow’s nodes
o Look for neck masses
Respiratory system:
o Look for signs of pneumonia (aspiration)
o Tracheal deviation due to mass effect
Abdominal:
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o Look for metastatic sites in case of esophageal ca like the liver.
o Look for ascites
o Palpable epigastric mass for GEJ cancers
Integumentary system:
o Changes in the skin may suggest a diagnosis of scleroderma
Neurologic examination:
o Cranial nerve pathologies suggest functional dysphagia.
o Look for generalized neuromuscular diseases.
Investigation
Baseline
Diagnostic:
1. Barium Esophagram:
A. Pre-Endoscopy
It is performed in patients with the following:
o History/clinical features of proximal esophageal lesion (eg, surgery for
laryngeal or esophageal cancer, Zenker's diverticulum, or radiation therapy).
o Known complex (tortuous) stricture (eg, post-caustic injury or radiation
therapy)
In these patients, the blind intubation of the proximal esophagus
during upper endoscopy may be associated with the risk of
perforation due to upper esophageal pathology
It is a three-phase study assessing mucosa, contour, and function of the esophagus
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o First phase: the double contrast phase, conducted
with the patient ingesting high density barium and
CO2 tablets in the upright position where the
mucosa is examined for strictures, ulcers or nodules.
It is not commonly used in Ethiopia; early
mucosal changes are not common in
Ethiopian setting.
o Next, esophageal function is assessed in the right anterior oblique (RAO) position
with the ingestion of low-density barium in single swallows at 20- to 30-second
intervals. For example, patient with diffuse esophageal spasm, corkscrew
esophagus can be appreciated.
o The final phase, the full-column technique, is performed with the patient in a
semi prone RAO position and low-density barium. Multiple quick swallows
produce a column of barium that fully distends the esophagus. This optimizes
imaging of the distal esophagus and can demonstrate small hiatal hernias, subtle
strictures, or distal rings
B. Post-Endoscopy:
To determine the underlying cause, exclude malignancy, and perform therapy (eg,
dilation of an esophageal ring) if needed.
2. Esophagoscopy: Esophagoscopy is used to
Visually assess mucosal and structural
esophageal abnormalities.
Take biopsies of epithelial abnormalities
(flexible fiberoptic esophagoscopy.)
Perform endoscopic resection, either mucosal
resection (EMR) or submucosal dissection (ESD)
Remove foreign body
Dilate stricture
Place endostents for inoperable carcinoma esophagus
Inject sclerosants for varices
3. Endoscopic Esophageal Ultrasound (EUS): it is used to
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Provide definition of the esophageal wall and
periesophageal tissue not possible to obtain with
routine fiberoptic esophagoscopy.
Evaluate abnormalities of the esophageal wall
and diagnosing non mucosal esophageal tumors.
For staging of esophageal cancer
Probes, which can be passed through the biopsy channel of flexible endoscopes,
can evaluate esophageal strictures that prevent passage of standard ultrasound
equipment
To take EUS-directed fine-needle aspiration (FNA) provides cytologic and
pathologic assessment of esophageal tumors, periesophageal masses, and
regional lymph nodes
4. 24-Hour Esophageal Manometry: is indicated
To establish the diagnosis of dysphagia when
obstruction and eosinophilic esophagitis
have been excluded
For placement of intraluminal devices such
as a pH probe
Before anti-reflux surgery; it is possibly
indicated for dysphagia after anti-reflux
surgery or therapy for achalasia
5. Chest X-ray
To look for aspiration pneumonia
To look for metastasis and pleural effusion
6. U/S abdomen
To look for liver and lymph nodes status in abdomen
To look for ascites
7. CT scan (95% accuracy)
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To look for local extension, nodal status, periesophageal /diaphragmatic/
pericardial (1%)/ vascular infiltration, obliteration of mediastinal fat and status of
tracheobronchial tree in case of upper third growth
8. PET scan (using 18 F-fluorodeoxyglucose (FDG))
Not commonly used
It is functional study
For staging
o It May down stage Tumors from Stage
III to IV in 20 % of Cases
o Better when used in PET CT; for the
anatomic description
For treatment response
9. Video assisted thoracoscopic approach
It can be used for staging
Differential Diagnosis
1. Esophageal Cancer
2. Gastroesophageal Reflex Disease (GERD)
3. Achalasia
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Discussion of the Differentials
Epidemiology
central Asian republics to North- In high incidence regions, SCC has no gender specificity
90 % of cases are SCC It is common in China, South Africa and Asian countries
Major risk factors are thought to It is less common in America and European countries.
include poor nutritional status, Incidence rates for adenocarcinoma of the esophagus
low intake of fruits and have been increasing dramatically; in contrast, rates for
vegetables, and drinking SCC have been steadily decreasing.
beverages at high temperature.
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Risk Factors
Hereditary factors:
o Familial aggregation of esophageal cancer has been described in regions with a
high incidence of esophageal squamous cell carcinoma (SCC).
o Hereditary conditions that increase the risk of esophageal cancer:
Peutz-Jeghers syndrome (PJS)
Germline mutations in the PTEN tumor suppressor gene
SCC:
o Geographic location
o Smoking
o Alcohol
o Dietary factors:
Drinking hot tea (60 to 64°C) or very Pickled vegetables and other food-products consumed
hot tea (≥65°C), and drinking tea within in high-risk endemic areas that are rich in N-nitroso
significantly associated with an High temperature beverages and foods may increase
increased risk of esophageal SCC the risk of esophageal cancer by causing thermal injury
to the esophageal mucosa
o The presence of specific preexisting esophageal diseases (such as achalasia and
caustic strictures)
10 - 17 % life time risk of developing SCC proximal to Achalasia cardia
site Follow up UGIE ever 5 years even if Achlasia is treated.
o Atrophic gastritis and other conditions that cause gastric atrophy are associated
with an approximately twofold increased risk of esophageal SCC (but not
adenocarcinoma)
o Prior gastrectomy
o HPV, particularly serotypes 16 and 18
o Use of oral bisphosphonates
o Current or past history of SCC of the head and neck (ie, oral cavity, oropharynx,
hypopharynx, or larynx)
o Poor oral hygiene particularly in areas where tobacco smoking and heavy alcohol
consumption are not major risk factors.
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Adenocarcinoma:
o Gastroesophageal Reflux disease (GERD) esophageal adenocarcinomas arise
from a region of Barrett's metaplasia.
o Smoking increases the risk of adenocarcinoma, particularly in patients with
Barrett's esophagus
o Obesity and metabolic syndrome
o Patients with acid hypersecretory states (such as Zollinger-Ellison syndrome) or
other conditions that are associated with gastroesophageal reflux (such as
surgical myotomy or balloon dilation of the lower esophageal sphincter or
scleroderma), may be at increased risk
Clinical Manifestations
Early symptoms of esophageal cancer may be subtle and nonspecific.
o Transient "sticking" of meat, hard-boiled eggs, or bread, which can be easily
overcome by the patient with careful chewing, may precede frank dysphagia.
o Approximately 20 percent of patients experience odynophagia (painful
swallowing)
o Patients may also notice retrosternal discomfort or a burning sensation.
o The dysphagia gradually progresses from solids to liquids.
Weight loss:
o Weight loss is mainly due to changes in diet to accommodate the dysphagia
o From tumor-related anorexia
Less commonly:
o Regurgitation of saliva or food uncontaminated by gastric secretions can occur
in patients with advanced disease.
o Hoarseness and/or cough if the recurrent laryngeal nerve is invaded by either
the primary tumor or associated nodal metastasis
o Aspiration pneumonia
o Chronic gastrointestinal blood may result in iron deficiency anemia (in 10%)
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However, patients seldom notice melena, hematemesis, or blood in
regurgitated food.
Similarly, acute upper gastrointestinal bleeding is rare and is a result of
tumor erosion into the aorta or pulmonary or bronchial arteries.
o Tracheobronchial fistulas direct invasion of the mainstem bronchus
Late complication of esophageal cancer.
Life expectancy is less than four weeks following the development of
this complication.
o Patients may present with signs or symptoms referable to distant metastatic
disease.
The most common sites of distant metastases in patients with
esophageal cancer are the liver, lungs, bone, and adrenal glands
Adenocarcinomas most frequently metastasize to intraabdominal sites
(liver, peritoneum), while metastases from SCCs are usually
intrathoracic.
Definitive Diagnosis
The diagnosis of esophageal cancer requires a histologic examination of tumor tissue
Biopsy:
o Endoscopic: early esophageal cancers appear as superficial plaques, nodules, or
ulcerations while advanced lesions appear as strictures, ulcerated masses,
circumferential masses or large ulcerations
o Endoscopic resection: if the tumor has a diameter of ≤2 cm, if it involves less
than one-third of the circumference of the esophageal wall and if it is limited to
the mucosa of the esophagus
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Staging
Accurate clinical staging of both local tumor extent and the presence or absence of
distant metastases is critical for estimating prognosis and selecting the appropriate
treatment strategy.
Locoregional Staging:
o Endoscopic ultrasound (EUS) is the preferred method for locoregional staging
Evaluation of distant metastasis:
o Contrast-enhanced computed tomography (CT) of the neck, chest, and abdomen
o Positron emission tomography (PET)/CT
Then the TNM staging system is used universally.
Table 3.2: Esophagus and esophagogastric junction cancers TNM staging AJCC UICC 2017
Primary Tumor (T)
T category T criteria
TX Tumor cannot be assessed
T0 No evidence of primary tumor
Tis High-grade dysplasia, defined as malignant cells confined to the epithelium
by the basement membrane
T1 Tumor invades the lamina propria, muscularis mucosae, or submucosa
T1a Tumor invades the lamina propria or muscularis mucosae
T1b Tumor invades the submucosa
T2 Tumor invades the muscularis propria
T3 Tumor invades adventitia
T4 Tumor invades adjacent structures
T4a Tumor invades the pleura, pericardium, azygos vein, diaphragm, or
peritoneum
T4b Tumor invades other adjacent structures, such as the aorta, vertebral body,
or airway
Regional lymph nodes (N)
N category N criteria
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NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in one or two regional lymph nodes
N2 Metastasis in three to six regional lymph nodes
N3 Metastasis in seven or more regional lymph nodes
Distant metastasis (M)
M category M criteria
M0 No distant metastasis
M1 Distant metastasis
Prognostic stage groups
T N M Stage group
Tis N0 M0 0
T1 N0-1 M0 I
T2 N0-1 M0 II
T3 N0 M0 II
T3 N1 M0 III
T1-3 N2 M0 III
T4 N0-2 M0 IVA
Any T N3 M0 IVA
Any T Any N M1 IVB
Management
Early presentation: only in 20% of the cases, curative surgery can be done
o Radical esophagectomy (Proximal extent of resection 10 cm above the
macroscopic tumor and distal is 5 cm from macroscopic distal end of tumor.
Proximal stomach has to be removed commonly with sufficient removal of
contiguous structures)
o LN involvement Curative resection + radiotherapy + chemotherapy
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Remaining patients (80%) Palliation is done:
o If patient is not fit for major surgery
o If there is blood spread
o If there is spread to adjacent organ
o If there is peritoneal/liver spread.
o To relieve pain and dysphagia
o To prevent aspiration and bleeding
Palliation procedures:
o External or intraluminal RT (Brachytherapy)
o Traction tubes through open surgery
o Pulsion tubes through endoscopes
o Endoscopic laser
o Chemotherapy
o Trans hiatal esophagectomy
Prognosis:
Not good (5-year survival rate is only 10%) because of:
o Early spread o Aggressiveness
o Longitudinal lymphatics o Difficult to approach
o Late presentation.
o Nodal involvement carries bad prognosis
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3.1.2 Achalasia
Epidemiology………………………………………….................114
Etiology…………………………………………............ …………..114
Clinical Manifestation……………………………………………..114
Diagnosis………………………………………….......................115
Management………………………………………….................116
Epidemiology
Uncommon disorder
It has an annual incidence of approximately 1.6 cases per 100,000 individuals and
prevalence of 10 cases per 100,000 individuals.
Men and women are affected with equal frequency.
Is common between the ages of 25 and 60 years, but can occur at any age.
Etiology
Idiopathic: This occurs due to absence or degeneration of Auerbach's plexus
throughout the body of the esophagus leading to improper integration of the
parasympathetic impulse.
Acquired variety is seen in South American countries caused by Trypanosoma cruzi
Chaga’s disease. This organism destroys the ganglion cell of Auerbach’s plexus.
Stress and emotional factors.
Vitamin deficiencies are also associated with this disease.
Clinical Manifestations
The classic triad of presenting symptoms consists of dysphagia, regurgitation, and
weight loss.
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o However, heartburn, postprandial choking, and nocturnal coughing are also
seen commonly.
The dysphagia that patients experience begins with liquids and progresses to solids.
The dysphagia progresses slowly over years and patients adapt their lifestyle to
accommodate the inconveniences that accompany this disease.
Patients often do not seek medical attention until their symptoms are quite
advanced will present with marked distension of the esophagus.
Regurgitation is frequent, and there may be overspill into the trachea, especially at
night.
It is also known to be a premalignant condition of the esophagus.
Diagnosis
Esophagram
o Shows dilated esophagus
with a distal narrowing
referred to as the classic
“bird's beak” or “rat tail”
appearance of the barium-
filled esophagus.
o The gastric gas bubble is
usually absent.
o It is not a sensitive test for
achalasia, as it may be
interpreted as normal in up
to one-third of patients
Manometry
o It is the gold standard test; the manometry tracings show five classic findings:
The LES will be hypertensive with pressures usually above 35 mm Hg.
The LES fails to relax with deglutition.
The body of the esophagus will have a pressure above baseline.
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The body will also have simultaneous mirrored contractions with no
evidence of progressive peristalsis
Low-amplitude waveforms indicating a lack of muscular tone.
Endoscopy
o Is performed to evaluate the mucosa for evidence of esophagitis or cancer.
o Little contribution to the diagnosis of achalasia.
Management
Is directed towards relieving the obstruction caused by the LES, however, all are
palliative treatments and can’t reverse the degeneration of ganglion cells.
It can be accomplished by:
o Mechanical disruption of the muscle fibers of the LES:
Pneumatic dilatation:
Involves stretching the cardia with a balloon
Over four to six years, nearly one-third of patients have
symptom relapse and require retreatment.
Perforation is the major complication.
Modified Heller’s cardiomyotomy:
Includes only anterior myotomy with laparoscopic approach in
preference.
Usually a partial fundoplication is added to reduce the risk of
gastro-esophageal reflux.
o Pharmacological reduction in LES pressure:
Injection of botulinum toxin:
It acts by interfering with cholinergic excitatory neuronal
activity at LES.
The effect is not permanent.
Oral nitrates or calcium channel blockers:
Are ineffective for long-term use.
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3.1. 3. Gastro-Esophageal Reflex Disease (GERD)
Risk Factors……………………………………………………….…117
Clinical Manifestation…………………………………………..118
Diagnosis……………………………………………………………..118
Management……………………………………………………….119
Risk Factors
It is due to varied anatomical and physiological factors.
Anatomical Factors:
o Obesity
o Altered length of intra-abdominal esophagus.
o Alteration of phreno-esophageal ligament.
o Altered obliquity of E-G junction.
o Reduced pinching action of right crus of diaphragm.
o Alteration in normal mucosal rosette at E-G junction.
o Alteration in sling mechanism of gastric musculature.
Physiological Factors:
o Reduced LES pressure. Resting pressure is decreased by secretin,
cholecystokinin, glucagon, calcium channel blockers, coffee, fatty meal.
o Altered transient relaxation period in LOS.
o Reduced esophageal clearance mechanism.
o Delayed gastric emptying due to diabetes, neuromuscular block, gastroparesis,
and medications.
o Increased gastric distension and gastric acid hyper secretion.
Others
o Alcohol, smoking, stress, lifestyle
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Clinical Manifestation
Diagnosis
Diagnosis can be based on symptoms alone in patients with the classic symptoms.
Patients may require additional evaluation if they have alarm features (like: new
onset of dyspepsia in a patient older than 60, anorexia, unexplained weight loss,
dysphagia, evidence of GI bleeding), risk factors for Barrette’s esophagus or
abnormal gastrointestinal imaging performed for evaluation of their symptoms.
In patients without the classic symptoms other disorders must be excluded.
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o Barium swallow in trendelenburg’s position can demonstrate the reverse flow
of barium in to the lower end of the esophagus.
o Endoscopy to exclude other diseases and to assess any mucosal injury.
o Mucosal biopsy to confirm metaplastic transformation.
o Esophageal manometry is used to assess the function of LES.
o 24 hours esophageal pH monitoring is the gold standard. PPI should be
stopped for 3 weeks prior to pH monitoring.
Management
Life style changes
o Stop smoking and excessive consumption of alcohol.
o Avoid tea, coffee and chocolate.
o A modest degree of head-up tilt of the bed.
o Small frequent meals and avoidance of constricting clothing.
Medical management
o In a patient whose history and examination are consistent with GERD. It would
be prudent to check for chronic anemia and to prescribe a 6-week course of
acid suppression therapy.
o Double dose of a proton pump inhibitor is the initial approach to medical
management. If the symptoms persist after a trial of medical therapy, a more
extensive evaluation would be indicated.
o The medications available to treat acid reflux include antacids, motility agents,
histamine-2 (H2) blockers, and proton pump inhibitors.
Surgical treatment indications:
o Failed medical management and noncompliance with medical therapy
o Severe esophagitis and benign stricture
o Barrett's columnar-lined epithelium (without severe dysplasia or carcinoma)
o Upper respiratory symptoms including hoarseness, laryngitis, wheezing,
nocturnal asthma, cough, aspiration, or dental erosion
Preoperative evaluation
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Upper endoscopy, esophageal manometry, and assessment of esophageal
length and degree of hiatal herniation are the most useful tests in making
surgical decisions
Procedures
o Hill’s posterior gastropexy
Intra-abdominal fixation of OG junction (cardia) into median arcuate
ligament to augment the effect of LOS, to enable the effective esophageal
peristalsis.
Modified Hill’s uses the preaortic fascia and the condensation of the crus as
the anchor for the repair.
Fewer side effects than fundoplication.
o Fundoplication
Mobilize the lower esophagus and wrap the fundus of the stomach around it
either totally or partially.
Most of the antireflux operations are now done a laparascopic approach.
Total Fundoplication
360° fundal wrap around the distal esophagus with division of the
short gastric vessels (“floppy”).
Tends to be associated with slightly more short-term dysphagia but is
the most durable repair in terms of long-term reflux control.
It also creates an over competent cardia, resulting in the gas bloat
syndrome where the stomach feels with air and the patient feels very
full after small meals and pass excessive flatus. It has been overcome
with the floppy Nissen technique in which the fundoplication is loose
around the esophagus and is kept short in length.
Partial Fundopliction
Whether performed posteriorly (Toupet) or anteriorly (Dor, Watson),
has fewer short-term side effects, although this is sometimes at the
expense of a slightly higher long-term failure rate. (does not cause gas
bloat syndrome)
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3.2 Chest Trauma
Case Discussion……………………………….121
Introduction……………………………………121
History …………………………………………..122
Physical Examination………………………124
Investigation…………………………………..125
Differential Diagnosis……………….…….127
Discussion of the differentials…………128
Case Discussion
A 24-year-old male patient presents to the emergency after he sustained a stab injury to
the back. Prior to his admission, he had profuse bleeding and lost consciousness as a
result. Upon arrival, he was unresponsive and tachycardic. After he gained consciousness
he noticed shortness of breath that is worsened by sleeping on the right side and relieved
when intranasal oxygen was supplied; and a severe type of stabbing chest pain. Physical
examination revealed pale conjunctivae, signs of fluid collection in the lower 2/3rd of his
left lung field, pressure bandages covering the stab wound posteriorly and chest tube
inserted in the left anterio-lateral chest
Introduction
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Mechanisms that provide the amount of energy needed to produce significant blunt
thoracic trauma are associated with head, abdominal, or extremity injuries should
be ruled out in the history.
Types: blunt/penetrating
o Blunt trauma: includes high-speed deceleration injury, crush injuries, falling
down accidents, assaults, sports mishaps, and blast injuries
o Penetrating:
High velocity: Bullet injuries
Low velocity: Stab injuries
History
Elaborate the symptoms that follow the injury: the commonest symptoms patients
experience after chest injury are
o Shortness of breath
o Chest pain: pleuritic (aggravated by taking deep breath or coughing)
o Loss of consciousness following a profuse bleeding: check the table below
Ask about the mechanism of injury, elaborate the type of the trauma the patient
sustains:
o For bullet injury: ask if the patient remembers the type of gun used, if they
can estimate the distance from the shooter, precisely where they were shot
and the number of times they were shot.
o For stab injury: ask if the patient remembers they type of material, where
they stabbed precisely (to anticipate the type of organ damage), and how
many times they were stabbed.
Ask for any associated symptoms
o Tachypnea, tachycardia, hypotension, tracheal deviation away from the side
of the injury, neck vein distention tension pneumothorax
o Fever
o Palpitations, lightheadedness and easy fatigue
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o Swelling of the face of the upper torso and extremity subcutaneous
emphysema
o Coughing up of blood or change in voice (hoarseness)
o Pain during swallowing, inability to swallow or vomiting up of blood
o Bluish discoloration of the lips or fingers or cold extremities
o Extremity weakness, pain/numbness/tingling sensation, urinary or bowel
incontinence Spinal cord injury
Assess any risk factors
o Ask history of alcohol consumption
o Known Seizure disorders
Care before referral
o Blood transfusion
o Wound care
o The type of medications given and if chest tube was inserted
Normal (Maintained
Blood
Extreme tachycardia
Heart rate
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Mental
Physical Examination
General appearance:
o Check if the patient is acutely sick looking: in respiratory distress (check for
oxygen line) or well looking
Vital sign:
o Temperature: febrile if infected
o Respiratory rate: tachypneic if the patient develops tension pneumothorax
o Pulse rate: tachycardic if the patient develops tension pneumothorax
o Blood pressure: hypotensive if the patient is in shock
o Oxygen Saturation:
HEENT:
o Head: check if there is an associated head trauma (particularly in a poly
trauma patient)
o Eyes: look for conjunctival pallor
o Mouth and lips: look for cyanosis and dry buccal mucosa
Respiratory system:
o Inspection: check if there is a reduced chest movement in one side,
intercostals or sub costal retractions or use of accessory muscles of
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respiration, a chest tube inserted (refer to the short case discussion section
on how to report)
o Palpation: feel if the trachea is central, if tactile fremitus is normal and
comparable and if there is any tenderness
o Percussion: look for dullness or hyper resonance
o Auscultation: check if the breath sounds are vesicular or not and if well heard,
reduced or absent; if there are added sounds or vocal resonances; if bowel
sounds were heard in the lower chest area (diaphragmatic injury).
Cardiovascular system:
o Veins: reduced venous pressure in the jugular veins
o Hypotension and distended veins at the same time is a near confirmatory
sign of Obstructive Shock
Abdominal:
o Look for associated abdominal trauma (particularly in a poly trauma patient)
Integumentary system:
o There might be reduced skin turgor if the patient is in shock
o Check if there are pressure bandages covering the injury site if so focus on the
wound care and describe the lesion underneath the bandages.
Neurologic examination:
o Detailed examination particularly if spinal cord injury is suspected due to
trauma to the back
o Check for the tone, power, sensation and sphincter tone.
Investigation
Do not send unstable patients for investigation.
If there is a need two doctors and a nurse should accompany the patient with
necessary resource at hand and get prepared to do CPR any time
1. Chest Radiography
First line diagnostic modality
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A systematic review of the film should reveal suspected and unsuspected injures.
It is helpful to:
o Rule out the presence of any foreign bodies.
o Rule out fractures of the bony thorax, including the ribs, clavicles, spine,
and scapulae because fractures of the thoracic cage indicate significant
energy transfer to the patient;
Those of the upper ribs trauma to the great vessels
Those of the clavicle pulmonary or cardiac contusions.
o Examine the lung fields for:
Pneumothorax Pulmonary
Hemothorax contusion
o Check for mediastinal widening, pneumomediastinum, or shifting:
Highly suggestive of aortic transection, tracheobronchial or
esophageal injuries, or tension pneumothorax or hemothorax.
o To examine the soft tissues for subtle subcutaneous air or foreign bodies.
o To check for the width of the cardiac silhouette
Raised suggests tamponade.
2. Chest CT:
It is not essential for every patient with chest trauma and should not be
performed in the severely hemodynamically unstable patient or in the presence
of obvious life-threatening injuries.
However, it may reveal injuries not seen clearly on plain radiographs such as:
o Diaphragmatic injuries o Pneumothorax
o Pulmonary contusions o Pneumomediastinum
o Aortic disruption o Hemothorax
It can also be used to exclude diagnoses made by the less sensitive chest
radiograph
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3. Ultrasonography:
E-FAST: extended focused assessment for the sonographic evaluation of the
trauma patient
Uses an extension of the right and left upper quadrant views to include the right
and left hemithoraces
o Aid in the diagnosis of hemothorax or pneumothorax
4. 12 lead ECG
5. Echocardiography
Diagnostic tool for detecting injuries, wall motion abnormalities, effusions,
valvular or septal defects, and particularly chamber rupture.
This should be performed in all patients with an abnormal ECG or who are
hemodynamically unstable
6. CT Angiography
More sensitive than echocardiography in the diagnosis of aortic and great vessel
injuries: gold standard
Differential Diagnosis
3.2.1 Pneumothorax
Introduction…………………………….129
Clinical Manifestation………………129
Investigation……………………………129
Management…………………………..129
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Introduction
Clinical Manifestation
Investigation
The supine chest radiograph has high specificity for diagnosing a pneumothorax but
its sensitivity is variable.
Ultrasound may be a more sensitive initial screening tool
For patients with a risk for pneumothorax (has a history of pleuritic pain, dyspnea
and rib fracture revealed on examination) whose initial radiograph does not reveal
a pneumothorax, repeat the radiograph in six hours.
Management
Simple Pneumothorax: refer to the chest tube section under short case discussion
Tension Pneumothorax: refer to the needle thoracostomy section under short case
discussion
Open Pneumothorax:
3.2.2 Hemothorax
Introduction………………………………………..130
Clinical Manifestation………………………….131
Investigation………………………………………..131
Management……………………………………….132
Introduction
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o Internal mammary arteries
o Lacerated lung
Injuries leading to massive hemothorax include:
o Aortic rupture o Injury to hilar structures
o Myocardial rupture
Clinical Manifestation
Typical signs and symptoms include:
o Shortness of breath o Reduced tactile fremitus
o Pleuritic type of chest pain o Dull to percussion
o Bulged chest wall o Absent breath sounds
o Reduced chest expansion
o Signs and symptoms of shock might also occur depending on the degree of
hemorrhage (refer Table 3.3).
Investigation
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Management
Introduction……………………………………………….132
Clinical Manifestation………………………………...133
Investigation………………………………………………133
Management……………………………………………..134
Introduction
Clinical Manifestation
Classic symptoms include:
o Dyspnea o Cyanosis
o Tachypnea o Hypotension
o Hemoptysis
Physical examination can demonstrate
o Inspiratory rales
o Decreased breath sounds on the affected side
Investigation
Chest radiograph:
o Irregular, non-lobular opacification of the pulmonary parenchyma on chest
radiograph is the diagnostic hallmark.
o About one-third of the time the contusion is not evident on initial
radiographs
Do chest CT
Chest CT:
o CT scan is the study of choice; it is more sensitive than radiography in
detecting a pulmonary contusion
o Contusions evident on CT but not plain CXR have better outcomes
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Management
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Case Discussion
A 20-year-old man with no significant past medical history presented to his primary care
physician for chest discomfort and cough. Two months prior to presentation, he reported
having an unremarkable viral syndrome which resolved with no medical intervention. His
primary care physician prescribed a short course of antibiotics for empiric treatment of
pneumonia with some initial improvement in symptoms. His chest discomfort returned
and he developed progressive dyspnea on exertion. Physical examination was
unremarkable. Imaging studies reveal left-sided mediastinal mass on chest x-ray and a
rounded, well-demarcated mass in the superoanterior mediastinal compartment on CT.
Introduction
A mediastinal mass can be an incidental finding in patients who undergo plain chest
radiography or advanced imaging studies, such as CT or MRI.
Symptoms, if present, may be due to direct mass effect of the mediastinal anomaly
or to systemic effects of the illness.
In general, malignant lesions are more likely to be symptomatic
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History
Identification: Age
o In infants and children: neurogenic tumors and enterogenous cysts are the
most common mediastinal masses
o In adults: neurogenic tumors, thymomas, and thymic cysts are most
frequently encountered lesions
Commonest complaints: because of the mass effect are:
o Cough o Hemoptysis
o Stridor o Shortness of breath
o In children: respiratory difficulty and recurrent pulmonary infection
mostly symptomatic
o Pain
Dull aching pain: commonly
Severe pain is typically a sign of advanced invasive disease
o Dysphagia esophageal compression
o Hoarseness Recurrent laryngeal nerve involvement
o Vascular compression: Superior vena cava
Facial, neck and upper extremity swelling
Dyspnea
Chest pain, upper extremity pain
Mental status changes
o Hypotension Tamponade physiology or cardiac compression
o Horner syndrome (Ptosis, miosis, anhidrosis) Sympathetic ganglion
involvement
o Weakness or paralysis involvement of the spinal cord
Elaborate the chief compliant
o Ask the progression of the symptom: slow growth over the course of years
(eg, thymoma in some patients) or rapid expansion (eg, lymphoma)
Ask if there are any systemic effects:
o Fever, night sweats, and weight loss can be present in the case of
lymphoma
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o Could also be due to a variety of paraneoplastic syndromes, such as
myasthenia gravis with thymoma.
o Symptoms of thyrotoxicosis
o Symptoms of hyperparathyroidism
Ask associated symptoms
o Abnormalities in other parts of the body (eg, testicular masses with germ
cell tumors)
o Others are mentioned in the discussion of the differential diagnosis
section below
Physical Examination
Look for the signs of paraneoplastic syndromes like
o Myasthenia gravis o Hyperparathyroidism.
o Thyrotoxicosis
Assess metastatic sites in case of thymic cancer (mentioned in the discussion of the
differentials section)
Besides check:
o General appearance: chronically sick looking in cases of carcinomas
o Vital sign: patients can be febrile or tachycardic
o Lympho glandular system: Check for lymphadenopathy, look for neck masses,
do scrotal examination in males
o Respiratory system: tracheal deviation due to mass effect, signs of pleural
effusion (metastasis)
o SVC obstruction Syndrome:
o Engorged neck veins and Puffy face
o These patients need early intervention either by chemo,
radiation or surgery
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Investigation
a. Lab studies:
If there are systemic symptoms:
o Thyroid function test
o Calcium, phosphate and PTH
For thymic tumors:
o Anti-acetylcholine receptor antibodies may be positive in some
patients and indicate presence of myasthenia gravis.
If paraganglionic tumor suspected:
o Fractionated 24-hour urinary metanephrines and catecholamines
If non-seminomatous germ cell tumor is suspected:
o Alpha-fetoprotein (AFP) elevated levels of AFP (malignant)
Specifically, 60 to 80 % of dysembryomas are serum AFP positive.
o Beta-human chorionic gonadotropin (beta-hCG) is associated with
seminoma (10 percent) and non-seminomatous (30 to 50 percent) germ
cell tumors.
Lactate dehydrogenase (LDH):
o May be elevated in patients with non-seminomatous dysembryoma
o Generally, not as specific as AFP or beta-hCG
o May also be elevated in patients with lymphoma.
b. Imaging studies:
Chest X-ray
Chest CT:
o CT with contrast is typically used to evaluate abnormalities seen on plain
radiographs and to:
Confirm the presence of a mediastinal mass
Provide detailed information regarding the mediastinal
abnormality including its location, size or relationship to other
structures
Check tissue characteristics, including presence of fat, fluid, or
calcifications (eg, teratoma)
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o Careful on giving Iodinated contrast for Thyroid Origin tumors as it may
convert Subclinical thyrotoxicosis to overt.
Chest and/or cardiac gated magnetic resonance (MR) imaging:
o Useful in distinguishing compression versus invasion where this distinction
can be difficult on CT
o For example: particularly in cases of large anterior mediastinal masses
Positron emission tomography (PET):
o For a mediastinal mass that is suspected to be a lymphoma
o To identify a preferred biopsy site
o To monitor response to treatment
o There can be false positive results for nonmalignant conditions such as
teratoma and thymic cysts
Spine MRI:
o To provide a detailed evaluation of posterior mediastinal masses adjacent
to the spine.
o MR is better than CT for determining whether a mass extends into the
neural foramina or spinal canal, which is important for surgical planning
Tissue Diagnosis: biopsy
o Percutaneous Both anterior and posterior mediastinal masses can often
be biopsied under CT guidance
o Endobronchial — Endobronchial biopsy (EBUS) is reasonable to consider
when the mediastinal mass is located immediately adjacent to an airway.
o Surgical
When percutaneous or endobronchial biopsy is not possible or
cannot provide adequate tissue to definitively establish a
diagnosis, surgical biopsy may be necessary.
It is known as Chamberlain's Incision
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Differential Diagnosis
1. Thymoma
2. Bronchogenic cyst
3. Neurogenic tumors
Other differentials for each compartment are mentioned in the table below
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Discussion of the Differentials
3.3.1 Thymoma
Introduction……………………………………..…………….141
Epidemiology…………………………………..……………..141
Clinical Manifestation………………………………….....142
Diagnosis………………………………………..………………142
Management………………………………………………....142
Introduction
Clinically present as one of the three:
o An incidental finding identified on imaging in an asymptomatic patient
o Because of local (thoracic) symptoms mass effect
o Due to symptoms from a paraneoplastic syndrome
Metastasis of thymic carcinoma is commonly to:
o Kidney o Adrenals
o Extrathoracic LNs o Thyroid
o Liver o Bone
o Brain
Epidemiology
Thymic tumors are rare neoplasms that arise in the anterior mediastinum
In adults, thymomas and thymic carcinomas are the most common neoplasms
arising in the thymus.
Thymomas account for about 20 percent of mediastinal neoplasm
Most thymoma patients are between 40 and 60 years of age, and there is a similar
incidence in men and women
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Clinical Manifestation
Thoracic symptoms:
o Chest pain
o Shortness of breath
o Cough
o Phrenic nerve palsy
o Superior vena cava syndrome
o Pleural or pericardial effusions are the most common manifestation of more
disseminated disease
Paraneoplastic syndrome:
o The most common paraneoplastic syndrome is myasthenia gravis
o Rarely:
Addison's disease, Cushing syndrome, panhypopituitarism, thyroiditis
Agranulocytosis and hemolytic anemia
Alopecia areata, pemphigus or scleroderma
Diagnosis
Imaging studies
Definitive diagnosis of a thymoma or thymic carcinoma requires a tissue diagnosis
Management
Resectable disease:
o Those with completely encapsulated tumors
o Those with tumors invading readily resectable structures:
Mediastinal pleura
Pericardium
Adjacent lung
o Surgery is indicated as the initial treatment for such patients.
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o Patients should be evaluated for evidence of myasthenia gravis
If signs or symptoms are present Should be treated medically prior
to surgery
Potentially resectable disease
o For patients in whom a complete resection is not considered feasible as the
initial treatment, those with tumor invasion into:
The innominate vein
Phrenic nerve(s)
Heart/great vessels
o Multimodality therapy incorporating preoperative chemotherapy and
postoperative RT is indicated
Such disease is considered potentially resectable if neoadjuvant
therapy allows for a partial or complete response.
Unresectable disease
o Patients who present with:
Extensive pleural
Pericardial metastases
Unreconstructable great vessel or heart involvement
Tracheal involvement
Technically unresectable disease
Distant metastases.
o Systemic therapy, radiotherapy, or chemoradiotherapy may be indicated for
such patients
Additionally, such treatments are offered to those who are medically
unfit for surgery due to age or comorbidity.
Treatments are individualized according to the patient’s extent of
disease, symptoms, and performance status.
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Short Case Discussion
Content By:
Samuel Mesfin
Edited By:
3.4. Chest Tube……..……..……..……..……..……..……145
Samuel Mesfin 3.5. Needle Thoracostomy……..……..……..……..….158
Reviewed By: 3.6. Tracheostomy…….…….……..……..……..……..…160
Dr. Ephraim Teffera
(General and Cardiothoracic 3.7. Video QR Codes……..……..……..……..……..……168
Surgeon)
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3.4. Chest Tube
Describe what you see.…………………………...145
Introduction……………………..………………………145
Indications……………………..…………………………146
Contraindications……………………..………………147
Equipment………………………………………………..147
Chest tube size and selection……………..…….148
Preparation ……………………………………..………150
Insertion techniques………………………..……….151
Complications…………………………………………..155
Chest tube Management…………………………..155
Chest Tube removal………………………..………..157
Introduction
A chest tube (thoracic catheter, thoracostomy tube) is a sterile flexible plastic tube
with a number of drainage holes that is inserted through the chest wall and into the
pleural space or mediastinum.
A patient may require a chest drainage system anytime the negative pressure in the
pleural cavity is disrupted, resulting in respiratory distress.
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o Negative pressure is disrupted when air or fluid enters the pleural space.
o A small amount of fluid or air can be absorbed by the body without a chest
tube. A large amount of fluid or air will require drainage.
Tube thoracostomy is a common procedure in which a tube is placed through the
chest wall into the pleural cavity:
o Primarily to drain air or fluid
o To instill agents to induce pleurodesis or to treat empyema.
Indications
Insertion of a chest tube is indicated in either emergency or nonemergency
situations
Table 3.8: Indications of Tube Thoracostomy
Emergency Non-emergency
Pneumothorax Pleural Effusion:
In all patients on mechanical ventilation Malignant pleural effusion
Bronchopleural fistula Recurrent pleural effusion
When pneumothorax is large Sterile effusion
In a clinically unstable patient Infected or inflammatory effusion
For tension pneumothorax after needle o Empyema
decompression o Parapneumonic effusion
When pneumothorax is recurrent or Chylothorax
persistent Hemothorax following chest trauma
When pneumothorax is secondary to chest Biliary-pleural or bronchobiliary fistula
trauma o Following combined injury of the
When pneumothorax is iatrogenic, if large liver, diaphragm, and lung
and clinically significant most commonly
due to central line placement
Massive hemothorax (>1.5L) Treatment with sclerosing agents or pleurodesis
for the treatment of refractory effusion
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Esophageal rupture with gastric leak into pleural Postoperative care after:
space o Coronary bypass
o Thoracotomy
o Lobectomy
Contraindication
Equipment
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1 or 2 % lidocaine
Needles (size 25 and size 18-21) and syringes
for anesthetizing the skin
Scalpel, with No. 10 or 11 blade
Three Kelly clamps
Straight scissors
Chest tube
Silk suture (1 to 0)
Petroleum gauze
Drain sponges
Elastic tape
Sterile drapes, gown and gloves
Mask, protective eyewear
2 % chlorhexidine/povidone iodine
Drainage system
Tube Selection:
Chest tubes of silicone (Silastic) are preferred over older latex rubber tubes because the
later:
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o Had fewer drainage holes
o Are not well visualized on chest radiographs
o Produced more pleural inflammation
o Have been associated with latex allergy
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Preparation
Anterior border of the latissimus dorsi, The actual insertion site should be one intercostal
Posterior border of the pectoralis major space above the chest-tube incision site in order
to deal with possible pleuro-cutaneous fistula
Superior border of the fifth rib4th to 5th
which is a rare occurrence.
ICS at midaxillary line.
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o Draw up more lidocaine solution in a 20-ml syringe. Using a 21-gauge
needle, anesthetize the deeper subcutaneous tissues and intercostal
muscles.
Locate the rib lying below the intercostal space where the tube will be inserted,
and continue to anesthetize the periosteal surface.
o Use 3ml/kg to calculate the amount of lidocaine solution that may be
used to ensure optimal analgesia (based on %).
Ex: 2% Lidocaine for a 50Kg person:
2% = 2gm in 100ml 2000mg in 100ml 20 mg/ml
3ml/kg x 50kg 150ml 7.5 ml of 2% Lidocaine
o While anesthetizing the rib, find the superior aspect of the rib and use
this to bevel or “march” the needle on top of it.
Using continued negative suction as the needle advances, with the needle
beveled on top of the rib, confirm entry into the pleural space when a flash of
pleural fluid enters the chamber of the syringe.
If a pneumothorax is being evacuated:
o The syringe may only fill with air.
o Stop advancing the needle and inject any remaining lidocaine to fully
anesthetize the parietal pleura.
o You may feel the decrement in pressure when you breach the pleura
even if nothing is coming out.
Withdraw the needle and syringe completely
Insertion Techniques
Blind insertion of a chest tube is dangerous in a patient with pleural adhesions from
infection, previous pleurodesis, or prior pulmonary surgery guidance by ultrasound or
CT scan without contrast is preferred.
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Prophylactic antibiotics are warranted for chest tubes placed in the setting of trauma,
particularly in patients with penetrating injury.
Incision and Dissection
An incision 1.5 to 2.0 cm in length should be made parallel to the rib.
o Use the Kelly clamp or artery forceps to cut through the subcutaneous layers
and intercostal muscles
o The path should traverse diagonally up toward the next superior intercostal
space.
Once you have dissected through the subcutaneous tissues, find the surface of the rib
lying below this space with the dissecting instrument.
Then slide the instrument straight up, until you find the top edge of the rib.
Use this to bevel or balance the dissecting instrument as you dissect the intercostal
muscles
Once you reach the parietal pleura, gently push the dissecting instrument through it.
o You may also digitally penetrate the pleura to avoid puncturing
adjacent lung tissue, using your index finger to explore the tract.
Once your finger enters the pleura, withdraw the Kelly clamp. Use your finger to palpate
within the pleural layer and ensure that the lung falls away from the pleura.
o If it does not, this may indicate the presence of an adhesion, so tube insertion
may be difficult.
Tube Insertion
Once the distal tip of the tube has passed
through the incision, unclamp the Kelly
clamps or forceps and advance the tube
manually.
Aim the tube:
o Apically for evacuation of a
pneumothorax
o Basally for evacuation of any fluid.
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Securing the Tube
Mattress or interrupted sutures should be used on both sides of the incision
to close the ends.
Tape the tube to the side of the patient and wrap a petroleum-based gauze
dressing around the tube.
Cover this gauze with several pieces of regular sterile gauze, and secure the
site with multiple pressure dressings.
Connect the distal end of the chest tube to a sterile pleural drainage system.
Once the tube is connected, unclamp the distal end:
o If there is a pneumothorax, bubbling may be seen
o If there is a large pleural effusion, it will begin collecting.
Do not reclamp the chest tube, once released, unless the pleural drainage
system is being changed.
Radio-opaque marking o Reclamping the tube may lead to the redevelopment of a
on thoracostomy tube
pneumothorax and may create a tension pneumothorax.
Seldinger technique
Chest tubes can also be placed using a trocar, which is a pointed metallic bar used
to guide the tube through the chest wall.
This method is less popular due to an increased risk of iatrogenic lung injury.
Placement using the Seldinger technique, in which a blunt guidewire is passed
through a needle (over which the chest tube is then inserted), has been described.
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Functionality of chest tube
Continuous bubbling in the bottle
Look for oscillations
o Oscillation is the proof of functionality not bubbling It may not be present
in most patients
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Complications
Technical
o Incorrect positioning of the tube, which causes ineffective drainage.
o Intermittent tube blockage from clotted blood, pus, or debris
Insertion related
o Pain
o Solid organ Puncture
Lung (commonest), heart, spleen, liver, stomach, colon, and diaphragm
o Bleeding and hemothorax
Commonly from intercostal artery perforation but can also be from
perforation of major vascular structures such as the aorta or
subclavian vessels
o Intercostal Neuralgia
From trauma to the neurovascular bundles
o Subcutaneous emphysema
Position related
o Mal-position
o Re-expansion pulmonary edema (RPE)
Usually arises after rapid reexpansion of a lung that has been collapsed
for at least three days
Patients developing RPE typically present soon after chest tube
placement with cough, dyspnea, and hypoxemia, but the clinical
presentation can be delayed for up to 24 to 48 hours.
Infection
o Drainage site infection
o Pneumonia
o Empyema
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Managing initial drainage: amount should be assessed on a regular basis (hourly, in
the setting of trauma).
o An immediate drainage of 20 mL/kg or the accumulation of >3 mL/kg per
hour of blood an indication for thoracotomy to identify and manage
thoracic vascular injury
o To minimize the likelihood of developing RPE, limit initial fluid drainage to 1.5
liters by clamping the chest tube and waiting at least one hour before
draining additional fluid.
Tube:
o If a closed-suction system becomes disconnected:
The tube should be cleaned with an antiseptic and the tubing
reconnected.
If a new closed-suction apparatus is immediately available, the new
one should be connected
The chest tube should not be clamped to avoid tension
pneumothorax.
o If the chest tube is no longer draining and there is a suspicion that it is full of
clot or debris, the tube cleared of obstruction by other maneuvers
Hold the chest tube near its insertion site with the non-dominant hand
Compress the tube between the first and second fingers of the
dominant hand Gently pull toward the drainage system
If stripping the tube once or twice does not clear the tube
Twisting the tube 360 degrees
Pulling the tube out 1 to 2 cm
Passing a sterile endotracheal tube suction catheter
Injecting a small volume of sterile saline with a few drops of
povidone-iodine
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Chest Tube Removal
Technique:
o Two people may need to participate so that one can instruct the patient and pull
the tube while the other can quickly occlude the insertion site.
o Cut the skin sutures, using sterile technique.
o Have additional strong nylon or silk sutures ready in case additional sutures are
required to seal the hole.
o Instruct the spontaneously breathing patient to perform a forced Valsalva
maneuver or to inhale to total lung capacity after a full exhalation.
If the patient is being fully mechanically ventilated, removal should be
timed to end-expiration.
o One operator can pull the tube out while the other quickly occludes the site with
gauze, adds additional sutures to close the opening, and secures the site with a
pressure dressing.
o A chest radiograph 12 to 24 hours after removal is recommended; this
should be done sooner if there is clinical suspicion of a residual air leak or a new
pneumothorax.
o It will take about 3 to 4 weeks for your incision to heal completely
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3. 5. Needle Thoracostomy
Introduction……………………..……………………..158
Equipment………………………………..……………..158
Indications and Contraindications…………….159
Techniques……………………………………………….159
Complications………………………..…………………159
Aftercare………………..………………..………………160
Introduction
Equipment
A 14- or 16-gauge needle (an over-the-needle catheter is best)
o 8-cm needles are more successful than 5-cm
needles but increase the risk of injury to
underlying structures
Transfusion or LP set needle could also work
Sterile gown, mask, gloves
Cleansing solution such as 2% chlorhexidine solution
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Indication and Contraindication
Technique
We perform this on the affected side in the midclavicular
line through the second intercostal space with one of any
readily available kits.
o The angiocatheter from the kit is placed first, which
allows for immediate decompression.
Complications
Because these catheters are small-bore thin-walled catheters
o They are prone to kinking
o They may not completely relieve a tension pneumothorax
They can also be dislodged
o Leading to reaccumulation of air and recurrent tension pneumothorax.
o Immediately following needle decompression, a standard thoracostomy tube
should be placed
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Others:
o Lung laceration, bleeding, infection, air embolism
o Intercostal neuralgia due to injury of the neurovascular bundle
Aftercare
Chest x-ray should be done to confirm expansion of the lung and proper placement of
the chest tube and insert a chest tube as soon as possible
3.6. Tracheostomy
Introduction………………………………….………….161
Types of Tracheostomy…………………...……….162
Functions of Tracheostomy……………………….162
Indications……………………..…………………………163
Contraindications………………………….………….163
Equipment………………………………………………..164
Techniques………………………………….…………..165
Post- Op Care…………………………………………..165
Decannulation………………………………………….166
Complications…………………………………………..167
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Introduction
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Types of Tracheostomy
Emergency tracheostomy
Elective or tranquil tracheostomy
Permanent tracheostomy
Percutaneous dilatational tracheostomy
Mini tracheostomy (cricothyroidotomy)
Based on level: Thyroid isthmus lies against II, III
High and IV tracheal rings
o Above the level of thyroid isthmus
o Only indication - carcinoma of larynx
Mid
o Preferred one; through the II or III tracheal rings
o Entail division of the thyroid isthmus or its retraction upwards or downwards
to expose this part of trachea.
Low
o Below the level of isthmus.
o Trachea is deep at this level and close to several large vessels; also, there are
difficulties with tracheostomy tube which impinges on suprasternal notch
Functions of Tracheostomy
Alternative pathway for breathing
Improves alveolar ventilation in cases of respiratory insufficiency
Protects the airways by using cuffed tube, tracheobronchial tree is protected against
aspiration of:
o Pharyngeal secretions
o Blood, as in hemorrhage from pharynx, larynx or maxillofacial injuries
Permits removal of tracheobronchial secretions
Intermittent positive pressure respiration (IPPR)
o If IPPR is required beyond 72 hours, tracheostomy is superior to intubation.
To administer anesthesia
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Indications
1. Respiratory obstruction.
Infection
Trauma
Neoplasms of larynx, pharynx, upper trachea, tongue and thyroid
Foreign body
Laryngeal edema
Congenital anomalies such as Laryngeal web, cysts, tracheoesophageal fistula
Bilateral choanal atresia
2. Retained secretions.
Inability to cough from coma of any cause or spasm or paralysis of respiratory
muscles
Painful cough from chest trauma, pneumonia or multiple rib fractures
Aspiration of pharyngeal secretions due to bulbar polio, polyneuritis, bilateral
laryngeal paralysis
3. Respiratory insufficiency: Chronic lung conditions
Contraindications
Emphysema
Chronic bronchitis
Bronchiectasis
Atelectasis
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Relative contraindications to percutaneous tracheostomy include:
Age under 15 years of age
Uncorrectable bleeding diathesis
Gross distortion of the neck from hematoma
Tumor
Thyromegaly
Scarring from previous neck surgery
Documented or clinically suspected tracheomalacia
Evidence of infection in the soft tissues of the neck
Obese and/or short neck which obscures landmarks
Inability to extend the neck because of cervical fusion
Rheumatoid arthritis, or other causes of cervical spine instability
Equipment
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Technique
Position: Supine with a pillow under the shoulders so that neck is extended
Inject anesthesia
A vertical incision in the midline of neck, extending from cricoid cartilage to just above
the sternal notch
o This is the most favored incision and can be used in emergency and elective
procedures.
o It gives rapid access with minimum of bleeding and tissue dissection
After incision, tissues are dissected in the midline. Dilated veins are either displaced or
ligated
Strap muscles are separated in the midline and retracted laterally.
Thyroid isthmus is displaced upwards or divided between the clamps, and suture-ligated
Trachea is fixed with a hook and opened with a vertical incision in the region of 3rd and
4th or 3rd and 2nd rings
Confirmation of trachea:
o 5 ml syringe containing 4 % Lignocaine taken, its needle inserted into trachea &
aspirated Air bubbles confirm presence of needle in trachea.
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Decannulation
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Complications
Acute/Immediate:
Postoperative hemorrhage
Aspiration of blood
Injury to recurrent laryngeal nerve
Injury to apical pleura (Pneumothorax)
Injury to oesophagus (May cause tracheoesophageal fistula)
Obstruction:
o Percutaneous tracheostomy tubes can become partially obstructed by the
posterior membranous trachea following initial placement
Intermediate Complications
Haemorrhage
Displacement of tube
o Due to use of improper size tube
Blocking of tube
o Due to excessive crusting/poor humidification
Subcutaneous emphysema and pneumothorax
o Due to imperfect positioning of fenestrated cannula and posterior wall
perforation
Tracheitis/Tracheobronchitis with crusting in trachea
Pulmonary infections
o Due to compromised airway defense mechanism
Wound infection & granulation
Chronic:
Haemorrhage
o Due to erosion of major vessels especially innominate or bracheocephalic
artery
Tracheal stenosis
o Due to tracheal ulceration and infection
Tracheoarterial fistula
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o Due to erosion of trachea by tip of the tube
Reduced phonation and Laryngeal stenosis
o Due to perichondritis of cricoids cartilage
Tracheoesophageal fistula Difficult decannulation
Keloid/Unsightly scar at tracheostomy site
Chest Tube
Needle Thoracostomy
Tracheostomy
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Part 4: Urology
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4.1. Bladder Outlet Obstruction
Case Discussion……………………………………………170
History…………………………………………………….....170
Differential Diagnosis…………………………………..171
Discussion of the Differential Diagnosis……….171
Complication……………………………………………….198
Case Discussion
62 years old male man present with frequency urgency nocturia hesitancy and dribbling of
2-year duration. He has no associated hematuria, fever or flank pain. On physical
examination he is well nourished and has stable vital sign and DRE of the prostate reveals
enlarged firm, smooth, well circumscribed prostate which is mobile on the underlying
rectal mucosa.
History
Differential Diagnosis
1. BPH 5. Bladder stone
2. Prostatic ca 6. Bladder neck stenosis
3. Bladder ca 7. Bladder neck hypertrophy
4. Urethral stricture 8. Neurogenic-bladder
Introduction
Benign enlargement of prostate which occurs after 50 years, usually between 60 and
70 years.
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Involves median and lateral lobe (transitional zone)
It involves adenomatous zone of prostate, i.e. submucosal glands
Epidemiology
BPH is one of the most common disease in ageing men
Prevalence increase with age being 50% in 6th decade of life and raising to 80% in
9th decade of life
Risk Factors
Increased Age
Family history
Presence of circulating androgen
Diet: conception of soya rich food decrease risk of BPH
Clinical Manifestation
History
Ask if there are lower urinary tract symptoms
Often mixed obstructive and irritative symptoms
Intensity of symptoms doesn’t relate to size of the prostate
Focus on
o Onset, duration and frequency of symptoms
o Precipitating factors
o Sexual history
o Medication intake:
Anti-histamines
Anti-hypertensives
Anti-cholinergic
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Tricyclic antidepressants
o Previously attempted Rx
Assess severity of symptoms using International prostate symptom score
Physical examination:
Focus on
o Suprapubic palpation for distension or tenderness
o Palpation of kidney for possible hydro nephrotic kidney
o Sign of anemia
o DRE: assesses the prostate for
Size Measure (by finger) & approximate it if reachable
Contour Medial sulcus
Consistency Nodules
Fixity
Possible findings
Enlarged smooth firm and well-defined prostate – BPH
Enlarged nodular hard irregular prostate which may be fixed to
rectal mucosal – Prostatic ca
Investigation
Urine analysis Acid phosphatase
Urine culture Prostate specific antigen (PSA)
Abdominopelvic US Renal function test
Transrectal US (most sensitive) Serum electrolyte
Cystoscopy Urodynamics(Optional)
Management
Urethral catheterisation for Patient with acute retention
Medical management.
o Alpha blockers such as terazosin, doxazosin, tamsulosin, and alfluzasin
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Inhibit smooth muscle contraction of prostate reduce the
bladder neck resistance so as to improve the urine flow.
o 5-Alpha reductase inhibitors such as finasteride and dutasteride.
Inhibits conversion of testosterone to dihydro-testosterone.
Effective in bigger prostates (above 50gms).
Surgical management
o Indications for Surgery
Moderate and severe LUTS according to IPSS
Failed medical treatment
Acute retention of urine.
Chronic retention of urine with residual urine more than 200 ml.
Complications like hydroureter, hydronephrosis, stone
formation, recurrent infection, bladder changes.
Haematuria.
o TURP: Possible complications include:
Significant hematuria (temporary), urethral stricture, retrograde
ejaculation and subsequent infertility, sexual dysfunction
(occasionally), or even urinary incontinence after the procedure
Transurethral resection syndrome, caused by absorption of the
hypotonic irrigating solution that is infused into the prostatic
venous system during the procedure. This can cause
hypervolemia and hyponatremia, which leads to confusion, visual
disturbances, and cardiac arrhythmias.
o Open prostatectomy is used when the prostate is too large (over 100
grams) to remove transurethrally.
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4.1. 2. Prostatic Cancer
Introduction………………………………………….175
Epidemiology………………………………………..175
Risk factors…………………………………………..176
Clinical Manifestations………………………….176
Investigation…………………………………………176
Staging………………………………………………….177
Management………………………………………..179
Introduction
The most common malignant tumour in men over 65 years.
Occurs in peripheral zone in prostatic gland proper, i.e. commonly in posterior
lobe.
o So, prostatectomy for BPH does not confer protection against
development of carcinoma prostate
Incidence of prostate cancer in men over 80 years is 70%.
Histology is an adenocarcinoma
Epidemiology
Grading of carcinoma is based on dedifferentiation as proposed by Gleason.
Prostate cancer is the second most common cancer diagnosed in men and fifth
leading cause of cancer death worldwide.
Incidence of prostate cancer in men over 80 years is 70%.
African Americans men have higher incidence rate and more aggressive type of
prostate cancer
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Risk Factors
Age
Family history
Life style: high fat food
Obesity
Clinical Manifestations
History:
Commonly asymptomatic
Bladder outlet obstruction with possible obstructive and irritative symptoms
Haematuria
Pelvic pain, back pain, arthritic pain in sacroiliac joint— features of secondaries
Features of renal failure
Features of anemia
Physical examination:
On per rectal examination, prostate feels hard, nodular, irregular often with loss of
median groove
Patients with advanced diseases may have
o Weight loss
o Bony tenderness
o Lower extremity lymph edema
o Adenopathy
o Over distended bladder
Investigations
PSA level Plain X-ray, KUB
Acid phosphatase Trans rectal ultrasound (TRUS)
Hg% and peripheral smear Trans rectal prostatic biopsy
Liver function test CT and MRI for staging
Rena function test
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Staging
<20
≥20
Any value
Prognostic stage groups
T N M PSA Grade Group Stage
group
cT1a-c, cT2a N0 M0 <10 1 I
pT2 N0 M0 <10 1 I
cT1a-c, cT2a, pT2 N0 M0 ≥10 <20 1 IIA
cT2b-c N0 M0 <20 1 IIA
T1-2 N0 M0 <20 2 IIB
T1-2 N0 M0 <20 3 IIC
T1-2 N0 M0 <20 4 IIC
T1-2 N0 M0 ≥20 1-4 IIIA
T3-4 N0 M0 Any 1-4 IIIB
Any T N0 M0 Any 5 IIIC
Any T N1 M0 Any Any IVA
Any T Any N M1 Any Any IVB
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Management
Management depends on the tumour grade, stage and the life expectancy of the
patient according to age and comorbidities
Options include
1. Watchful waiting 4. Radiotherapy
2. Active surveillance 5. Androgen deprivation
3. Radical prostatectomy therapy
Local disease
o Radical prostatectomy o Androgen deprivation
o Radical radiotherapy therapy
Advanced diseases
o Palliation therapy
o hormonal ablation
Surgical Bilateral surgical orchiectomy
Pharmacological luteinizing hormone-releasing hormone
agonist, antiandrogens, such as flutamide and cyproterone.
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Introduction
Many bladder cancer patients survive but they experience multiple recurrences.
o As a consequence, there are a relatively large number of people alive
with a history of bladder cancer.
o In middle-aged and older adult men, bladder cancer is the second
most prevalent malignancy after prostate cancer
Types
Primary:
a. Transitional cell carcinoma (90%);
b. Squamous carcinoma arising in an area of metaplasia (7%);
c. Adenocarcinoma (uncommon, but may occur in urachal remnants)
(2%);
d. Sarcomas (rare).
Secondary: direct invasion from adjacent tumours, i.e. colonic, renal,
ovarian, uterine, prostatic tumours.
Epidemiology
Bladder cancer is the most common malignancy involving the urinary system
The ninth most common malignancy worldwide
United States and Western Europe:
o Urothelial (previously known as transitional cell) carcinoma is the
predominant histologic type (90%)
Other areas of the world, such as the Middle East:
o Non-urothelial histologies are more frequent Schistosomiasis
Typically diagnosed in older individuals
o Median age at diagnosis of 69 years in men and 71 in women
o The age of onset is younger in current smokers than in never-smokers
o Rarely, in children and young adults, where it usually presents with low-
grade, non-invasive disease
Environmental exposures account for most cases of bladder cancer.
o "Field cancerization"
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The surface epithelium (urothelium) that lines the mucosal surfaces of
the entire urinary tract is exposed to potential carcinogens that are
either excreted in the urine or activated from precursors in the urine
by hydrolyzing enzymes.
This effect is one hypothesis to explain the multifocal occurrence that
is a characteristic feature of urothelial carcinomas of both the urinary
bladder and the upper urinary tract.
o Monoclonality hypothesis
In the majority of cases, multifocal urothelial carcinomas are
monoclonal.
This supports their presumed origin from a single genetically altered
cell, which then spreads through the urothelium via intraluminal
seeding or intraepithelial migration
Risk Factors
Established:
Cigarette smoking:
o The extent of smoking appears to be related to the aggressiveness of bladder
cancer:
Heavy smokers (≥30 pack years) are more likely to have a high-grade
tumor and to have muscle invasive disease at their original
presentation compared with non-smokers
o Smoking cessation Smoking cessation decreases but does not eliminate
the increased risk of bladder cancer
o Secondhand smoke Exposure to secondhand smoke in women appears to
be a risk factor for the development of bladder cancer
Occupational carcinogen exposure:
o Metal workers o Leather workers
o Painters o Textile and electrical
o Rubber industry workers workers
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o Miners o Excavating-machine
o Cement workers operators
o Transport operators o Paints, plastics or hair dyes
Drinking water:
o Trihalomethanes (THMs) are formed as a by-product when chlorine or
bromine is used to disinfect water for drinking and may have adverse health
effects at high concentrations.
o High concentrations of arsenic in drinking water and the subsequent
development of bladder cancer
Miscellaneous:
Chronic Cystitis:
o Recurrent or chronic bladder infections and those who have an ongoing
source of bladder inflammation like prolonged indwelling catheters in the
setting of
Spinal cord injury
Have a higher risk of bladder cancer
Bladder calculi
compared with the general population
Neurogenic bladder
o In this setting, there is a substantially higher incidence of non-urothelial
cancers, especially squamous cell carcinoma
o Leads to Cancer by:
Repeated chronic irritation
Obstructive uropathy Bacterial superinfection Production of
nitrosamines in the acidic urine Induction of bladder cancer
Inflammatory cells ROS
HPV:
o High risk serotypes of HPV, especially HPV 16
Upper urinary tract cancer
o Urothelial cancers of the renal pelvis and ureter are thought to be due to the
same etiologic factors as urothelial cancer of the bladder
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o Patients with urothelial cancer of the upper urinary tract are at high risk for
the subsequent development of urothelial cancer of the urinary bladder as
well as contralateral upper urinary tract malignancy
Bladder augmentation
o Augmentation cystoplasty is occasionally used to treat neurogenic bladder,
and may also be undertaken if the bladder does not develop to a sufficient
size to allow for continence
o Patients who undergo a bladder augmentation procedure (including both
ileocystoplasty and gastrocystoplasty) appear to be at increased risk for the
subsequent development of urothelial cancer.
o The cumulative risk is estimated to be approximately 1 percent, with a latent
period of less than 20 years
o These cancers may arise in the residual bladder urothelium or in the intestinal
mucosa of the augmented bladder.
o Tumors have included urothelial carcinomas, adenocarcinomas, and at least
one case of signet cell carcinoma
o Screening: annual cystoscopy beginning 10 years after the bladder
augmentation
Iatrogenic:
Radiation therapy
Cyclophosphamide:
o Acrolein, a urinary metabolite of cyclophosphamide, is thought to be
responsible for both hemorrhagic cystitis as well as bladder cancer
o The uroprotectant mesna inactivates urinary acrolein
Analgesics:
o has been linked to an increased risk of urothelial carcinoma, particularly of
the renal pelvis
Genetics:
High risk: affected relatives were diagnosed before age 60 years and never-smokers
P53 and RB mutations
Protective:
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Clinical Manifestations
An increase in total fluid intake may dilute excreted urinary carcinogens and reduce
contact time with the urothelium.
Delayed Diagnosis due to:
o Similarity of the symptoms to those of benign disorders (urinary tract
infection, cystitis, prostatitis, passage of renal calculi)
o Symptoms are often intermittent
History:
Hematuria: intermittent, gross, painless, and present throughout micturition.
The point at which gross hematuria is noted during urination can be helpful in localizing its source:
o Hematuria occurring primarily at the beginning of urination urethral source.
o Blood that is only noticed as a discharge between voiding or as a stain on
undergarments, while the voided urine itself appears clear the urethral meatus or the
anterior urethra.
o Terminal hematuria, with blood appearing towards the end of voiding the bladder neck or
prostatic urethra.
o Hematuria occurring throughout voiding anywhere in the urinary tract, including the bladder,
ureters, or kidneys.
Initial symptoms:
Painless hematuria: Commonest
Irritative voiding symptoms (frequency, urgency, dysuria)
Metastasis
Autopsy is rare: most become symptomatic eventually
Pain:
o Usually the result of locally advanced or metastatic tumors.
o Its distribution is related to the size and location of the primary tumor or its
metastases
Flank pain may result when a tumor obstructs the ureter at any level (bladder, ureter, or renal pelvis).
o Usually is associated with muscle invasive disease or large noninvasive tumors at the
ureteral orifice
Suprapubic pain is usually a sign of a locally advanced tumor that is either directly invading the
perivesical soft tissues and nerves or obstructing the bladder outlet urinary retention.
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Hypogastric, rectal, and perineal pain can be signs of disease invading the obturator fossa, perirectal
fat, presacral nerves, or the urogenital diaphragm.
Abdominal or right upper quadrant pain may signal the presence of abdominal lymph node or liver
metastases.
Bone pain may indicate the presence of bone metastases.
Significant and persistent headache or disordered cognitive function may suggest the presence of
intracranial or leptomeningeal metastases
Voiding symptoms
Storage symptoms are most common in patients with carcinoma in situ (CIS) of the
bladder
May also result from:
o Functional decrease in the bladder capacity
o Detrusor overactivity
o Invasion of the trigone
o Obstruction of the bladder neck or urethra
Irritative voiding symptoms:
o Eg: daytime and/or nocturnal frequency, urgency, dysuria, or urge
incontinence
o Occur in approximately one-third of patients.
o The complex of dysuria, frequency, and urgency in particular is highly
suggestive of bladder CIS.
Obstructive voiding symptoms:
o Less common and may be due to tumor location at the bladder neck or
prostatic urethra.
o Symptoms include straining, an intermittent stream, nocturia, decreased
force of stream, and a feeling of incomplete voiding.
o On occasion, gross hematuria may result in "clot retention”.
Constitutional symptoms:
Symptoms such as fatigue, weight loss, anorexia, and failure to thrive are usually
signs of advanced or metastatic disease and denote a poor prognosis.
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In rare cases, patients may have constitutional symptoms due to renal failure caused
by bilateral ureteral obstruction
Physical Examination:
Must include digital rectal examination in men and a bimanual examination of the vagina and rectum
in women.
Although the physical examination is unremarkable in most patients, abnormal findings that can be
seen include the following:
o A solid pelvic mass may be felt in advanced cases.
o Induration of the prostate gland can sometimes be felt on digital rectal examination if the
bladder cancer involves the bladder neck and Invades the prostate.
o An attempt to palpate the base and lateral walls of the bladder should be made, looking for
induration or fixation.
o Inguinal adenopathy can be present, although the inguinal region is not a common site of node
metastases
o Nodularity in the periumbilical region can be seen in advanced lesions involving the dome of the
bladder. This is often seen with urachal cancers, which typically are adenocarcinomas rather than
urothelial tumors
Abdominal examination may reveal the presence of substantially enlarged paraaortic lymph nodes or
hepatic metastases
Investigation
Urinalysis:
Include a microscopic and gross examination as well as a dipstick chemical test.
Nonrefrigerated urine should be examined within 30 minutes of collection.
The average individual excretes approximately 30,000 red blood cells (RBCs) per
hour:
o Equates to approximately 1 RBC per high-power field (HPF) on microscopic
examination
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o Hematuria is usually not considered significant unless there are more than 3
RBCs per HPF.
Color: Urinary pigments that can mimic hematuria include:
o Betalain contained in beets (beeturia)
o Phenazopyridine, a urinary analgesic
o Vegetable dyes
o Urates
o Free myoglobin or hemoglobin
o Serratia marcescens
o Phenolphthalein, which used to be a common component of many over-
thecounter laxative
Specific gravity
o Affects the stability of white blood cells or RBCs
o When the urinary flow rate is high and the urine is very dilute RBCs are
lysed and therefore will not be present on microscopic examination, even in
the presence of pathology.
Cystoscopy:
The gold standard for the initial diagnosis and staging of bladder cancer.
Any visible tumor or suspicious lesion seen at the initial (diagnostic) cystoscopy:
o Do biopsy or resect transurethrally to determine the histology and depth of
invasion into the submucosa and muscle layers of the bladder
In patients who presented with a positive urine cytology and whose initial
cystoscopy showed no visible tumor (or suspicious lesion) within the bladder:
o Biopsy of apparently normal appearing urothelium, prostatic urethra, and
selective catheterization of the ureters/renal pelvis with urine specimens for
cytology from the upper tract is required.
For patients with documented high-risk disease confirmed on a diagnostic
transurethral resection of bladder tumor (TURBT);
o Repeat resection may be indicated to eliminate the risk of understaging
Procedure:
o Bimanual exam under ansthesia
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o Insert cystoscope and take urine sample for cytology
o Irrigate the bladder with sterile saline Visualize
Cytology:
Specificity >98 but poor sensitivity for low grade tumors
Urine biomarkers
Abdomino-pelvic CT with and without contrast:
Should include delayed images to identify defects in the collecting system
CT may demonstrate:
o Extravesical extension
o Nodal involvement in the pelvis or retroperitoneum, visceral, pulmonary, or
osseous metastasis
o Tumor involvement or obstruction of the upper urinary tract
Disadvantages:
o It may miss tumors <1 cm in size, particularly those in the bladder trigone or
dome
o It cannot differentiate depth of bladder-wall invasion (ie, mucosal versus
lamina propria or muscularis propria)
o Difficult to distinguish inflammatory or iatrogenic edematous
changes from true extravesical tumor extension
o Identification of nodal involvement is relatively low
MRI:
Gadolinium-enhanced MRI may be superior to CT to detect superficial and multiple
tumors, extravesical tumor extension, and surrounding organ invasion
It is difficult to tolerate by claustrophobic patients and cannot be used in patients
with pacemakers or other metallic foreign bodies.
Ultrasonography:
US can
o Confirm the presence of a soft tissue mass
o Evaluate the upper tracts for renal parenchymal disease
o Detect hydronephrosis
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o To differentiate a non-radiopaque stone from a soft tissue mass by difference
in echogenicity
But usually cannot determine depth of invasion, extravesical extension, or nodal
status.
Metastatic:
Commonly to lung, liver and bone
Imaging of the chest for all patients with muscle-invasive bladder cancer
o CXR: insensitive for lesions <1 cm
o Metastatic lesions are typically non-calcified soft tissue densities
Bone scan and imaging of the brain are reserved for symptomatic patients
Staging
Clinical:
o From bimanual exam and imaging studies as well as pathology results from
the cystoscopic biopsy or TURBT
o Jewett, strong and marshall system
o Broadly classified in to
1. Non-muscle invasive bladder cancer
2. Muscle invasive bladder cancer
3. Carcinoma in situ
Pathologic:
o TNM system, which is based upon pathologic studies of cystectomy
specimens
o This staging system is applied to urothelial carcinoma, squamous cell
carcinoma, undifferentiated carcinoma, and adenocarcinoma arising in the
bladder.
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Table 4.2: Bladder Cancer TNM staging AJCC UICC 2017
Primary Tumor (T)
T category T criteria
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Ta Noninvasive papillary carcinoma
Tis Urothelial carcinoma in situ: "Flat tumor"
T1 Tumor invades lamina propria (subepithelial connective
tissue)
T2 Tumor invades muscularis propria
pT2a Tumor invades superficial muscularis propria (inner half)
pT2b Tumor invades deep muscularis propria (outer half)
T3 Tumor invades perivesical soft tissue
pT3a Microscopically
pT3b Macroscopically (extravesical mass)
T4 Extravesical tumor directly invades any of the following:
Prostatic stroma, seminal vesicles, uterus, vagina, pelvic wall,
abdominal wall
T4a Extravesical tumor invades directly into prostatic stroma,
uterus, vagina
T4b Extravesical tumor invades pelvic wall, abdominal wall
Regional lymph nodes (N)
N category N criteria
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N2 Multiple regional lymph node metastasis in the true pelvis
(perivesical, obturator, internal and external iliac, or sacral
lymph node metastasis)
N3 Lymph node metastasis to the common iliac lymph nodes
Distant metastasis (M)
M category M criteria
M0 No distant metastasis
M1 Distant metastasis
M1a Distant metastasis limited to lymph nodes beyond the
common iliacs
M1b Non-lymph-node distant metastases
Prognostic stage groups
T N M Stage group
Ta N0 M0 0a
Tis N0 M0 0is
T1 N0 M0 I
T2a N0 M0 II
T2b N0 M0 II
T3a, T3b, T4a N0 M0 IIIA
T1-T4a N1 M0 IIIA
T1-T4a N2, N3 M0 IIIB
T4b Any N M0 IVA
Any T Any N M1a IVA
Any T Any N M1b IVB
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Management
Non-invasive tumour
o For patients with non-muscle invasive bladder cancer, conservative
management may allow the preservation of a functional bladder based upon
transurethral resection of bladder tumor (TURBT), potentially combined with
adjuvant intravesical therapy.
o However, this approach must be balanced against the risk of recurrence or
progression
o Intravesical chemotherapy including doxorubicin, mitomycin and adriamycin
can be used
o BCG Immunotherapy
Invasive bladder tumour
o Surgery
Radical cystectomy
Partial cystectomy
o The only potentially curative treatment for MIBC is radical cystectomy with
regional lymphadenectomy
o Radiotherapy
Indications for cystectomy:
o Any of the following represents a strong indication to proceed to cystectomy:
Muscle invasive bladder cancer
T1 tumors with lymphovascular invasion
Variant histologies, including micropapillary transitional cell
carcinoma, sarcoma, squamous cell carcinoma, or adeno-
carcinomas
T1, grade 3 tumors that were incompletely resected
Prostatic duct/acinar CIS
Women with bladder neck and/or urethra CIS
o Any of the following represents a relative indication to proceed. However,
decisions regarding cystectomy should be individualized based on the surgical
risks of the patient:
P a g e 192 | 548
Ta or T1 high-grade plus CIS; T1b tumors (ie, deep involvement of
lamina propria)
Persistent T1, grade 3 tumors identified on reresection
Recurrent or persistent disease within 6 to 12 months of initiating
treatment with BCG
Large-volume Ta, low-grade disease
o Cystectomy is also indicated for bladder cancer patients crippled by
symptoms related to bladder pathology (eg, intolerable urinary frequency,
pain, incontinence, and hemorrhage) that cannot be adequately managed
medically.
Radical cystectomy:
o Entails removal of the bladder, adjacent organs, and regional lymph nodes.
o In men, radical cystectomy generally includes removal of the prostate and
seminal vesicles as well as the urinary bladder.
o In women, removal of the uterus, cervix, ovaries, and anterior vagina is
usually performed en bloc with the bladder.
o Patients who have undergone radical cystectomy for urothelial bladder cancer
are at risk for the development of distant metastases as well as second
primary urothelial tumors in the renal pelvis, ureters, or urethra
Urinary diversion:
o Removal of the bladder requires that the urinary flow be redirected, which
may take one of several forms:
o A non-continent cutaneous diversion, in which the urine flows from the
ureters through a segment of bowel (usually ileum, termed an ileal conduit)
to the skin surface as a stoma
Then it is collected in an external appliance.
o A cutaneous continent reservoir may be constructed to avoid the need for
an external appliance.
The patient self-catheterizes at regular intervals to empty the
reservoir.
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o An orthotopic neobladder may be formed from a segment of bowel and
attached to the urethra, enabling the patient to void through the urethra.
Continent diversions may facilitate maintenance of patient
perceptions of quality of life and self-image and increase their
acceptance of radical cystectomy.
Metastatic Disease:
o Advances in the management of advanced urothelial (transitional cell)
carcinoma using cisplatin-based combination chemotherapy led to
improved survival
o But there was only limited further progress until the development of
checkpoint inhibition immunotherapy
Pharmacological luteinizing hormone-releasing hormone
agonist, antiandrogens, such as flutamide and cyproterone.
Introduction………………………………………..195
Etiology……………………………………………….195
Clinical Manifestation………………………….196
Investigation………………………………………..196
Management……………………………………….197
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Introduction
Etiology
Congenital
Inflammatory
a. Post-gonococcal:
It is most common 70%
Gonococcal stricture occurs one year after infection
Retention develops only 10-15 years later
Common in the bulb of urethra especially in the roof
o Here multiple strictures are common
o Proximal stricture is the narrowest
b. Tuberculous
c. Other infection (urethritis
Traumatic:
Bulbous (due to a straddle type of trauma)
Membranous (due to pelvic fractures)
Post instrumentation:
Catheter Dilator
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Cystoscope
Postoperative:
Prostate surgery (4%)
Clinical Manifestations
History
Voiding symptoms especially poor urinary stream
Irritative symptoms such as dysuria and frequency
retention and often with overflow
Physical examination
Perineal hematoma
High riding prostate Sign indicating urethral
injury after trauma
Blood at the meatus
Investigation
Urine analysis
Urine culture
Urethroscopy
Urethrography
o Retrograde retrogram must be done before attempting to catheterize the
patient
Urodynamic studies
Renal function test
IVP
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Management
Introduction
Neurogenic bladder is the loss of normal function of the bladder secondary to
damage to part of the nervous system
Causes include:
o Traumatic spinal cord injury o Multiple sclerosis,
o Spinal cord neoplasm o Cerebral palsy
o Spina bifida o Parkinson disease
o Stroke
Clinical Manifestations
History:
Urinary incontinence Frequent UTI
Urinary retention Urinary urgency
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Urinary frequency.
Physical examination:
Neurologic examination including:
o Anal tone
o Bulbocavernous muscle reflex
Investigation
Tests to locate the neuroanatomic lesion (CT and MRI of brain, spine)
Urine analysis and urine culture
Cystoscopy To rule out other
Post void residual urine volume (PVR) causes of BOO
Ultrasound
Management
Behavioural therapy
Medical management
o Anticholinergic therapy o Prophylactic antibiotics
Surgical management
o Bladder augmentation o Botulinum toxin Injection
Case Discussion
A 60 years old man present to emergency department with sudden onset, sever flank pain
which radiate to his back. He has no associated symptoms and physical examination was
unremarkable except that he was changing his position frequently due to the pain.
Introduction
Formation stone in urinary tract
Include nephrolithiasis, ureterolithiasis and bladder stones
Cause include genetic and environmental factors
Types of stone
o Oxalate stones (75%) o Cystine stones (2%)
o Phosphate stones (10-15%) o Xanthine stones
o Urate stones
o Most stones are mixed and contain organic matrix
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Epidemiology
Risk Factors
Family history or previous history of urolithiasis
Dietary risk factors
o Vitamin A deficiency o Diet rich in protein
o Dehydration
Environmental
o Hot climate
Inadequate urinary drainage and urinary stasis
Infection
Medical history
o Hyperparathyroidism o HTN
o Gout o Obesity
o Hyperoxaluria o Immobilisation from any
o Cystinuria (Autosomal cause, e.g. paraplegia
recessive) o Medication intake
o Low urinary citrate level
Surgical history such as Gastric by-pass surgery
History
Asymptomatic
Pain: depend on position of the stone
o Renal stone: acute renal colic, sudden onset of severe pain originating in
the flank radiating anteriorly and inferiorly
o Stone obstructing ureteropelvic junction:
Mild to severe flank pain without radiation
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Irritative voiding symptoms
Suprapubic pain
o Stone within ureter:
Abrupt onset of sever, colicky pain in the flank and ipsilateral lower
abdomen radiation to testicle or vulvar area
Intense nausea with or without vomiting
o Upper ureteral stones: pain radiates to flank or lumbar
o Mid ureteral stone: pain radiate anteriorly and caudally
o Stone in the bladder:
Mostly asymptomatic Positional urinary retention
Hematuria: gross or microscopic
Nausea and vomiting:
o As a result of compression of renal capsule
Fever is usually absent in uncomplicated urolithiasis
Physical Examination
Complications
Hydronephrosis Renal loss due to long standing
Abscess formation obstruction
Urinary fistula formation Increased risk of small cell
Ureteral scarring and stenosis carcinoma
Ureteral perforation
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Differential Diagnosis
Pyelonephritis RCC
Pyonephrosis Bladder ca
Renal trauma
Pelvic inflammatory diseases
Renal TB
Investigations
Urine analysis, urine culture
RFT, serum electrolyte, parathyroid hormone and phosphorus.
CBC
CRP
Ultrasound
o Detect stone in kidney and bladder
o Assess obstructive changes
o Assess parenchyma loss
Plain abdominal x ray (KUB)
o Detect up to 90% of the stones
IVP
CT scan
Management
Expectant treatment
o For stone <5mm
Extracorporeal shock wave lithotripsy (ESWL)
Ureteroscopy
Percutaneous nephrolithotomy (PCNL)
Open surgery rarely required (<5%); if the non-invasive options are available
Medical therapy
o Dissolution of calculi through alkalization of urine
For uric acid and cysteine stones
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o Chemoprophylaxis
Limitation of dietary component
Stone formation inhibitors (intestinal calcium binders)
Augmentation of fluid intake (goal being a urine output of 2L
per 24 hours)
Case Discussion…………………………………………203
Introduction……………………………………………..204
Epidemiology…………………………………………….205
Risk factors………………………………………………..206
Clinical Manifestation………………………………..207
Differential Diagnosis…………………………………208
Investigation……………………………………………..208
Staging……….……………………………………………..209
Management……………………………………………..211
Case Discussion
A 48 years old women present with flank pain of 1-year duration. She also had fever weight loss
and night sweet of a month duration. She had no LUTS or hematuria and on physical
examination she was febrile and had right renal mass.
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Introduction
Renal Neoplasms:
Can be primary or secondary
o Secondary renal neoplasms are usually clinically insignificant and discovered
at postmortem examination
Primary:
o Arising from/within the renal cortex 80 to 85 %
o Transitional cell carcinomas of the renal pelvis approximately 8%
o Wilms' tumor 5 to 6 %
o Parenchymal epithelial tumors (oncocytomas, collecting duct tumors, and
renal sarcomas) occur infrequently
o Renal medullary carcinoma (seen in sickle cell disease) rare
RCC
It is an adenocarcinoma arising from renal tubular cells
The most common site is proximal renal tubule
RCC types:
Clear cell (75 to 85 percent of tumors)
o Sporadic deletion of chromosome 3p or associated with von Hippel-
Lindau disease
o Arise from the proximal tubule
o Macroscopically, they may be solid or less commonly, cystic
o Has abundant lipid and glycogen
Papillary (chromophilic) (10 to 15 percent)
o Originates from the proximal tubule
Type I: Typically presents as stage I or II disease Favorable
prognosis
Type II: Typically presents as stage III or IV disease Aggressive
poor prognosis
Chromophobe (5 to 10 percent)
o Lack abundant lipid and glycogen
o Originate from the intercalated cells of the collecting system
o Early presentation good prognosis
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Oncocytic (3 to 7 percent)
o Consist of a pure population of oncocytes, which are large well-
differentiated neoplastic cells with intensely eosinophilic granular
cytoplasm that is due to a large number of mitochondria
o Benign: well encapsulated, rarely invasive/ metastasize
o Originate from the intercalated cells of the collecting system
Collecting duct (Bellini's duct) (very rare)
o Younger patients
o Frequently aggressive
o They commonly present with gross hematuria
o Includes renal medullary carcinoma
< 5 % Unclassified
o Includes lymphomas, soft tissue sarcomas (eg, leiomyosarcoma,
liposarcoma) and carcinoids
o Translocation carcinomas:
o Fusion of the TFE3 gene to a number of other genes
o Occur at a younger age compared with other RCCs
Common in North America
Epidemiology
Men > than Females by 50%
6th – 8th decade (mean age is 64)
Early (<40) genetic
Extent:
o Localized 65% o Metastasis 16%
o Regional (LNs) 16% o Unstaged 3%
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Risk Factors
Established:
Smoking, HTN, Obesity
Acquired cystic disease:
o 35 to 50 percent of chronic dialysis patients RCC in 6%
Occupational Exposure:
o Cadmium o Petroleum by-products
o Asbestos
Analgesics:
o Aspirin o Acetaminophen
o NSAIDS
Cytotoxic chemotherapy in childhood
Chronic Hepatitis infection CKD RCC
Sickle cell disease
Stone
Genetics if:
o Young age
o Treated for previous RCC
o Strong family history (first degree relatives with a tumor, onset before the
age of 40, and bilateral or multifocal disease)
o Chromosome 3 abnormalities
o Inherited PKD.
Factors that modify risk:
DM
PKD
Dietary factors
o Nitrite from processed meat sources
Prior radiation therapy
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Clinical Manifestations
Differential Diagnosis
Pyelonephritis Adrenal tumour
Polycystic kidney disease Retroperitoneal tumour
Solitary cyst of kidney Bladder cancer
Investigation
Initially Abdominal US: criteria for a simple cyst
o The cyst is round and sharply demarcated with smooth walls
o There are no echoes within the cyst ("anechoic")
o There is a strong posterior wall echo, indicating good transmission through a cyst
If all of these criteria are fulfilled No further evaluation is needed
likelihood of a malignancy is extremely small
CT before and after injection of iodinated contrast
o Simple cyst: Bosniak category I
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Hairline thin wall (has a smooth appearance without a clearly
delineated wall)
Has no enhancement with intravascular contrast
Does not contain septa, calcification, or solid components
Has the density of water (less than 20 Hounsfield units)
o Malignancy: Bosniak category IV
Thickened irregular walls or septa and enhancement after
contrast
MRI: When,
o US and CT are non-diagnostic
o Radiographic contrast cannot be administered because of allergy or poor
renal function
o Identify the presence and/or extent of involvement of the collecting system
and/or inferior vena cava.
Biopsy:
o Mostly: Nephrectomy or partial nephrectomy
o Occasionally: biopsy of a metastasis.
o Percutaneous biopsy: more limited except for a small renal mass if there is a
high index of suspicion for a metastatic lesion to the kidney, lymphoma, or a
focal kidney infection.
Staging
Abdominal CT
Others:
o Bone scan: only in patients with bone pain and/or an elevated ALP
o Chest CT: pulmonary or mediastinal lymph node metastases.
o MRI: the inferior vena cava and right atrium involvement
o PET or PET/CT
Solid renal masses less than 3 cm were once thought to represent benign
adenomas; distinctions based upon size are no longer used.
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Then TNM Staging
P a g e 210 | 548
M category M criteria
M0 No distant metastasis
M1 Distant metastasis
Prognostic stage groups
T N M Stage group
T1 N0 M0 I
T1 N1 M0 III
T2 N0 M0 II
T2 N1 M0 III
T3 NX, N0 M0 III
T3 N1 M0 III
T4 Any N M0 IV
Any T Any N M1 IV
Screening:
Not recommended because of the low prevalence except for patients with:
o Inherited diseases like VHL syndrome and tuberous sclerosis.
o End-stage renal disease, who have been on dialysis for three to five years
or more.
o A strong family history of RCC
o Prior kidney irradiation.
Management
Localized disease:
This includes stage I, II, and III
Surgery is curative in the majority of patients
May require a radical nephrectomy or a partial nephrectomy
o To preserve renal parenchyma for appropriately selected patients
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Surgery may be carried out through:
o A conventional approach or
o A minimally-invasive approach such as laparoscopy
In carefully selected patients who present with a resectable primary tumor and
a concurrent single metastasis:
o Surgical resection of the metastasis, in conjunction with radical
nephrectomy, may be curative
Other ablative procedures for patients with relatively small renal masses who
are not surgical candidates:
o Cryotherapy
o Radiofrequency ablation [RFA]
Advanced Disease:
RCC is known to be chemo and radio resistant.
In general, systemic therapy (immunotherapy, molecularly targeted agents),
surgery, and radiation all may have a role depending upon
o The extent of disease
o Sites of involvement
o Patient-specific factors
The choice of treatment for patients with advanced disease should consider
prognostic risk factors
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4.4. Urologic Trauma
Case Discussion……………………………………….…..213
Introduction………………………………………….……..213
Epidemiology……………………………………….………214
History…………………….………………………….……….214
Physical Examination……………….………..…………215
Investigation…………………………………….………….216
Differential Diagnosis……………………………….….218
Discussion of the Differentials……………………..219
Management……………………………………………….229
Complications…………………………….………………..231
Case Discussion
A 20-year-old patient was apparently healthy 04 hours back at which time he sustained a motor
vehicle crush accident to his pelvis. He was a passenger sitting in the front seat and sustained
side impact vehicle collision. Since the accident he complains of abdominal pain and inability to
void. On his physical examination he has blood at the urethral meats, suprapubic tenderness
and high riding prostate on digital rectal exam.
Introduction
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Epidemiology
It may result in high morbidity if not properly identified and managed. The diagnosis
of genitourinary trauma typically relies on patient history, physical examination,
urinalysis, and imaging (CT, cystoscopy, retrograde urethrogram.
10% of the 2.8 million trauma patients hospitalized yearly in the US sustaining
genitourinary injuries
The majority of renal, bladder, and posterior urethral trauma is from blunt
mechanisms, most commonly motor vehicle collisions.
Most ureteral and anterior urethral injuries are iatrogenic
History
1) What is the mechanism of injury?
Blunt injuries vs. penetrating?
motor vehicle collision
o Speed of vehicle
o Crush or not: Crush injury to the pelvis- posterior urethral injury
Falls
o Height of fall o Landing condition
Gunshot injury
o Type of gun o Distance of shooting
Assaults: know type of weapon
Sports injury
History of instrumentation:
o TURP o Endoscopic surgery
o Radical prostatectomy
Self-inflicted: foreign body insertion may damage urethra
2) Chief complaint and associated symptoms
Hematuria
o Neither specific or sensitive in urologic trauma
o Seen in renal and bladder trauma
o In bladder trauma, 82% have this symptom
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o Clot in damaged kidney and maybe delayed as clot dislodges
Flank pain: renal trauma or if ureter has been ligated
Abdominal mass: urinoma
Abdominal pain
o Nonspecific in urologic trauma
Inability to void Perineal pain- urethral injury
Prolonged postoperative fever or overt urinary sepsis
Ileus – due to urine in peritoneal cavity in ureter injury
o Diffuse, persistent abdominal pain
o Nausea and/or vomiting
o Delayed passage of or inability to pass flats
o Inability to tolerate an oral diet
3) Previous medical history
History of Renal disease
4) Concomitant injury
Head injury: history of Loss of consciousness
Spinal cord injury: incontinence Fracture
5) Assess for complications
Bleeding Stricture and recurrent stenosis
Infection Urethro-cutaneous fistful
urinary fistula Impotence
hypertension Uroascites
Incontinence: common in bladder injury, very rare in urethral injury (2%)
Physical Examination
General appearance: in distress? Bleeding? Conscious?
Vital: look for hemodynamic instability and sepsis
Renal trauma:
Obvious penetrating trauma and bullet entry or exit at the lower thorax, upper
abdomen, flanks and back
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Flank tenderness Fractured ribs
Flank ecchymosis Meteiorism
Abdominal distension 24–48 hours after renal injury is probably as a result of
retroperitoneal hematoma implicating splanchnic nerves
Ureter injury:
Abdominal mass (urinoma)
Signs of ileus (abdominal distention)
Drainage of fluid from drains, abdominal wound or vagina
Bladder injury:
bruises over the suprapubic region
abdominal distention Abdominal Tenderness
Urethral trauma:
Posterior urethral trauma
o Blood at the urethral meats o Palpable pelvic hematoma
o Suprapubic tenderness o Perianal and suprapubic
o Palpable full bladder contusions
o Pelvic fracture
o DRE: “high-riding” prostate or a “butterfly” perineal hematoma
Anterior urethral trauma
o Blood may be present at the end of the penis and a hematoma around the
site of the rupture
o Tender perineum
o Scrotum swelling and a ‘butterfly wing’ pattern of bruising
Investigation
1) laboratory
Urine analysis
o For Hematuria; Gross or microscopic (> 5 rbc/ hpf)
Serial hematocrit
o For continuous follow up
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Creatinine measurement
o Indicates preexisting renal abnormality if increased (if taken within 1
hr of trauma)
2) Imaging
Ultrasound
o For initial evaluation of renal injury
o Can show laceration but can’t assess the renal function status
o Doppler ultrasound or ultrasound with contrast to determine blood
flow to the kidney
CT scan
o More accurately defines the location of injuries
o Easily detects contusions and devitalized segments
o Visualizes the entire retroperitoneum and any associated
hematomas, also arterial extravasations and pre-existing
abnormalities
IVP
o Should only be performed when CT scan is not available
o Can be used to confirm function of the injured kidney and presence of
the contralateral kidney.
o Can be used to diagnose ureteral injury
o Incomplete visualization of the entire ureter
o Ureteral deviation or o Urinary extravasation
dilation o Hydronephrosis.
MRI
o Accurate in finding perirenal hematomas, assessing the viability of
renal fragments, and detecting preexisting renal abnormalities
Failed to visualize urinary extravasation on initial
examination.
Not the first choice in managing the patient with trauma
Radionuclide scan
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o Helpful to document renal blood flow in the trauma patient with
severe allergy to iodinated contrast material
o In following up repair of renovascular trauma
CT urography
o Best study for detecting ureteral injuries
o Delayed ipsilateral nephrogram
o Lack of contrast in the distal ureter
o Contrast extravasation o Periureteral urinoma
o Hydronephrosis
Retrograde ureterogram
o Is the most sensitive radiographic test for ureteral injury.
o Most commonly used to diagnose initially missed ureteral injuries,
because it allows the simultaneous placement of a ureteral stent if
possible.
Cystography
o Very accurate (>90%) in bladder injury
o Can distinguish intraperitoneal from extra peritoneal rupture.
CT cystography
o Has the highest sensitivity
o Correctly assess other visceral injuries in a polytraumatized patient
o It has the drawback:
Of being expensive
It can’t not differentiate urine from ascites and also adequate distension
Extravasation of contrast material is an issue leading to high false
positive results
Retrograde urethrography: gold standard for urethral injury
Differential Diagnosis
Renal Injury Bladder Injury
Ureter Injury Urethral Injury
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Discussion of the Differentials
Epidemiology……………………………………………….219
Etiology………………………………………………………..219
Clinical Manifestation…………………………………..220
Investigation…………………………………………………220
Epidemiology
Kidney is the most commonly injured organ in the genitourinary system.
Seen in up to 5% of all trauma cases, and in 10% of all abdominal trauma cases.
Associated with young age and male gender with incidence of about 4.9 per 100,000
Etiology
Renal trauma is most often an acute condition caused by a blunt abdominal injury
and may, if severe, represent a urological emergency.
Blunt injury could be:
o Motor vehicle collision
o Falls
o Assault
o Sports injury
Renal trauma could occur following penetrating injuries: tend to be more severe and
less predictable.
o Stab wounds
o Gunshot wounds
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Clinical Manifestations
The classical symptoms of renal trauma are hematuria and pain in the affected
side following injury.
Associated symptoms
o Bruising o Hematoma
o Possible accompanying injuries
E.g., rib fracture with motion-dependent pain
o Meteiorism
Abdominal distension 24–48 hours after renal injury is probably as a
result of retroperitoneal hematoma implicating splanchnic nerves
o Flank tenderness o Abdominal tenderness
o Flank ecchymosis o Palpable mass
Patients may also be asymptomatic
Some may have nonspecific symptoms like nausea and vomiting in venous
occlusions.
Investigation
CT with IV contrast of the abdomen/pelvis
o Is used to assess renal and accompanying injuries or intra-abdominal fluid
retention.
Mild trauma generally only requires monitoring, while high-grade injury may
require emergency surgery and intensive care
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4.4.2. Ureteral Trauma
Epidemiology……………………………………………..222
Etiology………………………………………………………222
Clinical Manifestation………………………………..223
Investigation………………………………………………223
Epidemiology
Etiology
Penetrating stab and gunshot wounds and external injury from high-speed blunt
mechanisms contribute to the overall incidence; 95% are penetrating and 5%are
blunt injuries
External trauma
o Ureteral injuries are often subtle and clinicians must maintain a high index of
suspicion to prevent a delay in diagnosis and comorbidity.
o The presence of massive force injuries in the patient with blunt trauma
should increase the level of suspicion for ureteral injury.
Surgical Injury
o Any abdominopelvic surgical procedure, whether gynecologic, obstetric,
general surgical, or urologic, can potentially injure the ureter
Crushing from misapplication of a clamp
Ligation with suture
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Transection (partial and complete)
Angulation of the ureter with secondary obstruction
Ischemia from ureteral stripping
Resection of ureteral segment (recently one of the common causes
of ureteral injury are perforations, lacerations and avulsions
sustained during ureteroscopy for stones)
Ureteral injuries are often subtle and clinicians must maintain a high index of
Clinical Manifestations
suspicion to prevent a delay in diagnosis and comorbidity.
Hematuria is a nonspecific indicator of urologic injury
Fever, leukocytosis, and local peritoneal irritation are the most common signs and
symptoms of ureteral injury and always should prompt CT examination.
Investigation
CT urography with delayed images is the best study for detecting ureteral injuries.
Retrograde ureterogram is the most sensitive radiographic test for ureteral injury
Table 4.5: AAST Grading (American Association for the Surgery of Trauma)
Grade Description
I Contusion or hematoma without devascularization
II Laceration; less than 50% transection
III Laceration; 50% or greater transection
IV Laceration; complete transection with less than 2cm of devascularization
V Laceration; avulsion with greater than 2cm of devascularization
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4.4.3. Bladder Trauma
Epidemiology……………………………………………..224
Etiology………………………………………………………224
Clinical Manifestation…………………………………225
Investigation………………………………………………226
Epidemiology
Due to the protected deep-seated position of the urinary bladder in the bony pelvis,
bladder injuries are quite uncommon.
They constitute less than 2% of abdominal injuries necessitating surgical
intervention.
However, the incidence of blunt trauma is rising as a result of modern transportation
preferences.
The presence of a bladder injury signifies the severity of trauma and is usually
associated with serious injuries to various other organ systems.
Etiology
Blunt trauma
o Accounts for 67%–86% of traumatic bladder ruptures
o The most common cause (90%) of bladder rupture by blunt trauma is motor
vehicle accident followed by falls, industrial trauma/pelvic crush injuries and
blows to the lower abdomen.
o A urine-filled bladder is particularly susceptible in this kind of conditions;
when trauma occurs after drinking alcohol. In contrast, an empty bladder is
usually well protected.
o Approximately 83-95% of patients with bladder injuries from blunt trauma
have associated pelvic fractures.
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Penetrating trauma
o Most commonly due to gunshot wounds (85%).
o Stab injuries account for (15%) of the cases.
Iatrogenic trauma
o Rare
o Following gynecological, obstetric and general surgery procedures:
transurethral or pelvic surgery
Idiopathic
o This type of condition which may result from combination of overdistended
bladder with minimal trauma.
Clinical Manifestations
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It commonly presents with:
o Peritoneal irritation
o Sudden severe pain in the hypogastrium, often accompanied by
syncope.
o Shock subsides, abdomen distended, no desire to micturate
o Rise in serum creatinine through peritoneal resorption of urinary
creatinine
Investigation
Retrograde cystography or retrograde CT cystography:
o Severity of injury can be graded
o Can distinguish intra peritoneal from extra peritoneal rupture.
o Extra peritoneal bladder injuries usually resolve with catheterization,
while intra peritoneal injury requires surgery, which can help to prevent
peritonitis and urosepsis
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4.4.4. Urethral Trauma
Epidemiology……………………………………………….227
Etiology………………………………………………………..227
Clinical Manifestation…………………………………..228
Investigation………………………………………………..228
Epidemiology
Uncommon
10% of male patients and up to 6% of female patients with pelvic fractures
Girls younger than 17 years of age have a higher risk for urethral injury compared
with women, perhaps because of greater compressibility of the pelvic bones
In children, injuries are less common but are more likely to extend proximally to
the bladder neck because of the rudimentary nature of the prostate.
Etiology
External blunt
Pelvic fracture:
o Most common cause of posterior urethral injury
o Road traffic accidents, falls from a height, crush injuries
Straddle injury:
o E.g. forceful contact of perineum with bicycle cross-bar*), kick to
perineum; penile fracture
o Most common cause of anterior urethral injury
External penetrating
Gunshot—rare; stab—rare.
Internal, iatrogenic:
Endoscopic surgery Radical prostatectomy
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TURP Penile surgery
Catheter balloon inflated in
urethra
Internal, self-inflicted
Foreign bodies inserted into urethra—rare
Clinical Manifestations
Patient usually complain of hematuria, Inability to void despite urge and
suprapubic pain
The common findings on physical examination include:
o Blood at the urethral meatus
o Socrotal hematoma
o Perineal tenderness
o High-riding prostate on PR exam
o Palpably distended bladder
Investigation
Retrograde urethrography is gold standard to investigate urethral injury.
Table 4.7: AAST classification
Type Description Appearance
1 contusion blood at the urethral meatus; normal urethrogram
2 Stretch injury Elongation of the urethra without extravasation on urethrography.
3 Partial disruption Extravasation of contrast at injury site with contrast visualized in
the bladder
4 Complete disruption Extravasation of contrast at injury site without contrast visualized
in the bladder, <2cm urethral separation
5 Complete disruption >2cm urethral separation or extension to prostate or vagina
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Management of Urologic Trauma
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RenalUreteral
Trauma:Trauma
Penetrating
Bladder Trauma
For extraperitoneal
o Foley catheter drainage
o Rest
o Prophylactic antibiotic
For intraperitoneal
o Surgical exploration
Urethral Trauma
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Complications of Genitourinary Injury
Early:
o Bleeding
o Infection, abscess
o Urinary extravasation, urinoma
Cyst containing urine that forms outside the urinary tract following
trauma or a surgical procedure
o Renal hypertension
Delayed:
o Bleeding
o Hydronephrosis
o Calculus formation
o Chronic pyelonephritis
o Hypertension
o Arteriovenous fistula
o Urethral stricture
o Urinary incontinence
o Sexual dysfunction
o Loss of function in the affected kidney:
As a result of hydronephrosis or renal artery stenosis
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Short Case Discussion
Content By:
Enas Hassen
Samuel Mesfin 4.5. Urethral Catheterization………………………………….…………233
Edited By: 4.6. Suprapubic Cystostomy……………………………….…………….236
Samuel Mesfin
Reviewed By: 4.7. Hypospadias…………………………………………………….………..238
Dr. Abeselom Lemma 4.8. Video QR Codes.………………………………………………………..247
(Urologist)
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4.5. Urethral Catheterization
Introduction………………………………………………..233
Types…………………………………………………….......233
Indications…………………………………………………..234
Contraindications………………………………………..234
Equipment…………………………………………………..234
Technique……………………………………………………235
Removal………………………………………………………235
Complication……………………………………………….235
Introduction
Urethral catheterization is a routine medical procedure that facilitates direct
drainage of the urinary bladder.
It may be used for diagnostic purposes (to help determine the etiology of various
genitourinary conditions) or therapeutically (to relieve urinary retention, instil
medication, or provide irrigation).
Types
Straight tip
Coude tip
3-way catheter
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Indications
Diagnostic
o To collect uncontaminated urine specimen
o Urine output monitoring
o Imaging of urinary tract
Therapeutic
o Acute urinary retention
o Chronic obstruction causing hydronephrosis
o Intermittent bladder decompression
For neurogenic bladder
o Immobilized pt and unconscious pt
o Pt with urinary incontinence
o Intravesical pharmacologic therapy
Contraindications
Absolute: Urethral injury secondary to pelvic or straddle injury
Relative:
o Urethral stricture o Recent surgery
Equipment
Catheter tray with:
o Povidone-iodine
o Sterile cotton ball
o Lubrication gel
o Sterile glove
o Sterile drape
o Urethral catheter
Catheter type and size
o Adults: Foley catheter 16F-18F
o Adult male with obstruction at the urethra: Coude tip (18F)
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o Adults with gross hematuria: Foley catheter (20-24F) or 3-way irrigation
catheter (20-30F)
o Children : Foley, to determine size divide child’s age by 2 and then add 8
o Infants younger than 6 months – Feeding tube (5F) with tape
Drainage bag
Technique
Consider prophylactic antibiotics: valvular
heart disease or acute prostatitis.
Consider intraurethral anesthetic.
Position: supine, frog leg or knees flexed.
Locate meatus.
Apply antiseptic.
Removal
Deflate the balloon by aspirating contents with 10cc syringe from side port.
Withdraw catheter gently, taking care not to splash from tip
Complications
Infection
Paraphimosis
Bladder perforation
Bladder Fistula (urethral injury)
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4.6. Suprapubic Cystostomy
Introduction…………………………………………………236
Indications……………………………………………………236
Contraindications…………………………………………236
Technique…………………………………………………….237
Complication………………………………………………..237
Introduction
Cystostomy is the general term for the surgical creation of an opening into the bladder;
it may be a planned component of urologic surgery or an iatrogenic occurrence.
Often, however, the term is used more narrowly to refer to suprapubic cystostomy or
suprapubic catheterization.
Indications
Acute urinary retention in which urethral catheter can’t be passed. For example:
o Uretral stricture
o Bladder neck contracture secondary to previous surgery.
Urethral trauma
Management of complicated genitourinary tract infection
Contraindications
Requirement for long term urinary diversion (e.g neurogenic bladder)
Absolute contraindication
o Distended bladder which is not easily palpable and can’t be localized by ultra-
sonographic assistant
o History of bladder Ca
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Relative contra indication
o Coagulopathy
o Pelvic cancer with or without history of irradiation
o Pervious lower abdominal or pelvic surgery
o Placement of orthopaedic hardware for pelvic fracture repair
Technique
Percutaneous
Open
Complications
Early complication
o Inadvertent bowel injury o Vascular injury
o Bleeding o Post-operative diuresis
Intraperitoneal extravasation
Extra peritoneal extravasation
Latex allergy
Refractory hematuria
Wound infection
Urosepsis
Bladder stone
Tube calcification and
malfunction
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4.7. Hypospadias
Introduction………………………………………………….……238
Risk Factors…………………………………………………….….238
Classification……………………………………………………..239
Epidemiology……………………………………………………..240
Physical Examination………………………………………...240
Diagnosis……………………………………………………………241
Discussion of the Case………………………………………..242
Management……………………………………………………..244
Complications…………………………………………………….246
Introduction
Hypospadias is a congenital anomaly of the male urethra that results in abnormal
ventral placement of the urethral opening. The location of the displaced urethral
meatus may range anywhere within the glans, the shaft of penis, the scrotum, or
perineum
Hypospadias is defined as a combination of any or all of the following associated
penile anomalies:
o Ectopic urethral meatus
o Penile curvature (chordee)
o Ventral foreskin deficiency with incomplete foreskin closure around the glans,
leading to the appearance of a dorsal hooded prepuce
Risk Factors
In most cases of hypospadias the cause is unknown.
Reported risk factors include the following
o Advanced maternal age
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o Preexisting maternal diabetes mellitus
o Gestational age before 37 weeks
o History of paternal hypospadias
o Exposure to smoking and pesticides
o Placental insufficiency (low placental weight and pathology)
o Prematurity o In-vitro fertilization
o Fetal growth restriction
Classification
Based on the examination, the penile anatomy can be classified into the following
categories for hypospadias based on the appearance of the foreskin, urethral
location, and the presence and degree of penile curvature
o Normal
o Forme fruste of hypospadias (incomplete or partial presence of hypospadias)
Approximately 10 percent of hypospadias
o Standard hypospadias
Ectopic urethral meatus that is accompanied by a classic dorsal
hooded foreskin without fusion of the foreskin to the scrotum with a
normal penile length
Normal glans size (≥14 mm at maximal diameter)
Variable penile curvature (approximately 65 percent of hypospadias).
o Severe hypospadias
Ectopic urethral meatus located in the scrotum or perineum and/or an
abnormally small glans size (<14 mm at maximal diameter) and severe
curvature (approximately 20 percent of hypospadias)
o Less common variants:
Chordee without hypospadias and megameatus with a normal
appearing foreskin (approximately 5 percent of hypospadias).
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Epidemiology
Physical Examination
General
The newborn examination begins with an overall assessment of the child and
identification of any associated congenital anomalies that would suggest a possible
syndromic cause of hypospadias. Examples include:
o Anridia associated with Wilms tumor
o Hand-foot-mouth anomalies
o Ocular telorism, asymmetry of the skull and laryngoesophageal defects
o Cryptophthalmos and cutaneous syndactyly are features of Fraser syndrome
that is also associated with genitourinary anomalies.
o Other findings that have been associated with hypospadias include:
Ear tags/deformities Club feet
Digit abnormalities Spinal abnormalities
Cardiac anomalies Imperforate anus
Genital examination
The key aspect of the genital examination is direct visualization of the penis and
glans, hence adequate lighting is obligatory. The examination includes:
o Assessment of the stretched penile length, which should be 2.5 to 3.5 cm in a
full term male.
To measure the penile length, the glans penis is held with the thumb
and forefinger and the penis is fully stretched until point of increased
resistance is reached.
The measurement is taken using a ruler or caliper from the pubic
ramus (making sure the suprapubic fat pad is depressed) to the distal
tip of the glans penis over the dorsal side.
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o Assessment regarding any evidence of penile curvature, and if so, the degree
of curvature.
The severity of curvature is classified by the assessment of the
curvature when the penis is fully erected as follows:
Normal No curvature to 15 degrees
Mild 15 to 40 degrees
Moderate 40 to 80 degrees
Severe 80 degrees
o Assessment of the foreskin to ensure complete and circumferential
development of the foreskin without any ventral asymmetry or deficiency.
If the foreskin is normally circumferential, it is unlikely that a
significant hypospadias requiring surgery is present.
If the foreskin is not properly formed, the presence of an ectopic
urethral meatus along the ventral shaft of the penis should be sought
after and identified.
o Determination of the presence of both testicles in the normal dependent
position in the scrotum.
Diagnosis
The diagnosis of hypospadias is generally made during the newborn genital
examination
Physical findings consistent with the diagnosis include:
o Abnormal foreskin resulting in an incomplete closure around the glans
leading to the appearance of a dorsal hooded prepuce.
o Abnormal penile curvature (chordee).
o The appearance of "two urethral openings":
The first in the normal position at the end of the glans
The second, the abnormally located true urethral meatus.
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Discussion of the Case
P a g e 242 | 548
The severity of hypospadias increases as the position of the displaced urinary
meatus increases from the normal position at the tip of the glans and with increasing
penile curvature.
o Distal – The most common location for an ectopic urethral meatus is at the
proximal glans, coronal margin, or just below the coronal margin
Patients with distal standard hypospadias typically have a normal-size
penis and glans, and dorsal hooded foreskin due to deficient ventral
foreskin with or without mild penile curvature.
o Proximal – The more severe variant of standard hypospadias occurs when the
urethral meatus is proximally located along the penile shaft, at the
penoscrotal junction or within the scrotum.
These patients often have moderate amounts of penile curvature. They
have a normal size penis and glans, and a classic dorsal hooded foreskin
without fusion of the foreskin to the scrotum, which distinguishes them
from patients with the more severe hypospadias variant.
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4.7.4. Uncommon Hypospadias
Management
Urologic referral and correction are reserved for those patients in whom there is a
potential functional issue including:
o Significant deflection of the urinary stream
o Inability to urinate from a standing position
o Erectile dysfunction due to penile curvature leading to intercourse difficulties
o Fertility issues due to sperm deposition difficulties
Urologic referral is not needed for patients with mild defects; this includes patients
with:
o Forme fruste of hypospadias (incomplete or partial presence of hypospadias)
o Standard distal hypospadias (eg, urethral opening at the proximal glans,
coronal margin, or just below the coronal margin) and without penile
curvature.
o Neonatal circumcision should be avoided in patients with:
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Hypospadias where the foreskin is asymmetric with abnormal
development on the ventral aspect of the penis:
This anatomical configuration is not conducive to a safe
neonatal circumcision
Standard and severe forms of hypospadias:
o The foreskin needs to be preserved and reserved for use during
the hypospadias reconstruction to prevent fistula formation
In severe cases: to reconstruct the new urethra.
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Excess dorsal foreskin is transferred to the ventral side of the
penis, as this tissue is required for the second stage.
The second operation is performed at least six months later, after
healing is complete from the first procedure.
In this stage, the urethra is reconstructed using the transferred
dorsal skin that is now on the ventral aspect of the penis in a
manner similar to the primary tubularization.
o In any of the procedures, the addition of a complete covering layer over the
newly constructed urethra is recommended, as this reduces the risk of
developing a urethral fistula
o Choice of surgical procedure — for standard hypospadias, the procedure of
choice is primary tubularization, and when necessary, incision of the urethral
plate.
Complications
Urethral fistula
o The most common complication following hypospadias surgery is
urethrocutaneous fistula, which is characterized as two urinary streams
because of the extra urethral opening.
o It is reported in approximately 4 to 20 percent of patients, depending on the
severity of their hypospadias
o Fistula correction requires a second operation that is performed six months
after the initial procedure.
Urethral stricture:
o It is due to tightening of the reconstructed urethra within the glans, which is
referred to as meatal stenosis.
o These children will have symptoms of straining or pushing on urination and a
thin or fine urinary stream.
o Correction of a urethral stricture requires a second operation at least six
months following the prior surgery.
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Urethral diverticulum:
o Urethral diverticulum is due to outpouching of the reconstructed urethra.
o These children can have ballooning of the ventral aspect of the penis on
urination and dribbling from retained urine after they void.
o Correction of a urethral stricture requires a second operation, ideally, at least
six months following the prior surgery, unless recurrent infection requires
more immediate intervention.
Suprapubic Cystostomy
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Part 5: Gastrointestinal Surgery
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5.1. Liver Abscess
Case Discussion………………………………………………….249
History …………………………………………….……………….249
Physical Examination…………………………………………251
Investigation……………………………………………………..252
Differential Diagnosis………………………………………..253
Discussion of the Case……………………………………….254
Case Discussion
A 50-year-old male patient complains of gradual onset dull aching RUQ pain of 1-month
duration with radiation to the right shoulder. He has associated high grade intermittent
fever, chills and rigors. In addition, he developed productive cough of blood tinged
sputum, SOB and pleuritic chest pain. He has history of drinking areke for >20 years. On
physical examination there were signs of pleural effusion and tender hepatomegaly.
History
1) Describe the pain (PQR^2ST)
2) Duration: if acute more likely – pyogenic, if chronic- amoebic, hydatid
3) Ask for Associated symptoms:
Fever, chills – if high grade fever (pyogenic)
Loss of appetite, weight loss
Yellow discoloration
Symptoms of anemia (blurring of vision, palpitations)
Change in bowel habit – prior hx of dysentery (amoebic in 3-9%)
Respiratory symptoms (cough, chest pain) due to diaphragm irritation
4) Asses for risk factors
Low socioeconomic, immune suppression -amoebic
Age, sex – older male risk of HCC and abscess
Alcohol, cigarette history- HCC
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Contact with jaundiced person, blood transfusion or MSP- Hepatitis for HCC
Travel history and history of ingestion water or food contaminated with dog
feces- hydatid cyst
Abdominal trauma or prior history of surgery- pyogenic
Fever and jaundice (ascending cholangitis) – pyogenic
DM, underlying pancreatic or hepato-biliary disease-pyogenic, DM for HCC
OCP use- adenoma of the liver
Symptoms of cirrhosis(hematemesis, tarry stool, jaundice) - HCC
5) Rule out differential
Contact with chronic coughed or previous TB treatment -TB
Hemoptysis, bone pain, bleeding from other site – HCC
Constitutional symptoms of malignancies (weight loss, fever, loss of appetite) –
HCC
Jaundice, pale stool, dark urine, itching sensation -biliary disease or hydatid
Urinary complaints (dysuria, hematuria)- pyelonephritis?
6) Rue out complications
Cough, SOB, pleuritic chest pain- pleural effusion and pneumonia
Secondary infection
Generalized abdominal pain – peritonitis
Copious brown sputum – rupture to bronchus
Symptoms of OJ-hydatid cyst complication
Headache, dizziness & decreased level of consciousness – hydatid cyst cerebral
involvement
7) Ask Treatment in between the symptoms:
Route of treatment
Frequency per day
For how long it was taken
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Physical Examination
General appearance:
Vital:
HEENT:
Lymphoglandular System:
LN enlargement – HCC
Parotid enlarged, testicular atrophy, gynecomastia – HCC on top of cirrhosis
Respiratory:
Follow the steps and do detailed examination to check for signs of pleural effusion
and pneumonia as complication
CVS:
GI:
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Perform a detailed and meticulous abdominal examination, which includes:
inspection, auscultation, palpation and percussion.
Note the Site, Size, shape, surface, edge, consistency, mobility and attachments,
bimanual palpability and pulsatile nature of any palpable mass.
Also look for stigmata of cirrhosis (spider angioma), stigmata of HCC (bruit over the
liver, friction rub, liver will be irregular, nodular and hard in consistency).
In liver abscess you will appreciate: tender hepatomegaly: soft, smooth, regular,
mobile
In hydatid: non tender, round border, smooth surface and enlarged liver with
typical hydatid thrill
Integumentary:
CNS:
Investigation
CBC: increased total WBC in abscess and hydatid cyst
o Eosinophilic: hydatid
o Neutrophil count increased if pyogenic
Raised ESR and CRP
Abdominal ultrasound & US guided aspiration: establishes diagnosis
o Pyogenic:
Round or oval hypoechoic lesions with well-defined borders and a variable
number of internal echoes.
o Hydatid cysts
Are well-defined hypodense lesions with a distinct wall.
Ring-like calcifications of the pericysts are present in 20% to 30% of cases.
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As healing occurs, the entire cyst calcifies densely, and a lesion with this
appearance is usually dead or inactive.
Daughter cysts generally occur in a peripheral location within the main cyst
and are typically slightly hypodense compared with the mother cyst.
CT followed by FNAC: when in doubt
o Pus for gram stain, culture and sensitivity
o Pyogenic: hypodense with peripheral enhancement and may contain air-fluid
levels indicating a gas-producing infectious organism.
CXR: for empyema thoracic, perforated viscous
Stool exam:
o Amoebic cyst, culture and sensitivity for typhoid bacilli
Serologic testing (indirect hemagglutinin test):
o 90-95% amoebic abscesses
Sigmoidoscopy:
o Shows flask shaped ulcer in amoeba
AFP and metastasis workup: HCC
Plain x-ray:
o Speckled calcification of hydatid cyst
ERCP:
o If there is OJ following hydatid cyst
Differential Diagnosis
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Discussion of the Differentials
Introduction
Epidemiology
Liver abscesses are the most common type of visceral abscess
The annual incidence of liver abscess has been estimated at 2.3 cases per 100,000
populations and is higher among men than women (3.3 versus 1.3 per 100,000).
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Risk Factors
Diabetes
Underlying hepatobiliary or pancreatic disease
Liver transplant
Geographic and host factors may also play a role:
o For example, a primary invasive liver abscess syndrome due to K.
pneumoniae has been described in East Asia.
Independent risk factors for mortality include:
o Need for open surgical drainage
o The presence of malignancy
o The presence of anaerobic infection
Microbiology
Approximately 40% of abscesses are monomicrobial, an additional 40% are
polymicrobial, and 20% are culture-negative.
The most common infecting agents are gram-negative bacteria:
o Escherichia coli is found in two thirds of cases
o Other common organisms include:
Streptococcus Klebsiella
faecalis Proteus vulgaris
Anaerobic organisms such as Bacteroidesfragilisalso are seen frequently.
In patients with endocarditis and infected indwelling catheters:
o Staphylococcus and Streptococcus species are more commonly found.
Arise from:
- Ascending infection-infected and obstructed biliary tree
- Haematogenous
- Localized liver necrosis-trauma, local ablative therapies
- Cryptogenic
- Impaired biliary drainage
- Subacute bacterial endocarditis
- Infected indwelling catheters
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- Dental work
- The direct extension of infections such as diverticulitis or Crohn’s disease into
the liver.
Clinical Manifestations
Fever
Abdominal pain and tenderness,
o Usually localized to the right upper quadrant and may include pain, guarding,
rocking tenderness (pain caused by gently rocking the patient's abdomen), and
even rebound tenderness
Nausea and vomiting
Anorexia and weight loss
Hepatomegaly and Jaundice
Diagnosis
Imaging
o CXR Elevated diaphragm, pleuraleffusion, atelectasis, sub-diaphragmatic
air-fluid level
o U/S and CT –localize the abscess and guide percutaneous treatment
Management
The Goal
1) Complete drainage of pus and infected debris.
2) Initiation of adequate antibiotic therapy.
3) Resolution of the underlying cause.
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Treatment options ranges from antibiotic therapy alone to major operative
interventions.
Blood samples should be obtained before starting antibiotics if possible.
Broad-spectrum parenteral therapy must begin as soon as possible.
o Antibiotics – 4-6 weeks ceftriaxone [G +ve and -ve] plus metronidazole
[anaerobe]
o Drain: indication failure to respond to antibiotics, abscess> 6cm, impending
rupture
Percutaneous
Laparoscopic
Open-drainage /resection [when most part of liver affected]
Treat the underlying cause- e.g biliary obstruction
PCD is performed when:
o The pus is too thick to be aspirated
o The abscess is greater than 5 cm in diameter
o The wall is thick and non-collapsible
o The PLA is multi-loculated
o Failure of PCD may occur in as many as 10% of patients.
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5.1.2. Amoebic Liver Abscess
Introduction …………………………………………………………….258
Epidemiology…………………………………………………………...258
Risk Factors………………………………………………………………259
Clinical Manifestation……………………………………………….259
Diagnosis………………………………………………………………….260
Management……………………………………………………………261
Introduction
Amebic liver abscess is the most common extra intestinal manifestation of
amebiasis.
Amebae establish hepatic infection by ascending the portal venous system
Epidemiology
Amebic liver abscess (and other extra intestinal disease) is 7 to 10 times more
common among adult men than other demographic groups, despite equal gender
distribution of colonic amebic disease.
It is observed most frequently in the fourth and fifth decades of life.
The reasons for these observations are not fully understood; suggested mechanisms
include hormonal effects and a potential role of alcoholic hepatocellular damage in
creating a nidus for portal seeding.
In developed countries, amebiasis is generally seen in migrants from and travelers to
endemic areas.
Amebiasis is relatively uncommon among short-term travelers, but amebic liver
abscesses can occur after travel exposures as short as four days.
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Risk Factors
Clinical Manifestations
One to two weeks of right upper quadrant pain and fever (38.5 to 39.5ºC).
o Pain may be referred to the epigastrium, the right chest, or the right
shoulder.
o The pain is usually dull but may be pleuritic or aching.
Cough Malaise
Sweating Hiccoughs
Anorexia and weight loss
Concurrent diarrhea is present in less than one-third of patients
o Some patients report history of dysentery within the previous few months.
Jaundice occurs in less than 10 percent of patients
Physical examination reveals hepatomegaly and point tenderness over the liver in
approximately 50 percent of cases.
Rupture of liver abscess can occur into any adjoining space or organ; extension into
the chest occurs almost four times as often as extension into the peritoneal cavity.
o In up to 7 percent of cases peritonitis and hepatic vein and inferior vena cava
thrombosis
Patients with secondary cardiac or pulmonary involvement may present with
symptoms primarily due to these complications.
Occasionally patients have a more chronic presentation:
o Fever o Abdominal pain
o Weight loss o Hepatomegaly
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Diagnosis
Lab
o A leukocytosis (>10,000/mm3) without eosinophilia.
o Alkaline phosphatase
Elevated (80 percent of cases)
o Hepatic transaminases
May also be elevated.
o Amebic Serology:
Highly sensitive and specific in the differentiation b/n PLA and ALA.
An indirect hemagglutinin test (IHAT) 90% sensitive.
EIA detects antibodies specific for E. histolytica in ~ 95% of pnts with
extraintestinalamebiasis.
Currently: ELISA and IHATappear to be the most reliable tests, with
sensitivity and specificity > 95%
Imaging
o CXR
Elevation of the right dome of the diaphragm
Atelectasis of the right lung
Pleural effusion
Gas in the biliary tree or liver parenchymal.
o US:
Preferable diagnostic test (90% accuracy).
Round or oval, with well-defined margins.
Single:
80%: right lobe 6%: caudate lobe
10%: left lobe
The remaining are multiple abscesses.
CT scan:
o Does not add to the diagnostic accuracy
o Is helpful in differentiating amebic from pyogenic abscesses and in identifying
simple cyst & necrotic tumor.
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Management
Chemotherapy
Metronidazole is the drug of choice for ALA (500-750 mg TID for 7 -10 days) with
cure rate >90%.
Luminal agent: Paromomycin, iodoquinoldiloxanide furoate.
Emetine hydrochloride reaches amebicidal concentrations in tissues rather than
intestine.
Aspiration or PCD indicated
1. Age older than 55 years,
2. Abscess greater than 10 cm in diameter, and
3. Failure of medical therapy after 7 days
4. Failure to differentiate PLA from ALA
5. Abscesses that extended into the peritoneal cavity.
Open laparotomy indicated
1. Doubtful diagnosis
2. Concomitant hollow viscus perforation with fistulation: in life-threatening
hemorrhage or sepsis
3. Failure of conservative management.
Treat the complications
1) Pulmonary complications:
o Thoracocentesis
o Pulmonary decortication If amebic empyema complicated by secondary
infection.
o Lung abscess: Postural drainage, bronchodilators, and anti- amebic drugs
may suffice.
2) Vascular and Pericardial Involvement
o Pericardial thickening or pericardial effusion: Aspiration of a left-sided ALA.
o Cardiac Tamponade: Pericardiocentesis + drainage of liver abscess & anti-
amebic drugs
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5.2. Obstructive Jaundice (OJ)
Case Discussion……………………………………………..262
History ………………………………………………………….262
Physical Examination…………………………………….264
Investigation…………………………………………………265
Differential Diagnosis……………………………………267
Discussion of the Case…………………………………..267
Discussion of the Differentials……………………….272
Case Discussion
A 55-year-old male soldier who presented with dull aching generalized abdominal pain of
2-month duration. He has associated nausea, vomiting and loss of appetite. He had yellow
discoloration of the eye and palm. In addition, he had clay colored stool, dark urine and
itching at night. He also had alcohol and smoking habit.
History
1) Chief complaints and associated symptoms
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Age and sex: Cholelithiasis-30-50 of age and usually female, 50-70 years
periampulary cancer more likely
Previous history of malignancy
History of previous gallbladder surgery- may lead to bile strictures and jaundice, also
endo prosthesis or stents cold be risk factors
Look for the 5 F’s – risk for stone
Alcohol, drugs and medication:
o OCP, hormone replacement therapy are a risk factor for cholelithiasis
o Alcohol abuse risk for pancreatic cancer
Past history of DM
Known gallstone disease
3) Rule out differential
Pain
o Colicky: sharp RUQ pain which occurs after having a heavy meal or during the
night usually waking the patient from sleep. It may radiate to the right
scapular area or the chest. It may last from 15 minutes to a few hours –
choledocholithiasis
o Painless or dull aching persistent pain: pancreatic head cancer back pain-
retroperitoneal extension of PCa
Acuteness of symptoms: perampullary ca has shorter duration (1-3) months
Color of jaundice: deep yellow (choledocholithiasis), greenish yellow (perampullary
Ca)
Anemia symptoms: light headedness, malaise, dizziness, fatigue, palpitations -
perampullary Ca
Early satiety, vomiting, belching: pancreatitis or biliary stricture
Family history of jaundice
Round worm infestation: Ascaris
History of contact with a jaundiced patient, transfusion, drug abuse/needle sharing,
needle-stick injuries, sexual contact – rule out pre-hepatic and hepatic cause of
jaundice
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4) Rule out complication
Chariots triad and Reynolds pentad
Encephalopathy following liver decompensation
Diarrhea of recent onset- liver failure
Bone pain, neck lump, dyspnea: periampulary cancer metastasis
Urinary symptoms and edema: renal failure
Physical Examination
General appearance
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o Hepatomegaly: is common in both hepatic and post hepatic jaundice. Palpation
of an enlarged irregular liver suggests cancer and a shrunken nodular liver is
likely to be due to cirrhosis.
o Murphy’s sign
– Mucocele projecting downwards and forwards from below the liver just
– Empyema lateral to the outer border of rectus muscle (Below the 9th rib
Investigation
Laboratory Studies
Imaging:
Plain x-ray:
o Shows radiopaque gallstones in 10% of the patients Mercedzbenz sign
Ultrasonography: Initial imaging modality of choice; shows
o Biliary calculi
o Size and thickness of Gall bladder
o Presence of inflammation around GB
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o Size of Common Biliary Duct
o Stones within the biliary tree
Preferred for GB stones rather than CBD stones
CT:
o The modality of choice in the staging of cancers of the liver, gall bladder, bile
ducts and pancreas.
o It is inferior to u/s to diagnose stones
MRCP: replaced ERCP
ERCP: gold for CBD stone removal
PTC: to diagnose pathologies in higher level above cystic duct
Barium meal follow through:
o Periampulary ca - inverted 3 sign
o Pancreatic head tumor – pad sign
Differential Diagnosis
1. Congenital: Biliary atresia, choledochal cyst
2. Inflammatory: Ascending cholangitis, sclerosing cholangitis
3. Obstructive: Common bile duct (CBD) stones, biliary stricture, parasitic infestation
4. Neoplastic: Carcinoma of head of pancreas, periampulary carcinoma, cholangio-
carcinoma, Klatskin tumor
5. Extrinsic compression: Compression by lymph nodes
Jaundice is a generic term, which describes yellow pigmentation of the skin, mucous
membrane or sclera. It can be caused by pre-hepatic, hepatic and post hepatic
causes.
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Obstructive jaundice is strictly defined as a condition occurring due to a block in the
pathway between the site of conjugation of bile in liver cells and the entry of bile
into the duodenum through the ampulla
Normal serum bilirubin level is from 0.3-1.0 mg/dL.
o Conjugated: 0.1- 0.3mg/dl
o Unconjugated: 0.2-0.7mg/dl
Jaundice is clinically detected in sclera when serum bilirubin is greater than 2.5-
3mg/dl.
Jaundice is clinically detected in skin/mucus membrane when serum bilirubin is
greater than 6.0mg/.
Globin Fe2+, CO
HO Bilirubin
Hemoglobin Heme Biliverdin
(insoluble) Spleen
O2, H2O,
NADPH NADP+
Bilirubin-albumin
conjugate Blood
Bilirubin
Liver
Bilirubin diclucorinide
Excreted
Physiology
Normal secretory pressure of bile is 15-25cm of water.
At 35cm of water, there is suppression of bile flow.
High pressure leads to cholangiovenous and cholangiolymphatic reflux of bile.
Dilation of bile duct and intra hepatic biliary radicals (IHBR)
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Pathophysiology
Increase in biliary pressure leads to
o Disruption of tight junctions between hepatocytes and bile duct cells with
increased permeability
o Reflux of bile contents in liver sinusoids
o Neutrophil infiltration, increased fibro genesis and deposition of reticulin fibers in
portal triad
o Reticulin fibers get converted to type 1 collagen
o Laying down of collagen fibers leads to hepatic fibrosis obstruction of sinusoids and
secondary biliary cirrhosis and portal hypertension
o Fibrosis can also lead to atrophy of obstructed liver.
Causes:
A. In the lumen of duct C. Outside the wall
B. In the wall of duct 1. Benign
1. Congenital 2. Malignant
2. Acquired
Clinical Classification:
Table 5.3: Clinical Classification
Type 1 (Complete) Type 2 (Intermittent)
Malignancy of Head of Pancreas Choledocholithiasis
Ligation of Common Bile Duct Periampulary tumor
Cholangiocarcinoma Duodenal diverticula
Parenchymal Liver Disease Choledochal Cyst
Papillomas of the bile duct
Intrabiliary parasites
Hemobilia
Clinical Presentation:
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Pruritus
Clay colored stools, High colored urine
RUQ pain and tenderness
Biliary colic
Steatorrhea, Bleeding tendency
Icterus
Nausea/Vomiting, Anorexia, Weight loss
High grade fever with chills
Diagnosis:
The sensitivity of history, physical examination, and blood tests alone range from
70% to 95%, whereas the specifity is approximately 75%.
The overall accuracy of clinical assessment of hepatic and post-hepatic causes of
jaundice ranges from 87%-97%.
Complications:
Can be due the underlying pathologies or due to procedures for management.
Cholangitis Renal failure
Cholecystitis Liver failure
Hypoprotenemia and Malnutrition Acute pancreatitis
Liver abscess Reccurent stone
Septicemia Coagulation factor defect
Biliary cirrhosis
Management:
1) Pre-op:
Fluid and electrolyte:
o Intravenous administration of 5% dextrose saline followed by 10% mannitol
or loop diuretics to prevent renal failure (12-24 hours prior to surgery)
Nutrition:
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o High protein high carbohydrate and low fat diet through enteral route to
increase the glycogen reserve
Coagulopathy:
o Intramuscular vitamin K(1-10mg), Fresh frozen plasma
Endotoximia:
o Broad spectrum Antibiotic prophylaxis, Lactose, Early enteral nutrition
Pain management
Cholestyramine and antihistamine for symptomatic relief of pruritus
Antiemetics are given to minimize nausea and vomiting
2) Surgical
Cholidocolithiasis
o Sphincterotomy & ductal clearance, followed by laparoscopic
cholecystectomy or
o Found with intraoperative cholangiogram during cholecystectomy,
laparoscopic CBD exploration via the cystic duct or with formal
choledochotomy
Pancreatic ca
o Palliative
o Pain>narcotic
o Jaundice and pruritus
Endoscopic sphincterotomy
+
Stenting with percutaneous trans-hepatic biliary drainage
Cholidochoduodenostomy
Cholidochojejunostomy
Cholecystojejunostomy
o Surgical resection > whipple’s resection
o Adjuvant therapy: Chemotherapy, Radiotherapy
Cholangiocarcinoma
o Biliary decompression + cholecystectomy (to prevent cholecystitis)
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Discussion of the Differentials
5.2.1. Choledocholithiasis
Introduction …………………………………………………………….272
Epidemiology……………………………………………………………272
Risk Factors………………………………………………………………272
Clinical Manifestation…………………………………………….…272
Diagnosis……………………………………………………………….…274
Introduction
It refers to the presence of gallstones within the common bile duct (CBD).
Epidemiology
The exact incidence and prevalence of Choledocholithiasis are not known, but it has
been estimated that 5 to 20 percent of patients have CBD stones at the time of
cholecystectomy, with the incidence increasing with age.
Risk Factors
In the setting of bile stasis (eg, patients with cystic fibrosis)
Elderly patients with large bile ducts and periampullary diverticular
Patients with recurrent or persistent infection involving the biliary system
Clinical Manifestations
Patients with CBD stones may be asymptomatic or present with pain and liver test
abnormalities with or without evidence of complications.
o Asymptomatic presentation
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In such patients, the diagnosis is typically made when imaging studies are
obtained for unrelated reasons, when a patient is being evaluated for
abnormal liver tests, or when an intraoperative cholangiogram is obtained
during cholecystectomy.
o Pain and liver test abnormalities
Patients with uncomplicated CBD stones typically have pain and abnormal
liver tests, but are afebrile and do not have other abnormal laboratory tests.
Symptoms
Right upper quadrant or epigastric pain
o The pain is often more prolonged than is seen with typical biliary colic and
resolves with either spontaneous passage or removal of the CBD stone.
o Some patients have intermittent pain due to transient blockage of the CBD
(ball-valve effect).
nausea, and vomiting
Complicated Choledocholithiasis
Acute cholangitis
o Charcot's triad:
Fever
Right upper quadrant pain
Jaundice
o Leukocytosis
o Bacteremia and sepsis may lead to hypotension and altered mental status
(Reynolds' pentad)
Biliary pancreatitis
o Pain o Vomiting
o Nausea o Elevated liver tests
o Elevations in serum amylase and lipase (by definition >3 times the upper limit
of normal)
o Imaging findings suggestive of acute pancreatitis.
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Diagnosis
Patients with at least one very strong predictor or both strong predictors are considered high-risk.
Patients who do not qualify as high-risk, but who have at least one of the strong or moderate
predictors are considered intermediate-risk. Patients with no predictors are considered low-risk.
High-risk
o Proceed directly to ERCP
Intermediate-risk
o If the patient is a surgical candidate, proceed to laparoscopic
cholecystectomy with intraoperative cholangiography or ultrasonography.
o If the patient refuses surgery, is not a surgical candidate, or is post-
cholecystectomy, further imaging with an MRCP or EUS is recommended.
o If no CBD stones are seen on MRCP but suspicion remains for bile duct
stones, proceed to EUS.
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o If no CBD stones are seen by EUS, proceed to laparoscopic cholecystectomy in
patients who are surgical candidates (assuming cholelithiasis has been
confirmed by transabdominal or endoscopic ultrasound).
o If a stone is seen on MRCP or EUS proceed to ERCP, followed by laparoscopic
cholecystectomy (in surgical candidates) either during the same
hospitalization or electively.
Low-risk
o If stones or sludge are present within the gallbladder and the patient is a
good surgical candidate, proceed to laparoscopic cholecystectomy without
imaging of the CBD preoperatively or intra-operatively.
Introduction
The commonly used term "pancreatic cancer" usually refers to a ductal
adenocarcinoma of the pancreas (including its subtypes), which represents about
85 percent of all pancreatic neoplasms.
Approximately 60 to 70 percent of exocrine pancreatic cancers are localized to the
head of the pancreas, while 20 to 25 percent are in the body/tail and the remainder
involve the whole organ.
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Epidemiology
Pancreatic cancer is the fourth leading cause of cancer-related death in the among
both men and women.
The majority of these tumors (85 percent) are adenocarcinomas arising from the
Risk Factors
ductal epithelium.
Pathology
History of partial gastrectomy or cholecystectomy
Helicobacter pylori and Hepatitis B virus
Of the several subtypes of ductal adenocarcinoma, most share a similar poor long-
term prognosis, with the exception of colloid carcinomas, which have a somewhat
better prognosis.
The more inclusive term "exocrine pancreatic neoplasms" includes all tumors that
Clinical Manifestations
are related to the pancreatic ductal and acinar cells and their stem cells (including
pancreatoblastoma), and is preferred.
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Pancreatic head tumors more often present with jaundice, steatorrhea, and weight
loss
The most common presenting symptoms are pain, jaundice, and weight loss.
o The pain
Insidious in onset, and has been present for one to two months at the
time of presentation.
Rarely, pain develops very acutely, as a result of an episode of acute
pancreatitis due to tumor occlusion of the main pancreatic duct
Typical gnawing visceral quality is generally epigastric, radiating to the
sides and/or straight through to the back.
Severe back pain should raise suspicion for a tumor arising in the body
and tail of the pancreas
Intermittent and made worse by eating or lying supine.
It is frequently worse at night. Lying in a curled or fetal position may
improve the pain.
o Jaundice
Usually progressive,
May be accompanied by pruritus, darkening of the urine, and pale stools.
Painless jaundice has been more favorable prognosis
Early sign in tumors arising from the pancreatic head
Jaundice secondary to a tumor in the body or tail typically occurs later in
the course of the disease, and may be secondary to liver metastases.
Unexplained superficial thrombophlebitis, which may be migratory (classic
Trousseau’s syndrome) is sometimes present.
o It reflects the hypercoagulable state that frequently accompanies pancreatic
cancer (more commonly in tumors of tail or body of the pancreas).
Atypical diabetes mellitus may be noted
Signs of metastatic disease
o An abdominal mass or ascites
o Left supraclavicular lymphadenopathy (Virchow's node)
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Diagnosis
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5.2.3. Cholangiocarcinoma
Introduction ………………………………………………….…………279
Epidemiology……………………………………………………………279
Pathophysiology……………………………………………………….279
Risk Factors………………………………………………………………280
Clinical Manifestation………………………………………….……280
Diagnosis…………………………………………………………….……281
Introduction
Cholangiocarcinomas arise from the intrahepatic or extrahepatic biliary epithelium.
More than 90% are adenocarcinomas, and the remainders are squamous cell
tumors.
The etiology of most bile duct cancers remains undetermined.
Epidemiology
Incidence in most Western countries ranges from 2 to 6 cases per 100,000 people
per year.
The highest annual incidences are in Japan, at 5.5 cases per 100,000 people
Pathophysiology
Cholangiocarcinomas tend to grow slowly and to infiltrate the walls of the ducts,
dissecting along tissue planes.
Local extension occurs into:
o The liver/ porta-hepatis
o Regional lymph nodes of the celiac and pancreatico-duodenal chains.
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Risk Factors
Infections:
o Liver flukes
o Ascaris
o H.pylori
IBD
o Cholangiocarcinoma generally develops in patients with long-standing
ulcerative colitis and primary sclerosing cholangitis.
Chemical exposure:
o Workers of aircraft, wood and rubber industires
Miscellaneous: choledochal cyst
Bile duct adenoma
Obesity
Clinical Manifestations
Diagnosis
1. Ultrasound
May demonstrate biliary duct dilatation and larger hilar lesions.
Patients with underlying primary sclerosing cholangitis (PSC) may have limited
ductal dilatation secondary to ductal fibrosis.
Doppler ultrasound may show vascular encasement or thrombosis.
2. CT
Resembles ultrasound in that it may demonstrate ductal dilatation and large mass
lesions.
Evaluates for pathologic intra-abdominal lymphadenopathy.
Helical CT scans are accurate in diagnosing the level of biliary obstruction.
3. Magnetic resonance imaging (MRI)
Demonstrates hepatic parenchyma
MR cholangiography enables:
o Imaging of bile ducts
o In combination with MR angiography, permits staging (excluding vascular
involvement)
o Hepatic involvement can also be detected.
4. Biopsy
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5.3. Colorectal Cancer
Case Discussion…………………………………………………..282
History …………………………………………………………..…..282
Physical Examination…………………………………….…….284
Investigation…………………………………………………….…285
Differential Diagnosis………………………………………….285
Discussion of the Case…………………………………….…..287
Case Discussion
A 70-year-old man was seen in the surgical outpatient clinic complaining of a 3-month
history of loose stools. He normally opens his bowels once a day, but has recently been
passing loose motions up to four times a day. The motions have been associated with the
passage of blood clots and fresh blood mixed within the stools. His appetite has been
normal, but he reports a 2-stone weight loss. The past history was otherwise
unremarkable. His father died from cancer at the age of 45 years, but he is unsure of the
origin. On physical exam, there was no pallor or lymphadenopathy is present. The
abdomen is soft and non-tender with no palpable masses. Digital rectal examination is
normal.
History
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4) Look for complications
urinary complaints (pneumaturia, fecaluria, recurrent UTI, hematuria)
jaundice, ascites, difficulty breathing (metastasis)
Intestinal obstruction symptoms (constipation, vomiting, abdominal distension,
pain)
Generalized peritonitis
Physical Examination
Physical examination may usually be unrevealing except in advanced disease.
General appearance:
o chronically sick looking, acutely sick looking if there is obstruction
vital signs:
o BP low &HR high if there is excessive bleeding,
o temp high if there is secondary infection or pericolic abscess
HEENT
o EYE: pale, icteric
Lymphadenopathy- supraclavicular
Chest
o Sign of metastasis (pleural effusion)
Abdomen
o abdominal mass due to the tumour and/or hepatomegaly,
o signs of ascites
o abdominal tenderness
o PR: mass,blood,fixation (a sigmoid tumour may prolapse into the pouch of
Douglas)
o GU
o Faecal matter coming out of vagina or urethra(in case of fistula)
Locomotor system
o Edema (hypoalbuminaemia)
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Investigation
Lab:
CBC: WBC, Hb&Hct ESR stool exam: occult blood
Electrolytes LFT,RFT,
BUN & Cr CEA- diagnostic if >1000IU
Imaging
ECG
CXR
US for liver secondary
CT of abdomen
Double contrast barium enema
Colonoscopy(gold standard)
Flexible sigmoidoscopy: useful in supplementing barium investigations where
diagnosis is difficult due to diverticular disease.
Differential Diagnosis
1. Ulcerative colitis
2. Diverticular disease
3. Intestinal TB
4. Irritable bowel syndrome
5. Other dynamic and adynamic causes of bowel obstruction (volvulus, band, adhesion,
intussusception, ileus, etc…)
6. AVM (arterio venous malformation)
7. Ischemic bowel disease
8. Hemorrhoids
9. Dysenteries and other causes of diarrhea and change in bowel habit
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Table 5.4: Causes of Constipation
Organic Painful anal cause Adynamic bowel Drugs Habit and diet
obstruction
Carcinoma of Fissure in ano Hirschsprung’s aspirin Dyschezia
colon Prolapsed piles disease Opiate analgesics Dehydration
Diverticular Senility Anticholinergics starvation
disease Spinal cord Ganglion blockers Lack of bulk in diet
injury/ disease
myxoedema
Parkinson
disease
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Discussion of the Case
Introduction ……………………………………………………….……287
Epidemiology……………………………………………………….……287
Risk Factors…………………………………………………………….…287
Pathology………………………………………………………………...289
Clinical Manifestation……………………………………………….289
Spread of the disease..……………………………………………..290
Staging……………………………………………………………………..290
Management……………………………………………………………293
Introduction
Colorectal carcinoma is the most common malignancy of the gastrointestinal tract.
Epidemiology
The incidence is similar in men and women and has remained fairly constant over
the past 20 years; however, the widespread adoption of current national screening
programs is gradually decreasing the incidence of this common and lethal disease
Risk Factors
Aging
o It is the dominant risk factor for colorectal cancer, with incidence rising
steadily after age 50 years.
o However, individuals of any age can develop colorectal cancer, so symptoms
such as a significant change in bowel habits, rectal bleeding, melena,
unexplained anemia, or weight loss require a thorough evaluation.
Hereditary risk factors
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o Approximately 80% of colorectal cancers occur sporadically, while 20% arise
in patients with a known family history of colorectal cancer.
Environmental dietary factors
o The observation that colorectal carcinoma occurs more commonly in
populations that consume diets high in animal fat and low in fibre
o A diet high in saturated or polyunsaturated fats increases risk of colorectal
cancer while a diet high in oleic acid (olive oil, coconut oil, fish oil) does not
increase risk.
o In contrast, a diet high in vegetable fibreappears to be protective.
o A correlation between alcohol intake and incidence of colorectal carcinoma
has also been suggested.
o Ingestion of calcium, selenium, vitamins A, C, and E, carotenoids, and plant
phenols may decrease the risk ofdeveloping colorectal cancer.
o Obesity and sedentary lifestyle seems to increase
Inflammatory Bowel Disease.
o It is hypothesized that chronic inflammation predisposes the mucosa to
malignant changes, and there is some evidence that degree of inflammation
influences risk.
o In general, the duration and extent of colitis correlate with risk.
Primary sclerosing cholangitis
Family history of colorectal cancer.
Other Risk Factors
o Cigarette smoking is associated with an increased risk of colonic adenomas,
especially after more than 35 years of use.
o Patients with:
History of uretero-sigmoidostomy
Acromegaly
History of pelvic radiation
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Pathology
Microscopically:
Clinical Manifestations
1. Local effects
Change in bowel habit is the most common symptom, either constipation or
diarrhoea or the two alternating with each other.
o The diarrhoea may be accompanied by mucus (produced by the excessive
secretion of mucus from the tumour) or bleeding, which may be bright,
melaena or occult.
Intestinal obstruction due to a constricting neoplasm commonly found in the left.
Perforation of the tumour, either into the general peritoneal cavity or locally with
the formation of a pericolic abscess, or by fistulae into adjacent viscera
2. Effect of secondary deposit:
Jaundice,
Abdominal distension due to ascites and hepatomegaly.
3. Malignant features
Weight loss
Anemia
Loss of appetite
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Spread of the Disease
Local spread
o Tumour can spread in a longitudinal, transverse or radial direction.
o It spreads round the intestinal wall and usually causes intestinal obstruction
before it invades adjacent structures.
Lymphatic spread
o Lymph nodes draining the colon are grouped as follows:
N1: nodes in the immediate vicinity of the bowel wall;
N2: nodes arranged along the ileocolic, right colic, midcolic, left colic and
sigmoid arteries;
N3: the apical nodes around the superior and inferior mesenteric vessels.
Bloodstream spread
o Accounts for a large proportion (30–40%) of late deaths.
o Metastases are carried to the liver via the portal system, sometimes at an early
stage before clinical or operative evidence is detected (occult hepatic
metastases).
Staging
Transcoelomic spread: Rare
Duke’s Classification
A: confined to the bowel wall
B: through the bowel wall but not involving the free peritoneal serosal surface;
C: lymph nodes involved.
D: implies either advanced local disease or metastases to the liver.
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Table 5.6: Colorectal Cancer TNM staging AJCC UICC 2017
Primary Tumor (T)
T category T criteria
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ: intramucosal carcinoma (involvement of lamina propria with no
extension through muscularis mucosae)
T1 Tumor invades the submucosa (through the muscularis mucosa but not into the
muscularis propria)
T2 Tumor invades the muscularis propria
T3 Tumor invades through the muscularis propria into pericolorectal tissues
T4 Tumor invades the visceral peritoneum or invades or adheres to adjacent organ or
structure
T4a Tumor invades through the visceral peritoneum (including gross perforation of the bowel
through tumor and continuous invasion of tumor through areas of inflammation to the
surface of the visceral peritoneum)
T4b Tumor directly invades or adheres to adjacent organs or structures
Regional lymph nodes (N)
N category N criteria
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 One to three regional lymph nodes are positive (tumor in lymph nodes measuring ≥0.2
mm), or any number of tumor deposits are present and all identifiable lymph nodes are
negative
N1a One regional lymph node is positive
N1b Two or three regional lymph nodes are positive
N1c No regional lymph nodes are positive, but there are tumor deposits in the
o Subserosa
o Mesentery
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o Non-peritonealized pericolic, or perirectal/mesorectal tissues
N2 Four or more regional nodes are positive
N2a Four to six regional lymph nodes are positive
N2b Seven or more regional lymph nodes are positive
Distant metastasis (M)
M category M criteria
M0 No distant metastasis by imaging, etc, no evidence of tumor in distant sites or organs.
(This category is not assigned by pathologists.)
M1 Metastasis to one or more distant sites or organs or peritoneal metastasis is identified
M1a Metastasis to one site or organ is identified without peritoneal metastasis
M1b Metastasis to two or more sites or organs is identified without peritoneal metastasis
M1c Metastasis to the peritoneal surface identified alone/with other site or organ metastases
Prognostic Stage Groups
T N M Clinical Stage group
Tis N0 M0 0
T1, T2 N0 M0 I
T3 N0 M0 IIA
T4a N0 M0 IIB
T4b N0 M0 IIC
T1, T2 N1/N1c M0 IIIA
T1 N2a M0 IIIA
T3, T4a N1/N1c M0 IIIB
T2, T3 N2a M0 IIIB
T1, T2 N2b M0 IIIB
T4a N2a M0 IIIC
T3, T4a N2b M0 IIIC
T4b N1-N2 M0 IIIC
Any T Any N M1a IVA
Any T Any N M1b IVB
Any T Any N M1c IVC
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Management
Preoperative:
The bowel is cleared by enemas and oral stimulant laxatives (e.g. Picolax).
Metronidazole and gentamicin (or a cephalosporin) is given at the time of surgery.
The haemoglobin level is checked and blood transfusion given if necessary.
1. Operative:
Principle wide resection of the growth with regional lymphatics.
In the unobstructed case, the bowel can be prepared beforehand and primary
resection with restoration of continuity can be achieved.
In the obstructed case, in which bowel preparation is contraindicated, the primary
goal is to relieve obstruction.
It may be possible to achieve primary resection with restoration of continuity at the
same time, but the poor vascularity and high incidence of colonic anastomotic
breakdown means that this is undertaken only after serious consideration.
The options would be to use an extended right colonic resection round to the splenic
flexure, or bring out a defunctioning colostomy or ileostomy.
2. Postoperative
Adjuvant chemotherapy with 5 - fluorouracil (5 - FU), in combination with folinic
acid, may reduce the risk of recurrent disease.
For metastatic disease:
o The combination of 5 - FU together with folinic acid and irinotecan may
prolong survival.
Follow - up cross - sectional imaging is performed to detect local recurrence and
liver metastases:
o If there is metastasis to one lobe of the liver in the absence of other disease
resect the affected liver lobe.
Follow - up surveillance colonoscopy is undertaken at intervals to detect new
tumors and local recurrence.
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5.4. Gastric Outlet Obstruction (GOO)
Case Discussion……………………………….………..……294
History……………………………………………………………294
Physical Examination……………………………………..295
Investigation………………………………………………….296
Differential Diagnosis…………………………………….298
Management…………………………………………………298
Discussion of the Case……………………………………299
Case Discussion
This is a 65-year-old, male who came with of vomiting of 8 months duration. The Vomiting
was projectile, non-bilious and non-blood tinged. There was associated burning epigastric
pain of 2 years duration along with nausea, weight loss, easy fatigability and anorexia. On
physical examination, the patient was chronically sick looking with pale conjunctiva and
palms. Abdominal examination showed a decreased bowel sounds in addition to a 7x7,
tender, hard mass in the epigastric area that moves with respiration.
History
The cardinal symptoms a patient with GOO are:
o Nausea and vomiting
Physical Examination
General Appearance
o Chronically ill looking
o Malnourished with evidence of weight loss
o Dehydrated with signs like:
Oliguria Confusion
Dry skin Irritability
Sunken eye ball Fainting
Rapid heartbeat
Rapid breathing On Vital sign
Decreased BP
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Lymphoglandular system:
o The left supraclavicular lymph node can be enlarged (Virchow's node) in cases
of a metastatic gastric cancer.
o Periumbilical lymph node might also be palpable (Sister Mary Joseph's node) in
cases of metastatic gastric cancer.
Abdominal examination
o Visible gastric peristalsis: This can be elicited by asking the patient to drink a
glass of water.
o A distended abdomen with tympanitic mass may be appreciated in the
epigastric area and/or left upper quadrant as the stomach dilates.
o Succussion splash can also be experienced.
It is a sloshing sound heard with a stethoscope rested over the upper
abdomen during a sudden movement of the patient.
It is reflective of retained gastric material.
Is done after 3 hrs.
A palpable abdominal mass is noted in a minority of patients.
Investigation
Laboratory studies
May be normal or nonspecifically abnormal.
Serum electrolyte:
o Hypokalemic hypochloremic metabolic alkalosis:
Prolonged vomiting leads to loss of hydrochloric acid.
Bicarbonate is increased in the plasma to compensate the loss.
Potassium shifts to the extracellular compartment due to alkalosis.
With continued vomiting, sodium is preserved while potassium is
excreted by the kidneys hypokalemia.
CBC:
o Anemia may be seen in patients with:
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Peptic ulcer disease Large gastric polyps
Primary or metastatic malignant diseases
Serum tumor markers:
o CA 19-9 and/or CEA:
Can be elevated in patients with pancreatic cancer.
Can also be elevated in other malignancies involving the gastrointestinal
tract, as well as some benign conditions.
Imaging
Plain abdominal X-ray:
o The gastric bubble and the proximal duodenum can be enlarged.
o Air may be absent in the small bowel.
Contrast studies:
o With water-soluble contrast or barium studies.
o In complete GOO the contrast won’t pass to the small bowel.
o Although not specific it can give clues to the underlying etiology.
o The stomach should be decompressed first to minimize risks of aspiration.
Abdominal CT scan:
o Can show gastric distention o Air-fluid level
o The retained contents in the o Can suggest the specific causes
gastric lumen
Endoscopy:
o Useful to identify a specific cause and in therapeutic procedures.
o The stomach should be decompressed first to decrease risk of aspiration.
o Patients should fast for at least 4 hrs.
o Parenteral PPIs should be given to reduce gastric secretions and inflammation.
o Endoscopic biopsy:
Can confirm a diagnosis and exclude malignant diseases.
It can show false negative results if the tumor is extraluminal or does not
involve the mucosa.
Surgical specimens are better to diagnose gastroduodenal tuberculosis.
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Differential Diagnosis
Management
Principles of management:
o Correcting the metabolic abnormality.
o Treating the mechanical cause.
Correcting the metabolic abnormality:
o Rehydration with an IV isotonic saline:
To allow kidney to correct the acid-base abnormality.
o Replacement of K, Ca, and Mg.
In anemic patient blood transfusion may be considered.
Gastric decompression
o Should be done with nasogastric tube or large bore nasogastric tubes.
IV proton pump inhibitors should be administered to:
o Decrease gastric secretion.
o Improve inflammatory response.
Definitive treatment is based on the underlying etiology.
It includes:
o Stenting o Endoscopic balloon dilation
o Chemotherapy o Surgery
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Discussion of the Differentials
Introduction ……………………………………………………………299
Epidemiology…………………………….……………………………..299
Etiology…………………………………….………………………………300
Clinical Manifestation……………………………………………….301
Diagnosis………………………………………………………………….303
Management……………………………………………………………305
Introduction
Peptic ulcers are defects in the gastrointestinal mucosa that extend through the
muscularis mucosae.
Corrosive effect of acid & proteolytic effect of pepsin are responsible.
Common sites are:
o First part of duodenum o Stoma after gastric resection
o Lesser curvature of stomach
Less common:
o Distal esophagus
o Meckel’s diverticulum, which contains ectopic gastric epithelium
It can be an acute or chronic ulceration.
Epidemiology
H. pylori infection determines the disease burden.
o The ulcer incidence in H. pylori-infected individual ulcer incidence is around
1% per year, which is 6-10x higher than for uninfected individual.
In developing countries:
o Most children get infected before the age of 10.
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o More than 80% of adults are infected before the age of 50.
In developed countries:
o Infection before the age of 10 is uncommon.
o It is around 10% in those between 18 and 30 years of age.
o It is around 50% in those older than age 60.
The peak age incidence in gastric ulcer is older than duodenal ulcer.
The sex incidence is equal for gastric ulcers unlike duodenal ulcers with a slight
predilection of men.
Gastric ulceration is substantially less common than duodenal ulceration.
Etiology
There are 2 major factors:
o Helicobacter pylori infection, and
o Non-steroidal anti-inflammatory drugs (NSAIDs): The risk of PUD is dependent
on factors like:
Prior history of ulcer Genetic predisposition
Dose Comorbidities: cardiovascular
Duration of action disease
Duration of therapy
Co-therapy with drugs that enhance toxicity
Advanced age of the patient (generally above 75 years)
Other unusual causes include:
o Drugs other than NSAIDs:
Acetaminophen Sirolimus
Bisphosphonates Spironolactone
Glucocorticoids SSRIs
Clopidogrel Chemotherapy
o Hormonal or mediator-induced:
Gastrinoma Carcinoid syndrome
Systemic mastocytosis Myeloproliferative disorders
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Antral G-cell hyperfunction
o Postgastric surgery and postprocedure ulceration
o Other infections like:
Herpes simplex virus type I Candidiasis
Cytomegalovirus
o Radiation therapy
o Inflammatory and infiltrating disease like:
Sarcoidosis Crohn disease
o Idiopathic
Clinical Manifestations
Patients with PUD usually come with a complaint of dyspepsia which is an upper
abdominal pain or discomfort.
o It is seen in almost 80% of patients.
o It is described as gnawing or burning in nature and may radiate to the back.
o It is intermittent.
o Duodenal ulcer pain:
It is considered to occur 2-5 hrs after a meal and at night (between
about 11 PM and 2 AM).
It is relieved by eating food or taking antacids.
It is aggravated by hunger.
Gastric ulcer pain occurs immediately after a meal.
o The Symptoms are periodical which may be related to the spontaneous
healing of the ulcer.
o They may disappear for weeks or months to return again.
Other possible manifestations include:
o Vomiting: becomes more prominent with stenosis occurrence.
o Heart burn
o Bleeding:
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It may be acute which may present with nausea, hematemesis, or
melena. In rare cases, with hematochezia and orthostatic
hypotension if it is massive.
It may be chronic which may present with microcytic anemia.
o Alteration in weight:
Patients with gastric ulcer are often underweight unlike duodenal
ulcer patients.
o Gastric outlet obstruction: occurs as a complication of PUD located in the
pyloric channel or duodenum.
o Penetration and fistulization: is one of the complications of PUD in which the
peptic ulcers penetrate through the bowel wall without a free perforation.
The pain typically becomes more intense with longer duration
Is frequently referred to the lower thoracic or upper lumbar spine
region.
It is not relieved by food or antacids.
This change in symptom pattern may be gradual or sudden.
Gastrocolic or duodenocolic fistulas can present with halitosis,
feculent vomiting, postprandial diarrhea, dyspepsia, and weight loss.
o Perforation: present with sudden severe, diffuse abdominal pain.
Occurs in 2-10% of patients.
Duodenal perforations are the commonest next to prepyloric
ulcerations.
Stages of perforation:
Stage 1:
Chemical peritonitis on the first 2-4 hrs after a leak of duodenal and gastric
contents especially HCl followed by agonizing pain +/_ coffee ground
vomitus, Melina.
Pale & anxious pt, increase pulse, Normal BP
Guarding and rigidity of abdomen
Rebound tenderness all over the abdomen.
Absent liver dullness & often bowel sound
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Stage 2:
It is also called stage of reaction/stage of delusion/illusion.
It lasts for 3 to 6 hrs.
There is improvement of symptoms.
But signs are worse feeble pulse, hypotensive, shifting dullness plus
guarding, absent bowel sounds.
Stage 3
Bacterial peritonitis
Severely ill ,dehydrated, toxic with Hippocratic face in shock
Hypovolemic and septicemic
Distended abdomen with guarding and generalized tenderness.
On physical exam:
o For uncomplicated PUD findings are few and non-specific.
o Patients might present with signs of GOO mentioned above.
o In perforation patient might appear with:
Fever Dehydration
Tachycardia Ileus
o Abdominal examination reveals
Exquisite tenderness Guarding
Rigidity Rebound tenderness
Diagnosis
H pylori testing: is essential in all patients with peptic ulcer.
Endoscopic or invasive tests for H pylori include:
o A rapid urease test: is test of choice.
Tests the bacterial product urease on the biopsy specimen.
o Histopathology
Sensitivity is about 95% and specificity 99%.
o Culture:
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Sensitivity is about 80% and specificity 100%.
Non-invasive tests:
o Serology/ Fecal antigen test: detects H pylori antigens in stool.
It lacks specificity when blood is present in the stool due to cross
reactivity with blood constituents.
This test cannot be used to assess eradication after therapy because
the antibody titers can remain high for a year or more.
o Urea breathe test:
It is based on the ability of H. pylori to hydrolyze urea.
Its sensitivity and specificity are both greater than 95%.
In the presence of H pylori infection, after ingestion of the carbon
isotope- labeled urea, urea will be metabolized to ammonia and
labeled bicarbonate which is excreted in the breath as labeled carbon
dioxide.
False-negative results can occur if the test is done too soon after
treatment, so it is usually best to test 4 weeks after therapy is finished.
It is the method of choice to document eradication.
Upper endoscopy:
o It is the most accurate diagnostic test.
o Benign ulcers features:
Smooth, regular, rounded edges, with a flat, smooth ulcer base often
filled with exudate.
o Malignant ulcer features:
An ulcerated mass protruding into the lumen.
Folds surrounding the ulcer crater are nodular, clubbed, fused, or stop
short of the ulcer margin.
Overhanging, irregular, or thickened ulcer margins.
o Biopsy should be taken of ulcers with malignant features.
Upper Gastrointestinal Radiography:
o It requires the demonstration of barium within the ulcer crater.
o With single-contrast: 50% of duodenal ulcers may be missed.
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o With double-contrast studies: 80% to 90% of ulcer craters can be detected.
o Malignant ulcers appear: large, interrupted, fused, or nodular mucosal folds
approaching the margin of the crater, irregular filling.
Management
Principles:
o Relieve symptoms o Prevent recurrence
o Heal ulcer o Prevent cause
Lifestyle modifications:
o Avoiding cigarette smoking
It retards ulcer healing.
o Discontinuation of aspirin or NSAIDs, if possible.
o Decreasing usage of alcohol
It damages the mucosa
o Decreasing usage of coffee
It strongly stimulates acid secretion.
Medical management:
o H2 -receptor antagonists:
Most ulcers can be healed within few weeks.
Some patients are relatively refractory to the conventional dose.
o Proton pump inhibitors:
Majority of benign ulcers heal within 2 weeks.
Most patients become asymptomatic within few days.
They are safe to use.
Relapse after therapy cessation occurs.
o Antacids:
Most effective when ingested 1 hour after a meal.
If taken on an empty stomach, the antacids are emptied rapidly and
have only a transient buffering effect.
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o Eradication of Helicobacter pylori:
It is associated with higher healing rates of ulcer.
Eradication of infection should be confirmed four or more weeks after
the completion of therapy.
In patients with risk factors for macrolide resistance, we use bismuth
quadruple therapy including:
PPI
Bismuth subcitrate or Bismuth subsalicylate
Tetracycline (500 mg)
Metronidazole (250 to 500 mg)
In patients without risk factors for macrolide resistance, we use
clarithromycin-based triple therapy including:
PPI
Clarithromycin(500mg) and
Amoxicillin (1 gram) or Metronidazole (500 mg)
Surgical management:
The four classic indications for surgery are:
o Intractability o Perforation
o Hemorrhage o Obstruction
The surgical procedures used are:
1. Vagotomy +/- drainage: includes:
Truncal vagotomy:
o Is the most common operation performed for duodenal ulcer disease.
o It is usually done together with a drainage procedure.
Selective vagotomy
Highly selective/parietal cell vagotomy
o Preserves the vagal innervation of the gastric antrum so that there is
no need for routine drainage procedures.
2. Gastric resection:
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A. Truncal Vagotomy and Antrectomy:
The most common indication is gastric ulcer.
Relative contraindications include cirrhosis, extensive scarring of the
proximal duodenum, and previous operations on the proximal duodenum.
It is far more effective at reducing acid secretion and recurrence.
It requires reconstruction of GI continuity:
o Gastroduodenostomy/ Billroth I procedure or
o Gastrojejunostomy/ Billroth II procedure
B. Subtotal Gastrectomy :
Rarely performed today.
Done in patients with:
o Underlying malignancies
o Recurrent ulcerations after truncal vagotomy and antrectomy.
Restoration of GI continuity is done with:
Billroth II anastomosis
Roux-en-Y gastrojejunostomy
Introduction ……………………………………………………………308
Epidemiology……………………………………………………………308
Risk Factors………………………………………………………………309
Clinical Manifestation………………………….……………………311
Diagnosis…………………………………………….……………………312
Staging…………………………………………………....………………313
Management……………………………………………………………315
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Introduction
Epidemiology
4th most common cancer in men
5th most common cancer in women
Globally:
o 8% of all cancers and 10% of deaths.
o Peak age is around 60-84 years.
o Male : Female=2:1
o Blacks are affected twice as whites
o High incidence in low socioeconomic status
o 95% are Adenocarcinomas.
o Over all declining is related to distal stomach; however, proximal is
increasing.
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o Fatality to case ratio 70%
o Incidence highest
Eastern Asia South America
Eastern Europe
o Lowest:-Northern and Southern Africa
In Ethiopia:
o TAH 1992-96: 96pts operated, 437 GIT Cancer patients
22% of GIT Cancers M:F = 2.4:1
Mean age 48 yrs
o World Health Ranking:
6th most common cancer 3rd cause of ca death
Risk Factors
Environmental factors:
o Diet:
Salt and salt-preserved foods:
A potential synergistic effect of salt and H. pylori.
By damaging stomach mucosa and increasing the risk of
carcinogenesis.
Nitroso compounds
o Obesity
o Smoking
o Occupational exposures:
Coal and tin mining
Steel and iron processing
Rubber manufacturing industries
o Helicobacter pylori:
Triggers inflammation at the corpus mucosa that results in atrophy and
intestinal metaplasia.
Six fold increase in the risk of adenocarcinomas distal to the cardia.
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o Regular use of NSAIDs
It has been inversely associated with the risk of distal gastric
adenocarcinoma.
o Epstein-Barr virus
o Alcohol
o Socioeconomic status:
Distal gastric cancer is high in low socioeconomic status.
Proximal gastric cancer is high in higher socioeconomic class.
o Gastric surgery
o Cancer survivors who received abdominal irradiation
o Reproductive hormones:
Gastric ca is lower in women suggesting a protective role of reproductive
hormones in women.
Host-related factors
o Blood group:
Blood group A has 20% increased risk than those of group O, B, or AB.
o Familial predisposition:
Hereditary (familial) gastric cancer accounts for 1-3% of the global
burden.
It comprises:
Hereditary diffuse gastric cancer (HDGC)
Gastric adenocarcinoma and proximal polyposis of the stomach
(GAPPS)
Familial intestinal gastric cancer (FIGC).
o Gastric polyps: many have malignant potential.
o Gastric ulcer:
Approximately 25% of patients have a history of gastric ulcer.
All gastric ulcers should be followed to complete healing
Those that do not heal should undergo resection.
o Pernicious anemia:
2-6 fold increased risk.
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Clinical Manifestations
Symptoms:
It lacks specific symptoms early in the course of the disease.
The most common symptoms are:
o Weight loss:
Is due to decreased intake, which may be attributed to anorexia,
nausea, abdominal pain, early satiety, and dysphagia.
o Persistent abdominal pain:
Epigastric area
It is non-radiating
It is not relieved by food ingestion
Early in the disease: vague and mild
As it progresses: severe and constant
Dysphagia
o Occurs in proximal gastric ca.
Nausea and early satiety:
o Due to tumor mass
o Due to poor distensibility in linitis plastica with diffuse mural involvement.
Gastric outlet obstruction:
o Occurs in an advanced distal tumor.
Occult GI bleeding is frequently seen
o Results in iron deficiency anemia.
Overt bleeding occurs in 20% of cases.
Physical signs:
Most commonly associated with locally advanced or metastatic disease.
o Patient may present with signs of anemia:
Pale conjunctivae, skin pallor and the like.
o Virchow's node:
Palpable left supraclavicular lymph nodes.
Is the most common finding of metastatic disease.
o Irish node:
A left axillary node.
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o Sister Mary Joseph's node:
A periumbilical nodule
o Palpable abdominal mass:
Present in long-standing and advanced disease.
o Blumer's shelf:
Peritoneal metastasis to the pouch of douglas which is palpable by
rectal examination.
o Krukenberg's tumor:
Metastasis to ovary leading to an enlarged ovary.
o A metastasis to the liver can lead to hepatomegaly.
Other clinical features like jaundice, ascites, and cachexia can also
occur.
o If peritoneal carcinomatosis occurs ascites can be a manifestation.
o Signs GOO mentioned above can occur is there is obstruction.
Paraneoplastic syndromes such as:
o Dermatomyositis
o Acanthosis nigricans Poor prognostic features.
o Circinate erythemas
Diagnosis
Laboratory Tests:
o CBC: to look for anemia and for the need of pre-operative blood transfusion.
o Liver function test: if there is metastasis to the liver.
Endoscopy:
o Helps to determine the anatomic location and extent of a lesion.
o Biopsy can be taken.
During endoscopy adds to its clinical utility.
A single biopsy has a sensitivity of 70% seven biopsies from the ulcer
margin and base has a sensitivity of greater than 98%.
A combination of strip and bite biopsy techniques: to diagnose linitis plastica.
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o Brush cytology:
Increases the sensitivity of single biopsies
If bleeding with biopsy is a concern.
Barium studies:
o Shows irregular filling defect and infiltrating lesions.
o False-negative results can occur in as many as 50% of cases.
o It has 14% sensitivity in early gastric ca.
o “Leather-flask" appearing stomach: can be seen in case of linitis plastica.
Ultrasound and CT-scan:
o Useful to rule out secondaries on liver, ovaries and other sites.
o To look for an enlarged nodes, and detect ascites.
Laparoscopy:
o To stage disease.
o Picks up peritoneal secondaries; detect occult metastases, organ
invasion.
o Can be used to take :
Biopsy of peritoneum and Peritoneal lavage for cytology
nodes Laparoscopic US
o It will avoid unnecessary laparotomy.
o It is more accurate than CT.
Staging
There are two major classification systems currently in use for gastric cancer:
o The Japanese classification
The most elaborate; it is based upon refined anatomic location,
particularly of the lymph node stations
o The American Joint Committee on Cancer (AJCC) and the Union for
International Cancer Control (UICC) classification:
The more widely used staging system, It is based upon tumor, node,
and metastasis (TNM) classifications, refer the table below
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Table 5.8: Stomach Cancer TNM staging AJCC UICC 2017
Primary Tumor (T)
T category T criteria
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ: Intraepithelial tumor without invasion of the lamina propria, high-
grade dysplasia
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Prognostic stage groups
T N M Clinical Stage group
Tis N0 M0 0
T1 N0 M0 I
T2 N0 M0 I
T1 N1, N2, or N3 M0 IIA
T2 N1, N2, or N3 M0 IIA
T3 N0 M0 IIB
T4a N0 M0 IIB
T3 N1, N2, or N3 M0 III
T4a N1, N2, or N3 M0 III
T4b Any N M0 IVA
Any T Any N M1 IVB
Management
Aims of surgery:
o Palliative resection or bypass:
For bleeding or obstruction
o Curative resection when possible.
Resection is considered curative if:
No evidence of gross or residual tumor.
No involvement of serosa, no T3 or T4 tumor.
o No evidence of metastatic tumor.
Management of gastric ca is a multidisciplinary Approach:
o Surgery o Radiotherapy
o Chemotherapy
Surgery:
o It is the treatment of choice for carcinoma stomach.
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o The most common procedure is gastrectomy (total, subtotal or distal)
Signs of in-operability:
o Distant metastasis o Hard nodular liver (secondaries)
o Malignant ascites o Peritoneal seedling like
o Sr. Mary joseph’s nodes krukenberg
o Fixed to pancreas and retro peritoneum
o Celiac, para-aortic, supraclavicular LNs
Endoscopic:
o Excision of early gastric Ca
o Haemostatic for bleeding lesions
o Endoscopic palliation (stent placement)
o Recannalization of neoplastic obstruction
Surgical treatment; gastric resection:
o The most important determinant of resectability is the stage of the disease
o Type of procedure is determined by:
Growth pattern on biopsy Location of LN metastasis
Site and macroscopic size of lesion in stomach
o Type of procedure
Subtotal gasterectomy:
For an early or well circumscribed T2 Ca
If the proximal edge is>2cm from esophagogastric junction
A 5cm clearance is required for more infiltrative lesions.
Total gasterectomy:
If the proximal distance from the junction is<5cm or
If it is diffuse with submucosal infiltration.
o Recommendations of UIAC &Japanese Research Society:
Proximal 3rd:
Extended gasterectomy + distal esophagectomy.
Distal 3rd:
Subtotal gasterectomy (intestinal) & Total gasterectomy (diffuse).
Middle 3rd:
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Total gasterectomy
o In all cases:
Excision of the greater and lesser omentum is undertaken with the
anterior leaf of the omental bursa (lesser sac).
Duodenum should be divided at least 2cm beyond the pylorus.
o If it is adherent to adjacent structures removal of part or whole of the organs
en block is necessary to obtain a macroscopically free margin.
o Reconstruction GI continuity is by Roux-en Y jejunal loop.
o Jejunal interposition pouches to improve nutritional intake.
Lymphadenectomy:
o Extended to reduce regional recurrence
o Allows more accurate staging and better prediction of survival.
o Radicality of dissection D1,D2,D3 is categorized by level of complete node
groups excised:
D1 resection:
Removal of perigastric lymph nodes.
Done when nodes are not involved (N0).
D2 resection:
Removal of group N1&N2 Nodes (left gastric/ common
hepatic/splenic/retropancreatic)
Adjuvant and Neoadjuvant therapies
o Surgery is principal Rx
o Advanced disease has limited outcome.
o Chemo and Radiotherapy does not prolog 5yr survival (used for palliation).
o Neoadjuvant chemotherapy:
Allow downstaging of disease to increase respectability.
Decrease micrometastatic disease burden prior to surgery.
Determine chemotherapy sensitivity.
Reduce the rate of local and distant recurrences.
Palliative treatment:
o Radiotherapy:
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Relief from bleeding, obstruction, and pain in advanced disease.
o Surgery:
Wide local excision Gastrointestinal bypass
Partial gasterectomy
o Combined chemo radiation o Endoscopic laser therapy
o Endoluminal stenting and Feeding jejunostomy
Case Discussion
A 54-year-old man presents to the emergency department with a 4-day history of abdominal
distension, central colicky abdominal pain, vomiting and constipation. On further questioning
he says he has passed a small amount of flatus yesterday but none today. He has had a previous
right-sided hemicolectomy 2 years ago for colonic carcinoma. He lives with his wife and has no
known allergies. On physical exam His blood pressure and temperature are normal. The pulse is
irregularly irregular at 90/min. He has obvious abdominal distension, but the abdomen is only
mildly tender centrally. The hernia orifices are clear. There is no loin tenderness and the rectum
is empty on digital examination. The bowel sounds are hyperactive and high pitched. Chest
examination finds reduced air entry basally. P a g e 318 | 548
History
Physical Examination
Vital signs
o Fever and tachycardia- strangulating obstruction.
o Hypotension- dehydration and strangulation
HEENT
o Dry mucous membranes – dehydration
Abdomen
o surgical scars
o Look for hernia sites
o Auscultation may reveal high-pitched or hypoactive bowel sounds- not very
helpful.
o Tenderness to light percussion, rebound, guarding, and localized tenderness-
peritonitis
o Tympany is usually present due to air-filled loops of bowel or stomach.
o Abdominal mass
An abscess Volvulus Tumor
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o Central lump which hardens on pulsation- intussusception
o DRE:
Empty rectal vault, but occasionally a rectal mass can be the cause of
obstruction.
Gross or occult blood- with intestinal neoplasm, ischemia, and
intussusception
Etiology
In our setup: volvulus and hernia
In western setup: adhesion
1. Adhesions 6. Inflammatory bowel disease
o Common after previous 7. Radiation enteritis
abdominal/gynaecological 8. Intussusception
surgery 9. Trauma
2. Malignancy 10. Early post op obstruction
3. Strictures 11. Superior mesenteric artery
4. Incarcerated hernia syndrome: unusual cause
5. Gallstone ileus
Investigation
Lab
The urea nitrogen and creatinine and the hematocrit- degree of dehydration.
CBC
o Leukocytosis with leftward shift may indicate the presence of strangulation.
o Hb- low in malignancy and dehydration
Serum electrolyte:
o Metabolic alkalosis can be seen in patients who have frequent emesis
o Lactic Acidosis can result if the bowel becomes ischemic or if dehydration is
severe enough to cause hypoperfusion of the gut and other tissues.
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o Serum lactate: is elevated in mesenteric ischemia and is a sensitive, though
not specific, marker of strangulation in SBO
Imaging:
Plain abdominal X-ray: upright chest film
o Dilated small bowel loops (>3 cm in diameter)
o Multiple air-fluid levels seen on upright films
o Paucity of air in the colon.
Small bowel series
o Standard for determining whether an obstruction is partial or complete
o Inferior to CT in the detection of closed-loop obstruction or ischemic
o Rarely offer any indication of the etiology of the obstruction
CT scan
o Abdominal pathology can be detected
o Closed-loop or strangulating obstruction detected in some cases
o The diagnosis of obstruction is made when
There is a discrepancy in the caliber of proximal and distal small bowel
Absence of air or fluid in the distal small bowel or colon- complete
obstruction.
Distended, fluid-filled, sometimes C-shaped or U-shaped loop of bowel
with prominent mesenteric vessels converging on the point of torsion
or incarceration- Closed-loop obstruction
o Advanced small bowel ischemia can be recognized by intestinal pneumatosis
and hemorrhagic mesenteric changes.
Ultrasonography:
o Is more sensitive and specific than plain films for the diagnosis of small
bowel obstruction but not as accurate as CT
o For pregnant patients or as a bedside test for the critically ill
P a g e 322 | 548
Differential Diagnosis
1. Paralytic ileus
Paralytic ileus occurs to some degree after almost all open abdominal operations
and can also be caused by peritonitis, trauma, and intestinal ischemia.
It is exacerbated by electrolyte disorders, particularly hypokalemia.
As the intestine becomes distended, the patient experiences many of the symptoms
of obstruction described above, despite the absence of a mechanical obstruction.
On radiologic examination there is air in the colon and rectum, and by CT or small
bowel series there is no demonstrable obstruction.
2. Intestinal pseudo-obstruction
It is a chronic condition characterized by symptoms of recurrent abdominal
distention.
The colon is generally affected more than the small intestine.
No mechanical cause can be demonstrated in these patients, and they frequently
have a history of several previous operations for bowel obstruction during which no
cause for obstruction could be found.
Laparotomy should be avoided in these patients; once diagnosed, the preferred
treatment is nasogastric suction, correction of any metabolic abnormalities, and in
some cases parenteral nutrition
Management
Aims of treatment
o To relieve obstruction
o To correct dehydration
o To prevent recurrence
o To control peritonitis and to save life
1. Supportive management: partial SBO due to metastatic intraabdominal malignancy,
recurrent adhesive obstruction, obstructing radiation enteritis, or during the early
postoperative period.
Limiting oral intake
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Nasogastric decompression is achieved by the passage of a non-vented (Ryle)
or vented (Salem) tube.
Fluid and electrolyte replacement -Hartmann’s solution or normal saline
Antibiotics: if complicated
2. Surgical treatment
Relief of obstruction -- delayed until resuscitation is complete (no sign of
strangulation or evidence of closed-loop obstruction)
Adequate exposure is best achieved by a midline incision (If the site of
obstruction is unknown, see diagram below)
Incarcerated inguinal hernia- an inguinal incision even if bowel resection is
required
Operative treatment of most other types of small bowel obstruction requires
laparotomy or laparoscopy for exploration.
Growth/gangrene
Viable Bowel Gangrene No gangrene
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Table 5.9: Difference between Viable and Non-viable Bowel
Viable Non-viable
Circulation Dark changes to lighter color Dark color
Visible pulsation in mesenteric arteries No detectable pulsation
General Appearance Shiny Dull and lustreless
Intestinal Musculature Firm Flabby, thin and friable
Peristalsis maybe observed No peristalsis
Small bowel obstruction (SBO) occurs when the normal flow of intestinal contents is
interrupted
Pathogenesis
The hallmark of SBO is dehydration and its sequelae.
P a g e 325 | 548
When normal luminal flow of intestinal contents is interrupted, the small intestine
proximal to the obstruction begins to dilate as intestinal secretions are prevented
from passing distally.
This has a number of consequences that depend, in part, upon the site and the
degree of obstruction.
o Patients with proximal obstruction (jejunum) experience repeated bouts of
nausea and emesis and typically cease taking in food or liquids orally.
o These features are less prominent in patients with distal obstruction (ileum).
Swallowed air and gas from bacterial fermentation accumulates, adding to the
dilatation.
Bacterial overgrowth occurs in the proximal small bowel, the contents of which are
normally nearly sterile, and therefore the emesis can become feculent due to
bacterial overgrowth.
As the process continues, the bowel wall becomes edematous and the intestine's
normal absorptive function is lost so that even more fluid is sequestered in the
bowel lumen.
Secretion of fluid into the lumen of the proximal dilated bowel increases. With
worsening edema of the intestine, there is transudative loss of fluid into the
peritoneal cavity.
o The end result is increasing dehydration with concomitant electrolyte
derangements and decreased urine output.
o Tachycardia, oliguria, azotemia, and hypotension can result from progressive
dehydration.
In more proximal obstruction, emesis causes the loss of fluid containing Na, K, H, and
Cl, resulting in metabolic alkalosis.
Strangulation complicates from 7 to 42% of bowel obstruction and occurs when
bowel wall edema and increasing intraluminal pressure compromise perfusion to a
segment of intestine.
o Necrosis ensues, with concomitant fever and leukocytosis, which will
eventually lead to perforation unless the process is interrupted.
P a g e 326 | 548
o Necrosis of the small bowel during obstruction is most commonly caused by
twisting of the mesentery (such as in volvulus) from an adhesive band acting
as the point of fixation.
o Mortality is significantly increased in the setting of strangulation.
o Strangulation of the intestine almost always occurs in the setting of complete
obstruction.
o Obstruction of the small intestine can be complete or partial.
o One exception to that rule is a Richter's hernia, a condition in which only part
of the circumference of a segment of intestine passes through a hernia
orifice.
In such cases strangulation can occur without complete obstruction of
the lumen.
A closed-loop obstruction occurs when a segment of intestine is obstructed in two
locations, creating a segment with no proximal or distal outlet.
o If undetected, closed-loop obstruction can rapidly progress to strangulation.
o In this setting, there may only be a short segment of intestine that is
distended, making the diagnosis difficult because of minimal abdominal
distention.
It is therefore of utmost importance to determine whether a bowel obstruction is
complete or partial, and whether strangulation of the intestine is impending or has
occurred.
The location and cause of obstruction are of secondary importance, although in rare
circumstances this information may affect subsequent management decisions.
Diagnosis:
The diagnosis of SBO is generally made based upon clinical and radiographic features
It must be distinguished from non- obstructing causes of bowel dilatation.
See above for more.
P a g e 327 | 548
5.6. Large Bowel Obstruction (LBO)
Case Discussion……………………….………………………….…328
History……………………………………………….…………….……328
Physical Examination………………………….…………….……329
Investigation……………………………………………….….……..330
Management………………………………………………..……….332
Differential Diagnosis……………………………………….……333
Discussion of the Differentials…………………………..……334
Case Discussion
This is a 77 years old male patient who presented with inability to pass feces and flatus for
7 days duration which was accompanied by abdominal distension. He had the same
complaint starting 10 years back with 3-month recurrence with one episode lasting for not
more than a day. He also has history of abdominal pain, nausea and vomiting. The patient
is conscious and chronically ill looking. The vitals are within normal range. There is a
sagittal scar extending from the umbilicus till the pubic symphysis.
History
Risk factors:
o Ask risk factors for malignancy (colonic cancer or non-colonic like pancreatic
cancer, ovarian cancer, and lymphoma )
o Prior abdominal surgery adhesive large bowel obstruction
o Repeated bouts of intestinal inflammation strictures; examples include:
diverticulitis, sequelae of ischemic colitis and inflammatory bowel disease.
o Benign conditions that lead to rectal stenosis like inflammatory bowel
disease, tuberculosis, suppository use, radiotherapy, fibrosis due to
endometriosis, lymphogranuloma venereum, and postoperative stricture.
P a g e 328 | 548
Clinical Features:
o Acute Obstruction:
Abdominal Pain:
- Infraumbilical and cramping type with paroxysms of pain occurring
every 20 to 30 minutes.
- Pain in the low pelvis may be due to rectal tenesmus as a sign of
rectal obstruction.
- Focal abdominal pain may indicate peritoneal irritation due to
ischemia or colonic necrosis, whereas a sudden relief of pain followed
by a progressive worsening of pain may relate to intestinal
perforation.
Nausea and/or vomiting: particularly with proximal colonic obstruction
Bloating
Obstipation
o Chronic obstruction:
Progressive change in bowel habits, typically over weeks to months.
A change in bowel habits associated with unintentional weight loss over
the same period is suggestive of malignancy.
Physical Examination
Patients with colorectal obstruction, particularly those with a delayed presentation,
may have signs of dehydration, shock, or even abdominal compartment syndrome
from severe colonic distention.
Check features of toxemia or septicemia: tachycardia, tachypnea, fever
Abdominal examination:
o Inspection: check for abdominal distention, which can be particularly
dramatic for distal complete obstructions.
o Auscultation: increased/high pitched metallic sounds; if fatigue occurs or
gangrene develops, bowel sounds are not heard—silent abdomen.
P a g e 329 | 548
o Palpation: check for abdominal tenderness, initially localized but later
becomes diffuse
o PR Examination: Shows empty, dilated rectum, often with tenderness. If
rectal growth is the cause for obstruction, it may be palpable.
Investigation
Lab studies
o Serum electrolytes
There is derangement of most of the electrolytes (hypokalemia,
hyponatremia, hypochloremia) in case of intestinal obstruction which
needs to be corrected preoperatively.
Strangulation may be associated with deranged potassium, amylase or
lactate dehydrogenase.
o Complete blood count
Low hemoglobin indicates underlying malignancy.
Increases total WBC count indicates infection and sepsis (perforation).
Definitive diagnosis
1. Plain abdominal X-ray Gas shadows appear earlier than fluid
Upright position: Air fluid levels:
levels, so if fluid levels are pronounced,
Multiple in small bowel obstruction
the obstruction is advanced.
Two big in sigmoid volvulus
Isolated air fluid level at the area of left colon suggests malignant
obstruction at the recto sigmoid bowel.
Supine position:
Indicates the distal limit of the obstruction
Central distension indicates small bowel obstruction
Peripheral distention indicates large bowel obstruction
Valvulae Conniventes in small bowel
Haustrations in large bowl.
P a g e 330 | 548
Caecum has no haustrations:- It appears as a round gas shadow in the
right iliac fossa.
Lateral erect X Ray:
To see gas in the rectum, absence of gas in the rectum is suggestive of
complete mechanical obstruction
Anteriorly located bowel distension is suggestive of small bowel
obstruction.
Posteriorly located distension is suggestive of large bowel obstruction
2. Sigmoidoscopy If the obstruction is in the distal segment
When large amount of colonic air of the colon it usually does not give rise to
extends down to the rectum, flexible or small bowel fluid levels unless advanced,
rigid sigmoidoscopy will readily exclude whereas in proximal colonic obstruction
a rectal or distal sigmoid obstruction. may do so in the presence of an income-
petent ileocaecal valve.
3. Barium Enema: With water soluble contrast material.
Bird’s beak appearance in sigmoid volvulus.
Apple core appearance in colonic malignancy.
To differentiate large bowel obstruction from pseudo-obstruction, which is a
severe impairment in the ability of the intestines to push food through, is by
using a limited water soluble enema should be undertaken.
But contrast studies with enema are contraindicated in case of perforation.
4. Ultrasound
Sonographic evidence has been established for small bowel and colonic
obstruction.
o Simultaneous observation of distended and collapsed bowel
segments.
o Free peritoneal fluid
o Inspissated intestinal content
o Paradoxical pendulating peristalsis
o Highly reflactive fluid within the bowel lumen
o Bowel wall edema between serosa and mucosa
P a g e 331 | 548
o A fixed mass of aperistaltic, fluid filled, dilated intestinal loops.
Advantages of US includes:
o Is well suited to critically ill patients, because it can be performed at
the bedside
o Is relatively inexpensive
o Is easy and quick to perform
o Can provide a great deal of information about the location, nature,
and severity of the obstruction
5. CT Scan of the Abdomen:
It can ascertain level of obstruction
It can assess the severity of the obstruction and determine its cause.
It can detect closed loop obstruction and early strangulation.
It can detect inflammatory and neoplastic processes both outside and inside
peritoneal cavity.
Can visualize small amounts of intraperitoneal air or pneumatosis cystoides
intestinalis not seen in the conventional films.
Accuracy higher than 95% sensitivity and more than 94% specificity.
When CT Scanning is not diagnostic, small bowel follow through examination
with dilute barium is often useful.
Management
Preoperative management includes correction of dehydration and electrolytes as
well as relief of symptoms ones the diagnosis is settled.
A- Aspiration: - With Ryle’s tube (NGT)
This is the most important step in the management of intestinal obstruction.
It helps in decreasing the distension
Prevents vomiting
Prevents respiratory complications, such as aspiration during and following general
anesthesia.
B- Bowel care: - No Purgatives
P a g e 332 | 548
Nothing is given by mouth because purgation can cause perforation
C- Charts
Temperature
Pulse
Respiration rate
Intake and output measurement
o In cases of conservative management such as obstruction due to adhesion,
change in temperature and increasing pulse rate, suggest perforation and
gangrene.
o These patients have to be operated immediately.
D- Drugs
To cover gram-positive, gram negative & anaerobic microorganisms.
E- Exploratory Laparotomy
To check and treat the obstruction depending on the
F- Fluids
Should be given before, during and after surgery.
It forms the most the most important treatment of intestinal obstruction.
Differential Diagnosis
1. Volvulus
2. Neoplasm
a. Benign b. Malignant
3. Stricture
a. Diverticular disease b. Ischemic
4. Congenital
a. Anorectal malformation b. Congenital megacolon
5. Impaction Bands
P a g e 333 | 548
Discussion of the Differentials
5.6.1. Volvulus
Introduction ……………………………………………………………334
Epidemiology…………………………………………………………..334
Risk Factors………………………………………………………………334
Clinical Manifestation………………………………………………335
Diagnosis………………………………………………………………….336
Management……………………………………………………………336
Introduction
A volvulus is a twisting or axial rotation of a portion of bowel about its mesentery.
o >180° torsion- obstruction of lumen.
o >360°torsion-vascular occlusion of mesentery Thrombosis Ischemia.
Epidemiology
Sigmoid volvulus accounts for two thirds to three fourths of all cases of colonic
volvulus.
o Cecal and transverse colon volvulus cover the rest.
It usually occurs in older adults with a mean age of 70 years at presentation.
It has been reported in patients with
o Crohn disease o Chagas disease
o Pregnancy
Risk Factors
Older age
Loaded colon due to high residue diet.
Diverticulitis with a band or adhesion
P a g e 334 | 548
Chronic constipation
Anatomic factors
o A long redundant and pendulous colon
o Long mesentery
o Narrow attachment at the base
Clinical Manifestations
Majority of patients present with:
o Insidious onset of slowly progressive abdominal pain which is usually
continuous and severe, with a superimposed colicky component during
peristalsis.
o Nausea
o Abdominal distension which starts from the left iliac fossa and extends to the
rest.
o Constipation.
o Vomiting usually occurs several days after the onset of pain.
A distended tympanic abdomen with tenderness on palpation is a common physical
finding.
Rarely, compromise of the blood supply to the sigmoid colon may result in gangrene,
peritonitis, and sepsis.
If perforation and/ or peritonitis develop EXPECT:
o Fever o Abdominal guarding
o Tachycardia o Rigidity
o Hypotension o Rebound tenderness
P a g e 335 | 548
Diagnosis
Management
The goal of treatment of sigmoid volvulus is to reduce the sigmoid volvulus and to
prevent recurrent episodes.
o First we have to perform the aforementioned principles of management.
o Then deflation of the gut should be done with a flexible sigmoidoscopy or
rigid sigmoidoscopy and insertion of a flatus tube which should be secured
for 24 hours:
To reduce the chance of recurrent volvulus in the acute setting.
o Take X-ray to make sure that the decompression has occurred.
o In the elderly there is a high death rate
~80 per cent at two years
P a g e 336 | 548
If further surgical management is done unlike young patients who
require an elective surgical intervention after week to avoid
recurrence.
o If this method fails, the volvulus is untwisted at laparotomy and the bowel
is decompressed via a rectal tube threaded upwards from the anus and if
viable, it can be fixed to the lateral wall of abdomen or pelvis—
sigmoidopexy.
But resection of the segment and anastomosis is preferable.
P a g e 337 | 548
5.7. Acute Abdomen
Case Discussion……………………………………………………….338
Introduction…………………………………………………………….338
History ……………………………………………………………………338
Physical Examination…………………………………………….…342
Investigation……………………………………………………………343
Management…………………………………………………………..346
Discussion of the Differentials…………………………………346
Case Discussion
A 22-year-old male presents to the emergency room with abdominal pain, anorexia,
nausea, and low-grade fever. Pain started in the mid-abdominal region 6 hours ago and is
now in the right lower quadrant of the abdomen. The pain is steady in nature and
aggravated by coughing. Physical examination reveals a low-grade fever (100.5°F [38°C])
and pain on palpation at right lower quadrant (McBurney sign).
Introduction
It refers to signs and symptoms of abdominal pain and tenderness.
o Previously undiagnosed pain that arises suddenly.
o Less than 7 days duration usually less than 48 hrs.
o If the abdominal pain persists for more than 6 hours it is most likely surgical.
History
Age
o Infants and children: Intussusceptions, Mid gut Volvulus, Incarcerated
hernia, Hirschsprung's disease
o Young: Appendicitis, ovarian/Testicular torsion
P a g e 338 | 548
o Adult: Acute pancreatitis, acute cholecystitis, perforation
o Elderly: intestinal ischemia and infarction, diverticulitis, and sigmoid volvulus
and carcinoma of the colon causing obstruction.
Sex
o Ectopic pregnancy, PID, and twisted ovarian cyst are only seen in females.
o Acute cholecystitis and primary peritonitis are common in females.
o Volvulus, intussusception, and perforated peptic ulcer are common in males.
Elaborate the chief complaint
o Pain is the most common compliant of patients with acute abdomen.
o Onset and duration
Sudden onset(within seconds): perforation, rupture, infarction, stone,
and torsion
Rapidly accelerating pain (within minutes):
- Colic syndromes: biliary colic and ureteral colic.
- Inflammatory processes: acute appendicitis, pancreatitis, and
diverticulitis.
- Ischemic processes: mesenteric ischemia, strangulated intestinal
obstruction, and volvulus.
Gradual onset with increasing in intensity(over several hours):
- Inflammatory conditions: appendicitis and cholecystitis.
- Obstructive processes: nonstrangulated bowel obstruction and
urinary retention.
- Other mechanical processes: ectopic pregnancy and penetrating
or perforating tumors.
Quality of pain
o Colicky: gripping in nature which starts and stops abrubtly and occurs due to
spasm of hollow viscus.
o Dull: deep ache felt in an area, but does not stop the patient from daily
activity.
Initial periumblical pain of appendicitis
o Burning: peritonitis.
P a g e 339 | 548
o Lancinating: piercing or stabbing sensation.
Acute pancreatitis
o Tearing: causing continued or repeated pain or distress.
Dissecting aneurysm
Timing
o Intermittent Colicky/Crampy/ pain: SBO, ureteric stone
biliary colic is an exception
o Persistent, sharp and steadily increasing: infectious or inflammatory process
(e.g., appendicitis).
Location and radiation
o Solid organ visceral pain: generalized in the involved quadrant.
o Appendicitis: diffuse periumbilical pain later shifts to the right lower
abdomen.
o Perforated ulcer, ruptured aortic aneurysm or pancreatitis: may radiate to
the back.
o Genitourinary pain: starts at the flank and radiates to the groin.
Alleviating and aggravating factors
o Diffuse peritonitis:
Worsened by any movement, deep breathing, coughing, or sneezing;
relieved by lying still.
o Intestinal obstruction:
Transient relief after vomiting. Eating may worsen it.
o Acute pancreatitis:
Exacerbated by lying down and relieved by sitting up.
o Non-perforated duodenal ulcer:
Relieved by eating or taking antacids.
o Eating worsens the pain of bowel obstruction, biliary colic, pancreatitis,
diverticulitis, or bowel perforation.
Ask for any associated symptoms:
o Nausea and vomiting.
P a g e 340 | 548
It occurs before the onset of pain in non-surgical conditions like
classic presentation of It occurs after the onset of pain in surgical conditions like appendicitis,
acute appendicitis which pancreatitis, colics.
has been described as pain It is repetitive and profuse in acute pancreatitis and acute intestinal
first, vomiting next and obstruction.
Physical Examination
General appearance
o Acute peritonitis: Patient stays still in the bed in supine position without
moving.
o Colic: restless and unable to find a comfortable position.
Patients with ureteral colic may writhe in pain or walk around the
examination room.
o Biliary obstruction: jaundice
o Septic: weak and lethargic
Vital
o Fever: once patient develops septicemia fever might not be present.
o Hypotension or tachycardia:
It remains normal during the initial phases of appendicitis,
pancreatitis, and peritonitis and develops when sepsis occurs.
In intestinal obstruction it is due to dehydration.
Abdominal examination
o Inspection- Look for any:
Distention: is gradually progressive in acute intestinal obstruction and
acute peritonitis.
Hernia: because they are common causes of intestinal obstruction.
Surgical scars, Bulging masses
Areas of erythema, ecchymosis: bruising around the umbilicus
(cullen’s sign) and around the flank (Grey Turner’s sign) is a feature of
acute hemorrhagic pancreatitis.
Movement with respiration: a diffuse restriction of movement is seen
in a diffuse peritonitis unlike appendicitis and cholecystitis with
localized limitation of movement.
P a g e 342 | 548
Visible peristalsis: step ladder peristalsis is a typical feature of small
bowel obstruction.
o Auscultation-
Hyperactive: in early phases of intestinal obstruction.
Absent bowel sound: is a typical feature of diffuse peritonitis.
o Palpation
Tenderness:
McBurney’s tenderness McBurney’s tenderness
is typical of acute Rebound tenderness indicates an inflamed parietal
appendicitis which is of peritoneum.
spinoumbilical line at Mass
rd
junction of medial 2/3 Guarding and rigidity: indicates an inflamed parietal peritoneum.
rd
and lateral 1/3 . Organomegally
Thoroughly search for hernias
o Percussion:
Tympanic Vs dull,
Signs or fluid collection,
Obliteration of liver dullness: due to bowel perforation.
Rectal examination
o Tenderness or a mass on the right pelvic side wall is sometimes seen in
appendicitis.
o Look for a mass in the rectum and occult blood in the stool specimen.
Other
o Pelvic examination o Testicular/scrotal
Investigation
Laboratory studies
CBC (with differentials):
o Leukocytosis typically suggests an infectious or inflammatory process like
peritonitis.
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Acute appendicitisis is not ruled out with a normal WBC count.
o Anemia suggests either acute or acute on chronic bleeding.
o Increase in hematocrit may indicate hemoconcentration due to dehydration.
Serum electrolyte:
o Hypochloremic hypokalemic metabolic alkalosis occurs in recurrent vomiting.
o Metabolic acidosis (lactic acidosis) and hyperkalemia can occur in bowel
ischemia.
LFT and Liver enzymes:
o Conjugated hyperbilirubinemia, mildly elevated transaminases is expected in
choledocholithiasis, cholangitis, and gallstone pancreatitis.
o Highly elevated transaminases and mild cholestasis can be seen in hepatic
abscess.
Pancreatic enzymes (Lipase and amylase):
o A three-fold elevation in lipase is diagnostic of acute pancreatitis. Amylase is
less specific and may be elevated in other conditions like bowel obstruction
and PUD.
Urinalysis:
o The presence of hematuria, nitrates, and/or urinary crystals should raise
suspicion for a UTI and/or nephrolithiasis.
o Mild pyuria may be present in acute appendicitis because of relationship of
appendix with the right ureter.
β-hCG urine and serum test:
o Should be performed in every woman of reproductive age, regardless of
current contraception use to rule out undiagnosed intrauterine pregnancy
and ectopic pregnancy.
RFT:
o Elevated urea may indicate prerenal azotemia.
o Elevated creatinine is a relative contraindication for IV contrast
administration.
Serum Lactate:
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o Elevated in hypotension/shock like in acute pancreatitis and bowel infarction
due to bowel obstruction/mesenteric ischemia.
Cultures:
o If urinalysis indicates a UTI we do urine cultures.
o Blood cultures in patients with suspected sepsis.
NB. Patients with obvious signs of diffuse peritonitis do not require further diagnostic
imaging and should proceed straight to surgical management.
Imaging studies:
Plain abdominal X-ray:
o Gas under diaphragm is visible in case of perforation.
o Multiple air fluid levels can be seen in intestinal obstruction.
o In the presence of acute peritonitis ground glass appearance can be seen.
o Shows abnormal calcifications:
About 5% of appendicoliths, 10% of gallstones, and 90% of renal
stones contain sufficient amounts of calcium to be radiopaque.
Pancreatic calcifications can be seen in many patients with chronic
pancreatitis.
Ultrasonography:- is preferred for:
o The bedside evaluation of unstable patients.
o Suspected pregnancy and to evaluate for other acute gynecologic disorders
such as:
tubo-ovarian abscess,
ruptured corpus luteum cyst, or
Ovarian torsion.
o It is also preferred for the initial evaluation of suspected acute cholecystitis
and ureteral stones with hydronephrosis
CT-scan:
o It is preferred and can provide a definitive diagnosis in up to 90% of patients
with acute severe abdominal pain
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o It can be falsely negative early in the course of acute pancreatitis, mesenteric
ischemia, cholecystitis, appendicitis, and diverticulitis, especially if performed
without contrast.
MRI imaging:
o It is not widely used yet in the diagnostic work-up of patients who present
with acute abdominal pain.
o Its main advantage is that it lacks ionizing radiation exposure.
Management
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Introduction
Epidemiology
It is common in the second and third decades of life.
The incidence is approximately 233/100,000 population and is highest in the 10 to
19 year-old age group.
Male to female ratio is 3:2.
The lifetime incidence is around 8.6% in male and 6.7% in women.
Etiology
The etiology of appendicitis still doesn’t have a unifying hypothesis.
Although it is associated with the growth of both aerobic and anaerobic organisms,
the initiating event is controversial.
Obstruction of the appendix lumen:
o The lumen of the appendix is small in relation to its length, and this
configuration may predispose to closed-loop obstruction and gives a fertile
ground for overgrowth of bacteria.
o And the continued secretion of mucus leads to intraluminal distention and
increased wall pressure which produces the visceral pain sensation
experienced by the patient as periumbilical pain.
o Subsequent impairment of lymphatic and venous drainage leads to mucosal
ischemia.
o These findings in combination promote a localized inflammatory process that
may progress to gangrene and perforation.
o Inflammation of the adjacent peritoneum gives rise to localized pain in the
right lower quadrant.This can occur due to:
Faecolith (Appendicolith): is composed of inspissated faecal
material, calcium phosphates, bacteria and epithelial debris.
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A fibrotic stricture
Neoplasm of caecum near the base.
Intestinal parasites, particularly Oxyuris vermicularis (pinworm), can
proliferate in the appendix and occlude the lumen.
Non obstructive theory:
o Diffuse inflammation of the appendix due to different kinds of bacteria.
Dietary factors:
o Decreased intake of dietary fiber and increased consumption of refined
carbohydrate.
Familial susceptibility:
o A long retrocecal appendix is more susceptible to appendicitis since there
is a decreased blood flow to the tip.
Abuse of purgatives
Clinical Manifestations
Clinical syndromes of acute appendicitis:
o Acute catarrhal (non-obstructive) appendicitis and
o Acute obstructive appendicitis:
Is characterized by a more acute course.
There may be a generalized abdominal pain from the start.
The temperature may be normal and vomiting is common.
The classic symptoms of acute appendicitis are:
o Abdominal pain: is the most common symptom.
The pain at first is a periumblical colicky type of abdominal pain which
is a visceral pain and later it is shifted to the right iliac fossa which is
more intense, constant and somatic in nature as the inflammation
progresses.
It is aggravated by coughing or sudden movement.
It is known as a migratory pain and is the most reliable symptom; but
is present in only about half of the patients.
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Atypical pain is more common in the elderly
o Anorexia: is a useful and constant clinical feature, particularly in children.
o Nausea and vomiting: if they occur, usually follow the onset of pain and is
nonfrequent. It is due to reflex pylorospasm.
After the first 6 hours, slight pyrexia (37.2– 37.7°C) with a corresponding increase in
the pulse rate to 80 or 90 is usual, but not in 20% of patients.
In many patients, initial features are atypical or nonspecific, and can include:
o Indigestion
o Flatulence
o Bowel irregularity
o Diarrhea: if the appendix is at post-ileal or pelvic position.
o Generalized malaise
o Urinary frequency: Inflamed appendix may come in contact with bladder and
can cause bladder irritation.
NB. The symptoms of appendicitis vary depending upon the location of the appendix.
Signs:
McBurney's point tenderness:
o Is described as maximal tenderness at the spinoumbilical line over the
junction of medial 2/3rd and lateral 1/3rd.
o Has a sensitivity of 50-94% and specificity of 75-86%.
Rovsing's sign:
o It is also called indirect tenderness.
o Refers to pain in the right lower quadrant with palpation of the left lower
quadrant. It is due to displacement of colonic gas and small bowel coils
impinging up on the inflamed appendix.
o Has sensitivity of 22-68% and specificity 58-96%.
The psoas sign:
o Is associated with a retrocecal appendix.
o This is manifested by right lower quadrant pain with passive right hip
extension due to irritation of the right psoas muscle.
o Has a sensitivity of 13-42% and specificity 79-97%.
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The obturator sign:
o Is associated with a pelvic appendix.
o Flexion of the right hip and knee followed by internal rotation produces a
right lower quadrant pain due to irritation of obturator internus muscle.
o Has a sensitivity of 8% and specificity of 94%.
Blumberg’s sign:
o Is rebound tenderness over the right iliac fossa due to inflammation of the
parietal peritoneum.
Cough tenderness: it is due inflammation of the parietal peritoneum.
o Is usefull in differentiating acute appendicitis form ureteric colic.
Per rectal examination shows tenderness over the right side of the rectum.
o Often infection gets localized by omentum, dilated ileum and parietal
peritoneum leading to appendicular mass.
o Most often suppuration occurs in the localized area resulting in appendicular
abscess.
Special features:
Acute Appendicitis in Infancy:
o Is rare, but has a higher chance of perforation with a higher mortality rate.
o Diffuse peritonitis can develop rapidly because of the underdeveloped
greater omentum.
Acute Appendicitis in Children:
o Peritonitis occurs early due to absence of localization.
o Dehydration and septicemia are common.
o Almost all children have vomiting as a symptom.
In Elderly
o Gangrene and perforation occur much more frequently.
o Localization is poor and so peritonitis occurs early due to lax abdominal wall.
o Has a higher mortality rate.
In Pregnancy
o The appendix is pushed to the right upper quadrant during pregnancy.
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o However, pain in the right lower quadrant of the abdomen remains the
cardinal feature, but can also be localized at mid or even the upper right side
of the abdomen.
o Leads to an increased rate of maternal mortality and also leads to premature
labour and fetal loss.
Diagnosis
Laboratory tests
o WBC count with differential:
A very high WBC count suggests a complicated appendicitis with
perforation or gangrene.
A completely normal leukocyte count and differential is found in about
10% of patients with acute appendicitis.
o Serum C-reactive protein (CRP)
o Serum pregnancy test in women of childbearing age
Alvarado score:
o The diagnosis of acute appendicitis is essentially clinical.
Table 5.11: Alvarado (MANTRELS) score
Symptoms Points
Migratory right lower quadrant pain 1 point
Anorexia 1 point
Nausea or vomiting 1 point
Signs
Tenderness in the right lower quadrant 2 point
Rebound tenderness in the right lower quadrant 1 point
Elevated temperature >37.5°C (>99.5°F) 1 point
Laboratory values
Leukocytosis of WBC count >10 x 109/L 1 point
Shift to Left (>75% neutrophils) 2 point
Total score 10
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Score less than 5: Not sure.
Score between 5-6: Compatible. Abdominal ultrasound or contrast-
enhanced CT examination further reduces the rate of negative
appendicectomy.
Score between 6-9: Probable.
Score more than 9: Confirmed
Abdominopelvic CT-scan:
o Is recommended as the preferred test in the imaging evaluation of suspected
appendicitis in adults.
o Intravenous contrast is recommended unless there is contradiction like:
Renal insufficiency
History of hypersensitivity reaction to iodinated contrast.
o Demonstrates higher diagnostic accuracy than ultrasound or MRI.
o The imaging features of acute appendicitis on abdominopelvic CT are:
Enlarged appendiceal double-wall thickness (>6 mm)
Appendiceal wall thickening (>2 mm)
Periappendiceal fat stranding
Appendiceal wall enhancement
Appendicolith (seen in a minority of patients)
Ultrasound:
o Useful to rule other causes.
o It is preferred over CT-scan in children and pregnant women.
o Advantages:
Lack of ionizing radiation and intravenous contrast.
Can be performed at the bedside.
o Disadvantage:
Has a lower diagnostic accuracy than CT or MRI.
Compression over the appendix can cause significant patient
discomfort in patients with appendicitis.
Rates of indeterminate exams are high.
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o Imaging features of acute appendicitis on ultrasound include
Noncompressible appendix with double-wall thickness diameter of >6
mm
Focal pain over appendix with compression
Appendicolith
Increased echogenicity of inflamed periappendiceal fat
Fluid in the right lower quadrant
MRI:
o Is preferred over CT in:
Pregnant women.
Older children who can cooperate with the exam
Plain abdominal X-ray:
o Is not recommended in the diagnostic workup of suspected appendicitis.
o The exam does not visualize the appendix.
o It can be used to rule out other causes of acute abdomen like intestinal
obstruction.
Surgical exploration:
o Is done when clinical suspicion for appendicitis is high but imaging studies are
negative, nondiagnostic, or unavailable.
Management
Catarrhal(non-obstructive) appendicitis:
o Are now treated with conservative management.
o They should generally be hospitalized for treatment with intravenous
antibiotics, bed rest, intravenous fluids, and bowel rest.
o For outpatient management, antibiotics are administered and the course is
followed closely.
o However there is an approximately 15% recurrence rate within one year.
o This approach should also be considered in patients with high operative risk
(multiple comorbidities).
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Preoperative preparation:
o They require adequate hydration with intravenous fluids (isotonic saline or
ringer lactate).
o Correction of electrolyte abnormalities.
o Administration of perioperative antibiotics:
Is important for preventing wound infection and intra-abdominal
abscess following appendectomy.
Should be given within a 60-minute "window" before the initial
incision for patients proceeding directly from the emergency room to
the operating room.
o The patient's vital signs and urine output should be closely monitored; a Foley
catheter may be required in severely dehydrated patients.
Appendicectomy:
Gridiron incision:
o Is made at right angles to spinoumblical line, its centre being along the line at
McBurney’s point.
Rutherford Morison incision:
o Is used when a better access is required. It is an oblique muscle cutting
incision with its lower end over McBurney’s point and extending obliquely
upwards and laterally as necessary.
Lanz incision:
o Is a transverse skin crease. It has a better exposure and extension is easier to
make.
Lower midline abdominal incision:
o Is done when the diagnosis is in doubt.
Laparoscopic Appendicectomy
Is superior over open approach in:
o Management of suspected appendicitis is as a diagnostic tool, particularly in
women of child-bearing age.
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o Lower rate of wound infections.
o Less pain on postoperative days.
o Shorter duration of hospital stay.
o In obese patients
But it inferior in:
o Has a higher rate of intra-abdominal abscesses
o It requires a longer operative time.
1. Ischemia:
a. Ovarian torsion
b. Testicular torsion
c. Mesenteric ischemia
d. Strangulated hernia
e. Ischemic colitis
2. Obstruction:
a. Small bowel obstruction
b. Large bowel obstruction
3. Hemorrhage:
a. Solid organ trauma
b. Leaking or ruptured arterial aneurysm
c. Ruptured ectopic pregnancy
d. Hemorrhagic pancreatitis
e. Intestinal ulceration
4. Perforation:
a. Perforated GI ulcer and cancer
b. Boerhaave’s syndrome
c. Perforated diverticulum
5. Infection:
a. Appendicitis
b. cholecystitis
c. Meckel’s diverticulitis
d. Hepatic abscess
e. Diverticular abscess
f. Psoas abscess
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5.7.2. Acute Cholecystitis
Introduction …………………………………………………………….357
Epidemiology……………………………………………………………357
Etiology…………………………………………………………………...358
Clinical Manifestation………………………………………………359
Diagnosis………………………………………………………………… 359
Management……………………………………………………………361
Introduction
The term cholecystitis refers to inflammation of the gallbladder.
It can be:
o Acute cholecystitis:
Refers to a syndrome of right upper quadrant pain, fever, and
leukocytosis. It can be:
Calculus cholecystitis:
Is an obstructive cholecystitis due to gallstones.
It is more common.
Acalculous cholecystitis:
Less often, without gallstones.
It has a more fulminant course and more commonly
progresses to gangrene, empyema, or perforation.
o Chronic cholecystitis:
It develops over time and be discovered histologically following
cholecystectomy.
Epidemiology
The distribution and incidence of acute cholecystitis follow that of cholelithiasis
because of the close relationship between the two.
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It occurs in approximately 20% of patients with biliary colic if they are left
untreated.
However incidence is falling likely due to early treatment of symptomatic
gallstones.
It is 3 times more common in women than in men up to the age of 50 years, and
is about 1.5 times more common in women than in men thereafter.
Etiology
Cholecystolithiasis accounts for 90%–95% of all causes of acute cholecystitis.
o The “5F ” Risk factors for cholelithiasis can be an indirect factors:
Female gender Fat
Forty Fair
Fertile
o Common to all individuals with these “5Fs” are high levels of estrogen and
progesterone which leads to reduction in gallbladder contractility and bile
stasis.
o Hemolytic anemia, surgery, and drugs can also be risk factors.
Acalculous cholecystitis accounts for the remaining 5%–10%.
Although the exact etiology is unclear, gallbladder stasis and ischemia have been
implicated as causative factors.
o Risk factors are:
Older age Total parentral nutrition
Diabetes Prolonged fasting
HIV infection Immobility
Vascular disease ICU patient
Critically ill patients after trauma, burns and major operations.
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Clinical Manifestations
Diagnosis
Laboratory tests
o WBC count with differential: there is leukocytosis with a left shift which is an
increased number of band forms.
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Ultrasonography
o Finding calculi on ultrasound in the presence of right upper quadrant
abdominal pain and fever suggests an acute cholecystitis but is not
diagnostic.
o Additional sonographic features include:
Gallbladder wall thickening (greater than 4 to 5 mm) or edema (double
wall sign).
A "sonographic Murphy's sign" can be elicited which can confirm that
the inspiratory arrest is indeed due to the gallbladder.
o It has a sensitivity of 84% and specificity of 99%.
Cholescintigraphy/HIDA scan:
o Is indicated if the diagnosis remains uncertain following ultrasonography.
o A 99mTc-hepatic iminodiacetic acid is injected intravenously and is excreted
into the biliary tree within 30-60 minutes.
o In acute cholecystitis edema of the cystic duct prevents the dye from entering
the gallbladder. The test is positive if the gallbladder is not visualized.
o It has a sensitivity of 90-97% and specificity of 71-90%.
o False positive results occur in:
Cystic duct obstruction with a stone or tumor.
Severe liver disease.
Patients with total parenteral nutrition.
Biliary sphincterotomy.
Hyperbilirubinemia.
o False negative results are uncommon but can occur if the obstruction is
incomplete.
Abdominal CT-scan:
o Is usually unnecessary.
o It can easily demonstrate gallbladder wall edema.
o It is useful when we suspect acute cholecystitis complications like:
Emphysematous cholecystitis
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Gallbladder perforation
o It may fail to detect gallstones because many stones are isodense with bile.
Management
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5.7.3. Acute Pancreatitis
Introduction …………………………………………………………….362
Epidemiology……………………………………………………………363
Etiology…………………………………………………………………...363
Clinical Manifestation………………………………………………364
Diagnosis…………………………………………………………………365
Management…………………………………………..………………367
Introduction
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Epidemiology
Although rare in kids, it may occur at any age, with a peak in young men and older
women.
There is no sex predilection.
The annual incidence is 4.9-35/100,000 population.
It is the leading gastrointestinal cause of hospitalization in the United States.
The mortality rate has decreased due to advancement in diagnostic and therapeutic
interventions.
Etiology
The two major causes are:
o Biliary calculi: accounts for 50–70% of patients, and
o Alcohol abuse: accounts for 25% of cases.
Other causes include:
o Mechanical ampullary obstruction:
Biliary sludge Ampullary stenosis
Ascariasis Periampullary diverticulum
Pancreatic or periampullary cancer
Duodenal stricture or obstruction.
o Toxic:
Ethanol Scorpion venom
Methanol Organophosphate poisoning
o Metabolic:
Hyperlipidemia (types I, IV, V) Hypercalcemia
o Drugs:
Corticosteroids Valproic acid
Azathioprine Thiazides
Asparaginase Oestrogens
o Infection:
Viruses: mumps, coxsackie, hepatitis B, CMV, varicella-zoster, HSV,
HIV
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Bacteria: mycoplasma, Legionella, Leptospira, salmonella
Fungi: aspergillus
Parasites: toxoplasma, cryptosporidium, Ascaris
o Hyperparathyroidism: causing hypercalcemia
o Trauma:
Blunt or penetrating abdominal injury
Iatrogenic injury during surgery or ERCP (sphincterotomy)
o Congenital: Cholodochocele type V
o Vascular:
Ischemia Atheroembolism
Vasculitis (polyarteritis nodosa, SLE)
o Genetic: CFTR and other genetic mutations
o Miscellaneous:
Post ERCP Renal transplantation
Pregnancy Alpha-1-antitrypsin deficiency
Clinical Manifestations
Pain is the cardinal symptom.
o It has an acute onset and is persistent for several hours or days, severe and is
often felt over the epigastric abdominal area, but can also be felt over either
of the upper quadrants.
o The pain radiates to the back in approximately 50% of patients in a” belt like”
manner.
o It may be partially relieved by sitting up or bending forward.
There is retching, nausea and repeated vomiting which may persist for several hours
in 90% of patients.
o The retching may persist despite the stomach being kept empty by
nasogastric aspiration.
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There may also be dyspnea and hiccoughs, in case of diaphragm irritation and
pleural effusion.
On physical exam: it varies with the severity.
o The patient might appear well or in severe cases gravely ill with profound
shock, toxicity and confusion.
o Tachypnoea is common,
o Tachycardia is usual, and hypotension may be present.
o The body temperature is often normal or even subnormal, but frequently
rises as inflammation develops.
o Mild icterus can occur due to obstructive jaundice caused by
choledocholithiasis or edema of the head of the pancreas.
o On abdominal exam:
There is epigastric tenderness and guarding.
They may also have abdominal distention and hypoactive bowel
sounds due to an ileus secondary to inflammation.
An epigastric mass can also be palpated due to inflammation.
Although not pathognomonic for acute pancreatitis bruising around
the umbilicus (cullen’s sign) and around the flank (Grey Turner’s sign)
can also be present.
o In 10–20 % of patients’ plural effusion, pulmonary edema and pneumonitis
are present.
Diagnosis
Laboratory tests:
o Serum amylase:
It rises within 6 to 12 hours of the onset.
It has a half-life of approximately 10 hours.
It returns to its normal level within 3-5 days in uncomplicated cases, so
a normal serum amylase level doesn’t exclude acute pancreatitis.
An elevation of 3-4 times above the normal is indicative of the disease.
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o Serum lipase:
It rises within 4-8 hours of the onset.
It peaks at 24 hours.
It returns to its normal level within 8-14 days.
It elevates earlier and last longer as compared with elevations in
amylase
It is more sensitive and specific test than amylase.
o Trypsinogen activation peptide (TAP):
Is elevated in acute pancreatitis.
It useful in detection of early acute pancreatitis and as a predictor of
the severity of acute pancreatitis.
Plain erect chest and abdominal radiographs:
o Are not diagnostic.
o Non-specific findings in pancreatitis include:
A generalised or local ileus (sentinel loop),
A colon cut-off sign: reflects a paucity of air in the colon distal to the
splenic flexure due to functional spasm of the descending colon
secondary to pancreatic inflammation.
A renal halosign.
Occasionally, calcified gallstones or pancreatic calcification may be
seen.
o A chest radiograph may show a pleural effusion and, in severe cases, a diffuse
alveolar interstitial shadowing may suggest acute respiratory distress
syndrome.
Abdominal ultrasound:
o The pancreas appears diffusely enlarged and hypoechoic.
o Gallstones may be visualized in the gallbladder or the bile duct.
o To rule out acute cholecystitis as a differential diagnosis.
Abdominal CT-scan:
o Findings with the use of an intravenous contrast are:
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Focal or diffuse enlargement of the pancreas with heterogeneous
enhancement.
Can distinguish interstitial from necrotising pancreatitis
If done three or more days after the onset, it can detect the presence
and extent of pancreatic necrosis and local complications and predict
the severity of the disease.
MRI:
o On contrast-enhanced, failure of the pancreatic parenchyma to enhance
indicates the presence of pancreatic necrosis.
o Can yield similar information to that obtained by CT and has a higher
sensitivity for the diagnosis of early acute pancreatitis and can better
characterize the pancreatic and bile ducts and complications of acute
pancreatitis.
o MRCP is comparable to ERCP for the detection of choledocholithiasis.
Management
Assessment of severity should be done first.
o Helps to predict the pts course and Complications.
o Identify patients who need admission to the ICU.
o Guides use of prophylactic antibiotics, urgent bile duct imaging and early
ERCP.
o There are different scores like:
Atlanta criteria and APACHE II scoring system
MODS score SIRS score
Ranson criteria CT severity index
o They have low specifictiy and positive predictive value but good negative
predictive value.
Supportive treatment:
o Aggressive fluid and electrolyte replacement (Crystalloids)
o Blood sugar control: Sliding scale insulin
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Table 5.12: RANSON CRITERIA
At admission Within 24hrs
Age > 55yrs HCT drop > 10 Number Mortality
<2 1%
WBC > 16,000 BUN > 5
3-4 16%
Glucose > 200 Arterial PO2 < 60mmHg
5-6 40%
LDH > 350IU/L Base deficit > 4mEq/L
7-8 100%
AST > 250IU/L Serum Ca < 8
Fluid sequestration > 6L
o Pain control:
Adequate pain control requires the use of intravenous opiates.
o Pancreatic rest / Nutrition:
For Patients with mild pancreatitis can often be managed with
intravenous hydration alone since recovery occurs rapidly unlike
patients with severe pancreatitis which need nutritional support.
o Organ support
o Antibiotics:
Are not recommended in acute pancreatitis as a prophylaxis
Can be given if extra-pancreatic infection is suspected.
o Prompt identification and treatment of Complications.
In acute pancreatitis that require intervention include:
o Local complications o Infected Pancreatic necrosis
o Pancreatic necrosis with persistent Symptoms
o Persistent /symptomatic Pseudocyst
The types of intervention are:
o Percutaneous o Surgical (laporascopic or open)
o Endoscopic
Treatment of Biliary stone associated pancreatitis:
o Early ERCP for selected patients:
Concomitant cholangitis Bil >5mg/dl
Persistent biliary obstruction Severe biliary pancreatits
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5.8. Perianal Emeregency
Case Discussion………………………………………………………….369
Introduction……………………………………………………………….369
Differential Diagnosis…………………………………………………369
Discussion of the Differentials……………………………………370
Case Discussion
A 28-year-old man presents to the emergency department complaining of anal and lower-
back pain for the previous 36 h. He has tried taking simple analgesics with no benefit. The
pain is progressively getting worse and he is now finding it uncomfortable to walk or sit
down. He is otherwise fit and well and smokes 10 cigarettes a day. On physical
examination, Inspection of the anus reveals a 3cm by 3 cm swelling at the anal margin.
The swelling is warm, exquisitely tender and fluctuant. There is no other obvious
abnormality.
Introduction
Differential Diagnosis
o Anorectal abscess
o Anal fissure
o Fistula inano
o Thrombosed hemorrhoid
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Discussion of the Differentials
Introduction ……………………………………………………….370
Epidemiology………………………………………………………370
Risk Factors…………………………………………………………371
Clinical Manifestation…………………………………………371
Investigation……………………………………………………….372
Management…………………………………………………..….373
Introduction
Perianal and perirectal abscesses are common anorectal problems.
The infection originates most often from an obstructed anal crypt gland:
o The resultant pus collects in the subcutaneous tissue, intersphincteric
plane, or beyond (ischiorectal space or supralevator space) various types
of anorectal abscesses form.
Once diagnosed, anorectal abscesses should be promptly drained surgically.
An undrained anorectal abscess can continue to expand into adjacent spaces as well
as progress to generalized systemic infection.
Epidemiology
The mean age of presentation is 40 years
o Range from 20 to 60
Adult males are twice as likely to develop an anorectal abscess and/or fistula
compared with females
30 to 70 % of anorectal abscesses are associated with a concomitant anorectal
fistula
30 to 40 % of patients develop an anorectal fistula after undergoing treatment for an
anorectal abscess
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Risk Factors
Sexually transmitted infections and an infected anal fissure are common cause of
anal abscesses.
Some other risk factors include:
o Crohn’s disease o Diabetes
o Ulcerative colitis
o A compromised immune system due to illnesses like HIV
o Anal sex
It can increase the risk of anal abscesses in both men and women
o Use of the medication:
Prednisone or other steroids
o Current or recent chemotherapy
Clinical Manifestations
History:
The classic locations of anorectal abscesses, listed in order of decreasing frequency,
are as follows:
o Perianal
o Ischiorectal
o Intersphincteric
o Supralevator
The clinical presentation correlates with the anatomic location of the abscess.
Almost all perirectal abscesses are associated with perirectal pain:
o It is indolent in nature.
o It is exacerbated by movement and increased perineal pressure from sitting
or defecation.
o Associated with the pain patients may also complain of dull perianal
discomfort and pruritus
Those with an ischiorectal abscess often present with:
o Systemic fevers and chills
o Severe perirectal pain and fullness consistent with the more advanced nature
of this process.
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External signs are minimal and may include
o Erythema
o Induration
o Fluctuance.
Physical Examination:
Patients with anorectal abscesses usually have normal vital signs on initial evaluation
o Only 21% reporting fevers or chills (most likely to be Ischiorectal)
Physical examination in case of perianal abscess demonstrates
o A small, erythematous, subcutaneous mass near the anal orifice.
o It is usually well-defined and fluctuant
On digital rectal examination (DRE):
o A fluctuant, indurated mass may be encountered.
Optimal physical assessment of an ischiorectal abscess may require anesthesia to
alleviate patient discomfort that would otherwise limit the extent of the
examination.
Patients with an intersphincteric abscess present with rectal pain and exhibit
localized tenderness on DRE.
Physical examination may fail to identify an intersphincteric abscess.
Anal abscesses are most often diagnosed through a physical exam
Investigation
CBC:
o WBC might be elevated in case of ischiorectal abscess because systemic
symptoms are more manifested.
Imaging:
o CT, Ultrasound and MRI:
Imaging studies are not usually necessary in the evaluation of
patients with an anorectal abscess
Clinical suspicion of an intersphincteric or supralevator abscess may, however,
require confirmation by means of CT, anal ultrasonography, or MRI.
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o As a rule, use of anal ultrasonography is limited to confirming the presence
of an intersphincteric abscess
This modality can also be used intraoperatively to help identify a
difficult abscess or fistula.
Management
Perianal abscesses almost always require surgical drainage, even if they have
spontaneously discharged
Patients with diabetes
Immunosuppression
Evidence of systemic sepsis
Substantial local cellulitis require urgent drainage
In uncomplicated cases, offer incision and drainage within 24 hours
Drainage leads to an open cavity that typically takes 3-4 weeks to heal
Persistent failure to heal may indicate an underlying fistula
Antibiotics are only indicated:
o If there is extensive overlying cellulitis
o If the patient is immunocompromised.
Introduction …………………………………………………….……374
Risk Factors…………………………………………………….………374
Clinical Manifestation……………………………………….……375
Investigation……………………………………………………….…375
Management…………………………………………………………375
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Introduction
Fistula in ano is an abnormal tract or cavity with an external opening in the perianal
area by identifiable internal opening.
Goodsall’s rule to identify the internal opening offistula in ano suggests that:
o Fistulas with an external opening anteriorly connect to the internal
opening by a short, radial tract.
o Fistulas with an external opening posteriorly track in a curvilinear fashion
to the posterior midline.
o However, exceptions to this rule often occur if an anterior externalopening
is greater than 3 cm from the anal margin.
Such fistulas usually track to the posterior midline.
Risk Factors
Previous anorectal abscess Radiation therapy for prostatic ca.
Trauma Actinomycosis
CD ( Crohn’s disease) TB
Anal fissures LGV
Anal carcinoma
Parks classification for fistula in ano
1. Inter sphincteric 3. Trans sphincteric
2. Supra sphincteric 4. Extra sphincteric
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Clinical Manifestations
History:
Patients often provide a reliable history of previous pain, swelling, and spontaneous
or planned surgical drainage of an anorectal abscess.
Signs and symptoms of fistula-in-ano, in order of prevalence, include the following:
o Perianal discharge o Diarrhea
o Pain o Skin excoriation
o Swelling o External opening
o Bleeding
A review of symptoms may reveal the following in patients with a fistula in ano:
o Abdominal pain o Changes in bowel habit
o Weight loss
Physical examination:
The examiner should observe the entire perineum, looking for an external opening
that appears as an open sinus or elevation of granulation tissue.
Spontaneous discharge of pus or blood via the external opening may be apparent or
expressible on digital rectal examination.
Digital rectal examination (DRE) may reveal:
o A fibrous tract or cord beneath the skin
o It also helps to delineate any further acute inflammation that is not yet drained.
Investigation
Lateral or posterior induration suggests deep postanal or ischiorectal extension.
Laboratory or imaging studies are not done in routine fistula in ano
o Physical examination findings remain the mainstay of diagnosis.
Management
Drainage
Eradicating the fistulous tract
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5.8.3. Anal Fissure
Introduction ……………………………………………………….……376
Epidemiology……………………………………………………………376
Risk Factors……………………………………………………………...376
Clinical Manifestation………………………………………….……377
Management……………………………………………………………378
Introduction
An anal fissure is a painful linear tear or crack in the distal anal canal
o In the short term, usually involves only the epithelium
o In the long term, involves the full thickness of the anal mucosa.
Acute if <6Wks
Epidemiology
Risk Factors
Clinical Manifestations
History:
The symptoms of an anal fissure are relatively specific, and the diagnosis can often
be made on the basis of the history alone.
Typically, the patient reports severe pain during a bowel movement
o The pain lasting several minutes to hours afterward.
o The pain recurs with every bowel movement, and the patient commonly
becomes afraid or unwilling to have a bowel movement
This leads to a cycle of worsening constipation, harder stools, and
more anal pain.
Patients note bright-red blood on the toilet paper or stool.
o Occasionally, a few drops may fall in the toilet bowl, but significant bleeding
does not usually occur with an anal fissure.
Physical examination:
Initially, the fissure is just a tear in the anal mucosa and is defined as an acute anal
fissure.
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If the fissure persists over time, it progresses to a chronic fissure that can be
distinguished by its classic features.
o The fibers of the internal anal sphincter are visible in the base of the chronic
fissure
o An enlarged anal skin tag is present distal to the fissure
o Hypertrophied anal papillae are present in the anal canal proximal to the
fissure.
Management
Conservative treatment to minimize anal trauma
o Bulk agents
o Stool softeners
o Warm sitz baths
o Analgesic creams
Surgical treatment for chronic fissures that failed
medical therapy
o Lateral sphincterotomy
o To decrease spasm of internal sphincter by
dividing a portion of the muscle.
5.8.4. Hemorrhoids
Introduction…………………………………………………….……..379
Risk Factors…………………………………………………….……….379
Clinical Manifestation……………………………………….…..…379
Differential Diagnosis……………………………………….……..380
Investigation…………………………………………………….….….380
Management……………………………………………………….….381
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Introduction
Risk Factors
Constipation Family history
Straining Chronic diarrhea
Pregnancy prolonged toilet sitting
o Postpartum hemorrhoids from Colon malignancy
straining during labor IBD
Low fiber diet Heavy weight lifting
Clinical Manifestation
History
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The presence of pruritus or any discharge should also be noted.
Inflammatory bowel diseases need to be ruled out as the cause of symptoms.
Physical Examination
Differential Diagnosis
Condylomaacuminata Proctitis
Anal fissure Rectal prolapsed
Anal fistula Colorectal ca
Anal abscess
Investigation
Lab Studies
o CBC( infection, anemia)
Imaging Studies
o Anoscopy o Flexible sigmoidoscopy
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Management
Conservative Rx
o Give stool softener
o Advice on
High fiber diet Avoidance of straining
Increasing fluid intake Good hygiene
Non-surgical
o Rubber band ligation o Sclerotherapy
o Infrared photo-coagulation
Surgical
o Excision of thrombosed external hemorrhoids
o Operative hemorrhoidectomy
Case Discussion………………………………………………..……382
Introduction………………………………………………….………382
History ………………………………………………………….………382
Physical Examination……………………………………….……383
Investigation…………………………………………………………383
Evaluation of Special Injuries..………………………………385
Management…………………………………………………………387
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Case Discussion
18-year-old girl has sustained a falling down and she is now complaining of generalized
abdominal pain and left shoulder-tip pain. Examination of her chest is normal, initially; her pulse
rate is 110/min with a blood pressure of 84/60 mmHg. She is slightly drowsy and her GCS is 14.
On examination of the abdomen, there is an abrasion on the left side beneath the costal margin
with tenderness in the left upper quadrant. There is no evidence of any other injuries. The
patient is given 2 L of intravenous fluids and the blood pressure improves to 130/90 mmHg.
Introduction
Abdominal trauma is seen quite often in the Emergency Department and can result
from blunt or penetrating mechanisms.
Blunt abdominal trauma (BAT) is frequently encountered in the form of motor vehicle
crashes (MVCs) (75%), followed by falls and direct abdominal impact.
There are two main kinds of Penetrating abdominal trauma (PAT):
o Stab Wounds (SW) and Gun Shot Wounds (GSW)
o SWs are more common than GSWs, however they have a lower mortality rate
compared with GSWs.
o The higher energy transfer and missile trajectory with multiple bullet fragments
from GSWs leads to increased morbidity and mortality compared to stab
wounds.
History
For MVCs speed of collision, position of colliding car to each other, position of patient
in the car, seatbelt use, and extent of damage (intrusion, windshield damage,
difficulty of extrication, air-bag deployment) are important elements to elicit.
With respect to falls, height of fall is very important.
In gunshot wounds, the type of gun, distance from the shooter, and number of shots
heard are all relevant.
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For stab wounds, it is prudent to obtain information on the type of weapon
used.
AMPLE” history (Allergies, Medications, Past Medical History, Last Oral Intake
and Events Preceding the Incident).
The AMPLE history can be obtained at the same time as the physical exam
portion of the secondary survey if the patient is alert and cooperative.
Physical Examination
The abdomen should be examined by inspection, auscultation, palpation, and
percussion.
The abdominal exam should detail exit and entry wounds, number of wounds,
any evisceration, ecchymosis and deformity, in addition to tenderness.
The perineum, rectum and genitalia should all be examined at this point.
A rectal exam can alert the provider to a high riding prostate, lack of rectal
tone, or heme-positive stools.
The stability of the pelvis should also be assessed during the physical exam.
When assessing a trauma victim, it is important to be aware of factors that
make a physical exam unreliable.
These factors include altered mental status, intoxication and distracting
injuries.
The most important way to make your physical exam reliable is to perform it
serially, noting important changes as the patient is reexamined.
Investigation
Plain films:
o Will be ordered on all abdominal trauma patients.
o Chest and abdominal X ray should be ordered.
o Cervical and Lumbar spine films may be useful as well.
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CT Scan:
o The most common and the most accurate diagnostic modalities for
penetrating and blunt abdominal injury.
o Should only be performed if the patient is hemodynamically stable
o If there is an absolute indication for exploratory laparotomy*, don’t
waste time with a CT.
Focused abdominal sonography for trauma (FAST):
o A series of ultrasound reading looking for bleeding in the abdomen (as
well as in pericardium if there is bleeding can be non-hypovolemic cause
of hypotension.)
o Performed in most patients.
o Ideal for non-stable patients because of its relative efficiency.
Diagnostic peritoneal lavage:
o DPL is used as a method of rapidly determining the presence of
intraperitoneal blood.
o It is particularly useful if the history and abdominal examination of an
unstable patient with multisystem injuries are either:
Unreliable (eg, because of head injury, alcohol, or drug
intoxication) or
Equivocal (eg, because of lower rib fractures, pelvic fractures,
or confounding clinical examination).
o DPL results are considered positive in a blunt trauma patient:
If 10 mL of grossly bloody aspirate is obtained before infusion
of the lavage fluid or
If the siphoned lavage fluid contains more than 100,000 red
blood cells (RBCs)/µL, more than 500 white blood cells
(WBCs)/µL, elevated amylase content, bile, bacteria, vegetable
matter, or urine.
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Evaluation of Specific Injuries
The liver, spleen, and kidney are the organs predominantly involved following blunt
trauma, although the relative incidence of hollow visceral perforation, and lumbar
spinal injuries increases with improper seat-belt usage.
Diagnosis of injuries to the diaphragm, duodenum, pancreas, genitourinary system,
and small bowel can be difficult.
Most penetrating injuries are diagnosed at laparotomy.
Blunt tears can occur in any portion of either diaphragm, although the left
hemidiaphragm is most often injured.
Abnormalities on the initial chest x-ray include elevation or “blurring” of the
hemidiaphragm, hemothorax, an abnormal gas shadow that obscures the
hemidiaphragm, or a gastric tube positioned in the chest.
However, the initial chest x-ray can be normal in a small percentage of patients.
Suspect this diagnosis for any penetrating wound of the thoracoabdominal, and
confirm it with laparotomy, thoracoscopy, or laparoscopy.
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5.9.3. Pancreatic Injuries
Pancreatic injuries often result from a direct epigastric blow that compresses the
pancreas against the vertebral column.
An early normal serum amylase level does not exclude major pancreatic trauma.
Conversely, the amylase level can be elevated from nonpancreatic sources.
Double-contrast CT may not identify significant pancreatic trauma in the immediate
postinjury period (up to 8 hours).
o It may be repeated, or other pancreatic imaging performed, if injury is
suspected. Surgical exploration of the pancreas may be warranted following
equivocal diagnostic studies.
Blunt injury to the intestines generally results from sudden deceleration with
subsequent tearing near a fixed point of attachment, particularly if the patient’s seat
belt was positioned incorrectly.
A transverse, linear ecchymosis on the abdominal wall (seat-belt sign) or lumbar
distraction fracture (i.e., Chance fracture) on x-ray should alert clinicians to the
possibility of intestinal injury.
Although some patients have early abdominal pain and tenderness, the diagnosis of
hollow viscus injuries can be difficult since they are not always associated with
hemorrhage.
Injuries to the liver, spleen, and kidney that result in shock, hemodynamic
abnormality, or evidence of continuing hemorrhage are indications for urgent
laparotomy.
Solid organ injury in hemodynamically normal patients can often be managed
nonoperatively.
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Admit these patients to the hospital for careful observation, and evaluation by a
surgeon is essential.
Concomitant hollow viscus injury occurs in less than 5% of patients initially
diagnosed with isolated solid organ injuries.
Management
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3. Patient selection:
4. Control of hemorrhage and contamination
Simple ligation of blood vessels
Shunting of major arteries and veins
Drainage
Temporary stapling of bowel
Therapeutic packing
Closure
5. Resuscitation continued in ICU: to correct the triad
6. Definitive treatment
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Short Case Discussion
5.10. Ostomy.………………………..………………..…...391
Content By:
Nanati Jemal 5.11. T-Tube.………………………..…..……………..…..397
Mikiyas Mesay
Edited By: 5.12. Hernia.………………………..………….……..…...400
Samuel Mesfin
5.13. Nasogastric Tube (NGT)………………………..420
5.14. Video QRs…………………………………………….425
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5.10. Ostomy
There is pink and fleshy stoma opening through a single circular opening in the Right
lower quadrant. It is not foul smelling and skin irritation wasn’t seen. There is yellow
watery discharge continuously coming out and its amount is not predictable due to
unattached bag. The patient appears emaciated but not dehydrated
What kind of ostomy is it?
o Ileostomy
Has watery discharge
Not foul smelling
The site is RLQ
Emaciated
Introduction
An ostomy is surgery to create an opening (stoma) from an area inside the body to
the outside.
It treats certain diseases of the digestive or urinary systems.
It can be permanent, when an organ must be removed.
It can be temporary, when the organ needs time to heal.
The organ could be the small intestine, colon, rectum, or bladder.
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With an ostomy, there must be a new way for wastes to leave the body.
The part of the bowel that is seen on the abdomen surface is called a stoma.
Types of Ostomy
Tracheostomy Cecostomy
Esophagostomy Nephrostomy
thoracostomy Ureterostomy
Gastrostomy Cystostomy
Jejunostomy Vesicostomy
Ileostomy T-tube
Colostomy
Classify ostomies
o Based on role
o Permanent o Temporary
o Based on type
o End o Loop
o Spectacle o Double barrel
o Temporary indication
Indications
o Gangrenous LBO o Penetrating injuries
o Hemodynamic instability
Trauma, sepsis
o Perianal fistfuls
o High risk leak
Malnourished, immunosuppressed
o Permanent indication
o Rectal excision o Proctocolectomy
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Complications
o Early
o Leakage o Stromal necrosis
o Skin irritation o Stromal retraction
o Late
o Stromal stenosis o Parastomal hernia
o Stromal prolapse
Specific Ostomies
5.10.1. Colostomy
Introduction …………………………………………………………….393
Classification…………………………………………………………….393
Indication…………………………………………………………………394
Complication……………..…………………………………………….395
When to Close..………………………………………………………..395
Introduction
Colostomy: is an iatrogenic fistula between the colon and the skin:
o colo-cutaneous fistula.
Classification
Based on surgical construction
o Loop:
o Penetrating abdominal injury o Perianal injury
o Descending colon diverticula o Congenital megacolon
Double barrel
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Spectacle:
o In ARM o Fistula
End:
o In sigmoid volvulus o volvulus
o Gangrenous
Indications
Temporary
o Trauma
Perianal injury with or without sphincter
Penetrating injury with colonic trauma
o Inflammatory
IBD
High type perianal fistula
o Obstruction
Malignancies
Sigmoid volvulus
Pelvic mass
Congenital:
- ARM
- Hirschsprung’s Disease
Permanent
o Unresponsive incontinence
o APR
o Perianal fistula
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Complications
Early
o Bleeding o Necrotic distal end
Late
o Prolapse o Fecal impaction
o Retraction o Infection
o Hernia o Irritation of skin (95%bile)
o Diarrhea o Depression
When to Close?
At 6-12 weeks
5.10.2. Illeostomy
Introduction …………………………………………………………..396
Indication……………………………………………………………….396
Complication……………..…………………………………………..396
How to differentiate Stomas………………………………….397
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Introduction
Ileostomy - the bottom of the small intestine (ileum) is attached to the stoma.
This bypasses the colon, rectum and anus.
Indications
Child Young adult
Meconium ileus Cohn’s
Illeal Artesia Illeal TB perforation
Long segment HST Typhoid perforation
Complicated volvulus Malignancy
Intussusception Primary volvulus
Gangrenous volvulus
Complications
Immediate
Bleeding’
Necrosis (if double barrel and it clamped branching vessels)
Spillage
Local and adjacent organ injury
Fluid and electrolyte derangement (ileostomy bypasses the fluid absorbing
capability of the colon)
Early
Bleeding Skin irritation Hernia
Infection Retraction Malnutrition
Necrosis Diarrhea
Late
Adhesion Infection
Stenosis Bleeding
Diarrhea (skin contamin-ation Fecal Impaction
and GI microflora) Psychological impact
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How to Differentiate Stomas
5.11. T-Tube
Introduction……………………………………………………………398
Indications……………………………………………………………..398
Placement………………………………………………………………398
Management………………………………………………………….399
Complications…………………………………………………………400
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Introduction
Indications
After Laparoscopic /open Choledochotomy
o Access for postoperative stone retrieval or cholangiography or
choledochoscopy
After biliary tree manipulation
Injury to the common bile duct
Drainage of bile in the setting of CBD or papillary edema
Persistent Duodenal Fistula
Hepaticojejunostomies in the setting of liver transplantation
Pancreaticoduodenectomy
Tracheal stenosis.
Montgomery T tube in ventilator-dependent patients
Placement
A) Prepare T-tube by cutting two limbs at lengths that will not transverse into the left
or right hepatic duct proximally or into the duodenum distally
Excise the back wall of the horizontal portion of the T (to minimize the risk
of tube occlusion and to facilitate tube removal).
B) T-tube should be inserted to the supra-duodenal portion of the common bile duct
The incision on the common bile duct should be vertical.
C) After the incision, the stone is removed followed by T-tube insertion
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D) The remainder of the duct is closed with fine
absorbable sutures around the tube.
Leave enough redundancy in the
intraperitoneal portion of the tube to
avoid tension (and possible tube
disgorgement) in the event of
significant postoperative abdominal
distension.
E) The long segment will be drawn externally in the right upper quadrant and will be
connected to a plastic bag, to be placed under the bed.
It also important to concomitantly drain the Morrison’s pouch, also known
as the sub-hepatic space.
Post-Operative Management
Complications
In situ
o Fluid and electrolyte o Tube dislocation
imbalance o Tube retention
o Early dislodgment o bacteremia
With removal of the T-tube
o Bile leaks o Biliary peritonitisSepsis
5.12. Hernia
Introduction…………………………………………………………401
Precipitating Factors……………………………………………402
Surgical Pathology….……………………………………………403
Basic Feature………………………………………………………404
Complications……………………………………………………..404
Discussion….…………………………………….…………………406
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Introduction
P a g e 401 | 548
Precipitating Factors
P a g e 402 | 548
Surgical Pathology
P a g e 403 | 548
Basic Features
Complications
1. Irreducibility:
When the contents of the sac cannot be completely emptied from the sac
because of:
o Adhesion formed between the contents and the sac or between the
contents themselves;
o Growth of the omentum within the sac;
o Narrowing of the neck of the sac because of fibrosis, e.g., following
continuous pressure of truss;
o Retention of faeces in the large intestine occupying the sac.
In a simple irreducible hernia, though the contents cannot be reduced, the blood
supply remains intact, and there are no symptoms of intestinal obstruction
2. Obstruction:
Irreducibility+ obstruction of the lumen of the contained bowel leading to
intestinal obstruction. The features are:
o The hernia is irreducible but painless.
o Cough impulse may be present.
o Features of intestinal obstruction are present.
o Can precipitate strangulation if not treated early.
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Hernia is one of the commonest causes of intestinal obstruction. So, hernial sites
should always be examined in a patient presenting with intestinal obstruction.
3. Strangulation:
Irreducibility + features of intestinal obstruction + arrest of blood supply to the
contained intestine leading to gangrene.
The features are:
o The hernia is irreducible and painful.
o The sac is tense and tender.
o Cough impulse absent.
o Features of intestinal obstruction present - pain abdomen, vomiting,
abdominal distension, rebound tenderness.
Strangulation is more likely to happen in a hernia with a narrow neck.
Most strangulated herniae are therefore either inguinal or femoral, because
these herniae have narrow necks.
Often, the sac contains the greater omentum which may become gangrenous
due to arrest of blood supply showing the features of strangulation but without
the features of intestinal obstruction.
Strangulation without obstruction also noted in Richter's hernia.
4. Reduction-en-masse:
Sometimes, during forceful manual reduction of irreducible hernia, the
contents together with the covering sac gets pushed forcibly back into the
abdominal cavity; the bowel within the sac may be strangulated by the neck of
the sac.
Thus, the symptoms of obstruction or strangulation may not be relieved
5. Incarceration:
Incarcerated hernia is a variety of irreducible hernia where the content of the sac
is large gut containing faeces.
The large gut is fixed in the sac because of its size or adhesions.
Here, the hernia can be indented like putty with the fingertip pressure because
of the scybalous content of the gut.
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Though the hernia is irreducible, obstruction or strangulation rarely occur.
6. Inflammation
E.g., tuberculosis of the sac
7. Compression or torsion of the omentum within the sac:
The omentum may become gangrenous due to arrest of blood supply
showing the features of strangulation but without features of intestinal
obstruction.
8. Collection of fluid in the hernial sac-hydrocele of the hernial sac.
9. Maydl's hernia
10. Sliding hernia
11. Recurrent hernia
Introduction
This is the most common type of abdominal hernia in both males and females.
There are two types:
1. Indirect or oblique inguinal 2. Direct inguinal hernia
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Surgical Anatomy
Inguinal canal
The hernia sac enters the inguinal canal through the deep inguinal ring lateral to
the inferior epigastric artery.
The neck of the sac is lateral to the inferior epigastric artery.
Indirect hernia is usually congenital due to persistence of patent processus
vaginalis; it appears at or soon after birth or may appear in adolescence.
Indirect hernia may be acquired when the sac is formed as an outpushing of the
abdominal peritoneum through the deep ring.
The acquired variety may occur at any age in adult life due to increased intra-
abdominal pressure following strenuous exercises, heavy weight lifting, straining
at defaecation (chronic constipation) or at micturition (enlarged prostate,
stricture urethra) or at coughing (chronic bronchitis).
The indirect hernia may be subdivided into:
1. Incomplete
2. Vaginal or Complete hernia
Incomplete
• Bubonocele
o The processus vaginalis is closed proximal to the superficial inguinal ring.
o The hernia is limited in the inguinal canal and so appears as an inguinal
swelling.
• Funicular Incomplete hernia
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o Here the processus vaginalis is closed at its lower end, so the sap of the
hernia is separate from the sac of tunica vaginalis.
o The sac is closed and extends beyond the superficial inguinal ring but
stops above the testis.
o The testis lies below the hernia and can be felt separately from the
contents of the hernial sac
o Most of the indirect inguinal herniae belong to this category and are
commonly seen in adults.
o It is usually acquired but may be congenital.
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Direct Inguinal Hernia
The hernia protrudes directly through the posterior wall of the inguinal canal in
the Hesselbach's triangle.
The direct hernial sac lies outside the cord (cf indirect inguinal hernia) - behind,
above or below the cord.
The neck of the sac lies medial to the inferior epigastric artery- a differentiating
point at operation from indirect hernial sac where the neck of the sac lies lateral
to the artery.
Direct herniae are mostly acquired in nature.
It is found predominantly in the elderly males due to increased intra-abdominal
pressure leading to increased wear and tear of the conjoined tendon.
A direct inguinal hernia seldom comes out through the superficial inguinal ring
and thus it is unusual for the sac to descend into the scrotum.
The neck of the direct hernial sac is wide and therefore the hernia appears
immediately on standing and disappears again immediately when the patient
lies down.
Moreover; because of this wide neck obstruction or strangulation is extremely
rare.
P a g e 409 | 548
Diagnostic Criteria
History
1. Age: It occurs in all ages, from birth to elderly. Indirect hernia is more common in
younger and adult life. Direct hernia is more common in elderly people.
2. Sex: Common in males
3. Symptoms:
History of swellings in the groin – inguinal swelling which is gradually
increasing in size.
o The swelling becomes more prominent on standing or straining and
gets smaller or disappears on lying or on manipulation, unless it is
complicated.
• The swelling may expand and extend down to the scrotum - inguinoscrotal
swelling.
• The swelling may be asymptomatic – the hernia may be accidentally
discovered during a medical checkup.
Local discomfort or pain which gets worsened on strenuous effort.
o The pain may be aching sensation in the groin due to the stretching
of the deep inguinal ring by the protruding viscus.
o The pain may be dragging indicating omentocele. As the omentum is
attached to stomach and supplied by Tl2 nerve, the pain may be
referred to the umbilicus.
o Sudden severe pain in the hernia with vomiting and irreducibility
indicates obstruction of the hernia.
• History of chronic strain e.g., cough, constipation and difficulty in passing
urine should be enquired as these may be the cause of hernia formation.
Physical examination:
The patient should be examined first in the standing position and then in lying down
position (supine), if necessary.
1. Inguinal swelling- indirect hernia: bubonocele or direct hernia; Inguinoscrotal
swelling - indirect hernia: funicular or vaginal hernia
2. Shape: A bubonocele or direct hernia is globular in shape. A funicular or vaginal
hernia is usually pyriform in shape.
3. Expansile impulse on coughing - visible and palpable: present.
P a g e 410 | 548
4. Non-tender if uncomplicated
5. Consistency - depends on the contents of the sac: soft, elastic and fluctuant,
resonant on percussion - if it contains gut. Firm and doughy, non-fluctuant and
dull on percussion - if it contains omentum.
6. Getting above the swelling in presence of inguinoscrotal swelling.
• To differentiate a scrotal swelling from inguinoscrotal swelling.
• With the patient standing, normally the spermatic cord is palpated
between the thumb and the fingers at the root of the scrotum.
o In case of scrotal swelling e.g., hydrocele, the spermatic cord
can also be felt easily, above the swelling= so. getting above the
swelling is possible.
o In inguinoscrotal Swelling. 5micular and complete indirect
hernia the spermatic cord cannot be felt nakedly, because iris
covered anterolaterally by the sac, so getting above the
swelling is not possible. On complete reduction of swelling, one
can feel the cord at the root of the scrotum.
7. Relation of the sac with pubic tubercle: To differentiate inguinal from femoral
hernia.
• Inguinal hernia- the swelling is situated above and medial to the pubic
tubercle.
• Femoral hernia-the swelling is situated below and lateral to the pubic
tubercle.
8. Reducibility: All hernia are reducible unless complicated.
• On lying down - the direct hernia usually reduces immediately and
spontaneously, but indirect hernia usually requires manipulation.
• A direct hernia reduces directly backwards.
• An indirect hernia reduces in an upward, backward and lateral direction.
• During reduction confirm the contents of the sac
o If there is gurgling sound, it is an enterocele; if the sac feels
doughy, it is omentocele.
o In enterocele, during reduction the first part of the content is
difficult to reduce but the latter part is easy to reduce.
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o In omentocele, during reduction the first part is easy to reduce
while the latter part is difficult to reduce.
• After reduction:
o Note the relation of the sac with the pubic tubercle.
o Note the reappearance of the swelling on straining or coughing:
ln indirect hernia, the swelling reappears gradually and
steadily in medial and downward directions.
In direct hernia, the swelling reappears immediately
straightforward exactly where it was observed before.
9. Deep ring occlusion test:
• Identification of deep inguinal ring - it lies1 cm above the femoral pulse
felt below the inguinal ligament.
• After the reduction of hernia, the deep ring is occluded by the pressure of
the thumb and the patient is asked to cough:
o Indirect hernia - the swelling does not reappear, so the test is
positive.
o Direct hernia - the swelling reappears immediately, so the test is
negative.
10. Invagination test:
• After the hernia is reduced, the tip of the index finger can be invaginated
into the neck of the scrotum and then pushed inside the inguinal canal
through the superficial inguinal ring - the patient is then asked to cough
o Indirect hernia - a thrust will be felt at the tip of the finger.
o Direct hernia - a thrust will be felt at the pulp of the finger.
Invagination test helps to diagnose an early case of incomplete hernia. It also
helps to differentiate bubonocele and direct hernia from femoral hernia.
Invagination test is not a must.
When necessary, it should be performed very gently not to cause any pain to the
patient.
This test cannot be done in female as the labial skin is thick and not lax.
11. Examine the opposite side also to exclude hernia. Direct hernia is often
bilateral.
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12. Examine the testis, epididymis & spermatic cord.
13. Examine the tone of abdominal muscles by head or leg rising test. Also look for
Malgaigne bulging. Valsalva maneuver may be used to check the tone of the
abdominal muscles.
14. Note for any evidence of chronic straining like chronic bronchitis, enlarged
prostate (per rectal examination), stricture urethra (palpation of bulbar urethra
for thickening).
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above and broad base below
Appearance of the Slowly appears on straining or coughing Easily pops out on standing, straining or
swelling coughing
Reducibility Gradually reduces, may need Usually reduces immediately and
manipulation spontaneously on lying down
Direction of reduction Reduces upwards, then laterally and Reduces upwards and backwards
backwards
Deep ring occlusion Positive i.e. the swelling does not appear Negative i.e. swelling reappears
test after reduction when the patient coughs.
Release of occlusion The swelling appears first in the middle The swelling reappears straight forward
followed by coughing of the inguinal region and the follows exactly where it was before
medially and ultimately turns down to
the neck of scrotum
Obstruction/ Common due to narrow neck of the sac Rare due to wide neck of the sac
strangulation
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5.12.2. Femoral Hernia
Introduction …………………………………………………….………415
Surgical Pathology…………………………………………………….415
Diagnostic Criteria ……………………………………………………416
Introduction
It is the protrusion of the extraperitoneal fat and peritoneum with or without
abdominal contents through the femoral canal. In this hernia the sac passes through
the femoral ring and enters the femoral canal.
Surgical Pathology
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• Due to abdomen (fascia of Scarpa) to the fascia lata of the thigh at the
lower border of the fossa ovalis, the sac cannot pass down in the thigh.
• So, the sac courses, and when enlarging it courses upward over the
inguinal ligament and external oblique aponeurosis and thus the distal
part of the sac overlies the inguinal ligament and occupies the inguinal
region.
• The shape of the sac then becomes retort-shaped.
Diagnostic Criteria
1. Age- middle aged to elderly
2. Sex: More common in females.
3. Symptoms:
• The patient complains of dragging pain in the groin.
• Usually she or he presents with a small globular swelling in the groin. It
becomes more prominent on standing or straining but may disappear on lying
down.
• An obese lady may present with the features of intestinal obstruction or
strangulation of an unnoticed femoral hernia.
• Examination: the femoral hernia should be examined in the similar
manner as in inguinal hernia. Ask the patient to stand up, note the exact
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position of the lump, try to determine the exact anatomical relations of
the lump to the inguinal ligament and pubic tubercle and then note if the
lump has a cough impulse and whether it is reducible.
4. Position- A round or oval swelling below the medial end of the inguinal ligament-
at or below the groin crease.
5. Palpation: The neck of the lump is situated below and lateral to the pubic
tubercle (cf. Inguinal hernia).
6. Cough impulse: Both visible and palpable, may be absent in many femoral hernias
because the contents are adherent to the peritoneal sac.
7. Reducibility: Often partial. When complete it reduces directly upwards and
backwards.
8. Inguinal canal examination, e.g., invagination test – empty
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5.12.3. Incisional Hernia
Introduction ……………………………………………………………418
Predisposing Factors………………………………………………..418
Introduction
• AKA: Postoperative hernia, Ventral hernia
• An abdominal incisional hernia is one where the peritoneal sac herniates through
an acquired scar in the abdominal wall, usually caused by a previous surgical
operation or an accidental trauma.
• Scar tissue is inelastic and can be stretched easily if subjected to constant strain.
• Contents of such hernia are usually bowel and/ or omentum
Predisposing Factors
1. Some subjects:
Obese individuals with poor musculature.
Diabetic patients.
Malnutrition: severe anemia. hypoproteinemia. avitaminosis, e.g., vitamin
C deficiency.Patients with cachexia and advanced malignant disease.
Patients with any chronic source of straining,
2. Some operations:
Operation for peptic perforation or appendicular perforation.
Operation in case of peritonitis.
Operation for visceral cancer.
Pancreatic resection operation.
3. Some incisions:
Kocher’s subcostal incision for cholecystectomy causing injury to the ninth
and tenth thoracic nerves.
McBurney's incision for appendicectomy causing injury to the ilio-inguinal
nerve.
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Battle's para-rectal incision for appendicectomy.
Midline infraumbilical incision e.g., during caesarean section.
4. Some faults during operation:
Division of motor nerves supplying the muscles around the wound.
Defective closure of the laparotomy wound, e.g., failure of suturing the
abdominal wounds in anatomical layers; suturing under tension causes
pressure necrosis of intervening tissues.
Inadequate haemostasis during operation leading to wound haematoma
which becomes more vulnerable if infected.
Wound closed with non-absorbable suture materials like nylon, prolene
are followed by a lesser incidence of incisional hernia than the wound
closed with absorbable sutme like catgut.
Drainage tubes brought through the main laparotomy wound and left
behind for a long time. (lntraperitoneal drains should always be brought
out through a separate stab incision.)
5. Some post-operative complications:
Severe post-operative abdominal distensions causing tension over the
suture line.
Persistent postoperative cough – causing tension over the suture line.
Post-operative peritonitis - because there is a chance of wound infection
and abdominal distension.
Wound infection.
Wound haematoma.
Too early removal of sutures.
Too early resumption of strenuous labour.
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5.13. Nasogastric Tube (NGT)
Introduction…………………………………………………………420
Indications……………………………………………………………420
Contraindications….…………………………………………… 421
Equipment……………………………………………………………422
Placement……………………………………………………………423
Complications………………………………………………………424
Introduction
Indications
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Indication for Pediatric Patients
Acute gastric dilatation
Upper GI bleeding
Decontamination of poisoned children
Intussusceptions in children
Growth failure & poor weight gain
Caustic esophageal injury
Treatment of appendicitis
Inpatient Treatment of pneumonia
DKA in children
Suckling & swallowing disorders in newborn
Fluid & electrolyte therapy
Contraindications
Absolute contraindications
Severe midface trauma
With midface trauma, you run the risk of the NG tube going through
the cribriform plate of the ethmoid bone; if this happens, then the
NG tube will be in the cranial vault with fatal results
Recent nasal, throat, or esophageal surgery.
NG tubes should only be placed by a surgeon if being used for a
patient who's undergone recent nasal, throat, or esophageal
surgery. The risk of reopening the suture line is too great and can
lead to serious post-op complications.
Relative contraindications
Coagulation abnormalities
The mucosal lining of the nasal passages is extremely thin and very
vascular. If your patient has an uncorrected coagulation
abnormality, you run the risk of epistaxis during NG tube insertion.
Severe epistaxis is a true medical emergency; it can lead to airway
compromise and/or aspiration of blood.
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Esophageal varices
The fact that the veins are so close to the surface of the esophagus
makes it easy for them to start bleeding upon NG tube insertion.
Esophageal stricture
The scar tissue isn't as pliable as normal esophageal tissue, making
it easier to become damaged with the insertion of invasive tubes
Alkaline ingestion
With an NG tube in place, the cardioesophageal sphincter can't
completely close, increasing the risk of reflux of the alkaline
substance into the esophagus, causing further damage.
Contraindications in the pediatric population
Congenital birth defects affecting the gastrointestinal tract, most specifically
cleft lip and/or cleft palate.
Recent esophageal or gastric surgery
Head trauma with possible basilar skull fracture
Equipment
Glove
NG tube
Lubricant
cup with water
Syringe & stethoscope
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Placement
P a g e 423 | 548
14. Confirm placement per your facility's
policy. Ways to check placement include
aspirating gastric contents and testing it with pH
paper (a pH of 5.5 or less indicates gastric acid), or
obtaining a chest X-ray.
Special consideration: Average gastric pH is 1 to 3;
with patients who are taking medication for acid
reduction, the pH can be higher than 4.
15. Once placement is confirmed, tape the
tube more securely to the patient's nose.
Complications
Pharyngeal discomfort
Erosion of the naris
Sinusitis
Nasotracheal intubation causing pneumothorax and pulmonary placement
Gastritis
Perforation and bleeding
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5.14. Video QRs
Stoma
NG Tube Insertion
Groin Hernias
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Part 6: Pediatric Surgery
Content By:
Samuel Mesfin
6.1. Approach to Scrotal Swelling……………………427
Edited By:
Samuel Mesfin 6.2. Video QRs………………..………………………………438
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6.1. Approach to Scrotal Swelling
Case Discussion………………………………………………….…427
Introduction………………………………………………………...427
History………………………………………………………………...428
Physical Examination……………………………………….....429
Diagnostic Approach…………………………………………….431
Discussion of the Differentials………………………………431
Case Discussion
A 13-year-old boy was presented to the pediatric emergency with a 2-week history of
swelling of the right scrotal contents, of simple evolution. During the previous 48hrs, his
symptoms worsened by the appearance of acute scrotal pain. He had no known testicular
or scrotal abnormalities. There were no fevers, abdominal pain, nausea or vomiting. He
had no significant past medical, past surgical or family history. The examination revealed a
soft abdomen but with an erythematous right hemiscrotum that was swollen, tense and
particularly painful during its palpation
Introduction
The most common causes of painless scrotal swelling in children and adolescents include
hydrocele and inguinal hernias that are not incarcerated.
Less common causes are varicocele, spermatocele, localized edema from insect
bites, nephrotic syndrome (swelling is usually bilateral), and rarely, testicular
cancer
Scrotal swelling and testicular masses warrant prompt evaluation.
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History
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o Is there abdominal pain associated with decreased appetite,
nausea, and/or vomiting?
These symptoms can be nonspecific but may represent referred
pain associated with testicular torsion.
o Has the patient had fever?
Fever suggests orchitis due to infections such as coxsackie virus,
mumps, or brucellosis.
Fever is also seen in some patients with epididymitis.
Physical Examination
Inspection
o The first step is to inspect the penis, pubic hair, and inguinal area while
the patient is standing.
o The examiner should notice the presence or absence of any ulcers,
papules, urethral discharge, piercings, tattoos, pubic hair infestation, or
lymphadenopathy.
o Ulcers, papules, discharge, and lymphadenopathy may suggest a sexually
transmitted infection.
o Piercings and tattoos may provide a portal of entry for skin and soft tissue
infection.
o The position of the testicles (eg, high versus low and horizontal versus
vertical) should be evaluated.
The left testicle usually lies slightly lower than the right testicle.
o Patients with varicoceles should also be examined in the supine position.
This maneuver will help to differentiate idiopathic from secondary
varicocele.
Idiopathic varicocele usually is more prominent in the upright
position and disappears when the patient is supine, whereas
secondary varicocele usually does not get much smaller with
change in position from upright to supine.
Palpation
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o The examiner should palpate the entire testicular surface by gently rolling
it between his or her thumb and forefingers.
o The testicle should have the consistency of a hard-boiled egg.
o The epididymis should be palpated in the posterolateral position and
followed to the spermatic cord
o The examiner should note any swelling or tenderness along any of these
structures; if swelling is noted, transillumination may help to determine if
it is cystic or solid in nature.
o Transillumination is performed by placing a light source at the base of the
scrotum.
o Fluid-filled masses (eg, hydrocele or spermatocele) will transfer the light
and cause the scrotum to glow; solid masses (eg, torsed testicle) will not.
Cremasteric reflex
o It should be assessed by stroking the upper thigh while observing
the ipsilateral testis.
o Normal response is cremasteric contraction with elevation of the
testis.
o The reflex is present in the majority of healthy boys between the
ages of 30 months and 12 years
o It is almost always absent in patients with testicular torsion, may
help to distinguish this condition from other causes of scrotal pain
Prehn sign (testicular elevation)
o Prehn reported that elevation of the scrotal contents relieves the pain in
patients with epididymitis and aggravates or has no effect on the pain in
patients with the emergency condition, testicular torsion.
o However, Prehn sign may not be a reliable distinguishing feature between
testicular torsion, epididymitis, and other diagnoses in children.
Ancillary studies
o In addition to the genital examination, abdominal and rectal examinations
are indicated if clinical suspicion exists for an abdominal or rectal mass,
metastatic visceral disease, or prostatitis.
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Diagnostic Approach
P a g e 431 | 548
Although the clinical and radiographic evaluations may be normal at the time of
presentation in a boy with an intermittent torsion that has been reduced,
findings may be present to varying degrees on physical examination and imaging.
6.2.3. Epididymitis
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6.2.4. Scrotal Trauma
6.2.5. Hydrocele
A hydrocele is a collection of peritoneal fluid between
the parietal and visceral layers of the tunica vaginalis.
Hydroceles may be communicating or
noncommunicating.
o Communicating hydroceles usually develop as a
result of failure of the processus vaginalis to close
during development; the fluid around the testis is
peritoneal fluid
o Noncommunicating hydroceles have no
connection to the peritoneum; the fluid comes
from the mesothelial lining of the tunica vaginalis
Hydroceles are common in newborns (whether related to delayed closure of a
patent processus vaginalis or fluid trapped at the time of testicular descent is not
known)
o The majority of hydroceles in neonates resolve spontaneously, usually by
the first birthday
o In older children and adolescents, noncommunicating hydroceles may be
idiopathic or may occur secondary to epididymitis, orchitis, testicular
P a g e 433 | 548
torsion, torsion of the appendix testis or appendix epididymis, trauma, or
tumor (reactive hydroceles).
Patients with hydroceles present with a cystic scrotal mass.
A hydrocele that communicates with the peritoneal cavity may increase in size
during the day or with the Valsalva maneuver.
Noncommunicating hydroceles are not reducible and do not change in size or
shape with crying or straining.
In patients with testicular pain and scrotal swelling, the hydrocele may arise from
epididymitis, orchitis, testicular torsion, torsion of the appendix testis or appendix
epididymis, testicular rupture, testicular hematoma, or tumor as the primary
etiology (reactive hydroceles);
Doppler ultrasonography is usually necessary to evaluate these patients further.
The diagnosis of hydrocele can be made by physical examination and
transillumination of the scrotum that demonstrates a cystic fluid collection.
Communicating hydroceles are often reducible; noncommunicating hydroceles are
not.
Doppler ultrasonography may be necessary to evaluate the testicle and rule out a
primary cause.
Surgical repair is indicated for hydroceles in newborns that persist beyond one year
of age, for communicating hydroceles, and for idiopathic hydroceles that are
symptomatic or compromise the skin integrity.
The management of hydrocele in a neonate or child younger than one year of age
usually is supportive
Hydroceles that are present in newborns, whether communicating or
noncommunicating, usually resolve spontaneously by the first birthday, unless they
are accompanied by an inguinal hernia
Communicating hydroceles in older patients rarely resolve and pose a risk for
development of incarcerated inguinal hernia.
Surgical repair of communicating hydrocele is usually undertaken on an elective
basis
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6.2.6. Varicocele
P a g e 435 | 548
This maneuver will help to differentiate idiopathic or primary from secondary
varicocele.
o Primary varicocele usually is more prominent in the upright position and
disappears in supine
o Secondary varicocele usually does not get much smaller with change in
position from upright to supine.
If the varicocele persists in the supine position, has acute onset, or is right-sided
(secondary varicocele), then processes that cause inferior vena caval (IVC)
obstruction must be ruled out with Doppler ultrasonography.
These processes include:
o IVC thrombus
o Right renal vein thrombosis with clot propagation down the IVC
o Abdominal mass (eg, retroperitoneal tumors, kidney tumors, or
lymphadenopathy)
Varicocele grade does not correlate well with abnormal semen analysis or infertility
in adults
Most varicoceles in adolescents are managed conservatively with observation.
o When more aggressive treatment is necessary, varicoceles are repaired
through surgical ligation or testicular vein embolization.
These procedures should be considered under the following circumstances
o Affected testicular volume is less than that of the unaffected testicle (a
difference in size of >10 to 15 percent or >2 mL when assessed by
ultrasonography);
o Loss of testicular volume is associated with a decreased sperm count
o Testicular growth arrest can be reversed with varicocele repair
To alleviate symptoms: Pain, heaviness, swelling.
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6.2.7. Spermatocele (Epididymal Cyst)
P a g e 437 | 548
o Other common signs are testicular enlargement or swelling. Many patients
also report an aching feeling in the lower abdomen or scrotum.
o On examination, intrascrotal malignancies usually are firm, nontender
masses that do not transilluminate unless accompanied by a reactive
hydrocele.
o Some patients may have gynecomastia. The clinical presentation of
testicular cancer and advanced or metastatic testicular cancer are discussed
in more detail separately.
Diagnosis
o Scrotal ultrasound is the initial diagnostic test of choice
o Although pathology is the definitive diagnostic test, scrotal ultrasound may
help to distinguish intrinsic from extrinsic testicular lesions.
o Several conditions may mimic neoplasia on ultrasound, including
inflammation, hematoma, infarct, fibrosis, and tubular ectasia of the rete
testis.
o In cases in which the ultrasound is inconclusive, magnetic resonance
imaging (MRI) may help differentiate benign from malignant lesions.
Scrotal Swelling
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Part 7: Neurosurgery
P a g e 439 | 548
7.1. Head Injury
Case Discussion……………………………………….…440
Introduction………………………………………………440
History..…………………………………………………….441
Physical Examination…………………………………443
Investigation……………………………………………..446
Management…………………………………………….447
Discussion of Case…………………………………….449
Case Discussion
A 15-year-old boy is brought to the emergency department by his parents. He had been playing
with his friends and accidentally he was struck on the head by stone by one of his friends
approximately half an hour before admission. He lost consciousness briefly, but was able to walk
from the scene. He is complaining of a severe headache, and has vomited three times. He is mildly
confused. He has no previous medical history, and he is not on any medication. The physical
examination reveals a pulse rate of 58/min and a blood pressure of 180/110 mmHg. During the
course of the examination he becomes drowsy and his Glasgow Coma Score (GCS) drops to 3/15.
He has a ‘boggy swelling’ over the right temple.
Introduction
Head injury is the leading cause of death and disability from childhood to early
middle age.
Road traffic accidents are the leading cause of head injury, being responsible for up
to 50 per cent of cases.
Risk factors include male sex, recreational drugs (including alcohol and substance
abuse) and youth, with a peak at 15–30 years of age.
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History
Identification:
Chief complaint:
Duration
HPI:
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Table 7.1: Grading post traumatic amnesia
Grade Duration
Grade 1 or Slight less than 1 hour
Grade 2 or Moderate 1-24hours
Grade 3 or Severe 1-7days
Grade 4 or Fatal more than 7days
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Physical Examination
P a g e 443 | 548
- Skull fracture with or without CSF leak
Ear
- Bleeding through the - CSF leak
ear - Hearing loss
Eyes
- Periorbital - Visual difficulty
ecchymoses
Nose
- Bleeding via the nose - Difficulty in smelling/
- CSF leak Anosmia
Mouth
- Fluid/blood
o Chest Examination:
Sub conjunctival hemorrhage:
It is very important to examine the chest since
- It is deep to conjunctiva most head injuries are associated with other life
- Does not move with conjunctiva threatening injuries such as heamothorax,
- Points towards the cornea with tension pneumothorax.
invisible posterior limit Follow the standard steps:
- Conjunctival edema can occur Inspection – bruise, symmetry, scar
Palpation – position of the trachea, tactile
Superficial conjunctival hemorrhage:
fremitus, tenderness
- It is confirmed by its mobility with Percussion – resonance
the conjunctiva Auscultation- check breath sounds
- Has visible posterior limit
o Abdomen
Look for associated injury such as bleeding, Spleenic rupture
Rectal examination paying special attention to the anal tone (spinal injury)
o GUT
High ridding prostate (uretheral ruputre)
o MMSE
Limb fracture, bleeding
o CNS
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Conciousness – assessed with GCS (refer to table 7.2 below)
Mental status
Cranial nerve examination—focus on the following
- Pupillary size and reactivity:
Asymmetrical sluggish response: may suggest partial third
nerve dysfunction on that side implying uncal herniation as a
result of a mass on the ipsilateral side of sluggish pupil
As the third nerve becomes increasingly compromised the
ipsilateral pupil will become fixed and dilated.
- Anosmia (CN-I):
Associated with rhinorrhea ->This pts are @ risk of ascending
meningitis
- CN VI palsy:
Raised ICP
- CN VII & VIII palsy:
Basal skull fracture
A peripheral nerve examination should record…
- Muscle tone - Reflexes
- Muscle strength - Sensory loss
Table 7.2: Glasgow Coma Scale (GCS)
Examination of the whole patient in head
Eye opening injury
Spontaneous 4
Cervical spine injury is common in
Response to verbal command 3 patients with head injuries
Response to pain 2 Even obtunded patients should move
No eye Opening 1 all four limbs
Best verbal response Check and record power, tone and
Oriented 5 sensation in the peripheral nerves
Confused 4 Log roll to check the whole spine for
Inappropriate words 3 steps and tenderness
Incomprehensible sounds 2 Perform a rectal examination to check
No verbal response 1 for anal tone and anal wink
Best motor response Check for priapism
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Obeys command 6
Localizing response to pain 5
Withdrawal response to pain 4
Flexion to pain 3
Extension to pain 2
No motor response 1
Total 15
Investigation
Labratory workup:
o CBC - Haemoglobin, PCV
o Blood type and cross match
o Coagulation study - PT/PTT
o Serum electrolytes
Hyponatremia which can be due to SIADH or cereberal salt wasting
Elevated sodium level indicate simple dehydration or DI
o Blood sugar level (RBS)
o Blood gas analysis
o Toxicology screening for drugs
o Blood alcohol level
o Renal function test
Diagnostic imaging Studies
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o Plain skull x-ray
o CT scan without contrast
Is ideal investigation to identify intracranial injuries
Usually plain CT is done in emergency situation
o MRI is very useful and senstive
o Angiography
o Electromyography and NCS
o Brain tissue oxygen sensor
o Intraparenchymal fiberoptic pressure transducer
National Institute for Health and Clinical Excellence (NICE)guidelines for computed
tomography (CT) in head injury.
o GCS <13 at any point
o GCS 13 or 14 at 2 hours
o Focal neurological deficit
o Suspected open, depressed or basal skull fracture
o More than one episode of vomiting
o Any patient with a mild head injury over the age of 65 years or with a
coagulopathy, for instance warfarin use, should be scanned urgently
o Dangerous mechanism or injury or antegrade amnesia >30 minutes warrants
CT within 8 hours
Management
Priorities:
Minimize secondary brain injury
o ABCs
o A = Airway – is he protecting his airway?
GCS< 9 = unable to protect airway Intubate
Hypercapnia causes vasodilation, increasing ICP
o C spine immobilization and avoid head tilt to open the airway
o B = Breathing – is it compromised
E.g. any secondary lung injuries?
Administer O2
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Hypoxemia causes vasodilation, increasing ICP
o C = Circulation – is it adequate?
Maintain systolic BP> 90 mm Hg
Medical Management:
ABC’s
o Ensure Adequate Oxygenation/ Ventilation
PaCO2 – normal (35 mm Hg)
o IV Fluids
Isotonic – NS or Ringer’s
Goal: Euvolemia
Medical Management: Mannitol
Hyperventilation
Head Elevation
o Anti-Seizure Medication:
If severe head injury (GCS ≤ 8)
Penetrating head injury
History of seizure disorder
Antibiotics
ICP Monitoring and Management
Surgical Management
o Burrhole o Craniectomy
P a g e 448 | 548
Discussion of the Case
Classification………………………………………….…449
SCALP Laceration……………………………………..450
Skull Fracture…………………………………………..451
Brain Injuries..……………………………………….…453
Classification
Head injury include any trauma to scalp, skull and brain
SCALP laceration
Skull fracture
o Open or closed o Vault or Basal skull
o Linear or depressed fracture
Intracranial bleeding
o Epidural hematoma
o Subdural hematoma
o Intraparenchymal hematoma/bleeding
Brain injury could be either
o Primary injury: could be focal or diffuse
o Secondary injury
Based on GCS
o Minimal – GCS 15/15, no loss of conciousness
o Mild – 13-15/15 , loss of consciousness <5minutes
o Moderate – 9-12/15, loss of consciousness >5 minutes, CT finding-
contussion, laceration, heamatoma , Focal neurologic deficit such as
seizure,weakness, speech difficulty, memory, cranial deficit
o Severe – GCS 5-8/15
o Critical GCS <5
Based on clinical type
o OPEN – fracture of the skull associated with tear of the dura and the
arachinoid resulting in CSF leakage (either to the external enviroment or
through the base of skull, otorrhea, rhinorrhea)
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Result in intracranial infection which could be generalised
meningitis or focal infections such as subdural empyema, brain
abcess, osteomyelitis of the skull.
If intracranial air can be seen on the x-ray, then the dura has
been breached too.
o CLOSED – associated with no leakage
Subpericranial blood clot infection may result in pott’s puffy tumor
o This classification helps to identify who has the likelyhood of developing
infective complication.
Based on type of injury
o Blunt:
Acceleration Decceleration
o Penetrating:
Gunshot injury
SCALP Laceration
Introduction:
The most minor type of head trauma
Scalp is highly vascular Profuse bleeding
Major complication is infection
Physical examination:
The following attributes of the wound should be noted:
o Length of laceration in centimeters
o Depth of laceration:
Epidermis
Dermis
Subcutaneous fat
Muscle
Bone
o Shape of laceration:
Linear Stellate
Curvilinear Corner
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o Presence of gross contamination or visible foreign bodies
o The presence of skin loss
Investigation:
Patients with clinical findings that suggest the presence of a foreign body or
bony injury need appropriate imaging:
o Plain radiograph
o Head CT without contrast
Management:
Direct pressure initially controls the bleeding, allowing close inspection to the
injury
Simple laceration Copiously irrigate & close primarily
Laceration
o Short or a single layer:
Percutaneous suture
Laceration
o Long or has multiple arms:
Debridement and closure in the OR
Skull Fracture
Introduction:
Skull fracture can be:
Open or Closed
o A closed fracture:
Is covered by intact skin
Do not normally require specific treatment.
o An open, or compound fracture
Associated with disrupted overlying skin
Require repair of the scalp and operative debridement.
Depressed or Non-Depressed
o Depressed fracture
Inner and outer cortices of the skull are disrupted and fragment is
pressed toward the brain.
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Occur when trauma of significant force drives a segment of the skull
below the level of the adjacent skull
The sharp edges of the bones can lacerate dura,brain or vessels
Increased risk of infection, neurologic deficit, late onset epilepsy
Craniotomy is required to elevate the fracture.
However, fractures overlying dural venous sinuses require restraint.
Because surgical exploration leads to life threatening hemorrhage
from lacerated sinuse.
o Llinear fracture
Mostly skull vault fracture is a single fracture that most often
extends through the entire thickness of the calvarium.
They occur most often in the temporoparietal, frontal, and occipital
regions.
Location:
Vault
Across midline…involve sagittal sinus
Basilar skull fractures
o Anterior skull base facture
o Middle skull base fracture
o Posterior skull base fracture
Physical signs of skull fractures:
Anterior cranial fossa
o Nasal bleeding
o Orbital haematoma(Racoon eyes)
o Cerebrospinal fluid rhinorrhea
o Cranial nerve injuries, nerves I – VI
Middle cranial fossa
o Orbital haematoma o Bleeding from the ear
o Cerebrospinal fluid otorrhoea (rare)
o Cranial nerve injuries, nerves VII and VIII
Posterior cranial fossa
o Bruising over the suboccipital region, which develops after a day or two
(Battle’s sign)
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o Cranial nerve injuries – nerves IX, X and XI (rare)
Investigation:
Halo test
o Is simple test used to detect CSF.
o Allow a drop of the fluid to fall on an absorbent surfaceIf blood is mixed
with CSF
The drop will form a double ring, with a darker center spot
containing blood components surrounded by a light halo of CSF.
Beta transferrin test
o Carbohydrate-free isoform of transferrin exclusively found in the CSF
Management:
Skull base fractures requiring intervention include those with an associated
cranial nerve deficit or CSF leak.
NG tube insertion is contraindicated in skull base fracture
Indications for craniotomy include:
o Depression greater than the cranial thickness
o Intracranial hematoma o Frontal sinus involvement
Brain Injuries
TBI is best understood as a complex process that is composed of overlapping
phases, including primary injury and its evolution, secondary injury, and recovery.
• Occurs at the time of insult; direct and indirect impact to the brain parenchyma
• Shearing secondary to motion of the brai relative to the fixed skull and dura (DAI)
Primary Injury • Vascular injury: torn bridging veins, arterial dissections, etc... and it is not amenable to treatment
• The constellationof cellular and biochemical processses that are set in motion by the primary
injury; evolve over the subsequent hours and days
Secondary
Injury • Significant cause of post traumatic neurological disability
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Table 7.3 Categorization of Head Injury Severity
Minimal Mild Moderate Severe
GCS = 15 GCS = 14 GCS = 9-13 GCS = 5-8 Critical TBI
No loss of Conscious- Or Or GCS = 3-4
ness (LOC) GCS = 15 plus either brief LOC ≥ 5 min
No amnesia LOC (<5 min) or impaired Or
alertness of memory Focal neurologic deficit
Traumatic Brain
Injury
Non-focal
Focal Lesions
Lesions
Contusions/
Epidural Subdural Diffuse Axonal Diffuse Cerebral
intraparenchym
Hematomas Hematomas Injury (DAI) Edema
al Hematomas
1. Concussion:
Temporary neuronal dysfunction due to non penetrating trauma
Clinical features include:
o Confusion o Vertigo
o Amnesia – specially o Nausea and vomiting
amnesia of the event is o Vacant state
very common o Delayed verbal
o Loss of consciousness expression
o Headache o Inability concentrating
o Dizziness o Disorientation
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Normal head CT; there is no apparent parenchymal damage
Deficit resolve over minutes to hours
For grading refer to the table below
Second-impact syndrome:
o Occurs when the brain swells rapidly, and catastrophically, after a person suffers
a second concussion before symptoms from an earlier one have subsided.
Table 7.4: Concussions grading according to Colorado grading system
Grade 1 Head trauma patients with confusion only
Grade 2 Patients with amnesia
Grade 3 Patients who lose consciousness
2. Contusion:
Bruise of the brain
It is due to break down of small vessels and extravasation blood into the brain
The frontal, occipital and temporal lobes are commonly involved
On CT scan, the contused areas appear bright
Edema develops around the contusion and creates mass effect
Coup injury:
o Occurs under the site of impact with an object
Countercoup injury:
o Occurs on the side opposite to the area that was hit.
o Occurs with decceleration of the brain against the skull
Coup and contrecoup injuries can occur individually or together.
The management for contussion is aimed at preventing or reducing swelling
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C. Subarachnoid Hemorrhage
Is bleeding into the space between subarachnoid membrane and pia matter
It can occur spontaneously (ruptured cerebral aneurysm which is the most
common cause) or due to head trauma
Signs and symptom include sudden onset severe headache (thunderclap
headache or the worst headache of my life), loss of consciousness, hemiparesis
seziure, nausea or vomiting, meningismus
It carries poor prognosis if associated with loss of consciousness
D. Intraparenchymal hemorrhage
Most often associated with hypertensive hemorrhage or arteriovenous
malformations (AVMs)
Indications for craniotomy include:
o Any clot volume >50 cm3 or a clot volume >20 cm3 with referable
neurologic deterioration (GCS 6–8)
o Associated midline shift >5 mm or basal cistern compression
Management
Indications in administration of mannitol in E/ R
1. Evidence of intracranial hypertension
2. Evidence of mass effect (focal deficit, e.g. hemiparesis)
3. Sudden deterioration prior to CT (including pupillary dilatation)
4. After CT, if a lesion that is associated with increased ICP is identified
5. After CT, if going to O.R.
6. To assess “salvageability”: in patient with no evidence of brainstem function,
look for return of brainstem reflexes
Contraindications:
1. Prophylactic administration is not recommended due to its volume-
depleting e ect. Use only for appropriate indications (see above)
2. Hypotension or hypervolemia: hypotension can negatively influence
outcome. Therefore, when intracranial hypertension (IC-HTN) is present,
first utilize sedation and/or paralysis, and CSF drainage. If further measures
are needed, fluid resuscitates the patient before administering mannitol.
Use Hyperventilation in hypovolemic patients until mannitol can be given
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3. Relative contraindication: mannitol may slightly impede normal coagulation
4. CHF: before causing diuresis, mannitol transiently increases intravascular
volume. Use with caution in CHF, may need to pre-treat with furosemide
(Lasix®): bolus with 0.25–1 gm/kg over <20 min (for average adult: ˜ 350 ml
of 20% solution). Peak occurs in ˜ 20 minutes.
Light sedation e.g. codeine 30-60mg IM q 4hrs (Same as heavy sedation, see below)
PRN
Unenhanced head CT scan for ICP problems Rule out surgical condition
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7.2. Spinal Injury
Case Discussion…………………………………………460
Introduction……………………………………………..460
History……………………..………………………………461
Physical Examination………..………………………462
Investigation………………………………….…………464
Management……………………………………………465
Complication……………………………………………466
Discussion of Case……………………………………466
Case Discussion
A 35-year-old man came to the hospital by ambulance after gunshot injury to the lumbar spine.
The injury occurred when he was involved in war. He was shot with an AR- 15 rifle, and the bullet
went through the victims back. He has lost consciousness after the accident and remained
unconscious for three hours. After the incident, his bilateral lower limbs showed no muscle
contraction with sensory loss. His vitals are PR- 120, BP- 180/90, RR- 30. Examination of the lumbar
spine shows penetrating wound around L2.
Introduction
Evaluation of a patient with suspected spinal cord injury begins with primary
survey which focuses on assessment of life threatening conditions ABCs
Suspected spinal injury:
o High speed o Neurologic deficit
o Unconscious o Spinal tenderness
o Multiple injuries
On secondary survey detailed history and physical examination is obtained.
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History
Physical Examination
Vital signs:
o Vital signs including heart rate, blood pressure, respiratory status, and
temperature require ongoing monitoring.
o Pulse oximetry is important to identify hypoxia.
Identification of shock:
o Hypotensive shock
Low BP, tachycardia, cold clammy skin. Mx- resucitation
o Neurogenic shock:
Low BP, normal heart rate or bradycardia, warm peripheries
Occurs in acute spinal cord injuries above T6
Associated neurologic deficit
Due to disruption of autonomic pathway(sympathetic)
causing decreased vascuar resistance(unopposed vagal
stimulation)
Diligent search for source of heamorrhage must be completed
before attributing hypotension to neurogenic shock
Treated with ionotrops, avoid fliud overload
o Spinal shock:
Initial loss of all neurological function
Characterized by hypotonia, paralysis, areflexia
Usually lasts 24hrs after spinal cord injury
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Chest examination:
o Carefully evaluate respiratory rate, chest wall expansion,
Degree of respiratory dysfunction abdominal wall movement, cough, chest wall and/or
depends on: pulmonary injuries (such as
pneumothorax,hemothorax).
Preexisting pulmonary
o Inspection: look for poor chest wall expansion, pallor,
comorbidty
cyanosis, paradoxic movement of the chest wall,
Level of spinal cord injury
increased accessory muscle use.
Associated chest wall or lung
o Palpation: look for chest wall tenderness, tracheal
injury
deviation (pneumothorax, hemothorax)
o Percussion: check if there is dullness or hyperresonance
o Auscultaion: check if there is decreased air entry, rales, rhonci
Abdominal examination:
o Follow the steps and do detailed examination.
o Check for seat belt mark Indicate high energy injury.
Spine exam:
o Apply the formal spinal log roll.
o Logrolling the patient to systematically examine each spinous process of
the entire axial skeleton from occiput to the sacrum can help identify
and localize injury.
o “ Skeletal level of injury – level of greatest verteberal damage on
radiograph.”
o Inspection – swelling, erythema, wounds - stabbed site or penetrating
o Palpation- tenderness, swelling, palpable step or gap
Neurological examination - focus on:
o Motor function (out of 5)
o Sensory function-Sensation, position and vibration
o Deep tendon and superficial abdominal reflexes
o Rectal exam
Anal tone
Voluntary anal contraction
Perianal sensation
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Investigation
Labratory workup
CBC ->Hg and/or hematocrit serially taken to dectect or monitor blood loss
Arterial blood gas-> to evaluate adequacy of oxygenation and vantilation
Serum lactate -> to monitor perfusion status
Urine analysis -> to detect any associated genitourinary injury
Diagnostic imaging
Plain radiograph:
o X-ray Guidelines (cervical) AABBCDS
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o AP and lateral, open mouth
Adequacy, Alignment
Bone abnormality, Base of skull
Cartilage
Disc space
Soft tissue
CT is better for occult fractures and identifying details of fracture.
CT scanning remains the most sensitive imaging modality in spinal trauma.
MRI is good to identify those injuries with no bony involvement.
o Posttraumatic disc prolapse
o Hematoma
o Soft tissue and ligament injury
Flexion-extension films for stability in patient with no deficit.
Management
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o Many spinal injuries can be managed non opertatively using external
support.
o Absolute indication for surgery in spinal trauma is deteriorating
neurologic function
Neurological deficit: Deficit >Decompression
o Cord can be compressed by bone or disc. Surgical decompression is
necessary.
o Reduce post traumatic syrnix formation
Introduction…………………………………………...467
Classification ………………………………………….467
Specific Local Spinal Injuries..………………….471
M
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Introduction
Classification
Spinal cord injuries are classified as
o Primary or Secondary
o Temporary (Spinal shock) or Permanent (Immediate it Delayed)
o Complete or Incomplete
Primary Injury:
o Direct insult to neural component, which occurs at the time of initial
trauma.
o The injury could be directly from:
Flexion Rotation or traction
Extension Axial loading
Compression of the cord by fragment bone or disc material.
Secondary Injury – due to
o Haemorrhage, oedema and ischaemia
o Hypotension, hypoxia or spinal instability
o Persistent compression of the neural elements.
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o Management of a spinal cord injury must focus on minimizing secondary
injury
Complete:
o No function below the level of injury
o Sensation and voluntary movement around S4/5 is absent.
o In the acute phase, the classic syndrome of complete spinal cord
transection at the high cervical level consists:
Respiratory insufficency
Quadriplegia with upper and lower
extremity areflexia
Ansthesia below the affected level
Neurogenic shock (hypothermia and
hypotension without compensatory
tachycardia)
Loss of rectal and bladder sphincter tone
Urinary and bowel retention leading to
abdominal distention, ileus and delayed
gastric empyting.
This constellation of symptoms is called
spinal shock.
o Horner syndrome is also present with higher lesions, ie:
Ipsilateral ptosis Anhydrosis
Miosis
o Lower cervical level injury spares respiratory muscles
o Higher thoracic lesions lead to paraparesis, but autonomic symptoms are
still marked
o Lower thoracic and lumbosacral cord lesions, hypotension is not present
but urinary and bowel retention are.
o The presence of priapism after spinal shock phase indicates the presence
of complete spinal cord injury and is marker for progression to complete
cord injury.
Incomplete
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o Is preservation of sensation around S4/5 distribution and voluntary anal
control?
o Includes phenomenon called Sacral sparing.
o Some of incomplete injuries are the following:
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Taumatic injury is usually caused by severe neck hyperextension.
o It is characterized by initial quadriplegia replaced over minutes by leg
recovery.
o In addition to the distal morethan proximal arm weakness (man in a barrel
syndrome), bladder dysfunction, patch sensory loss below the level of the
lesion, and considerable recovery occur.
In older patients neck hyperextension in prexisting cervical stenosis.
In the young patients neck flexion is common cause.
Most common causes are falls and vehicle accidents
3. Brown Sequard Syndrome:
Injury to half the cord at a given level with
loss of motor control and proprioception
ipsilaterally and loss of nociception and
thermoception contralaterally.
Typically it is due to stab injury or
gunshot.
Carries good prognosis
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Table 7.6: American Spinal Injury Association Scale (ASIA) Impairment Scale (AIS)
Grade Criteria
A Complete cord injury.
No motor or sensory function is preserved in the sacral segments S4-5.
B Sensory incomplete.
Sensory but not motor function is preserved below the neurologic level and includes the
sacral segments (light touch or pin prick at S4-5 or deep anal pressure)
No motor function is preserved more than three levels below the motor level on either side
of the body.
C Motor incomplete.
Motor function is preserved below the neurologic level and more than half of key muscle
functions below the neurologic level of injury have a muscle grade <3 (Grades 0 to 2).
D Motor incomplete.
Motor function is preserved below the neurologic level and at least half (half or more) of
key muscle functions below the neurologic level of injury have a muscle grade ≥3.
E Normal
Sensation and motor function are graded as normal in all segments and the patient had
prior deficits.
Patients without an initial spinal cord injury do not receive an AIS grade.
Introduction …………………..………………….……472
Types of Injury………….……………………….…….473
Management………….……………….………………474
Introduction
The peripheral nervous system extends throughout the body and is subject to
injury from a wide variety of trauma.
Four major mechanisms of injury to peripheral nerves:
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o Laceration - Knives, passing bullets, or jagged bone fractures may lacerate
nerves.
o Stretched - Adjacent expanding hematomas or dislocated fractures may
stretch nerves.
o Compression - Expanding hematomas, external orthoses such as casts or
braces, or blunt trauma over a superficial nerve may compress or crush
nerves
o Contusion - Shock waves from high velocity bullets may contuse nerves.
The following four characteristics make a nerve segment more vulnerable:
o Proximity to a joint o Being fixed in position
o Superficial course
o Passage through a confined space
Types of Injury
According to Seddon classification:
Neurapraxia:
o Temporary failure of nerve functions
without physical axonal disruption.
o No Axon degeneration
o Recovery occurs in hours to months,
often in the 2- to 4-week range.
Axonotmesis:
o Disruption of axons and myelin.
o The surrounding connective tissues, including endoneurium, are intact.
o The axons degenerate proximally and distally from the area of injury.
o Distal degeneration is known as Wallerian degeneration.
o Axon regeneration within the connective tissue pathways can occur,
leading to restoration of function.
Axons regenerate at a rate of 1 mm per day.
Significant functional recovery may occur for up to 18 months.
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o Scarring at the site of injury from connective tissue reaction can form a
neuroma and interfere with regeneration.
Neurotmesis:
o Disruption of axons and endoneurial tubes.
o Peripheral collagenous components, such as the epineurium, may or may
not be intact.
o Proximal and distal axonal degeneration occurs.
o Effective axonal regeneration depends on the extent of neuroma
formation and on the degree of persisting anatomic alignment of the
connective tissue structures.
Management
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7.4. Brain Tumor
Case Discussion……………………………………….475
Introduction……………………………………………475
History.……………………………………..…………...476
Physical Examination………………………………479
Investigation…………………………………………..480
Differential Diagnosis……………………………..481
Management………………………………………….481
Discussion of Case………………………………….483
Case Discussion
A 57-year-old male patient complains of progressive visual loss of 8 years duration and complete
blindness of 6years duration. He has associated severe bilateral headache which gets worse at
night and vomiting of ingested matter. In addition, he has had fecal and urinary incontinence of 6-
month duration. Other than that he has no history of ABM, trauma and chronic medical illness. On
physical examination, there was cranial nerve deficit of cranial nerve 2, 3, 4 and 6.
Introduction
Brain tumors may originate from neural elements within the brain, or they may
represent spread of distant cancers.
Primary brain tumors arise from CNS tissue and account for roughly half of all
cases of intracranial neoplasms.
The remainders of brain neoplasms are caused by metastatic lesions.
In adults, two thirds of primary brain tumors arise from structures above the
tentorium (supratentorial), whereas in children, two thirds of brain tumors arise
from structures below the tentorium (infratentorial).
Gliomas, metastasis, meningiomas, pituitary adenomas, and acoustic neuromas
account for 95% of all brain tumors.
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History
Manifestations depend on the cause of the symptoms, which may comprise any of the
following:
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o Seizures are common in patients with supratentorial meningioma,
affecting anywhere from 10% to 50% of individuals with these lesions,
and are frequently the presenting symptom.
o A Jacksonian pattern (ie, one in which a focal seizure begins in one
extremity and then progresses until it becomes generalized) is
distinctive in suggesting a focal structural lesion of the cortex.
o Any middle-aged or elderly patients presenting with a first seizure
should have CNS tumor high in the differential diagnosis
Fixed visual changes TIA symptoms
Speech deficits
Focal sensory abnormalities
5) Look for Manifestations of brain tumor may reflect the tumor site
Frontal lobe
o Mental status changes, especially memory loss and decreased alertness
o Sleeping longer, appearing preoccupied while awake, and apathy.
Temporal lobe neoplasms
o Depersonalization o Emotional changes
o Dejavu sensation o Behavioral disturbances
o Auditory/olfactory
affection
Partial lobe
o Contralateral loss of motor/sensory
o Homonyms hemianopsia
o Apraxia
Occipital lobe
o Contralateral loss of vision
An acoustic neuroma
o Intermittent (then o Disequilibrium
progressive) hearing loss o Tinnitus.
Posterior fossa tumors
o Irritability o Headache
o Unsteadiness o Vomiting
o Ataxia o Progressive obtundation
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Supratentorial tumors in children
o Seizures o Speech difficulties
o Hemiparesis o Intellectual disturbance
o Visual field cuts
Infratentorial symptoms
o Increased ICP due to hydrocephalus
Headache Ataxia
Nausea Vertigo
Vomiting Diplopia
Papiledema
o Local symptoms
Cerebllar hemisphere- intention tremor, ataxia
Cerebllar vermis- truncal ataxia, broad based gait
Brain stem
Pituitary adenomas
o Non-functional pituitary adenomas remain asymptomatic until they are
large enough to encroach the optic chiasm and disturb normal vision.
o Most hyper secretory pituitary adenomas secrete prolactin,
Women noting an amenorrhea galactorrhea syndrome.
Men with complain of headache, visual problems, and
impotence.
6) Asses for risk factors
Occupation:
o Agricultural: herbicides, pesticides
o Electrical workers: EMF exposure
Diets: N-nitroso compounds (NOCs)
Infection: toxoplasma in astrocytoma and meningioma
Radiation history
Family history
Head trauma: for meningioma
7) Rule out differentials
History of chronic cough or exposure to a known TB patient- TB
VDRL status and sexual history- neurosyphilis
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Travel hx and hx of ingestion water or food contaminated with dog feces, Right
upper quadrant pain - hydatid cyst
History of cough and bloody vomiting, bone pain, breast lump etc- brain
metastasis
Stroke in acute settings
Physical Examination
Based on their location, intracranial tumors may produce a focal or generalized
deficit, but signs may be lacking (especially if the tumor is confined to the frontal
lobe) or even falsely localizing.
Papilledema:
o More prevalent with pediatric brain tumors, reflects an increase in ICP of
several days or longer.
o Not all patients with CNS tumors develop papilledema.
Diplopia:
o Result from displacement or compression of the sixth cranial nerve at the
base of the brain.
Parinaud syndrome:
o May occur with pineal tumors
o Impaired upward gaze
Tumors of the occipital lobe specifically may produce homonymous hemianopia or
partial visual field deficits.
Anosmia may occur with frontal lobe tumors.
Brainstem and cerebellar tumors
o Cranial nerve palsies o Nystagmus
o Ataxia, incoordination o Pyramidal signs
o Sensory deficits on one or both sides of the body.
Tumors in the region of the cerebellopontine angle:
o May impair the functions of the three cranial nerves that traverse this
region: facial, cochlear, and vestibular.
o Acoustic neuromas most commonly originate from the vestibular nerve
(part of cranial nerve VIII).
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Investigation
Laboratory
CBC: for anemia and rule out differentials
Coagulation studies
Serum electrolyte: to check for Hypercalcemia
Metabolic studies: SIADH
Tumor markers
o Human chorionic gonadotropin (hCG)
o Alpha-fetoprotein
o Carcinoembryonic antigen (CEA)
o S-100 protein
Imaging
Important information to gain from neuro imaging
o Age
o Location
o Multicentricity
o Architecture
o Contrast enhancement
o Bilateral hemisphere involvement
o Interaction with surrounding tissue
Gadolinium-enhanced magnetic resonance imaging (MRI):
o It is the preferred modality because of its resolution and enhancement
with contrast agents.
Head and spine computed tomography (CT):
o If MRI cannot be performed (e.g., in patients with metallic implants,
embedded devices, or claustrophobia)
o It cannot adequately assess lesions in the posterior fossa and spine.
o White areas = areas that absorb or “attenuate” the passage of x-ray beam
(acute hematoma, bone, calcium = hyperdense/ attenuating)
o Black areas = areas that do not absorb or “attenuate” the passage of x-ray
beam (fat, air, CSF, edema = hypodense/ attenuating)
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Differential Diagnosis
Management
Principles:
o Careful history, physical o Chemotherapy
and investigation o Radiotherapy
o steroids o Surgery
o Mannitol
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Craniotomy for supratentorial tumors
Position: (depends on location of tumor)
Pre-op embolization (by neuroendovascular interventionalist) for some vascular
tumors including some meningiomas
Equipment:
o Microscope o Image guidance system
o Ultrasonic aspirator
Blood availability: type and cross match
Post-op: ICU
Consent
o Procedure: surgery through the skull to remove as much of the tumor as is
safely possible
o Alternatives: nonsurgical management, radiation therapy for some tumors
o Complications: usual craniotomy complications plus inability to remove all
of the tumor
1. Astrocytoma:
• Astrocytic tumors are the most common primary
intra-axial brain tumor.
• The best-established causes for brain tumors are
syndromic (familial diseases…) and post-radiation
therapy
• The major cause of morbidity with low-grade
astrocytomas is dedifferentiation to a more
malignant grade.
• GBM is The most common primary brain tumor
• It is also the most malignant astrocytoma
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2. Meningioma:
• Meningiomas are the most common primary
intracranial tumors. They are usually slow
growing, extra-axial tumor, circumscribed (non-
infiltrating), benign lesions.
• Arise from arachnoid cap cells (not dura)
o Most commonly located along falx,
convexity, or sphenoid bone
o Most are cured if completely removed
3. Pituitary tumors:
• Most are benign adenomas arising from the
anterior pituitary (adenohypophysis)
• Presentation: most commonly present due to
hormonal effects (includes: hyperprolactinemia,
Cushing’s syndrome, acromegaly…)
• Mass effect (most commonly: bitemporal
hemianopsia from compression of optic chiasm)
• As an incidental finding, or infrequently with pituitary apoplexy
• Prolactinoma is the only type for which medical therapy (DA agonists) may be the
primary treatment.
• For other tumor types, options primarily consist of surgery (transsphenoidal or
transcranial), or XRT
• Most primary pituitary tumors are benign adenomas which arise from the
anterior pituitary gland
• Microadenoma: A pituitar y tumor < 1 cm diameter.
• Macroadenomas: Tumors >1 cm diameter.
4. Metastasis to brain:
• Those commonly involving brain include:
I. Lung cancer: small-cell IV. Renal cell
II. Breast V. Lymphoma
III. Melanoma VI. GI
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7.5. Neural Tube Defects (NTDs)
Case Discussion……………………………….…….485
Introduction…………………………………….…….485
History…………………….……………………….…..486
Physical Examination………………….…….……487
Investigation……………………………………….…488
Management………………………………………….489
Complications………………………………………..489
Discussion of Case………………………………….490
Case Discussion
Introduction
Neural tube defects (NTDs) are congenital malformations of the neural tube,
caused by failure of the neural tube to close at the end of the fourth week after
conception. Neural tube defects are typical examples of a multifactorial
congenital malformation.
The neural tube is the structure from which the skull, brain, spinal cord and
nerves will develop, as well as the spinal column (made up of vertebrae).
If the neural tube fails to close at the head end, the defect results in
anencephaly or an encephalocoele. If it fails to close lower down along the
spine, the result is spina bifida.
There are several anatomic types of NTDs, which affect either the spine or
cranium. They can be classified as open (neural tissue exposed) or closed
(neural tissue not exposed). Open NTDs often involve both the spine and
cranium, while closed NTDs are usually localized and confined to the spine.
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History
P a g e 486 | 548
o Bowel & Bladder incontinence
o Loss of sensation in perianal region
o No motor weakness
Mid lumbar region –
o weakness of lower limbs
o loss of sensation
Sudden onset of pain, motor and sensory loss, and bladder dysfunction after an
acute trauma (e.g., fall, motor vehicle accident, placement in lithotomy
position).
o May be related to tethering of the cord (the distal end of the spinal cord
is fixed in position).
Ask for symptoms of CNS infections
o A patient with a dermal sinus also can present with bacterial meningitis
or spinal abscess.
o Neuro-enteric or dermoid cysts also can present with repeated bouts of
aseptic meningitis due to leaking of the contents into the spinal
subarachnoid space.
Ask for symptoms of spinal cord compression
o Seen in a patient with a closed NTD such as a congenital dermal sinus
with an intraspinal dermoid cyst or a neuro-enteric cyst
Ask for medical co morbidities
o The prevalence depends on the level and severity of the lesion
o Urologic abnormalities (i.e., UTI and nephrolithiasis) are the most
common issues among adults with NTDs.
o Scoliosis, pain, epilepsy, and pressure ulcers are also often reported in
adult patients with myelomeningocele.
Physical Examination
1) A complete neurological assessment of the newborn with an open NTD
Measurement of head circumference
Assessment of general vigor (especially cry and sucking)
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Upper extremity motor function, anal sphincter, and urinary stream, as well as
thorough motor and sensory examination of the lower extremities and trunk.
o Observation of muscle bulk
o Spontaneous active movements
o Movements in response to stimulation
o Assessment of muscle tone by palpation.
o Extent of muscle weakness and paralysis
o Deep tendon reflexes and anocutaneous reflex (anal wink)
2) Inspect the spine for:
The size and site of the lesion: whether it is leaking CSF.
The shape of the defect
Health and laxity of the surrounding skin and soft tissue
The presence of early spinal deformity (eg, kyphosis)
3) Attention to the following features
Level of the spinal cord neurologic deficit
Associated SC anomalies, such as split cord malformation
Signs of hydrocephalus
Evidence of brainstem compression (from the Chiari II)
4) Evaluation for associated abnormalities
Clubfeet Kyphosis
Flexion or extension contractures of hips, knees, & ankles
Other congenital abnormalities
Investigation
N.B. postnatal diagnosis is usually done through clinical examination.
Maternal serum alpha-fetoprotein
o Abnormal MSAFP tests are typically followed by an ultrasound exam to
assess for possible NTD, confirm gestational age, fetal viability, number of
fetuses, and so on.
Aminocentesis
Ultrasonography
o Used antenatally for neural tube defect (NTD) screening.
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MRI
o Study of choice for imaging neural tissue and for identifying contents of
the defect in the newborn
o This allows for visualization of associated anomalies, both intraspinal and
intracranial
o Rarely used
CT scan
o To determine the presence or absence of hydrocephalus or other
intracranial anomalies
o Usually reserved for adults or older kids with spina bifida occulta due to its
high radiation.
Management
Medical management:
o keep the newborn warm
o Cover the defect with a sterile wet saline dressing.
o Antibiotics for meningitis & UTI
o Recurrent catheterization o Anticonvulsants
Surgical management:
o Fetal surgery
o The newborn with an open NTD should undergo prompt closure of the
defect.
o Hydrocephalus- should have a ventriculoperitoneal shunt placed
o Symptomatic Chiari malformations: should undergo suboccipital
craniotomy and decompression of the posterior fossa and tonsils.
o Syrinx- needs a laminectomy and placement of a syringosubarachnoid stent
to divert the CSF out of the central canal.
Complications
Infection
Bladder dysfunctions
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Discussion of the Case
Classification……………………………………………490
Anencephaly……………………………………………490
Encephalocoele……………………………………....491
Spina Bifida……………………………………………..491
Classification
Anencephaly
Anencephaly (no brain) is the most
serious of all neural tube defects and
always results in stillbirth or early
neonatal death.
The top (vault) of the skull is absent,
exposing the brain, which is malformed.
The cerebral hemispheres do not
develop with anencephaly.
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Encephalocoele
Spina Bifida
Spina bifida (split spine) is an opening in the spinal column due to failure of
closure of the bony vertebral arches. Spina bifida may occur anywhere down the
spinal column. There are three forms of spina bifida:
o Spina bifida with Meningomyelocoele (spina bifida cystica): this is the
most severe form
o Spina bifida with Meningocoele (spina bifida aperta): a less severe than
meningomyelocoele.
o Spina bifida occulta. This is the least severe form as it only involves the
bony spine.
A) Spina bifida with Meningomyelocoele
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It is an open neural tube defects
Neural tissue (spinal cord and nerves) and the
coverings of the spinal cord (the meninges) bulge
through the opening.
o The skin over this defect does not close, but
the defect may be covered by a thin
membrane which tears easily.
o The neural tissue that bulges through the bony
defect is usually damaged, resulting in nerve
abnormalities below the level of the defect.
Myelomeningocele patients often have hydrocephalus and a Chiari II
malformation, an abnormal downward herniation of the cerebellum and brain
stem through the foramen magnum
Common findings include weakness and atrophy of the lower extremities, gait
disturbance, urinary incontinence, constipation, and deformities of the foot.
o Myelomeningoceles arising from the high lumbar cord usually cause
total paralysis and incontinence, while those arising from the sacral
cord may have only clawing of the foot and partial urinary function
loss
B) Spina bifida with Meningocoele
Only the coverings of the spinal cord (the meninges)
protrude through the defect, forming a sac which is
filled with cerebrospinal fluid (CSF).
The spinal cord and nerves are normal and do not
bulge through the opening.
o There is no associated spinal cord or nerve
damage.
o The meningocoele usually is covered on the
outside by skin (closed neural tube defect).
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Spina bifida occulta is congenital absence of posterior
vertebral
o The spinous process is always missing
o The laminae may be missing to various
degrees, but the underlying neural tissues are
not involved elements
Spina bifida occulta is a closed neural tube defect.
Spina bifida occulta is found in 25% of the general
population
It is asymptomatic unless associated with other developmental abnormalities
The spinal cord and meninges are normal and do not
protrude through the defect.
o The defect may be covered by an overlying
abnormality such as a midline patch of hair, a
lipoma or a dimple.
7.6. Hydrocephalus
Case Discussion………………………………………494
Introduction……………………………………………494
Clinical Manifestations…………………………...495
Investigation…………………………………………..496
Management………………………………………….496
Complications………………………………………..496
Discussion of Case………………………………….497
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Case Discussion
Baby Aster is delivered by caesarean section and transferred to the pediatric intensive care unit
(PICU). On admission to the nursery: Temperature: 37° C (98.6° F) Pulse: 144 beats/minute,
Respirations: 40 breaths/minute. She has bulging fontanels and a high-pitched cry. Her head
circumference is 42 cm and her chest circumference is 35 cm. In the lumbar region of her spine,
the she has a sac-like projection.
Introduction
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Clinical Manifestation
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Investigation
Management
Medical Management: Diuretics
Surgical management:
o Surgery Principle
To reduce the CSF production
To by-pass the blockage to normal CSF flow (ventriculoperitoneal [VP]).
To drain CSF externally
To drain CSF to another absorptive viscus
To treat the cause (remove the obstruction)
o Surgery Contraindication (Lober’s criteria)
Paraplegia Congenital anomaly
Kyphoscoliosis Intracranial birth injury
Gross hydrocephalus Ventriculitis
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Discussion of the Case
Classification……………………………………………….497
Communicating Hydrocephalus…………….......497
Non-communicating Hydrocephalus ……….…497
Congenital Hydrocephalus………………………....498
Acquired Hydrocephalus……………………………..498
Classification
Using two methods
o Communicating (non-obstructive) vs. Non-communicating (obstructive)
o Congenital vs. Acquired
Communicating Hydrocephalus
Obstruction at the level of the arachnoid granulations
constitutes communicating hydrocephalus
It is caused by:
o Meningitis
o Subarachnoid hemorrhage- may cause
transient hydrocephalus
Non-communicating Hydrocephalus
It is obstruction of CSF pathways
The ventricles proximal to the obstruction dilate, while
those distal to the obstruction remain normal in size.
It can be caused by:
o Intracranial cysts with no evidence of bleed at diagnosis
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o Triventricular hydrocephalus due to radiologically apparent aqueductal stenosis
o Membranous obstruction of aqueduct
o Asymmetrical hydrocephalus, due to atresia of the foramen of Monro
o Obstruction of fourth ventricle outlets
They may present precipitously and require urgent shunting to prevent herniation.
Congenital Hydrocephalus
Congenital is caused by:
o Stenosis of the cerebral aqueduct
o Chiari malformation
o Myelomeningocele
o Intrauterine infections
o Neural tube defects—MM, Chari-malformation
o Isolated hydrocephalus: caused by aqueductal
stenosis
o Dandy-Walker: caused by atresia of the foramina of
Luschka and Magendie
o Choroid plexus papilloma or carcinoma
Acquired Hydrocephalus
Acquired is caused by:
o Infections
o Post-hemorrhagic hydrocephalus: hemorrhage
into the subarachnoid space or, less commonly,
into the ventricular system, by ruptured
aneurysms, arteriovenous malformations,
trauma, or systemic bleeding disorders.
o Secondary to masses & spinal tumors
o Post op
o Low pressure hydrocephalus
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7.7. Video QRs
Neurologic Examination
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Part 8: Orthopedics
Content By:
Matyas Wondwossen
Nanati Jemal 8.1. Fracture ………………………………………………501
Edited By:
Samuel Mesfin 8.2. Bone Tumor…………………………………………510
Reviewed By:
Dr. Matiyas Seid
(Orthopedic Surgeon)
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8.1. Fracture
Case Discussion……………………………………………………501
Clinical Manifestation………………………….………………501
Investigation……………………………………………………….504
Discussion of the Case………………………………………...504
Principles of Management…………………………………..508
Complications……………………………………………………..509
Case Discussion
A 23-year-old man is brought into the emergency department by ambulance after coming
off his motorcycle. He was travelling at approximately 45 mph and hit a stationary car.
There is no other history available and he is in significant pain.
Clinical Manifestation
History:
N.B: For patients without apparent life-threatening injuries who appear appropriate for
office management, assessment begins with a focused history. Analgesia is sometimes
needed before a history can be obtained.
Age
o Both extremes of age have increased tendency for fracture
o Younger age is important for bone healing
Sex
o Menopausal females at risk of fracture
o Males more prone to accidents and are risk takers
Assess for chief complaints
o Pain, Swelling, Bruising, Loss of function and deformity
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o Duration and site of the injury
Asses for risk factors
o Injuries
o occupation: contraction workers, drivers, high risk sport athletes, ballerinas
o Other Comorbidities: diabetes mellitus, arteriovascular disease, anemia,
hypothyroidism, malnutrition (eg, vitamin C or D deficiencies, inadequate
protein intake),
o Excessive chronic alcohol: intoxication clues to severe due to loss of
protective reflexes.
o Specific medications may also impair fracture healing: nonsteroidal anti-
inflammatory drugs, glucocorticoids, and certain antibiotics (eg,
ciprofloxacin)
Describe the mechanism and degree of injury in trauma
o Road traffic accident
Ask if the patient was restrained: airbag + seatbelt
Was the patient in the front seat or back?
Was the patient a passenger or pedestrian?
death in passengers/pedestrians, severe casualties, burn associated
with the accident, rolled car
o Gunshot
Nature of the incident
Accident or assault
Type of gun
distance
o Falling down accident
height
landing condition
Why?
Accident at work Suicide
Intoxication pushed
Look for associated injuries: Did you injure any other part of your body?
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o Shortness of breath
o Blood in the urine
o Altered sensibility
Significant past injuries or surgeries in the affected area
Family history
Last meal (in case an injury requiring urgent surgery is identified) and medical
care given prior to coming to the hospital
Physical examination
Follow trauma protocol and Do ABCDE
General appearance, level of awareness, GCS
Check vital signs
Evaluate overlying skin: intact skin, bleeding, bruising,
Look, feel and move for signs of fracture
o Visible or palpable deformity
o Local swelling
o Visible bruising (ecchymosis) from escape of blood from the fracture
surfaces and periosteum
o Marked local tenderness over bone
o Marked impairment of function
Is there a wound communicating with the fracture? -skin integrity
Is there any impairment of circulation distal to the fracture? -color, warmth,
pulse, capillary return, nerve conductivity
Is there any evidence of nerve injury? Is there any evidence of visceral injury?
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Investigation
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Introduction
Stress Fracture
Stress fractures are due to loads that stress (either
compress or stretch) a bone but would not individually be
expected to cause it to break.
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Even then the fracture itself may show only as a faint hairline crack, usually more or
less transverse in direction: only rarely is there any displacement of the fragments.
More striking than the fracture is the zone of callus that surrounds it.
Faint—seen only as a haze near the bone—this new bone may eventually form a
dense fusiform mass about the site of fracture.
Pathologic Fracture
It occurs through a bone that is already weakened
by disease.
Often the bone gives way from trivial violence, or
even spontaneously.
In many cases the patient, when directly
questioned, will admit to having suffered pain or
discomfort in the region of the affected bone for
some time before fracture.
Causes
Infections:
o Pyogenic osteomyelitis (usually in chronic form)
Tumors:
Miscellaneous: Simple bone cyst
Congenital disorders:
o Osteogenesis imperfect (fragilitas ossium)
Diffuse rarefaction of bone:
o Senile osteoporosis o Infantile rickets
o Cushing syndrome
Disseminated tumors:
o Multiple myeloma
Miscellaneous:
o Paget’s disease o Gaucher’s disease
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Open Fracture
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Hip
Femoral neck Proximal femur fracture between the trochanters and the
fracture femoral head
Interochanteric Proximal femur fracture extending between the greater and
fracture lesser trochanters
Foot
Jones fracture Acute fracture in the metaphyseal-diaphyseal area of the
proximal 5th meta-tarsal (often confused with avulsion or stress
fractures)
Principles of Management
Initial management
A) Airway and cervical position
B) Breathing
C) Circulation
D) Disability (neurological, GCS)
E) Exposure
F) Open Fracture
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ward off infection from the organisms that must inevitably remain even after the
most meticulous cleansing.
Supplementary treatment
Broad-spectrum antibiotic, such 3rd generation cephalosporin
Prophylaxis against tetanus
Precautions: - in severe open fractures, with perhaps considerable loss of blood,
there is a greater liability to shock, and appropriate measures of resuscitation are
often required
Complications
Life-threatening Conditions:
o Femur fractures that disrupt the femoral artery or its branches are potentially
fatal
o Pelvic fractures can damage pelvic arteries or veins causing life-threatening
hemorrhage.
o Hip fractures, particularly in the elderly, may prevent ambulation, resulting in
potentially life-threatening complications, such as pneumonia,
thromboembolic disease, and possibly rhabdomyolysis.
o Patients with multiple rib fractures are at substantial risk for pulmonary
contusion and related complications.
Arterial injury
Nerve injury
Compartment syndrome
Thromboembolic disease
Osteomyelitis
Nonunion
o Incomplete healing of a fracture where the cortices of the bone fragments do
not reconnect
Malunion
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o When a fracture heals with a deformity (eg, angulation, rotation, incongruent
joint surface)
Complex regional pain syndrome:
o Complex Regional Pain Syndrome (CRPS), also known as Reflex Sympathetic
Dystrophy (RSD)
o It is a complex disorder of the extremities characterized by localized pain,
swelling, limited range of motion, vasomotor instability, skin changes, and
bone demineralization.
Fat embolism syndrome:
o FES typically manifests 24 to 72 hours after injury with dyspnea, tachypnea,
and hypoxemia.
o Neurologic abnormalities and a petechial rash may be present.
o Severe respiratory distress and death can occur.
Post Traumatic Arthritis
Case Discussion……………………………………………..511
Clinical Manifestation…………………………………….511
Investigation………………………………………………….512
Differential Diagnosis…………………………………….516
Discussion of the Case………..…………………………517
Principles of Management…………………………….520
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Case Discussion
A 14-year-old male patient presented with right knee swelling of 03 month duration. The
swelling was initially small in size, later it increase to attend the current size. Associated
with the swelling he has also intermittent Right knee pain for the past 10 weeks, the pain
and swelling has grown more regular in the last week. Further interview reveals that the
patient plays on a youth soccer team, and his knee feels especially painful during practice.
His parents attributed the symptoms to “growing pains,” as the patient’s height and
weight have been increasing appropriately for his age, and he has had no known skeletal
diseases—nor any serious conditions—prior to onset of the pain, no compliant in other
system. On Physical examination, Vital signs were normal on MSK examination there is
8x6 cm, palpable mass on the anterior aspect of the right proximal tibia. Which is tender
to palpation, mobile, not adherent to the adjacent structure.
Clinical Manifestation
History
Age: you can narrow down your differentials based on age
Chief complaint
o Localized pain or swelling of a few weeks' or months' duration
Asymptomatic in most benign tumors
Mild pain which is aggravated by exercise and is often worse at night:
malignant tumors
Ask for associated bleeding
o Thyroid and kidney metastasis is highly vascular
Ask for signs of infection
o Fever
o Tenderness
o discharge
Rule out Malignant metastasis to Bone
o Ask if there is breast lump, discharge or any prior breast cancer diagnoses
o Ask for anterior neck swelling, heat or cold intolerance- thyroid cancer
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Investigation
Lesion:
1. Osteoid, chondroid or fibrous (ground glass)
2. What is the lesion doing to the bone? (sclerotic/lytic/mixed/calcification)
3. What is the bone doing to the lesion? (periosteal reaction/Codman’s triangle/onion skinning)
Margins:
1. Well defined (narrow zone of transition) - slow growing – less aggressive
2. Poorly defined (wide zone of transition – likely progressive (malignant)
3. Cortical breach
You should be able to comment on radiographs if the likely diagnosis is non-aggressive or
aggressive lesion
Although a definite diagnosis may not be expected, there should be an appropriate
recognition and work up for a potentially malignant condition.
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Table 8.3: X-ray features of common tumors
Giant cell tumor Soap bubbles
Osteochondroma Exostosis
Osteosarcoma Sunburst appearance
Ewing sarcoma Onion skin periosteum, moth eaten
Chondrosarcoma Moth eaten butterfly shape
Osteoid osteoma Nidus (hole)<1.5 cm
Osteoblastoma Nidus (hole)>1.5 cm
CT-scan:
o To evaluate disease extent
Radionuclide bone scans or total body
positron emission tomography (PET)
o To evaluate the entire skeleton for
the presence of multiple lesions
MRI
o For nerve conduction test
o For soft tissue tumor
o To look for prognosis
Tumor markers
Biopsy: the indications for biopsy are:
o Whenever there is significant doubt as to the diagnosis of a benign or
malignant lesion
o When the histologic distinction among possible diagnoses could alter the
planned course of treatment
o When definitive confirmation of the diagnosis is required before undertaking
a hazardous, costly, or potentially disfiguring treatment
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Work-Up of Suspected Neoplasm
Local staging: MRI of whole limb (to assess spread of tumour, compartments involved, check
for skip lesions and look for neurovascular proximity)
Systemic workup:
o CT chest
o Abdomen and pelvis to identify primary or metastatic lesions
Bone scan - to check for skeletal metastases
Don’t fix fracture until sure of pathology
Staging vs. Grading:
o Stage – degree of spread of the tumor
o Grade – Degree of cellular differentiation
Biopsy:
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Principles of biopsy:
Must be performed by or under direct instruction of surgeon at specialist bone tumor unit
Tract removable within definitive incision
Extensile longitudinal incision
If using LA, then judicious use to avoid seeding
Tourniquet use only with gravity exsanguination, should be deflated prior to definitive closure
Direct to bone do not follow planes
Don’t contaminate > 1 compartment
Enough tissue from periphery of tumour to avoid area of central necrosis
Meticulous haemostasis to avoid seeding
Send in a formalin container
If a drain is inserted, it should come out through or in line the surgical incision
Do not forget to biopsy every infection and culture every tumour
Sutures close to wound margin to allow inclusion for excision of tract later
Differential Diagnosis
1) Bone tumor
2) Abscess
3) Metastasis to the bone
4) Bone cyst
5) Osteomyelitis
6) Fibrous dysplasia
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Discussion of the Case
Introduction…………………………………………………..517
Osteosarcoma…………………………………………….….518
Chondrosarcoma……………………………………………518
Ewing Sarcoma……………………………………………….519
Other Tumors…………………………………………………519
Introduction
Bone tumors can be classified as primary and secondary.
Secondary bone tumor is the most common
Primary bone tumors can be classified into:
o Bone forming
Osteoma
Osetoid osteoma
Osteoblastoma
Osteosarcooma
o Cartilage forming
Osetochondroma
Enchondroma
Chnodromyxoid fibroma
Chondroblastoma
Chondrosarcoma
o Miscellaneous tumors
Ewing sarcoma
Giant cell tumor of bone
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8.2.1. Osteosarcoma
8.2.2. Chondrosarcoma
A condition of middle aged and older adults
Bones of pelvis, proximal femur, proximal humerus
Is usually of low or intermediate grade.
Cartilage can be recognized on imaging because it tends to
grow in nodules, has a very high-water content (making it
bright on T2 weighted MRI and dark on CT scan), and
deposits mineral in dense "rings and arcs" whose density
can focally exceed cortical bone.
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8.2.3. Ewing Sarcoma
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Management
1. Chemotherapy
Induces apoptosis
Targets rapidly dividing cells, such as those found in neoplasms, therefore not
effective against slow dividing cells
o E.g. Cartilage
Lack of specificity – therefore other rapidly dividing cells also affected
o E.g. lining of gut, bone marrow, hair, and skin
Eliminates micro-metastases in lungs
Indications:
o Osteosarcoma
o Ewing's sarcoma
o Metastatic soft tissue sarcoma
6 – 12 weeks pre-op and 6 – 12 months postop
Agent specific side effects:
o Doxorubicin (cardiac toxicity)
o Ifosfamide: (neurological toxicity)
o Cyclophosphamide: (myelosuppression and urotoxicity)
o Bleomycin: (pulmonary fibrosis)
2. Radiotherapy
Production of free radicals leading to direct genetic damage
Indications:
o Ewing Sarcoma
o Lymphoma of bone
o Multiple Myeloma
o Soft tissue sarcoma
Metastatic bone disease - breast & prostate
o Radio-resistant: renal & GI metastases
Complications:
o Delayed bone healing o Sarcoma
o Infection o AVN
o Fracture o Growth arrest
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3. Surgical excision
Indications for surgery in benign tumors:
Thinning of >50% of cortex
Mass effect
Types of surgery:
o Intralesional: Excisional biopsy for benign lesions
o Marginal:
Resection passes through reactive zone
Outside tumour pseudocapsule where inflammatory and tumour
cells are present
Between cancer and normal tissues, micro-metastasis may persist
o Wide:
Outside reactive zone with cuff of normal tissue
Intra-compartmental possibility of skip lesions
Careful planning of surgical approach to ensure tumour clearance
o Radical:
En-bloc excision of entire compartment
Reconstruction endoprosthesis, custom-made or modular
o Amputation: When Vascular/neurological invasion present
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Short Case Discussion
Content By:
Matyas Wondwossen
Nanati Jemal 8.3. Fracture management…………………………………523
Edited By:
Samuel Mesfin
8.4. Talipes Equinovarus
Reviewed By: (Idiopathic Club-Foot)..…………………………………529
Dr. Matiyas Seid
(Orthopedic Surgeon)
8.5. Video QRs………………..…………………………………534
P a g e 522 | 548
8.3. Fracture Management
Principles……………………………………………….523
Plaster of Paris……………………………………….524
Continuous Traction……………………………….525
External Fixation………………………………….…526
Internal Fixation…………………………………….528
Principles
A. Reduction
Restoration of fracture fragment to acceptable position
o Aim for adequate apposition and normal alignment
o There are two methods closed or open
In many fractures reduction is unnecessary, either because there is no displacement
or because the displacement is immaterial to final result.
1. By closed manipulation- most commonly used, under generalized or local
anesthesia,
2. By mechanical traction with or without manipulation
Closed reduction principles
o All displaced # should be reduced
o Analgesia & muscle relaxation
o Correct length, rotation & angulation
o Use splints initially
o Immobilize it above and below #
3. By open operation
B. Immobilization
Indication:
1. To prevent displacement or angulation of the fragments
2. To prevent movement that might interfere with union
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3. To relieve pain
Methods: -
1. By a plaster of Paris (POP) or another external splint
2. By continuous traction
3. By external fixation
4. By internal fixation
Holding reduction is usually no problem and patients with tibial fractures can bear
weight on the cast.
However, joints encased in plaster cannot move and are liable to stiffen.
Stiffness can be minimized by:
o Delayed splintage – that is, by using traction until movement has been
regained, and only then applying plaster; or
o Starting with a conventional cast but, after a few weeks, when the limb can
be handled without too much discomfort, replacing the cast by a functional
brace which permits joint movement.
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Types of application of POP
Posterior gutter:
o The POP is applied only posteriorly and the rest
is covered by bandage.
o It allows expansion, thus helping to decrease risk
of compartment syndrome.
Circular cast:
o The POP spans the whole
circumference of the limb, making it
better at stabilizing the fracture
fragments.
o But it has higher risk for compartment
syndrome.
Indications
o Undisplaced fractures
o Tolerable displacement
o Closed reduction of displacement possible
o Fracture in children (Upper and lower extremities)
Complications
o Tight cast
o Pressure sores
o Abrasion or laceration of the skin.
Continuous Traction
Traction is applied to the limb distal to the fracture, so as to exert a continuous pull
in the long axis of the bone, with a counterforce in the opposite direction (to
prevent the patient being merely dragged along the bed).
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Traction includes:
o Traction by gravity:
This applies only to upper limb injuries.
Thus, with a wrist sling the weight of the
arm provides continuous traction to the
humerus.
o Skin traction:
Skin traction will sustain a pull of no more
than 4 or 5 kg.
Holland strapping or one-way-stretch
Elastoplast is stuck to the shaved skin and
held on with a bandage.
The malleoli are protected by Gamgee
tissue, and cords or tapes are used for
traction.
o Skeletal traction:
A stiff wire or pin is inserted – usually
behind the tibial tubercle for hip, thigh and
knee injuries, or through the calcaneum
for tibial fractures – and cords tied to them
for applying traction.
External Fixation
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Internal Fixation
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8.4. Talipes Equinovarus (Idiopathic Club-Foot)
Introduction………………………………………………….529
Pathological Anatomy…………………………………..529
Epidemiology………………………………………………..530
Etiology…………………………………………………….…..530
Clinical Manifestation……………………………………531
Deformities…………………………………………….…….532
Investigation…………………………………………………532
Management…………………………………………..……533
Introduction
The term ‘talipes’ is derived from talus (Latin = ankle bone) and pes (Latin = foot).
Equinovarus is one of several different talipes deformities; others are talipes
calcaneus and talipes valgus.
In the full-blown equinovarus deformity the heel is in equinus, the entire hindfoot in
varus and the mid and forefoot adducted and supinated.
The abnormality is relatively common, the incidence ranging from 1–2 per thousand
births; boys are affected twice as often as girls and the condition is bilateral in one-
third of cases.
Pathological Anatomy
The neck of the talus points downwards and deviates medially, whereas the body is
rotated slightly outwards in relation to both the calcaneum and the ankle mortise.
The posterior part of the calcaneum is held close to the fibula by a tight calcaneo-
fibular ligament, and is tilted into equines and varus; it is also rotated medially
beneath the ankle.
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The navicular and entire forefoot are shifted medially and rotated into supination
(the composite varus deformity).
The skin and soft tissues of the calf and the medial side of the foot are short and
underdeveloped.
If the condition is not corrected early, secondary growth changes occur in the
bones; these are permanent.
Epidemiology
Even with treatment the foot is liable to be short and the calf may remain thin.
The most common birth defect
o 1/1000 Caucasians, 3/1000 Polynesians
o Female: Male = 2: 1
o Bilateral in 50%
Underlying bone problem are
Deformed talus, which it is flexed and medially deviated
Etiology
Calcaneus is in varus and rotated medially around talus
Navicular and cuboid are displaced medially
Multifactorial
o Neurogenic theory:
Histochemical abnormalities secondary to denervation changes in
various muscle groups of the leg/ foot
o Neurogenic imbalance deformity:
Defect in nerve supply (the incidence of varus and equinovarus
deformity in spina bifida is approximately 35%)
o Myogenic theory:
Primary muscle defect.
Predominance in type I muscle fibres and fibre type IIB deficiency
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o Congenital constriction bands/rings
o Retracting fibrosis:
Increased fibrous tissue in muscles and ligaments
Clinical Manifestation
Examine the whole child to exclude associated abnormalities:
o Myelomeningocele o Polio
o Intraspinal tumour o CP
o Diastematomyelia
Usually obvious at birth; the foot is both
turned and twisted inwards so that the sole
faces posteromedial.
The ankle is in equinus, the heel is inverted
and the forefoot is adducted and supinated;
sometimes the foot also has a high medial
arch (cavus), and the talus may protrude on
the dorsolateral surface of the foot.
The heel is usually small and high, and deep creases appear posteriorly and medially;
some of these creases are incomplete constriction bands.
o In some cases, the calf is abnormally thin.
The infant must always be examined for associated disorders such as congenital hip
dislocation and spinabifida.
X-rays are used mainly to assess progress after treatment.
Look for any associated developmental syndrome:
o Arthrogryposis o Diastrophic dysplasia
Examine the spine (neurological cause)
Pulses: Usually present but vascular dysgenesis
is possible (absent dorsalis pedis artery)
Examine foot creases: Medial, plantar, posterior
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Deformities
Investigation
Radiographs not routinely taken in a newly diagnosed presenting infant but may be
of value if the case is resistant to therapy or other pathologies
o E.g. congenital vertical talus) is suspected
Dorsiflexion lateral (Turco view):
o Shows hindfoot parallelism between talus and calcaneus
Lateral:
o Talo-calcaneal angle < 250
o Tibio-calcaneal angle > 900
AP:
o Talo-calneal (Kite) angle < 200
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Management
Aim of treatment: painless functional plantigrade foot without need of orthotic shoe
in the 1st year
Ponseti – Spanish physician worked in Iowa in 1950s
o 90 % success
o Start at 7 days - can be used in children up to 10 years
o Lasts for 6-8 weeks
o Serial weekly above knee casting with knee in 90 degree flexion
Cast manipulation using head of talus as fulcrum
o Cavus corrected first by dorsi-flexing first ray, increase supination – foot looks
worse
o Forefoot abducted
o Adduction and varus corrected simultaneously (varus corrected with hindfoot
abduction)
o Finally, equinus corrected – once anterior calcaneum is abducted from under
talus)
Kite error (Fulcrum at calcaneo-cuboid joint, which prevented correction of hindfoot)
Post-reduction abduction splinting is required to maintain the position for 23 hours
per day (full-time splinting) for 3 months and then 12 hours per day (night-time
splinting) until age 5 (or as close to this as canrealistically be achieved)
Traditionally, this involved Denis Browne boots and bar; however, Mitchell boots are
gaining popularity as they are well tolerated by infants (and therefore, their parents)
Residual equinus requires tendoachilles release in 90 %
Aim for at least 150 dorsiflexion
Done under LA (full division)
Cast for further 3 weeks while tenotomise heals
Cochrane:
o Ponseti technique produce better short-term outcomes compared to Kite’s
Posteromedial soft tissue release and Achilles tendon lengthening
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8.5. Video QRs
Article on Clubfoot Etiology and Treatment
Fracture Management
Bone Tumor
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Index
Abdomen Renal, 203 Fractures, 501
Acute pancreatitis, 362 Skin, 15 Fracture Management, 523
Colorectal cancer, 282 Cardiac tamponade, 262 Gait, 476
Gallstones, 357 Charcot’s triad, 273 Gallbladder, 265, 274
Intestinal obstruction, 319, 328 Chest trauma, 121 Gallstones (cholelithiasis), 357, 361
Intussusceptions, 338, 441 Cleft lip and palate, 43 Gastric cancer, 307
LUTS, 183, 283 Club foot (congenital talipes Aetiology and risk factors, 309
Abdominal trauma, 381 equinovarus), 529 Chemotherapy, 315
Advanced Trauma Life Support Colorectal cancer, 282 Clinical features, 311
(ATLS), 387 Clinical features, 282 Imaging, 312
Anorectal abscess, 370 Epidemiology, 287 Incidence, 308
Appendicectomy, 354, 419 Investigation, 285 Investigations, 312
Bladder cancer, 179 Management, 293 Radiotherapy, 315
Bladder outflow obstruction, 170 Pathology, 289 Surgery, 316
Bladder cancer, 179 Risk factors, 287 Subtotal gastrectomy, 316
Bladder trauma, 224 Spread, 290 Total radical gastrectomy, 316
BPH, 171 Staging, 290 Gastric outlet obstruction, 294
Neurogenic bladder, 197 Cystoscopy, 188 Gastric ulcers, 309, 310, 319
Prostatic Cancer, 175 Debridement, 12 Glasgow Coma Scale
Urethral stricture, 194 Digital rectal examination (GCS), 443, 444, 445
Brain injury, 440 (DRE), 375 Goitre, 76, 77, 78, 80, 82
Brain tumours, 475 Ductal carcinoma in situ Retrosternal, 75, 89
Breast carcinoma, 65 (DCIS), 67 Toxic, 78
Burns, 24 Dysphagia, 98 Goitrogens, 77
Cancer External fixation, 526 Graves’ disease, 79, 80, 86
Bone, 511 Extradural haematoma, 456 Haematuria, 174, 185
Bladder, 180 Extremity trauma, 398 Haemorrhoids, 369, 378
Colorectal, 282 Compartment Haemothorax, 130, 146, 149
Esophageal, 107 syndrome, 507 Hamartomas, 49
Gastric, 307 Fractures, 501 Hartmann’s procedure, 387
Prostatic, 175 Follicular carcinoma, 82 Head injury, 440
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Hernias, 400, 406, 415, 418 Lung cancer, 484, 512 Parkland formula, 34
Hydronephrosis, 174, 201 Melanoma, 22 Penetrating injuries, 6, 152, 394, 467
International Prostate Symptom Meningioma, 475, 477 Peptic ulcers, 297, 299
Score (IPSS), 174 Nasogastric tubes, 420 Perforation, 302, 303, 326
Intestinal obstruction, 318, 328 Nephrolithiasis, 199 Plaster of Paris, 524
Intracranial pressure (ICP), 445, 448 Neural tube defects, 485 Pleural effusion, 251, 260, 284
Intussusceptions, 338, 441 Neurogenic shock, 461, 468 Prepuce, 238, 244
Jaundice, 250, 262 Nipple, 60, 63, 64 Priapism, 445, 468
Keloid scars, 10 Nocturia, 170, 185 Primary survey, 387, 443
Liver Osteosarcoma, 518 Prostate
Abscess, 254, 258 Paget’s disease, 68, 92 Prostate cancer, 175
Hydatid cyst, 250, 253 Pancreas Prostatectomy, 174, 175
Metastases, 253, 264 Pancreatic carcinoma, 276 Rectal bleeding, 283, 379
Trauma, 386 Pancreatitis, 362 Renal calculi/stones, 199, 428
Tumours, 249, 250 Papillary carcinoma, 82 Renal cell carcinoma, 203
Lower urinary tract symptoms Paradoxical respiration, 465 Retrograde ureterogram, 218
(LUTS), 174, 203 Paralytic ileus, 30, 323 Urinary catheterization, 233
Screening, 183, 212, 446 Subarachnoid hemorrhage, 458
Skin cancer, 15 Testes, 432, 435 Wound healing
Skin grafts, 12, 34 Thyroid, 71, 86 Abnormal, 10
Skull fractures, 445, 451 Tracheostomy, 160 Burns, 24
Small intestines, 323, 326 Transurethral resection of Contractures, 10
Smoking, 14, 45, 58, 108 Prostate (TURP) Delayed, 12
Spinal cord injury, 460 Complications, 174 Infected wounds, 10
Staging, 21, 111, 177 Tumor, nodes, metastases Primary intention, 9
Strangulation, 321, 326 (TNM) staging, 177, 190, 210 Secondary intention, 9
Strictures, 328, 332, 412 Ureteroscopy, 202, 223 Wound management, 10
Subdural haematoma, 454, 456 Urethra
Tension pneumothorax, 128 Stricture, 231, 234
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