Surgery final

59

Principles of history taking

● Identify the reason for consultation – the presenting complaint

● Determine the onset, duration and evolution of the symptoms

● Deduce the most likely organ or system affected

● Refine the history with relevant direct questions

● Establish relevant past, social, family, drug and allergy history

● Complete with a thorough review of other systems

● Devise a list of differential diagnoses

ources of abdominal symptoms

● Abdominal pain, weight loss, anorexia or vomiting, jaundice, alteration of bowel habit, and blood loss
or anaemia are the common clinical presentations of abdominal pathology

● Occult malignancies may have atypical presentation

Pain is the most common of all abdominal symptoms

Classic presentations of abdominal pathology

● Obstructive and inflammatory pathology must be excluded in patients with abdominal pain and
altered bowel habit

● Closed-loop obstruction with tenderness in the right iliac fossa is indicative of imminent caecal
rupture

● Caecal cancer classically presents with anaemia

● Patients who have had previous abdominal surgery may have adhesions

● Check carefully for small incarcerated hernias, particularly femoral, in obese patients

The abdominal wall and parietal peritoneum are innervated by the somatic nervous system, whereas
the abdominal organs and visceral peritoneum are innervated by the autonomic nervous system.

Nerves responsible for abdominal pain

● Abdominal wall and parietal peritoneum are supplied by the somatic nerves

● Abdominal organs and the visceral peritoneum are supplied by the autonomic nervous system

● Skin, muscles and parietal peritoneum are supplied by the iliohypogastric and ilioinguinal nerves
and the lower six intercostal nerves

● Afferent pain fibres from the abdominal organs and visceral peritoneum travel with sympathetic
nerves

central part of the diaphragmatic peritoneum is supplied by the phrenic nerve (C4); therefore, pain
arising in this region is referred to the tip of the shoulder

. Unlike somatic pain, autonomic pain is deep and poorly localised. T1-l2

Somatic parietal peritoneum, the pain becomes sharp and localizes

when the patient takes a deep breath, the tenderness in the right subcostal region is markedly
increased, causing the patient to stop breathing; this is Murphy’s sign. h acute cholecystiti

Specific characteristics of abdominal pain

● Visceral pain arises from ischaemia, muscle spasm or stretching of the visceral peritoneum

● Autonomic pain, deep and poorly localised, is referred to the equivalent somatic distribution of that
nerve root from T1 to L2

● When an inflamed organ touches the parietal peritoneum, pain is then localised to the segmental
dermatome of the abdominal wall

● The pain in the parietal peritoneum may radiate to back or front along the dermatome

Colicky abdominal pain ● Pain of ‘small bowel colic’ comes in waves and disappears completely in
minutes when the peristaltic wave ceases ● Pain of biliary colic is insidious in onset, reaches the peak in
half an hour or so and does not ease off completely between spasms ● Pain of ureteric colic is intense
lasting one to two minutes of the ureter

Nine sites of abdominal pain: 1, right subcostal;( R hypochondrium) 2, epigastrium; 3, left subcostal; 4,
right flank( lumbar); 5, periumbilical; 6, left flank; 7, right iliac fossa; 8, suprapubic/hypogastrium; 9, left
iliac fossa.
Abdominal examination the following sequence: inspection, palpation, percussion and auscultation.

Inspection Scars, abdominal distension, visible peristalsis or abdominal masses, dilated veins, pulsation
or abdominal wall swelling suggestive of hernia should all be carefully sought.
for Grey Turner’s sign – skin discoloration of the flanks due to retroperitoneal haemorrhage in severe
acute pancreatitis and leaking abdominal aortic aneurysm.

Cullen’s sign – discoloration around the umbilicus – may indicate severe acute pancreatitis, ruptured
ectopic pregnancy or trauma to the liver.

healthy patient the spleen is not normally palpable. supine patient.just like liver

Auscultation High-pitched bowel sounds are heard during early stages of mechanical intestinal
obstruction. Distal part absent

Aortic and iliac bruits are heard when blood flows through a stenosis.

A succussion splash is a sound like ‘shaking a half-filled bottle with water’ and is found most often in
patients with gastric stasis due to gastric outlet obstruction.

In generalised peritonitis, bowel sounds will not be heard or be very few and far between.

Inspection of hernia sites, examination of genitalia, inspection of anal region and digital rectal
examination for abdominal pain

60

Ab wall Its major function is to protect the enclosed organs , role is mobility, being able to flex, extend,

Anteriorly the two powerful rectus abdominis muscles extend vertically from ribs to pelvis. join, the
linea alba,

natural weaknesses the lumbar triangles and the posterior wall of the inguinal canal

Other examples are: oesophagus → hiatus hernia, femoral vessels → femoral hernia, obturator nerve →
obturator hernia, sciatic nerve → sciatic hernia.

inguinal hernia (indirect) also occurs through the developmental failure of the processus vaginalis to

Herniation at the umbilicus structures passing through the abdominal wall in fetal life and
developmental failure of closure.

Weakness of abdominal muscles sharp trauma surgery , stabing , blunt trauma or tearin

Causes of hernia ● Basic design weakness ● Weakness due to structures entering and leaving the
abdomen ● Developmental failures ● Genetic weakness of collagen ● Sharp and blunt trauma ●
Weakness due to ageing and pregnancy ● Primary neurological and muscle diseases ● ? Excessive intra-
abdominal pressure
constipation, prostatic symptoms, excessive coughing in respiratory disease and obesity. common in
pregnancy due to hormonally induced laxity of pelvic ligaments.

Types of hernia by complexity ‘

● Occult – not detectable clinically; may cause severe pain ● Reducible – a swelling that appears and
disappears ● Irreducible – a swelling that cannot be replaced in the abdomen, high risk of complications
● Strangulated ischaemic and may infarct. The hernia is then said to have– painful swelling with vascular
compromise, requires urgent surgery ● Infarcted – when contents of the hernia have become
gangrenous, high mortality

special circumstance (Richter’s hernia) only part of the bowel wall enters the hernia.

An interstitial hernia occurs when the hernia extends between the layers of muscle and not directly
through them. This is typical of a spigelian hernia (see below under Spigelian hernia). An internal

An internal hernia is a term used when adhesions form within the peritoneal cavity.

most cases a cough impulse is felt. Gentle pressure is applied to the lump and the patient is asked to
cough. If an impulse is felt this is due to increased abdominal pressure

physical exam Checks ● Reducibility ● Cough impulse ● Tenderness ● Overlying skin colour changes ●
Multiple defects/contralateral side ● Signs of previous repair ● Scrotal content for groin hernia ●
Associated pathology

● A swelling with a cough impulse is not necessarily a hernia ● A swelling with no cough impulse may
still be a hernia

a hiatus hernia and diaphragmatic hernia may be seen on a chest radiograph.

Ultrasonography is very useful in the early postoperative period when a haematoma or seroma may
develop, and be difficult to distinguish from

Computed tomography is helpful in complex incisional hernia,

Investigations ● Plain radiograph – of little value ● Ultrasound scan – low cost, operator dependent ● CT
scan – incisional hernia ● MRI – good in sportsman’s groin with pain ● Contrast radiology – especially for
inguinal hernia ● Laparoscopy – useful to identify occult inguinal hernia

Reduction of hernia content is essential for a successful repair.

Excision and closure of the peritoneal sac are ideal but not essential.

During laparoscopic repair of incisional hernia, surgeons will often leave the sac in situ after reducing the
hernia contents, and simply fix a mesh over the neck to prevent recurrence.

Mesh type : GROSS STRUCTURE ( net ) SYNTHETIC(synthetic polymers of polypropylene, polyester or

polytetrafluoroethylene (PTFE) ,non absorba

Synthetic meshes are very strong and early meshes were much stronger than a human abdominal wall,

All meshes provoke a fibrous reaction.

‘biological meshes’ that are sheets of sterilised, decellularised, non-immunogenic connective tissue.

from human or animal dermis, bovine pericardium or porcine intestinal submucosa.age

Mesh characteristics ● Woven, knitted or sheet ● Synthetic or biological – mainly synthetic ● Light,
medium or heavyweight – lightweight becoming more popular ● Large pore, small pore – large pore
causes less fibrosis and pain ● Intraperitoneal use or not – non-adhesive mesh on one side ● Non-
absorbable or absorbable – mainly non-absorbable

Positioning the mesh

just outside the muscle in the subcutaneous space (onlay); ● within the defect (inlay) – only
applies to mesh plugs in small defects; ● between fascial layers in the abdominal wall
(intraparietal or sublay); ● immediately extraperitoneally, against muscle or fascia (also
sublay); ● intraperitoneally.
At open surgery all of these planes are used but laparoscopic surgeons currently use only
intraperitoneal or extraperitoneal planes
infection limits the use of mesh, particularly heavyweight types.
Inguinal hrnia
The congenital inguinal hernia is known as indirect, oblique or lateral whereas the acquired
hernia is called direct or medial. There is a third ‘sliding’ hernia that is acquired but is lateral
in position
Sliding inguinal hernia : occurs at the deep inguinal ring lateral to the IE vessels.
Occasionally, both lateral and medial hernias are present in the same patient (pantaloon
hernia).
landmark the deep inguinal ring at the mid-inguinal point. Gentle pressure is applied at this
point and the patient asked to cough. If the hernia is controlled with pressure on the deep
inguinal ring then it is likely to be indirect/lateral and if the hernia appears medial to this
point then it is direct/medial.

Diagnostic difficulties
lymph node groin mass or an abdominal mass , Large scrotal hernias may be misdiagnosed as
a hydrocele , cases require urgent investigation by either ultrasonography or CT.

children who have lateral hernias with a persistent processus, it is sufficient just to remove
and close the sac. This is called a herniotomy. In adult surgery, herniotomy alone has a high
recurrence rate and some form of muscle strengthening is added (herniorrhaphy).
OPEN FLAT MESH REPAIR , OPEN PLUG/DEVICE/COMPLEX MESH REPAIR , OPEN
PREPERITONEAL REPAIR
OPEN PREPERITONEAL REPAIR : The totally extraperitoneal (TEP) approach is more widely
used than the transabdominal preperitoneal (TAPP) approach.

Operations for inguinal hernia ● Herniotomy ● Open suture repair Bassini Shouldice Desarda ● Open flat
mesh repair Lichtenstein ● Open complex mesh repair Plugs Hernia systems ● Open preperitoneal repair
Stoppa ● Laparoscopic repair TEP TAPP

Complications ● Early pain, bleeding, urinary retention, anaesthetic related ● Medium seroma, wound
infection ● Late chronic pain, testicular atrophy

Sportsman’s hernia : almost entirely restricted to young men who play contact sports such as football
and rugby.

Femoral hernia : The female pelvis has a different shape to the male, increasing the size of the femoral
canal and the risk of hernia. low-weight, elderly women.

The iliac artery and vein pass below the inguinal ligament to become the femoral vessels in the leg.

The walls of a femoral hernia are the femoral vein laterally, the inguinal ligament anteriorly, the pelvic
bone covered by the iliopectineal ligament (Astley Cooper’s) posteriorly and the lacunar ligament
(Gimbernat’s) medially

Femoral hernia ● Less common than inguinal hernia ● It is more common in women than in men ● Easily
missed on examination ● Of cases 50% present as an emergency with very high risk of strangulation
The hernia appears below and lateral to the pubic tubercle and lies in the upper leg rather than in the
lower abdomen.

Differential diagnosis femoral hernia ● Direct inguinal hernia ● Lymph node ● Saphena varix ● Femoral
artery aneurysm ● Psoas abscess ● Rupture of adductor longus with haematoma

LOW APPROACH (LOCKWOOD) , simplest operation for a femoral hernia , THE INGUINAL APPROACH
(LOTHEISSEN) , HIGH APPROACH (McEVEDY)

VENTRAL HERNIA : to hernias of the anterior abdominal wall. Umbilical–paraumbilical ● Epigastric ●

Incisional ● Parastomal ● Spigelian ● Lumbar ● Traumatic

Umbilical hernia in children , Common in infants and most resolve spontaneously ● Rarely strangulate

Umbilical hernia in adults

Conditions that cause stretching and thinning of the midline raphe (linea alba), such as pregnancy,
obesity and liver disease

Epigastric hernia : hernias arise through the midline raphe (linea alba) any where between the xiphoid
process and the umbilicus, usually midway.

. Incisional hernia a defect in the musculofascial layers of the abdominal wall in the region of a
postoperative scar.

Spigelian hernia. through a defect in the spigelian fascia, which is the aponeurosis of transversus
abdominis. Most spigelian hernias appear below the level of the umbilicus near the edge of the rectus

sheath, but

Lumbar hernia , A lumbar hernia must be distinguished from: ● a lipoma; ● a cold (tuberculous) abscess
pointing to this position; ● a pseudo-hernia due to local muscular paralysis. Lumbar pseudo-hernia

Parastomal hernia When surgeons create a stoma, such as a colostomy or ileostomy, they are effectively
creating a hernia by

Traumatic hernia , abdominal stab wound , abdominal stab wound , secondary to muscle atrophy that
occurs as a result of nerve injury or other traumatic

UMBILICAL CONDITIONS IN THE ADULT ,: Chronic infection , Chronic fistula

Patent urachus A connection between the urinary bladder and umbilicus usually presents in later life.

Abdominal compartment syndrome : of high intra-abdominal pressures that , occur in severe

intraabdominal sepsis, such as pancreatitis and also aortic aneurysm rupture. High , Tension-releasing
incisions, equivalent to a fasciotomy,

Desmoid tumour : a hamartoma

Fibrosarcoma

61

PERITONITIS

a primary ‘spontaneous’ peritonitis, in which a pure infection with streptococcal, pneumococcal or

haemophilus bacteria occurs.

Paths to peritoneal infection ● Gastrointestinal perforation, e.g. perforated ulcer, appendix,

diverticulum ● Transmural translocation (no perforation), e.g. pancreatitis, ischaemic bowel, primary
bacterial peritonitis ● Exogenous contamination, e.g. drains, open surgery, trauma, peritoneal dialysis ●
Female genital tract infection, e.g. pelvic inflammatory disease ● Haematogenous spread (rare), e.g.
septicaemia

Bacteria from the gastrointestinal tract

The biliaryand pancreatic tracts are also normally free from bacteria,

gallstones. Peritoneal infection , Gram-negative bacteria contain endotoxins , Clostridium perfringens,

exotoxins. Bacteroides spp.

Microorganisms in peritonitis Gastrointestinal source ● Escherichia coli ● Streptococci ● Enterococci ●

Bacteroides spp. ● Clostridium spp. ● Klebsiella pneumoniae Other sources ● Chlamydia trachomatis ●
Neisseria gonorrhoeae ● Haemolytic streptococci ● Staphylococci ● Streptococcus pneumoniae ●
Mycobacterium tuberculosis and other species ● Fungal infections

The greater sac of the peritoneum is divided into (1) the subphrenic spaces, (2) the pelvis and (3) the
peritoneal cavity proper. TheThe last is divided into a supracolic and an infracolic compartment by the
transverse colon and transverse mesocolon,

Diffuse (generalised) peritonitis

Speed of peritoneal contamination is a prime factor. 2Stimulation of peristalsis by the ingestion .

virulence of the infecting organism, Young children have a small omentum, which is less effective in
localising infection. Disruption of localised collections may occur with injudicious handling, e.g. appendix
mass or pericolic abscess. ● Deficient natural resistance (‘immune deficiency’)
Clinical features of peritonitis ● Abdominal pain, worse on movement, coughing and deep respiration ●
Constitutional upset: anorexia, malaise, fever, lassitude ● GI upset: nausea ± vomiting ● Pyrexia (may be
absent) ● Raised pulse rate ● Tenderness ± guarding/rigidity/rebound of abdominal wall ●
Pain/tenderness on rectal/vaginal examination (pelvic peritonitis) ● Absent or reduced bowel sounds ●
‘Septic shock’ (systemic inflammatory response syndrome [SIRS] and multi-organ dysfunction syndrome
[MODS]) in later stages , hiccup

Diagnostic

Urin analysis UTI , ecg , Baseline urea and electrolytes (U&Es) for treatment. ● Full blood count for white
cell count (WCC). ● Serum amylase estimation may establish the diagnosis of acute pancreatitis

radiograph to demonstrate free subdiaphragmatic gas perforation and peritonitis ; tomography (CT) is
increasingly used to identify the cause of peritonitis ; Ultrasonography has undoubted value in certain
situations such as pelvic peritonitis in women and localised right upper quadrant peritonism.

Causes of bile peritonitis ● Perforated gall bladder secondary to inflammation or obstruction (especially
empyema) ● Post-cholecystectomy: Cystic duct stump leakage Leakage from an accessory duct in the
gall-bladder bed Bile duct injury T-tube drain dislodgement (or tract rupture on removal) ● Following
other operations/procedures: Duodenal injury Leaking duodenal stump post gastrectomy Leaking
biliary–enteric anastomosis Leakage around percutaneously placed biliary drains ● Blunt or penetrating
hepatobiliary or duodenal trauma

Spontaneous bacterial peritonitis (SBP; sometimes called primary bacterial peritonitis) is an acute
bacterial infection of ascitic fluid.

Clinical features usually include local symptoms and/or signs of peritonitis, GI upset (secondary to ileus,
e.g. nausea and vomiting), signs of systemic inflammation (hyper- or hypothermia, chills, tachycardia
and tachypnoea ± signs of septic shock), worsening liver and renal function, hepatic encephalopathy and
GI bleeding.

diagnosis is made by paracentesis, an increased neutrophil of , gram-negative bacteria, usually E. coli,

and gram-positive cocci (mainly streptococci and enterococci). a third-generation cephalosporin, e.g.
cefotaxime, Complications of SBP, e.g. septic shock, GI bleeding and hypoalbuminaemia,

Primary pneumococcal peritonitis Haemophilus spp., group A streptococci and a few gram-negative
bacteria.

that the is route of infection sometimes via the vagina and fallopian tubes. At other times, and always in
boys, the infection is blood borne and secondary to respiratory tract , useful. Laparotomy or laparoscopy
may be used. Should the exudate be odourless sticky
Tuberculous peritonitis , where Mycobacterium avium-intracellulare is , patients with extrapulmonary
TB and includes intraperitoneal, GI tract and solid organ disease forms, with TB peritonitis being a
common site-specific (ileocaecal is

Tuberculous peritonitis ● Acute (may be clinically indistinguishable from acute bacterial peritonitis) and
chronic forms ● Abdominal pain, sweats, malaise and weight loss are frequent ● Ascites common, may
be loculated ● Caseating peritoneal nodules are common – distinguish from metastatic carcinoma and
fat necrosis of pancreatitis ● Intestinal obstruction may respond to anti-tuberculous treatment without
surgery

Familial Mediterranean fever (periodic peritonitis)

Familial Mediterranean fever (periodic peritonitis) is characterised by abdominal pain and tenderness,
mild pyrexia, polymorphonuclear leukocytosis and, occasionally, pain in the thorax and joints.

Risk in history of undergone appendicectomy , affected. Mutations in the MEFV (Mediterranean fever)
gene

Clinical features of an abdominal/pelvic abscess Symptoms ● Malaise, lethargy – failure to recover from
surgery as expected ● Anorexia and weight loss ● Sweats ± rigors ● Abdominal/pelvic pain ● Symptoms
from local irritation, e.g. shoulder tip/hiccoughs (subphrenic), diarrhoea and mucus (pelvic), nausea and
vomiting (any upper abdominal) Signs ● Increased temperature and pulse ± swinging pyrexia ● Localised
abdominal tenderness ± mass (including on pelvic exam)

Pelvic abscess

most common site of abscess formation, apendicx and fallopian tube infection , pelvic pain, diar-

rhoea and the passage of mucus in the stools

Investigation and management ; dranage , (viginal , but chok , rectal)

Abdominal abscess 4 space: 1 the left subphrenic space; 2, left subhepatic space/lesser sac; 3,

right subphrenic space; 4, right subhepatic space.

Clinical future : pain ,fever sweting , anorexia hiccup, tenderness

Investigation : X- Ray( colaps lung plural effiusion , empyema ) – us or ct guide dranage

Ascites is defined as an accumulation of excess serous fluid within the peritoneal cavity.

Capillary pressure may be increased because of generalised water retention, cardiac failure, constrictive
pericarditis or vena cava obstruction. Capillary

Plasma colloid osmotic pressure may be lowered in patients with reduced nutritional intake, diminished
intestinal absorption, abnormal protein losses or defective protein synthesis, such as occurs in cirrhosis.
Peritoneal lymphatic drainage may be impaired, resulting in the accumulation of protein-rich fluid.
Causes of ascites Transudates (protein <25 g/L) ● Low plasma protein concentrations: Malnutrition
Nephrotic syndrome Protein-losing enteropathy ● High central venous pressure: Congestive cardiac
failure ● Portal hypertension Portal vein thrombosis Cirrhosis Exudates (protein >25 g/L) ● Peritoneal
malignancy ● Tuberculous peritonitis ● Budd–Chiari syndrome (hepatic vein occlusion or thrombosis) ●
Pancreatic ascites ● Chylous ascites ● Meigs’ syndrome

Clinical f: more 1.5 L fluid , dull percisssion , aspiration

Chylous ascites : the ascitic fluid appears milky because of an excess of chylomicrons (triglycerides).
Most cases are associated with malignancy, usually lymphomas; other causes are cirrhosis, TB, filariasis,
nephrotic syndrome, abdominal trauma (including surgery), constrictive pericarditis, sarcoidosis and
congenital lymphatic abnormality.

Carcinomatosis peritonei L: a common terminal event in many cases of carcinoma

Pseudomyxoma peritonei This rare condition occurs more frequently in women. The abdomen is filled
with a yellow jelly, large quantities of which are often encysted.

Pseudomyxoma peritonei This rare condition occurs more frequently in women. The abdomen is filled
with a yellow jelly, large quantities of which are often encysted. Inflammation , the coagulation cascade.

The most common adhesion-related problem is small bowel obstruction (SBO).

PREVENTUION : Minimising the production of ischaemic tissue by careful surgical technique, including ,
drugs including antiinflammatory drugs such as aspirin and steroids, some hormones, anticlotting
agents, antibiotics, vitamin E an9).

Rutherford Morison called the greater omentum ‘the abdominal policeman’.

Torsion of the omentum is a rare emergency and consequently is seldom diagnosed correctly.mistake
appendicitis can cause ischemia

The term ‘misty mesentery’ indicates a pathological increase in mesenteric fat attenuation at CT

Mesenteric cysts: clinical features : Cysts occur most commonly in adults with a mean age of 45 years ●
Twice as common in women as in me ● Rare: incidence around 1 per 140 000 ● Approximately a third of
cases occur in children younger than 15 years ● The mean age of children affected is 4.9 years ● The
most common presentation is of a painless abdominal swelling with characteristic physical signs there is
a fluctuant swelling near the umbilicus the swelling moves freely in a plane at right angles to the
attachment of the mesentery (Tillaux’s sign) (Figure 61.12) there is a zone of resonance around the cyst
● Other presentations are with recurrent attacks of abdominal pain with or without vomiting (pain
resulting from recurring temporary impaction of a food bolus in a segment of bowel narrowed by the
cyst or possibly from torsion of the mesentery) and acute abdominal catastrophe, due to: torsion of that
portion of the mesentery containing the cyst rupture of the cyst, often as a result of a comparatively
trivial accident haemorrhage into the cyst infection
Mesenteric tumours Benign ● Lipoma ● Fibroma ● Fibromyxoma Malignant ● Lymphoma ● Secondary
carcinoma Tumours

Causes of retroperitoneal fibrosis Benign ● Idiopathic (Ormond’s disease) ● Chronic inflammation ●

Extravasation of urine ● Retroperitoneal irritation by leakage of blood or intestinal content ● Aortic
aneurysm (inflammatory type) ● Trauma ● Drugs (chemotherapeutic agents and previously
methysergide) Malignant ● Lymphoma ● Carcinoid tumours ● Secondary deposits (especially from
carcinoma of stomach, colon, breast and prostate)

70

ANATOMY OF THE LARGE INTESTINE

The colon is distinguished from the small bowel by having fat-filled peritoneal tags known as appendices
epiploicae and the taenia coli. haustrations.

the superior mesenteric artery from the caecum to the distal transverse colon and the inferior
mesenteric artery and its branches more distally. Adjacent

Absorption of nutrients including glucose, fatty acids, amino acids and vitamins can also take place in the
colon.water vitk d

TUMOURS OF THE LARGE INTESTINE

Benign : Adenomatous polyps , Familial adenomatous polyposis

Classification of intestinal polyps. Inflammatory Inflammatory polyps (pseudopolyps in UC) Metaplastic

Metaplastic or hyperplastic polyps Hamartomatous Peutz–Jeghers polyp Juvenile polyp Neoplastic
Adenoma Tubular Tubulovillous Villous Adenocarcinoma Carcinoid tumour

The term ‘polyp’ is a clinical description of any protrusion of the mucosa.

Colorectal cancer – adenocarsinoma

Risk factors : genes mutation , ditery habit ( meat products) animal fat , alchol smoking - right ( anemia .
weoght loos , ischmia smaller ) left ( ileuse perforation , more common , bigger

Type : anullar , tubular , ulcer, cauliflower )

Dukes’ staging for colorectal cancer ● A: invasion of but not breaching the muscularis propria ● B:
breaching the muscularis propria but not involving lymph nodes ● C: lymph nodes involved. Dukes
himself never described a stage D, but this is often used to describe metastatic disease

TNM classification for colonic cancer ● T Tumour stage T1 Into submucosa T2 Into muscularis propria T3
Into pericolic fat or subserosa but not breaching serosa T4 Breaches serosa or directly involving another
organ ● N Nodal stage N0 No nodes involved N1 1-3 nodes involved N2 Four or more nodes involved ●
M Metastases M0 No metastases M1 Metastases

Symptom: rectal bleeding bowl habit change , anemia , pain constipation

Surgical pr : hemicolectomy

‘inflammatory bowel disease’ (i.e. ulcerative colitis [UC] and Crohn’s disease [CD].

Ulcerative colitis: the rectum and colon , ages of 20 and 40.rectal bleeding discharge pain bowl habit
change, can cause arthritis , ankiylosis , skin erythematous nodusoum , mucusa and submocusa

Mild disease is characterized by fewer than four stools daily, with or without bleeding. There are no
systemic signs of toxicity. ● Moderate disease corresponds to more than four stools daily, but with few
signs of systemic illness. There may be mild anaemia. Abdominal pain may occur. Inflammatory markers,
including erythrocyte sedimentation rate and C-reactive protein, are often raised. ● Severe disease
corresponds to more than six bloody stools a day and evidence of systemic illness, with fever,
tachycardia, anaemia and raised inflammatory markers. Hypoalbuminaemia is common and an ominous
finding. ● Fulminant disease is associated with more than 10 bowel movements daily, fever, tachycardia,
continuous bleeding, anaemia, hypoalbuminaemia, abdominal tenderness and distension, the need for
blood transfusion

Distinguishing ulcerative colitis (UC) and Crohn’s disease (CD).

UC CD Macroscopic Distribution Colon/rectum Anywhere in the gastrointestinal tract Rectum Always

involved Often spared Perianal disease Rare Common Fistula formation Rare Common Stricture Rare
Common Microscopic Layers involved Mucosa/submucosa Full thickness Granulomas No Common
Fissuring No Common Crypt abscesses Common Rare

Colonoscopy and biopsy has a key role in diagnosis and management:

OPERATIVE TREATMENT FOR UC

Subtotal colectomy( rmove all colon except sigmoid and anastomosis with small gut)

End ileostomy ( end ilum on sufuce of abdimenal wall)

ileoanal anastomosis with pouch ( J ,S ,W type )

Crohn’s disease.

Mostly small but colon also and anywhere in GIT , Colonic strictures The presence of skip lesions, rectal
sparing, non-caseating granulomas or perianal disease will point to CD. irregular Crohn’s stricture with
polypoid mucosa may be almost indistinguishable from malignancy ,full thicness

Infection with Campylobacter jejuni

Intestinal amoebiasis Entamoeba histolytica has a worldwide distribution and is transmitted mainly in
contaminated drinking water. Colonic ulcer , perforation bleeding hemmot=rage stricture , treatment
metronidazol

Colonic diverticula Diverticula (hollow out-pouchings) are a common structural abnormality. They

Congenital. All three coats of the bowel are present in the wall of the diverticulum (e.g. Meckel’s
diverticulum). 2 Acquired. There is no muscularis layer present in the diverticulum (e.g. sigmoid
diverticular disease).

deficient in dietary fibre.collagen ddisorder, symptom: oain inflammation , perforation , obstructure h

Complications of diverticular disease ● Diverticulitis ● Abscess ● Peritonitis ● Intestinal obstruction ●

Haemorrhage ● Fistula formation

degree of infection has a major impact on outcome in acute diverticulitis.

Hinchey classification of complicated diverticulitis. Grade I Mesenteric or pericolic abscess Grade II Pelvic
abscess Grade III Purulent peritonitis Grade IV Faecal peritonitis

Investigation colonoscopy P see the opening of divertocula

Operative procedures for diverticular disease: Hartmann’s procedure (sigmoid resection with formation
of left iliac fossa colostomy and closure of the rectal stump)

COLOSTOMIES A colostomy (or ileostomy) stoma is a planned opening made in the colon (or small
intestine) to divert faeces and flatus to the abdominal wall where they can be collected in an external
appliance. Loop colostomy , end colostomy

Stomas ● May be colostomy or ileostomy ● May be temporary or permanent ● Temporary or

defunctioning stomas are usually fashioned as loop stomas ● An ileostomy is spouted; a colostomy is
flush ● Ileostomy effluent is usually liquid whereas colostomy effluent is usually solid ● Ileostomy
patients are more likely to develop fluid and electrolyte problems ● An ileostomy is usually sited in the
right iliac fossa ● End-colostomy is usually sited in the left iliac fossa ● Whenever possible patients
should be counselled and sited by a stoma care nurse before operation

Stoma complications ● Skin irritation ● Prolapse ● Retraction ● Ischaemia ● Stenosis ● Parastomal

hernia ● Bleeding ● Fistulation

Illnesses associated with constipation ● Neurological conditions ● Parkinson’s disease ● Multiple

sclerosis ● Diabetic nephropathy ● Spinal cord lesion ● Endocrine conditions ● Hypothyroidism ●
Hypercalcaemia

Drugs that can cause constipation ● Benzodiazepines ● Carbamazepine ● Chlorpromazine ●

Cholestyramine ● Iron ● Opiates, particularly codeine and morphine ● Tricyclic antidepressants ● Statins

irritable bowel syndrome (IBS) : but abdominal discomfort, bloating, irregularity of bowel habit and
passage of mucus are common.
55

The right main bronchus (RMB) is shorter, wider and nearly vertical compared with the left main
bronchus (LMB). As a consequence, inhaled foreign bodies are more likely to enter the right main
bronchus than the left (Figure

(Pneumothorax

is the presence of air outside the lung, within the pleural space. It must be distinguished from bullae or
air cysts within the lung. Bullae

into primary spontaneous pneumothorax (PSP) and secondary spontaneous pneumothorax (SSP).

Tension pneumothorax is when (independent of aetiology) there is a build up of positive pressure within
the hemithorax, to the extent that the lung is completely collapsed, the diaphragm is flattened, the
mediastinum is distorted and, eventually, the venous return to the heart is compromised.

surgical emphysema (or subcutaneous emphysema) occurs when air/gas is located in the
subcutaneous tissues (the layer under the skin). This usually occurs in the chest, face or
neck. The most serious cause is a ruptured oesophagus.

Primary spontaneous pneumothorax : be tall and have a family history , due to leaks from small
blebs, vesicles or bullae, at the apex of the upper lobe or on the upper border of the lower or
middle lobes.
Secondary spontaneous pneumothorax: This occurs when the visceral pleura leaks as part of
an underlying lung disease; any disease that involves the pleura may cause pneumothorax,
including tuberculosis, any degenerative or cavitating lung disease and necrosing tumours.
with sharp pleuritic pain and breathlessness. TheBleeding and tension pneumothorax can
occur.
use of small bore (10–14Fr) chest drains, intercostal tube connected
The safest site for insertion of a drain (Figure 55.8) is in the triangle that lies: ● anterior to the
mid-axillary line; ● above the level of the nipple; ● below and lateral to the pectoralis major
muscle. 5th ics above the rib ( below the rib nerve , vessl , toward the apex but for plural
effiusion toward base of lung_)
Surgical management of pneumothorax Pleurectomy and pleurodesis
Pleural effusions are divided into exudates and transudates, depending on protein content
(more (exudates) or less (transudates) than 30g/L), and characterised further according to
glucose content, pH and lactate dehydrogenase content.
● Elevated pulmonary capillary pressure.
● Reduced intravascular oncotic pressure.
Accumulation of pleural protein due
● Excessive permeability of the capillaries
Pleural effusion is a common complication of cancer. lung cancer; ● pleural involvement with
primary or secondary malignancy; ● mediastinal lymphatic involvement.
Pleural infection and empyema :end stage of pleural infection
and three phases of empyema are described: In the exudative phase, 2 the fluid thickens to
what is known as the fibrinopurulent phase. 3. The organising phase causes the lung to be
trapped by a thick peel or ‘cortex’ for which
Thoracoscopy or video-assisted thoracoscopic surgery (VATS)
55.4 Uses of bronchoscopy. Diagnostic Confirmation of disease: carcinoma of the bronchus;
inflammatory or infective processes Investigative Tissue biopsy Preoperative assessment
Before lung resection Before oesophageal resection Persistent haemoptysis Therapeutic
Removal of secretions Removal of foreign bodies Stent placement, endobronchial resection,
etc.
Causes of airway narrowing. Intraluminal Inhaled foreign body Neoplasm000000000000
Intramural Congenital stenosis Fibrous stricture (post-intubation or tuberculosis) Extramural
Neoplasm (thyroid cancer, secondary deposits) Aortic arch aneurysm

54

CARDIOPULMONARY BYPASS : open heart surgery

The heart is approached mainly by a median sternotomy. thymus and pleurae are dissected from the
pericardium and the pericardium is opened. Before cannulation for CPB, the patient is fully heparinised.
Other incisions that can be used include left or right anterolateral thoracotomy for

Arterial cannulation : ascending aorta, femoral artery or the axillary artery.

Venous cannulation: The venous pipe has end holes that sit in the inferior vena cava and side holes that
sit in the right atrium (to take drainage from the superior vena cava). Alternatively, the superior and
inferior vena

The methods of myocardial protection include intracoronary infusion of a cardioplegic solution

(antegrade), infusion via the coronary sinus (retrograde), intermittent cross-clamp fibrillation and total
circulatory arrest.

Cardioplegic solutions contain potassium as the arresting agent.

. Cold (4–10ºC) isotonic crystalloid or blood solutions aid myocardial protection by reducing metabolic
requirements through local hypothermia. Warm cardioplegic solutions, on the other hand, may facilitate
better myocardial repair recovery postoperatively by aiding activation of intramyocardial enzymes.

intermittent cross-clamp fibrillation is a versatile and cost-effective method of myocardial

protection, with the immediate postoperative outcome comparable to cardioplegic arrest in first-
time coronary artery bypass graft (CABG)
safe. Difficulties can occur during cannulation (aortic dissection or atrial injury), at the start of CPB
(oxygenator failure) and at the end of CPB (coagulopathy). Many

Potential complications of CPB ● Bleeding disorders ● Infection ● Air embolism ● Intestinal

ischaemia/infarction ● Microembolisation ● Myocardial depression ● Neurological dysfunction ●
Pancreatitis ● Postcardiotomy syndrome ● Pulmonary injury ● Systemic organ dysfunction ● Vascular
injury

coronary arteries are branches of the ascending aorta, arising from ostia in the aortic sinuses above the
aortic valve, the right from the anterior sinus and the left from the left posterior sinus

branches, the left anterior descending artery (LAD) or anterior interventricular artery and
obtuse/marginal (OM) branches of the circumflex artery. The LAD is the most frequently diseased
coronary artery and most often bypassed during CABG surgery.

The right coronary artery (RCA) passes from its origin anteriorly between the right atrial appendage and
the pulmonary trunk and courses in the atrioventricular groove around the margin of the right ventricle.
It usually forms an anastomosis with the circumflex artery at the junction of the right and left atria and
the interventricular septum (the crux). It continues as the posterior descending artery or interventricular
artery.

The question of anatomical dominance is determined by the artery that supplies the posterior
descending artery.

Coronary angiography ● ‘Gold standard’ for imaging of anatomy ● Demonstrates extent, severity and
location of stenoses ● Reduction in diameter of >70% is considered severe (90% reduction in cross-
sectional area) ● Demonstrates quality and size of distal arterial tree ● Aids diagnosis of ischaemia ●
Evaluates suitability for surgery ● Aids in prognostic assessment

Indication for surgery ● >50% stenosis of the left main stem (‘critical left main stem disease’) ● >50%
stenosis of the proximal left anterior interventricular artery ● Two or three main coronary arteries
diseased (‘triple-vessel disease’) ● Poor ventricular function associated with multivessel disease

The long saphenous vein is the most common vein used Venous grafts Alternative vein conduits include
the short saphenous vein or upper limb veins such as the cephalic vein;

Arterial grafts The left internal mammary artery (LIMA), or internal thoracic artery, the radial artery as a
second

Allen’s test ● The patient makes a tight fist while the surgeon compresses both distal and ulnar arteries
digitally; this squeezes blood from the hand ● The hand is then relaxed and compression of the ulnar
artery is released; the speed of returning colour to the hand is assessed ● If colour returns in 5–7 s,
patency and collateral flow from the ulnar artery is confirmed

Biological valves include homograft (or allograft) valves, removed from cadavers; autografts, a patient’s
own valve; and, most commonly, heterografts (or xenografts) prepared
Causes of mitral valve disease Stenosis ● Rheumatic heart disease (common) ● Calcification of valve or
chordae ● Congenital (rare) Regurgitation ● Rheumatic heart disease ● Valve prolapse ● Left ventricular
dilatation or hypertrophy ● Ischaemia ● Bacterial endocarditis

Causes of aortic regurgitation according to predominant anatomical location of pathology Valve leaflet
disease ● Congenital, e.g. bicuspid valve leading to degenerative changes, occasionally with ventricular
septal defect ● Rheumatic heart disease ● Infective endocarditis Aortic wall pathology ● Inflammatory,
e.g. connective tissue disorders such as ankylosing spondylitis, systemic lupus erythematosus,
rheumatoid arthritis ● Systemic disease, e.g. tertiary syphilis ● Degenerative, e.g. Marfan syndrome,
aortic root dissection, senile aortopathy, leading to aortic root/annular dilatation

Causes of aortic valve disease Stenosis ● Congenital ● Rheumatic heart disease ● Acquired calcification
and fibrosis of valve or chordae tendineae with age Regurgitation ● Rheumatic heart disease ● Infective
endocarditis ● Congenital ● Inflammatory: Systemic lupus erythematosus Rheumatic ankylosing
spondylitis ● Dilatation of aortic root: Marfan syndrome Dissection ● Systemic disease: Syphilis
Ulcerative colitis

(Atrial septal defects ASDs) Common defects ● Ostium secundum: fossa ovalis defect (approximately
70% of ASDs) ● Ostium primum: atrioventricular septal defect (approximately 20% of ASDs) ● Sinus
venosus defect: often associated with anomalous pulmonary venous drainage (approximately 10% of
ASDs) ● Patent foramen ovale: common in isolation, usually no left-toright shunt (not strictly an ASD)
Rarer defects ● Inferior vena cava defects: a low sinus venosus defect and may allow shunting of blood
into the left atrium ● Coronary sinus septal defect: also known as unroofed coronary sinus, with the left
superior vena cava draining to the left atrium as part of a more complex lesion

Types of ventricular septal defects (VSD) Perimembranous defect ● Also called conoventricular VSD; the
most common defect (70–80%), usually located within the membranous septum and may extend to the
tricuspid valve annulus or base of the aortic valve Muscular defect ● Also called trabecular VSD; occurs
in 10% of cases and is located within the membranous septum and often multiple Atrioventricular defect
● Also called atrioventricular canal-type or inlet defect; occurs in 5% of cases and is located in the
atrioventricular canal beneath the tricuspid valve Subarterial defect ● Also called outlet or subarterial
VSD; occurs in 5–10% of cases and lies within the conal septum immediately beneath the pulmonary
valve annulus.

bulge or ballooning in the wall of a blood vessel.A true aneurysm is a localised dilatation of a
blood vessel involving all layers of the vessel, whereas a false aneurysm has compressed supporting
tissue as its wall, and is usually the result of a defect in the vessel intima (from trauma, dissection or
previous surgery). Aneurysms are described as fusiform when the whole circumference is affected or
saccular when only part of the circumference is involved.

most common aetiology is atherosclerosis,

Aortic dissection This occurs when a defect or flap occurs in the intima of the aorta, resulting in blood
tracking into the aortic tissues splitting the medial layer and creating a false lumen. It most commonly
occurs in the ascending aorta

Predisposing factors for aortic dissection ● Age ● Hypertension ● Marfan syndrome ● Pregnancy ●
Other connective tissue disorders, for example Ehlers–Danlos syndrome, giant cell arteritis, systemic
lupus erythematosus ● Coarctation of the aorta ● Turner or Noonan syndromes ● Aortic cannulation
site (iatrogenic)

develop. If the pressure exceeds the pressure in the atria, compression will occur, venous return will fall
and the circulation will be compromised. This state of affairs is called ‘tamponade’.

The clinical features are low blood pressure with a raised jugular venous pressure and paradoxical pulse.
Kussmaul’s sign

Emergency treatment of pericardial tamponade is aspiration of the pericardial space.

Pericarditis Infection and inflammation may also affect the pericardium. Acute pericarditis usually occurs
following a viral illness. Treatment is with non-steroidal anti-inflammatory drugs

Atrial myxoma This is the most common benign cardiac mass in adult.

Rhabdomyoma This is the most common benign cardiac tumour in childern.

14

A simple system for checking radiographs Label Name of patient Site Date of examination Side (check
marker) What part is the film centered on? Does the film cover the whole area required? Is there more
than one view? Quality Is the penetration appropriate? Compare How have the appearances changed
from previous images? Conclude Is the diagnosis clear? Is further imaging needed?

Contrast media : Potential problems include allergic reaction and nephrotoxicity.

higher-density tissues result in a greater reduction in the number of x-ray photons and reduce the
amount of blackening caused by those photons. In terms of conventional radiographs,

It is cheap, universally available, easily reproducible and comparable with prior examinations and, in
many instances, has a relatively low dose of ionising radiation in contrast to more complex
examinations.

uses fluorescent screens to allow real-time monitoring of organs and structures as opposed to the
‘snapshot’ images obtained with radiographs.

Motility of the bowel can also be assessed in this way. Fluoroscopy angiography

such as musculoskeletal and breast ultrasound. Dedicated transducers have also been developed for
endocavitary ultrasound, such as transvaginal scanning and transrectal ultrasound of the prostate,
allowing high-frequency

principle forms the basis of Doppler ultrasound, whereby velocities within major vessels, as well as
smaller vessels in organs such as the liver and the kidneys, can be measured. Doppler imaging is widely
used in the assessment of arterial and venous disease, gynaecological , and testicular disorders,

Ligament, tendon and muscle injuries are also probably best imaged in the first instance by ultrasound
Ultrasound Strengths ● No radiation ● Inexpensive ● Allows interaction with patients ● Superb soft-
tissue resolution in the near field ● Dynamic studies can be performed ● First-line investigation for
hepatic, biliary and renal disease ● Endocavitary ultrasound for gynaecological and prostate disorders ●
Excellent resolution for breast, thyroid and testis imaging ● Good for soft tissue, including tendons and
ligaments ● Excellent for cysts and foreign bodies ● Doppler studies allow assessment of blood flow ●
Good real-time imaging to guide interventional biopsies and drainages Weaknesses ● Interpretation
only possible during the examination ● Long learning curve for some areas of expertise ● Resolution
dependent on the machine available ● Images cannot be reliably reviewed away from the patient

Computed tomography Strengths ● High spatial and contrast resolution ● Contrast resolution enhanced
by ability to image in multiple phases, including arterial, venous and delayed ● Rapid acquisition of
images in one breath-hold ● Imaging of choice for the detection of pulmonary masses ● Allows global
assessment of the abdomen and pelvis ● Excellent for liver, pancreatic, renal and bowel pathology ●
Three-dimensional reconstruction allows complex fracture imaging ● Multiplanar reconstruction and
three-dimensional imaging, ● e.g. CT angiography and colonoscopy ● Ability to guide intervention such
as percutaneous biopsy and drainage Weaknesses ● High radiation dose ● Poor soft-tissue resolution of
the peripheries and superficial structures ● Patient needs to be able to lie flat and still

Magnetic resonance (MR) imaging Strengths ● No ionising radiation ● Excellent soft-tissue contrast ●
Best imaging technique for Intracranial lesions Spine Bone marrow and joint lesions Evolving use ●
Staging ● MRCP ● MR angiography ● Breast malignancy ● Pelvic malignancy ● Cardiac imaging ● MR
enterography ● Diffusion-weighted imaging Weaknesses ● Absolute contraindications Ocular metallic
foreign bodies Pacemakers Cochlear implants Cranial aneurysm clips Cochlear implants Cranial
aneurysm clips ● Relative contraindications First trimester of pregnancy Claustrophobia ● Long scan
times so patients may not be able to keep still, especially if in pain ● Limited availability ● Expensive

Types of imaging ● Radiographs are the best first-line test for bone lesions and fractures ● MRI is good
for diagnosing bone marrow disease, occult fractures and tendon and soft-tissue disorders ● CT enables
visualisation of the fine detail of bony structures ● CT gives the best three-dimensional information on
fractures ● Ultrasound has better resolution in accessible soft tissues and can be used dynamically ●
Ultrasound is the best method of distinguishing solid from cystic lesions ● Ultrasound is the only method
for locating non-metallic foreign bodies ● Ultrasound is the best method for detecting muscle hernias

Radionuclide imaging Strengths ● Allows functional imaging ● Allows imaging of the whole body ● Bone
scan has a high sensitivity for metastatic bone disease, fractures and infection ● PET scanning is valuable
in the detection of metastatic cancer Weaknesses ● Specific agents are required for specific indications
● Often non-specific and an abnormal result may require further imaging ● Generally poor spatial
resolution

Trauma imaging ● Initial imaging is either radiography or CT ● At least two views are needed for
radiographs ● Use CT for spine, intra-articular or occult fractures

Imaging techniques for joint disease ● Radiographs are good for assessing established articular disease ●
Synovitis can be detected using ultrasound or contrastenhanced MRI ● Early damage to articular
cartilage is difficult to image by conventional methods ● Rotator cuff lesions are best studied using
ultrasound or MRI ● Destructive lesions are best studied first on plain radiographs ● MRI is best for
staging tumours ● Biopsy can be guided by fluoroscopy, CT or ultrasound
Imaging of aggressive lesions in bone ● Plain radiographs are important as a first investigation ● MRI is
best for local staging ● Bone scintigraphy or whole-body MRI for solitary or multiple lesion
determination ● CT detects lung metastases ● Fluoroscopy, CT, MRI or ultrasound can be used to guide
the biopsy

Imaging of soft-tissue lesions ● Ultrasound is the best for screening; it is often the only imaging required
● MRI is best for local staging and follow-up ● Doppler ultrasound can assess vascularity cheaply and
effectively ● Ultrasound is useful for biopsy

Imaging of potentially infected bone and joint ● Plain radiographs may be needed to exclude bone
erosion ● Ultrasound is sensitive for an effusion, periosteal collections and superficial abscesses and can
be used for guided aspiration ● CT is useful in established infection to look for sequestrum ● MRI is
useful to define the activity of osteomyelitis, early infection and soft-tissue collections ● Bone scans are
sensitive but of low specificity ● Complex nuclear medicine studies are useful in negative MR
examinations or equivocal cases

appropriate). Together, the patient and the surgeon select the course of action that seems best.

consent form is intended to serve as legal documentation of these discussions between the physician
and the patient.

In patients with cirrhosis, the Child-Pugh classification and Model for End-stage Liver Disease (MELD)
score should be calculated to assist in preoperative risk assessment. The ChildPugh class is based on the
serum bilirubin and albumin levels, prothrombin time, and severity of encephalopathy and ascites

The MELD score is based on serum bilirubin, serum creatinine, and the international normalized ratio
(INR) and is calculated by the formula:

Gastrointestinal Tract Tubes :

Nasogastric tubes are usually used to evacuate the gastric contents. They are most commonly used in
patients who have ileus or obstruction.

Nasoenteric tubes are usually intended for feeding.

Nasobiliary(biliary tree when there is an obstructing process (stone, tumor, stricture) , T-tubes are
placed within the common bile duct for the purpose of drainage.

Respiratory Tract Tubes: Chest tubes are placed into the pleural cavity to evacuate air (pneumothorax),
blood (hemothorax), or fluid (effusion). Endotracheal tubes (longterm mechanical ventilation

Urinary Tract Tubes: “Foley” catheters, are placed to straight drain.

Surgical Drains Closed suction , Sump suction drains, Passive tubes

Deep Vein Thrombosis Prophylaxis : Virchow’s three risk factors for venous thrombosis: stasis,
hypercoagulability, and endothelial injury. Low-dose unfractionated heparin is as effective in this
population as lowmolecular-weight heparin and is usually less expensive.
POSTOPERATIVE COMPLICATIONS

Malignant Hyperthermia : This produces violent and sustained muscle contraction and rigidity, heat
production, and acidosis. Muscle necrosis and rhabdomyolysis may occur. The the first sign. Masseter
muscle rigidity is seen , Tachycardia, cyanosis, and muscle rigidity are prominent features. Compartment
syndromes may develop. Rhabdomyolysis may produce myoglobinuria. Dantrolene,

Atelectasis : colaped lung . Management of postoperative atelectasis should begin preoperatively,

Surgical Wound Failure : Dehiscence, or acute surgical wound failure resulting in disruption of the fascial
closure, is acute mechanical failure of the surgical closure.

Fever

directly, this information to the care of patients. In both males and females, TBW is directly proportional
to muscle mass, which is about 70% water, and inversely related to fat, which is about 10% water.

two ECF subdivisions, plasma and interstitial space.

plasma (Table 2-1), sodium is the chief extracellular cation , compartment, the intracellular dominant
cations are potassium and magnesium and the dominant anions

Sodium resorption in exchange for potassium and hydrogen ion secretion in the distal tubules is a direct
effect of the adrenal cortical hormone aldosterone.

. Extracellular volume reduction, particularly in the intravascular space, is a potent stimulus for
aldosterone release.

The potassium level, which is usually inversely related to serum sodium concentrations, is the most
sensitive stimulator of aldosterone,

Adrenocorticotropic hormone (ACTH) can also stimulate aldosterone production,

Antidiuretic hormone (ADH, Vasopressin) peaking between 2 and 4 o’clock in the morning, and to a
lesser extent in the early afternoon.

There is increased ADH secretion in response to decreased blood volume; increased plasma osmolarity;

mEq/L. Potassium excretion is directly related to circulating levels of aldosterone, cellular and
extracellular potassium content, and tubular urine flow rates. Acid–base disturbances also exert a
significant influence.

Acid–Base Balance : Buffering systems , Pulmonary ventilation changes , Renal tubular function,

Maintenance • Resuscitation • Replacement

Crystalloid solutions are used initially to replace whole blood losses, but packed red blood cells and
colloid solutions may also be used. Ringer’s Lactate or normal saline solution should be used to replace
the isotonic fluid sequestered in injured tissue.
due to loss of plasma into the interstitial compartment due to burns, sepsis, and local or systemic
inflammatory response to injury. Fluid losses from the gastrointestinal tract (e.g., vomiting, diarrhea,
nasogastric suction)

The use of normal saline is acceptable as a replacement fluid with the caveat that if one is using large
amounts of normal saline, one risks hyperchloremia and worsening acidosis. Lactated Ringer’s is usually
the preferred solution for large-volume resuscitation.

. Ringer’s Lactate is the fluid of choice for blood loss and should be given with a 3:1 ratio because there
is little oncotic gradient, and the egress of the isotonic fluid from the intravascular to the extracellular
space is rapid.

“fluid overload” and “volume excess” involving inflammatory response syndromes or sepsis, the patient
may develop peripheral edema or pleural effusions , of congestive heart failure

compartments, treatment might be as simple as fluid or sodium restriction. If symptoms are severe, the
patient may need diuresis along with replacement of potassium losses.

acidosisbe life threatening. At pH < 7.2, there , As a result, cardiac function may be depressed and lethal
arrhythmias may occur. In addition, potassium is transported to the extracellular space, and can rise to
clinically significant levels, resulting in dysrhythmias.

Respiratory Acidosis Respiratory acidosis is the result of retention of CO2 because of pulmonary alveolar
hypoventilation. It can be acute or chronic. Acute causes are typically respiratory depression as a result
of narcotics, sedatives, muscle relaxants, or anesthetic agents. Decreased respiratory effort due to pain
from surgical incisions, or trauma, altered mechanics of the chest wall due to rib fractures, can also
cause hypoventilation. contusions and lacerations of the lung, pneumonia, or pulmonary edema , Airway
obstruction from a foreign body, misplaced or obstructed endotracheal tube, laryngospasm,

chronic respiratory acidosis is most often caused by advanced lung disease such as COPD.

respiratory cause if the Paco2 is abnormal and the Paco2 and pH change in opposite directions.

acute respiratory acidosis are caused by hypercapnia, and the accompanying hypoxia.

narcosis. This can occur with the administration of supplemental oxygen. In chronic compensated
respiratory acidosis, the stimulus to breathe is hypoxia,

TREATMENT: administering supplemental oxygen, or by instituting mechanical ventilation or simply

improving pain control since many patients have enough postoperative pain that their breathing is
inhibited, resulting in decreased ventilation and subsequent hypercapnia.

Metabolic acidosis can be acute or chronic. One cause of metabolic acidosis is loss of bicarbonate from
the extracellular space. This may be due to diarrhea, intestinal fistula, biliary fistula, or pancreatic fistula.

Chronic bicarbonate losses occur with renal dysfunctions, ureterointestinal anastomosis, decreased
mineralocorticoid activity, and the use of the diuretic acetazolamide,
activity. The second major cause of metabolic acidosis is an increased acid load. Lactic acidosis, occurs
with shock, is due to the production of lactic acid as the body responds to the insult with anaerobic
metabolism , clearance. Ketoacidosis that occurs with untreated hyperglycemia is another cause for
metabolic acidosis, toxins. Liver failure can result in metabolic acidosis when the liver decompensates to
the point where lactate and citrate that are normally produced by the body cannot be metabolized.
Likewise, renal failure can cause metabolic acidosis when the kidney fails to retain bicarbonate as a
result of injury to the tubules.

Normal anion gap is approximately 12 ± 3 mEq/L.

Treatment Identifying the underlying disorder causing metabolic acidosis and correcting it expeditiously
are critical.

Regardless of the cause, a pH more than 7.45 indicates an alkalosis is present.

Respiratory alkalosis is present when an increase in pHa is related to alveolar hyperventilation and a
reduced PaCO2. is common in surgical patients and may be caused by apprehension, pain that does not
impede respiratory effort , acidosis), hypoxia, fever, brain injury, sepsis, and liver failure that results in
elevated serum ammonia. Hypocapnia is also common in patients who are mechanically ventilated.

ventilated. The compensatory mechanism for respiratory alkalosis is renal excretion of bicarbonate,
which is slow, or limited in surgical

Diagnosis Acute respiratory alkalosis may appear similar to hypocalcemia with paresthesias, carpopedal
spasm, and Chvostek’s sign. Potassium, magnesium and calcium, and phosphate metabolism are all
disturbed in alkalotic states. The

correct the underlying cause of the hyperventilation. In the patients who are mechanically ventilated, a
decrease alveolar ventilation by changing respiratory rate or tidal volume will correct

hyperventilation. Chronic respiratory alkalosis usually is asymptomatic and does not require treatment.

Metabolic alkalosis occurs when the pH is elevated in association with an elevated serum bicarbonate

It is one of the most common acid–base abnormalities in surgical patients. Renal and gastrointestinal
losses of potassium and chloride result in hypochloremic, hypokalemic metabolic alkalosis. The infusion
of excess bicarbonate can also cause metabolic alkalosis. Also, the administration of loop diuretics

The kidneys’ response to metabolic alkalosis initially results in alkaline urine as bicarbonate is excreted.
With hypochloremic, hypokalemic metabolic alkalosis, the loss of electrolytes and the kidney’s
mechanism of saving potassium, absorbing bicarbonate instead of chloride and excreting hydrogen ion
will result in paradoxical aciduria. As the kidney reabsorbs the bicarbonate ion, the compensatory
mechanism fails. The correction requires replacement of chloride and potassium ions.

Presentation and Diagnosis The clinical problems associated with metabolic alkalosis are manifestations
of hypochloremia, hypokalemic, and intravascular volume deficiency. This may be caused by
gastrointestinal or renal losses and result in paralytic ileus, cardiac dysrhythmias, and digitalis toxicity.

Treatment The treatment of metabolic alkalosis requires replacement of electrolytes (particularly

chloride and potassium) and of fluids specific to the type of loss,
Most metabolic alkalosis is chloride responsive

Bleeding may occur in the presence of a deficiency of any of the factors of the coagulation pathways,
except factor XII.

Platelet count, prothrombin time (PT), and activated partial thromboplastin time (aPTT)

The PT measures the ability of the blood to form stable thrombi. It evaluates the adequacy of factors VII,
X, and V; prothrombin; and fibrinogen , Its most common use is to monitor oral anticoagulation with
warfarin

The aPTT evaluates the adequacy of fibrinogen, prothrombin, and factors V, VIII, IX, X, XI, and XII in the
intrinsic and common pathways (see Figure 4-2). It is the most commonly used test to monitor the
effectiveness of unfractionated heparin therapy. The aPTT cannot be used to monitor most low
molecular weight heparins

disorder. A newly found prolonged bleeding time may be caused by any of the following disorders: 1.
Thrombocytopenia 2. Abnormal platelet function because of a. Medication (e.g., aspirin) b. Dense
granular disorders of platelets 3. von Willebrand disease (congenital or acquired)

All anticoagulants : vitamin K antagonist (Coumadin) and heparins, both unfractionated and low
molecular weight. A new class of anticoagulants, direct factor Xa inhibitors (Fondaparinux),

Platelet-Inhibiting Drugs

irreversibly inhibit platelet : includes aspirin and clopidogrel (Plavix).

Residual heparin that remains after cardiopulmonary or peripheral vascular bypass surgery can cause
significant oozing or overt bleeding. Shock

Disseminated Intravascular Coagulatio : etiology of DIC 1release of tissue debris, extensive

endothelial ,damage , blockage of the reticuloendothelial sys , severe liver disease;, malignancy

diagnosis of DIC : prolonged APTT; (2) prolonged PT; (3) hypofi brinogen-

emia; (4) thrombocytopenia; and (5) the presence of fi brin and

fi brinogen split (FDP) products and positive d-dimers.

Whole blood is separated into (1) red cells, (2) white cells, (3) platelets, and (4) plasma.

antigen. Type AB has both antigens, and type O has neither antigen. Type O is the most common, and
type AB is the least , the D antigen on the surface of red blood cells, this person is Rh positive.

Red blood cell transfusions are available as (1) whole blood, (2) packed red blood cells, (3) washed red
blood cells, (4) leukoreduced red blood cells, and (5) divided or pediatric unit red blood cells.
Transfusion of packed red cells is indicated when the red blood cell mass is decreased

Packed red blood cells are typically stored frozen between 1°C and 6°C. One unit of packed red blood
cells contains about 200 mL of red cells and 30 mL of plasma in a total volume of about 310 mL.
Transfusion of Fresh Frozen Plasma: use. FFP contains all of the required coagulation factors in
physiologic concentrations (note: the coagulation factors are not concentrated). FFP does not contain
red cells, leukocytes, or platelets. FFP does not require crossmatch prior to use, but donor and recipient
must be ABO compatible. Rh status is not considered.

Platelet transfusion is indicated for patients who have clinical coagulopathy and either an absolute
thrombocytopenia or a relative thrombocytopenia due to platelet dysfunction.

Complications of Blood Component Therapy

Metabolic Derangements , Immunologic Transfusion Reactions , Transmission of Infectious Agents ,

Immunologic Transfusion Reactions

of shock often use systolic hypotension (<90 mm Hg) as the defining variable. According

hypovolemic/hemorrhagic, septic, cardiogenic, and neurogenic shock

predominant: (1) shock is secondary to inadequate oxygen delivery; (2) shock is secondary to a toxic
cellular insult that can progress even when suffi- cient oxygen is delivered.

Tissue injury and the associated inflammatory response result in the production or activation of cellular
molecules (i.e., cytokines, superoxide radicals, prostaglandins, adhesion molecules) that promote local
cellular activation, tissue repair, and host defenses. The result is systemic inflammation that can cause
organ malfunction and shock.

stated, hypoperfusion begets inflammation, and inflammation begets hypoperfusion.

Preload is the magnitude of myocardial stretch, the stimulus to muscle contraction that is described by
the FrankStarling mechanism , Preload is most appropriately measured as end-diastolic volume.

central venous pressure [CVP] for the right side of the heart and pulmonary capillary wedge or
pulmonary artery occlusion pressure [PAOP] for the left side of the heart)

Ventricular afterload is determined primarily by the resistance to ventricular ejection that is present in
either the pulmonary (pulmonary vascular resistance) or systemic arterial tree (systemic vascular
resistance).

Increased Venous Return Increased MSP, Increased vascular volume ,Increased vascular tone, External
compression Trendelenburg position (increased MSP in lower extremities and abdomen), Decreased CVP
Negative pressure respiration Decreased venous resistance Decreased venous constriction

Diminished Venous Return Decreased MSP Hypovolemia Vasodilation Increased CVP Intracardiac
Congestive heart failure Cardiogenic shock Tricuspid regurgitation Right heart failure Extracardiac
Positive pressure respiration PEEP

MSP, mean systemic pressure; CVP, central venous pressure (right atrial pressure); RV, venous
resistance; and RA, arterial resistance. This equation (including
Normal Inflammation

Coagulation( Platelets) , Early inflammation Polymorphonuclear leukocytes (first few hours) , Later
inflammation Monocytes (days) macrophages, Collagen and mucopolysaccharide Fibroblasts (maximum
deposition 7–10 days) , Capillary budding Endothelial cells (maximum 7–10 days)

Functions of Inflammatory Cells

Platelets Coagulation, release PDGF, IL-1 ‫و‬,Polymorphonuclear leukocytes Phagocytosis, especially

microbes, release IL-1, IL-8, Macrophage Phagocytosis; stimulate fibroblast migration and growth;
stimulate endothelial cell migration and growth; release FGF, PDGF, IL-1, IL-6, TNF, TFG-β, TGF-
α ,Fibroblast Collagen deposition, Endothelial cells Release of adhesion molecules Capillary budding

Neurohumoral Response to Hypoperfusion

INCREASEDö ACTH Cortisol Aldosterone Growth hormone; epine, norep, dopam, glucagon , renin ,
angiote

deacresedÖ insulin , tzroxin ,

The primary etiologies of hypoperfusion states in surgical patients are decreased venous return and
decreased myocardial function

Decreased Venous Return: Hypovolemia

Etiologies of Hypoperfusion Decreased venous return,, Hypovolemia, Pericardial tamponade, Tension

pneumothorax ,Increased abdominal pressure, Bowel obstruction, Tension pneumoperitoneum, Massive
bleeding ,Diagnostic laparoscopy Ascites

Common Etiologies of Hypovolemia: Hemorrhage , Severe inflammation or infection Trauma

Pancreatitis or other causes of peritonitis Burns, Vomiting or other intestinal losses Excessive diuresis
Inadequate oral intake

Cellular Effects of Hemorrhagic Shock Diminished transmembrane potential difference ,Increased

intracellular sodium, Decreased intracellular ATP, Increased intracellular calcium

Hypovolemic hypoperfusion that is severe enough to cause hypotension is associated with metabolic
acidosis that is recognized either from serum electrolytes or, more precisely, arterial blood gases and
blood lactic acid concentration. Elevated serum blood urea nitrogen (BUN) and creatinine levels that

Treatment of Hypovolemia : In general, two types of fluid, crystalloid and colloid, are used for volume
replacement

Fluids for Hypovolemia Resuscitation: Crystalloid Isotonic Ringer’s lactate 0.9% saline Hypertonic saline,
Colloid Red blood cells, Fresh frozen plasma, Albumin ,Processed human protein Low–molecular-weight
dextran Hydroxyethyl starch

Decreased Venous Return: Tension Pneumothorax ,Tension pneumothorax ,reduces venous return by
producing an extracavitary increase in CVP and by increasing venous resistance in the chest.
Decreased Venous Return: Increased Abdominal Pressure

Treatment of Cardiogenic Shock : Reversal of underlying disease : Coronary artery bypass Valve
replacement Rx myopathy Repair ventricular septal defect . Reduce preload: Decrease water intake
Diuretics Venous dilation Nitroglycerin Calcium channel blockers Narcotics , Reduce afterload
Nitroprusside Antihypertensives Diuretics Narcotics , Increase contractility Intravenous inotropes
Increase arterial oxygen Supplemental O2 Mechanical ventilation Intraaortic balloon pump

Cardiogenic shock is associated with chest x-ray evidence of hydrostatic pulmonary edema, metabolic
acidosis (lactic acidosis), increased CVP and PAOP, and elevated BUN and creatinine.

always, treatment is based on the etiology. Arrhythmias are usually the most readily treated etiology of
severe cardiac impairment

Decreased Venous Return: Pericardial Tamponade

primary mechanism for decreased venous return during pericardial tamponade is an extracavitary
increase in CVP. The

the systemic inflammatory response syndrome (SIRS),

beneficial, severe tissue injury from a variety of causes (Table 5-19) can result in inflammation distant
from the original disease (systemic inflammation).

To meet the definition of SIRS, a patient must have two or more of the following conditions: (1)
temperature >38.5°C or <36°C; (2) heart rate > 90 beats/minute; (3) respiratory rate >20 breaths/minute
or Paco2 < 32 Torr; and (4) total leukocyte count >12,000 cells/mm, <4,000 cells/mm3 , or >10%
immature forms.rediuced cardiac output

Etiologies of Systemic Inflammation : Infection (meets definition of sepsis) ,Trauma , Burns

Ischemia/reperfusion: regional or total body Pancreatitis Drug reactions Hemolytic transfusion reactions

Circulatory Disorders in Severe Inflammation: Reduced Cardiac Output Hypovolemia Peripheral

vasodilation Increased capillary permeability, local or total body Intracellular migration of fluid
Sequestration in gastrointestinal tract lumen Myocardial depression Increased pulmonary vascular
resistance Hypoxia Platelet emboli Thromboxane release Serotonin release White blood cell aggregation
Deficits in the microcirculation Gastrointestinal tract Renal

A PRACTICAL GUIDE TO THE PATIENT IN SHOCK : patient is recognized to be in shock, the guiding
principles are to: (1) provide an excellent circulation and (2) treat severe inflammation.

severe hypotension and marked tachycardia

Characteristics of the Patient Who Is at Risk for Shock : Trauma or burn Vascular catastrophe—ruptured
aneurysm ,Acute cardiac disease ,Acute abdominal disease ,Severe extraabdominal infection

Common Laboratory Abnormalities With Shock : Metabolic acidosis, Elevated BUN and
creatinine ,Leukocytosis or leukopenia ,Elevated blood glucose, Decreased platelet count Decreased
ionized calcium
7.

PHASES OF WOUND HEALING

The substrate phase is also known as the inflammatory phase, lag phase, or exudative phase.

Proliferative Phase: The primary cell in this phase is the fibroblast, which produces collagen.

Maturation Phase (Remodeling)

Primary Intention: sututer , infection

Secondary Intention: leave it ipen

Delayed primary::initaly leave it open after 5 days no infection we close it

Steps in Wound Care 1. Sterile preparation and draping 2. Administration of local anesthetic 3.
Hemostasis 4. Irrigation and débridement 5. Closure in layers 6. Dressing and bandage

(0). The more zeros, the smaller the suture. Suture size number 1 is larger than 0, which in turn is larger
than 2-0 (00). Suture can be as small as 9-0 or 10-0. A 3-0 or 4-0 suture is used for skin on the torso and
extremities, whereas a 5-0 or 6-0 suture is appropriate

Suture Material: nylon , polyester, silk, catuge, polyproplin

Four types of chronic wounds are generally encountered in clinical practice: pressure ulcers, venous
stasis ulcers, arterial insufficiency ulcers, and diabetic neuropathic ulcers.

Clean 3 Atraumatic, no gastrointestinal (GI) or genitourinary system (GU) or respiratory track (R)
involvement

Clean–Contaminated 8 Minor sterile breaks, entrance into GI, GU, or R tract without significant
contamination

Contaminated 15 Entrance into GI, GU, or R tract with spillage of contents, traumatic wounds with soil
and particulate matter

Dirty 35 Infection within tissue, that is, abscess

Pressure Ulcers : neurologically impaired patients , chronic spinal cord injury , pressure ulceration are
the heel, sacrum, and ischial tuberosities

Pressure Sore Classification/Grade: Grade 1 This is a nonblanching erythematous area on intact skin.
Grade 2 Partial-thickness skin loss with the involvement of the epidermis and/ or the dermis. This is
usually superficial and can appear as a blister or abrasion. Grade 3 Full-thickness skin loss with necrosis
of subcutaneous tissue that can extend to the fascia. Grade 4 Full-thickness skin loss with necrosis.
Destruction can involve muscle, bone, and tendons.

Venous stasis ulcers are the most common chronic wounds developing in adults

Venous ulcers generally are super- ficial wounds in the anteromedial aspect of the leg (“gaiter zone”),
not involving the foot. The
 Venous ulcers1) decreased skin perfusion as a consequence of elevated venous pressures in the
capillaries and (2) decreased delivery of oxygen and glucose to tissues as a consequence of edema and
protein deposition in the interstitium.

Management of venous ulcers starts with compression,

Arterial insufficiency ulcers result from atherosclerotic obstruction of the main conduit arteries
supplying the lower extremity, although other causes of occlusion such as thromboembolism may apply

extend into deeper structures to expose bone or tendon. Typically, arterial ulcers involve the toes, which

wounds. The presence of black, infarcted skin or multiple wounds should strongly raise the suspicion for
arterial disease. Pedal pulses are usually absent,

Management of arterial wounds : interventions to improve tissue perfusion. endovascular balloon

angioplasty or stenting,

Diabetic neuropathic ulcers result : Motor neuropathy , causes sensory deficits, and a lack of proper
protective reflexes , wound. Elevated glucose in poorly controlled diabetes independently retards
wound healing and inhibits the leukocyte response to infection;

include Charcot’s foot, which is a collapse of the midfoot with plantar subluxation of the ruined bones,
and clawing of the toes with plantar subluxation of the metatarsal heads

diabetic neuropathic ulcers are found at a site of increased weight bearing, such as a subluxed plantar
surface of a metatarsal head, the heel, or on the dorsal surface of a toe that is rubbing against a shoe.

10

Epidermal burns (“first-degree burns”) involve only the epidermis. only supportive care, which consists
of pain control (oral analgesics), adequate oral fluids, and application of a soothing topical compound
such as ‫و‬injured epidermis peels off, revealing new skin beneath.

Partial-thickness burns (“second-degree burns”) extend into but not through the dermis.

Superficial partial-thickness burns : present with reddened skin that forms distended blisters comprised
of epidermis and filled with proteinaceous fluid that escapes from damaged capillaries. usually very
painful,

Deep partial-thickness injuries : Coagulation necrosis of the upper dermis ‫و‬dry, thickened texture.
Erythema is often absent, often waxy white. vary in the amount of pain they produce;

very deep wounds cause destruction of many dermal nerve endings and are less painful than more
superficial injuries. Such wounds heal badly,

During the first 24 to 48 hours postburn, burn wounds develop a coating of dead tissue, coagulated
serum, and debris called eschar.

Full-thickness burns (“third-degree burns”) occur when all layers of the skin are destroyed. These
wounds are usually covered with dry, avascular coagulum, no sense no nerve , any color, from waxy
white in the case of chemical burns, to a completely black, charred surface from flame injury. dark red
color, but the surface is dry and does not blanch with pressure. injuries require skin grafting

“fourth-degree” burns, is sometimes used to describe injuries that extend to bone.

Inhalation injury is a unique complication of injury from flames and smoke that is an important facet of
burn treatment. cause severe morbidity and mortality , The treatment of inhalation injury is largely
supportive. Endotracheal intubation to secure the swelling airway is mandatory. Ventilator support with
positive end expiratory pressure (PEEP) is most helpful in combating the airway collapse.

CO poisoning is a common cause of immediate death in patients injured in building fires,

many physicians divide burn care into three periods: Resuscitation, Wound Closure, and Rehabilitation.

Resuscitation Period: This period lasts for the first 24 to 48 hours , for isotonic crystalloid fluid (lactated
Ringer’s solution) to be given at an initial rate determined , of choices (from 2 to 4 mL of lactated
Ringer’s solution per kilogram body weight for every percent TBSA that is burned).

Lund and Browder chart. This diagram extent of burn injuries.

Fluid accumulating beneath the constricted eschar of a deep burn increases tissue hydrostatic pressure,
sometimes to the point that circulation is compromised. Frequent evaluation of extremity pulses,
sensory and motor function, and pain is essential to diagnose the progressive ischemia of a
compartment syndrome. The treatment of this problem is escharotomy, an incision made through the
rigid, leathery eschar to relieve the compression produced by ongoing edema,

Skin graft Two techniques are used: fascial and tangential excision.

patient’s own skin, termed autograft. Autografting can be performed using full-thickness or split-
thickness skin grafts. Full-thickness

invasive infection, termed burn wound sepsis. Infection (Sulfamylon), and silver sulfadiazine

Nutritional Support

Rehabilitation Phase : the adage that rehabilitation begins at the time of injury,

24

Biopsy : including fine-needle aspiration biopsy (FNAB), core-needle biopsy, excisional biopsy, and
incisional biopsy.

FNAB consists of removing cells from a suspicious mass using a thin or fine needle. FNAB has a higher
false-negative rate

Core-needle biopsy is removal of tissue from a suspicious mass using a larger needle

Excisional biopsy refers to the complete removal of a lesion, while incisional biopsy refers to partial
removal of a lesion.
Imaging techniques, such as ultrasonography or computed tomography (CT), can direct the biopsy

More invasive diagnostic methods include upper and lower GI tract endoscopy and endoscopic
retrograde cholangiopancreatography (ERCP). Laparoscopy, thoracoscopy, and mediastinoscopy may be
performed

Tumor, Node, Metastasis (TNM) staging system. grades: Grade 1 = well differentiated (low grade), Grade
2 = moderately differentiated (intermediate grade), and Grade 3 = poorly differentiated/anaplastic (high
grade).

prostate cancer, hormonal interventions include orchiectomy or the administration of stilbestrol (a

synthetic estrogen), luteinizing-hormone-releasing hormone (LHRH) analogues (gonadorelins), or
antiandrogen drugs (cyproterone or flutamide). In breast cancer, interventions include oophorectomy or
administration of tamoxifen (antiestrogen), progestogens (megestrol), LHRH (gonadorelin) antagonists,
or aromatase inhibitors.

Skin cancer

Basal cell : head and neck , upper lip ,nodular redish telengectasis , ulcerative

Squamouse cell: plantar aspect of foot , cauliflower

Melanoma is classified into four main morphologic subtypes: superficial spreading melanoma, nodular
melanoma, lentigo maligna melanoma, and acral lentiginous melanoma.

A = Asymmetry: One-half of the skin lesion does not match the other half. B = Border: The edges are
ragged, irregular, or blurred. C = Color: There is variation in the color with differing shades of brown,
black, or blue. D = Diameter: The lesion is larger than 6 mm (the size of a pencil eraser). E = Evolution:
The lesion has grown or changed since the last evaluation.

Leg in women , trunk back in men

Lesions that are occasionally confused with cutaneous melanoma include junctional nevi, compound
nevi, intradermal nevi, blue nevi, BCCs, seborrheic keratoses, dermatofibromas, and subungual
hemorrhage.

The Breslow system is the other method for assessing melanoma thickness.

The Clark system for primary melanoma is based on the histologic level of invasion of the tumor.

SARCOMA Adult soft tissue sarcomas are rare tumors derived from embryonic mesoderm. Bone , soft
tissue

Angiosarcoma , gastrointestinal sarcoma , rhombomyosarcoma , liposarcoma , fibrosarcoma ,

synovialsarcoma ,

Limb, chest ab , head and neck

Kaposi’s Sarcoma

Kaposi’s sarcoma (KS) was largely limited to elderly Jewish men of Mediterranean descent and to people
from sub-Saharan Africa. With the AIDS epidemic, Kaposi’s sarcoma (KS) was largely limited to elderly
Jewish men of Mediterranean descent and to people from sub-Saharan Africa. With the AIDS epidemic,

Kaposi’s sarcoma lesions initially appear as flat, blue patches that resemble a hematoma. Later, they
become raised, rubbery nodules. Non-AIDS KS is typically found on the lower extremities AIDS-related
KS often begins in the perioral mucosa. The palate is the most common site.

Aids related KS is often multifocal, with rapid spread to the lymph nodes. It often involves the
gastrointestinal tract, presenting as GI bleed, obstruction, and dysphagia. Other mucosal surfaces

Surgical excision or local radiation is effective for small, localized lesions. Liposomal doxorubicin is the
licensed agent for the treatment of disseminated or unresectable KS. Patients with AIDS-related KS
should also be treated concurrently with multiple antiretroviral therapy through consultation with an
infectious disease specialist. The tolerability of liposomal doxorubicin can be poor in this population due
to their poor performance status, concurrent opportunistic infections, and the toxicities from
antiretroviral therapy. Responses to liposomal doxorubicin can be observed rapidly and dramatically
after a few treatments. Recent literature suggests that once the CD4 count is 400 or above and most of
the lesions either regress or are asymptomatic, liposomal doxorubicin can be stopped. Further
regression occurs, which is likely due to reconstitution of the immune system. Local radiation shrinks
these lesions and provides palliation. Treatment includes single-drug regimens with vinblastine or VP-16.

).