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Acute Cholecystitis: Etiology

• Stagnation of gallbladder contents is a predisposing factor.
• Acute obstructive (calculus) accounts for 95% of cases.
• Acute non-obstructive (non-calculus) accounts for 5% of cases, often due to major burns, trauma, or gallbladder dyskinesia.
• Common organisms include E. coli, streptococcus faecalis, Klebsiella, and bacteroids.
• Clostridia welchii (rare) leads to emphysematous cholecystitis.
• Salmonella typhi causes typhoid cholecystitis.
• Direct spread along biliary ducts is the most common route of infection in obstructive cholecystitis.
• Hematogenous route via the cystic artery and lymphatic route are other possible, but rare, routes of infection.
• Chronic cholecystitis obstructing the cystic duct by stone and adhesions is the most common predisposing factor, leading to infection and then acute cholecystitis.

Acute Cholecystitis: Pathology

• Calcular cholecystitis progresses through several stages.

Catarrhal Inflammation

• Localized to the mucous membrane with congestion, the gallbladder distends with mucus and bile (mucocele).

Suppurative Inflammation

• Secondary bacterial invasion occurs, with the gallbladder distending with pus (empyema = pyocele).
• Omentum and surrounding viscera adhere to the inflamed gallbladder.
• Adhesions are first fibrinous, and may later become fibrous.

Gangrenous Stage

• Septic thrombosis and gangrene can occur if obstruction and inflammation is severe.

• Non-calculus cholecystitis follows similar stages but mucocele and pyocele do not occur.

• Gangrene and perforation are less common, and the inflammatory process is slower in non-calculus cholecystitis.

Acute Cholecystitis: Clinical Presentation

• Risk factors: "Fatty, Forty, Filthy, Fertile, Females (5 F)."

Symptoms:

• Severe paroxysmal colicky pain in the right hypochondrium, radiating to the right shoulder and scapular area.
• If acute infection is superadded pain becomes continuous and throbbing aggravated by movement, coughing, and associated with high fever, rigors, and excessive sweating.
• Nausea and vomiting is also present
• Constipation and distension can also occur

Signs:

General

• Toxic look (patient is flushed)
• Coated tongue
• High temperature
• Tachycardia
• Tinge of jaundice occurs in a few cases results from
  • Ulceration of GB mucosa with absorption of concentrated bile.
  • Stone in Hartmann’s pouch pressing upon CBD (Mirizzi’s $ I) or erosion of stone into CBD (Mirizzi’s $ II)
  • Stone or edema in CBD.
  • Spasm of sphincter of oddi.
  • Ascending cholangitis, reactive hepatitis.

Abdominal

• Limitation of abdominal mobility with respiration in the right hypochondrium.
• Tenderness and rigidity in the right hypochondrium.
• Positive Murphy's sign: inspiratory arrest upon palpation.
• Boas's sign: hyperesthesia over the right 9th-11th ribs posteriorly.
• Distended and palpable gallbladder if empyema or mucocele is present.

Features of Mucocele:

• Patient is relatively well.
• Normal temperature.
• Little tenderness and rigidity over swelling.

Features of Empyema:

• Very ill patient.
• Feverish.
• Marked tenderness and rigidity.

Acute Cholecystitis: Complications

• Chronic acute inflammation subsides, and the gallbladder becomes the site of chronic cholecystitis and stone formation with recurrent acute exacerbations.

Perforation

• Fundus farthest away from blood supply is the most common site of perforation.
• Neck can perforate from pressure necrosis of an impacted stone.

Low Incidence of Perforation in Acute Cholecystitis:

• High incidence if: The gallbladder is capacious and distensible
• Has good blood supply
• Has thickened wall of GB in acute cholecystitis on top of chronic cholecystitis

High Incidence of Rupture in Acute Cholecystitis:

• Is gangrenous
• Typhoid GB
• Diabetic
• Immunosuppressed

Spread of Infection

• General septicemia, toxemia, and pyemia.
• Local cholangiohepatitis and pancreatitis.

Intestinal Obstruction

• By obturation (gallstone ileus) due to internal fistula allowing passage of a stone to the intestine.
• Small stones pass with stool.
• Large stones obstruct the terminal ileum.

Investigations:

Laboratory

• CBC: leucocytosis is present
• LFTs: serum bilirubin and ALK may be elevated

Radiology

Ultrasound

• Investigation of choice
• Detects 90% of radio-lucent gallstones
• Gallstones appear as hyperechoic shadows

Plain X-Ray

• Radio-opaque gallstones in the right hypochondrium (10%)
• Mercedes Benz or Seagull signs containing gas fissures within the stone
• Emphysematous gallbladder with gas in the GB and its wall
• Porcelain gallbladder with calcifications in the wall
• Used to exclude other causes of acute abdomen

Biliary Radionuclide Scanning or HIDA Scan

• HIDA labeled with 99Tc is administered IV which dye is then taken by hepatocytes and excreted in the bile with serial films taken, normally concentrated in the GB
• If CBD is visualized while the gallbladder is not seen diagnostic if acute cholecystitis
• Normal scan excludes acute cholecystitis
• In hepatocellular disease there is typically a delay in excretion
• Obstructing jaundice shows no shadow and no fecal radioactivity after 24 hours
• Advantages are that it is non-invasive, can be done with bilirubin up to 20mg%, and can be done in children and pregnancy

CT Scan

• Less sensitive than ultrasonography
• Can exclude other causes of acute abdominal pain
• Demonstrates thickening of the gallbladder wall, pericholecystic fluid, presence of gallstones, and air in the gallbladder wall

Oral & IV Cholecystography

• Is only of historical significance and is not done now

Differential Diagnosis:

• Exclude other causes of acute abdomen.

Treatment: Conservative Treatment

• Admission to the hospital.
• Absolute rest while in the semi-sitting position
• Administration of analgesics and antispasmodic drugs.
• Antibiotics: 2nd or 3rd generation cephalosporin and metronidazole.
• For patients with allergies: aminoglycoside and metronidazole.
• Maintain fluid and electrolyte balances through parenteral feeding with continuous IV dextrose-saline solution.
• Rest the inflamed gallbladder, biliary, and pancreatic systems through aspiration of gastric contents for 3-5 days. Also application of Kaolin poultices or hot fomentation on the right hypochondrium.
• Monitor patient generally with pulse, temperature, vomiting and general condition, and locally with pain, tenderness, rigidity, mass, peritonitis.

Conservative treatment for 2-3 days, look to see if either:

• Improves: continue treatment with oral fluids, semi-solids, then light solids.
• Cholecystectomy should take place 6 weeks later
• Worsens: signs of failure should be noted and signs of failure included: Rising pulse rate because it is a dangerous sign, but also persistent vomiting/fever Increasing jaundice and pain as well as spreading peritonitis should all lead to urgent cholecystectomy

Treatment: Surgical Treatment

Routine Early Operation

• Performed after 48 hours of preparation with parental fluids, gastric suction and antibiotics
• Indications include emphysematous gallbladder, empyema or perforated gallbladder, diabetic patient with cholecystitis, old patients >60 years that don't improve within 24 hours, typhoid gallbladder, patients receiving corticosteroids, and uncertain diagnosis

Emergent Operations

• Cholecystectomy
• Subtotal cholecystectomy if cholecystectomy is considered hazardous. Posterior wall left in situ and attached to liver bed, with the cystic duct secured from within by a purse-string suture
• Cholecystostomy in presence of massive adhesions with gallbladder contents evacuated, gangrenous patches excised, and 22F foly's catheter inserted into the gallbladder
• Mini cholecystostomy to aspirate inflammation after localization with Ultrasound, with local anesthetic