GI Drs For Pedi&Surgical Nsg-Merged

Asrat Weldeyes Health Science Campus
School of Nursing and Midwifery

Department of Nursing
Medical Surgical Nursing for Nursing

Students
By: Bantalem T. (BSc, RN, MSN in AHN)

Gastrointestinal disease
disorders
Overview
♦ Overview of anatomy and physiology of the GI system
♦ Assessment of gastrointestinal system (4hrs)
♦ Hx
♦ Abdominal Assessment
♦ Common diagnostic procedures
♦ Therapeutic procedures
Anatomy and physiology over view
 The gastrointestinal system includes

 The alimentary canal
Mouth  Accessory organs
Esophagus Salivary glands
Stomach Liver
Small intestine Pancreas
Large intestine and Gallbladder and
Rectum Ducts
4 By: Bantalem T(MSc) 2/14/2024

Anatomy and physiology over view…
 The alimentary canal is a hollow tube lined with mucous
membrane.
 The gastrointestinal system functions
 To digest food
 Absorb nutrients
 Propel the contents through the lumen and
 Eliminate the waste products.

 For simplicity and understanding, the alimentary canal can be
dividing into three parts:
 The Upper gastrointestinal tract  the Mouth, Oesophagus
and Stomach.
 The Middle GIT  Small intestine.
 The Lower GIT  Large intestine.
 The Fourth part (accessory) - Structures- salivary glands, liver,
gallbladder, and pancreas

 Both mechanical and chemical digestion processes begin in the
mouth.
 Chewing, movement through the gastrointestinal tract and
churning within the stomach are parts of the mechanical
process.
 Saliva, hydrochloric acid, bile and other digestive enzymes all
contribute to the chemical process of digestion.

 The esophagus extends from the oropharynx to the stomach.
 At the top of the esophagus is the upper esophageal sphincter
(UES).
 This prevent the influx of air into the esophagus during
respiration.
 At the bottom of the esophagus is the lower esophageal
sphincter (LES)
 This prevent the reflux of acid from the stomach into the
esophagus.

 The contents of the esophagus empty into the stomach
through the cardiac sphincter.
 The stomach secretes
Gastrin  promotes secretion of pepsinogen
Hydrochloric acid, pepsin, and lipase,  aid digestion and
Mucous  helps protect the stomach lining.

 The liver is a very vascular organ located in the right upper

quadrant of the abdomen under the diaphragm.
 It has two main lobes that are comprised of smaller lobules.

 Function:
stores a variety of vitamins and minerals.
Metabolizes proteins
Synthesizes plasma proteins, fatty acids and
triglycerides
Stores and releases glycogen.
detoxifies foreign substances such as alcohol, drugs or
chemicals.
Forms and secretes bile to aid in digestion of fat

 The gall bladder is a small receptacle that holds bile until it is
needed.
 It is located on the inferior aspect of the liver.
 The pancreas is located retroperitoneally in the upper abdomen
near the stomach
 It extends from just right of midline to the left toward the
spleen.

 The pancreas has both endocrine and exocrine functions.
 The endocrine functions
 Secretion of insulin
 Secretion of glucagon
 The exocrine function includes
 Secretion of trypsin, lipase, amylase, and chymotrypsin to aid
in digestion.

 The Gastrointestinal tract lumen is also composed of four
layers.
Mucosa (inner layer)
sub mucosa
Muscularies
Serosa.
Muscularies (longitudinal and circular )
The largest serosa is peritoneum
Most of abdominal organs are covered by peritoneum

 The small intestine is comprised of the duodenum, jejunum,
and the ileum.
 Duodenum  attaches to the stomach, is about one foot long
and C-shaped and curves to the left around the pancreas.
 The common bile duct and pancreatic duct enter here.
 Jejunum  is between the duodenum and ileum and is about
eight feet long.

Anatomy and physiology overview…
 Ileum is up to twelve feet long, depending on the size of

the patient.
 Ileocecal valve  separates the ileum from the large
intestine.
 The appendix is found at this juncture.

Anatomy and physiology overview…
 The large intestine can be broken down into
The ascending colon
Transverse colon
Descending colon and
Sigmoid colon.
 The sigmoid colon joins the rectum and ultimately the anal canal

Diagnostic procedures of GI disorder
 History taking
 Physical examination
 Laboratory tests
 CBC and electrolyte
 stool examination
o Occult blood
o Ova and parasites
o Stool culture
o Stool for lipids

Diagnostic …
 Radiographic tests
 X-ray study is performed to visualize abdominal organs.
 This test can reveal abnormalities such as tumours,
obstruction, abnormal gas collectives and strictures.

Diagnostic …
 Upper gastro-intestinal series (Barium) swallow.
 An upper series permits radiologic visualization of the
oesophagus, stomach, duodenum and jejunum.
 It can aid in the detection of structures, ulcers, tumors,
polyps, hiatal hernias and motility problems.
 Preparation:
 Instruct the patients NPO for 6 to 8 hours before test.
 Procedure: clients drink a radiopaque contrast medium
(barium) while standing in front of a fluoroscopy.

Diagnostic …
 Lower gastrointestinal series (Barium enema)
Is performed to visualize the position, movements, and filling
of the colon.
This test aid in the detection of tumors, diverticulum, stenosis,
obstruction, inflammation, ulcerative colitis and polyps.
 Preparation:
 Adequate bowel preparation
 Placing the client on a low-residue, clear liquid
 NPO for 6 to 8 hrs.
 Laxative
 Cleansing enema.

Diagnostic …
 Endoscopy
Is the direct visualization of the GI system by means of a
lighted, flexible tube.
More accurate than radiologic examination because the
physician can directly observe source of bleeding and surface
lesions and determine the status of healing tissue.

Always seek knowledge

GI Disorders ------

Diseases of the mouth and related structures
 DENTAL PLAQUE AND CARIES
 Tooth decay:
 Is an erosive process that begins with the action of bacteria on
fermentable carbohydrates in the mouth,
 It is the most common problem affecting the teeth.
 Dental decay can occur in anyone.
 Older adults are subject to decay

Tooth decay Cont`d…
Risk Factors
 Poor oral hygiene, poor health and perhaps a diet high
in simple or refined sugars also play a role.
 Drug-induced or age-related oral dryness
 Plague formation

Disorders in the oral cavity…
 The extent of damage to the teeth depends on
The presence of dental plaque
The strength of the acids
The ability of the saliva to neutralize the acids
The length of time the acids are in contact with the teeth
The susceptibility of the teeth to decay

Disorders in the oral cavity …
 Dental decay begins with a small hole, usually in a fissure (a
break in the tooth’s enamel) or in an area that is hard to clean.
 Left unchecked, the decay extends into the dentin. Because
dentin is not as hard as enamel,
 Decay progresses more rapidly and in time reaches the pulp of
the tooth.
 An abscess may form
 Soreness and pain usually occur with an abscess.
 As infection continues the patient’s face may swell, and there
may be pulsating pain.

 The extent of damage and the type of treatment is
determined by X-ray.
 Treatment
 Fillings
 Dental implants and
 Extractions.

 Prevention
Practicing effective mouth care
Reducing the intake of starches and sugars (refined
carbohydrates)
Applying fluoride to the teeth or drinking fluoridated water,
Refraining from smoking
Controlling diabetes

Periodontal diseases
 Infections and inflammation of the gums and bone that surround
and support the teeth.
 The most common cause of tooth loss among adults
 Gingivitis (inflammation of the gums)
 Periodontitis ( involves the soft tissue and bone supporting
the teeth)

Periodontal disease
Periodontitis
 The periodontium is the tissue that surrounds and supports the
teeth
 Periodontitis: an inflammation of the periodontium
 Cause
 Bacterial plaque
 Dental malocyusion
 Caries
 Dietary deficiencies
 Systemic diseases such as diabetes

Pathophysiology
 When develops, the inner layer of the gum and bone pull
away from the teeth and form pockets.
 Small spaces between teeth and gums collect debris and
can become infected.
 The body’s immune system fights the bacteria as the
plaque spreads and grows below the gum line.
 Weaken and break down bone and collective tissue that
hold teeth in place.
 Pockets deepen and even more gum tissue and bone are
destroyed.
 Tooth loss
Cont`d…
 C/M:
 Inflamed or swollen gums
 Pain when chewing,
 Poor tooth alignment,
 Clear pockets between teeth and gums
 Bright red, sometimes purple gums
 Pain when the gums are touched
 Receding gums, which make the teeth look longer
 Pus between the teeth and gums

Cont`d…

Cont`d…
 RX:
 The main aim of treatment is:
 To clean out bacteria from the pockets around the teeth and
prevent further destruction of bone and tissue.
 Good oral hygiene
 Good oral hygiene should be followed daily, even if the teeth
and gums are healthy, to prevent infection.
 Proper dental care involves brushing teeth at least twice a day
and flossing once a day.
 Scaling and cleaning

Cont`d…
 Prescription antimicrobial mouth rinse, such as
chlorhexidine: To control bacteria
 Antiseptic chip: This is a small piece of gelatin that is filled with
chlorhexidine.
 Antibiotic gel: This gel contains doxycycline, an antibiotic
 Antibiotic microspheres: Very small particles containing
minocycline
 Enzyme suppressant: Keeps destructive enzymes in check
with a low-dose of doxycycline.
 Oral antibiotics: for acute or locally persistent periodontal
infection

Cont`d…
 Flap surgery: to remove calculus in deep pockets, or to
reduce the pocket so that keeping it clean is easier.
 Bone and tissue grafts: This procedure helps regenerate
bone or gum tissue that has been destroyed
 Compln
 Loss of teeth
 Respiratory disease, rheumatoid arthritis, coronary artery
disease and problems controlling blood sugar in diabetes

Cont`d…
 Gingivitis:
 Inflammation of gums
 It commonly occurs because a film of plaque, or bacteria,
accumulates on the teeth.
 The earliest form of periodontal disease

Cont`d…
 There are two main categories of gingival diseases:
 Dental plaque-induced gingival disease:
 Caused by plaque, systemic factors, medications, or malnutrition.
 Non-plaque induced gingival lesions:
 Caused by a specific bacterium, virus, or fungus.

Cont`d…
By course
1. Acute Gingivitis:-it is sudden onset and short duration can be
painful.
2. Recurrent Gingivitis:-re appears after eliminated by medical
treatment or eliminated spontaneously.
3.Chronic Gingivitis:-show in onset and longer duration and
painless inflammation persists and resolves and normal areas
become inflamed

Cont`d…
 Classification based on distribution
 Localized gingivitis
 Confined to gingiva of single tooth
 Generalized gingivitis
 Involves the entire mouth

Cont`d…
 Causes and risk factors
 Accumulation of bacterial plaque
 Changes in hormones:
 Some diseases:
 Drugs:

Pathophysiology
 Accumulation of bacterial plaque between and around the teeth.
 The plaque triggers an immune response
 Lead to the destruction of gingival, or gum, tissue.
 Lead to further complications, including the loss of teeth.

Pathophysiology
 When plaque is not removed adequately, it can harden into
calculus, or tartar, at the base of the teeth, near the gums.
 This has a yellow color.
 Calculus can only be removed professionally.
 Plaque and tartar eventually irritate the gums, causing
gum inflammation around the base of the teeth.
 This means that the gums might easily bleed.

Cont`d…
 C/M:
 Bright red or purple gums
 Tender gums that may be painful to touch
 Bleeding from the gum when brushing
 Halitosis
 Inflammation swelling of gums
 Soft gums

Cont`d…
 DX: clinically
 Mgt:
► Removal of decayed tooth, structures and their replacement with
restorative barriers
► Tooth extraction and the fitting of dentures
► Brush your teeth at least twice a day and Floss daily.
► Replace your toothbrush every three months.
► Use a natural mouthwash.
► Visit your dentist at least once a year

Cont`d…
 Prevention
 Good hygiene with frequent brushing and regular flushing
 Correct techniques , regular checkups and intervention
 Restricting the amount of simple sugar in the diet.
 Adequate or supplemental vitamin to reduce plague
 Oral health.

Periapical Abscess
 Called as an abscessed tooth
 Involves a collection of pus in the apical dental periosteum and
the tissue surrounding the apex of the tooth
 The abscess may be acute or chronic.
 An acute periapical abscess arises from an infection, usually
secondary to dental caries.
 The infection of the dental pulp extends through the apical
foramen of the tooth to form an abscess around the apex.
 A chronic periodontal abscess occurs from a slowly
progressive infectious process.

Cont`d…

Cont`d…
 C/M:
 The abscess produces a dull, gnawing, continuous pain, often with
a surrounding cellulitis
 Edema of the adjacent facial structures, and mobility of the
involved tooth.
 The gum opposite the apex of the tooth is usually swollen on
the cheek side.
 Swelling and cellulitis of the facial structures may make it
difficult for the patient to open the mouth.
 There may also be a systemic reaction, fever, and malaise.

Cont`d…
 Mgt:
 Aspiration or drill an opening into the pulp chamber to relieve
pressure and pain and to provide drainage.s.
 Tooth extraction or root canal therapy
 Antibiotics, in the presence of overt spreading infection
 Analgesics

Cont`d…
Stomatitis
 Inflammation of oral tissue
 C/M:
 mild redness, edema
 If severe
o Painful ulceration
o Bleeding
o pain interfere with nutritional in take, communication and
willingness to maintain oral hygiene

Cont`d…
 Types of stomatitis include:
 Canker sore: A single pale or yellow ulcer with a red outer ring
or a cluster of such ulcers in the mouth, usually on the
cheeks, tongue, or inside the lip.
 Usually last 5 to 10 days
 Tend to come back
 Not associated with fever
 Cold sores : Also called fever blisters, cold sores are fluid-filled
sores that occur on or around the lips.
 Painful, contagious
 Usually gone in 7 to 10 days
 Associated with cold or flu-like symptoms

Cont`d…
 Mouth irritation.
 Biting your cheek, tongue, or lip
 Wearing braces or having a sharp, broken tooth
 Chewing tobacco
 Burning one's mouth from hot food or drinks
 Having gum disease (gingivitis) or other type of mouth
infection
 Having hypersensitivity to certain things, such as foods or
medicines
 Drugs such as chemotherapy, Radiation
antibiotics, medications used for rheumatoid arthritis,
or epilepsy medications.

Cont`d…
 RX:
 Oral hygiene
 Avoid foods that are difficult to chew or too hot or too spicy
to reduce further trauma
 Lips are lubricated
 Topical antifungal and anesthetic to promote healing and
minimize discomfort
 Analgesics
 Maintain adequate fluid and food intake
 Antibiotics

Parotitis
 Parotid glands are the saliva producing glands buried within each
cheek
 Saliva comes out usually at the level of the upper back teeth
 Parotitis is an inflammation of one or both parotid glands
 Cause
 Staphylococcus aureus, except in mumps (viral)
 Acute bacteria parotitis:
 An acute inflammatory response to bacterial infection which
cause redness, pain, swelling and tenderness over the gland on
the side of the cheek.

 Rx
 Correction of fluids
 Antibiotics
 Analgesics
 Chronic recurrent parotitis
 Refers to repeated episodes of discomfort and swelling of the
parotid gland often after eating.
 It is treated conservatively
 Gland massage
 Stimulate flow of saliva (lemon juice)
 Antibiotics
 Surgery –remove the gland

Cont`d…
 Viral parotitis
 The commonest viral cause of parotitis is mumps.
 Usually affected 4 to 10 years old
 Causes painful swelling of both parotid glands
 Recurrent parotitis in children
 Distention of the duct and the same symptoms as acute
bacterial parotitis in this case it is self limiting.

Cont`d…

Cancer of the oral cavity
 Cancer of the oral cavity is one of the most common
malignancies, especially in developing countries, but also in the
developed world.
 Squamous cell carcinoma (SCC) is the most common histology
 About 50,000 people in the U.S. get oral cancer each year, 70% of
them men

Causes
 Tobacco smoking:
 contains many carcinogenic molecules, especially polycyclic
hydrocarbons and nitrosamines.
 A directly proportional effect exists between the pack years
of tobacco used and the risk of SCCOC.
 Alcohol intake:
 Alcohol and tobacco seem to have a synergtistic effect in the
etiology of oral and oropharyngeal SCC.
 However, alcohol is linked to an increased risk of cancer even
in non-smokers.

Causes
 Human papilloma virus
 Herpes simplex virus
 Human immune deficiency virus
 Other factors such as
 poor oral hygiene
 wood dust exposure
 dietary deficiencies
 red meat and salted meat consumption have been linked
oral cancer

Pathophysiology
 Squamous cell carcinomas (SCC) constitute more than 90% of all
oral cancer.
 Other malignant tumors can arise from the epithelium, connective
tissue, minor salivary glands, lymphoid tissue, and melanocytes or
metastasis from a distant tumor.
 A variety of premalignant lesions have been associated with
development of SCC.
 The more common premalignant lesions including leukoplakia,
erythroplakia, oral lichen planus, and oral submucous fibrosis have
varying potential for malignant transformation

Leukoplakia
 Is a clinical term defined as a ―white patch or plaque that cannot
be characterized clinically or pathologically as any other disease.
 This lesion is usually associated with smoking and alcohol use.
 Dysplastic changes are seen in only 2–5% of patients.

Oral cancer
 Risk factors for malignant transformation include presence of
 dysplasia
 long duration of leukoplakia
 location on the tongue or floor of mouth,
 leukoplakia in non-smokers, size greater than 2cm
 Erythroplakia is a ―bright red velvety patch that cannot be
characterized clinically or pathologically as being caused by any
other condition

C/M:
 Pain is a common symptom in oral cancer patients, representing
30–40% of their main complaints.
 Occasionally patients may present with cervical lymphadenopathy
without any other symptoms
 It is very important to establish an early diagnosis in OSCC, and
it must be suspected in patients with single oral lesions persisting
for more than 3 weeks.

C/M:
 The clinical presentation of these early malignant lesions
is usually in the form of an erytholeukoplastic lesion.
 It consists of red or red and white areas with a slight
roughness and is well-demarcated.
 Ulceration in advanced stage

C/M:
 Lump
 In these advanced stages, exophytic tumours with warty
surfaces, poorly defined boundaries, and hard to
palpation may be seen.

Dx:
 The initial workup consists of diagnosis by biopsy.
 Accessible lesions may be adequately biopsied in the clinic
using punch forceps, core needle or fine-needle aspiration.
 Some patients will require examination under general
anesthesia to access posteriorly located lesions, or to
complete a physical exam limited by pain.

Dx cont`d…
 Radiographic imaging is crucial for evaluation of the
relation of the tumor to adjacent bone and for assessing
regional lymph nodes.
 CT scan is the study of choice for evaluation of bone
and neck nodes, especially early cortical involvement and
extracapsular nodal spread.
 MRI provides complementary information about soft
tissue extent
 perineural invasion and is also helpful for evaluating the
extent of medullary bone involvement because adult
marrow is normally replaced by fat.
Rx:
 Surgical resection is the treatment of choice for SCCOC.
 Surgical resection allows accurate pathologic staging,
with information about the status of margins, tumor
spread and histopathologic characteristics
 Adjuvant radiotherapy ± chemotherapy is used for
specific indications in regionally advanced tumors.

Disorders of the Esophagus
 DYSPHAGIA
 It is a difficulty of swallowing and is the most common symptom
of esophageal disease.
 This symptom may vary from an uncomfortable feeling in the
upper esophagus to acute pain on swallowing (odynophagia).
 Obstruction of food and even liquids may occur anywhere along
the esophagus.

Disorders of the Esophagus…
 Often the patient can indicate where the problem is located in
the esophagus.
 Pathologic conditions of the esophagus, includes
Motility disorders (achalasia, diffuse spasm)
Gastro esophageal reflux
Hiatal hernias
Diverticulation
Perforation
Foreign bodies
Chemical burns
Benign tumors and carcinoma.

 ACHALASIA
 Achalasia is absent or ineffective peristalsis of the distal
esophagus
 It is accompanied by failure of the esophageal sphincter to
relax in response to swallowing.
 Achalasia may progress slowly and occurs most often in
people 40 years of age or older.

 Cause include the following:
 Primary (idiopathic)
 Degeneration and loss of ganglion cells cause a defect in the
innervations of the esophagus
 Resulting absence of complete LES relaxation and absence of
peristalsis

 Clinical manifestation
 Difficulty in swallowing both liquids and solids.
 Sensation of food sticking in the lower portion of the
esophagus.
 Food regurgitation( commonly in advanced stage).
 Weight loss can be a late manifestation.

 Chest pain and heartburn (pyrosis).
 Pain may or may not be associated with eating.
 There may be secondary pulmonary complications from
aspiration of gastric contents.

 Treatment
 There is no curative treatment for achalasia
 The aim is to decrease the LES pressure either
chemically(medications) or mechanically (by forceful
stretching) .
 Smooth muscle relaxants such as
 Calcium channel blockers and
 Nitrates, have been used with limited success.

Ex. Nifedipine, 10–20 mg, or isosorbide dinitrate, 5–10
mg solution
Forceful dilation of the LES using balloons, pneumatic
(forceful) dilation
Pneumatic dilation has a high success rate
Is effective in 85%cases , with 3–5% risk of perforation or
bleeding.

Nursing care of pt’s with achalasia
 The patient should be instructed to eat slowly and to drink
fluids with meals
 Semisoft ,warm foods are better tolerated than cold, hard foods
,the client should avoid hot, iced foods as well as alcohol and
tobacco
 All foods should be chewed thoroughly to add saliva to mixture,
providing lubrication and allowing the bolus to pass more easily
 To prevent nocturnal reflux of food the client should sleep with
head of the bed elevated.

Esophageal diverticulum
 An esophageal diverticulum is a protruding pouch in the lining
of the esophagus.
 It forms in a weak area of the esophagus.
 The pouch can be anywhere from 1 to 4 inches in length.
 There are three types of esophageal diverticula (plural of
diverticulum), based on where they’re located:
 Zenker’s diverticulum. develops near the top of the
esophagus.
 Midthoracic diverticulum. This type occurs in the middle part
of the esophagus.
 Epiphrenic diverticulum. This type is located in the lower part
of the esophagus.

Causes
 The exact causes of esophageal diverticula is unknown. Some
people are born with it, while other develop it later in life.
 In adults, it’s often associated with increased pressure within the
esophagus.
 This pressure causes the lining to protrude in a weakened area.
 Potential causes of this increased pressure include:
 malfunction of the sphincters on either end of the esophagus
 inflammation from outside the esophagus
 food not moving properly through the esophagus
 malfunctioning of the swallowing mechanism

Clinical presentation
 Common symptoms of an esophageal  chronic cough
diverticulum include:  bad breath
 Difficulty swallowing
 chest pain
 Feeling like food is caught in the
 neck pain
throat
 weight loss
 Regurgitating food when bending over,
 vocal changes
lying down, or standing up
 Pain when swallowing

Dx
 Barium swallow. You’ll be asked to swallow a solution
containing barium, which shows up on an X-ray or CT scan. This
allows to track the movement of fluid through your esophagus.
 Gastrointestinal endoscopy. For this procedure, your doctor
inserts a thin, flexible tube with a camera at the end through your
mouth and down your throat in order to view your esophagus.
 Esophageal manometry. This technique measures the timing
and strength of the contractions of your esophagus.
 24-hour pH test. This test measures the pH in your esophagus
over a 24-hour period to check for signs of stomach acid or bile in
the esophagus.

Rx
Nonsurgical treatment
© Mild esophageal diverticula can usually be managed through
lifestyle changes, such as:
© Thoroughly chewing your food
© Eating a bland diet
© Drinking lots of water after eating to help with digestion.
© Over-the-counter antacids can also help with mild symptoms
Surgical management:-
 Surgically removing the diverticulum by using endoscopy

Hiatal hernia
 Some times also known as a diaphragmatic or esophageal hernia.
 A part of the stomach protrudes up through the diaphragm near
the esophagus into the chest.
 Patients may be asymptomatic or have daily symptoms of gastro
esophageal reflux disease (GERD).

Hiatal hernia…
 The hernia may be
 A sliding hiatal hernia:- is known as type I hernia.
 Accounts about 90% of total hiatal hernia
 Allows movement of the upper portion of the stomach
including the lower esophageal sphincter up and down
through the diaphragm.
 These patients typically have symptoms of GERD.

Hiatal hernia …
 Etiology. The actual cause of sliding hernia is unknown
 Predisposing factors
 Structural changes, such as weakening of the muscles in the
diaphragm around the esophagogastric opening
 Factors that increase intraabdominal pressure:
 e.g Obesity, pregnancy, ascites, tumors, tight corsets, intense
physical exertion and heavy lifting on a continual basis
02/14/2024
2/14/2024 By: Bantalem T(MSc)
Hiatal hernia …
 Other predisposing factors are
 Increased age
 Trauma
 Poor nutrition and
 A forced recumbent position

94
Hiatal Hernia …
 C/M:
 In sliding hernia 50% patients are asymptomatic
 Heart burn, Regurgitation
 Dysphagia
 Substernal pain, burning, non radiating, position dependent
epigastric pain, substernal tightness
 Symptoms may be exacerbated by gastric irritants(alcohol,
tobacco, caffeine)

95
Hiatal hernia…
 A rolling hernia:- known as Paraesophageal (type II)
hernia.
 Portion of the stomach protrudes up through the diaphragm,
but the lower esophageal sphincter area remains below the
level of the diaphragm.
 These patients do not generally suffer from reflux.

Hernia …
 Type II(paraesophageal hernia),Rolling hernia accounts 10% of
the total hernia
 Depending on the extent of herniation, Paraesophageal hernia is
further classified as types II, III, or IV(which has the greatest
herniation)
 Gastro esophageal junction is blow the diaphragm

97
Hiatal Hernia …

98
Hernia …
 Clinical Manifestations
 A sense of fullness after eating
 Does not have symptoms of reflux
 Chest pain
 Reflux usually does not occur, because the gastroesophageal
sphincter is intact.
 Complication for both (type I and II)
 Hemorrhage, obstruction, and strangulation can occur with
any type of hernia.

99
Hernia …
 Nursing Management
 Frequent, small feedings that can pass easily through the
esophagus.
 No food intake several hours before bed
 Weight reduction
 Sleep with head at 300
 Avoid gastric irritants, alcohol, tobacco and caffeine
 Regular use of anti acids

100
Hernia …
 The patient is advised not to recline for 1 hour after eating, to
prevent reflux or movement of the hernia,
 Elevate the head of the bed 10- to 20-cm blocks to prevent the
hernia from sliding upward.
 Avoid lifting and straining
 If overweight, the patient should be encourage to lose weight

101
Esophageal cancer
 Esophageal carcinoma (EC) is the eighth most common cancer
and the sixth leading cause of cancer‐related deaths
worldwide.
 China, unfortunately, locates in the highest-risk area (often
referred to as the ―esophageal cancer belt‖) spanning from
northern Iran through the Central Asian republics and into
northern China.

Esophageal cancer
 Esophageal cancer is a disease in epidemiologic transition.
 Until the 1970s, the most common type of esophageal
cancer in the United States was squamous cell carcinoma,
which has smoking and alcohol consumption as risk
factors.
 Since then, there has been a steep increase in the
incidence of esophageal adenocarcinoma, for which the
most common predisposing factor is gastroesophageal
reflux disease (GERD).

Epidemiology
 Esophageal cancer is more common among men than
among women.
 The lifetime risk of esophageal cancer in the United
States is about 1 in 132 in men and about 1 in 455 in
women.
 Esophageal cancer makes up about 1% of all cancers
diagnosed in the United States, but it is much more
common in some other parts of the world, such as Iran,
northern China, India, and southern Africa.

Histologic type
 There are two main types of esophageal cancer. One type
is squamous cell carcinoma.
 Squamous cells line the inner esophagus,
and cancer developing from squamous cells can occur along
the entire esophagus.
 The other type is called adenocarcinoma. This is cancer that
develops from gland cells.

Risk factors
 Age
 The chance of getting esophageal cancer increases with
age. Less than 15% of cases are found in people younger
than age 55.
 Gender
 Men are more likely than women to get esophageal
cancer.
 Gastroesophageal reflux disease
 The stomach normally makes strong acid and enzymes to
help digest food.

Risk factors
 In some people, acid can escape from the stomach up
into the lower part of the esophagus.
 Smoking
 Barrett’s esophagus
 Alcoholism
 Obesity

Signs and symptoms
 Difficulty or pain when swallowing
 Weight loss
 Pain in the chest, behind the breastbone
 Coughing
 Hoarseness
 Indigestion and heartburn

Diagnosis
 Signs and symptoms
 Medical history
 Barium swallow study
 Endoscopy
 Biopsy

Treatment
 As with many cancers, esophageal cancer treatment has a
greater chance of success if the cancer is caught early.
 Surgery . Part or all of the esophagus may be removed.
 Radiation therapy. Kills cancer cells with radiation.
 Chemotherapy. Powerful drugs that attack cancer cells
throughout the body
 Targeted therapy and immune therapy

Stay motivated
and
Study hard!

Gastric disorders
Gastritis
 Inflammation of the gastric or stomach mucosa

 A common GI problem
 about 2 million visits to outpatient clinics annually in the US
 It affects women and men about equally
 More common in older adults
Gastritis
 Can be :
 Acute gastritis: lasting several hours to a few days
 Chronic gastritis: Resulting from repeated exposure to
irritating agents or recurring episodes of acute gastritis

Causes
 Acute gastritis may be classified as
 Erosive: caused by local irritants such as aspirin and other
nonsteroidal anti-inflammatory drugs (NSAIDS) (e.G., Ibuprofen
[motrin]); alcohol consumption; and gastric radiation therapy
 nonerosive: caused by an infection with helicobacter pylori
 Ingestion of strong acid or alkaline
 Stress-related gastritis
 Reflux of duodenal content

C/M:
 Epigastric pain or discomfort,
 Dyspepsia (indigestion)
 Anorexia, hiccups, or nausea and vomiting
 Bleeding, which may manifest as blood in vomit acute
 Melena (black, tarry stools)
 Hematochezia (bright red, bloody stools)
o Fatigue
o Pyrosis (a burning sensation in the stomach and esophagus that
moves up to the mouth; heartburn) after eating
o Belching, a sour taste in the mouth, early satiety
o Anorexia, or nausea and vomiting
o Intolerance to spicy or fatty foods
Dx:
 Endoscopy and histologic examination of a tissue specimen
obtained by biopsy
 Complete blood count (CBC)
 Diagnostic measures for detecting H. pylori infection

Rx:
 Fluids
 Modifying the patient’s diet, promoting rest, reducing stress,
 Avoidance of alcohol and NSAIDS
 Initiating medications that may include antacids, H2 blockers, or
proton pump inhibitors
 H. Pylori may be treated with selected drug combinations (a
proton pump inhibitor, antibiotics, and sometimes bismuth salts)

Peptic Ulcer Disease
PUD
 PUD is an excavation (hollowed-out area) that forms in the
mucosal wall of the stomach, in the pylorus, duodenum, or in the
esophagus
 Results from the digestive action of HCl & pepsin
 More common in people b/n 40 & 60 years
 Incidence
 Is relatively uncommon in women of childbearing age
 Is almost equal to that in men after menopause
 Can occur without excessive acid secretion
 Ulcers are defined as breaks in the mucosal surface >5 mm in
size, with depth to the sub-mucosa

Damage of gastric mucosa from irritants

Types of PUD
Depending on the degree of mucosal involvement
i. Acute PUD
 Associated with superficial erosion and minimal inflammation
ii. Chronic PUD
 Is of long duration, eroding through the muscular wall with the
formation of fibrous tissue
 Present continuously for many months or intermittently
throughout the person’s lifetime
 Is at least four times as common as acute erosion
Depending on the location of erosion
a. Gastric ulcer (GU)
b. Duodenal ulcer (DU)

Cause
 Infection with H. pylori
 Excessive secretion of HCl in the stomach because of:
 Psychological stress (e.g., anxiety) and physiological stress
(like in case of burn, shock, surgery)
 Caffeinated beverages
 Ingestion of hot, rough, or spicy foods
 Alcohol
 Smoking

Cause Cont’d…
 Ulcerogenic drugs
 Tumors, like in case of Zollinger-Ellison syndrome (ZES)–
produce excessive amounts of the hormone gastrin
 GERD- resulting esophageal ulcer
 Familial tendency-genetic link– those with blood type O
 Pregnancy appears to protect women from the developing ulcers

Pathophysiology
Acids, bile salts, aspirin, ischemia, H. pylori
Breakdown of gastric mucosal barrier
Acid back-diffusion into mucosa

Histamine release
from damaged
Destruction of mucosal cells
mucosa
 Acid & Pepsin release

 Vasodilation
 Capillary
Further mucosal erosion permeability
Destruction of B/Vs
Bleeding
 Loss of plasma
proteins into gastric
lumen
125 ULCERATION
By: Bantalem T(MSc)  Mucosal edema
2/14/2024
C/Ms Cont’d…
Dull, gnawing pain or a burning sensation in the mid-
epigastrium or in the back
Pain of duodenal ulcer origin Pain of gastric ulcer origin

 Burning‖ or ―cramping‖  Located high in the epi-
 Often located in the mid- gastrium
epigastrium region beneath  Occurs about 1/2 to 1 hours
the xyphoid process after meals
 Back pain  Can be burning‖ or ―gaseous‖
 Usually relieved by eating

C/Ms Cont’d…
 Sharply localized tenderness
Around the epigastrium or
Slightly to the right of the midline
 Pyrosis (heartburn)
 Emesis often containing undigested food eaten many hours earlier
 Bleeding– melana (tarry stools)
 Abdominal distention

Emergency Complications
3 major emergency complications
1. Hemorrhage
2. Perforation
3. Gastric outlet obstruction

Complications Cont’d…
1. Hemorrhage
 Is the most common observed
 Cause
 Erosion of the granulation tissue found at the base of the
ulcer during healing
 Erosion of the ulcer through a major blood vessels

2. Perforation
 The 2nd most common complication
 Commonly seen in large penetrating DUs
 Occurs with ulcer penetrating the serosal surface, with spillage
of either gastric or duodenal contents in to the peritoneal cavity
 S/S
 Sudden, severe upper abdominal pain that quickly spread
throughout the abdomen
 Shallow and rapid respiration
 Usually absent bowel sounds
 Nausea and vomiting

3. Gastric outlet obstruction
 Is the least common ulcer-related complication
 Cause
 Inflammation and edema in the peri-pyloric region
 S/s
 Long history of ulcer pain
 Pain
 Short duration or completely absent
 More generalized upper abdominal discomfort that
becomes worse towards the end of the day as the fills and
dilates
 May be relieved by belching or by self-induced vomiting
S/s of Gastric outlet obstruction
 Vomiting- which is very common and often projectile
 Constipation- as result of dehydration
 Swelling in the upper abdomen as a result of dilation of
stomach
 Loud peristalsis may be heard

Duodenal vs Gastric Ulcers
Duodenal Ulcer Gastric Ulcer
Lesion
 Superficial; smooth margins;  Penetrating
round, oval, or cone shaped
Incidence
 Age 30–60  Usually 50 and over
 Male: female 2–3:1  Male: female 1:1
 80% of peptic ulcers  15% of peptic ulcers
Risk Factors
 H. pylori, alcohol, smoking,  H. pylori, gastritis, alcohol,
By: Bantalem T(MSc)
133 stress smoking, use of NSAIDs, stress
2/14/2024
GUs Vs DUs Cont’d…
Duodenal Ulcer Gastric Ulcer
Signs, Symptoms, and Clinical Findings
 Hypersecretion of HCl  Normal—hyposecretion of HCl
 May have weight gain  Weight loss may occur
 Pain occurs 2-3 hrs after a  Pain 1⁄2 -1 hr after a meal
meal  Rarely occurs at night(30-40%)
 Often awakened b/n 1-2 AM(50-80%)  May be relieved by vomiting
 Ingestion of food relieves pain  Ingestion of food does not help
 Vomiting is uncommon  Vomiting common
 Hemorrhage less likely  Hemorrhage more likely
 Melena more common than  Hematemesis more common
hematemesis than melena
 More likely to perforate
Malignancy Possibility

134 Rare
By: Bantalem T(MSc)  common 2/14/2024
Diagnosis
 Fiberoptic endoscopy
 To visualize inflammatory changes, ulcers, and lesions
 To obtain a biopsy of the gastric mucosa
 Upper GI barium-contrast study
 Gastric secretory studies
 CBC – determine anemia secondary to bleeding
 Liver enzyme studies
 Stool tests – for the presence of blood
 Serologic test for antibodies to the H. pylori

Management
Aim of the treatment
1. To decrease the amount of gastric acidity
2. To enhance mucosal defense mechanisms
3. To minimize the harmful effects on the mucosa

Mgt Cont’d…
Conservative management/minimum medical treatments
Adequate rest
Dietary interventions
Medications
Elimination of smoking
Long-term follow-up care

Mgt Cont’d…
Lifestyle modifications
 Adequate physical and emotional rest
 A quite, calm environment
 Elimination of stress
 Moderate in daily activity

Mgt Cont’d…
Nutritional Management
 Avoiding irritant foods and beverages
 Hot, spicy foods and pepper
 Alcohol
 Carbonated beverages
 Tea and coffee
 Foods high in roughage, such as raw
fruits, salads, and vegetables may
irritate an inflamed mucosa

Nutritional Mgt Cont’d…
 Milk
 Milk proteins and calcium are stimulant to gastric acid
production
 Can neutralize gastric acidity
 Contains prostaglandins and growth factors which protect
the GI mucosa from injury
NB:
i. No specific diet seems totally appropriate in the treatment of
ulcer disease
ii. Each patient should be instructed to eat and drink foods and
fluids that do not cause and distressing or harmful side effects

Mgt Cont’d…
Pharmacologic Therapy
1. Neutralizing agents – Antiacids
 Are the initial drugs of choice
 Decrease gastric acidity and the acid content of chyme reaching
the duodenum
 Block the conversion of pepesinogen to pepsin by raising the
pH to above 3.5
 Some (like Al(OH)3) can bind to bile salts and decrease their
effects on the gastric mucosa
Examples: Aluminum hydroxide and magnesium trisilcates

Pharmacologic Mgt Cont’d…
II. Antisecretory
a. Histamine H2-receptor antagonists
 Inhibit the action of histamine at histamine H2 receptor cells to
reduce the secretion of gastric acid and total pepsin output
Ex: cimetidine, famotidine, nizatidine, ranitidine
b. Proton pump inhibitors (H+, K+-ATPase inhibitors)
 Inhibit the H+, K+-ATPase enzyme systemat at the secretory
surface of the gastric parietal cells.
 Block the last step of acid production
Ex: Omeprazole, Lansoprazole, Rabeprazole

III. Cytoprotective
Sucralfate
 Accelerate healing
 Doesn’t have acid neutralizing effect
 Should be given at least 30 minutes before or after an
antiacid
Misoprostol
 Is a synthetic prostaglandin
 Protects the gastric mucosa
 s mucus production and bicarbonate levels
Bismuth subsalicylate
 Suppresses H. pylori bacteria

IV. Antibiotics for H. pylori
 Tetracycline + proton pump inhibitor + bismuth salts
 Amoxicillin + clarithromycin + proton pump inhibitor
 Metronidazole + clarithromycin + proton pump inhibitor
 Clarithromycin + proton pump inhibitor + amoxicillin

PUD Rx-- FMHACA-Ethiopia
I. PUD only
First Line
Omeprazole
20 mg P.O. QD for 4 weeks (DU) or 8 weeks (GU)
Alternatives
Cimetidine
400 mg P.O. BID, with breakfast and at night, OR
800 mg at night for 4 - 8 weeks
OR
Ranitidine
150 mg P.O. BID OR 300 mg at bedtime for 4-6 weeks
Maintenance therapy: 150 mg at bedtime.
OR
145Famotidine, 40
By: Bantalem mg, P.O. at night for 4-6 weeks
T(MSc) 2/14/2024
II. PUD associated with H. pylori
First Line
Amoxicillin, 1g, P.O. BID
PLUS
Clarithromycin, 500mg P.O. BID 7 to 14 days
PLUS
Omeprazole, 20mg P.O. BID (OR 40mg QD)
Alternative
Clarithromycin, 500mg P.O. BID
 PLUS
Metronidazole, 500mg, P.O. BID
PLUS
Omeprazole,
146 By: Bantalem T(MSc)20mg P.O. BID OR 40mg QD for 7-14 days
2/14/2024
Mgt Cont’d…
Surgical Management
Usually recommended for:
 Patients with intractable ulcers
 Those that fail to heal after 12 to 16 weeks of medical
treatment
 Life-threatening hemorrhage, perforation, or obstruction
 Those with ZES not responding to medications
Types
1. Pyloroplasty- the pylorus, is cut and resutured, to relax the muscle and widen
the opening into the intestine.
2. Vagotomy
3. Antrectomy
Gastroduodenostomy – billroth I
147 Gastrojejunostomy
By: Bantalem T(MSc) – Billroth II 2/14/2024
Cont`d…

Nursing Interventions
1. Relieving Pain
Patient education:
 To take the prescribed drugs
 To avoid aspirin, foods and beverages that contain caffeine
 To eat meals at regularly paced intervals in a relaxed setting
 Teaching relaxation techniques to help manage stress and
pain
 Enhance smoking cessation efforts

Nsg Interventions Cont’d…
2. Maintaining Optimal Nutritional Status
 Assesses the patient for malnutrition and weight loss
 Advise the patient about the importance of complying with the
medication regimen and dietary restrictions

3.Teaching Patients Self-Care
 Factors that will help or aggravate the condition
 Drug information
 Avoiding foods that exacerbate symptoms and potentially acid-
producing foods
 Eating meals at regular times and in a relaxed setting
 Avoiding overeating
 Irritant effects of smoking on the ulcer and cessation of
smoking

Teach about the S/S of complications:

i. Hemorrhage
 cool skin, confusion, ed heart rate, ed BP, labored
breathing, blood in stool
ii. Penetration and perforation
 Severe abdominal pain, rigid and tender abdomen,
vomiting, ed temp, ed HR
iii. Pyloric obstruction
 Nausea and vomiting, distended abdomen, abdominal
pain
Quiz
 Write 6 Differentiate features of DU From GU(3pt)?
 List at least 3 complications of PUD(2pt)?
 Write at least four factors of gastritis(2pt)?
 Write the first line treatment option for PUD with H.
pylori infection(1pt)?
 Write the aim of PUD treatment(2pt)?

Pyloric stenosis
 Pyloric stenosis is a thickening or narrowing of the pylorus

 Rarely occurs in adults
 The common cause of intestinal obstruction in infancy
 Called hypertrophic pyloric stenosis
Cont`d…
 Causes
 The causes of pyloric stenosis are unknown
 Sex. Pyloric stenosis is seen more often in boys — especially
firstborn children — than in girls.
 Premature birth. Pyloric stenosis is more common in babies
born prematurely than in full-term babies.
 Smoking during pregnancy. This behavior can nearly double
the risk of pyloric stenosis.
 An adjacent ulcer, cancer, or adhesions after an abdominal
surgery

Cont`d…

C/M:
 Vomiting after feeding (projectile vomiting)
 Persistent hunger
 Stomach contractions.
 Dehydration.
 Changes in bowel movements
 Weight problems

Cont`d…
 Dx:
 Electrolyte
 Ultrasound: the gold standard for diagnosing pyloric stenosis
 Gastrointestinal series
 Rx:
 Pyloromyotomy

Cont`d…
Complications
 Dehydration. Frequent vomiting can cause dehydration and a
mineral (electrolyte) imbalance. Electrolytes help regulate many
vital functions.
 Stomach irritation. Repeated vomiting can irritate your baby's
stomach and may cause mild bleeding.
 Jaundice. Rarely, a substance secreted by the liver (bilirubin) can
build up, causing a yellowish discoloration of the skin and eyes

Gastric Cancer
Gastric Cancer
 Gastric cancer is a more common diagnosis among older adults
 The fifth most common cancer diagnosis, with the highest
incidence in Eastern Asia
 A diet high in smoked, salted, or pickled foods and low in fruits
and vegetables may increase the risk of gastric cancer
 H. pylori infection is a major risk factor the development of
gastric cancer.
 It is estimated that 60% of all gastric cancers worldwide are
attributed to H. pylori infection
 The 5- year survival rate for all patients with gastric cancer is
only about 29%.

Pathophysiology
90 to 95% of gastric ca are adenocarcinomas, which arise from the
mucus-producing cells of the inner-most lining of the stomach
Gastric cancer begins with a lesion involving cells on the top layer
of the stomach mucosa.
The lesion then penetrates cells in the deeper layers of the
mucosa, submucosa, and stomach wall.
Eventually the lesion infiltrates the stomach wall and extends to
organs or structures adjacent to the stomach.
Lymph node involvement and metastasis tend to occur early due
to the abundant lymphatic and vascular networks of the stomach.

C/M:
Symptoms of early-stage
pain that is relieved by antacids, resembling those of benign
ulcers
Symptoms of advanced disease are similar to those of peptic
ulcer disease
Fatigue often occurs as a result of the cancer itself or blood
loss from the lesion infiltrating the stomach or surrounding
tissue

Dx:
 Palpable as a mass- in advanced gastric cancer
 Ascites and hepatomegaly (enlarged liver) may be apparent if the
cancer cells have metastasized to the liver.
 Sister Mary Joseph’s nodules- sign of a GI malignancy, usually a
gastric cancer
 Esophagogastroduodenoscopy
 barium x-ray examination of the upper GI tract may also be
performed
 Endoscopic ultrasound
 Computed tomography (CT) scanning
 CBC
Rx:
 Surgery to control the cancer growth or for the palliation of
symptoms,
 Chemotherapy: chemotherapeutic agents often include
fluorouracil (5-FU), carboplatin (paraplatin), capecitabine
(xeloda), cisplatin
 Targeted therapy: in case of advanced gastric cancer
 Radiation therapy.

Gastric surgery Complications
 Bile reflux:
 Manipulation or removal of the pylorus
 Gastric outlet obstruction:
 Due to arrowing (stenosis) or scar tissue (stricture)
formation at the surgical anastomosis site
 Bleeding result haemorrhagic shock
 Dumping syndrome

Acute abdomen
Called a surgical abdomen

× Characterized by an acute onset of abdominal pain that does
not have a traumatic etiology.
× Most typically requires swift surgical intervention.
 Appendicitis
 Intestinal obstruction
 Peritonitis
 Volvulus
 Intussusceptions
Appendicitis

Introduction
The Appendix
 A small, finger-like appendage about 8 to 10 cm long
 Attached to the cecum just below the ileo-cecal valve
 Fills with food and empties regularly into the cecum
 appendix is prone to obstruction and is particularly vulnerable to
infection
 Because it empties inefficiently and its lumen is small

Definition
 Appendicitis- is an inflammation of the vermiform appendix
Etiology
 Obstruction of the lumen by:
 A fecalith (accumulated feces)
 Foreign bodies
 Worms (e.g., Pinworms, ascaris)
 Intramural thickening caused by lymphoid hyperplasia
 Tumors of the cecum or appendix

Pathophysiology
Obstruction

Distension

Venous engorgement

Accumulation of mucus and bacteria (pus)

Gangrene

Perforation

Clinical Manifestations
 Vague epigastric or peri-umbilical pain
 Progressing to RLQ
 May be accompanied by:
 A low-grade fever
 Nausea and vomiting
 Loss of appetite
 Local tenderness is elicited at McBurney’s point when pressure
is applied
 Guarding the abdominal area by lying still with the right leg
flexed at the knee

McBurney’s point and test of Rovsing’s sign

Possible signs of Appendicitis
Rebound
a. Rebound tenderness tenderness: Suggests
b. Rovsing’s sign & referred rebound peritoneal
tenderness inflammation, as from
 Press deeply and evenly in the LLQ appendicitis
 Then quickly withdraw your fingers
Pain in the RLQ during left-sided pressure

 Positive Rovsing’s sign
RLQ pain on quick withdrawal
 Referred rebound tenderness
c. Positive Psoas Sign
Psoas Sign: 2 methods
1st Method
 Place your hand just above the patient’s right knee
 Ask the patient to raise that thigh against your hand (extending
right thigh)
2nd Method
 Ask the patient to turn onto the left side
 Then extend the patient’s right leg at the hip
 Flexion of the leg at the hip makes the psoas muscle
contract; extension stretches it

Possible Appendicitis-- Psoas Sign
Cont’d…

Possible Appendicitis…
d. Positive Obturator Sign
 Flex the patient’s right thigh at the hip, with the knee bent, and
rotate the leg internally at the hip
 This maneuver stretches the internal obturator muscle

Possible Appendicitis-- Obturator Sign

C/Ms Cont’d…
 The extent of tenderness depends on the location of the inflamed
appendix
Pain on defecation suggests that the tip of the appendix is
resting against the rectum.
Pain in urination suggest that the tip is near to the bladder
If tip is in the pelvis can be elicited only on rectal examination.

Acute Complications
a. Perforation
 The most common and generally occurs 24 hours after the
onset of pain
b. Peritonitis
c. Abscess

Diagnosis
 History
 Complete physical examination
 Lab tests
CBC—ed WBCs (neutrophils >75%)
Serum electrolyte profile
 Abdominal x-ray films, ultrasound studies, and CT scans
 U/A- R/O genitourinary conditions

Mgt
 Surgery is indicated if appendicitis is diagnosed
 Antibiotics and intravenous fluids
 To correct or prevent fluid and electrolyte imbalance and
dehydration, until surgery is performed
 Used for 6 to 8 hrs before the appendectomy
 If the appendix has ruptured and there is evidence of
peritonitis or an abscess
 Analgesics after diagnosis
 Appendectomy

Nursing Mgt
Patient preparation for surgery
 IV infusion to replace fluid loss and promote adequate renal
function
 Antibiotic therapy to prevent infection
 Enema is not administered because risk of perforation
 Avoid self-treatment like the use of laxatives and enema to
prevent perforation
 Cold compress to the RLQ to decrease blood flow to the area
and impend the inflammatory process
 Heat is never used because it may cause the appendix to rupture

Nsg Mgt Cont’d…
Postoperative care
 Placing the patient in a semi-Fowler position
 Opioid, usually morphine sulfate
 Oral fluids as tolerated
 Food is provided as desired and tolerated on the day of surgery
 Ambulation begins the day of surgery or the first postoperative
day
 Discharge on the first or second postoperative day
 Normal activities are resumed 2 to 3 weeks after surgery

Peritonitis
 Is an inflammation of the peritoneum
Causes
 The most common causative organisms:
Escherichia coli
Klebsiella
Proteus
Pseudomonas
 Others organisms:
Streptococci spp
Staphylococci
Pneumococci

Cause Peritonitis Cont’d…
It can result from
 Diseases of the GI tract
 From the internal reproductive organs (females)
 External sources
 Injury or trauma (e.g., gunshot wound, stab wound)
 Extension from the inflammation of retroperitoneal organs like
the kidneys
 Appendicitis
 Perforated ulcer
 Diverticulitis
 Bowel perforation
 Abdominal surgical procedures

Cont`d…
 Primary peritonitis: called spontaneous bacterial peritonitis
 occurs as a spontaneous bacterial infection of ascitic fluid.
 Secondary peritonitis:
 occurs secondary to perforation of abdominal organs with
spillage that infects the serous peritoneum.
 Tertiary peritonitis:
 occurs as a result of a suprainfection in a patient who is
immunocompromised.

C/M:
 Symptoms depend on the location and extent of the
inflammation
S/S include:
 Pain
 At first diffuse type
 Tends to become constant, localized, and more intense near
the site of the inflammation.
 Usually aggravated by movement

C/Ms Cont’d…
 The affected area of the abdomen becomes extremely tender and
distended, and the muscles become rigid
 Rebound tenderness
 Nausea and vomiting
 Peristalsis is diminished
 Increased temperature and pulse rate
 Almost always an elevated leukocyte count

Dx
 Lab tests
 Increased leukocyte count
 ed Hemoglobin and hematocrit blood loss
 Serum electrolyte studies
 Abdominal x-ray
 CT scan of the abdomen
 Peritoneal aspiration and culture
 Reveal infection and identify the causative organisms

Complications
1. Sepsis-- the major cause of death
2. Shock because of septicemia or hypovolemia
3. Intestinal obstruction with bowel adhesion as a result of the
inflammatory process
4. Wound evisceration/dehiscence and abscess formation
S/S
 Tender or painful abdomen
 Feeling as if something just gave way

Mgt
 Administration of several liters of an isotonic solution
 Analgesics
 Anti-emetics
 Intestinal intubation and suction
 Oxygen therapy by nasal cannula or mask

Mgt Cont’d…
 Large doses of IV broad-spectrum antibiotic until the specific
organism causing the infection is identified
 Third-generation cephalosporins
 Cefotaxime
 Ceftriaxone
 Patients with primary bacterial peritonitis (PBP) usually
respond within 72 hours to appropriate antibiotic therapy

Mgt Cont’d…
Surgery
 To remove the infected material and correct the cause
 Includes:
 Excision (i.e., appendix)
 Resection with or without anastomosis (i.e., intestine)
 Repair (i.e., perforation)
 Drainage (i.e., abscess)

Intestinal Obstruction
 A partial or complete blockage of the bowel that prevents the
normal flow of intestinal contents through the intestinal tract.
 Two types:
Mechanical obstruction
Functional obstruction

Types of Intestinal Obstruction Cont’d…
A. Mechanical Obstruction
 Cause:
 Intra-luminal obstruction or
 Obstruction from pressure on the intestinal walls
 Accounts for 90% of intestinal obstructions
Examples:
1. Adhesions (50%)
 Loops of intestine become adherent to areas that heal slowly
or scar after abdominal surgery
 May produce a kinking of an intestinal loop

2. Hernias (15%)
 Protrusion of intestine through a weakened area in the
abdominal muscle or wall
 May result in complete obstruction of intestinal lumen and
obstruction of blood flow to the area
3. Intussusception
 One part of the intestine slips into another part located below
it
 Results in narrowing of intestinal lumen

Types of Intestinal Obstruction
Cont’d…
Intussusception
Hernia
4. Volvulus
 Bowel twists and turns on itself
 Results in obstruction to intestinal lumen and accumulation
of gas and fluid in the trapped bowel
5. Others include:
 Neoplasms (15%)
 Stenosis
 Strictures
 Abscesses

Volvulus of the sigmoid colon

B. Functional Obstruction
 Intestinal musculature cannot propel the contents along the
bowel as result of neuromuscular or vascular disorders
Examples:
 Paralytic ilues (the most common)
 Amyloidosis
 Muscular dystrophy
 Endocrine disorders such as diabetes mellitus
 Neurologic disorders such as Parkinson's disease

Small Intestine Obstruction
Accumulate of fluid, gas & intestinal contents proximal to the obstruction

Abdominal distention and retention of fluid

Reduced absorption of fluids and stimulation of more gastric secretions

Increased fluid in the lumen

Increased intraluminal pressure

Increase venous and arteriolar capillary pressure
Fluid and electrolyte extravasation
 to the peritoneal cavity
Increased capillary permeability
Edema, congestion, necrosis
 Circulating blood
Perforation of the intestinal wall
Hypovolemic Shock
204
Peritonitis
By: Bantalem T(MSc) 2/14/2024
C/M:
 Crampy pain that is wavelike and colicky
 Severe, steady pain strangulation
 In the absence of strangulation, the abdomen is not tender
 Passing blood & mucus, with no fecal matter & no flatus
 Signs of dehydration evident
 Intense thirst, drowsiness, generalized malaise, aching, and a dry
tongue and mucous membranes
 Abdominal distension
 Nausea and vomiting

C/Ms Cont’d…
 Vomiting
 Bilious rapid projectile vomiting
obstruction located high in the small bowel
 Vomiting of fecal material
Obstruction below the proximal colon or in the ileum
 Progression of the vomiting
 Vomiting the Stomach contents
 Then the bile-stained contents of the duodenum & the
jejunum
 Finally, with each paroxysm of pain, the darker, fecal-like
contents of the ileum

Diagnosis
 History and physical examination
 Abdominal x-ray studies
 CT-scan
 Ultrasound
 Biopsy
 Laboratory studies
 CBC
 ed WBCs
Strangulation or perforation
 ed hemoglobin or hematocrit
Bleeding from neoplasm or strangulation with
necrosis
 Serum electrolyte profile
Medical Mgt
 Decompression of the bowel through a naso-gastric or small
bowel
Surgical intervention
 IV therapy before surgery to replace the depleted water, sodium,
chloride, and potassium
 Include:
 Repairing the hernia
 Dividing the adhesion
 Removing the portion of affected bowel and anastomosis

Large Bowel Obstruction
Attributes to15% of intestinal obstructions
Commonly occur in the sigmoid colon
The most common causes:
Carcinoma
Diverticulitis
Benign tumors

Pathophysiology
► As in small bowel obstruction, large bowel obstruction results in
an accumulation of intestinal contents, fluid, and gas proximal to
the Obstruction.
► Obstruction in the large bowel can lead to severe distention and
perforation unless some gas and fluid can flow back through the
ileal valve.
► If the blood supply is cut off, however, intestinal strangulation and
necrosis (tissue death) occur; this condition is life threatening.
► In the LBO, dehydration occurs more slowly than in the SBO b/c
the colon can absorb its fluid contents.
► Adenocarcinoid tumors account for the majority of large bowel
obstructions
210
C/M:
 Unlike small intestine symptoms develop and progress relatively
slowly
 Obstruction in the sigmoid colon or the rectum
 Constipation in patients
 Distention of the abdomen
 Visible outlining of loops of large bowel through the
abdominal wall
 Crampy lower abdominal pain
 Fecal vomiting
 Symptoms of shock may occur

Dx
 See under small bowel obstruction
 Barium enema
 To locate large intestinal obstruction
 Not used if perforation is suspected

Mgt
 Colonoscopy
Inspection of the interior surface of the colon
To untwist and decompress the bowel.
 Temporary or permanent colostomy
 Ileoanal anastomosis
 To remove the entire large colon
 Rectal tube
 To decompress an area that is lower in the bowel

Cont`d…
Always give attention

Inflammatory bowel disease
 IBD is a group of chronic disorders:

 Crohn’s disease (i.e., regional enteritis)
 Ulcerative colitis that result in inflammation or ulceration
(or both) of the bowel
Crohn’s Disease (Regional Enteritis)
 It is a subacute and chronic inflammation of the GI tract wall
that extends through all layers
 Characterized by periods of remission and exacerbation
 Histopathologic changes can occur anywhere in the GI tract
 Most commonly occurs in the distal ileum and the ascending
colon.

Pathophysiology
 The inflammatory process begins with crypt inflammation and
abscesses, which develop into small, focal ulcers.
 Lesions then deepen into ulcers, separated by edematous patches,
creating a characteristic cobblestone appearance
 Fistulas, fissures, and abscesses form as the inflammation extends
into the peritoneum.
 Granulomas can occur in lymph nodes, the peritoneum, and
through the layers of the bowel in about half of patients.

Pathophysiology
 Diseased bowel segments are sharply demarcated by adjoining
areas of normal bowel tissue.
 These are called skip lesions, from which the label regional
enteritis is derived.
 As the disease advances, the bowel wall thickens and becomes
fibrotic, and the intestinal lumen narrows.
 Diseased bowel loops sometimes adhere to other loops

Cont`d…
 Causes
 There's no known cause of Crohn's disease.
 Certain factors may increase risk of developing the condition:
 Autoimmune disease:
 Bacteria in the digestive tract may cause the body's immune
system to attack your healthy cells.
 Genes: Inflammatory bowel disease (IBD) often runs in
families

Cont`d…
 Prominent right lower quadrant abdominal pain and diarrhea
unrelieved by defecation.
 Crampy abdominal pain.
 Abdominal tenderness and spasm
 weight loss, malnutrition, and secondary anemia occur
 Fever and leukocytosis
 Chronic symptoms include diarrhea, steatorrhea, anorexia

Cont`d…
 Barium study of the upper GI tract
 A ―string sign‖ on an x-ray image of the terminal ileum,
indicating the constriction of a segment of intestine.
 CT scan and MRI: more accurately assess bowel and pelvic
disease
 CBC
 HCT and Hgb levels , WBC

Cont`d…
Complications
 Intestinal obstruction
 Perianal disease, fluid and electrolyte imbalances,
 Malnutrition from malabsorption
 Fistula and abscess formation

Ulcerative Colitis
 A chronic ulcerative and inflammatory disease of the mucosal and
submucosal layers of the colon and rectum.
 Characterized by unpredictable periods of remission and
exacerbation with bouts of abdominal cramps and bloody or
purulent diarrhea.
 The inflammatory changes typically begin in the rectum and
progress proximally through the colon

Pathophysiology
 It affects the superficial mucosa of the colon
 Chxed by multiple ulcerations, diffuse inflammations, and
desquamation or shedding of the colonic epithelium.
 Bleeding occurs as a result of the ulcerations.
 The mucosa becomes edematous and inflamed.
 The lesions are contiguous, occurring one after the other.
 The bowel narrows, shortens, and thickens because of muscular
hypertrophy and fat deposits.

Cont`d…
 C/M:
 The clinical course is usually one of exacerbations and
remissions.
 Diarrhea, with passage of mucus, pus, or blood
 Left lower quadrant abdominal pain
 Intermittent tenesmus.
 The bleeding , anemia, and fatigue
 Anorexia, weight loss, fever, vomiting, and dehydration
 Extraintestinal manifestations
 skin lesions , eye lesions, joint abnormalities and liver disease

Dx:
 Abdominal x-ray :
 Determining the cause of symptoms.
 Colonoscopy is the definitive screening test
 Reveal friable, inflamed mucosa with exudate and ulcerations.
 Biopsies :
 Determine histologic characteristics of the colonic tissue and
extent of disease.
 CT scanning, MRI, and ultrasound:
 Identify abscesses and perirectal involvement
 lab test low HCT and Hgb and elevated WBC, low albumin levels
 Stool examination for parasites and other microbes

Cont`d…
Complications
 Toxic megacolon
 Fever, abdominal pain and distention, vomiting, and fatigue.
 Does not respond within 72 hours to medical management ,
surgery is required
 Perforation
 Bleeding as a result of ulceration, vascular engorgement, and
highly vascular granulation tissue

Cont`d…

Rx:
Oral fluids and a low-residue, high-protein,
high-calorie diet with supplemental vitamin therapy and iron
replacement
Prescribed to meet nutritional needs, reduce inflammation, and
control pain and diarrhea.
Avoid foods that exacerbate diarrhea.
Avoid cold foods and smoking.

Rx: Cont`d…
 Antidiarrheal and antiperistaltic medications
 Aminosalicylates such as sulfasalazine
 For mild or moderate inflammation
 to prevent or reduce recurrences
 Immunomodulators : limit your immune system’s reaction.
 Antibiotics complications such as abscesses or fistula formation
 Corticosteroids are used to treat severe and fulminant disease
patients.

Rx: cont`d…
 Common indications for surgery in patients with:
o ulcerative colitis:
 presence of colon cancer, Megacolon,severe, intractable
bleeding; or perforation
o Crohn’s disease:
 Recurrent partial intestinal obstructions; complete intestinal
obstructions; intractable fistulas or intractable abscesses

Cont`d…
 Strictureplasty: widens and shortens the intestines
 Bowel resection, portions of damaged intestine are removed.
 Ostomy : a hole through which your body can eliminate
waste.
 colectomy .
 proctocolectomy : colon and rectum.

Hernia
 When an internal organ or other body part protrudes through the
wall of muscle or tissue that normally contains it.
 Most hernias occur within the abdominal cavity, between the chest
and the hips
 Inguinal hernia the common one:
 Direct inguinal hernias: protrude through the back wall of the inguinal
canal
 Indirect hernias: protrude through the inguinal ring

Cont`d…

Cont`d…
 Causes
 A combination of pressure and an opening or weakness of muscle
or fascia
 Muscle weakness is present at birth, it occurs later in life.
 Anything that causes an increase in pressure in the abdomen
Lifting heavy objects without stabilizing the abdominal muscles
Diarrhea or constipation
Persistent coughing or sneezing

Cont`d…
 C/M:
 Swelling or bulge in the groin or scrotum (the pouch that
contains the testicles).
 Increased pain at the site of the bulge.
 Pain while lifting.
 Increase in the bulge size over time.
 A dull aching sensation.
 A sense of feeling full or signs of bowel obstruction

Cont`d…
 Dx:
 PE and imaging studies
 Rx:
 Moving the herniated tissue back into place
 Repairing the weak area where the hernia occurred

Hemorrhoid
♦ Hemorrhoids are dilated portions of veins in the anal canal
♦ Very common, affecting approximately 38.9% of adults in the
United States.
♦ Hemorrhoids are classified into two types:
♦ Internal hemorrhoids: Those above the internal sphincter
♦ External hemorrhoids: Those appearing outside the external
sphincter

Hemorrhoid con't…
 Based on degree of prolaps
 First-degree internal hemorrhoids
o Do not prolapse out of the canal but are characterized by
prominent vascularity.
 Second-degree hemorrhoids
o Prolapse outside of the canal during bowel movements or
straining, but reduce spontaneously.
 Third-degree hemorrhoids
o Prolapse out of the canal and require manual reduction.
 Fourth-degree hemorrhoids
o Irreducible even with manipulation.

Cont`d…
Risk Factors
 Pressure building up in your lower rectum can
affect blood flow and make the veins there swell.
∆ Pushing during bowel movements
∆ Straining
∆ Extra weight, like obesity
∆ Pregnancy,: uterus pressure on veins
∆ A diet low in fiber

C/M:
 Blood on your poop, on toilet paper after wipe, or in the toilet
bowl
 Tissue that bulges outside the anal opening (prolapse).
 Pain
 Bleeding
 Itching
 Swelling

Dx:
 Physical exam: For lumps, swelling, irritation
 Digital rectal exam
 To check muscle tone and feel for tenderness, lumps, or other
problems.
 Anoscopy: Anal canal.
 Sigmoidoscopy: Lower colon with a flexible lighted tube
 Colonoscopy. large intestine with a long, flexible tube

Rx:
 Lifestyle changes can often relieve mild hemorrhoid symptoms
within 2 to 7 days.
 High fiber diet and foods like fruit, vegetables, and grains.
 Avoid straining during defication
 Drinking more water can make it easier to go.
 Warm sitz baths for 20 minutes several times a day may also
make you feel better.
 Surgery

Anal Fistula
 An anal fistula is a tiny, tubular, fibrous tract that extends into the
anal canal from an opening located beside the anus in the
perianal skin
 Usually result from an abscess.
 May develop from trauma, fissures, or Crohn’s disease.
 Purulent drainage or stool may leak constantly from the
cutaneous opening.
 passage of flatus or feces from the vagina or bladder, depending
on the location of the fistula tract.
 Untreated fistulas may cause systemic infection with related
symptoms

Anal fissure
A longitudinal tear or ulceration in the lining of the anal canal
usually just distal to the dentate line.
Caused by the trauma of passing a large, firm stool or from
persistent tightening of the anal canal
Other causes include childbirth, trauma
Painful defecation, burning, and bleeding characterize fissures
Bright red blood
Dietary modification with addition of fiber supplements, stool
softeners

Anorectal Abscess
 Caused by obstruction of an anal gland with dried debris,
resulting in retrograde infection.
 People with Crohn’s disease or immunosuppressive conditions
such as AIDS are particularly susceptible to these infections.
 Many of these abscesses result in fistulas
 Dull perianal discomfort and itching, and increased pain with
defecation
 Rx: Prompt surgical treatment to incise and drain the abscess

Always say
I can do today
better than yesterday

Gastroenteritis
 An acute inflammation of the gastric and intestinal mucosa
 It is most commonly due to bacterial, viral, protozoa or parasitic
infection.
 It may also be caused by irritation due to chemical or toxin
exposure or allergic response.

Gastroenteritis…
 Symptoms may be self-limiting or may need prescription
medication to resolve the illness.
 Older or debilitated patients may have more severe symptoms
or require hospitalization due to dehydration.

Gastroenteritis…
 C/M
Anorexia, Malaise, Nausea & vomiting
Diarrhea—watery, soft, may be mixed with mucous or blood
Abdominal pain
Abdominal distention
Fever due to infection
Headache due to viral illness
Signs of dehydration

Gastroenteritis…
 Lab finding
CBC may show leukocytosis or eosinophilia (parasites).
Electrolytes show imbalance due to GI loss.
BUN and creatinine elevated due to dehydration.
Stool for ova and parasites show positive with parasitic
infection.

Gastroenteritis…
 Medical management
 Monitor intake and output.
 Replace fluids lost.
 Administer antiemetic medication for symptom relief:
 Prochlorperazine
 Trimethobenzamide

Gastroenteritis…
 Administer anti diarrheal medications for symptom relief:
 Loperamide
 Diphenoxylate
 Kaolin-pectin
 Bismuth subsalicylate
 Need to allow organism one way out of gastrointestinal system
(either antiemetic or ant diarrheal).

Gastroenteritis…
 Administer antimicrobials for infectious cause:
 ciprofloxacin
 Metronidazole
 Intravenous fluids to correct dehydration

Nursing intervention
Monitor vital signs for changes.
Monitor intake and output.
Assess skin and mucous membranes for signs of dehydration.
Assess abdomen for bowel sounds, tenderness
Teach the patient about the risks of communicability

Hepatic Disorders
Hepatic Dysfunction
 Hepatic dysfunction results from damage to the liver’s
parenchymal cells by:
 Directly from primary liver diseases
 Indirectly from obstruction of bile flow or derangements of
hepatic circulation

The most common and significant symptoms
of liver disease
Jaundice
Portal hypertension, ascites, and varices
Nutritional deficiencies
Hepatic encephalopathy or coma

Jaundice/Icterus
 Is yellowish-tinged or greenish-yellow discoloration of the body
tissues, including the sclerae, mucosa and the skin as result of
abnormal elevation of bilirubin concentration in the blood.
 Is a symptom rather than a disease
 Becomes clinically evident when the serum bilirubin level
exceeds 2.0 mg/dL
 May result from impairment of:
 Hepatic uptake
 Conjugation of bilirubin
 Excretion of bilirubin into the biliary system

Types of Jaundice
Hemolytic Hepatocellular
Hereditary
Obstructive
hyperbilirubinemia

Bilirubin Metabolism

I. Hemolytic/ Pre-hepatic Jaundice
 Results from an increased destruction of the red blood cells
 Flood the plasma with unconjugated bilirubin so rapidly
 The liver cannot excrete the bilirubin as quickly as it is formed
Causes
 Hemolytic transfusion reactions
 Sickle cell crisis
 Hemolytic anemia

Hemolytic Jaundice Cont’d…
 If prolonged it may result in:
 The formation of pigment stones in the gallbladder
 Extremely severe jaundice (>20 to 25 mg/dl) poses a risk for
brain stem damage
Lab Tests
 ed fecal and urine urobilinogen
 Urine is free of bilirubin

II. Hepatocellular/ hepatic Jaundice
 Caused by the inability of damaged liver cells to:
 Take up bilirubin from the blood or
 Conjugate or
 Excrete normal amount of bilirubin from the blood
Cirrhosis
 Patients may be mildly or severely ill

Hepatocellular Jaundice Cont’d…
Causes of cellular damage
Infection by viral hepatitis or other viruses
Medication or chemical toxicity or alcohol
Hepatic carcinoma
Lab Tests:
 ed unconjugated serum bilirubin
 ed AST & ed ALT levels

III. Obstructive / Post-hepatic Jaundice
 Is due to impended or obstructed flow of bile
A. Intra-hepatic obstruction
 May involve obstruction of the small bile ducts within the liver
 Can be caused by
 Pressure on these channels from inflammatory swelling of the
liver (hepatitis, cirrhosis, tumors)
 Inflammatory exudates within the ducts themselves

Obstructive Jaundice Cont’d…
B. Extra-hepatic obstruction
 Caused by occlusion of the bile duct by a gallstone, an
inflammatory process, a tumor, or pressure from an enlarged
organ

Clinical Findings
Bile backed up into the liver

Reabsorbed into the blood

Carried throughout the entire body

Staining the skin, mucous membranes, and sclera
 Deep orange and foamy urine
 Light or clay-colored stool
 The skin may itch intensely
 Intolerance to fatty foods
Lab tests:
 AST, ALT levels generally rise only moderately
 ed conjugated and unconjugated bilirubin
 ed urine bilirubin

Hereditary Hyperbilirubinemia
♦ Increased serum bilirubin levels
♦ Resulting from any of several inherited disorders
♦ Gilbert syndrome
♦ is a familial disorder characterized by an increased level of
unconjugated bilirubin that causes jaundice.
♦ Occur when UGT enzyme activity is low
♦ Serum bilirubin levels are increased, liver histology and liver
function test results are normal, and there is no hemolysis.
♦ This syndrome affects 3% to 8% of the population,
predominantly males

The Portal Venous System

Portal hypertension (PHpn)
 Normal pressure in the portal vein is 5 to 10 mmHg

 PHpn is increased pressure throughout the portal venous
system
 PHpn is commonly associated with hepatic cirrhosis
 It can also occur with noncirrhotic liver disease like thrombosis,
or clotting in the portal vein

PP Alcohol Abuse, Infection, Drugs, Bilary Obstruction
Destruction of Hepatocytes
Replacement of destroyed liver cells gradually by scar tissue
The amount of scar tissue exceeds that of the functioning liver tissue
Fibrosis/Scar Jaundice
Impaired blood and lymph flow

ed pressure in the venous & sinusoidal channels
Fatty infiltration—fibrosis/scar
Ascites
Portal Hypertension
Splenomegaly
Esophageal varices
PHpn C/Ms
 GI bleeding/ Varices
 Spleenomegally
 Ascites
 Hepatic encephalopathy

Ascites
 Ascites is the accumulation of fluid in the peritoneal cavity
Risk factors
 Cirrhosis—for 80% of cases
 Renal factors: stimulation of RAA system
 Other conditions like
 Congestive heart failure
 Nephrosis

PP Portal Hypertension/Resistance Esophageal Varices
to Blood Flow
Leakage of plasma into Vasocongestion within Hemorrhoids

liver lymphatics
intestinal vasculature
Production of liver
Transudation of plasma Development of collateral
lymph with high protein
into the abdominal cavity venous vessels
Leakage of lymph
into abdominal
Ascites Persistence of amine
cavity with osmotic neurotransmitters
gradient between
lymph & ECF Leakage of plasma Redistribution of blood flow—
out of vascular space reduced renal perfusion
 Intravascular oncotic pressure Stimulation of

RAA system
 Albumin production
276 By: Bantalem T(MSc) Sodium and water

2/14/2024
Hepatocyte Dysfunction retention
 ed abdominal girth
 Bulging of flanks
 Shifting dullness
 Fluid wave/trill
 Everted umbilicus (severe)
 Rapid weight gain
 SOB
 Visible striae and distended veins over the abdominal wall
 Decreased urine output

Assessing for abdominal fluid wave

Diagnosis
 History
 Physical Examination
 Diagnostic paracentesis (50 to 100 mL)
 The fluid should be examined for its gross appearance; protein
content, cell count, and differential cell count should be
determined
 Cytologic analysis : strong clinical suspicion for malignancy

Management of Ascites
Dietary Modification
Diuretics- spironolactone, Lasix
Bed rest
Paracentesis
Insertion of a peritoneovenous shunt
 A connection between the peritoneal cavity and the systemic
venous circulation via a shunting tube placed subcutaneously
connected with a one-way pressure valve
relieves ascites by transferring fluid through a one-way valve
from the peritoneal cavity into the superior vena cava

Cont`d…
 Transjugular intrahepatic portosystemic shunt (TIPS)
 Method of treating ascites in which a cannula is threaded into
the portal vein by the transjugular route.
 Used to treat the complications of portal hypertension

Esophageal Varices
 A complex of longitudinal tortuous and extremely dilated
sub-mucosal veins at the lower end of the esophagus, enlarged
and swollen as the result of portal hypertension
 The vessels are especially susceptible to hemorrhage.
 Bleeding or hemorrhage from esophageal varices occurs in
approximately one third of patients with cirrhosis and varices

Factors that contribute to hemorrhage
 Muscular exertion from lifting heavy objects
 Straining at stool
 Sneezing, coughing, or vomiting
 Esophagitis
 Irritation of vessels by poorly chewed foods or course foods or
irritating fluids
 Reflux of stomach contents (especially alcohol)
 Salicylates and any medication that erodes the esophageal
mucosa
 Liver cirrhosis

Pathophysiology of Esophageal Varices
Portal hypertension (caused by resistance to portal flow and increased portal
venous inflow)

Development of pressure gradient of >=12 mm Hg between portal vein and
inferior vena cava
(portal pressure gradient)

Venous collaterals develop from high portal system pressure to systemic veins in
esophageal plexus, hemorrhoidal plexus and retroperitoneal veins

Abnormal varicoid vessels form in any of above locations

Vessels may rupture causing life-threatening hemorrhage

C/M:
 Hematemesis
 Melena
 General deterioration in mental or physical status
 Symptoms of shock (cool clammy skin, hypotension,
tachycardia)

Mgt:
 Intravenous fluids with electrolytes and volume expanders
 Oxygen is administered to prevent hypoxemia/hypoxia
 Monitoring vital signs continuously
Pharmacologic Therapy
 Vasopressin (IV or intra-arterial)
 Propranolol and nadolol, beta-blocking agents that decrease
portal pressure
 Nitrates such as isosorbide

Hepatic Cirrhosis
 Characterized by irreversible chronic injury of the hepatic
parenchyma
 Extensive degeneration and destruction of the liver parenchyma
cells and by replacement of liver tissue by fibrous scar tissue.
 As necrotic tissue yields to fibrosis, this disease alters liver
structure and normal vasculature, impairs blood and lymph flow,
and ultimately causes hepatic insufficiency.

Cirrhosis
 Alcoholic cirrhosis. The most common type, this occurs in 30%
to 50% of cirrhotic patients, up to 90% of whom have a history of
alcoholism.
 Biliary cirrhosis. Biliary cirrhosis results in injury or prolonged
obstruction.
 Post necrotic cirrhosis. Post necrotic cirrhosis stems from
various types of hepatitis.
 Pigment cirrhosis. Pigment cirrhosis may result from disorders
such as hemochromatosis.
 Cardiac cirrhosis. Cardiac cirrhosis refers to cirrhosis caused
by right-sided heart failure.
 Idiopathic cirrhosis. Idiopathic cirrhosis has no known cause.

Cirrhosis
 Different types of cirrhosis have different causes.
 Excessive alcohol consumption. Too much alcohol intake is
the most common cause of cirrhosis as liver damage is associated
with chronic alcohol consumption.
 Injury. Injury or prolonged obstruction causes biliary cirrhosis.
 Hepatitis. The different types of hepatitis can cause pos
tnecrotic cirrhosis.
 Other diseases. Diseases such as hemochromatosis causes
pigment cirrhosis.
 Right-sided heart failure. Cardiac cirrhosis, a rare kind of
cirrhosis, is caused by right-sided heart failure.

Types of cirrhosis or scarring of the liver:
A. Alcoholic cirrhosis
 Frequently due to chronic alcoholism for decades, resulting in:
 Chronic inflammatory
 Toxic effects on the liver
 Blocking the normal metabolism of protein, fats, and
carbohydrates
 Scar tissue characteristically surrounds the portal areas
 Is the most common type of cirrhosis

Types of Cirrhosis Cont’d…
B. Postnecrotic cirrhosis
 There are broad bands of scar tissue as a late result of a
previous bout of acute viral hepatitis (hepatitis B or
hepatitis C)
C. Biliary cirrhosis
 Scarring occurs in the liver around the bile ducts
 Is the result of chronic biliary obstruction and infection
(cholangitis)
 Much less common

C/M:
Early manifestation
 Palpation of liver reveals a firm, lumpy, (nodular), usually enlarged
liver.
 GI disturbance – anorexia, nausea, vomiting……
 Hepatomegally
 Pain
Late manifestation
 Ascites, gastro intestinal bleeding from varices
 Encephalopathy, splenomegally, jaundice, skin lesion, Anemia
 Sodium and fluid retention

Dx:
 History
 Physical Exam
 Diagnostic Studies
Liver scans/biopsy- Detects fatty infiltrates, fibrosis, destruction
of hepatic tissues, tumors
Esophagogastroduodenoscopy (EGD)- demonstrate presence
of esophageal varices
Electrolytes: Hypokalemia, hypocalcemia

Dx:
 Increased Serum bilirubin
 Increased Serum ammonia: Because of inability to convert
ammonia to urea.
 Decreased Serum glucose: Impaired glycogenesis
 Decreased Serum albumin
 CBC: Hgb/Hct and RBCs may be decreased because of bleeding
 Increased BUN: Indicates breakdown of blood/protein
 Increased Liver enzymes:

Medical Mgt
Symptomatic management
 Antacids—to decrease gastric distress and minimize the
possibility of GI bleeding.
 Vitamins and nutritional supplements
 Potassium-sparing diuretics (spironolactone, triamterene)--to
decrease ascites
 Avoidance of alcohol

Hepatic Encephalopathy and Coma
Hepatic encephalopathy
 Is a life-threatening complication of liver disease occurring with
profound liver failure
 May result from the accumulation of ammonia and other toxic
metabolites in the blood
 Can occur in any condition in which liver damage causes ammonia
to enter the systemic circulation without liver detoxification
Hepatic coma represents the most advanced stage of hepatic
encephalopathy

Hepatic Encephalopathy cont’d…
 Normally, the liver converts ammonia in to glutamine, which is
stored in the liver and later converted to urea and excreted via
the kidneys.
 Blood ammonia rises when the liver cells are unable to perform
this conversion due to liver cell damage and necrosis.
C/M:
 From mild mental confusion like, unresponsiveness, forgetfulness,
trouble concentrating, or changes in sleep habits to deep coma.
 Simple tasks, such as handwriting, become difficult

 Asterixis or ―liver flap‖.
 The patient is asked to hold the arm out with the hand held
upward (dorsiflexed).
 Within a few seconds, the hand falls forward involuntarily and
then quickly returns to the dorsiflexed position.
 Dx
 Lab-results show elevated blood ammonia

Medical Management
 Principles of intervention in hepatic encephalopathy.
Reduce protein in the intestine
Prevent gastro-intestinal bleeding.
Reduce bacterial production of NH3 by neomycin
High cleansing enema to decrease bacteria.
Eliminate infection.
Intravenous administration of glucose to minimize protein
breakdown

Liver Abscess
 A mass filled with pus inside the liver

Cont`d…
 Amebic liver abscesses
 most commonly caused by Entamoeba histolytica.
 Occur in the developing countries of the tropics and
subtropics
 Pyogenic liver abscesses
 Much less common
 More common in developed countries

Pathophysiology
 Infection develops anywhere along the biliary or GI tract, infecting
organisms
 Reach the liver through the biliary system, portal venous system,
or hepatic arterial or lymphatic system.
 Most bacteria are destroyed promptly, but occasionally some gain a
foothold.
 The bacterial toxins destroy the neighboring liver cells, and the
resulting necrotic tissue serves as a protective wall for the
organisms.
 leukocytes migrate into the infected area.
 The results an abscess cavity full of a liquid containing living and
dead leukocytes, liquefied liver cells, and bacteria.

Cont`d…
 C/M:
 Fever with chills and diaphoresis, malaise, anorexia, nausea,
vomiting, and weight loss may occur.
 dull abdominal pain,
 tenderness in the RUQ of the abdomen
 Hepatomegaly, jaundice, anemia
 Sepsis and shock
 Dx:
 Aspiration of the liver abscess, guided by ultrasound, CT, or MRI

Cont`d…
Rx:
 IV antibiotic therapy
 Continuous supportive care b/c of the serious condition of the pt.
 percutaneous drainage
 Open surgical drainage

Cholecystitis
Cholecystitis
 Several disorders affect the biliary system and interfere with
normal drainage of bile into the duodenum.
 Is an acute or chronic inflammation oh the gall bladder.
 Calculous cholecystitis: A gallbladder stone obstructs bile
outflow.
 Acalculous cholecystitis. Acute inflammation in the absence of
obstruction by gallstones.
 Causes
 Gallbladder stone.
 Bacteria
 Alterations in fluids and electrolytes.
 Bile stasis

Pathophysiology:
 Calculous cholecystitis occurs when a gallbladder stone obstructs
the bile outflow.
 Bile remaining in the gallbladder initiates a chemical reaction;
autolysis and edema occur.
 Blood vessels in the gallbladder compressed, compromising its
vascular supply.
 Gangrene of the gallbladder with perforation
 Acalculous cholecystitis occurs after major surgical procedures,
orthopedic procedures, severe trauma, or burns.
 Alterations in fluids and electrolytes and alterations in regional
blood flow in the visceral circulation.
 Bile stasis and increased viscosity of the bile.

Cont`d…
C/M:
 Pain. Right upper quadrant pain occurs with cholecystitis.
 Leukocytosis. An increase in the WBC occurs because of the
body’s attempt to ward off pathogens.
 Fever. Fever occurs in response to the infection inside the body.
 Palpable gallbladder. The gallbladder becomes edematous as
infection progresses.
 Sepsis. Infection reaches the bloodstream and the body
undergoes sepsis.

Cont`d…
 Complications
 Empyema. An empyema of the bladder develops if the
gallbladder becomes filled with purulent fluid.
 Gangrene. Gangrene develops because the tissues do not receive
enough oxygen and nourishment at all.
 Cholangitis. The infection progresses as it reaches the bile duct.

Cont`d…
Dx:
 Biliary ultrasound
 Oral cholecystography (OCG)
 Endoscopic retrograde cholangiopancreatography (ERCP)
 Percutaneous transhepatic cholangiography (PTC)

Cont`d…
 Mgt:
 Fasting, to rest the gallbladder.
 IV fluids to prevent dehydration.
 Pain medication.
 Antibiotics to treat infection.
 Removing the gallbladder(Cholecystectomy)

Cholelithiasis
 Presence of one or more calculi (gallstones) in the gallbladder

 More prevalent with increasing age.
 Prevalence of gallstones ranges from
 5% to 20% in women between the ages of 20 and 55 years
 25% to 30% in women older than 50 years.
 Affects approximately 50% of women by the age of 70 years.
Pathophysiology
 There are two major types of gallstones:
► Pigment stones
 Form when unconjugated pigments in the bile precipitate to
form stones
 Account for about 10% to 25% of cases in the US.
 Stone formation increased in patients with cirrhosis, hemolysis,
and infections of the biliary tract.
 Pigment stones cannot be dissolved and must be removed
surgically

Pathophysiology Cont`d…
► Cholesterol stones
 account for most of the remaining 75% of cases of gallbladder
disease in the US.
 Cholesterol, which is a normal constituent of bile, is insoluble in
water
 Its solubility depends on bile acids and lecithin (phospholipids) in
bile.
 In gallstone-prone patients, there is decreased bile acid synthesis
and increased cholesterol synthesis in the liver,
 Resulting in bile supersaturated with cholesterol, which precipitates
out of the bile to form stones.

Cont`d…
 Epigastric distress, such as fullness, abdominal distention, and
vague pain in the RUQ of the abdomen
 Pain and Biliary Colic
 Jaundice
 Urine dark color

Cont`d…
Dx:
♦ Cholesterol increase in biliary obstruction decrease in
liver disease
♦ Abdominal X-Ray
♦ Ultrasonography
♦ Radionuclide Imaging or Cholescintigraphy:
 used successfully in the diagnosis of acute cholecystitis or
blockage of a bile duct

Cont`d…
Mgt:
 Dietary management
 Ursodeoxycholic acid (UDCA and chenodeoxycholic acid
(chenodiol - dissolve small, radiolucent gallstones
composed primarily of cholesterol
 Laparoscopic cholecystectomy

Pancreatitis
 Pancreatitis is inflammation of the gland parenchyma

of the pancreas
 Types
 Acute
 Chronic
Acute pancreatitis
 Presents as an emergency
An acute condition presenting with abdominal pain and is
usually associated with raised pancreatic enzyme levels in the
blood or urine as a result of pancreatic inflammation.
 The underlying mechanism of injury in pancreatitis is thought to
be premature activation of pancreatic enzymes within the
pancreas, leading to a process of autodigestion.

Acute pancreatitis
 Acute pancreatitis may be categorised as
Mild acute pancreatitis
• Interstitial edema of the gland and minimal organ dysfunction
• 80% of patients
• Mortality is around 1%

Acute pancreatitis cont’d…
 Severe acute pancreatitis
• Pancreatic necrosis, a severe systemic inflammatory response
and often multi-organ failure
• Mortality varies from 20% -50%
• About 1/3 of deaths occur in the early phase of the attack,
from multiple organ failure, while deaths occurring after the
first week of onset are due to septic complications

 Incidence
 Acute pancreatitis accounts for 3% of all cases of abdominal
pain among patients admitted to hospital in UK
 The disease may occur at any age, with a peak in young men and
older women

Etiology
 Anything that injures the acinar cell and impairs the secretion
of zymogen granules, or damages the duct epithelium and thus
delays enzymatic secretion, can trigger acute pancreatitis
 The two major causes of acute pancreatitis are biliary
calculi(50–70% ), and alcohol abuse(25%)
 ERCP
 Upper abdominal or cardiothoracic surgery
 Blunt abdominal trauma
 Tumours at the ampulla of Vater
 Hypercalcemia(It is important to check the serum calcium
level)

Etiology
 Patients have a tendency to suffer acute pancreatitis while in
their teens, progress to chronic pancreatitis in the next two
decades and have a high risk (possibly up to 40%) of developing
pancreatic cancer by the age of 70 years
Autoimmune
Viral infections(Coxsackie, mumps)
Drugs (corticosteroids, azathioprine, asparaginase and valproic
acid)
Idiopathic

 C/M:
 Pain is the cardinal symptom Characteristically develops quickly,
reaching maximum intensity within minutes rather than
hours and persists for hours or even days
 Frequently severe, constant and refractory to the usual doses
of analgesics
 Usually experienced first in the epigastrium but may be localized
to either upper quadrant or felt diffusely throughout the abdomen
 Radiation to the back in about 50% of patients
 Some patients may gain relief by sitting or leaning
forwards

 On examination:-
 Appearance -well or, gravely ill with profound shock, toxicity
and confusion
 Tachypnea , tachycardia , and hypotension may be present
 Temperature - normal or even subnormal, but frequently rises
as inflammation develops
 Mild icterus (biliary obstruction in gallstone pancreatitis, and
an acute swinging pyrexia suggests cholangitis)

 Bleeding into the fascial planes can produce bluish discoloration of
the flanks (Grey Turner’s sign) or
 Para umbilical ecchymosis (Cullen’s sign)-neither sign is
pathognomonic of acute pancreatitis.

 Investigations
 Typically, the diagnosis is made on the basis of the
clinical presentation and an elevated serum amylase level 3-
4x above normal is indicative of the disease
 A normal serum amylase level does not exclude acute
pancreatitis, particularly if the patient has presented a few days
later
 Serum lipase level provides a slightly more sensitive and
specific test than amylase

 Imaging
 Plain erect chest and abdominal radiographs
-Useful in the differential diagnosis
 Ultrasound
 To detect gallstones as a potential cause,
 rule out acute cholecystitis as a differential diagnosis
 determine whether the common bile duct is dilated
 CT is the best single imaging investigation
 Cross-sectional MRI
2/14/2024
330 By: Bantalem T(MSc)
 Management
• Mild attack of pancreatitis- conservative approach
Intravenous fluid administration
Frequent, but non-invasive, observation
A brief period of fasting in a patient who is nauseated and in
pain
Analgesics and anti-emetics
Antibiotics are not indicated
No drugs or interventions are warranted

 Severe attack of pancreatitis- more aggressive approach
Admit to a high-dependency or an intensive care unit and
monitored invasively
Adequate analgesia
Aggressive fluid resuscitation, guided by frequent
measurement of vital signs, urine output and central venous
pressure
Supplemental oxygen and serial arterial blood gas analysis
The haematocrit, clotting profile, blood glucose and serum
levels of calcium and magnesium should be closely monitored

 Complications
Pancreatic oedema, haemorrhage and, eventually, necrosis
As inflammatory mediators are released into the circulation,
systemic complications can arise, such as
Haemodynamic instability
Bacteraemia (due to translocation of gut flora)
Acute respiratory distress syndrome and pleural effusions
Gastrointestinal haemorrhage
Renal failure and
Disseminated intravascular coagulation (DIC)

Chronic pancreatitis
 A continuing inflammatory disease of the pancreas characterized
by irreversible morphological change typically causing pain
and/or permanent loss of function
 A prolonged and frequently lifelong disorder resulting from the
development of fibrosis within the pancreas
 A chronic inflammatory disease in which there is irreversible
progressive destruction of pancreatic tissue

Chronic pancreatitis cont’d…
 Etiology and pathology
 High alcohol consumption is the most frequent cause of

chronic pancreatitis, accounting for 60–70% of cases
 Only 5–10% of people with alcoholism develop chronic
pancreatitis
 Genetic and metabolic factors may play
Pancreatic duct obstruction(stricture formation after
trauma, after acute pancreatitis or even occlusion of the
duct by pancreatic cancer)
 Congenital abnormalities, such as pancreas divisum and
annular pancreas

 C/M:
o Epigastric and right subcostal pain(head of pancreas) , left
subcostal and back pain(left side of pancreas)
o In some patients, the pain is more diffuse
o Radiation to the shoulder, usually the left shoulder, occurs
o Nausea is common during attacks, and vomiting
o Weight loss
o The patient’s lifestyle is gradually destroyed by pain, analgesic
dependence, weight loss and inability to work
o Loss of exocrine function leads to steatorrhoea in more than
30% of patients
o Loss of endocrine function and the development of diabetes
336 o By: Bantalem T(MSc) 2/14/2024

Cont`d…
Investigations
Only in the early stages of the disease will there be a rise in
serum amylase
Abdominal X-ray - pancreatic calcifications
CT or MRI scan will show the outline of the gland, the
main area of damage
A glucose tolerance test evaluates pancreatic islet cell
function

 MRCP: identify the presence of biliary obstruction and the state
of the pancreatic duct
 ERCP is the most accurate way of elucidating the anatomy of
the duct
 Histologically proven chronic pancreatitis can, however, occur in
the setting of normal findings on pancreatography

Mgt:
 Most patients can be managed with medical measures
 Endoscopic, radiological or surgical interventions are indicated
mainly
 to relieve obstruction of the pancreatic duct, bile duct
or the duodenum, or in dealing with complications

Thank you
Genitourinary System Disorders
Prepared by: Tsegaye E

Debre Berhan University
Asratweldeyes Health Science College
Department of Nursing
Learning Objectives
• At the end of this lesson you will able to:
• Discuses the over view of anatomy and physiology of GUS
• Assess of clients with GUT problems
• Identify the diagnostic modalities for GU problems
• Discuss about fluid and electrolyte imbalance
• Discuss acid base imbalance
• Discuss about urinary tract disorders
• Discuss about common disorders of male reproductive organs
2/20/2024 2
The urinary system
• The renal system composed of
➢ Two kidneys: formation of urine
➢ Two ureters: transport urine from

the kidney to the bladder.
➢ Urinary bladder: provides

temporary storage reservoir for
urine.
➢ Urethra: transport urine from

bladder out of the body.
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Renal system…
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2/20/2024 5
The internal anatomy of a kidney.
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Nephrons
• Functional unit of kidney
• One million nephron in each kidney.
• Nephron has two parts
1. Glomerulus: contains glomerular capillaries covered by
Bowman’s Capsule;
• Function: Glomerular filtration.
2. Renal tubular system contains: Proximal convoluted tubule,
Loop of Henle, Distal convoluted tubule and Collected duct.
➢ Function: Reabsorption & secretion.
2/20/2024 7
(A) The anatomy of a nephrons, the functional unit of a kidney.
(B) A scanning electron micrograph of glomerular capillaries.
2/20/2024 8
Type of Nephron
There are two type of nephron
1. Cortical Nephrons
✓ Accounts about 80–85% of the nephrons
✓ Located in the cortex
✓ Have short loops of Henle that lie mainly in the cortex.
✓ Supplied with peritubular capillaries.
✓ Involved in the formation of diluted urine
2/20/2024 9
Type of Nephron…
2.Juxtamedullary Nephrons
❖ Few in number which account about 15–20% of the nephrons.
❖ Located in the medullary region
❖ Their renal corpus located in the cortex
❖ Have a long loop of Henle that deep the medulla
❖ Supplied with vasa recta.
❖ Involved in the formation of concentrated urine.
2/20/2024 10
2/20/2024 11
Functions of the urinary system
❖ Excretion: Eliminate metabolic nitrogenous waste product
(urea and creatinine), drugs, Toxins. from the body.
❖ Regulation function: water balance, electrolyte balance (Na,

K, Chlorine, bicarbonate, Ca, Mg), acid base balance.
❖ pH regulation: The kidneys control the proper balance of H

in the blood, thus helping to regulate the proper pH levels
in the body.
2/20/2024 12
Excretion---Urine formation
• Glomerular filtration; filter the plasma via the fenestrated
glomerular membrane into renal tubules.
• Tubular reabsorption; as the filter flows via the tubules,
reabsorption of needed substance.
• Secretion; secretion of unwanted substances into the renal
tubules.
2/20/2024 13
Excrete waste in urine
➢ Total daily UOP ≈ 0.72-2.4L.
➢ E.g., If pt drinks a large volume of fluid, UOP↑↑. But a pt
restricts water intake or intake of excessive solutes as Na, UOP↓↓.

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Work load of kidney---water balance
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Electrolyte balance and pH regulation…
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Other hormonal functions of the kidneys include:
• Secretion of the hormone erythropoietin in response to low
arterial oxygen tension, which travels to the bone marrow and
stimulates red blood cell production.
• Regulation of calcium and phosphorus balance by activate

vitamin D3 (calciferol), a compound that promotes intestinal
calcium absorption and regulates phosphate excretion.
(Cholecalciferol(skin) → Liver (25 hydroxi cholecalciferol →

Renal(1,25 Di hydroxi cholecalciferol → active form).
• Regulate Blood pressure by produce the enzyme renin.
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Renin angiotensin system
2/20/2024 18
Function….
❖ Hormones help regulate tubular reabsorption and secretion:
• Antidiuretic hormone (produced by the pituitary gland), acts

in the distal tubule and collecting ducts to increase water
reabsorption and urine concentration.
• Aldosterone (produced by the adrenal gland), affects tubular

reabsorption by regulating sodium retention and helping
control potassium secretion by tubular epithelial cells.
2/20/2024 19
ASSESSMENT OF CLIENTS WITH
URINARY TRACT PROBLEMS
2/20/2024 20
Assessment of urinary tract systems
• History taking
I. Current health status: When a patient has a renal disorder,
expect these common complaints/symptoms:
Pain
Identifying characteristics of genitourinary pain
Type Location
Kidney Costovertebral angle, may extend to umbilicus
Bladder Suprapubic area
Ureteral Costovertebral angle, flank, lower abdominal area, testis,
or labium
Prostatic Perineum and rectum
Urethra Male: along penis to meatus; Female: urethra to meatus
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Problems associated with changes in voiding
Problem Definition
Frequency Frequent voiding more than every 3 hrs
Urgency Strong desire to void
Dysuria Painful or difficult voiding
Hesitancy Delay, difficulty in initiating voiding
Nocturia Excessive urination at night
Incontinence Involuntary loss of urine
Enuresis Involuntary voiding during sleep
Polyuria Increased volume of urine voided
Oliguria Urine output less than 500 ml/day
Anuria Urine output less than 50 ml/day
Hematuria/pyuria RBCs/ WBCs in the urine
Proteinuria Abnormal amounts of protein in the urine
2/20/2024 22
Gastrointestinal Symptoms
➢ It often associated with urologic conditions because of

shared autonomic and sensory innervation and
renointestinal reflexes.
➢ The most common signs and symptoms are nausea,

vomiting, diarrhea, abdominal discomfort, and abdominal
distention.
➢ Urologic symptoms can mimic such disorders as

appendicitis, peptic ulcer disease, and cholecystitis.
2/20/2024 23
Unexplained Anemia
➢ Gradual kidney dysfunction can be insidious in its
presentation, although fatigue is a common symptom.
➢ Fatigue, shortness of breath, and exercise intolerance all
result from the condition known as “anemia of chronic
disease.”
II. Previous health status (past history)
– Explore all of the patient’s previous major/minor illnesses,
accidents or injuries, surgical procedures, and allergies.
– Assess the patient’s psychosocial status, level of anxiety,
perceived threats to body image, available support systems,
and sociocultural patterns.
2/20/2024 24
PH….
• Ask about a history of urologic related disorders such as HTN.
• Other questions to ask include:
• Have you ever had a urinary infection?
• Are you taking herbal medications or prescription, over the

counter, or recreational drugs?
• Do you have pain or burning on urination?
• Is initiating urination difficult?
• What color is your urine?
• Have you ever had a sexually transmitted disease (STD)?

2/20/2024 25
Cont…
• Family history
– For clues to risk factors, ask if blood relatives have ever

been treated for renal or cardiovascular disorders, diabetes,
cancer, or other chronic illness.
• Lifestyle patterns
– Investigate psychosocial factors that may affect the way the

patient deals with his condition.
– Marital problems, unstable living conditions, job insecurity,

and other stresses can strongly affect how he feels.
2/20/2024 26
Physical examination
• Begin the physical examination by documenting baseline V/S
and weighing the patient.
• Assess the specimen (urine) for color, odor, and clarity.
• Renal system affects many body functions, a systemic

assessment includes examination of multiple related body
systems using inspection, auscultation, percussion, and
palpation techniques.
Inspection: Renal system inspection includes examination of

the abdomen and urethral meatus.
2/20/2024 27
✓ Inspect Abdomen
• Help the patient assume a supine position with his arms
relaxed at his sides.
• Expose the patient’s abdomen from the xiphoid process to the
symphysis pubis, and inspect the abdomen for gross
enlargements or fullness by comparing the left and right sides,
noting asymmetrical areas.
• Ask about scars, lesions, bruises, or discolorations found on
abdominal skin.
2/20/2024 28
✓ Inspect Urethral meatus
• Help the patient feel more at ease during your
inspection by examining the urethral meatus last and
by explaining beforehand how you’ll assess this area.
• Be sure to wear gloves.
2/20/2024 29
Auscultation
• Auscultate the renal arteries in the Lt and Rt upper

abdominal quadrants by pressing the stethoscope bell
lightly against the abdomen and instructing the
patient to exhale deeply.
• Begin auscultating at the midline and work to the left.
• Then return to the midline and work to the right.
• Systolic bruits (whooshing sounds) or other unusual

sounds are potentially significant abnormalities.
2/20/2024 30
Percussion
• After auscultating the renal arteries,
• Percuss the patient’s kidneys to detect any tenderness and
• Percuss the bladder to evaluate its position and contents.
2/20/2024 31
Percussion…
2/20/2024 32
Palpation
• Palpation of the kidneys and bladder.
• Through palpation, you can detect any lumps, masses, or

tenderness.
• To achieve optimal results, ask the patient to relax his

abdomen by taking deep breaths through his mouth.
• In a normal adult, the kidneys usually aren’t palpable because

they’re located deep within the abdomen.
2/20/2024 33
Palpation…
• However, they may be palpable in a thin patient or in one with
reduced abdominal muscle mass, and the right kidney, slightly
lower than the left, may be easier to palpate altogether.
• Keep in mind that both kidneys descend with deep inhalation.
• An adult’s bladder may not be palpable either.
• However, if it’s palpable, it usually feels firm and relatively

smooth.
• When palpating urinary organs, use bimanual palpation,

beginning on the patient’s right side.
2/20/2024 34
Palpation…
2/20/2024 35
2/20/2024 36
Diagnostic Modalities for GU problems
❑ Urine studies, such as urinalysis and urine osmolality, can
indicate urinary tract infection (UTI) and other disorders
➢ Urinalysis: Performed on a urine specimen of at least 10 ml,

urinalysis can indicate urinary or systemic disorders.
✓ Macroscopic urinalysis
• Is the direct visual observation of the urine, noting its volume,

color, clarity….
• Normal urine is typically pale yellow and clear.
2/20/2024 37
Macroscopic urinalysis…
Macroscopic
urinalysis
2/20/2024 38
Dipstick chemical analysis
• Nitrite (suggestive of bacteria in urine).

• Bilirubin (possible liver disease or red blood cell break down).
• Urobilinogen (possible liver disease).
2/20/2024 39
Microscopic Urinalysis
2/20/2024 40
Microscopic Urinalysis
➢ Microscopic examination used to view elements that are not

visible without microscope. e.g cells
❑ Red Blood Cells: Hematuria is the presence of abnormal

numbers of red cells in urine due to:
➢ Glomerular damage
➢ Tumors
➢ Urinary tract stones
➢ Upper and lower urinary tract infections
2/20/2024 41
Two Types of Hematuria
• Gross hematuria means that the blood can be seen by the
naked eye.
• Microscopic hematuria means that the urine is clear, but blood
cells can be seen under a microscope.
2/20/2024 42
White Blood Cells
❑ Pyuria: refers to the presence of abnormal numbers of

leukocytes that may appear with infection in either the upper
or lower urinary tract or with acute glomerulonephritis.
➢ Usually, the WBC's are granulocytes
❑ Casts: Urinary casts may be made up of cells (such as WBCs,

RBCs, kidney cells) or substances such as protein.
➢ They are formed in the distal convoluted tubule and

collecting ducts of nephrons, then dislodge and pass into the
urine, where they can detected by microscopy.
2/20/2024 43
▪The factors which favor protein cast formation
✓Low flow rate of the filtrate
✓High salt concentration
✓Low pH
▪All of which favor protein denaturation and precipitation
2/20/2024 44
2/20/2024 45
Renal Function test
• Common tests of renal function include :
• Renal concentration tests (urine osmolality, specific gravity &

urine creatinine clearance).
• Serum creatinine and blood urea nitrogen levels.
– Urine osmolality: Normal urine osmolality 300–900

mOsm/kg/24 hr.
– Specific gravity: Evaluates ability of kidneys to

concentrate solutes in urine.
• The normal range is 1.010 to 1.025.

2/20/2024 46
• 24 Hours urine test (Creatinine clearance): provides an
approximation of the glomerular filtration rate.
• Blood urea nitrogen: End product of protein metabolism; it

affected by protein intake, tissue breakdown, and fluid volume
changes. Normal 7–18 mg/dL; Patients 60 yrs: 8–20 mg/dL.
2/20/2024 47
• Serum creatinine: a nitrogenous waste, results from muscle
metabolism of Creatine.
– Normal serum creatinine values for adult males 0.6-1.2

mg/dl; for adult females, 0.4-1 mg/dl.
– Creatinine levels greater than 1.5 mg/dl indicate 66% or

greater loss of renal function; levels greater than 2 mg/dl
indicate renal insufficiency.
• BUN-to-creatinine ratio: An elevated ratio is seen in

hypovolemia; a normal ratio with an elevated BUN and
creatinine is seen with intrinsic renal disease; about 10:1.
2/20/2024 48
Normal blood Chemistry Levels
2/20/2024 49
Radiologic and imaging studies
• Radiologic and imaging studies (ST scan, Excretory
urography, Kidney-ureter-bladder (KUB) radiography,
Magnetic resonance imaging, Radionuclide renal scan, Renal
angiography, Ultrasonography, Voiding cystourethrography).
• Other tests like Cystometry, Percutaneous renal biopsy,
Uroflowmetry).
2/20/2024 50
Renal Ultrasonography…
• Hydronephrosis
• Detection and surveillance of nephrolithiasis,
• Characterization of focal renal lesions, and workup of renal
failure and hematuria
• Renal colic
• Acute renal vein thrombosis
• Renal failure
• Renal mass
• Acute renal infection
• Renal trauma
• Urinary retention
2/20/2024 51
Fluid and Electrolytes
Learning Objectives:
❑ At the completion of this unit you will be able to:
• Describe normal distribution of body fluid
• Describe disturbances of fluid and electrolytes
• Explain about acid base balance and imbalance
2/20/2024 52
Introduction
• Fluids are located both inside the cells (intracellular fluid
[ICF]) and outside the cells (extracellular fluid [ECF]).
• ECF can be further divided into:
• Intravascular fluid, which is the plasma of the blood.
• Interstitial fluid is the water that surrounds the body’s cells and
includes lymph.
• Transcellular fluids such as cerebrospinal fluid, digestive

juices, and synovial fluid in joints.
2/20/2024 53
Cont…
➢ Total Body Water (TBW)
• 60% in an average young adult male & 50% in young adult

female.
• The highest percentage of TBW is found in newborns, with

approximately 80% of their total body weight.
• Fluid Balance: Fluid and electrolyte homeostasis is

maintained in the body via
• Neutral balance: input = output; Positive balance: input >

output; Negative balance: input < output.
2/20/2024 54
Normal distribution of body fluid
Fluid compartments
 60% of body weight
Intracellular fluid
Extracellular fluid
( 2/3)
( 1/3)
Skeletal muscle mass
Intravascular Interstitial fluid Transcellular fluid [<1% (1 L)]

25% (≈3L) of 75% (≈11-12
ECF L) of ECF CSF, pericardial, synovial,
Plasma Lymph intraocular, pleural, sweat and
digestive secretion
2/20/2024 55
Electrolytes
• Electrolytes have special physiological functions in the body
✓ Promote neuromuscular irritability,
✓ Maintain body fluid osmolarity,
✓ Regulate acid-base balance, and
✓ Distribute body fluids between the fluid compartments.
• The main electrolytes in body fluid are:
– Sodium , Potassium , Calcium, and Magnesium
– Chloride, Bicarbonate, Proteinate, and Phosphates.
2/20/2024 56
Approximate major electrolyte content in body fluid
Extracellular Fluid in mEq/L Intracellular Fluid in mEq/L
Cations Anions Cations Anions
Sodium 142 Chloride 103 Potassium 150 Phosphates 150
& Sulfates
Potassium 5 Bicarbonate 26 Mg 40 Proteinate 40
Calcium 5 Proteinate 17 Sodium 10 Bicarbonate 10
Mg 2 Organic 5
acid
Phosphates 2
Sulfates 1
Total 154 Total 154 Total 200 Total anions 200
cations anions cations
2/20/2024 57
Normal electrolyte values for adults in venous blood
Electrolytes Amount
Sodium 135-145 mEq/L
Potassium 3.5-5.0 mEq/L
Chloride 95-108 mEq/L
Calcium(ionized) 4.5-5.5 mEq/L
Magnesium 1.5-2.5 mEq/L
Phosphate-(phosphorus) 1.8-2.6 mEq/L

Serum osmolality 280-300 mOsm/kg water
2/20/2024 58
Movement of fluids and electrolytes in the body
• Fluids and electrolytes move in the body by active and

passive transport systems.
• Active transport depends on the presence of adequate cellular

ATP for energy e.g. Sodium-potassium pumps.
• Passive transport, no energy is expended specifically to move

the substances.
• The three passive transport systems are diffusion, filtration,

and osmosis.
• Plasma osmolality=[2x(Na)+(Glucose/18)+(urea/2.8)]
2/20/2024 • Plasma tonicity=[2x(Na)+(Glucose/18)] 59
Cont…
Diffusion is a process in which the substance moves from an area

of higher concentration to an area of lower concentration.
• E.g. of diffusion are the exchange of oxygen and carbon

dioxide.
2/20/2024 60
Filtration
• It is movement of water and solutes occurs from an area of

high hydrostatic pressure to an area of low hydrostatic
pressure.
• Filtration is promoted by hydrostatic pressure which is the
force that water exerts; sometimes called water pushing
pressure.
e.g. 1→ Glomerular filtration.
2→The passage of water and electrolytes from the arterial

capillary bed to the interstitial fluid.
2/20/2024 61
Osmosis…
• Osmosis is s diffusion of water caused by a fluid concentration
gradient .
• Three other terms are associated with osmosis:
❖Osmotic pressure is the amount of hydrostatic pressure

needed to stop the flow of water by osmosis.
❖ Oncotic pressure is the osmotic pressure exerted by

proteins (eg, albumin).
❖ Osmotic diuresis is the ↑↑ UOP caused by the substances

such as glucose, mannitol, or contrast agents.
2/20/2024 62
2/20/2024 63
Osmolarity & Osmolality
• Osmolarity is the concentration of fluid that affects the
movement of water between fluid compartments by osmosis.
• Tonicity (effective osmolarity) is the ability of all the solutes
to cause an osmotic driving force.
• Osmolarity measures the solute [(sodium, BUN and glucose)

//(urea, creatinine, and uric acid)] concentration per mOsm/L
in blood and urine.
• Osmolality, another term that measured per mOsm/Kg.
• Normal serum osmolarity is 280 -300 mOsm/L.

2/20/2024 64
Selected water and electrolyte solutions
• Fluids can be classified as isotonic, hypotonic, or hypertonic.
• Isotonic is fluid that has the same osmolarity as the blood.

e.g. 0.9% NaCl (NS), RL solution & 5% DW.
• Hypotonic solution has a lower osmolarity than blood.

e.g. 0.45% NaCl (half-strength saline)
• Hypertonic solutions exert greater osmotic pressure than

blood. e.g. [3% NaCl; 5% NaCl (hypertonic saline)].
2/20/2024 65
Fluid volume disturbances
A. Fluid volume deficit (hypovolemia): both water &
electrolyte, but dehydration is water loss alone.
Cause
➢ GI loss
➢ ↓↓ intake and third-space fluid shifts,
➢ Diabetes insipidus,
➢ Adrenal insufficiency,
➢ Osmotic diuresis,
➢ Hemorrhage.
2/20/2024 66
Sign/symptoms
• Wt loss, thirst, rapid, weak pulse and low BP.
• Dry skin, mm & poor skin turgor
• ↓UOP
• Constipation
• Disturbance in cellular function in the brain, heart, & kidney
➔ Coma & death
Diagnoses finding
➢ Elevated BUN, HCT, creatinine.
➢ Serum electrolyte changes.
2/20/2024 67
Treatment of FVD
• Fluid mgt
• Monitors fluid I&O
• Monitored Vital signs
• Monitored Skin and tongue turgor
• Monitor the urine specific gravity.
• Monitors mental function
2/20/2024 68
Fluid Excess (Hypervolemia)
• Fluid Excess is a retention of water & sodium.
Contributing factors
• Heart failure, renal failure, and cirrhosis of the liver,
• Intake of excessive NaCl
• Administration of sodium-containing fluids.
• Syndrome of inappropriate ADH
2/20/2024 69
Sign/symptoms
• ↑↑BP, bounding pulse, ↑↑RR and shallow, neck vein
distention, pitting edema, weight gain, and skin pale and cool.
• Dyspnea, crackles and ascites → CHF → PE → Organ failure

→ Death.
Diagnoses finding
• Decreased BUN & HCT.
• A chest x-ray may reveal pulmonary congestion.
• Decreased serum osmolality and sodium level
• Decreased urine sodium level
2/20/2024 70
Treatment
• Drug therapy (Diuretics),

• Monitor I/O, Wt & edema.
• Diet therapy: restriction of sodium intake.
• Positioning: semi(high)-fowler’s.
• Oxygen therapy
• Breath sounds are assessed
• Dialysis
2/20/2024 71
Acid-base balance
• The pH vary from 0 to 14, with 7 being neutral.
• The normal serum pH is 7.35 to 7.45, or slightly alkaline.
• A pH <6.9 or >7.8 is usually fatal.
• Three major mechanisms to control of acid-base balance are:

cellular buffers, the lungs, and the kidneys.
A. Cellular buffers
• Are proteins, hemoglobin, bicarbonate, and phosphates.
• These buffers act as a type of sponge to “soak up” extra H+ if

too acidic or release hydrogen ions if too alkaline.
2/20/2024 72
Acid-base balance…
B. The lungs
• The second line of defense to restore normal pH.
• When the blood is too acidic, the lungs “blow off” additional
carbon dioxide through rapid, deep breathing.
• This reduces the amount of carbon dioxide available to make

carbonic acid in the body.
• If the blood is too alkaline, the lungs try to conserve carbon

dioxide through shallow respirations.
2/20/2024 73
Acid-base balance…
C. The kidneys
• The slowest to respond to changes in serum pH, takes 24 to 48
hours compensate.
• The kidneys help to regulating the amount of bicarbonate.
• If the serum pH lowers, it reabsorb additional bicarbonate.
• If the serum pH increases, it excrete additional bicarbonate.
• The kidneys also buffer pH by forming acids and ammonium

(a base).
2/20/2024 74
Normal values for arterial and mixed venous blood
Parameter Arterial Blood Mixed Venous Blood
pH 7.35-7.45 7.32-7.42
PaC02 35-45 mm Hg 38-52 mm Hg
Pa02 70-100 mm Hg 24-48 mm Hg
HC03- 19-25mEq/L 19-25mEq/L
Oxygen saturation >94% >40-70%
2/20/2024 75
Acid-base imbalances
Respiratory Acidosis
• Acute respiratory acidosis is caused by hypoventilation and

chronic respiratory disease cause chronic respiratory acidosis.
• CO2 is not adequately “blown off” during expiration, causing

a build-up of CO2 that mixes with water to create a weak acid.
Cause
• Hypoventilation (asthma, pneumonia, COPD) or due to
inadequate chest expansion; Airway obstruction; trauma;
stroke.
• Respiratory depression due to opioids or benzodiazepines.
2/20/2024 76
• Signs and symptoms: Mental status is altered, confusion and
lethargy to stupor, dyspnea and coma and muscle weakness
worsens.
• Rx of respiratory acidosis is aggressive management of the

underlying respiratory problem.
• Oxygen, bronchodilator
• Mechanical ventilation
• Naloxone for opioid overdose
2/20/2024 77
Respiratory alkalosis
• It occurs when there is excessive loss of CO2 through
hyperventilation due to:
• Severely anxious or fearful, Salicylate toxicity like aspirin.
• Mechanical ventilation
• Pulmonary embolism
• High attitude, shock, pain or trauma.
• The serum pH is increased and the PaCO2 is very low.
• S/S is shortness of breath, dizziness, chest pain, numbness in

the hand or feet, ↑ heart rate and becomes weak and thready.
2/20/2024 78
Treatment of Respiratory alkalosis
• Treated by having patients hold their breath or rebreather their

own CO2 with the use of rebreathing mask.
• The underlying cause must also be treated.
• Pain medication, anti anxiety medication.
2/20/2024 79
Metabolic acidosis
• It can result from too much acid or too little HCO3 in the body.
• Caused by uncontrolled DM, end-stage renal failure, severe

diarrhea or prolonged nasointestinal suction and starvation.
• The serum pH decreases as the bicarbonate level decreases
• H+/K+ exchange when ↑H+ in the ECF will cause hyperkalemia.
• S/S similar to respiratory acidosis, except the respiratory pattern.
• Tachycardia, hypotension, weak pulse, dysarrithmias, kussmaul's

respirations and fruity odor breath.
2/20/2024 80
Treatment of Metabolic acidosis
• is based on management of the underlying disease.
• Sodium bicarbonate, Iv fluid and insulin for DKA
• Hemodialysis for Renal failure
2/20/2024 81
Metabolic alkalosis
• It results from excessive ingestion of bicarbonate or other
bases (sodium bicarbonate) or
• Antacid overdose or loss of acids (prolonged vomiting or

nasogastric suction) from the body.
• The serum pH is increased, as is bicarbonate.
• Hydrogen from the ICF moves into the blood in exchange for
potassium, which cause hypokalemia.
• Hypocalcemia may also accompany hypokalemia.
2/20/2024 82
Metabolic alkalosis……
• The S/S are related to hypokalemia and hypocalcemia.
– Tachycardia, dysrhythmias, muscle weakness and lethargy
• Treatment involves identifying the underlying cause.
• Vomiting---antiemetic
• Iv fluid and electrolyte replacement
2/20/2024 83
Composition
• The body attempts to composite for acid-base disorders in
such a way as to mitigate derangements of arterial pH.
• The primary metabolic disorder will result in respiratory

composition (timing of peak compensation is 1-24hrs).
• The primary respiratory disorder will result in metabolic

composition (timing of peak compensation is 12hrs-5days?).
• Composition does not return pH in normal and patient is never

overcompensate.
2/20/2024 84
Acid–base disorders and compensation
Disorder Initial event Compensation
Respiratory ↓pH, ↑PaCo2 ↑Excretion H+ and ↑reabsorption

acidosis ,↑or normal Hco3- by kidney (↑Hco3- →↑pH)
Hco3-
Respiratory ↑pH, ↓PaCo2 ↓Excretion of H+& ↓reabsorption
alkalosis ,↓or normal Hco3- by kidney(↓Hco3- →↓pH)
Hco3-
Metabolic ↓pH, ↓ Hco3-, Increase minute ventilation by
acidosis ↓or normal Hyperventilation with resulting
PaCo2 ↓PaCo2 → ↑pH
Metabolic ↑pH, ↑Hco3-, Decrease minute ventilation by
alkalosis ↑or normal Hypoventilation with resulting
PaCo2 ↑PaCo2 → ↓pH
2/20/2024 85
Pyelonephritis
✓ It is a bacterial infections that involves both the
parenchyma and the pelvis of the kidney, it may affect
one or both kidneys.
✓ It is frequently secondary to ureterovesical reflux
✓ It may be acute or chronic when it is chronic the kidneys

are scarred, contracted and non-functioning.
✓ Most commonly affect females with out

instrumentation.
2/20/2024 86
Etiology
❖The dominant etiologic agents

are gram (-) bacilli that are
normal inhabitant of intestinal
tract – the most common are
E.coli followed by proteus,
Klebsiella & Enterobacter.
2/20/2024 87
Mechanism of pyelonephritis
❖ The two routes by
which bacteria
reach the kidney.
✓ Hematogenous
infection
✓ Ascending
infection
2/20/2024 88
Mechanism…
❖ Pyelonephritis, an upper urinary tract infection, is a bacterial
infection of the renal pelvis, tubules, and interstitial tissue in one
or both kidneys.
❖ Bacteria reach the bladder through the urethra and ascend to the
kidney.
❖ It is frequently secondary to urine backup into the ureters usually

at the time of voiding.
❖ Urinary tract obstruction (e.g. Urinary stones, tumors, and

prostatic hypertrophy) is another cause.
2/20/2024 89
Acute Pyelonephritis
❖ Acute suppurative inflammation of the kidney
❖ There will be patchy interstitial suppurative inflammation,

intratubular aggregates of neutrophils & tubular necrosis.
• Acute pyelonephritis often occurs after bacterial contamination

of the urethra or after instrumentation.
• The course of acute Pyelonephritis is usually short
• Recurs & common either due to as a relapse of a previous

infection not eradicated or as a new infection.
– The infection may also progress to bacteremia.

2/20/2024 90
Risk factors
• Secondary infection
• Ascending infection secondary to ureteral reflux
• Instrumentation
• Obstruction
• Pregnancy
• Immuno - compromised
2/20/2024 91
Pathophysiology
• Pyelonephritis occurs when bacteria enter the renal pelvis
causing an inflammatory response and an increase in WBCs.
• Leads to edema and swelling of the involved tissue, beginning

at the papillae & some times spreading to the cortex.
• As the infection is treated and inflammation subsides, fibrosis

and scar tissue may develop, the calices become blunted with
scarring in the interstitial tissues.
• If infections reoccur, more and more scar tissue is developed,

fibrosis and altered tubular reabsorption and secretion lead to
decreased renal function.
2/20/2024 92
Figure 20-27 Acute pyelonephritis. Cortical surface shows
grayish white areas of inflammation and abscess formation.
2/20/2024 93
Complication
Three complication of acute pyelonephritis
▪ Papillary necrosis – as result of the inflammation, the

medullar blood supply is compromised & renal papillary
necrosis may occur particularly in diabetics, urinary tract
obstruction, sickle cell disease, or analgesic abuse.
▪ Pyonephrosis occurs when there is total or complete

obstruction & pus fills renal pelvis, calyces & ureter.
▪ Perinephric abscess – extension of suppurative

inflammation through renal capsule into perinephric tissue
2/20/2024 94
Papillary necrosis. Areas of pale-gray necrosis involve the
papillae(arrows).
2/20/2024 95
Pyonephrosis occurs when there is total or complete obstruction
& pus fills renal pelvis, calyces & ureter

2/20/2024 96
Perinephric abscess – extension of suppurative inflammation
through renal capsule into perinephric tissue
2/20/2024 97
• Develops quickly over hours to a day.
• Enlarged kidney with interstitial infiltrations
• Acutely ill with chills, fever, leukocytosis and pyuria
• Low back pain, flank pain, N/V, headache, malaise;
• Painful urination
• Pain and tenderness on CVA
• LUT involvement, such as dysuria and frequency
• Urine contains leukocyte (pyuria) & pus cast
• Definitive diagnosis is made by urine culture

2/20/2024 98
Diagnostic Assessment
• Urine culture
• Urinalysis:.
– Pyuria is a highly sensitive indicator of infection.
– Leukocyte esterase “dipstick” positivity is useful when
microscopy is not available.
– Pyuria without bacteriuria may indicate infection with
unusual organisms such as C. trachomatis or M.TB or may
be due to noninfectious causes such as calculi.
• Ultra sound to locate any obstruction in the urinary tract.
2/20/2024 99
Management
• Diet should represent intake from all food group and include an
adequate number of calories
• Fluid intake needs to be at least 2-3/day unless contraindicated.
Pharmacological treatment
• Analgesics: ibuprofen and acetaminophen
2/20/2024 100
A. Acute uncomplicated Pyelonephritis in non-pregnant
women: Mild and moderate acute uncomplicated pyelonephritis
• Goals of therapy are
1. Control of possible urosepsis
2. Eradication of the invading organism
3. Prevention of recurrences.
✓ Floroquinolone and β lactam/aminoglycoside

combination or an advanced spectrum β lactam IV.
First line: Ciprofloxacin, 500mg P.O., BID, oral for 7-10 days
Alternatives:
2/20/2024
Cotrimoxazole 960mg P.O, BID for 14 days OR 101
B. Severe acute uncomplicated pyelonephritis (high
fever, high white blood cell count, vomiting, dehydration, or
evidence of sepsis).
• First line:- Ciprofloxacin 400mg IV BID till patient improves
and continue oral ciprofloxacin 500mg, PO, BID, 10-14 days.
• Alternative:- Ceftriaxone, 2gm, IV, daily or 1gm, IV, BID till
patient improves and continue oral ciprofloxacin 500mg PO
BID, 10-14 days.
2/20/2024 102
Glomerulonephritis
• The kidney is particularly susceptible to nephrotic

injury by virtue of its
– Rich blood supply (20-25 % of CO)
– Ability to concentrate toxins in medullary

interstitium
2/20/2024 103
Cont….
✓ Glomerulonephritis is abroad term refers to a group
of kidney disease in which there is an inflammatory
reaction in the glomeruli.
✓ Glomerular disease includes glomerulonephritis, i.e.

inflammation of the glomeruli and glomerulopathies
when there is no evidence of inflammation.
✓ Glomerulonephritis is a subset of glomerulopathies.
2/20/2024 104
Cont..
• Numerous inflammatory and non inflammatory
diseases affect the glomerulus and lead to alteration in
glomerular permeability, structure and function
• The onset of symptom is usually sudden; recovery is

usually complete and quick.
• Most individuals with acute improve dramatically

within weeks and recover completely within 1-2 yr.
2/20/2024 105
Pathogenesis of GN
2/20/2024 106
Acute glomerulonephritis
❖ Acute GN is a bilateral inflammation of the glomeruli,
commonly following a streptococcal infection.
❖ It is also called Acute Nephritis, Glomerulonephritis and Post-
Streptococcal Glomerulonephritis.
❖ Predominantly affects children from ages 3 to 10.
❖ Incubation period is 2 to 3 weeks.
❖ The severity depends on the size, number, location, duration of
exposure, and type of antigen-antibody complexes.

2/20/2024 107
Causes AGN
• Inflammatory reaction in the glomeruli in most types of
glomerulonephritis IgG.
• Mostly group A streptococcal infection of the throat
precede to glomerulonephritis within 2 to 3 wks.
• Glomerulonephritis may also follow
– Impetigo
– Acute viral infection (URTI, mumps, varicella, Epstein
Barr Virus, hepatitis B & HIV infection)
2/20/2024 108
Clinical features
 Abrupt onset of:
 Hematuria (smoke or coffee colored urine).
 Non-nephrotic range proteinuria (<2 g in 24 hrs).
 Mild to moderate oedema (periorbital, sacral).
 Mild to severe hypertension (Sodium or water retention ).
 Transient renal impairment (oliguria<400ml/day, azotemia).
 Headache, Malaise, Fatigue, Lack of energy, Anorexia,
 Nausea, Vomiting if uremia from renal failure is present.
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Diagnostic tests
• Blood studies reveal elevated electrolyte, BUN, and creatinine
levels.
• Urine studies reveal RBCs, WBCs, mixed cell casts, and

protein.
• Elevated antistreptolysin-O titers, elevated streptozyme and

anti-DNase B titers verify recent streptococcal infection.
• A throat culture may also show group A beta-hemolytic

streptococci.
• KUB X-rays show bilateral kidney enlargement.
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Treatment
• The goals of treatment are the relief of symptoms and the
prevention of complications.
• Vigorous supportive care includes bed rest, fluid and dietary

sodium restrictions, and correction of electrolyte imbalances.
• Therapy may include diuretics such as furosemide to reduce

extracellular fluid overload and
• An antihypertensive such as Hydralazine.
• The use of antibiotics to prevent secondary infection or

transmission to others is controversial (penicillin).
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Nursing intervation
• Promote bed rest during the acute phase.
• Allow the patient to resume normal activities gradually; the

disorder usually resolves within 2 weeks.
• Monitor V/S, electrolyte, intake and output, and daily weight.
• Assess renal function daily through serum creatinine and BUN

levels, and urine creatinine clearance.
• Watch for and immediately report signs of acute renal failure

(such as oliguria, azotemia, and acidosis).
• Diet high in calories and low in protein, Na, K, and fluids.

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Nephrotic Syndrome
• Learning objectives: at the end of this lesson the student will
be able to:
➢ Define nephrotic syndrome.
➢ List the etiologies of nephrotic syndrome.
➢ Describe the clinical features of nephrotic syndrome.
➢ Identity complications of nephrotic syndrome..
➢ Understand the diagnostic approach of nephrotic syndrome.
➢ Understand the principle of management of nephrotic

syndrome.
2/20/2024 113
Definition
• The nephrotic syndrome is a clinical complex due to damage
of podocytes which results heavy (massive) proteinuria.
• Nephrotic syndrome is defined if all the following 1st three

clinical and laboratory findings are fulfilled:
1. Heavy proteinuria: urine protein >3g in 24hrs.
2. Hypoalbuminemia: serum albumin <3g/dl
3. Edema/anasarca
4. Hyperlipidemia and lipiduria and
5. HTN and minimal microscopic hematuria.

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Notice
o Proteinuria (nephrotic range) and edema are marked in

nephrotic syndrome than nephritic syndrome.
o Hypertension and Hematuria are marked in nephritic

syndrome than nephrotic syndrome.
o Some patients might have heavy proteinuria (>3g in 24hrs) but

do not have the other features of the nephrotic syndrome.
o They are said to have nephrotic range proteinuria, but not the
nephrotic syndrome.
o NS is not a single disease, It is a manifestation of several ds.

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Major cause of primary Major causes of secondary
nephrotic syndrome in adult nephrotic syndrome in adult
➢ Primary focal segmental ➢ Diabetic Nephropathy
glomerulosclerosis (FSGS) ➢ Autoimmune disease; SLE
➢ Minimal change disease (MCD) ➢ Infectious; HBV, HCV, Syphilis,
➢ Primary membranous nephropathy Schistosomiasis
(MN) ➢ Drugs; NSAIDs
➢ Primary Membranoproliferative ➢ Preeclampsia
glomerulonephritis (MPGN) ➢ Malignancy: Multiple myeloma,
lymphoma, carcinomas
• DM, Collagen vascular diseases and Amyloidosis (50 - 70% ).

• Primary glomerulopathies (Idiopathic):- account for 30 - 50%.
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Clinical manifestation
➢ Symptoms and signs related to the nephrotic state
➢ Proteinuria and hypoalbuminemia:- due to ↑↑ permeability of

the glomerular basement membrane.
➢ Edema:- Due to hypoalbuminemia
➢ Urine: excessive foaming
➢ Nail: white horizontal bands on the nail
➢ Hyperlipidemia:- ↑hepatic lipoprotein synthesis & ↑clearance.
➢ Hypercoagulability:- Due to loss of anti-thrombin III in the

urine, ↑fibrinogen production by the liver, ↑platelet aggregation.
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CF…
✓ Clinical features suggestive of specific secondary causes
• Diabetes: presence of diabetic retinopathy
• SLE: diffuse non-scarring hair loss, malar rash,

photosensitivity, polyarthritis
• Preeclampsia: 3rd trimester pregnancy or peripartal state with

high BP
• Multiple myeloma: bone pain, pathological fracture, anemia
• Lymphoma: Lymphadenopathy, splenomegaly
• Carcinomas: Local symptoms (breast lump, abdominal mass,

cough/hemoptysis, lymphadenopathy)
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Diagnosis
• Confirming significant proteinuria
✓ Quantify 24 hours urine protein.
✓ Comparing with urinary creatinine level on a single void urine.
✓ Measurement of urinary protein by a dipstick (+3 or +4

diagnostic if the first two are not available).
• Renal biopsy: to identify the underlying histopathologic.
• Minimal change diseases: accounts for 80% of children <10yrs
• Membranous glomerulopathy: accounts for 60-70% of adults.
• Focal segmental glomerulosclerosis

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Treatment
• The treatment of nephrotic syndrome involves:-
I. Specific treatment of the underlying morphologic entity
• Minimal change disease : Steroids , and cytotoxic drugs
• Membranous nephropathy : Not steroid responsive
II. Measures to control proteinuria:-
• Dietary protein restriction
• Angiotensin-converting enzyme (ACE) inhibitor
• Controlling hypertension below 130/80 reduces proteinuria.
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Rx….
III. Treatment of complications of nephrotic syndrome.
• Edema: should be managed cautiously by
– Moderate salt restriction & Loop diuretics.
• Thromboembolism: Anticoagulation is indicated for patients
with deep venous thrombosis, arterial thrombosis, and
pulmonary embolism.
– Heparin may not be effective because of urinary loss of
anti- thrombin III.
• Hyperlipidemia : may need lipid lowering agents
• Vitamin D deficiency: Vit-- D supplementation.
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Urolithiasis: Nephrolithiasis
• Brain storming
1. List the chemical type of
kidney stones?
2. How you would like to
work up a case suspected
to have nephrolithiasis?
3. What are the
conservative managements
of kidney stone?
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Nephrolithiasis…
• Nephrolithiasis is refers to kidney stones or renal calculi or
urolithiasis. In the ureter it is called ureterolithiasis, almost
always it originate from the kidney.
• Common sites of obstruction
❑ Uretro-pelvic junction
❑ Over the iliac artery/pelvic brim
❑ Uretero-vesical junction
• 80-85% of stones pass spontaneously
• Recurrence rate after 5 years is 50%

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Chemical types
• Calcium oxalate stones cover around ≈75% of renal stones.
• Calcium phosphate (≈15%).
• Uric acid (≈8%),
• Struvite stone (Mgpo4) (≈1%),
• Cystine stones (<1%).
• Many stones are a mixture of crystal types (e.g., calcium
oxalate and calcium phosphate) and also contain protein in the
stone matrix.
• Rarely, stones are composed of medications, such as acyclovir,
indinavir, and triamterene.
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Chemical types…
2/20/2024 125
Risk factors
✓ Dietary: Low fluid intake;
Protein rich diets/meat, fish eggs--lead to hyperuricemia;
Vit A deficiency--desquamation of renal epithelium--stone
formation.
✓ Environmental factors: Living in hot climate area
✓ Anatomical abnormalities which result in inadequate drainage
Horse shoe kidney, un-ascended kidney
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Risk factors…
✓ Medical conditions:
UTI due to prolonged catheterization,
Hyperparathyroidism (Pt literally pass their skeleton in their
urine), Gout (uric acid stone), crohn disease (hyper oxaluria &
magnesium malabsorption), Hypertension, obesity,
immobilization.
Some medications (Acyclovir, sulfadiazine, loop diuretics,
Gluco-corticosteroids).
2/20/2024 127
Risk factors…
✓ Previous nephrolithiasis –recurrence
✓ Surgery related:
Gastric bypass procedures,
Bariatic surgery,
Short bowel syndrome → Predispose to enhanced enteric

oxalate absorption, this in turn increases risk of stone
formation.
✓ Family history of nephrolithiasis
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Clinical Presentation
• May be clinically silent/asymptomatic.
• Symptomatic stones: pain in the flank area; produced when

stones pass from the renal pelvis into the ureter.
• Site of obstruction determine the location of the pain.
• Upper ureteral or renal pelvic obstructions lead to flank pain

which is dull aching to pricking type.
• Lower ureteral obstructions lead to colicky type of flank pain

with radiation from the loin to the groin area.
• The radiation is due to irritation of genitofemoral nerve.

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CF…
• The severity of the pain isn’t associated with the size of the
stone.
• Majority of symptomatic pts has microscopic/gross hematuria.
• Nausea and vomiting commonly accompany ureteral colic.
• At risk of recurrent UTI: dysuria, frequency, urgency, pyuria

(U/A), fever in case of upper UTI.
• Urinary urgency or frequency: obstruction is in the distal ureter.
▪Acute renal colic: the most excruciatingly painful event a person can endure
▪ Pain > child birth, broken bones, gunshot wounds, burns, surgery...
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2/20/2024 131
DDx
• Pyelonephritis
• Renal Cell Carcinoma (RCC)
• Perirenal abscess
• Bladder cancer
• Renal trauma
• Polycystic kidney disease
• Renal TB
• In females consider gynecologic cases: Ovarian torsion;
Ectopic pregnancy...
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Investigation
• Urinalysis:
– 24hrs urine profile, Hematuria, Leukocytes, bacteria,
– Crystals of calcium oxalate, cystine
– PH < 5→Uric acid stones;
– PH> 7 may suggest urea splitting organisms like proteus,

pseudomonas, klebsiella or struvite stones.
• CBC: Anemia(CKD), leukocytosis, Serum electrolytes, RFT
• Ultrasonography, KUB x-ray, Intravenous/Retrograde

pyelography, CT scan.
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Ultrasonography
2/20/2024 134
KBU x-ray
2/20/2024 135
Intravenous pyelography
2/20/2024 136
Retrograde pyelography CT scan
2/20/2024 137
Complications of nephrolithiasis
• Recurrent UTI
• Calculus hydronephrosis
• Pyonephrosis
• Squamous cell cancer
• Renal failure/in bilateral Struvite stones
– Bilateral Struvite calculi can lead to renal failure over years
because these stones typically are not symptomatic unless
they result in urinary tract obstruction or infection.

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Management
• Medical therapy
➢ Pain management: according to WHO pain mgt ladder.
2/20/2024 139
Cont…
• Non-opioids: Ibuprofen or other NSAID, pcm, or aspirin.
• Weak opioids: codeine, tramadol, or low-dose morphine.
• Strong opioids: morphine, fentanyl, oxycodone,
hydromorphone, buprenorphine.
• Dietary measures: Increase fluid intake and avoid excess salt,
protein intake.
• Alpha-adrenergic blockers: ureteral smooth muscle relaxing
effect
• Dissolution of calculi using sodium bicarbonate or potassium
citrate
2/20/2024 140
Surgical options
• 4mm -- can easily pass, >8mm -- unlikely to pass
• Obstructed, infected system
a. Non-invasive procedures
➢ Percutaneous nephrolithotomy(PNL)
➢ Extracorporeal shock wave lithotripsy (ECSWL)
b. Open surgery
➢ Pyelolithotomy--Indicated for stones in the renal pelvis
➢ Nephrolithotomy
2/20/2024 141
Cont…
Emergency department management of renal colic
✓ Secure IV line & give; Analgesics, fluid and antiemetic.
✓ Obstructed, infected system---needs emergent surgical

decompression.
Practical tip on conservative management

• Advise them to drink plenty of water (UOP=2L/day).
• Prescribe po analgestics to be taken during episodes of pain.
• Dietary modification.
• Check-up ultrasound every 3-6month to follow stone size.
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Renal Failure
• Learning objectives: at the end of this lesson the you will be
able to :
• Define acute renal failure.
• List the etiologies of acute and chronic RF.
• Describe the pathophysiology of acute and chronic RF.
• Identify the clinical manifestation of acute and chronic RF.
• Identify complications of acute and chronic renal failure.
• Understand the diagnostic approach of acute and chronic RF.
• Understand the management of acute and chronic RF.

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Renal Failure
• Kidney failure describes any condition that decreases
the kidney’s ability to function normally.
• Kidney failure is classified as acute kidney injury

(formerly known as acute kidney failure) or chronic
kidney disease based on onset and reversibility.
• CKD has a slow onset (months to years) and is

characterized by progressive, irreversible damage.
2/20/2024 144
Acute Renal Failure
• Acute renal failure also called acute renal injury is a syndrome
characterized by:
– Abrupt or rapid decline in renal filtration function (hours to

days).
– Which is marked by a rise in serum creatinine

concentration or azotemia (a rise in BUN concentration).
– Retention of nitrogenous wastes due to failure of excretion.
– Disturbance in extracellular fluid volume and
– Disturbance electrolyte and acid base homeostasis.

2/20/2024 145
ARF…
• Based on the amount of urine output acute renal
failure may be classified as:
– Anuric:- if urine volume is less than 100 ml/day.
– Oliguric:- if urine volume is less than 400 ml/day.
– Non-oliguric:- if urine volume is greater than or

equal 400 ml/day.
2/20/2024 146
Course of ARF
• Most cases of ARF are characterized by 4 distinct phases
1. Initiation /onset phase
• The initiation period begins with the initial insult and ends
when cellular injury and oliguria develops.
2. Oliguria phase (average 7 to 14 days)
• Increase in the serum concentration of wastes such as urea,

creatinine, organic acids, and the electrolytes K +, P -, and Mg +.
• Renal replacement therapy such as dialysis may be needed until

kidney function returns.
2/20/2024 147
Cont…
3. The diuretic phase
• Marked by a gradual increase in urine output, which signals

that glomerular filtration has started to recover.
• Urine output may be normal, or the patient may excrete large

amounts of dilute urine and should be observed closely for
dehydration, which may damage the kidney further.
• Laboratory values plateau and begin to decline.
4. Recovery phase (6 to 12 months): Cell regeneration and

gradual return of GFR to or toward normal.
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Etiologic classification of acute renal failure
A. Prerenal ARF: account for nearly 55% of all cases of ARF
I. Hypovolemia: Hemorrhage, burns, dehydration, GI fluid loss:
▪ Renal fluid loss: diuretics, osmotic diuresis, hypoadrenalism
▪ Sequestration in extravascular space
II. Low CO: Diseases of myocardium, valves, and pericardium;

arrhythmias; tamponade, pulmonary HTN, massive PE.
III. Altered renal systemic vascular resistance ratio
o Systemic vasodilatation: sepsis, anaphylaxis IV, ACEI drug
2/20/2024 149
AFR…
➔Renal hypoperfusion → Deprives kidney nutrients
→→→Intrarenal injury.
B. Intrinsic Renal ARF: account for nearly 40% of all ARF
I. Renovascular obstruction (bilateral or unilateral)
II. Infection:- Interstitial nephritis, Glomerulonephritis
III. Injury:- Acute tubular necrosis or ischemia.
V. Nephrotoxic drugs: NSAIDS, aminoglycosides,

Chemotherapy.
➔Decreased ability to filter blood, remove waste & excessive

water, maintain electrolyte levels.
2/20/2024 150
ARF…
C. Postrenal ARF (Obstruction): account for ~5% of ARF.
• Blockage in urinary tract after the kidney to the urethra that
prevents urine draining out of system.
• ↑↑pressure in kidney and ↑↑waste products; this decreases
kidney function.
I. Ureteric: Calculi, blood clot, sloughed papillae, cancer.
II. Bladder neck: Neurogenic, BPH, calculi, cancer, blood clot
III. Urethra Stricture, congenital valve, phimosis

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➢ Staging AKI: According to the Kidney Disease Improving Global
Outcomes staging.
Table. Staging of AKI according to KIDGO*

Stages Creatinine-based Urine-out put base
Stage 1 Increase from baseline: 1.5 - 1.9 times < 0.5 ml/kg/h for
(>50% but <100%) or >0.3mg/dl 6 – 12 hours
Stage 2 Increase from baseline 2.0 -2.9 Urine output < 0.5
times (>100% but < 300%) ml/kg/h for ≥ 12 hrs
Stage 3 Increase from baseline ➢ <0.3 ml/kg/h for
➢ 3 times (>300%) OR >24 hours OR
➢ >4.0 mg/dl Or ➢ Anuria for >12
➢ Initiation of RRT hrs
* KIDGO is a modification to RIFLE (Risk, Injury, Failure, Loss, ESRD) and AKIN.
2/20/2024 152
Pathophysiology
• Hypovolemia leads to glomerular hypoperfusion, but filtration
rate are preserved during mild hypoperfusion through several
compensatory mechanisms.
• During states of more severe hypoperfusion, these

compensatory responses are overwhelmed and GFR falls,
leading to prerenal ARF.
• Drugs that interfere with adaptive responses in the renal

microcirculation may trigger progression of prerenal ARF to
ischemic intrinsic renal ARF (ACE inhibitors, NSAIDS)
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Pathophysiology…
Intrinsic ARF
• Intrinsic renal ARF can complicate many diverse

diseases of the renal parenchyma.
• Most intrinsic renal ARF is triggered by ischemia

(ischemic ARF) or nephrotoxins (nephrotoxic ARF),
insults that classically induce acute tubular necrosis
(ATN).
2/20/2024 154
Signs and symptoms of Acute Renal Failure
Types of ARF Signs and symptoms
Prerenal ➢ Hypotension, Tachycardia, Dizziness, Thirst
Intrarenal ➢ Flank pain, Joint pain, Oliguria, Hypertension,
Headache, Confusion, Seizure.
Postrenal • Pain on flank, lower abdomen, groin and
genitalia.
• Oliguria, Distended bladder, Hematuria,
Peripheral edema.
2/20/2024 155
CM….
• Azotemia (increased serum creatinine, BUN, and
other nitrogenous waste products).
• Alterations in calcium and phosphorus balance and failure of

BP regulation and
• Erytheropoiesis with resulting anemia develop rapidly.
• ARF is usually asymptomatic and is diagnosed when screening

of hospitalized patients.
2/20/2024 156
Diagnostic Evaluation
➢ Urine analysis: many RBCs, Eosinophilia, casts.
➢ Urine and blood chemistry:
• Urine osmolarity & specific gravity
• Serum Creatinine level
• BUN
• Input and out put
• Assessment of electrolytes: Sodium, Potassium, Ca+ , Po4
• Hemoglobin & Hematocrit level to detect Anemia
➢ Radiography: Ultrasonography, Retrograde pyelography.

2/20/2024 157
Diagnostic Definition of AKI
➢ AKI is diagnosed if any one of the following criteria is
fulfilled.
☛ Increase in serum creatinine from the baseline by > 0.3mg/dl,

which is known to have occurred occur in <48 hours. Or
☛ Increase in serum creatinine by 50% (1.5-fold) form baseline,

which is known or presumed to have occurred within one
week (the prior 7 days). Or
☛ Urine output <0.5ml/kg/hr for ≥ 6 hours (for an average adult

<200ml/6hours).
2/20/2024 158
Complications of ARF
• Intravascular overload
• Electrolyte disturbance: Hyperkalemia, Hyponatremia,

Hyperphosphatemia, Hypocalcemia & Hypercalcemia.
• Metabolic acidosis
• Hyperuricemia
• Bleeding tendency
• Seizure: may occur related to uremia
• Chronic Renal failure

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Management of ARF
• Prevention: Because there are no specific therapies for
ischemic or nephrotoxic ARF, prevention is of paramount
importance.
• Preliminary measures: Exclusion of reversible causes,

correction of prerenal factors and maintenance of urine output
• Specific measures
➢ Prerenal ARF: The composition of replacement fluids for

treatment of prerenal ARF due to hypovolemia.
➢ Postrenal ARF: Transurethral or suprapubic bladder catheter,

2/20/2024 160
Mgt…
➢ Percutaneous catheterization of the dilated renal pelvis or
ureter.
• Supportive Measures
➢ Dietary management: High calorie food & decrease protein.
➢ Fluid and electrolyte management:
✓ Hypervolemia, Metabolic acidosis, Hyperkalemia,
Hyperphosphatemia, Hypocalcemia, Anemia, GI bleeding.
2/20/2024 161
Dialysis
• Dialysis replaces renal function until regeneration and repair
restore renal function.
• Hemodialysis and peritoneal dialysis are equally effective.
• Indications for dialysis
✓ When medical management fails to control
✓ Volume overload (Pulmonary edema and anuria)
✓ Severe hyperkalemia (>6.5mmol/l) or Intractable metabolic

acidosis.
✓ Progressive uremia as evidenced by rising BUN and Cr and

altered CNS function, Pericarditis.
2/20/2024 162
Dialysis…
2/20/2024 163
Urinary Retention
♪ Urinary retention is the inability to empty the bladder
completely during attempts to void.
♪ Chronic urine retention often leads to overflow

incontinence (from the pressure of the retained urine in
the bladder).
♪ Residual urine is urine that remains in the bladder after

voiding.
2/20/2024 Tsegaye E. (Bsc, Msc in AHN) 164

Cont…
♪ In a healthy adult younger than 60 years, complete
bladder emptying should occur with each voiding.
♪ In adults older than 60 years, 50 to 100 mL of residual

urine may remain after each voiding because of the
decreased contractility of the detrusor muscle.

Cause
✓ The most frequent causes of acute retention in male
o Bladder outlet obstruction (the commonest cause)
o Urethral stricture
o Acute urethritis or prostatitis
o Phimosis
✓ Cause of acute retention in female
❑Retroverted gravid uterus
❑Bladder neck obstruction (rare)

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✓ Cause of acute retention in both sex
▪ Blood clot ▪ Faecal impaction
▪ Urethral calculus ▪ Anal pain (hemorrhoidectomy)
▪ Rupture of the urethra ▪ Intensive postoperative analgesic
▪ Neurogenic (injury or treatment
disease of the spinal cord) ▪ Some drugs
▪ Smooth muscle cell ▪ Spinal anaesthesia

dysfunction associated with
ageing
2/20/2024 167
Clinical manifestation
♪ Primary manifestation of urinary retention is
⸸ Distended bladder & client's inability to void
⸸ Oliguria or anuria
⸸ Pain is present.
⸸ The bladder is visible, palpable, tender and dull to

percussion.
⸸ Potential neurological causes should be excluded by checking

reflexes in the lower limbs and perianal sensation.

Diagnostic Assessment
♪ Catheterization is the major diagnostic test if there is more than
250 to 500ml of urine in the bladder and the client has not been
able to void, retention is present.
♪ Cystoscopy - to determine the case for obstruction.

Management
♪ If obstruction causes the urinary retention the urethra will need to
be dilated or the occasion removed form long term relief.
♪ Urinary catheterization with either a straight or a retention catheter

is commonly used to treat retention.
♪ Cholinergic medications help stimulate bladder contraction, but

these drugs must never be used if mechanical obstruction is
present.
♪ The other option is to place a plastic suprapubic trocar and

cannula, which has a removable plastic strip on the side.
Surgical management
♪ Cystoplasty insert an elastic wedge into the area.
♪ Urethral instrumentation
♪ In a patient with a known excising urethra stricture, dilate the

stricture or carry out an optical urethrotomy or sometimes with
plastic repair (urethroplasty) is used.
♪ Suprapubic catheterization is also used when urethra

catheterization is difficult or dangerous.
♪ Such as:- patient with severely enlarged prostate; urethral

strictures; quadriplegics.
Benign Prostatic Hyperplasia
➢ Prostate gland
• A muscular gland just below the urinary bladder, the prostate
gland is about 3 cm high by 4cm wide by 2cm deep.
• It surrounds the first inch of the urethra as it emerges from the

bladder
• Prostate secretes an alkaline fluid that helps maintain sperm

motility
• The smooth muscle of the prostate gland contracts during

ejaculation to contribute to the expulsion of semen.
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BPH
• Benign Prostatic Hypertrophy is the hyperplasia of the prostate
gland on peri-urethral & transitional zone.
• BPH is prostate gland enlargement; about 50% of men older

than age 50 and 75% of men older than age 70 yrs.
BPH
2/20/2024 173
BPH---
• The cause is unknown but may be linked to
hormonal changes.
• As the prostate enlarges, the urethral opening narrows

and interferes with urine flow, causing urine
retention.
• Progressive bladder distention may cause a pouch to

form in the bladder that retains urine.
• Common cause of BOO in elderly.

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Risk factor of BPH
• Age 50 or older; Family history
• Other health problems i.e. Obesity, CVD
• No exercise; Erectile dysfunction
Precipitating factors
• Postponement of micturation: Common after heavy drinking of
alcohol in social gathering.
• Perianal pain, UTIs
• Medication intake which can induce retention E.g.,
antihistamines, antihypertensive, Anticholinergics, tricyclic
antidepressants ...
2/20/2024 175
Clinical presentation
• The voiding dysfunction that results from prostatic
enlargement & Bladder Outflow Obstruction and Lower
urinary tract symptoms.
I. Lower urinary tract symptoms
• Frequency, nocturia, hesitancy, cystitis, hematuria, fatigue,

nausea, vomiting, anorexia, and abdominal discomfort.
II. Voiding/obstructive symptoms
III. Storage/ irritative symptoms
2/20/2024 176
II. Obstructive /voiding symptoms
• Result from failure of the urinary bladder to empty urine when

the bladder is full.
• The patient will complain of
• A reduced force of the urinary stream
• Straining to empty (poor flow) and
• Sensation of poor bladder emptying
• Hesitancy
• Dribbling
2/20/2024 177
III. Irritative /storage symptoms
• Result from the failure of the urinary bladder to store urine

until the bladder is full.
• Frequent urination (put it in day to night ratio)
• Urgency (frequent urge to urinate)
• Nocturia
• Urge incontinence
2/20/2024 178
Physical examination
• Suprapubic area → Check for distended bladder
• Digital rectal examination
• Prostate: Size---Enlarged; Surface---Smooth; Consistency--

Firm; Contour---well defined; Fixity---Not fixed to rectal
mucosa; Medial sulcus---palpable.
• On DRE, also assess...Tenderness ---Prostitis
• Absence or presence of fluctuation --- Prostatic abscess
• Anal sphincter tone & bulbocavernous muscle reflex---

neurological disorder.
2/20/2024 179
American Urological Association Symptom Scoring Index
2/20/2024 180
Diagnostic test
• Hematologic studies: RFT, CBC, Serum electrolyte
• Urinalysis
• Urine culture
• Prostate Specific Antigen (PSA) can help to rule out prostatic
carcinoma;
• Post void residual volume (PVR) test and
• Cystoscopy, urethrography, excretory urography, trans rectal
ultrasonography
2/20/2024 181
Management
• For acute cases, treat acute urinary retention:
– Catheterize the patient or
– Suprapubic cystostomy (incision and catheter placement in

the bladder) and
– Arrange uro-surgical follow-up.
• Non-emergency case: Link to uro-surgical clinic.
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Algorithm for selection of treatment of BPH
2/20/2024 183
Uro-surgical management options
I. Watchful waiting
• Annual checkup for asymptomatic clients.
• For mild symptoms, follow 1 to 2 times yearly and offer

suggestions that help to reduce symptoms.
• Lifestyle changes for symptom relief
✓ Avoid alcohol or caffeinated beverages; Avoid antihistamines

and decongestants and
✓ Double void.
2/20/2024 184
II. Medical management for moderate symptoms
a. α adnergic blockers (e.g. prazosin, doxazosin,
tamsulosin , & terazosin) to relax the muscles.
b. Dutasteride 0.5mg/d (non-selective type I&II 5α-

reductase inhibitor) or Finasteride 5mg/d (selective
type II 5α-reductase inhibitor) to decrease the size of
the prostate.
c. Combination therapy
III. Surgical management

2/20/2024 185
Indications for surgery
• AUR
• Chronic urinary retention & renal impairment
– Hydroureter or hydronephrosis
– Residual urine≥200ml
– Uremic manifestations
• Complications of BOO. e.g., infection, stone...
• Severe symptoms bothering the pt and affect his quality of life.
• Failed medical treatments
2/20/2024 186
III. Surgical management for severs symptoms
• Transurethral incision of the prostate (TUIP)—Gold standard.
• Balloon dilation (urethroplasty)
• Transurethral laser resection
• Transurethral needle ablation, and microwave thermotherapy
▪ For very large prostate gland
✓ Open prostatectomy (>20 gm) → Retro-pubic prostatectomy-

- commonly used in Ethiopia currently.
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Surgical management ---
2/20/2024 188
Specific complications to BPH Surgery
➢ Urethral stricture
➢ Bladder damage: Bleeding (Hematuria); Bladder neck

contracture;
➢ Inability to urinate --- Bladder stone
➢ Incontinence
➢ kidney damage: Urinary tract infections
➢ Retrograde ejaculation
➢ Impotence
2/20/2024 189
Preoperative nursing interventions
• Explain the surgical procedure, perioperative
experience, and expected postoperative course to help
decrease the patient’s anxiety.
• Allow the patient to discuss fears and concerns about

postoperative urinary incontinence and impotence,
but assure him that they aren’t common after prostate
surgery, only after radical perineal resection.
2/20/2024 190
Postoperative nursing interventions
• Evaluate the patient’s pain and response to analgesia
• Explain to the patient that after transurethral resection of the
prostate (TURP) or prostatectomy, bladder spasms are typical;
explain to him that the sensation of needing to void is normal
and that avoiding straining may decrease the frequency and
intensity of bladder spasms.
• Observe and maintain the patency of the three-way irrigation
system; clots can obstruct the system and cause pain and
bladder spasms; if clots form, increase the flow of saline
solution to dilute the urine and allow the clots to flow out.
2/20/2024 191
Specific complications to BPH Surgery
✓ Bleeding
✓ Retrograde ejaculation
✓ Incontinence
✓ Impotence
✓ Urethral stricture
✓ Bladder neck contracture...
2/20/2024 192
Reading assignment
• Uretheral catheterization
• Supra-pubic cystostomy
• Bladder Exstrophy
• Incontinence of urine
2/20/2024 193
References
• Brunner and Suddarth‘s text book of medical surgical nursing, 11th edition.
• Linda D, Kathleen M, Mary E. Critical care nursing diagnosis and management,
9th edition.
• Ruth F. Craven, Constance J. Hirnle. Fundamentals of nursing: human health and
function.
• L. Williams, W., Brunner and suddarth’s textbook of medical surgical nursing. 12th
edition: 2010:volume 1.
• M. A. Papadakis, S.J.M., M. W. Rabow, Current medical diagnosis & treatment.
2016. fifth editions p. 962.
• Norman S. Williams MS. Bailey & Love’s short practice of surgery, 25th.
452
• Harrison’s principle of internal medicine 20th edition
• Bates’ Guide to Physical Examination and History Taking, 12th edition.
• Standard treatment guideline for general hospitals in Ethiopia, FMOH, 4th edition,
2021.
•
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2/20/2024 195
Learning Objectives
 Review anatomy and physiology of the nervous system
 Analyze the approach for nervous system examination
 Identify the common neurological manifestation
 Identify common neurological disorders, cause
Pathophysiology, clinical manifestation, medical and
surgical management
 Nursing care for patients with common neurological
disorders
The Nervous system consists of two divisions:
➢ The central Nervous system (CNS)
❖ The Brain and Spinal cord.
➢ The peripheral nervous system, made up of Cranial and Spinal
nerves.
• 12 Pairs of cranial nerves
• 31 Pairs of spinal nerves
• Carry info to and from the spinal cord
 A network of billions of nerve cells linked together in a highly

organized fashion to form the rapid control center of the body
The peripheral Nervous system divided into
➢The Somatic or Voluntary, Nervous system,
➢The Autonomic or Involuntary, Nervous
system,which includes; Para sympahetic and
sympathetic Nervous system
 The function of the Nervous system is to control all
motor, sensory, autonomic, cognitive, and behavioral
activities.
 Makes up 2% of your body weigh
 The brain is contained in the rigid skull, which protects it
from injury.
 The meninges is covers the brain and spinal cord.
 It provide protection, support, and nourishment to the brain
and spinal cord.
Brain has two hemisphere
1. Left side of the brain- controls the functions of the right
half of the body, and
2. The right side of the brain-controls the left half of the
body.(Exceptions to this rule are the eye and the ear,
which have bilateral cortical connections.)
Note: one side of the brain, usually the left hemisphere is
functionally dominant, in almost all right handed
individuals
 Brain is one of our largest organs, consists of the
following major divisions, named in ascending order
beginning with most inferior part:
I. Brain stem
A. Medulla oblongata - Transmits motor fibber from the
brain to the spinal cord and sensory fibber from the spinal
cord to the brain.
B. Pons - -Contain motor and sensory pathway and it is
abridge b/n the medulla and the cerebrum.-Also contain
centre for controlling heart, respiration
C. Midbrain- It contains sensory and motor pathways and
serves as a centre for auditory and visual reflexes.
II. Cerebellum- Is largely responsible for smoothness &
coordination of movement
• It controls balance position & fine movement
Ill. Diencephalon
. The embryonic diencephalon has three major derivatives:
the thalamus, hypothalamus, and epithalamiums.
IV. Cerebrum- responsible for an individual function and
intelligence
7
• General movement
• Visceral functions
• Perception
• Behavior
• Voluntary movement
• Interpretation of sensory data
• Lies inferior to the cerebrum and occupies the posterior cranial
fossa
• 2nd largest region of the brain. 10% of the brain by volume, but it
contains 50% of its neurons
• Has 2 primary functions:
1. Adjusting the postural muscles of the body
• Coordinates rapid, automatic adjustments, that maintain
balance and equilibrium
2. Programming and fine-tuning movements controlled at the
subconscious and conscious levels
• Refines learned movement patterns by regulating activity of
both the pyramidal and extrapyramidal motor pathways of
the cerebral cortex
 CSF, a clear and colorless fluid with a specific gravity of
1.007
 Is produced in the ventricles and circulates around the
brain and the spinal cord through the ventricular system.
 There are four ventricles: the right and left lateral, and the
third and fourth ventricles
 The fourth ventricle supplies CSF to the subarachnoid
space and down the spinal cord on the dorsal surface
CEREBRAL CIRCULATION
• The cerebral circulation receives 15% of the
cardiac output, or 750 mL per minute.
• The brain does not store nutrients and has a high
metabolic demand that requires the high blood
flow.
• The brain’s blood pathway is unique because it
flows against gravity;
• Its arteries fill from below and the veins drain from
above
 It serves as the connection between the brain and the
periphery.
 Approximately 45 cm (18 in) long and about the
thickness of a finger
 It extends from the foramen magnum at the base of the
skull to the lower border of the first lumbar vertebra.
 where it tapers to a fibrous band called the conus
medullaris.
 The spinal cord is an H-shaped structure with nerve cell
bodies (gray matter) surrounded by ascending and
descending tracts
 The anterior horns contain cells with fibers that form the
anterior (motor) root
 The posterior (upper horns) portion contains cells with
fibers that enter over the posterior (sensory)
SPINAL NERVES
The spinal cord is composed of;
 31 pairs of spinal nerves: 8 cervical,12 thoracic, 5 lumbar, 5
sacral, and 1 coccygeal.
 Each spinal nerve has a Ventral root(efferent/motor)and
Dorsal root(afferent/sensory)
1. Sensation
- Monitors changes/events occurring in and outside the
body. Such changes are known as stimuli and the cells that
monitor them are receptors.
2. Integration
- The parallel processing and interpretation of sensory
information to determine the appropriate response
3. Reaction
- The activation of muscles or glands (typically via the release
of neurotransmitters (NTs)
➢ The brain and spinal cord cannot be examined as directly as other
systems of the body.
➢ Much of the neurologic examination is an indirect evaluation that
assesses the function of the specific body part or parts controlled or
innervated by the nervous system.
 Health history
 Physical examination
 Examining the cranial nerves
 Examining the motor system
HEALTH HISTORY
 The health history must include details about the
• Onset, character,
• Severity, location,
• Duration, and frequency of symptoms and Signs;
associated complaints;
• Precipitating, aggravating,
• Relieving factors;
• Progression, remission, and
• Exacerbation; and the presence or absence of similar
symptom among family members
 Loss of consciousness
 Seizure ( convulsion )
 Syncope
 Weakness or paralysis of part of the body
 Abnormal body movements like tremor
 Neurologic pain
 Altered or loss of sensation
1. Mental status examination
2. Cranial nerves examination
3. Motor examination
4. Reflexes
5. Assessment of muscle coordination
6. Examination of posture, station and gait.
7. Examination for signs of meningeal irritation
MENTAL STATUS
I. Appearance and behaviour.
1. Observing the pt’s dress, grooming and personal
hygiene
2. Observing posture, gesture ,movements, facial
expressions, and motor activity.
3. Manner of speech and level of consciousness.
 ALERT- patient opens his eyes, looks you
- responds fully and appropriately to normal tone voice stimuli
Lethargy –patient opens his eyes ,looks a you in response to loud
voice and immediately falls asleep
 Obtundation-patient opens his eyes and looks at you in response
gentle shake
 STUPOR- patient responds to painful stimuli
- Has slow or absent verbal response
- Has minimum awareness of self and environment
 COMA- patient do not respond to any type of stimuli
II. Mood
 The appropriateness of the patient’s mood or affect is noted
E.g. If the patient smiles while experiencing excruciating chest pain,
this is considered as inappropriate mood.
III. Speech and language
❖ The patient’s speech reveals important information about his
mental function and emotional status.
➢ Throughout the interview, note the patient’s speech, including.
❑ Quantity: Is the patient talkative or silent?
❑ Rate. Is speech fast or slow?
❑ Loudness. Is speech loud or soft?
❑ Articulation /quality of Words
➢ Are the words spoken clear and distinct?

IV. THOUGHT AND PERCEPTION
❖ Observe logic, relevance, and coherence of the patient’s
thought processes as revealed in words.
❖ Any unusual aspects of perception such as:
✓ Illusions-Misinterpretations of real external stimuli.

✓ Hallucinations -Subjective sensory perceptions in the
absence of relevant external stimuli
v. Cognitive function:
 Orientation to time, place, and person.
 Assess the three aspects to memory, which usually becomes
obvious during the interview.
1. Immediate- recall by saying a series of numbers and
having the patient repeat them.
2.Recent memory- by asking the patient to recall something
after 5 minutes has elapsed.
3 . Remote memory- refers to events in the distant past
1. The first cranial (olfactory) nerve
 Arises from inferior side of the frontal lobe.
 It mediates the sense of smell.
 One can check the ability of the person to smell using a peel of
an orange/ lemon, checking each nostril separately.
2. The second cranial (Optic) nerve
 Arises from the retina and ends at the occipital visual cortex.
 It caries the sense of sight.
 It is tested by examination of:-
2.1 Testing of the visual fields
2.2 Visual acuity: - may be checked by snellen’s chart
2.3 Checking for colour vision
 Asking the individual to identify different colours in the
surrounding
3. Third, fourth, and sixth cranial nerves
➢ The third (oculomoter nerve) arises from the mid brain.
 Its functions are give motor supply to all extra ocular muscles
except lateral rectus and superior oblique.
➢ The fourth (Trochlear) nerve: - supplies the superior oblique
muscle.
➢ The sixth (Abducents)-nerve: - supplies the lateral rectus muscle.
 The third, fourth and sixth cranial nerves are checked
together.
 The first thing to do is inspect carefully to see if there is
 Ptosis: - drooping of the eyelid which is found in 3rd
nerve palsy.
 Abnormal eye position (strabismus), such patient may
complain of double vision
 Then test the movement of the eye balls in all directions
 The cornial light reflex test
4. The fifth cranial (Trigeminal) nerve:-
❖ It has motor and sensory components.
I. Motor branch: supplies the masseter, temporalis
II. Sensory branch: supplies mainly the skin of the face, anterior part
of the scalp, the mucous membrane of the mouth and cornea.
-It has three sub- branches:-
➢ Ophthalmic
➢ Maxillary and
➢Mandibular division
Examination of the fifth cranial nerve includes:
I. Motor examination
 Motor examination of jaw movement -Patient is asked to
extend the jaw, move it from side to side, and bite
strongly.
 Palpate the masseter and temporalis muscles as the
patient clamp to gether his teeth.
 Compare muscle tension bilaterally with teeth
compressed.
II. Sensory of the trigeminal nerve
 Sensory examination of the three divisions of the
trigeminal nerve-the examiner tests
 Light touch sensibility- with a cotton and pain by pricking
with a pin the patient’s forehead, the area of the mandible
and the maxilla.
 Corneal reflex- The patient is asked to look upward
while the examiner uses the wisp of cotton carefully and
to briefly stroke the cornea from the side and from
below. The normal response is blinking
5. The seventh (facial) nerve: - has two major functions
 Motor branch supplies all muscles of facial expression

 Sensory branch supplies taste buds of anterior 2/3 of the
tongue
Evaluation of the motor function
❖ Inspection for flattening of the nasolabial fold, facial
droop or asymmetry
❖ Then ask the patient to raise eye brows, •lose his eye
tightly against pressure, Smile or show upper teeth, puff
cheeks
The sensory portion of the seventh nerve:-
❖ Is tested by applying crystals of salt and sugar from two
moistened cotton applicators on different aspects of the
tongue.
6. The eighth (vestibule-cochlear) nerve: -
 It mediates the sense of hearing and also important for
rotational perception and keeping balance.
 Testing cochlear portion is done by assessing the ability to
hear using:-
 Whispered and spoken voice
Weber’s test- tests for lateralization:
✓ Place the vibrating tuning fork on top of the patient’s head
and, ask patient in which ear he hears it best.
✓ In conduction problems sound lateralizes to the abnormal
ear and in neural deafness to the normal ear.
Rinne’s test -to compare air conduction to bone conduction:
 Place the vibrating tuning fork on the mastoid bone with ear
closed first ,then place the “U” of vibrating tuning fork at the ear
as soon as patient reports no vibration from mastoid bone.
 In conductive deafness bone conduction is longer than air

conduction.
 In sensory neural hearing loss, sound is heard longer through the

air.
7. The ninth cranial (glosso pharyngeal) nerve
 Mediates taste sensation- from the posterior 1/3 of the
tongue
 Motor supplies- to muscles of the pharynx
Examination includes;
 Checking for taste over the posterior third of the tongue.
 A portion of the ninth nerve and a portion of the tenth nerve
are tested by the gag reflex, elicited by stimulating the
posterior tongue with a tongue depressor.
8. The tenth cranial (vagus) nerve
 Mediates Sensory and motor supply to the pharynx, larynx
together with the ninth nerve.
 Watching movement of the uvula, which normally rises to
the midline during phonation (“ah” reflex).
 If a unilateral lesion is present, the uvula will deviate
from the lesion to the side opposite.
 Hoarseness of the voice and difficulty in swallowing, as
well as repeated coughing after swallowing liquid,
suggest the possibility of vagal involvement
 In Cranial Nerve X paralysis, the soft palate fails to rise
and the uvula deviates to the opposite side.
9. The eleventh cranial (accessory) nerve:
 Innervates sternocleidomastoid and trapizius muscles.
 This nerve is evaluated by observing neck motion and by
testing the trapizius and sternocleidomastoid muscles.
 The patient is asked to keep his shoulders shrugged
while the examiner attempts to push them down.
 The patient is then asked to turn his chin against the
examiner’s resisting hand, first to one side and then
to the other.
 Functional impairment of the nerve is manifested by
weakness in these maneuvers.
10. Twelfth cranial (hypoglossal) nerve
 Innervates muscles of the tongue.
 It is evaluated by observing the movements of the tongue.
 Weakness that is secondary to hypoglossal nerve
involvement on one side is manifested by deviation of the
tongue toward the side of the lesion.
Inspection and Palpation
 comprehensive inspection and palpation of the motor
system includes evaluation of
• muscle size,
• strength
• and tone of muscles.
Inspection and palpation: muscle bulk
 Do the muscles look flat or concave, suggesting atrophy? If
so, is the process unilateral or bilateral? Is it proximal or
distal?
 Compare the size and contours of muscles
 atrophy results from diseases of the peripheral nervous
system
 flattening of the thenar and hypothenar eminences and furrow
between the metacarpals suggest atrophy
 suggests damage to the median and ulnar nerves, respectively.
 Test muscle strength against a resistance, using a 0 ‐ 5
scale
◦ Pull forearm towards upper arm
◦ Push forearm away from upper arm
Grade Strength
• 5- Full ROM against gravity & resistance muscle
strength
• 4-Full ROM against gravity & moderate amount
resistance, slight weakness
• 3- Full ROM against gravity only moderate muscle
weakness
• 2- Full ROM when gravity eliminated, severe weakness
• 1- Weak muscle contraction is palpated, no movement
noted, severe weakness
• 0- complete paralysis
 Impaired strength is called weakness (paresis).
 Absence of strength is called paralysis (plegia).
◦ Hemiparesis refers to weakness of one half of
the body; hemiplegia to paralysis of one half of
the body.
◦ Paraplegia means paralysis of the legs;
quadriplegia, paralysis of all four limbs
Inspection and Palpation: Muscle Tone
 When testing muscle strength, abnormalities in
muscle tone will become more evident:
◦ Lift legs up
◦ Push legs down
 Abnormal muscle tone findings can include:
◦ Limited range of motion

◦ Pain on motion
◦ Decreased resistance (flaccidity) or increased
resistance (rigidity), or spasticity
Gait
 Observe as a person walks, runs and returns.
 Normally the gait is smooth, rhythmic and effortless.
 Ask the person to walk a straight line in a heel- to- toe
fashion (tandem walking).
 Normally, the person can walk straight and stay
balanced.
 Abnormal-staggering loss of balance.
Vc v
heels
heel to toe
tip of
toes
Romberg test
 Ask the person to stand up with feet together and arms at
the sides.
 Once in a stable position, ask the person to close the eyes
and to hold the position. Wait about 20 seconds. Normal
posture and balance are maintained
 Positive Romberg's sign is loss of balancing with closing of
eyes that occurs with cerebellar ataxia and loss of vestibular
function.
 Ask the person to hop, first on one leg, then the other. This
demonstrates muscle strength, and cerebellar function
Rapid alternating movement (RAM)
 Ask the person to pat the knees with both hands, lift up,
turn hands over and pat the knees with the backs to hands.
 Then ask the person to do this faster. Normally, this is
done with equal turning and a quick rhythmic pace.
 Alternatively, ask the person to touch the thumb to each
finger on the same hands, starting with the index finger,
then reverse direction.
 Normally; this can be done quickly and accurately.
 abnormalities-Upper motor
neuron weakness and basal ganglia
Finger to finger Test
 With the person’s eyes open, ask to use the index
finger to touch your finger, then the person’s own
nose.
 After a few times move your finger to different spots.
 The person’s movement should be smooth and
accurate.
 Abnormal - misses the mark, dysmetria
Finger to nose test
 Ask the person to close the eyes and to stretch out the arms.
 Ask the person to touch the tip of his or her nose with each
index finger, alternating hands and increasing speed.
 Normally done with accurate and smooth movement
 Abnormal. Misses nose
Heel to shin test
 Lower extremity coordination by asking the person, who
is in a supine position, to place the heel on the opposite
knee, and run it down the shin from the knee to ankle.
 Normally moves the heel is a straight line down the shin.
 Abnormal- lack of coordination; heel falls off shin.
◦ Cerebellar disease, lost position sense

 Reflexes are rapid, automatic and predictable response of
the body to stimuli.
 Absent decreased or increased reflex responses may be
used as indicators of certain pathology in the body
 Reflex may be absent or decreased when
◦ Sensation is lost
◦ The relevant spinal segments are damaged
◦ The peripheral nerves are damaged
◦ There is the disease of muscles
◦ The neuromuscular junctions are diseased
 Increased reflex suggest central nervous system disease
 The following two groups of reflexes are usually included
in the general physical examination
➢ Deep tendon reflexes
◦ The biceps reflex
◦ The triceps reflex
◦ The knee-jerk reflex
◦ The ankle-jerk reflex
➢ Cutaneous reflex or superficial
 Plantar reflexes
 Abdominal reflexes
Neck rigidity
 With the patient supine, place your hand behind the patient
head and flex the neck forward until the chin touches the
chest if possible
 Normally the patient can easily touch his chest with his chin
 Pain in the neck and resistant to flexion may suggest
meningeal irritation
➢ Brudzinsk’s sign
◦ While flexing the patient neck forward above the hip and knee in reaction
to your maneuver
◦ Normally they should remain relax and motion less
◦ Flexion of the patient hip and knees while you are doing the maneuver
suggest meningeal irritation
➢ Kerning's sign
 Flex the patient (a supine position) leg both at the knee and the
hip, and then straighten the knee
 Normally the patient feel no pain except some discomfort behind
the knee felt by some people during full extension
 Bilateral pain and increased resistance to extending the knee
suggests meningeal irritation
✓ Describe the causes, pathophysiology, clinical
manifestations, medical ,surgical and nursing
management of :
➢ Increased intracranial pressure (ICP)
➢ Seizures/Epilepsy
➢ Headache(cephalgia)
➢ Cerebrovascular Disorder(stroke)
➢Head injury, Spinal cord injury
➢ Bell’s palsy(Facial paralysis)
➢ Parkinson’s diseases
Altered Level of Consciousness
 An altered level of consciousness (LOC) is apparent in the
patient who is not
• Oriented,
• Does not follow commands, or
• Needs persistent stimuli to achieve a state of alertness.
 Altered LOC is not a disorder itself; rather, it is a function
and symptom of multiple pathophysiologic phenomena.
 The cause may be neurologic (head injury, stroke),
toxicology (drug overdose, alcohol intoxication), or
metabolic (hepatic or renal failure, diabetic ketoacidosis).
Complications
◦ Respiratory failure,
◦ Pneumonia,
◦ Pressure ulcers, and
◦ Aspiration
Medical management
 Maintain a patent airway.
 Orally or nasally intubation, or
 A tracheostomy may be performed.
 An iv line opened to provide access for fluids and intravenous

medications.
 A feeding tube or a gastrostomy tube, is initiated to provided
nutritional support
 Treatment of the underlying causes.
❑ Nursing diagnoses
 Ineffective airway clearance related to altered level of
consciousness
 Risk of injury related to decreased level of consciousness
 Deficient fluid volume related to inability to take in fluids
by mouth
 Risk for impaired skin integrity related to immobility
 Impaired urinary elimination
❑ Goal
◦ Maintaining Airway
◦ Facilitating airway clearance
◦ Providing mouth care
◦ Prevention of injury
◦ Maintaining fluid volume
◦ Maintaining elimination
❑ Expected patient out comes
◦ Clear airway
◦ Experiences no injuries
◦ Attains/maintains adequate fluid status
◦ Maintains normal skin integrity
◦ Has no urinary retention
❑ Interventions
◦ Ensure ventilation
◦ Elevating the head of the bed to 30 degrees helps prevent
aspiration
◦ Positioning the patient in a lateral or semi prone position will
also help as it permits the jaw and tongue to fall forward, thus
promoting drainage of secretions.
◦ Suctioning and oral hygiene.
◦ For the protection of the patient, padded side rails are provided
and raised at all times.
◦ Hydration of the patient after examination
◦ Catheterization may be needed
◦ Bowel elimination should be maintained
 The rigid cranial vault contains brain tissue (1,400 g),
blood (75 ml), and CSF (75 ml).
 ICP is usually measured in the lateral ventricles;
normal ICP is 10 to 20 mm
 The volume and pressure of these three components are
usually in a state of equilibrium and produce the ICP.
 Because brain tissue has limited space to change,
compensation typically is accomplished by displacing or
shifting CSF, increasing the absorption of CSF, or
decreasing cerebral blood volume
 As ICP increases the complains decreases (as ICP
increases ,compensatory mechanism decreases)
➢ Common causes of increased ICP
 Head trauma(injury )
 Intracranial hemorrhage,
 Hematoma,cerebral edema
 Brain tumors.(increasing tissue volume)
 CNS infection
 Brain abscess
 Increased ICP from any cause
 Decreases cerebral perfusion,
 Stimulates further swelling (edema), and shifts brain tissue
through openings in the rigid dura,
 Resulting in herniation
 Decreased cerebral blood flow
• Increased ICP may significantly reduce cerebral
blood flow, resulting in ischemia and cell death.
• In the early stages of cerebral ischemia, the
vasomotor centers are stimulated and the systemic
pressure rises to maintain cerebral blood flow.
• Usually a slow bounding pulse and respiratory
irregularities accompany this.
 Cerebral edema
• Edema can occur in the gray, white, or interstitial matter.
• As brain tissue swells within the rigid skull, several
mechanisms attempt to compensate for the increasing ICP.
• These mechanisms include auto regulation and decreasing the
production and flow of CSF.
• Auto regulation refers to the brain’s ability to change the
diameter of its blood vessels automatically to maintain a
constant cerebral blood flow during alterations in systemic
blood pressure
✓change LOC (Early sign )
✓ Restlessness, confusion, or increasing drowsiness
✓Headache that is constant, increasing in intensity, and aggravated
by movement or straining.
✓Vomiting , papille edema
✓Double vision (diplopia)
✓ Vital sign changes are a late indication of Increased ICP.
Cushing’s response is a classic late sign of increased ICP.
✓ Cushing’s response (or Cushing’s triad) is Characterized
by bradycardia, bradypnea, and arterial
hypertension(increasing systolic blood pressure while
diastolic blood pressure remains the same),
✓ Widening pulse pressure.
Detecting Later Signs of Increased ICP
✓ LOC continues to deteriorate until the patient is comatose.
✓ Altered respiratory patterns develop, including Cheyne-Stokes
breathing
✓ Projectile vomiting may occur with increased pressure on the reflex
center in the medulla.
✓ Hemiplegia ( when pressure on the brain stem increases
 History and physical examination
 computed tomography (CT)scanning
 Magnetic resonance imaging (MRI)
 cerebral angiography
 Skull x ray
 Lumbar puncture is avoided in patients with increased
ICP because the sudden release of pressure can cause the
brain to herniation
DECREASING CEREBRAL EDEMA
1. Osmotic diuretics (mannitol) -may be given to dehydrate
the brain tissue and reduce cerebral edema.
 They act by drawing water across intact membranes, thereby
reducing the volume of brain and extracellular fluid.
 An indwelling urinary catheter is usually inserted to monitor
urinary out.
2.Corticosteroids - help reduce the edema surrounding brain
tumors. (eg, dexamethasone)
3.Other method for decreasing cerebral edema is fluid
restriction
• Limiting over all fluid intake leads to dehydration and
hemoconcentration
• Hyperventilation of the patient
• Elevating the patient’s head to optimize venous drainage
 Seizures are episodes of abnormal motor, sensory,
autonomic, or psychic activity (or a combination of these)
resulting from sudden excessive discharge from cerebral
neurons.
 A part or all of the brain may be involved
 Most seizures are sudden and transient
 Seizures can develop at any time during a person’s life, and
they can occur at any time.
 A seizure may be a symptom of epilepsy or other
neurological disorders such as a brain tumor or meningitis.
 Epilepsy is a chronic neurological disorder characterized by
repeated seizure activity
Causes – Idiopathic(70%)
• Genetic factor (Family History)
• Developmental defects
• Acquired hypoxemia of any causes, Fever (child hood)
• vascular insufficiency , Hypertension, stroke ,CNS infections,
• Metabolic and toxic condition
• Head trauma, Neoplasms,
• allergies
• Drugs, Alcohol
SEIZURE
Partial Generalized Unclassified

PARTIAL SELZURES
 Occurs with in discrete regions of the brain
 Consciousness is fully preserved during the seizure
 The clinical picture is relatively simple and is termed
simple partial if consciousness is not altered
 If symptom is more complex & the seizure is termed
complex partial seizure
1. Simple Partial Seizures
 Cause motor sensory autonomic or psychic symptom
without an obvious alteration in consciousness.
 Only a finger or hand may shake or the mouth may jerk
uncontrollably
 Pt. experiences a localized paresis for minutes or many
hours.
2. Complex Partial Seizures
• Impaired consciousness
• Unable to respond appropriately to visual or verbal commands
during the seizure.
• Begins with an aura (warning sign)
• Start of the ictal phase is often a sudden behavioral arrest or
motionless stare
GENERALIZED SEIZURE (GRAND MAL SEIZURE
 Arise from both hemispheres simultaneously
 Intense rigidity of the entire body followed by jerky
alternations of muscle relaxation and contraction
/generalized tonic clonic contraction.
Generalized tonic clonic Seizure
 Epileptic cry
 tongue is chewed & the pt. is incontinent of urine and stool
 Convulsive mov’t subside after 1 or 2 minute & the pt.
relaxes and lies in deep coma, noisy breathing and
abdominal-respiration
 Confusion and hard to arouse in post ictal period
 Complaining of headache
Absence Seizures (Petit Mal)
 sudden, brief lapses of consciousness with loss of postural
control.
 Typically lasts for only few seconds
 Conscious returns as suddenly as it was lost
 No post ictal confusion
 Usually begin in childhood (4-8yrs)
 Can occur hundreds of time per day
Atonic Seizures
 Sudden loss of postural muscle tone lasting 1-2 sec:
 Consciousness is briefly impaired
 No post ictal confusion
 Very brief seizure may cause only a quick head drop or
nodding mov’t while longer seizure will cause the pt. to
collapse.
Myoclonic Seizures
 Sudden and brief muscle contraction that involve one part
of the body or the entire body.
 Sudden jerking mov’t observed while falling asleep is
common physiologic form of myoclonus
 Pathologic – most commonly seen in association with
metabolic disorder degenerative CNS disease or brain
injury.
DIAGNOSTIC EVALUATION
 History
◦ Frequency, severity and factors that
precipitate them
◦ Events during pregnancy and child birth
◦ Illness or head injury
◦ Physical and neurological exam
 EEG / Electroencephalogram/
 CT. Scan, Skull x-ray, serum glucose, LP,
cerebral angiography
MANAGEMENT
 Individualized to meet the special needs of each
pt. and not just to manage and prevent seizure.
• 1st rule of RX – To protect the person from injury.
• 2nd rule of Rx – To treat any underlying disease
 Reduce the frequency of seizure
 Bring seizure under control
 Anticonvulsant Medications
E.g Phenytoin ,Carbamazepine ,Phenobarbital
 Anticonvulsant drugs should never be discontinued
abruptly; rather the dose should be slowly to prevent
seizure recurrence.
 Should started with single agent and minimum dose
 Surgical Rx if the cause is tumor, abscess
Nursing Management During a Seizure
 A major responsibility of the nurse is to observe and
record the sequence of symptoms.
 Preventing injury and supporting the patient.
 This includes supporting the patient not only physically
but also psychologically.
 Consequences such as distress, embarrassment, fatigue,
and depression can be devastating to the patient.
Nursing Management After a Seizure
 Document the events leading to and occurring during the seizure
and to prevent complications (eg, aspiration, injury).
 To prevent complications, the patient is placed in the side-lying
position to facilitate drainage of oral secretions and is suctioned, if
needed, to maintain a patent airway and prevent aspiration.
 Seizure precautions are maintained, including having available fully
functioning suction equipment with a suction catheter and oral
airway.
 The bed is placed in a low position with side rails up and padded if
necessary to prevent patient injury.
 It is a group of syndromes characterized by unprovoked,
recurring seizures.
 The most common syndromes being those with
generalized seizures and those with partial-onset seizures
 Epilepsy can be primary (idiopathic) or secondary,
when the cause is known
 epilepsy is a symptom of another underlying
condition such as a brain tumor
 Messages from the body are carried by the neurons
(nerve cells) of the brain by means of discharges of
electrochemical energy that sweep along them.
 These impulses occur in bursts whenever a nerve cell has
a task to perform.
 Sometimes, these cells or groups of cells continue firing
after a task is finished.
 Resultant dysfunction ranges from mild to devastating and
often causes unconsciousness.
 When these uncontrolled, abnormal discharges occur

repeatedly, a person is said to have an epileptic syndrome.
 Epilepsy is not associated with intellectual level.
 Epilepsy is not synonymous with mental retardation or

illness
 Intense rigidity of the entire body followed by alternating muscle
relaxation and contraction (generalized tonic–clonic contraction).
 Simultaneous contractions of the diaphragm and
 Chest muscles may produce a characteristic epileptic cry
 Tongue is often chewed
 incontinent of urine and stool.
 After 1 or 2 minutes, the convulsive movements begin to subside;
the patient relaxes and lies in deep coma, breathing noisily.
 The respirations at this point are chiefly abdominal.
 In the postictal state (after the seizure), the patient is often
confused and hard to arouse and may sleep for hours.
 Many patients complain of headache, sore muscles,
fatigue, and depression.
Medical Management
 Management differs from patient to patient because some forms of
epilepsy arise from brain damage and others are due to altered brain
chemistry.
Pharmacologic therapy
◦ Treatment is usually started with a single medication and
minimum dosage.
◦ Sudden withdrawal of these medications can cause seizures to
occur with greater frequency or can precipitate the development
of status epileptics.
Many medications are available to control seizures.
E.g:carbamazepine, clonazepam, phenobarbital, phenytoin
Surgical management
 Surgery is indicated for patients whose epilepsy results from
intracranial tumors, abscess, cysts, or vascular anomalies.
Nursing Interventions
 Preventing injury
• The patient should be placed on the floor and any obstructive items
should be removed.
• The patient should never be forced into a position, nor should anyone
attempt to insert anything into the patient’s mouth once a seizure has
activated.
• Patients on seizure precautions should have pads applied to side rails
while in bed
 Reducing fear of seizures
• Fear that a seizure may occur unexpectedly can be
reduced by the patient’s adherence to the prescribed
treatment regimen.
• Photic stimulation (bright flickering lights, television
viewing) may precipitate seizures; wearing dark
glasses or covering one eye may be preventive.
• Tension states (anxiety, frustration) induce seizures in
some patients
 Status epilepticus (acute prolonged seizure activity) is a
series of generalized seizures that occur without full
recovery of consciousness between attacks.
 continuous clinical or electrical seizures lasting at least 30
minutes, even without impairment of consciousness.
 Generalized seizures that occurs with out full recovery of
consciousness between attacks
 It is a medical emergency.
Cause or precipitated by:
• withdrawls of antisezure medication
• CNS infections
• Metabolic instability
• Tumors
• Trauma
• Stroke
• Fever
 Patient is having over convulsion
 After 30-35 min of uninterrupted seizure, the signs may
become increasingly subtle.
DIAGNOSTIC FINDINGS
 EEG
 History of epilepsy /seizure ,withdrawal of the drugs
 Blood tests
 Glucose, Electrolytes, LFT, RFT .
 To stop the seizures as quickly as possible.
 To ensure adequate cerebral oxygenation
 To maintain the patient in a seizure-free state.
Emergency supportive measures:
• Keep Airway patent and maintain breathing
• Secure IV line and take blood for lab
• Give glucose
Emergency Supportive measures.
 Keep airway patent and maintain breathing.
 secure IV line
 Take blood for laboratory investigation.
2. Control the seizure with anticonvulsant.
Diazepam IV 5-10mgIV.
Phenoytoin 20 mg/min if seizure continues.
General anesthesia with phentobarbitol, if seizure becomes
refractory.
Nursing Management
 The patient is turned to a side-lying position if possible to
assist in draining pharyngeal secretions.
 Suction equipment must be available because of the risk for
aspiration.
 During seizures, the patient should be protected from injury
using seizure precautions and monitored closely.
 No effort should be made to restrain movements.
 The patient having seizures can inadvertently injure nearby
people, so nurses should protect themselves
 Hypoxia
 Metabolic acidosis
 Hypotension
 Hyperthermia
 Irreversible neuronal injury
 Hypoglycemia
 Headache, or cephalgia is one of the most common of all
human physical complaints.
 Headache is a symptom; it indicate
 Organic disease (neurologic or other disease),
 A stress response,
 Vasodilatation (migraine),
 Skeletal muscle tension (tension headache), or a
combination of factors.
 The headache is preceded by a rise in plasma serotonin
which dilates the cerebral vessels.
 A primary headache no organic cause can be identified.
include
• Migraine,
• Tension-type, and
• Cluster headache.
 A secondary headache is a symptom associated with an
organic cause, such as a brain tumor or an aneurysm.
Migraine
 Is a symptom complex characterized by periodic and
recurrent attacks of severe headache.
◦ The cause is not clearly demonstrated, but
◦ it is primarily a vascular disturbance that occurs more
commonly in women and
 The typical time of onset is puberty, and the incidence is
highest in adults 20 to 35 years of age.
 It is triggered by
• Menstrual cycles
• Bright lights
• Stress
• Depression
• Sleep deprivation
• Fatigue
• Overuse of certain medications, and
• Certain foods containing tyramine, monosodium glutamate,
nitrites, or milk products.
 Use of oral contraceptives may be associated with
increased frequency and severity of attacks in some
women
 The Clinical Manifestations divided into four phases:
prodrome, aura, the headache, and recovery (headache
termination and postdrome).
 Prodrome. symptoms include
 Depression
 Irritability
 Feeling cold
 Anorexia
 Change in activity level
 Increased urination
 Diarrhea
2. Aura Phase.
▪ Is characterized by focal neurologic symptoms such as
▪ Visual disturbances (i.e, light flashes and bright
spots) are common and may be
▪ Hemianopic (affecting only half of the visual field).
▪ Numbness and tingling of the lips, face, or hands;
▪ Mild confusion;
▪ Slight weakness of an extremity;
▪ Drowsiness; and dizziness.
▪ Usually lasts less than an hours
3. Headache Phase
 As vasodilation and a decline in serotonin levels occur, a
throbbing headache intensifies over several hours.
 headache is severe and devastating and is often associated
with photophobia, nausea, and vomiting.
 Its duration varies, ranging from 4 to 72 hours.
4. Recovery Phase.
 In the recovery phase
• The pain gradually subsides.
• Muscle contraction in the neck and scalp is common,
with associated muscle ache and localized tenderness,
exhaustion, and
• Mood changes.
• Physical exertion exacerbates the headache pain.
• Sleep for extended periods.
Medical Management
 Therapy for migraine headache is divided into abortive
(symptomatic) and preventive approaches.
 The triptans, serotonin receptor agonists, are the most
specific ant migraine agents available.
 These agents cause vasoconstriction, reduce inflammation,
and may reduce pain transmission.
Tension headaches
 Tend to be more chronic than severe and are probably the
most common type of headache.
 Emotional or physical stress may cause contraction of the
muscles in the neck and scalp, resulting in tension
headache.
 The tension headache is characterized by
◦ A steady, constant feeling of pressure that usually
begins in the forehead, temple, or back of the neck.
◦ It is often band like or may be described as “a weight
on top of my head.”
 The medical management of an acute attack of tension
headaches may include 100% oxygen by face mask for 15
minutes, ergotamine tartrate, sumatriptan, or steroids
Cluster headaches
 severe forms of vascular headache.
 The pathophysiology of cluster headache is not fully
understood.
 Cluster headaches are unilateral and come in clusters of
one to eight daily, with excruciating pain localized to the
eye and orbit and radiating to the facial and temporal
regions.
 The pain is accompanied by watering of the eye and nasal
congestion.
 Inhalation of 100% oxygen
 NSAID
 Sumatriptan
 Preventions/prophylactic therapy
 Prednisolone , Lithium, Methysergide, Ergotamine, Sodium
valproate and verapamil
➢Cerebrovascular disorders (stroke)- term that refers to
any functional abnormality of the central nervous
system (CNS) that occurs when the normal blood
supply to the brain is disrupted.
➢It is third commonest cause of death in developed world
➢Following Coronary heart diseases and cancer.
➢It is a leading cause of disability.

Etiologic classification
Ischemic Hemorrhagic
CAUSES
 Large artery thrombosis
 Small penetrating artery ❖ Intracerebral hemorrhage
thrombosis ❖ Subarachnoid hemorrhage
 Cardiogenic embolic • Cerebral aneurysm
 Accounts  80% - 85% • Arteriovenous malformation
❖ Accounts  15% - 20%
can be divided into two major categories:
 ischemic stroke(85%), in which vascular occlusion and
significant hypoperfusion occur.
 it is termed “brain attack”
 It is a sudden loss of function resulting from disruption of
the blood supply to a part of the brain.
 Are subdivided in to different types
according to their cause:
A,THROMBOTIC(61%)
• large artery thrombosis : resulting from
narrowing of cerebral arteries due to
atherosclerosis.
• small penetrating artery thrombosis Also
called lacunar strokes b/c cavity created.
B. cardiogenic embolic stroke
• Areassociated with cardiac dysrhythmias,usually atrial
fibrillation.
• Emboli originate from the heart and circulate to the
cerebral vasculature.
• Most commonly the left middle cerebral artery
C,Cryptogenic and others
 strokes, which have no known cause.
D, Other strokes, can be from drugs - cocaine use,
coagulopathies,
Types
Embolic Thrombotic
❑ Blood clot travels to ❑Blood flow is blocked

the brain to the brain
14
8
Classification Coverage
1 Small penetrating artery 25%

thrombosis
2 Large artery thrombosis 20%
3 Cardiogenic embolic stroke 20%
4 Cryptogenic 30%
5 Other 5%
 Disruption of the cerebral blood flow
 Complex series of cellular metabolic events
 (ischemic cascade)
 Ischemic cascade begins when cerebral blood flow falls to
less than 25 ml/100 g/min.
 At this point, neurons can no longer maintain aerobic
respiration.
 Early in the cascade, an area of low cerebral blood flow
exists around the area of infarction.
 Sudden numbness or weakness of face, arm, or
leg(especially on one side of the body)
 Sudden confusion, trouble speaking, or understanding
 Sudden trouble seeing in one or both eyes
 Sudden trouble walking, dizziness, loss of balance, or
coordination
 Sudden severe headache with no known cause
 Numbness or weakness of the face, arm, or leg, especially on
one side of the body
 Confusion or change in mental status
 Trouble speaking or understanding speech
 Visual disturbances
 Difficulty walking, dizziness, or loss of balance or coordination
 Sudden severe headache
 Hemiplegia (paralysis of one side of the body)
 Hemiparesis, or weakness of one side of the body
Assessment and Diagnostic Findings
• Careful history and a complete physical and neurologic
examination.
• CT scan or MRI
• Prothrombin time, Platelet count
 Platelet-inhibiting medications (aspirin, clopidogrel)
decrease the incidence of cerebral infarction.
Surgical Management
 Carotid endarterectomy: is the removal of an
atherosclerotic plaque or thrombus from the carotid artery
to prevent stroke in patients with occlusive disease of the
extra cranial cerebral arteries.
Hemorrhagic (15%), in which there is extravasation of blood into
the brain.
1. intracranial hemorrhage
 Mainly associated with unrecognized or poorly controlled
hypertention.
2. subarachnoid hemorrhage.
 from ruptured intracranial aneurysm, or certain medications
(eg, anticoagulants and amphetamine)
 Patients generally have more severe deficits and a longer
recovery time compared to those with ischemic stroke .
 is a much common cause of stroke in developing countries
Intracerebral hemorrhage
 An intracerebral hemorrhage, or bleeding into the brain
 common in patients with hypertension and cerebral
atherosclerosis because degenerative changes from these
diseases cause rupture of the vessel.
 due to certain types of arterial pathology, brain tumor, and
the use of medications (oral anticoagulants, amphetamines,
and illicit drugs such as crack and cocaine).
 The bleeding is usually arterial and occurs most commonly
in the cerebral lobes, basal ganglia, thalamus, brain stem
(mostly the pons), and cerebellum.
 Interruption of further brain damage.
 Management of complication
 Admit the patients where close follow up can be given.
 continue follow up and maintenance of vital functions.
 Airway and ventilation.
 Controlling of blood pressure.
 Controlling body temperature.
 Fluid administration/hydration
 Adequate oxygenation of blood to the brain is
necessary to minimize cerebral damage.
 Blood pressure and cardiac output must be maintained
to sustain cerebral blood flow, and hydration
(intravenous fluids)
 Oxygen therapy, if necessary, should be given at an
adequate perfusion pressure.
 The patient is placed in a lateral or semiprone position
with the head of the bed slightly elevated to lower
cerebral venous pressure.
 Endotracheal intubation and mechanical ventilation
are necessary for patients with massive stroke
 If the patient is comatose or has impaired mental status
 changing the patients position every 2 hrs and avoid the
occurrence of bed sores.
 bladder and bowel care: if the patient has incontinence-
Inserting catheter.
 Infections such as aspiration pneumonia should be treated
with antibiotics.
Anti-platelet aggregation agents.
 Aspirin reduces the incidence of stroke and vascular mortality.

 General recommendation is to give 325 mg of ASA once daily.
 It may not help to resolve the already formed thrombus, but
ASA prevents recurrence of stroke.
Anticoagulants:
 use of Heparin or Warfarin .
 Low dose heperin can give for prevention of thromboembolism
 continue supportive measures.
 control very high blood pressure.
 surgical consultation is indicated for removing cerebelar
hematoma, as it may compress vital centers in the
brainstem.
 If patient is hypertensive
 Short acting antihypertensive drugs are preferred.
hydralazine 5-10 mg initial dose iv
 Diuretics to reduce cerebral edema
Subarachnoid Hemorrhage
✓ supportive measures include bed rest, sedatives,
analgesis, laxative.
✓ control of hypertension and
✓ Nifidipin (calcium channel blocker) is given to prevent
neurologic deterioration due to vasopasm.
Prevention of further stroke:
 control of hypertension.
 control blood sugar in diabetics.
 cessation of smoking.
 physical activity and weight reduction
Complications
• Cerebral Hypoxia and Decreased Blood Flow
• Increased ICP
• Vasospasm
• Systemic Hypertension
Head Injuries
 Head injury is a broad classification that includes injury to
the scalp, skull, or brain.
Scalp injury
◦ Isolated scalp trauma is generally classified as a minor head
injury.
◦ Trauma may result in an abrasion (brush wound), contusion,
laceration, or hematoma beneath the layers of tissue of the scalp
(subgaleal hematoma).
 The area is irrigated before the laceration is sutured to
remove foreign material and to reduce the risk for
infection.
 Subgaleal hematomas (hematomas below the outer
covering of the skull) usually absorb on their own and do
not require any specific treatment.
Skull fractures
 Skull fracture is a break in the continuity of the skull
caused by forceful trauma. It may occur with or without
damage to the brain.
 Skull fractures are classified as linear, comminuted,
depressed, or basilar.
 A fracture may be open, indicating a scalp laceration or
tear in the dura (eg, from a bullet), or closed, in which the
dura is intact
 Persistent, localized pain usually suggests that a
fracture is present.
 Basal skull fractures are suspected when cerebrospinal
fluid leaks from the ears (CSF otorrhea) and the nose
(CSF rhinorrhea).
 A halo sign (a bloodstain surrounded by a yellowish
stain) may be seen on bed linens or the head dressing
and is highly suggestive of a CSF leak.
 Drainage of CSF is a serious problem because meningeal
infection can occur if organisms gain access to the cranial
contents through the nose, ear, or sinus through a tear in the
dura.
 Bloody CSF suggests a brain laceration or contusion.
◦ Physical examination and evaluation of neurologic status
◦ Skull x-rays
◦ CT scanning
◦ MRI
Medical Management
 Non depressed skull fractures generally do not require
surgical treatment; however, close observation of the
patient is essential.
 In fractures involving the base of the skull the
nasopharynx and the external ear should be kept clean.
 Usually a piece of sterile cotton is placed loosely in the
ear, or a sterile cotton pad may be taped loosely under the
nose or against the ear to collect the draining fluid
 The patient who is conscious is cautioned against sneezing
or blowing the nose.
 The head is elevated 30 degrees to reduce ICP and promote
spontaneous closure of the leak.
 Depressed skull fractures need surgical treatment
 Persistent CSF rhinorrhea or otorrhea usually requires

surgical intervention.
 IV Antibiotic to prevent infection

Brain Injury
 Damage to the brain from traumatic injury takes two forms:
primary injury and secondary injury.
 Primary injury is the initial damage to the brain that results
from the traumatic event. This may include contusions,
lacerations, and torn blood vessels from impact,
acceleration/deceleration, or foreign object penetration.
 Secondary injury evolves over the ensuing hours and days after
the initial injury and is due primarily to brain swelling or
ongoing bleeding.
 Closed (blunt) brain injury occurs when the head accelerates
and then rapidly decelerates or collides with another object
(eg, a wall or dashboard of a car) and brain tissue is damaged,
but there is no opening through the skull and dura.
 Open brain injury occurs when an object penetrates the
skull, enters the brain, and damages the soft brain tissue in its
path (penetrating injury), or when blunt trauma to the head is
so severe that it opens the scalp, skull, and dura to expose the
brain.
Concussion
 Is shaking of the brain
 A concussion generally involves a period of unconsciousness

lasting from a few seconds to a few minutes.
 If the brain tissue in the frontal lobe is affected, the patient may
◦ exhibit bizarre
◦ irrational behavior,
 whereas involvement of the temporal lobe can produce temporary
◦ amnesia or disorientation.
 Treatment involves observing the patient for headache, dizziness,
lethargy, irritability, and anxiety.
Contusion
 Cerebral contusion is a more severe injury in which the
brain is damaged, with possible surface hemorrhage.
 Clinical signs and symptoms depend on the size of the
contusion and the amount of associated cerebral
edema.
 The patient may
◦ lie motionless, with a faint pulse,
◦ shallow respirations, and
◦ cool, pale skin.
◦ involuntary evacuation of the bowels and the bladder.
 Residual headache and vertigo are common, and impaired
mental function or seizures may occur as a result of
permanent cerebral damage.
Intracranial Hemorrhage
 Hematomas (collections of blood) that develop within the

cranial vault are the most serious brain injuries.
 A hematoma may be epidural (above the dura), subdural

(below the dura), or intracerebral (within the brain).
 Major symptoms are frequently delayed until the

hematoma is large enough to cause distortion of the brain
and increased ICP.
Epidural hematoma
 After a head injury, blood may collect in the epidural
(extradural) space between the skull and the dura
 This often results from fractures of the skull that cause
rupture or laceration of the middle meningeal artery,
which runs between the dura and the skull located just
inferior to a thin portion of temporal bone; hemorrhage
from this artery causes pressure on the brain
 An epidural hematoma is considered an extreme
emergency; marked neurologic deficit or even respiratory
arrest can occur within minutes.
 Treatment consists of making openings through the skull
(burr holes) to decrease ICP emergently, remove the clot,
and control the bleeding.
 A craniotomy may be required to remove the clot and
control the bleeding.
 A drain is usually inserted after creation of burr holes or a
craniotomy to prevent reaccumulation of blood.
Subdural hematoma
A subdural hematoma is a collection of blood between the
dura and the brain, a space normally occupied by a thin
cushion of fluid
 The most common cause of subdural hematoma is trauma,
but it may also occur from coagulopathies or rupture of an
aneurysm.
 is more frequently venous in origin and is due to the rupture
of small vessels that bridge the subdural space.
 may be acute, sub acute, or chronic, depending on the size
of the involved vessel and the amount of bleeding present.
Acute subdural hematomas
 Are associated with major head injury involving contusion
or laceration.
 Clinical symptoms develop over 24 to 48 hours.
 Signs and symptoms include changes in the level of
consciousness (LOC), pupillary signs, and hemiparesis.
 may be minor or even no symptoms with small collections
of blood.
 Coma, increasing blood pressure, decreasing heart rate, and
slowing respiratory rate are all signs of a rapidly expanding
mass requiring immediate intervention.
Subacute subdural hematomas
 Are the result of less severe contusion and head trauma.
 Clinical manifestations usually appear between 48 hours
and 2 weeks after the injury.
 Signs and symptoms are similar to those of an acute
subdural hematoma.
 If the patient can be transported rapidly to the hospital, an
immediate craniotomy is performed to open the dura,
allowing the subdural clot to be evacuated.
Chronic subdural hematomas
 Can develop from seemingly minor head injuries and are
seen most frequently in the elderly.
 The elderly are prone to this type of head injury secondary
to brain atrophy, which is an expected consequence of the
aging process.
 A chronic subdural hematoma resembles other conditions
and may be mistaken for a stroke.
 The bleeding is less profuse and there is compression of
the intracranial contents
 The blood within the brain changes in character in 2 to 4
days, becoming thicker and darker.
 In a few weeks, the clot breaks down and has the color and
consistency of motor oil.
 The brain adapts to this foreign body invasion, and the
clinical signs and symptoms fluctuate.
 There may be severe headache, which tends to come and
go; alternating focal neurologic signs; personality changes;
mental deterioration; and focal seizures.
 The treatment of a chronic subdural hematoma consists of
surgical evacuation of the clot.
 The procedure may be carried out through multiple burr
holes, or a craniotomy may be performed for a sizable
subdural mass that cannot be suctioned or drained through
burr holes.
Intracerebral hematoma
 Intracerebral hemorrhage is bleeding into the substance of
the brain.
 It is commonly seen in head injuries when force is exerted
to the head over a small area (bullet wounds; stab injury).
 These hemorrhages within the brain may also result from
systemic hypertension, which causes degeneration and
rupture of a vessel; rupture of a saccular aneurysm; vascular
anomalies; intracranial tumors; systemic causes, including
bleeding disorders such as leukemia, hemophilia, aplastic
anemia, and thrombocytopenia; and complications of
anticoagulant therapy.
 Surgical intervention by craniotomy or brain debridement
permits removal of the blood clot and control of hemorrhage.
Spinal Cord Injury
 Spinal cord injury (SCI) is a major health problem.
 The predominant risk factors for SCI include age, gender,
and alcohol and drug use.
 The vertebrae most frequently involved in SCI are the 5th,
6th, and 7th cervical (neck), the 12th thoracic, and the 1st
lumbar vertebrae.
 These vertebrae are the most susceptible because there is a
greater range of mobility in the vertebral column in these
areas.
Pathophysiology
 Damage to the spinal cord ranges from transient concussion to
contusion, laceration, and compression of the cord substance to
complete transection of the cord.
 SCIs can be separated into two categories: primary injuries and

secondary injuries.
 Primary injuries are the result of the initial insult or trauma and
are usually permanent.
 Secondary injuries are usually the result of a contusion or tear

injury, in which the nerve fibers begin to swell and disintegrate
 A secondary chain of events produces ischemia, hypoxia,
edema, and hemorrhagic lesions, which in turn result in
destruction of myelin and axons.
 These secondary reactions, believed to be the principal
causes of spinal cord degeneration at the level of injury,
are now thought to be reversible 4 to 6 hours after injury.
 Manifestations depend on the type and level of injury.
 The type of injury refers to the extent of injury to the
spinal cord itself.
 Incomplete spinal cord lesions are classified according to
the area of spinal cord damage: central, lateral, anterior, or
peripheral.
 “Neurologic level” refers to the lowest level at which
sensory and motor functions are normal.
 Below the neurologic level, there is total sensory and
motor paralysis, loss of bladder and bowel control (usually
with urinary retention and bladder distention), loss of
sweating and vasomotor tone, and marked reduction of
blood pressure from loss of peripheral vascular resistance.
 A complete spinal cord lesion can result in paraplegia
(paralysis of the lower body) or quadriplegia (paralysis of
all four extremities).
 Often the patient speaks of fear that the neck or back is
broken.
 A detailed neurologic examination is performed.
 Diagnostic x-rays (lateral cervical spine x-rays) and CT
scanning are usually performed initially.
 An MRI scan may be ordered
Management of Spinal Cord Injuries
 Pharmacologic therapy
◦ In some studies, the administration of high-dose
corticosteroids, specifically methylprednisolone, has
been found to improve motor and sensory outcomes if
given within 8 hours of injury.
 Respiratory therapy
 Oxygen is administered to maintain a high arterial
PO2
 If endotracheal intubation is necessary, extreme care
Should be taken.
 Skeletal fracture reduction and traction
• Management of SCI requires immobilization and reduction of
dislocations (restoration of normal position) and stabilization of the
vertebral column.
• Traction is applied to the tongs by weights, the amount depending
on the size of the patient and the degree of fracture displacement.
• Reduction usually takes place after correct alignment has been
restored.
Surgical Management
 Surgery is indicated in any of the following instances:
• Compression of the cord is evident.
• The injury results in a fragmented or unstable vertebral body.
• The injury involves a wound that penetrates the cord.
• There are bony fragments in the spinal canal.
• The patient’s neurologic status is deteriorating.
MENINGITIS
 Meningitis is an inflammation of the meninges, the
protective membranes that surround the brain and spinal
cord.
 Meningitis is classified as aseptic or septic.
 In aseptic meningitis, bacteria are not the cause of the
inflammation; the cause is viral or secondary to lymphoma,
leukemia, or brain abscess.
Risk Factors
◦ Tobacco use and viral upper respiratory infections (Otitis media
and mastoiditis)
◦ Persons with immune system deficiencies]
Pathophysiology
◦ Meningeal infections generally originate in one of two ways:
1. through the bloodstream as a consequence of other infections,
or
2. by direct extension, such as might occur after a traumatic
injury to the facial bones, or secondary to invasive procedures.
◦ Once the causative organism enters the bloodstream, it crosses the
blood–brain barrier and causes an inflammatory reaction in the
meninges.
◦ Headache and fever are frequently the initial symptoms.
 Fever tends to remain high throughout the course of the
illness.
 Signs of meningeal irritation:
◦ Neck rigidity (stiff neck) is an early sign.
◦ Any attempts at flexion of the head are
difficult because of spasms in the muscles of
the neck. Forceful flexion causes severe pain.
◦ Positive Kernig’s sign: When the patient is
lying with the thigh flexed on the abdomen,
the leg cannot be completely extended.
 Positive Brudzinski’s sign: When the patient’s neck is
flexed, flexion of the knees and hips is produced; when
passive flexion of the lower extremity of one side is
made, a similar movement is seen in the opposite
extremity.
 Seizures and increased intracranial pressure (ICP) are
also associated with meningitis
20
by sindew M lecturer (AMU) 2/20/2024 4
 History and Physical examination
 CSF analysis
 CT scanning or MIR
Medical Management
 Penicillin antibiotics (eg, ampicillin, piperacillin) or one
of the cephalosporin's (eg, ceftriaxone , cefotaxime
sodium) may be used.
 Vancomycin hydrochloride alone or in combination with
rifampcin may be used if resistant strains of bacteria are
identified
 High doses of the appropriate antibiotic are administered
intravenously.
 Dexamethasone has been shown to be beneficial as

adjunct therapy in the treatment of acute bacterial
meningitis and in pneumococcal meningitis if given 15
to 20 minutes before the first dose of antibiotic and every
6 hours for the next 4 days.
 Dehydration and shock are treated with fluid volume

expanders.
Nursing Management
• Neurologic status and vital signs are continually assessed.
• Pulse oximetry and arterial blood gas values are used to quickly
identify the need for respiratory support as the increasing ICP
compromises the brain stem.
• Insertion of a cuffed endotracheal tube (or tracheotomy) and
mechanical ventilation may be necessary to maintain adequate
tissue oxygenation.
• Rapid intravenous (IV) fluid replacement may be prescribed,
but care is taken to prevent fluid overload.

HERPES SIMPLEX VIRUS ENCEPHALITIS
 Encephalitis is an acute inflammatory process of the brain
tissue.
 Herpes simplex virus (HSV) is the most common cause of
acute encephalitis.
 There are two herpes simplex viruses, HSV-1 and HSV-2.
 HSV-1 typically affects children and adults and HSV-2
most commonly affects neonates
Pathophysiology
 There are two possible modes of HSV-1 infection.
 In most cases, primary HSV-1 infection of the buccal
mucosa occurs, followed by retrograde spread along the
trigeminal nerve to the brain.
 It is also believed that latent virus in brain tissue may
reactivate and result in encephalitis.
 The initial symptoms include fever, headache, confusion,
and behavioral abnormalities.
 The EEG demonstrates a specific wave pattern
 CSF analysis reveals a high opening pressure and low
glucose and high protein levels.
 MRI is the neuroimaging study of choice in the diagnosis
of HSV encephalitis as it can help identify lesions in the
temporal lobe.
Medical Management
 Acyclovir (Zovirax), an antiviral agent, is the medication
of choice in HSV treatment.
 The mode of action is the inhibition of viral DNA
replication.
 It is usually well tolerated by the patient.
 To prevent relapse, treatment should continue for up to 3
weeks
 Autoimmune nervous system disorders include
multiple sclerosis, myasthenia gravis, and
Guillain-Barré syndrome.
MULTIPLE SCLEROSIS
 Chronic, progressive, degenerative disorder of the CNS
characterized by disseminated demyelization of nerve
fibers of the brain and spinal cord
 Multiple sclerosis (MS) is an immune-mediated
progressive demyelinating disease of the CNS.
 Demyelination refers to the destruction of myelin,
 it results in impaired transmission of nerve impulses.
 MS typically presents in young adults ages 20 to 40, and it

affects women more frequently than men.
 Autoimmune activity results in demyelination, but the
sensitized antigen has not been identified
 Genetic predisposition is indicated by the presence of a
specific cluster (haplotype) of human leukocyte antigens
(HLA) on the cell wall.
Pathophysiology
 Sensitized T cells typically cross the blood–brain barrier;
 their function is to check the CNS for antigens and then
leave.
 In MS, the sensitized T cells remain in the CNS and
promote the infiltration of other agents that damage the
immune system
 The immune system attack leads to inflammation that
destroys myelin (which normally insulates the axon and
speeds the conduction of impulses along the axon) and
oligodendroglial cells that produce myelin in the CNS.
 Plaques of sclerotic tissue appear on demyelinated axons,
further interrupting the transmission of impulses
 Demyelinated axons are scattered irregularly throughout
the CNS.
 The areas most frequently affected are the
• Optic nerves,
• Chiasm, and
• Tracts; the cerebrum;
• The brain stem and
• Cerebellum; and
• The spinal cord.
 The primary symptoms most commonly reported are
◦ Fatigue, Spinal chord involvement
◦ Depression,
◦ Weakness,
◦ Numbness,
◦ Difficulty in coordination, Cerebellum
◦ Loss of balance, and pain.
 Visual disturbances due to lesions in the optic nerves or
their connections may include blurring of vision,
diplopia, and total blindness.
 Relapses may be associated with periods of emotional
and physical stress.
 MRI is the primary diagnostic tool for visualizing plaques.
Medical Management
 No cure exists for MS.
 The goals of treatment are to delay the progression of the disease,

manage chronic symptoms, and treat acute exacerbations.
 Three medications, referred to as the “ABC (and R) drugs,” are
currently the main pharmacologic therapy for MS.
 The interferons beta-1a (Avonex) and beta-1b (Betaseron) reduce
the frequency of relapse by 30% and decrease the appearance of
new lesions on MRI by 80%.
 Glatiramer acetate (Copaxone) also reduces the number of lesions
on MRI and the relapse rate.
MYASTHENIA GRAVIS
 Myasthenia gravis, an autoimmune disorder affecting the
monaural junction,
 is characterized by varying degrees of weakness of the
voluntary muscles.
 Women tend to develop the disease at an earlier age (20 to
40 years of age) compared to men (60 to 70 years of age),
and women are affected more frequently.
Pathophysiology
 In myasthenia gravis, auto antibodies directed at the
acetylcholine receptor sites
 Impair transmission of impulses across the myoneural
junction.
 Therefore, fewer receptors are available for stimulation,
 Resulting in voluntary muscle weakness that escalates with
continued activity.
 The initial manifestation of myasthenia gravis usually
involves
◦ the ocular muscles.
◦ Diplopia (double vision) and
◦ Ptosis (drooping of the eyelids) are common.
 Laryngeal involvement produces dysphonia (voice

impairment) and increases the patient’s risk for choking and
aspiration.
 Myasthenia gravis is purely a motor disorder with no effect
on sensation or coordination
Medical Management
 Anticholinesterase agents :Eg. Pyridostigmine bromide
(Mestinon) and neostigmine bromide (Prostigmin).
 Corticosteroids: Prednisone and dexamethasone.
 Cytotoxic medications : Azathioprine (Imuran),
cyclophosphamide (Cytoxan), and cyclosporine
SURGICAL MANAGEMENT
 Thymectomy (surgical removal of the thymus gland) can
produce antigen-specific immunosuppression
Nursing Management
• The patient is taught strategies to conserve energy.
• To minimize the risk of aspiration, mealtimes should
coincide with the peak effects of anticholinesterase
medication.
• In case of ptosis , to prevent corneal damage when
the eyelids do not close completely, the patient is
instructed to tape the eyes closed for short intervals
and regularly instill artificial tears.
• If the patient cannot swallow, nasogastric tube
feedings may be prescribed
GUILLAIN-BARRÉ SYNDROME
 Guillain-Barré syndrome is an autoimmune attack of the
peripheral nerve myelin.
 The result is acute, rapid segmental demyelination of
peripheral nerves and some cranial nerves, producing
ascending weakness with dyskinesia (inability to execute
voluntary movements), hyporeflexia, and paresthesias
(numbness).
 In 66% of cases, there is a predisposing event, most
often a respiratory or gastrointestinal infection,
although vaccination, pregnancy, and surgery have also
been identified as antecedent events.
 The antecedent event usually occurs 2 weeks before
symptoms begin.
Pathophysiology
• Guillain-Barré is the result of a cell-mediated immune
attack on peripheral nerve myelin proteins.
• The best-accepted theory is that an infectious organism
contains an amino acid that mimics the peripheral nerve
myelin protein.
• The immune system cannot distinguish between the two
proteins and attacks and destroys peripheral nerve
myelin.
• Weakness and diminished reflexes of the lower extremities.
• Quadriplegia
• Demyelination of the nerves that innervate the diaphragm and
intercostal muscles results in neuromuscular respiratory failure.
• Optic nerve demyelination may result in blindness.
• Glossopharyngeal and vagus nerve demyelination results in an
inability to swallow or clear secretions.
 Medical Management
• Guillain-Barré is a medical emergency,
requiring intensive care unit management.
• Respiratory therapy or mechanical ventilation
may be necessary to support pulmonary
function and adequate oxygenation.
• Plasma pheresis and IV
• Both therapies decrease circulating antibody levels
TRIGEMINAL NEURALGIA (TIC DOULOUREUX)
 Trigeminal neuralgia is a condition of the fifth cranial
nerve characterized by paroxysms of pain in the area
innervated by fifth cranial nerve .
 The pain ends as abruptly as it starts and is described as a
unilateral shooting and stabbing sensation.
 Associated involuntary contraction of the facial muscles
can cause sudden closing of the eye or a twitch of the
mouth, hence the name tic douloureux (painful twitch).
Cause
 Uncertain
 Chronic compression or irritation of the trigeminal
nerve
C/M
 Pain on face
 Pain stimulated by washing the face, shaving, brushing
the teeth, eating, and drinking.
 A draft of cold air and direct pressure against the nerve
trunk may also cause pain
Medical Management
• Antiseizure agents, such as carbamazepine
(Tegretol), relieve pain in most patients with
trigeminal neuralgia by reducing the
transmission of impulses at certain nerve
terminals.
• Carbamazepine is taken with meals.
• The patient is monitored for bone marrow
depression during long term therapy.
SURGICAL MANAGEMENT
◦ Micro vascular Decompression of the
Trigeminal Nerve
BELL’S PALSY
◦ Bell’s palsy (facial paralysis) is due to unilateral
inflammation of the seventh cranial nerve, which
results in weakness or paralysis of the facial muscles
on the affected side.
Couse
◦ unknown,
◦ possible causes may include vascular ischemia, viral
disease (herpes simplex, herpes zoster), autoimmune
disease, or a combination of all of these factors.
C/M
• increased lacrimation (tearing);
• painful sensations in the face, behind the ear, and
in the eye
• speech difficulties and may be unable to eat on
the affected side
 The patient may be unable to close the eyelid,
 Un able to wrinkle the forehead, smile, raise the eyebrow,
or close the lips effectively.
 The mouth is pulled toward the unaffected side
 Other vague initial symptoms are dry eye or tingling
around the lips with progression to the more recognizable
symptoms
 Drooling of saliva occurs, and the affected eye has
constant tearing.
 Sense of taste is lost over the anterior two-thirds of the
tongue.
 Speech difficulties are present.
 Fifty percent of these patients will have complete recovery
in a short period of time.
 Thirty five percent will have full recovery in less than 1
year
Management
• Corticosteroid therapy
• Facial pain is controlled with analgesic agents.
• Heat may be applied to the involved side of the face to promote
comfort and blood flow through the muscles.
• Electrical stimulation may be applied to the face to prevent muscle
atrophy.
 Moist heat with gentle massage to the face and ear also
eases pain.
 Provide warm, moist compresses prn.
 Massage face.
 Assist with facial exercises several times a day.
 Provide frequent mouth care
PARKINSON’S DISEASE
◦ Parkinson’s disease is a slowly progressing neurologic
movement disorder that eventually leads to disability.
◦ Parkinson’s disease affects men more frequently than
women.
Cause
◦ Unknown,
◦ Possible causative factors, including genetics,
atherosclerosis, excessive accumulation of oxygen free
radicals, viral infections, head trauma, chronic
antipsychotic medication use, and some environmental
exposures.
Pathophysiology
 The substantia nigra is a group of cells located within the
basal ganglia, which is situated deep within the brain.
 These cells are responsible for the production of
dopamine, an inhibitory neurotransmitter.
 Dopamine facilitates the transmission of impulses from
one neuron to another.
 Parkinson’s disease is caused by destruction of the cells of
the substantia nigra, resulting in decreased dopamine
production.
 Loss of dopamine function results in impairment of
semiautomatic movements.
 Acetylcholine, an excitatory neurotransmitter, is secreted
normally in individuals with Parkinson’s disease.
 The normal balance of acetylcholine and dopamine is
interrupted in these patients, causing a relative excess of
acetylcholine,
 which results in the tremor, muscle rigidity, and
bradyakinesia and loss of muscle movement) characteristic
of Parkinson’s disease.
 has a gradual onset and symptoms progress slowly .
 The three cardinal signs are tremor, rigidity, and
bradykinesia(abnormally slow movements).
 Other features include hypokinesia, gait disturbances, and
postural instability
TREMOR
• Resting tremor characteristically disappears with purposeful
movement but is evident when the extremities are motionless.
• The tremor may present as a rhythmic, slow turning motion of the
forearm and the hand and a motion of the thumb against the
fingers as if rolling a pill.
• Tremor is present while the patient is at rest; it increases when the
patient is walking, concentrating, or feeling anxious
 RIGIDITY
• Resistance to passive limb movement
characterizes muscle rigidity.
• Rigidity of the passive extremity increases
when another extremity is engaged in
voluntary active movement.
• Stiffness of the neck, trunk, and shoulders is
common.
• Early in the disease, the patient may
complain of shoulder pain.
BRADYKINESIA
• Hypokinesia (abnormally diminished movement) is also
common and may appear after the tremor.
• Micrographic (shrinking, slow handwriting) develops.
• The face becomes increasingly masklike and
expressionless and the frequency of blinking decreases.
• Dysphonia (soft, slurred, low-pitched, and less audible
speech)
Medical Management
 Antiparkinsonian medications act by:
1. Increasing striatal dopaminergic activity,
2. Reducing the excessive influence of excitatory
cholinergic neurons on the extrapyramidal tract, thereby
restoring a balance between dopaminergic and cholinergic
activities, or
3. Acting on neurotransmitter pathways other than the
dopaminergic pathway.Eg, Levodopa, carbidopa
 Anticholinergics Therapy
◦ Anticholinergics agents are effective in controlling tremor
and rigidity. They may be used in combination with
levodopa.
 Antiviral Therapy
◦ Amantadine hydrochloride (Symmetrel) is an antiviral
agent used in early Parkinson’s treatment to reduce
rigidity, tremor, and bradykinesia.
◦ It is thought to act by releasing dopamine from neuronal
storage sites.
 Dopamine Agonists
◦ Bromo criptine mesylate and pergolide (ergot derivatives) are
dopamine receptor agonists and are useful in postponing the
initiation of carbidopa or levodopa therapy.
 Monoamine Oxidase Inhibitors (MAO Inhibitors)

◦ These medications inhibits dopamine breakdown and is thought to
slow the progression of the disease.
 Antidepressants
◦ Tricyclic antidepressants (eg amitriptyline) may be
prescribed to alleviate the depression that is so common in
Parkinson’s disease.
 Antihistamines
◦ Diphenhydramine hydrochloride (Benadryl), orphenadrine
citrate (Banflex), and phenindamine hydrochloride (Neo-
Synephrine) have mild central anticholinergic and sedative
effects and may reduce tremors.
SURGICAL MANAGEMENT
◦ Thalamotomy and pallidotomy are effective in relieving
many of the symptoms of Parkinson’s disease.
◦ Huntington’s disease is a chronic, progressive, hereditary disease
of the nervous system that results in progressive involuntary chorei
form movement and dementia.
Pathophysiology
◦ The basic pathology involves premature death of cells in the
striatum of the basal ganglia, the region deep within the brain
involved in the control of movement.
• There is also loss of cells in the cortex, the region of
the brain associated with thinking, memory,
perception, and judgment, and in the cerebellum, the
area that coordinates voluntary muscle activity.
• Researchers now believe that a building block for
protein called glutamine abnormally collects in the
cell nucleus, causing cell death.
• The cells’ destruction results in a lack the
neurotransmitters gamma-amino butyric acid (GABA)
and acetylcholine, which inhibit nerve action.
• abnormal involuntary movement,
• Intellectual decline, and, often, emotional disturbance
• Speech is affected, becoming slurred, hesitant, often explosive,
and eventually unintelligible.
• Chewing and swallowing are difficult, and there is a constant
danger of choking and aspiration.
• Cognitive function is usually affected, with dementia usually
occurring.
• Bladder and bowel control is lost.
• Judgment and memory are impaired.
• Hallucinations, delusions, and paranoid thinking may be occurred.
Management
• Thiothixene hydrochloride (Navane) and haloperidol (Haldol),
which predominantly block dopamine receptors, improve the
chorea in many patients.
• Chorea also is lessened by Reserpine (depletes presynaptic
dopamine) and Tetrabenazine (reduces dopaminergic
transmission).
 Alzheimer’s disease is a progressive, irreversible,
degenerative neurologic disease that begins
insidiously and is characterized by gradual losses of
cognitive function and disturbances in behavior and
affect.
 Risk factors
◦ Advanced age; genetic factor
◦ Presence of Down syndrome
C/M
• Depression
• Anomia (cannot name objects)
• Loss of all voluntary activity
• Apathy, indifference, irritability
• Poor judgment in everyday activities
• Distractible; short attention span
• Wandering, hyperactivity, pacing, restlessness, agitation
• Disorientation to time, place, and person
• Loss of recent memory
 Medical Management
◦ Acetyl cholinesterase inhibitors (tacrine hydrochloride
(Cognex), donepezil (Aricept) and rivastigmine
(Exelon)): enhances acetylcholine uptake in the brain,
thus maintaining memory skills for a period of time
 The exact cause of post-polio syndrome is not known, but
researchers suspect that with aging or muscle overuse the
neurons not destroyed originally by the poliovirus cannot
continue generating axon sprouts.
 These new terminal axon sprouts reinnervated the affected
muscles following the initial insult but may be more
vulnerable as the body ages.
26
0
Management
◦ No specific medical or surgical treatment is available for this
syndrome.
◦ Patients need to plan and coordinate activities to conserve energy
and reduce fatigue.
◦ Rest periods should be planned and assistive devices used to
reduce weakness and fatigue.
26
1
 The cervical spine is subjected to stresses that result from
disk degeneration (from aging, occupational stresses) and
spondylosis (degenerative changes occurring in disk and
adjacent vertebral bodies).
 A cervical disk herniation usually occurs at the C5-6 and
C6-7 interspaces.
C/M
• Pain and stiffness may occur in the neck, the top of the
shoulders, and the region of the scapulae
• Paresthesia (tingling or a “pins and needles” sensation)
and numbness of the upper extremities.
• Cervical MRI usually confirms the diagnosis.
◦ Physical Examination
◦ MRI
Medical Management
◦ The goals of treatment are
1. to rest and immobilize the cervical spine to give
the soft tissues time to heal and
2. to reduce inflammation in the supporting tissues
and the affected nerve roots in the cervical spine.
◦ Bed rest (usually 1 to 2 days)
◦ Proper positioning on a firm mattress
◦ The cervical spine may be rested and immobilized by a
cervical collar, cervical traction, or a brace.
Pharmacologic therapy
◦ Analgesic
◦ Muscle relaxants
◦ Corticosteroids
Surgical management
◦ Surgical excision of the herniated disk (discectomy).
 Most lumbar disk herniations occur at the L4-5 or the L5-
S1 interspaces.
 Clinical Manifestations
• low back pain with muscle spasms
• Radiation of the pain into one hip and down into the leg .
• Pain is aggravated by actions that increase intraspinal fluid
pressure
• Weakness, alterations in tendon reflexes, and sensory loss
(paralysis).
 Assessment and Diagnostic Findings
• Physical Examination
• MRI
Medical Management
• The objectives of treatment are to relieve pain, slow disease
progression, and increase the patient’s functional ability.
• Bed rest for 1 to 2 days on a firm mattress
• NSAIDs and systemic corticosteroids
• Moist heat and massage
• Antidepressant agents
26
9
Surgical management
◦ Lumbar disk excision(discectomy ) through a
posterolateral laminotomy.
◦ Microdiscectomy
1. What are cardinal sign of parkinson’s disease?(2pt)
2. List two autoimmune disorder? (1pt)
3. What are medical management patient with lumbar
disk herniation?(2pt)
Approaching Patients with Disorders
of the Integumentary System
By: Belete N(BSc, MSc in AHN)

Jan 2024, AWHSC, DBU
MSN for Pediatrics and Surgical Nursing Students 1

Objectives
Describe the structure and function of the integumentary
system
Describe specific assessment to be made during P/E of the skin
Describe diagnostics modalities for skin disorders
Explain the etiology, C/M, medical and nursing management of

common integumentary disorders
Explain burn and related issues

The integumentary system is composed of
1. Skin
2. Hair (Protection, sensory perception, thermoregulation)
3. Nail (used for scratching or picking up objects)
4. Glands of skin
 Sebaceous glands (secrete sebum that lubricate hair and
skin)
 Sweat glands

Anatomy of the skin

Functions of the skin
Protection
Sensation
Fluid balance
Temperature regulation
Immune response function

Primary skin lesions
 Primary skin lesions are original lesions arising from previously normal
skin
Macule: Flat, non palpable skin color change

(< 1 cm, circumscribed border) E.g. Solar lentigo
Patch: Flat, non palpable skin color change

(>1 cm, may have irregular border)
Examples:Vitiligo , freckles, flat moles, petechia, rubella, port wine
stains, ecchymosis
Papule: Elevated, palpable, solid mass circumscribed border( <1cm)
Examples: Acne, Elevated nevi, warts, lichen planus, Eruptive xanthoma
Plaque: Elevated, palpable, solid mass circumscribed border

 It may be coalesced papules with flat top(>1cm)
Examples: Psoriasis, actinic keratosis
Nodule: Elevated, palpable, solid mass or cystic elevation >1 cm but <2 cm in
diameter extends deeper into the dermis than a papule
Examples: Lymphoma, squamous cell carcinoma, poorly absorbed injection,
dermatofibroma
Vesicle: Circumscribed, elevated, palpable mass containing serous fluid (< 1 cm)
Examples: Herpes simplex/zoster, chickenpox, poison ivy, second-degree
burn (blister)
Bulla: Larger blister, circumscribed, elevated lesion containing clear serous or
hemorrhagic fluid that is > 1 cm in diameter.
Examples: Pemphigus, contact dermatitis, large burn blisters, poison ivy,
bullous impetigo
Wheal: Elevated mass with transient borders (often irregular, size and color
vary) caused by movement of serous fluid into the dermis
Does not contain free fluid in a cavity (as, for example, a vesicle does)
Examples: Urticaria (hives), insect bites
Tumor : Elevated, palpable, solid mass or cystic elevation >2 cm in
diameter extends deeper into the dermis than a papule; tumors do not
always have sharp borders)
Examples: Larger lymphoma, carcinoma
Pustule: Pus-filled vesicle

Examples: Acne, impetigo, furuncles, carbuncles
Cyst: Encapsulated fluid-filled or semisolid mass in the subcutaneous

tissue or dermis
Examples: Sebaceous cyst, epidermoid cysts
 Pustule:Pus-filled vesicle or bull
 Examples:Acne,impetigo,furuncles,carbuncles
Cyst:Encapsulated fluid-filled or semisolid mass in the subcutaneous tissue or

dermis.
 Examples:Sebaceous cyst,epidermoid cysts

Secondary skin lesions
Secondary skin lesions result from changes in primary lesions
Erosion: Loss of superficial epidermis does not extend to dermis,

depressed, moist area)
Examples: ruptured vesicles, scratch marks.
Ulcer: Skin loss extending past epidermis, necrotic tissue loss, bleeding
and scarring possible
Examples: Stasis ulcer of venous insufficiency, pressure ulcer

Fissure: Linear crack in the skin, may extend to dermis
Examples: Chapped lips or hands, athlete’s foot
Scales: Flakes secondary to desquamated dead epithelium, flakes may

adhere to skin surface, Color varies (silvery, white), Texture varies (thick,
fine)
Examples: Dandruff, psoriasis, dry skin, pityriasis rosea
Crust: dried residue of serum, blood, or pus on skin surface

Examples: residue left after vesicle rupture: impetigo, herpes, eczema

Scar: skin mark left after healing of a wound or lesion
Represents replacement by connective tissue of the injured tissue
Young scars: red or purple
Mature scars: white or glistening
Examples: Healed wound or surgical incision
 Keloid: hypertrophied scar tissue

Secondary to excessive collagen formation during healing (elevated,
irregular, red)
Example: Keloid of ear piercing or surgical incision
Atrophy: Thin, dry, transparent appearance of epidermis.
Loss of surface markings, secondary to loss of collagen and elastin
Examples: Aged skin, arterial insufficiency
 Lichenification: Thickening and roughening of the skin

Accentuated skin markings
May be secondary to repeated rubbing, irritation, scratching.
Example: Contact dermatitis
Sinus: Channel that permits escape of pus or fluid

Assessment of the integument
Data obtained in the assessment provide the basis for identification

of actual or potential problems related to
Skin
Infections
Fluid and electrolyte balance
Nutritional imbalances
Inadequate tissue oxygenation

Assessment of the integument…
Patient history
Usual skin conditions
Usual appearance, colour, moisture, texture and integrity
Onset of the problem
Initial sites
Skin appearance at onset
Other symptoms during onset (pain, itching, discomfort…)

Changes since onset

Changes in location of lesions and appearance
Increase in size and new symptoms
Specific known cause
Contact with poisoning
Exposure to known allergen or stress

If cause is unknown

Recent exposure to sensitizing substances
• Metals, chemicals, detergents or poisonous plants
Use of drugs (penicillin…)
Occupation that may prone to skin conditions
Recreational activities (painting, camping or gardening )
Exposure to sun burn, frost bite

Alleviating factors
Medical or non medical (home remedies)
Psychological reaction to skin changes
Withdraw from social activities
Cosmetics for cover up
Previous trauma, surgery or prior skin disease

Physical Examinations
Skin can be examined by
Direct inspection and observation with adequate light
Palpation to gather data about certain types of lesions
General principles
Be prepared (privacy and comfort with adequate light)
Be systematic (head to toe)
Be thorough (address all body parts)
Be specific (inspection and then lesion specific examination)
Compare symmetrical parts
Record all data findings
Use appropriate technique
• Inspection
• Colour
• Redness, whiteness, bluish (cyanosis)
• Yellow (jaundice), brown (increased melanin deposits
• Lesion palpation for density, indurations, tenderness

Diagnostic evaluation for dermatologic problems
The diagnosis of a skin disorder is made chiefly by visual inspection, but some
skin disorders may require additional testing
A. Skin biopsy
A. Is performed to obtain tissue for microscopic examination
B. May be obtained by scalpel excision or by a skin punch instrument that
removes a small core of tissue
Indications
Biopsies are performed on skin nodules, plaques, blisters, and other
lesions
• To rule out malignancy and to establish an exact diagnosis
B. Skin scraping
Tissue samples are scraped from suspected fungal lesions with a
scalpel blade moistened with oil so that the scraped skin adheres to the
blade
The scraped material is transferred to a glass slide, covered with a
cover slip, and examined microscopically
 Indications
To diagnose Leprosy , Onchocerciasis , Leishmaniasis

C. Wood’s light examination
Wood’s light is a special lamp that produces long-wave ultraviolet rays, which
results in a characteristic dark purple fluorescence
The color of the fluorescent light is best seen in a darkened room, where it is
possible to differentiate epidermal from dermal lesions and hypo pigmented
and hyper pigmented lesions from normal skin
The patient is reassured that the light is not harmful to skin or eyes
Lesions that still contain melanin almost disappear under ultraviolet light,
whereas lesions that are devoid of melanin increase in whiteness with
ultraviolet light
D. Tzanck smear (Arnault Tzanck, Russian dermatologist, 1886-1954)
Used to examine cells from blistering skin conditions, such as herpes
zoster, varicella, herpes simplex, and all forms of pemphigus
The secretions from a suspected lesion are applied to a glass slide,
stained, and examined
E. Culture and sensitivity

To confirm the causative agent and drugs to which they are sensitive

F. Patch testing
Is performed to identify substances to which the patient has developed an
allergy
Involves applying the suspected allergens to normal skin under occlusive
patches
The development of redness, fine bumps, or itching is considered a weak
positive reaction
Fine blisters, papules, and severe itching indicate a moderately positive
reaction
Blisters, pain, and ulceration indicate a strong positive reaction
Common Diseases of the Skin
1. Inflammatory & allergic reactions of the Skin
 E.g. Pruritis/dermatitis, Acne & Hydradenitis suppurative
2. Bacterial skin infections ( Pyodermas)
E.g. Furuncles ,Carbuncles, Impetigo, Folliculitis.
3. Viral skin infections
E.g. Herpes zoster/Simplex, G.herpes, viral warts
4. Fungal (mycotic) skin infections
E.g. Tinea
5. Parasitic skin infestation.
E.g. Pediculosis ,scabies

6. Non infectious inflammatory dermatoses
E.g. Psoriasis, exfoliative dermatitis
7. Blistering diseases
E.g. Pemphigus, dermatitis herpetiformis, herpes gestationis
8. Toxic epidermal necrolysis & Stevens Johnsons Syndrome
9. Sepsis & ulceration
10. Benign tumors of the skin
E.g. Cyst, Actinic & Seborrheic keratosis, warts, keloids, dermatofibroma,
angiomas, lipoma & moles
11. Skin cancer
E.g. Basal & squamous carcinoma & malignant melanoma
12. Burn injury
Part I
Inflammatory & Allergic Reactions of the Skin

Dermatitis
Is an inflammation of the skin
It usually involves swollen, reddened and itchy skin
It is a common condition that isn't life-threatening or contagious
Causes
Allergies
Genetic factors
Physical and mental stress, and
Irritants can cause dermatitis

There are several types of dermatitis
Contact dermatitis
Neuro dermatitis
Seborrheic dermatitis
Stasis dermatitis
Atopic dermatitis (eczema)
Perioral dermatitis

Each has distinct signs and symptoms
Common signs and symptoms include redness, swelling, itching and skin
lesions
Neuro dermatitis
Typically develops in areas where something, such as a tight garment rubs
or scratches your skin
This irritation may lead you to rub or scratch your skin repeatedly in that
area
Common locations include ankles, wrist, outer forearm or arm, and the
back of your neck
Stasis dermatitis
Can occur when fluid accumulates in the tissues just beneath your
skin, & typically involves the lower leg
The extra fluid interferes with blood's ability to nourish the skin &
places extra pressure against the skin from underneath
Varicose veins & other chronic conditions that slow the return of
venous blood in legs often cause this fluid buildup

General mgt
Correcting the condition that causes fluid to accumulate in legs or ankles
Wearing elastic support hose or even having varicose vein surgery
Wet dressings to soften the thickened, fragile, skin & to control infection
 Perioral dermatitis
May be a form of the skin disorder rosacea, adult acne or seborrheic
dermatitis, involving the skin around the mouth or nose
The exact cause is unknown, but makeup, moisturizers, topical
corticosteroids or some dental products containing fluoride may play a
role
General mgt
Oral antibiotic
Ex. Tetracycline
Very mild corticosteroid cream (when stronger corticosteroids are
used, the condition may return temporarily when the medication is
stopped).

Contact dermatitis
An acute or chronic inflammatory disorder usually characterized by
well demarcated skin lesions and a history of exposure to some
suspected offending agent on the skin surface
It is also called occupational (industrial) dermatitis
Causes
Irritant substance which comes into direct contact with the skin
Ex: Detergents, hair metals, perfumes, strong acids & alkalis induce
irritant contact dermatitis
Clinical features
If lesions are
 Wet & oedematous = acute case
 Dry, thickened, & scaly = chronic case
Erythematous
Macular, papular or papulo -vesicular eruptions, chiefly involving the
exposed part of the body
Pruritus is common

Contact dermatitis of the feet and wrist
Atopic dermatitis/Eczema
Is the cutaneous expression of the atopic state
It is a chronic superficial inflammation of skin characterized by pruritis
Causes
 The exact cause is not known
Although it is activated by the immune system & is related to allergic
reactions, it is not the same as other allergic reactions
 People with eczema do have the IgE antibodies produced by the
immune system as part of allergic reactions
Contact with the external trigger (allergen) causes the skin to become
inflamed
Common triggering factors
Soaps, detergents, weather /hot, cold, humid, or dry/, environmental allergens,
jewelry, creams, food handling, clothing, sweating, gloves, rubbing, bacteria,
emotional or mental stress)
It is not contagious
Pathophysiology
Remains incompletely understood but a genetic predisposition is believed to
be important
 2/3rd of patients have family members with asthma, fever, and very dry skin
Predisposing factors
Bacterial, viral & fungal infection, food allergens, & environmental factors

Sign & symptoms
Pruritis, redness, papule
Thickening of skin which is common over face & neck, behind the knee
in the cubital fassae , & back of the hand
Secondary bacterial infections are common
DX
Clinical criteria for the dx of atopic dermatitis
Pruritis & scratching
Course marked by exacerbations & remissions
Lesions typical of eczematous dermatitis
Personal or family hx. of atopy (asthma) clinical course lasting > 6
weeks

Nursing interventions
A. Relief of pruritis
As heat tends to aggravate itching the room should be maintained at
comfortable temperature
The bed clothes & personal clothing should be light, loose, and cool .
Tepid bath may be helpful in alleviating the itching
Diversions, which are of interest to the individual, ex: reading, or
watching TV
Administering prescribed medication & observing adverse effects of
the drugs
B. Maintenance of fluid & nutritional balance
 Diet reach in protein ( to replenish losses & to promote healing)
Any known allergens must be eliminated from diet
C. Prevention of infection
 The nails should be kept short & clean
All dressings & applications of topical substances must be performed
aseptically
After bathing the skin should be gently patted dry
If the skin disorders is contagious, isolation precautions may be
implemented to prevent the spread of infection to others
D. Providing psychological support

Severe cases may causes distress & embarrassment to the sufferer
Medical management of atopic & contact dermatitis
Topical drugs
Oozing lesion should be treated with saline compresses or 1% gentian
violet 2-3 times /d for 2 days
Betamethasone dipropionate 0.05% cream 2 x/d for two weeks or
Dexamethasone 0.25% cream “ “ “ or
Hydrocortison acetate 1 % “ “ “
Systemic drugs
Promethazine 25 mg p.o./d Or
Predinisolone 10 -20mg po/d for 7-10 days (sever cases)
Conservative
Remove the substances causing the reaction, antibiotic to prevent
infections
Seborrheic dermatitis
Seborrheic dermatitis is a chronic inflammatory skin disorder
characterized by dry, moist or greasy scales overlying erythmatous
patches or plaques
The most common location is in the scalp where it may be recognized
as sever dandruff
Etiology
Unknown
Aggravated by hormonal influences, fatigue & anxiety, infection, &
genetic factors
Common in people with oily skin or hair, May come & go depending on
the season of the year
May occur during times of physical stress, travel or in people who have
neurological conditions, such as Parkinson's disease
In infants, this disorder is known as cradle cap
Clinical Features
Scaly patches surrounded by erythema
The scale may be yellow or greasy usually on the scalp & spread to face,
eyebrows, eyelids, ears, grains, axillae
There may be hair loss & secondary bacterial infections
General management
Frequently shampoo, & then carefully rinse the scalp.
Hydrocortisone 2% creams/lotions/ + White F ointment
Selenium sulfide 2.5% shampoo twice weekly
Antibiotics
Screening and diagnosis
Clinically by history, signs and symptoms
Skin test/Patch testing
Contact dermatitis or atopic dermatitis
Complications
Impetigo
Cellulitis
Scarring
Treatment
Dermatitis is best treated if the type is known
Symptomatic treatment is applied to even if the exact dermatitis type is
not known

General mgt
Antihistamines if itching is severe
Wet dressings
Hormonal drugs
Immuno-suppressants (tacrolimus and pimecrolimus)
Affects the immune system & may help maintain normal skin texture
(short duration)
Avoid irritating & drying substances such as perfumes or harsh detergents
Treat other rashes, especially fungal infections & other complications
Keep skin as moisturized as possible
Acne(Pimples, Spots, or “Zits”)
Is an inflammatory disease of the skin, caused by changes in the pilo
sebaceous units (hair follicle & its associated sebaceous gland)
Is a disease of the sebaceous follicles
Acne develops as a result of blockages in follicles
Hyper keratinization & formation of a plug of keratin and sebum is the
earliest change
Enlargement of sebaceous glands and an increase in sebum production
occur with increased androgen production
The micro comedo may enlarge to form an open comedo (blackhead) or
closed Comedo (whitehead)
N.B: Comedo: is a clogged (blocked) hair follicle (pore) in skin
Increased sebum production provides an environment for the overgrowth
of Propionibacterium acnes
The activity of bacteria (Propriono-bacterium acnes) within the

comedones releases free fatty acids from sebum, causes inflammation
within the cyst, and results in rupture of the cyst wall
An inflammatory reaction develops as a result of extrusion of oily and

keratinous debris from the cyst

Acne Causes
The cause is not fully known
Several factors are known to be linked to acne
Family history (partly hereditary)
Hormonal activity, such as menstrual cycles & puberty
Stress, through increased output of hormones from the adrenal
glands
Hyperactive sebaceous glands
Accumulation of dead skin cells
Skin irritation or scratching of any sort will activate inflammation
Use of
• anabolic steroids
• occlusive cosmetics
Any medication containing halogens, lithium, barbiturates, or androgens
Exposure to high levels of chlorine compounds, particularly chlorinated
dioxins, can cause severe, long lasting acne, known as Chloracne
Associations between acne exacerbation and diet (e.g, chocolate),
inadequate face washing, masturbation, and sex are unfounded
Acne will not occur by eating chocolate or greasy foods but worsen by
using oily skin products that clog pores
Acne is most common during adolescence, affecting more than 85% of
teenagers, but not infrequently also continues into adulthood
Types of acne
Acne vulgaris
Acne Rosacea

Acne vulgaris
The permissive factor for the expression of the disease in adolescence
is the increase in sebum production by sebaceous glands after puberty
Blockage of the follicular orifice by retention of sebum and keratinous
material
Usually a self-limited disorder of teenagers & young adults
Rare in adults (10 - 20%)
Common distribution : Face, upper back
The clinical hallmark of acne vulgaris is the comedone, which may be
closed (whitehead) or open (blackhead)
Often accompanied by inflammatory lesions of papules, pustules, or
nodules
May be scar in severe cases

Grading of acne
1. Grand I
 less than 10 Comedon, papule, pustule on the face
2. Grand II
 10-20 comedon papule pustule on the face
3. Grand III
 20-50 comedon papule pustule on the face
4. Grand IV
 >50 comedon papule pustule on the face
Acne rosacea
Inflammatory disorder affecting predominantly the central face, rarely
affecting pts <30 years of age
It is characterized by the presence of erythema, telangiectases (spider-
like blood vessels), and superficial pustules
It is not associated with the presence of comedones
It is more common in females
Common distribution : blush area of cheeks, nose, forehead, chin
Often, individuals with rosacea initially demonstrate a pronounced
flushing reaction
This may be in response to heat, emotional stimuli, alcohol, hot drinks,
or spicy foods
Signs & symptoms of acne vulgaris
 Whiteheads or blackheads or pimples
Papules and pustules are red lesion
Nodules are larger, deeper, and more solid than papules
Cysts are suppurative nodules & cystic acne can be painful
Scarring
Diagnosis
Diagnosis is by clinical examination
Treatment of acne vulgaris
Avoid skin products that clog the skin pores
Ex. Look for products that say "non comedogenic" on the label
Try not to scrub or pick at the pimples - draining pustules
Hormonal manipulation –decreasing sebaceous gland activity,
Decreasing the population of (kill) acnes by
Keep the skin clean
Wash skin once or twice a day with a gentle soap
Topical antibiotics
Benzoyl peroxide, Erythromycin, Clindamycin, or Tetracycline 250 mg po Qid
for one week Or Erythromycin 250 mg po Qid for one week)
Decreasing inflammation
Corticosteroids, Salicylic acid cream
Mild disease often responds to topical metronidazole or sodium

sulfacetamide
More severe disease requires oral tetracycline in doses ranging from
250 to 1000 mg/d
Topical glucocorticoids, especially potent agents, should be avoided
since chronic use of these preparations may elicit rosacea

Part II
Bacterial Infections of the Skin

Furunculosis (boil)
Boil (furuncle) is a skin disease caused by the inflammation of hair
follicles, thus resulting in the localized accumulation of pus & dead tissue
Individual boils can cluster together and form an interconnected
network of boils called carbuncles
In severe cases, boils may develop to form abscesses
Etiology
Staphylococcus auerus or streptococcus
Sign & symptoms
Red, shiny, & swollen pus-filled lump
Tenderness, warm&/or painful
When the lump is ready to rupture, a pointy white or yellow central
area is noticed
 Fever & swollen lymph nodes if sever
Diagnostic procedure
Clinically
Culture &
Sensitivity
Medical management
Surgical drainage(incision & drainage)
Systemic antibiotics
E.g. Cloxacillin 500 mg po QID for 7 days
Vitamin A & E supply for recurring cases
Hot wet soaks are used to localize the infection
Magnesium sulfate paste - can prevent the growth of bacteria and
reduce boils by absorbing pus and drying up the lesion

Nursing mgt
Instruct the client to never pick or squeeze a furuncle because drainage is
infectious & this cause spread of the infection to the surrounding tissue
Other care given is similar to that of care for pt. with skin d/o
 Risk groups are persons with:

Immuno-compromised–diabetes & AIDS
Immuno-suppressant medications
Immune system disorders
Poor hygiene or malnutrition (Vit - A or E deficiency)
Carbuncle
A carbuncle is an abscess of the skin & subcutaneous tissue representing
an extension of a furuncle that has invaded several follicles & large &
deep seated
Causative agent
Usually staphylococcal infection
Clinical Features
Painful lesion, fever, malaise
Common sites for the lesion/thick & inelastic skin
Back of the neck
Shoulder hips
Thigh
Dx:- Clinical sign & symptoms
Medical Mgt
Cloxacillin 50mg/kg/day for 2 wks
Extraction (surgical drainage) when pus is formed
Nursing interventions
Warm moist compresses increases vascularization & hasten resolution
of boils or carbuncle
Clean surround skin with disinfectant
Supportive Rxs (analgesics)
Pt education on prevention through improving hygienic env’t
Impetigo
Impetigo is a superficial skin infection, caused by:
Staphylococcus aureus – the most common, & produce a toxin
Streptococcus pyogenes
Both can live harmlessly on the skin until they enter through a cut or
other wound & cause an infection
Impetigo is more common in children (face, jaw, perioral…)
In adults, it is usually the result of injury to the skin
Impetigo is contagious, mostly from direct contact with someone who has
it, but sometimes from towels, toys, clothing or household items
And often spreads to other parts of the body
Bacteria that cause impetigo may enter through a break in the skin

Types of Impetigo
1. Non-bullous impetigo
 The most common form, caused by both staph and strep.
 Small blisters or scabs, then form yellow or honey-colored crusts
 Appears on the nose, face, arms, or legs and possibly swollen glands.
2. Bullous impetigo
 Blisters in various areas, particularly in the buttocks area.
 Caused by staph bacteria
 Producing a toxin that causes a break b/n the epidermis & the lower
layers of skin.
 Appear in various skin areas, esp. the buttocks, fragile & often break &
leave red, raw skin with a ragged edge.

Risk factors
Children ages 2 to 6 years & infants (most often infected)
Schools & child care settings
Direct contact with impetigo lesions or contaminated towels, bedding or
clothing
Crowded conditions
Warm, humid weather
Participation in sports that involve skin-to-skin contact
Having chronic dermatitis, especially atopic dermatitis
Older adults and people with diabetes or a compromised immune system
Diagnosis
Usually clinically
Differential diagnosis - tinea or scabies
It is important to note that not every blister or ooze means infection
Culture tests
Treatment
Hygienic measures - for minor cases
Gentle cleansing, removing crusts
Topical agents
GV applied 2-3x daily
Oral antibiotics:
Non bullous- Bez.Penicillin or Amoxicillin or erythromycin
For bullous - Cloxacillin, Dicloxacillin
Prevention
Keeping the skin clean
Treat cuts, scrapes, insect bites & other wounds
Wash the affected areas with soap & running water & cover lightly with
gauze
Wash clothes, linens & towels every day
Avoid sharing of clothes
Wear gloves when applying any antibiotic ointment
Cut an infected child's nails short to prevent scratching
Encourage the child to wash hands frequently
Complications
AGN (PSGN)
Rheumatic fever
Methicillin- resistant Staphylococcus aureus (MRSA) infection
Cellulitis
Lightening (hypopigmentation) or darkening (hyperpigmentation) of
the skin

Part III
Viral infections of the skin

Herpes zoster
Herpes zoster, also called shingles, is an infection caused by the varicella-
zoster virus, a member of a group of DNA viruses
The viruses causing chickenpox and herpes zoster are indistinguishable,

hence the name varicella zoster virus
The disease is characterized by

A painful vesicular eruption along the area of distribution of the
sensory nerves from one or more posterior ganglia

Clinical manifestations
The virus spreads along the nerve fibers to the particular area of the skin
supplied by the involved nerve (called a dermatome the area that a single
sensory nerve supplies in the skin)
Pain (burning, lancinating (i.e, tearing or sharply cutting), stabbing, or aching)
Itching, tingling, or burning, constant aching, or deep, shooting pain
Rash, the blisters that develop resemble the lesions of chickenpox –
unilaterally
Blisters follow the path of the nerve or only in certain areas supplied by the
nerve
The blisters eventually burst & begin to crust over and heal
The entire outbreak can last for 3-4 weeks
Scarring may result
The clinical course varies from 1 to 3 weeks
The healing time varies from 7 to 26 days
Herpes zoster in healthy adults is usually localized and benign
However, in immune-suppressed patients, the disease may be severe
and the clinical course acutely disabling

Minimize pain
Reduce viral shedding
Speed crusting of lesions and healing
Ease physical, psychological, emotional discomfort
Prevent viral dissemination or other complications
Antiviral treatment begun <72 hours accelerates healing of skin lesions,
decreases the duration of acute pain, and may decrease the frequency of
PHN(post herpetic neuritis)
Acyclovir
800 mg BID or 200mg five times daily for 7 days
Antihistamine to relieve itching
TTC or Amoxicillin for 7 days
Non-drug treatment
Do not scratch - for the risk of secondary infection & scarring
Apply cool tap-water compresses but must be stopped once the blisters
have dried
Keep the area clean with mild soap &water
Appling petroleum jelly can aid in healing
Acupuncture &electric nerve stimulation through the skin can be helpful for
some patients
Wear loose clothing to avoid extra pain from clothing rubbing against the
rash
Nursing management
The patient is taught how to apply wet dressings or medication to the
lesions and to follow proper hand hygiene techniques to avoid
spreading the virus
Diversionary activities and relaxation techniques are encouraged to
ensure restful sleep and to alleviate discomfort
Relatives, neighbors, or a home care nurse may need to help with
dressing changes and food preparation for patients who cannot care
for themselves or prepare nourishing meals
Complications
Post Herpetic neuritis (PHN)
Localized pain in the area of herpetic lesion that persists beyond
one month, even after the rash is gone
It is due to irritation of the nerves of sensation by the virus
It is severe & debilitating & occurs primarily in persons over the
age of 50
Cellulitis

Herpes simplex
Infection of the keratinized skin or mucous membrane by two closely
related DNA viruses designated herpes simplex virus type 1 (HSV-1) and
herpes simplex virus type 2 (HSV-2)
Affects more than half of the population during their life time
The viruses cause a wide variety of mucocutaneous infections and

produce both primary and recurrent infections
Herpes labialis is caused usually by HSV -1, and occasionally by HSV-2
Herpes genitalis commonly by HSV-2 and sometimes by HSV-I

Transmission is usually skin-skin, skin-mucosa, and mucosa skin contact.
Following a primary infection, the virus establishes a latent or dormant
state in the sensory ganglia
Recurrent disease is caused by reactivation of this dormant virus
The primary infection is more severe than recurrent disease
Precipitating factors for recurrence
Skin/mucosal irritation (UV radiation), altered hormonal milieu
(menstruation)
Fever, common cold,
Altered immune states
Site of infection
Genital herpes recurs more frequently than labial
Treatment
Acyclovir 200mg PO QID, 400mg TID, or 800mg BID for five days
Started within two days of the prodrome
Recurrences cannot be prevented

Warts
Common warts are non cancerous skin growths caused by direct contact
with a virus called the HPV (Human papilloma virus) causing a rapid
growth of cells on the outer layer of the skin
Signs & symptom

Small, fleshy, grainy bumps ,Flesh-colored, white, pink or tan
Rough to touch & usually painless
Often contain one or more tiny black dots, which are sometimes
called wart seeds but are actually small, clotted blood vessels
Treatment
Salicylic acid(Podophylin 1-2ml wipe after 1hr)
Apply protector before podophylin
Bleomycin 0.25-.5 unit/kg Q. week
Freezing (cryotherapy or liquid nitrogen therapy)
Freezing works by causing a blister to form around the wart
Then, the dead tissue sloughs off within a week or so
Minor surgery
Involves cutting away the wart tissue or destroying it by using an
electric needle in a process called electrodessication & curettage
Cryosurgery
Electro surgery, and
Curettage
Prevention
Don't brush, clip, comb or shave areas with warts to avoid spreading
the virus
Don't use the same file or nail clipper on warts as using on healthy
nails
Don't bite your fingernails if you have warts nearby fingernails
Don't pick at warts
Picking may spread the virus
Covering your child's warts with an adhesive bandage to
discourage picking
Keep the hands as dry as possible
Because warts are more difficult to control in a moist
environment
Wash hands carefully after touching warts
Part IV
Fungal Skin Infections/Mycosis

Ringworm
Types of ringworm
Tinea capitis
Ringworm of the scalp
A contagious fungal infection of the hair shaft
A common cause of hair loss in children
Round, scaly lesions on the scalp; may be red or swollen (inflammed)
Hair brittle; breaks easily at scalp
Itching of the scalp may be slight, or may not occur at all
Sometimes pus-filled lesions (pustules) on the scalp
May be extremely persistent, may resolve spontaneously at puberty,
&may recur
Tinea corporis
Ringworm of the body( trunk & extremities)
 Begins with erythematous macule advancing to rings of papules or
vesicles with central clearing
 Itching. May occur on the arms, legs, face, or other exposed body
areas. The border of the rash lesions looks scaly
 May extend to inner thighs & buttock areas
Most frequently occurs in young joggers, obese persons, &those with
tight clothing
Tinea cruris
Tinea of the groin & axillae ("jock itch")
Tends to have a reddish-brown color and to extend from the folds of
the groin down onto thighs
Tinea Corporis…

Tinea curies

Tinea pedis - "Athlete's foot"
Appear esp. b/n the 4th & 5th toes, on the heels & soles
It is the most common & perhaps the most persistent of the tinea
infections
It is rare before adolescence
May occur in association with other fungal skin infections tinea cruris
Tinea unguium (Onychomycosis) - Fungal nails
 Appear as yellow, thick, & crumbly, nail lacks luster, whole nail may be
destroyed
Diagnosis
Primarily based on the appearance & location of the lesion.
Skin scraping
A skin biopsy or culture
Tinea Pedis

Onychomycosis

Tinea Unguium

Treatment
Topical treatment
If fungus affects the skin of the body or the groin or foot antifungal creams can
clear the condition in two weeks or so
Whitfield’s ointment twice a day until the infection clears(2-3 wks) Or
Clotrimazole 1% cream 2-3 times daily until it heals or Amphotericin B lotions
apply twice daily until clearing
Systemic treatment
Some fungus infections do not respond well to external applications (scalp fungus
& fungus of the nails)
First line
Grisofulvin (10mg/kg), long term therapy 500 mg/d after fatty food (wt < 50 kg,
500 mg Bid
But, Tenia pedis - 4wks/ungium-4months/ = 500 mg BID(Microsize)
Second line
Ketoconazole (200 mg /d x 14 days)
Prevention
Keep the area clean
Shampoo hair 2-3 times a week & after hair cuts
Minimize sweat & moisture
Avoid contact with infected clothing, individuals, and pets

Tinea versicolor (Pityriasis versicolor)
Tinea versicolor is a common fungal infection of the skin
The fungus interferes with the normal tanning of the skin appears as a
tissue-thin coating
Healthy skin may normally have the fungus that causes this disorder
growing in its pores (the opening of the hair follicles)
It occurs when the fungus becomes overgrown
A number of factors may trigger this growth
Hot, humid weather; Excessive sweating
Oily skin
Hormonal changes
Immuno-suppression
The classic presentation of tinea versicolor is white, oval, or circular
patches on tan skin.
Tinea versicolor ….
Signs & symptoms
The only signs are patches of discolored skin that grow slowly and
prevent the skin from tanning.
The small scaly patches can be various colors, including white, pink,
tan or dark brown.
Usually affects the back, chest, neck or upper arms & can cause mild
itching.
Screening and diagnosis
Manifestations
Skin scrapings

Treatment
 Wash and dry the affected area, apply Antifungal creams, lotions or
shampoos
Ketoconazole 2% cream or shampoo or
Flucoconazole 50 mg/d for 2-4 wks(max 6wks) or
Miconazole 125 mg Qid
Avoid applying oil or oily products to the skin or wearing tight,
restrictive or non ventilated clothing
Sun exposure makes the fungal infection more apparent
Part V
Parasitic Skin Infestations

Pediculosis : lice infestation
Lice infestation affects people of all ages
Three varieties of lice infest humans
oPediculus humanus capitis (ie, head louse)
oPediculus humanus corporis (ie, body louse), and
o Phthirus pubis (i.e, pubic louse or crab louse)
Lice are called ectoparasites because they live on the outside of the
host’s body

Pediculosis Capitis
Head lice are found most commonly along the back of the head and
behind the ears
The eggs are visible to the naked eye as silvery, glistening oval bodies
that are difficult to remove from the hair
The bite of the insect causes intense itching
The resultant scratching often leads to secondary bacterial
infection, such as impetigo or furunculosis
The infestation is more common in children and people with long hair
Head lice may be transmitted directly by physical contact or indirectly
by infested combs, brushes, wigs, hats, and bedding
Lindane (1%,1-2oz apply for 4 mins) a shampoo/lotion containing or
Pyrethrin (1%) compounds with Piperonyl butoxide (Shampoo)
All articles, clothing, towels, and bedding that may have lice or nits
should be washed in hot water—at least 54°C (130°F) or
Dry-cleaned to prevent re-infestation
Upholstered furniture, rugs, and floors should be vacuumed
frequently
Combs and brushes are also disinfected with the shampoo. All family
members and close contacts are treated
The nurse informs the patient that head lice may infest anyone and are
not a sign of dirtiness
Because the condition spreads rapidly, treatment must be started
immediately
School epidemics may be managed by having all of the students shampoo
their hair on the same night
Students should be warned not to share combs, brushes, and hats
Each family member should be inspected for head lice daily for at least 2
weeks
The patient should be instructed that Lindane may be toxic to the central
nervous system when used improperly

Pediculosis Corporis and pubis
Pediculosis corporis is an infestation of the body by the body louse
This is a disease of unwashed people or those who live in close

quarters and do not change their clothing
Pediculosis pubis is extremely common
The infestation is generally localized in the genital region and is

transmitted chiefly by sexual contact

Chiefly involved are those areas of the skin that come in closest contact
with the underclothing (i.e, neck, trunk, and thighs)
Itching is the most common symptom of pediculosis pubis, particularly at
night
Reddish brown dust (ie, excretions of the insects) may be found in the
patient’s underclothing
Infestation by pubic lice may coexist with sexually transmitted diseases
such as gonorrhea, herpes, or syphilis
There may also be infestation of the hairs of the chest, armpit, beard, and
eyelashes
The patient is instructed to bath with soap and water, after which
Lindane (Gamabenzene hexachloride) cream 1% (washed after 4 mins) or
Permethrin 1% is applied to affected areas of the skin and to hairy areas,
according to the product directions
Complications, such as severe pruritus, pyoderma, and dermatitis, are
treated with antipruritics, systemic antibiotics, and topical corticosteroids

All family members and sexual contacts must be treated and
educated in personal hygiene and methods to prevent or control
infestation
The patient and partner must also be scheduled for a diagnostic
workup for coexisting sexually transmitted disease
All clothing and bedding should be machine washed in hot water
or dry-cleaned

Scabies
Is an infestation of the skin by the itch mite Sarcoptes scabiei
The disease may be found in people living in sub standard hygienic

conditions
It is also common in very clean individuals and among the sexually active,
although infestations do not depend on sexual activity.
The mites frequently involve the fingers, and hand contact may produce
infection

It takes approximately 4 weeks from the time of contact for the
patient’s symptoms to appear
The patient complains of severe itching caused by a delayed type of
immunologic reaction to the mite or its fecal pellets
During examination, the patient is asked where the itch is most
severe
A magnifying glass and a penlight are held at an oblique angle to the
skin while a search is made for the small, raised burrows
Crusted Scabies …

Assessment and diagnostic findings
The diagnosis is confirmed by recovering sarcoptes scabiei or the
mites’ byproducts from the skin
A sample of superficial epidermis is scraped off the top of the
burrows or papules with a small scalpel blade
The scrapings are placed on a microscope slide and examined
through a low-powered microscope to demonstrate the mite

Management
 Warm, soapy bath to remove the scaling debris
A scabicides, Benzyl Benzoate Lotion (BBL 25%) applied to the entire
body for 3-5 consecutive evenings Or
Sulphur (5%) applied to the entire body for 3 consecutive evenings. If
itching persists repeat the drug whereas,
If it persists one wk after the 2nd RX, use Calamine 5% lotion
Contacts should be traced

Patient education and home care consideration
The patient should wear clean clothing
All bedding and clothing should be washed in a very hot water
and dried on hot climate
All family member and cloth contacts should be treated
simultaneously to eliminate the mite
Bath should be taken before the first and last application of BBL.

Part VI
Non Infectious Inflammatory Dermatoses

Psoriasis
Is a chronic, noninfectious inflammatory skin disease; incurable disease, it
occurs in up to 1-3% of the total population (ages 15 to 35yrs)
It’s thought to be an autoimmune(T-cells) response and seems to have a
genetic basis.
The principal abnormality in psoriasis is an alteration of the cell kinetics of
keratinocytes
The exact mechanism is not known.
With psoriasis, the entire life cycle of skin takes only days
As a result, cells build up rapidly, forming thick silvery scales

The disease is most often diagnosed in people ages 15 to 35
It has a tendency to improve and recur periodically
Recurrence is often triggered by physical trauma (Koebner’s
phenomenon), stress, infections, and seasonal and hormonal
changes
Psoriatic arthritis may develop as a complication

Risk factors
Family history(50% pts)-the most significant
Other medical conditions - People with HIV, recurring infections
(strep throat)
Stress – B/se it can have a strong impact on the immune system
Obesity
Smoking - not only increases the risk but also the severity
Infections, such as strep throat or thrush
Injury to the skin, such as a cut or scrape, dog bite, or a severe
sunburn
Stress, Cold weather, Smoking, Heavy alcohol consumption .
Certain medications, including lithium (for bipolar disorder), high
blood pressure medications such as beta blockers, anti malarial
drugs and iodides
Two classifications
1. Non pustular forms
Plaque psoriasis
Guttate psoriasis
Psoriatic arthritis
2. Pustular forms
Pustular psoriasis
Pustolosis palmaris plantaris
Erythrodermic psoriasis
Von Zumbusch
Signs and symptoms (Psoriasis)
Psoriasis is characterized by thick silvery scales and itchy, dry, red patches
that are sometimes painful
The patient’s nails may be pitted, discolored, and crumbling
Positive Auspitz’s sign(Psoriasis, Actinic keratoses)
Lesions appear bilaterally and may range from mild to severe;
The scalp, face, elbows, knees, lower back, and genitalia are most often
affected
Diagnosis
 Diagnosis is based on the appearance of the lesions
Skin biopsy reveals proliferation of epidermal cells
Treatment (Psoriasis)
Treatment is palliative and aims to slow rapid turnover of the epidermis,
promote resolution of the lesions, and control the disease cycle
Psoriasis is incurable disease
Emollients Ex. Paraffin, Vaseline, 10% urea cream Bid
Coal tar lotion 2% + Salcyclicacid 5-10 % (to remove the scale) Bid or
Retinoids 0.1% cream or
Phototherapy
A/ UV-B 2-3 times/week for 12 months or
B/ UV-A + Psoralen(PUVA) 2-3 times/week for at least 6 weeks or

Methotrexate7.5-25 mg stat/week for 8-12 weeks
 Vitamin D 50 mg BID for 7 days
Complications (Psoriasis)
Severe itching, which can lead to thickened skin & bacterial skin
infections
Fluid & electrolyte imbalance in severe pustular psoriasis
Disability, esp. when associated with arthritis
 Low self-esteem
 Depression, stress, anxiety

Nursing interventions (Psoriasis)
Teach the patient about the disease; help identify disease triggers and
work with the patient to modify those triggers
Discuss treatment options and the need for consistency and
compliance to achieve results; acknowledge that treatments are often
time-consuming
Teach the patient about the possible need for frequent and
prolonged bathing to soften and remove scales, followed by
application of prescribed creams or ointments
Discuss establishing a skin care program, even when the disease isn’t
in the acute phase
Provide emotional support to the patient experiencing body image
concerns or depression related to this chronic disease
Provide comfort measures and treatment to relieve itching and pain
Reading Assignment (MTR)
1. Pemphigus vulgaris (PV)
2. Stevens-Johnson syndrome (SJS)
3. Toxic epidermal necrolysis (TEN)
4. Toxic shock syndrome (TSS)
5. Staphylococcal scalded skin syndrome (SSS)
6. Systemic Lupus Erythematous (SLE)

Additional Reading Assignment
Auto-immune integumentary diseases
Alopecia areata
Vitiligo
Albinism
Drug eruptions
Melanoma
Basal Cell Carcinoma (BCC)
Squamous Cell Carcinoma (SCC)
Plastic Surgery
Skin graft
Pemphigus vulgaris

SJS

SkinTumors
 Benign SkinTumors
 Malignant skin tumors
 Cysts
 Verrucae:Warts  Basal cell carcinoma

 Pigmented Nevi: Moles  Squamous cell Carcinoma
 Keloids
 Malignant melanoma
 Dermatofibroma
 Angiomas

Benign Skin Tumors
Cysts
 Cysts of the skin are epithelium-lined cavities that contain fluid or
semi solid material.
 Epidermal cysts (epidermoid cysts) occur frequently
 Described as slow-growing, firm, elevated tumors
 Found frequently on the face, neck, upper chest, and back.
 Surgical removal of the cysts provides a cure.

 Pigmented Nevi: Moles
 Moles are common skin tumors of various sizes & shades,
ranging from yellowish brown to black
 They may be flat, macular lesions or elevated papules or nodules

that occasionally contain hair.
 Most pigmented nevi are harmless lesions
 Nevi larger than 1 cm should be examined carefully.

 Keloids
 Keloids are benign overgrowths of fibrous tissue a t the site of a scar
or trauma.
 Dermatofibroma
 It is a common,benign tumor of connective tissue
 Occurs predominantly on the extremities.
 It is a firm, dome-shaped papule or nodule that may be skin colored
or pinkish brown.

Malignant Skin Tumor
 The most common types of skin cancer are

 Basal cell carcinoma (BCC) and
 Squamous cell(epidermoid) carcinoma (SCC).
 Malignant melanoma
 Skin cancer is diagnosed by biopsy and histologic evaluation.

Basal cell carcinoma (BCC)
 Generally appears on sun-exposed areas of the body
 BCC usually begins as a small, waxy nodule with rolled, translucent, pearly
borders
 The tumors appear most frequently on the face.
 BCC is characterized by invasion and erosion of adjacenttissues.
 A neglected lesion can result in the loss of a nose,an ear, or a lip.

153
Basal cell carcinoma (BCC)

154
Squamous Cell Carcinoma (SCC)
 SCC is a malignant proliferation arising from the epidermis.

 Usually appears on sun-damaged skin,
 It may arise from normal skin or from preexisting skin lesions.
 It is a truly invasive carcinoma, metastasizing by the blood or lymphatic
system
 Metastases account for 75% of deaths from SCC .

155
156
 Prognosis
 BCC is usually good because tumors remain localized.
 SCC depends on the incidence of metastases
 Usually, SCC arising in sun-damaged areas is less invasive
 Management
 The goal of Rx is to eradicate the tumor.
 The Rx method depends on the tumor location; type, depth; cosmetic

desires of the patient.
 Surgical excision and Radiation therapy.

157
Malignant Melanoma
 Is a cancerous neoplasm in which atypical melanocytes are present in
the epidermis and the dermis
 It is the most lethal of all the skin cancers; least common
 Responsible for about 3% of all cancer deaths
 Most melanomas arise from cutaneous epidermal melanocytes, but
some appear in preexisting nevi
Readingassignment :Typesof malignant melanomas

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Pigmentation Disorders
 Vitiligo
 Occurs when melanocytes in the skin are destroyed
 As a result,white patches appear on the skin in different parts

of the body.
 The precise cause of vitiligo is unknown
 Genetic factors appear to play a role.
 20-30 percent of patients may have a family history of the disorder.

160
 The depigmentation has a predilection for acral areas and
around body orifices (e.g., mouth, eyes, nose, anus).
 The diagnosis of vitiligo is based upon the clinical

presence of depigmented patches of skin

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 Management
o Repigmentation therapies include:
• Corticosteroids
• Ultraviolet light
o Pseudocatalase cream
o Surgery – minigrafting techiniques

163
An injury of the body result from the transfer of heat energy from
heat source to the body.
A burn is a coagulative necrosis of the surface layers of the body
It may vary in depth, size and severity

Causes
Scalds
Flame of fire
Electric current
Chemical burn
UV rays( sun burn)
Carelessness with matches and in cigarette smoking
Defective heating, cooking and electrical equipment

Epidemiology of Burn
A leading cause of unintentional death , second only to motor vehicle
crashes.
Scald burns account for 85% of total injuries and are most prevalent in
children younger than 4 years of age.
Scald injury remains the leading cause of hospitalization for burns.
Fires are a major cause of mortality accounting for up to 34% those
younger than 16 year.
Flame burns account for 13%; the remaining are electrical and chemical
burns.
Burn Injury…
Types of burn injury
1. Thermal injury
 Scald – spillage of hot liquids
 Flame burns
 Flash burns due to exposure of natural gas, alcohol,
combustible liquids
 Contact burns – contact with hot metals/objects/materials
2. Electrical injury
3. Chemical burns – acid/alkali
4. Cold injury — frost bite
5. Radiation
6. Inhalational
1.Thermal Injury
Scald Burns
Scalds from hot water are the most common cause of burn
Depth is proportional to temperature, duration of contact & thickness
of skin
Flame Burns
Next most common
House fires, smoking related fires, improper use of flammable liquids,
automobile accidents, ignition of clothing from stoves or space heaters,
fall into open fire
Thermal Injury…
Flash Burns
Explosion of natural gas, propane, gasoline & other flammable liquids
Depth depends on the amount and type of fuel
Clothing, unless it catch fire, is protective against flash burns
May be associated with thermal damage to the upper airway
Contact Burns
Result from contact with hot metals, plastic, glass or hot coals
Limited in extent & very deep
2. Electrical Burn
Mechanisms of injury :
 Direct effect of electrical current on body tissue
 Conversion of electrical energy to thermal energy, resulting in
deep and superficial burn
 Blunt mechanical injury from lightning strike ,muscle contraction
or fall
Unlike other burn injures in that visible area of tissue necrosis

represent only a small portion of destroyed tissue
 When current flows through the body, it takes the shortest and least
resistance pathway.
 If Hand to head –current goes through brain – respiratory
center paralysis (can die immediately),
If Hand to leg – current goes through heart- ventricular
fibrillation& cardiac arrest
If Hand to hand – current goes through chest wall muscles,
resulting continuous contractions or spasms of inter costal muscles
and diaphragm - leading to traumatic asphyxia
 Mechanisms of death from Electrical burn
If current travel through brain/ spinal cord, brain centers paralysis
and die and it interferes with respiration, asphyxial death
If current travel through heart ventricular fibrillation and cardiac
arrest
If current travel through the chest wall direct paralysis of chest
muscles and asphyxial death

Severity of electrical burn injury depends on
Amount of voltage
Tissue resistance
Current pathway (in door or out door)
Surface area in contact with the current
Length of time of sustained injury

3. Chemical Burns
Usually associated with industrial exposure.
Burning will continue as long as the chemical is on the skin.
Acids
Immediate coagulation-type necrosis creating an eschar
 Bases (Alkali)
Liquefactive necrosis with continued penetration into deeper
tissue resulting in extensive injury

4. Inhalation Injury
 It occurs after major fire burns- due to:

 Inhalation of heat
 Noxious gases and incomplete products of combustion

5. Radiation Exposure
Waves or particles of energy that are emitted from radioactive
sources
 Alpha radiation
 Large, travel a short distance, minimal penetrating ability

 Can harm internal organs if inhaled, ingested or absorbed
 Beta radiation
 Small, more energy, more penetrating ability

 Usually enter through damaged skin, ingestion or inhalation
 Gamma radiation & X-rays
 Most dangerous penetrating radiation

 May produce localized skin burns and extensive internal damage
Effect of Injury
Body response to burn
Burns < 25% TBSA- local response.
Burns > 25% TBSA- local and a systemic response and are
considered major burn injuries.
Due to the release of cytokines and other mediators into the
systemic circulation.

Systemic Response/ Pathophysiology
Hemodynamic instability resulting from loss of capillary
integrity and subsequent shift of fluid, sodium and protein
from intravascular compartment to interstitial space
Decreased cardiac out put
Tissue hypo perfusion
Target Organ failure

Cardiovascular response
Decreased cardiac out put
Decreased blood pressure
Hypovolemia
Greatest volume of fluid leaking occur in the 1st 24hr- 36hr and
peak value of 6 to 8hr

Effects on fluid electrolytes and blood volume
Blood volume decreases during burn shock and fluid loss occur
through evaporation (3-5 L)
Hyponatremia (ed Na+ level) very common in the 1st week of
burn injury
Initially hyperkalemia (from tissue destruction) then hypokalemia
with fluid shift & inadequate K+ replacement
Pulmonary response
Upper air way obstruction and systemic response hypoxia
182
Severity of burn injury
The severity of burn injury determined by many factors,

such as:
 Location
 Age
 Poor risk factors/ preexisting medical problems
 Nutritional status
 Extent of body surface are burned (BSAB)
Severity of burn injury…
Location
Burns of face, neck and areas of chest are severe
Burn involving special care areas are severe
Age
Very young and very old victims have high risk of mortality.
Those between age 5 and 40 have good prognosis and those age
<5 years and > 60 years have poor prognosis

Nutritional status
Good vs. mal-nourished
Poor risk factors/ preexisting medical problems

Renal disease
Diabetic mellitus
Cardiovascular disease
Pulmonary disease
Extent of body surface area burned-Estimating TBSA burned

Methods to estimate the TBSA
Palm method
In patients with scattered burns, a method to estimate the
percentage of burn is the palm method.
The size of the patient’s palm is approximately 1% of TBSA

Methods…
Rule of nines
Quick way to estimate the extent of burns
The system assigns percentages in multiples of nine to major body
surfaces
Head=9%
Trunk = 36%
Upper extremity each =9% , Lower extremity each= 18%
Perineum = 1%
Rules of Nines
4.5
4.5
18 18
4.5
4.5
4.5
9 9
4.5 4.5 4.5
1
18 18
9 9 9 9 1
7 7 7

Lund and Browder method
More precise method
Assign percentage to various anatomic parts, especially the head and
leg changes with growth.
Because of changes in body proportion with growth, the calculated
TBSA changes with age as well.
The initial evaluation is made on the patient’s arrival at the hospital.
Revised on the second & third post-burn days because the
demarcation usually is not clear until then.
Depth of burn
Depth of the tissue involved to burn is depends on:

Temperature of burning agent
 Duration of contact
For example, in the case of scald burns in adults, 1 second of
contact with hot tap water at 68.9°C (156°F)
May result a full thickness (third-degree) injury

Depth of Burn

Depth of Burn…
Burn can be classified in to three based on depth or layers of tissue

involved.
 Superficial partial thickness (1st degree burn)
 Deep partial thickness (2nd degree burn)
 Full thickness (3rd degree burn)

Superficial partial thickness (1st degree burn)
Resulting from overexposure to sun light, brief contact with hot

objects or scalding by hot water or steam
Tissue involved
Epidermis and portion of dermis (irritates dermis)
Sign and symptom

Tingling sensation
Pain may present (soothed by cooling)
1st degree Cont’d
Blister may be formed
Blenching with pressure
Redness or discoloration
Usually heals without scarring
Healing time
Rapid within a week

1st degree…

Deep partial thickness (second degree burn)
Resulting from very deep sunburn, contact with hot liquids and
objects and flash flame contact
Tissue involved
Total epidermis and Portion or total dermis
Sign and symptoms
Painful
Red and matted appearance
Blister (exudates fluids)

Mild to moderate edema
Intact hair follicle
Healing time -2-3 wks
 Full thickness (3rd degree burn)
Results from flame, prolonged exposure to hot liquid, electric current,
chemicals
Tissue involved
Epidermis, Dermis
Subcutaneous tissue
Underlying structures (bone, Joint, muscle…)
superficial Ⅱ0

superficial Ⅱ0

3rd degree…
Sign symptoms
White to red or brown to black in color
Pain less
Hematuria
complete loss of all layers of the skin
Hemolysis of RBC
Edema
Healing time- over month

Classifying the extent of burn injury based on TBSA
1. Minor Burn Injury
2. Moderate burn
3. Major burn
1. Minor Burn Injury
Second-degree burn of <15% TBSA in adults or <10% TBSA in children
Third-degree burn of less than 2% TBSA not involving special care
areas
Excludes all patients with electrical injury, inhalation injury, concurrent
trauma, all poor-risk patients
Moderate, Uncomplicated Burn Injury
 Second-degree burns of 15%–25% TBSA in adults or 10%–20% in
children
Third-degree burns of <10% TBSA not involving special care areas
Excludes electrical injury, inhalation injury, concurrent trauma, all
poor-risk patients.

Major Burn Injury
 Second-degree burns >25% TBSA in adults or >20% in children
All third-degree burns >10% TBSA
 All burns involving eyes, ears, face, hands, feet, perineum, joints
All inhalation injury, electrical injury, concurrent trauma, all poor-
risk patients

Burn Management
Burn management classified into three phases
1. Emergency phase /resuscitation phase
2. Acute or intermediate phase
3. Rehabilitation phase

Initial management “6C”
Clothing should be removed
Cooling of the part by running water for 20 minutes
Cleaning the part to remove dust, mud etc
Chemoprophylaxis – tetanus toxoid; antibiotics; local antiseptics
Covering with dressings by different methods
Comforting with sedation and pain killer

Emergency Phase /Resuscitation Phase
From onset of injury to the end of fluid resuscitations
Time to resolve immediate problems
Phase of: fluid loss

Edema formations
 Fluid mobilizations
Fluid loss in the form of evaporation reaches200ml/hr to 400ml/hr
in major burn
It may last up to five days but more usually 24-48hr
Care activity during Emergency phase …
Extinguishing of fire
Ensure ABC
Remove restricting objects from the area.
Cover the wound with sterile or clean cloth.
Prevent shock & fluid replacement

Fluid replacement and resuscitation
The corner stone in the survival of patient with burn
Oral and enteral resuscitation can be successful in adults with
<20% TBSA and children with <10% to 15% TBSA
 >20% TBSA in adult and all major electrical burn needs
immediate IV fluid replacement.

Formulas for fluid replacement in burn injury
Consensus Formula
Lactated Ringer’s solution (or other balanced saline solution):
2–4 ml x kg body weight x % TBSA burned
 Half to be given in first 8 hours
 Remaining half to be given over next 16 hours

Formulas for fluid replacement…
Evans Formula
Colloids: 1 mL x kg body weight x % TBSA burned
Electrolytes (saline): 1 mL x body weight x % TBSA burned
Glucose (5% in water): 2,000 mL for insensible loss
Day 1: Half to be given in first 8 hours; remaining half over next 16
hours
Day 2: Half of previous day’s colloids and electrolytes: all of
insensible fluid replacement.

Maximum of 10,000 mL over 24 hours.
2nd and 3rd degree burns exceeding 50% TBSA-calculated on the
basis of 50% TBSA.
Brooke Army Formula

Colloids: 0.5 mL x kg body weight x % TBSA burned
 Electrolytes (lactated Ringer’s solution): 1.5 mL x kg body weight
x % TBSA burned
Glucose (5% in water): 2,000 mL for insensible loss
Brook Army…
Day 1: Half to be given in first 8 hours; remaining half over next 16
hours
Day 2: Half of colloids; half of electrolytes; all of insensible fluid

replacement.
Maximum of 10,000 mL over 24 hours.
2nd and 3rd degree burns exceeding 50% TBSA-calculated on the
basis of 50% TBSA.

Parkland/Baxter Formula
Lactated Ringer’s solution: 4 mL x kg body weight x % TBSA
burned
Day 1: Half to be given in first 8 hours; half to be given over
next 16 hours
Day 2: Colloid is added
Is the widely used formula

The adequacy of resuscitation should be constantly assessed using
Vital signs
Urine output
Blood gases
Hb and haematocrit
Protein levels
Peripheral colour and temperature
Electrolytes

Acute/ intermediate phase
Starting from onset of diuresis to the closure of wound (begins 48 to
72 hours after the burn injury).
May take weeks to months
Common events are

Fever
Infections
Septicemic shock

Care activity during Intermediate Phase:
Continued assessment and maintenance of respiratory and circulatory
status,
Fluid and electrolyte balance
Gastrointestinal function
Infection prevention
Burn wound care (i.e. Wound cleaning, topical antibacterial therapy, wound
dressing, dressing changes, wound debridement and wound grafting)
Pain management and nutritional support

Rehabilitation Phase
Begins with the closure of wounds to until the patient assume self care.
May take early as one week to two or three month or over.
Rehabilitative care
Preventions of scar and contracture
Physical, occupational and vocational rehabilitations
Functional and cosmetic reconstructions
Psychological counseling

Watch for overhead electrical wires and underground wires when
working outside
Use caution when cooking
Keep a working fire extinguisher in your home

Prevention of Infection
Wound care: is care of burn wound by debridement and Wound
dressing
Debridement
The removal of nonviable tissue (eschar)
Removal of tissue contaminated by bacteria and foreign bodies,
thereby protecting the patient from invasion of bacteria
Removal of devitalized tissue or burn eschar in preparation for
grafting and wound healing

Types Wound Debridement
Natural Debridement
The dead tissue separates from the underlying viable tissue
spontaneously.
Mechanical Debridement
It involves the use of surgical scissors, scalpels, and forceps to
separate and remove the eschar
Chemical Debridement
Topical enzymatic debridement agents are available to promote
debridement of the burn wounds
Surgical debridement
An operative procedure involving either primary excision
(surgical removal of tissue) of the full thickness of the skin down
to the fascia or shaving of the burned skin layers
This method is followed by an application of a skin graft

Tetanus Prophylaxis
Burns are tetanus-prone wounds.
Depends on patient's current immunization status.
Previous immunization within 5 years requires no treatment
Immunization within 10 years requires a tetanus toxoid booster,
0.5 ml IM
Unknown immunization status requires human tetanus
immunoglobulin 250 to 500 units

Pain Relief
Psychological treatment
Give oral anti-pain for mild pain to moderate pain
Morphine sulfate IV if pain is severe

Surgical management Options
Escharotomy: cutting of burned skin to relieve underlying pressure

Incise along medial and/or lateral surfaces
Indication
Compromises of Circulation & ventilation
Circulation to distal limb is in danger due to swelling.
In circumferential chest burn, patient might not be able to expand
his chest enough to ventilate & compromises ventilatory motion,
and might need escharotomy of the skin of the chest.
Escharotomy

Fasciotomy: incision of fascia (thick white covering of muscles )
and often overlying skin
Blood flow to distal limb is improved.
Muscle can be inspected for viability.
Excision and grafting

Excision and grafting
Skin graft from the patient’s unburned skin or other to be placed
on the clean excised burn
Physiotherapy and Rehabilitations

Body and limb positioning
Splinting
 Exercises
 Gradual ambulation

Burn Complication
Immediate Complication
Hypovolemic shock and fluid electrolyte &,plasma loss
Cardiac arrhythmias and cardiac arrest
Infection and Sepsis
Metabolic Acidosis and decrease temperature
Renal & hepatic damage
Pulmonary complications due to inhalation injury

 Long Term Burn Complication
Burn wound may heal with some complications like scar and
contracture
Hypertrophic scar:
• Scars that stay within the area of the original burn injury
due to continued production of collagen
Keloid:
• Scars with extension into surrounding tissues
 Contracture: mostly burn contractures are preventable
 Because of pain, patients will assume flexed position.
It predisposes wounds to contracture formation
Contracture Preventive measures

Preventive positioning
Splinting / Casting
Gait Training
 Scar Management

Contracture…

Contracture…

General rules for burn prevention
Cooking on floor should be avoided as a rule
 Avoid use of unauthorized gas cylinders & local kerosene stove
Avoid loose clothing while cooking
Restrain playing of toddlers in kitchen
 Never hold a cup of hot liquid near infant/toddlers
Do not smoke in bed
Do not fall asleep while smoking

 Use of proper authorized gadgets for cooking
Handle chemicals (acids, alkaline) carefully
Beware of high tension wires and open electrical wires at home
Supervise children while lighting fire crackers
Keep matches and lighters out of the reach of children
Never leave children unattended around fire or in bathroom/bathtub
Set the water heater temperature no higher than 120°F

Nursing Diagnosis
Ineffective airway clearance related to edema and loss of ciliary

action (smoke inhalation)
Fluid volume deficit related to increased capillary permeability and

evaporative losses from the burn wound
Pain related to destruction of skin/tissue and emotional impact of

injury
Impaired skin integrity related to open burn wounds evidenced by

absence of viable tissue
Imbalanced nutrition, less than body requirements, related to hyper
metabolism & wound healing needs
Impaired physical mobility related to burn wound edema, pain & joint
contractures neuromuscular impairment
Anxiety related to situational crises (hospitalization, memory of the

trauma experience, threat of death or disfigurement)
Risk for infection related to loss of skin barrier and impaired immune
response

Goal
Maintain patent airway and adequate airway clearance
Restoration of optimal fluid and electrolyte balance and perfusion of vital
organs.
Control of pain
Improve skin integrity
Support in nutritional intake to meet metabolic needs
Maintain optimal physical mobility
Minimization of patient’s and family’s anxiety
Absence of infection
Nursing interventions
Ineffective airway clearance

Positioning of pt (Elevate head of bed)
Encourage coughing/deep-breathing exercises and frequent
position changes
Suction (if necessary) with extreme care
Provide humidified oxygen

Fluid Volume Deficient
Monitor vital signs. Note capillary refill and strength of peripheral
pulses.
 Monitor urine output at least hourly & weigh patient daily.
Administer calculated IV replacement of fluids, electrolytes,
plasma, albumin
Elevate head of patient’s bed and elevate burned extremities
Observe for symptoms of deficiency or excess of serum sodium,
potassium, calcium, phosphorus, and bicarbonate
Pain Management
Assess reports of pain, noting location/character and intensity
Administer analgesics
Elevate burned extremities periodically
Provide emotional support and reassurance

Impaired Skin Integrity
Assess/document size, color, depth of wound, noting necrotic
tissue
provide appropriate burn care and infection control measures.
Dressings

Imbalanced Nutrition
Auscultate bowel sounds, noting hypoactive/absent sounds.
Provide small, frequent meals and snacks
Encourage pt to view diet as a Rx and to make food/beverage
choices high in calories/protein.
Provide oral hygiene before meals
Insert small feeding tube for enteral feedings

Impaired Mobility
Maintain proper body alignment with supports or splints
Note circulation, motion, and sensation of digits frequently
Encourage patient participation in all activities as individually able
Incorporate pt with physical therapy, hydrotherapy, and nursing
care

Anxiety
Provide frequent explanations and information about care
procedures
Assess patient’s and family’s understanding of burn injury, coping
skills
Maintain adequate pain relief
Consider administering prescribed anti-anxiety medications

Risk for infection
Emphasize/model good hand washing technique for all individuals
coming in contact with patient
Use gowns, gloves, masks, and strict aseptic technique during
direct wound care
Examine wounds daily, note/document changes in appearance,
odor, or quantity of drainage
Monitor vital signs for fever
Administer topical agents as indicated
References
Color Atlas and Synopsis of Clinical Dermatology
Andrews‘ Diseases of the Skin Clinical Dermatology
Brunner and Suddarths`s Medical surgical text book 14th edition,

Philadelphia, 2018
Principles and practice of burn care. Sarabahi S, Tiwari VK, Goel A,

Gupta LC (eds). New Delhi. 2018
American Burn Association (www.ameriburn.org)

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Asrat Weldeyes Health Science Campus

School of Nursing and Midwifery

Medical Surgical Nursing for Nursing

By: Bantalem T. (BSc, RN, MSN in AHN)

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