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Types of gallstones:
  • Cholesterol stones
  • Pigment (brown/black) stones and
  • Mixed stones


Cholesterol stone:

Cholesterol is synthesized in liver. Its solubility is determined by relative concentration of cholesterol, bile salts and lecithin. Altered levels of cholesterol, lecithin, and bile salts in bile reduces the micelle concentration in the bile leading to precipitation of insoluble cholesterol, hence the stone formation.
Factors altering the cholesterol to bile salt ratio are obesity, high-calorie diets and certain medications. These increase the secretion of cholesterol and supersaturate the bile, increasing the lithogenicity of bile.

Pigment stone:
Types- black and brown
Black stones
composed of insoluble bilirubin pigment polymer mixed with calcium phosphate and calcium bicarbonate. Black stones accompany hemolysis (hereditary spherocytosis or sickle cell disease)
Brown stones-
 composed of calcium bilirubinate, calcium palmitate, calcium stearate and cholesterol. It is rare in gall bladder and usually forms in bile duct and are related to bile stasis and infected bile. Deconjugation of bilirubin deglucuronide by bacterial beta- glucuronidase  causes insoluble unconjugated bilirubinate to precipitate leading to stone formation.
Brown stones are also associated: Foreign body within the bile duct (e.g. endoprosthesis) 
Parasites (like Clonorchis sinensis and Ascaris  lumbricoides)

Cholesterol stone
Pigment stone
Clinical presentation:
Patient may be asymptomatic or presents with features of its complications.

Effects and complications of gallstones
In the gall bladder
Biliary colic
Acute cholecystitis
Chronic cholecystitis
    Empyema of the gall bladder
b. In the bile ducts
    Biliary obstruction
    Acute cholangitis
    Acute pancreatitis
c. In the intestine: Gallstone ileus ( intestinal obstruction)

Based on history, physical examination and confirmatory radiological studies such as transabdominal USG and radionucleide scans.

Asymptomatic gall stone: observation
If symptomatic or complication of gallstones: cholecystectomy
Prophylactic cholecystectomy is done in:
diabetic pt
those with congenital hemolytic anaemia
those who undergo bariatric surgery for morbid obesity

Acute Cholecystitis

Definition: acute inflammation of the gallbladder, usually caused by cystic duct obstruction by gallstones.

Biliary colic: severe right upper quadrant pain associated with nausea and vomiting. Pain may radiate to the chest. Pain is usually severe and last for minutes or several hours. Frequently, pain starts during the night, waking the patient. Dyspeptic symptoms may coexist and be worse after the attack. 
Right upper quadrant (RUQ) tenderness on palpation that is exacerbated during inspiration: Murphy’s Sign.
 Low-grade fever and leukocytosis

Murphy’s sign

1. USG: reveals presence or absence of gallstone and thickening of the gall bladder wall
2. Plain X-ray abdomen : 10% of gallstone are radiopaque
3. Blood: Leucocytosis
Moderately elevated liver function
4. Radioisotope scanning
Allows visualisation of biliary tree and gall bladder. GB is visualised within 30min of isotope injection. Non-visualization of GB is suggestive of Acute cholecystitis.

USG findings in Ac. Cholecystitis
  • After the diagnosis of acute cholecystitis is made, IV fluids, antibiotics, and analgesia should be initiated. 
  • Antibiotics should cover gram-negative aerobes as well as anaerobes. 
  • Cholecystectomy is the definitive treatment for patients with acute cholecystitis. 
  • Early cholecystectomy performed within 2 to 3 days of presentation  (if patients fail initial medical therapy and require surgery during the initial admission)
  • If early cholecystectomy not indicated: Interval or delayed cholecystectomy that is performed 6 to 10 weeks after initial medical therapy. 

Cholecystectomy: open or laparoscopic


i. Empyema of the gall bladder
ii. Gangrene of the gallbladder
iii. Perforation and peritonitis
iv. Fistula formation and gallstone ileus (small bowel obstruction by a large gallstone

Chronic Cholecystitis

Defnition: ongoing chronic inflammation of the gallbladder usually caused by gallstones
Micro: chronic inflammation and Rokitansky-Aschoff sinuses
Late complication: calcification of the gallbladder ("porcelain gallbladder")
T/t: Cholecystectomy

Rokitansky-Aschoff sinuses
Porcelain gallbladder
Acalculous Cholecystitis
  • Inflammation of the gall bladder in the absence of the stones.
  • Seen particularly in patients recovering from major surgery, trauma and burns.
  • Clinical picture similar to calculous cholecystitis.

T/t: Cholecystectomy

Empyema of the gall bladder

Definition: Presence of pus in the gall bladder


Sequel of acute cholecystitis
Infected mucoecele

Fever, toxicity
Pain and tenderness in Rt. Hypochondrium
The wall may become necrotic and perforate with the development of localised peritonitis


1. USG abdomen
2. Blood: leucocytosis

   Drainage and, later, cholecystectomy


A nontender, palpable gall bladder results from complete obstruction of the cystic duct with resbsorption of the intraluminal bile salts and secretion of uninfected mucus by the gall bladder epithelium 

Mucocele of gall bladder
Clinical presentations
  • Painless swelling in the right hypochondrium
  • O/E: Non tender, smooth, globular, palpable gall bladder
  • If infected, can cause empyema gall bladder

USG abdomen

T/t: cholecystectomy

Fistula In Ano

  • It is a track lined by granulation tissue which connects perianal skin superficially to anal canal or rectum deeply.

  • It usually occurs in a pre-existing anorectal abscess which burst spontaneously.


According to whether the internal opening is below or above the anorectal ring:
  • Low-level fistulae- Open into the anal canal below the anorectal ring.

  • High-level fistulae- open into the anal canal at or above the anorectal ring.

Anatomical classification (standard)
  • Subcutaneous

  • Submucous

  • Low anal

  • High anal and

  • Pelvirectal 

Park’s classification

  • Intersphincteric 

  • Trans-sphincteric (maybe high or low) and

  • Supralevator 

Clinical features
  • It presents with seropurulent discharge, along with skin irritation and one or more external opening may be present with induration of the surrounding skin.

  • Pain is not  a symptom as long as the opening is large enough for the pus to escape. But if the orifice is occluded pain increases until the discharge erupts.

  • Often it may heal superficially but pus may collect beneath forming an abscess which again discharges through same or new opening. Thus there may be two or more external openings, grouped together on the right or left of the midline, but when both ischiorectal fossas are involved then the opening is seen on each side which often intercommunicates.

Fistula In Ano

Goodsall’s rule
  • Fistulas with an external opening in relation to the anterior half of the anus is of direct type.

  • Fistulas with external openings in relation to posterior half of the anus, has a curved track may be of horse-shoe type, opens in the midline posteriorly and may present with multiple external opening all connected to a single internal opening.

Goodsall’s rule
Digital examination:

  • Internal opening can be felt as a nodule on the wall of the anal canal.


  • May show the internal opening of the fistula.
  • A hypertrophied papilla is suggestive that the internal orifice lies within the crypt related to the papilla.

Probing: not advisable


Low level fistulas:

  • Under G/A or spinal anaesthesia
  • Probe is passed through external opening up to the internal opening which is felt as an induration.
  • Fistula is opened along the probe using a knife.
  • Fibrous track along with unhealthy granulation tissue and additional external openings are excised.
  • Specimen is then sent to HPE

High level fistulas:

Surgery involves staged procedure:

Initial colostomy followed by definitive procedure. This prevents sepsis ans promotes faster healing.
Later closure of colostomy is done.

  • A slik or linen ligature is passed across the fistula and left in place with a tie.
  • This allows the fistula to granulate and heal from above and to close completely. 
  • Takes longer duration to heal.


  • Hypertrophy of the musculature of pyloric antrum, especially the circular muscle fibres, causing failure of pylorus to relax. 
  • Duodenum is normal.

  • Progressive hypertrophy of the circular muscles in the pyloric sphincter.
  • Not present at birth but occurs over 3 to 5 weeks.

Clinical Features
  • Common in 1st born male child.
  • Projectile vomiting (non bile-stained fluid)
  • Weight loss, child becomes emaciated and dehydrated.
  • Hypertrophied pylorus is palpated in the epigastrium (“olive”). It’s mobile, smooth, firm mass with  well defined borders.
  • Visible gastric hyperperistalsis.

Visible gastric hyperperistalsis
  •      Diagnosis can be made with test feed .
  •      USG is the investigation of choice- features present in the pyloric canal can be seen.

  •      GERD
  •      Feeding problems
  •      Raised ICP
  •      Duodenal atresia
  •      Intestinal obstruction


At first metabolic abnormalities should be corrected (i.e. dehydration with low Na+,Cl, K+ and metabolic alkalosis) with i.v dextrose, NS and K+.

  • Ramstedt’s operation:
  • Laparotomy is done
  • Hypertrophied muscle is cut along the whole length until the mucosa bulges out. Mucosa should not be opened.

Duodenal Atresia
  • Atresia is distal to entry of the common bile duct (occurs at the point of fusion between the foregut and midgut)
  • Association with Down syndrome

  • History of maternal polyhydramnios (cannot reabsorb amniotic fluid)
  • Vomiting of bile-stained fluid at birth

     "Double bubble sign": air in stomach and air in proximal duodenum
  •      Antenatal diagnosis can be made-USG
  •      Duodenoduodenostomy


Cholecystoses are chronic inflammatory conditions of the gallbladder with cholesterol deposits.

Types :

1)Cholesterosis (Strawberry Gallbladder)
Aggregations of cholesterol crystals in the mucosa or submucosa

2)Cholesterol polyposis (Gallbladder polyp)
Cholesterol laden polypoid projections in the mucosa

3)Cholecystitis  glandularis proliferans
Granulomatous thickening and hyperplasia of the gallbladder.

4)Diverticulosis of the gallbladder
Diverticula formation in the wall of the gallbladder

5)Gallbladder wall fistula

Strawberry gallbladder
Cholesterol polyposis (Gallbladder polyp)

Cholecystitis  glandularis proliferans

Clinical features

Features of cholecystitis like positive Murphy’s sign, dyspepsia.


  • USG abdomen
  • OCG
  • Isotope study


  • Cholecystectomy

Cystic fibrosis

Most common lethal genetic disorder
Defect: mutation of the chloride channel protein, cystic fibrosis trans-membrane conductance regulator (CFTR)

i. CFTR gene is located on chromosome 7
ii. Most common mutation is a deletion in amino acid position 508 (AF508)

  • defective chloride channel protein leads to abnormally thick viscous mucous, which obstructs the ducts of exocrine organs

Distribution of disease

i. Lungs
  • Recurrent pulmonary infections with P. aeruginosa and S. aureus . 
  • Chronic bronchitis
  • Bronchiectasis

ii. Pancreas

  •  Plugging of pancreatic ducts results in atrophy and fibrosis
  •  Pancreatic insufficiency
  •  Fat malabsorption 
  •  Malodorous steatorrhea
  •  Deficiency of fat-soluble vitamins

iii. Male reproductive system

  • Obstruction of the vas deferens and epididymis
  • May lead to male infertility

 iv. Liver:

  •  plugging of the biliary canaliculi may result in biliary cirrhosis

v. GI tract:

  • small intestinal obstruction (meconium ileus)


i. Sweat test (elevated NaCl)
ii. DNA probes


  • Chest Physiotherapy
  • Antibiotics
  • Mucolytics : N-acetylcysteine
  • Gene therapy

i. Mean survival: 30 years
ii. Most common cause of death is pulmonary infections

Anal Fissure

It is an ulcer in the longitudinal axis of the lower anal canal.

  • Midline posteriorly- most common (more common in males)
  • Midline anteriorly- next most common (more common in females)

  • Due to the curvature of the sacrum and rectum, hard fecal matter while passing down causes a tear in the anal valve leading to posterior anal fissure.
  • Anterior anal fissure is common in females due to lack of support to the pelvic floor.
  • Haemorrhoidectomy
  • IBD- esp. chron’s disease
  • STD

  • It can be acute and chronic. Fissure ends above at the dentate line.
  • Acute anal fissure
  • It is a deep tear in the lower anal skin with  spasm of anal sphincter with little inflammatory induration or edemaof its edges.
  • Chronic anal fissure
  • It has got inflamed, indurated margin with scar tissue.
  • Ulcer at its inferior margin is having a skin tag, which is edematous, acts like a guard-’ Sentinel Pile’
  • It can cause repeated infection-fibrosis-abscess foramtion-fistula formation.

Clinical features
  • Common in middle aged women, not in elderly.
  • Pain is severe in nature in acute type, whereas less severe in chronic.
  • Constipation, bleeding and discharge.
  • O/E
  • In standing cases there may be sentinel skin tag. Sentinel skin tag + typical Hx + tightly closed, puckered anus= pathognomonic. 
  • In chronic fissure, ulcer is felt with button like depression, induration and often sentinel pile.
  • The lower end of the fissure can be seen by gently parting the margins of anus.
  • Digital examination and proctoscopy is not possible in acute fissure in ano. 

Anal fissure

Sentinel pile

Differential Dx

  • Carcinoma of anus
  • Inflammatory bowel disease
  • Venereal diseases
  • Anal chancre
  • Tuberculous ulcer
  • Proctalgia fugax


Conservative t/t
  • NO- neurotransmitter that induces relaxation of the internal spchicter.
  • Glyceryl trinitrate- being nitric acid donor, when applied as an ointment causes relaxation of the sphincter and also improves blood flow- both aids healing. 
  • Use of laxatives and xylocaine surface anaesthetic.


Gentle dilatation of the sphincter under GA:
  • Can be used in young men with high pressure sphincter.
  • CI in pts. with weak sphincter.
  • If this method is ineffective or if the fissure is chronic with fibrosis, a skin tag or a mucus polyp, then surgery is done under GA(best) or LA.

Lateral anal sphincterotomy:
  • Here internal sphincter is divided away from the fissure either in right or left lateral positions.
  • Can be done in OPD basis under L/A.
  • Healing completes in 3 wks.
  • Good result for acute than chronic cases.
  • Small risk of incontinence.

Closed and open

Anal advancement flap:

  • Here excision of the edges of the fissure and mobilization of a square, full-thickness anal skin flap which is slided forward over the fissure and sutured in place.
  • Only little risk of damage to the underlying internal sphincter and incontinence is unlikely.

Acute pancreatitis

  • Acute pancreatitis is defined as 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.
  • Acute pancreatitis may recur.

Etiology and pathogenesis
  • Gallstones
  • Alcoholism
  • Post ERCP
  • Abdominal trauma
  • Following biliary, upper GI or cardiothoracic surgery
  • Ampullary tumors
  • Drugs (corticosteroids, azathioprine, asparaginase, valproic acid, thiazides, oestrogens)
  • Hyperparathyroidism
  • Hypercalcaemia
  • Pancreas divisum
  • Autoimmune pancreatitis
  • Hereditary pancreatitis
  • Viral infections (mumps, coxsackie B)
  • Malnutrition
  • Scorpion bite
  • Idiopathic


Activation of pancreatic pro enzymes (inactive enzymes)

Activation leads to auto digestion of the pancreas

Mechanisms of activation of pro enzymes
(1) Obstruction of the main pancreatic duct or terminal CBD
(a) Gall stones 
(b) Alcohol thickens ductal secretions.
    • Also increases duct permeability to enzymes
(2) Chemical injury of acinar cells
• Examples—thiazides, alcohol, triglyceride (> 1000mg/dl)
(3) Infectious injury of acinar cells
• Examples—CMV, mumps, coxsackie virus
(4) Mechanical injury of acinar cells
• Examples—seat belt trauma, posterior penetration of duodenal ulcer
(5) Metabolic activation of pro enzymes (e.g. hypercalcemia ischemia, shock)

Trypsin is important in the activation of pro enzymes.
(1) Proteases damage acinar cell structure.
(2) Lipases and phospholipases produce enzymatic fat necrosis.
(3) Elastases  damage vessel walls and produce hemorrhage.
(4) Activated enzymes also circulate in the blood.

Clinical features
  • Sudden onset of upper abdominal pain which is referred to back. Pain may be relieved or reduced by leaning forward.
  • Vomiting and high fever, tachypnoea with cyanosis.
  • Tenderness, rebound tenderness, guarding, rigidity and abdominal distension, severe illness.
  • There may be mild jaundice (due to cholangitis)
  • Features of shock and dehydration.
  • Oliguria
  • Grey turner’s , Cullen’s sign
  • Haematemesis/malaena due to duodenal necrosis, gastric erosions, decreased coagulability/ DIC

  • Serum amylase is very high or shows rising titre.
  • Serum lipase more specific than amylase.
  • LFT: Serum bilirubin, albumin, PT, alkaline phosphatase.
  • Blood urea and serum creatinine
  • Blood glucose
  • Serum calcium level
  • Arterial PO2 and PCO2 level to assess pulmonary insufficiency (or ARDS)
  • Urinary lipase estimation
  • Total count, haematocrit
  • Peritoneal tap fluid shows high amylase and protein level
  • Plain X-ray shows:

  1. Sentinel  loop- of dilated proximal small bowel.
  2. Distension of transverse colon with collapse of descending colon (colon cut off sign)
  3. Air-fluid level in the duodenum.
  • USG  and CT abdomen
  • MRI
  • MRCP
  • CXR for effusion and ARDS

Sentinel  loop- of dilated proximal small bowel

Colon cut off sign
  • Mild attack:
I.V fluid resuscitation

  • Severe attack:
Patient should be admitted to ICU
a. NPO until clinically improved
b. Aggressive fluid resuscitation with crystalloid solutions
c. Meperidine or fentanyl for pain
d. Nasogastric suction if vomiting severe
e. Oxygen

  • If gallstones are the cause of an attack or if the patient has jaundice, cholangitis or dilated CBD, urgent ERCP should be done within 72 hrs of the onset of symptoms.
  • Antibiotics are not indicated.
  • Some evidence shows that prophylactic antibiotics ( i.v cefuroxime, imipenem or ciprofloxacin plus metronidazole) can prevent local and septic complication but the duration of use should not exceed 14 days.

a. Pancreatic necrosis
(1) Systemic signs occur earlier than usual.
(2) Higher fever than usual: sinus tachycardia
(3) Greater degree of neutrophilic leukocytosis
(4) Peripancreatic infections occur in 40% to 70% of cases.

b. Pancreatic pseudocyst (20%)
(1) Collection of digested pancreatic tissue around pancreas
(2) Abdominal mass with persistence of serum amylase longer than 10 days
(3) Treatment
(a) If  less than 5cm, observe and follow with CT scan.
                   Most resolve without surgical intervention.
(b) If greater than 5cm, percutaneous drainage with CT or ultrasound guidance

c. Pancreatic abscess
(1) Clinical and laboratory findings
(a) Abdominal pain
(b) High fever due to sepsis
     Usually gram-negative infections such as E. coli or Pseudomonas
(c) Neutrophilic leukocytosis
(d) Persistent hyperamylasemia
(2) Diagnosis
(a) CT scan shows multiple radiolucent bubbles in retroperitoneum
(b) CT-guided aspiration of abscess identifies organisms.
(3) Treatment
(a) Surgical drainage
(b) Imipenem- cilastin

 d. Pancreatic ascites
(1) Usually caused by leaking of a pseudocyst
(2) Peritoneal fluid has high amylase level.
(3) Usually resolves spontaneously

e. May develop acute respiratory distress syndrome or disseminated intravascular coagulation (DIC)

f. Pancreatic calcifications

Acute intussusception

It is telescoping or invagination of one portion of bowel into the adjacent segment. (proximal into distal)

  • It is common in weaning period of child, between 3-9 mths.

  • In children- associated with Meckls diverticulum, polyp, HSP, etc.

  • In adolescents and adults- submucus lipoma, leiomyoma, polyps in jejunum (Peutz-Jeghar syndrome), other polyps and carcinoma with papillary projections.


  • Apex- is the one which advances.

  • Intussuscipiens- is the one which receives (outer sheath)

  • Intussusceptum- are the tube which advances (middle and inner sheath)

  • Apex and inner tubes will have compromised blood supply which lead to gangrene.

    Ischaemia leads to sloughing off of the apex which in turn lead to bleeding which mixes with mucus to produce the classic currant jelly that is passed per anum.

    Gangrene may lead to perforation and peritonitis.

  • Common at around 6 months.
  • Sudden onset of pain ( screaming with drawing up of the legs vomiting, with passage of currant-jelly stool.
  • It is recurrent.
  • When it gets reduced, child becomes asymptomatic.
  • On examination, a mass is felt on the left or right of the umbilicus which is sausage shaped with concavity towards umbilicus.
  • Right iliac fossa is empty (Sign of dance)
  • PR- Blood stained mucus maybe found on the finger.
          In extensive ileocolic and colocolic intussusception, the apex may be palpable or even protrude from the anus.
  • If unrelieved, pain becomes continuous with abdominal distension and profuse vomiting.
  • Ultimately small bowel obstruction or peritonitis secondary to gangrene may lead to death.

  • Plain x-ray abdomen

     Absent caecal gas shadow in ileoileal or ileocolic cases
  • Barium enema

     Shows typical claw sign. (for ileocolic and colocolic)
  • CT scan- maybe be done for ileoileal intussusception which shows small bowel mass.

  • Acute enterocolitis
  • HSP
  • Rectal prolapse


  • Ryles tube aspiration

  • IV fluids

  • Antibiotics

  • Catheterization

  • Surgery

Midline incision
Then reducing by squeezing the most distal part of the mass in cephalad direction.
In difficult cases- Cope’s method- little finger gently inserted into the neck of the intussusception and separation of adhesion is tried.
Thumb and finger are placed in such a way to deinvaginate the apex.
Gentle pressure is applied and gradually increased to reduce edema around the ileocaecal valve
In case of irreducible or gangrenous intussusception- mass excision.

Acute Abdomen and Appendicitis

The term acute abdomen refers to signs and symptoms of abdominal pain and tenderness, a clinical presentation that often requires emergency surgical therapy.

Nonsurgical Causes of Acute Abdomen

Endocrine and metabolic causes
  • Uremia
  • Diabetic crisis
  • Addisonian crisis
  • Acute intermittent porphyria
  • Hereditary Mediterranean fever
Hematologic Causes
  • Sickle cell crisis
  • Acute leukemia
  • Other blood dyscrasias
Toxins and Drugs
  • Lead poisoning
  • Other heavy metal poisoning
  • Narcotic withdrawal
  • Black widow spider poisoning

Surgical Acute Abdominal Conditions

  • Solid organ trauma
  • Leaking or ruptured arterial aneurysm
  • Ruptured ectopic pregnancy
  • Bleeding gastrointestinal diverticulum
  • Arteriovenous malformation of gastrointestinal tract
  • Intestinal ulceration
  • Aortoduodenal fistula after aortic vascular graft
  • Hemorrhagic pancreatitis
  • Mallory-Weiss syndrome
  • Spontaneous rupture of spleen
  • Appendicitis
  • Cholecystitis
  • Meckel's diverticulitis
  • Hepatic abscess
  • Diverticular abscess
  • Psoas abscess
  • Perforated gastrointestinal ulcer Perforated gastrointestinal cancer
  • Boerhaave's syndrome
  • Perforated diverticulum
  • Adhesion related small or large bowel obstruction
  • Sigmoid volvulus
  • Cecal volvulus
  • Incarcerated hernias
  • Inflammatory bowel disease
  • Gastrointestinal malignancy
  • Intussusception
  • Buerger's disease
  • Mesenteric thrombosis or embolism
  • Ovarian torsion
  • Ischemic colitis
  • Testicular torsion
  • Strangulated hernias

Acute Appendicitis

  • Obstruction of the lumen is the major cause. 
  • Obstruction may be due to inspissated stool (fecalith or appendicolith), lymphoid hyperplasia, vegetable matter or seeds, parasites, or a neoplasm
  • Obstruction of the appendiceal lumen contributes to bacterial overgrowth, and continued secretion of mucus leads to intraluminal distention and increased wall pressure.
  • Luminal distention produces the visceral pain sensation experienced by the patient as periumbilical pain.
  • Inflammation of the adjacent peritoneum gives rise to localized pain in the right lower quadrant.
  • perforation typically occurs after at least 48 hours from the onset of symptoms and is accompanied

Diagnosis/ Clinical features

  • Acute abdominal pain.
  • The typical presentation begins with periumbilical pain (due to activation of visceral afferent neurons) followed by anorexia and nausea.
  • The pain then localizes to the right lower quadrant as the inflammatory process progresses to involve the parietal peritoneum overlying the appendix.
  • This classic pattern of migratory pain is the most reliable symptom of acute appendicitis.
  • A bout of vomiting may occur, in contrast to the repeated bouts of vomiting that typically accompany viral gastroenteritis or small bowel obstruction.
  • Fever ensues, followed by the development of leukocytosis.
  • Occasional patients have urinary symptoms or microscopic hematuria, owing to inflammation of periappendiceal tissues adjacent to the ureter or bladder.
  • Most patients with appendicitis develop an adynamic ileus and absent bowel movements on the day of presentation, occasional patients may have diarrhea.
  • May present with small bowel obstruction related to contiguous regional inflammation.

Physical Examination

  • Pt. look ill and  lie still in bed.
  • Low-grade fever is common (∼38°C). 
  • Examination of the abdomen usually reveals diminished bowel sounds and focal tenderness with voluntary guarding.
  • The exact location of the tenderness is directly over the appendix, which is most commonly at McBurney's point (located one third of the distance along a line drawn from the anterior superior iliac spine to the umbilicus
  • Peritoneal irritation can be elicited on physical examination by the findings of voluntary and involuntary guarding, percussion, or rebound tenderness.
  • Pain in the right lower quadrant during palpation of the left lower quadrant (Rovsing's sign), pain on internal rotation of the hip (obturator sign, suggesting a pelvic appendix), and pain on extension of the right hip (iliopsoas sign, typical of a retrocecal appendix).
  • Rectal and pelvic examinations are most likely to be negative. However, if the appendix is located within the pelvis, tenderness on abdominal examination may be minimal, whereas anterior tenderness may be elicited during rectal examination as the pelvic peritoneum is manipulated. Pelvic examination with cervical motion may also produce tenderness in this setting.

iliopsoas sign

Obturator Sign

Rovsing’s sign

Laboratory Studies
  • The white blood cell count is elevated with more than 75% neutrophils.
  • Shift to left.

  • appendix of 7 mm or more in anteroposterior diameter, a thick-walled, noncompressible luminal structure seen in cross section 
  • In more advanced cases, periappendiceal fluid or a mass may be found.

Computed tomography (CT)
  • Classic findings include a distended appendix greater than 7 mm in diameter and circumferential wall thickening, which may give the appearance of a halo or target .

Diagnostic Laparoscopy
  • Although most patients with appendicitis will be accurately diagnosed based on history, physical exam, laboratory studies, and if necessary, imaging techniques, there are a small number in whom the diagnosis remains unclear.
  • For these patients, diagnostic laparoscopy can provide both a direct examination of the appendix and a survey of the abdominal cavity for other possible causes of pain.
Shift to left

  • Most patients with acute appendicitis are managed by prompt surgical removal of the appendix.
  • A brief period of resuscitation is usually sufficient to ensure the safe induction of general anesthesia.
  • Preoperative antibiotics cover aerobic and anaerobic colonic flora. For patients with nonperforated appendicitis, a single preoperative dose of antibiotics reduces postoperative wound infections and intra-abdominal abscess formation.
  • For patients with perforated or gangrenous appendicitis, we continue postoperative intravenous antibiotics until the patient is afebrile. 

Open appendectomy 
  • Transverse right lower quadrant incision (Davis-Rockey) or an oblique incision (McArthur-McBurney), Recently-Lanz incision, Rutherford Morison incision- ( Para and retrocaecal or fixed appendix)
  • For uncomplicated cases - transverse, muscle-splitting incision lateral to the rectus abdominis muscle over McBurney's point.
  • After the peritoneum is entered, the inflamed appendix is identified by its firm consistency and br the presence of taeniae coli.
  • The meso-appendix is divided between clamps and tied.
  • A heavy absorbable tie is placed around the base of the appendix clamped and divided.
  • An absorbable purse-string suture or Z stitch is placed into the cecal wall, and the appendiceal stump is inverted into a fold in the wall of the cecum. 

Division of  Mesoappendix

  • Ligation of the baseand division of the appendix,

Placement of purse-string suture or Z stitch, Inversion of the appendiceal stump.

Laparoscopic appendectomy
  •  A 10-mm port into the umbilicus, followed by a 5-mm port in the suprapubic midline region and a 5-mm port midway between the first 2 ports and to the left of the rectus abdominis muscle.
  • With the patient in Trendelenburg's position and rotated left-side down, then gently sweep the terminal ileum medially and follow the taeniae of the cecum caudad to locate the appendix, which is then elevated. The mesoappendix is divided.
  • Appendix is encircled with two heavy absorbable Endoloops cinched down at the base of the appendix and then a third Endoloop is placed about 1 cm distally and the appendix divided.

  • Location of port sites 
    for laparoscopic 

  • Division of the 

  • Placement of an 
    Endoloop encircling 
    the base of the 

  • Division of the 
    appendix between 

  • Ruptured appendix 
  • Peritonitis and 
  • Abscess