Acute Cholecystitis

Gallstone-Associated (Calculous) Cholecystitis

• Prevalence: Over 90% of cases result from gallstones obstructing the cystic duct.
• Pathophysiology:
  • Obstruction leads to bile stasis, increased gallbladder pressure, inflammation, and secondary bacterial infection.
  • Chronic gallstone disease may present as episodic biliary colic, with persistent obstruction leading to acute cholecystitis.
• Risk Factors:
  • Female sex (influence of hormonal factors)
  • Increasing age
  • Pregnancy
  • Obesity and rapid weight loss
  • Certain ethnic groups, including Native American and Hispanic populations
  • Use of hormonal therapy such as estrogen.
    
    

Non-Gallstone (Acalculous) Cholecystitis

• Incidence: Accounts for approximately 5-10% of cases.
• Predisposing Conditions:
  • Severe Illness: Common in critically ill patients, particularly those in intensive care.
  • Total Parenteral Nutrition (TPN): Leads to gallbladder stasis, with a high prevalence of biliary sludge formation in prolonged cases.
  • Major Surgery & Trauma: Severe burns, major surgical interventions, and septic states increase risk due to gallbladder ischemia.
  • Cardiac Events: Myocardial infarction and shock states contribute to gallbladder hypoperfusion.
  • Infectious Causes: Epstein-Barr virus, Salmonella, cytomegalovirus, and Cryptosporidium have been implicated.
  • Medication-Induced Factors: Ceftriaxone can precipitate with calcium to form biliary sludge, while ciclosporin reduces bile acid secretion, promoting stone formation.
    
    

Bacterial Involvement

• Secondary Role: Infection is typically a consequence rather than a primary cause of gallbladder inflammation.
• Common Pathogens:
  • Escherichia coli, Klebsiella, Enterococcus, Pseudomonas, Salmonella, and Bacteroides fragilis.
  • In up to 40% of patients, cultures from gallbladder specimens may be negative despite inflammation.
    
    

Mechanisms of Gallstone Formation

• Supersaturation & Precipitation: Imbalances in bile composition, including excess cholesterol or bilirubin, predispose to stone formation.
• Biliary Stasis: Reduced gallbladder motility, often seen with fasting, TPN, or systemic illness, increases risk.
• Nucleation of Cholesterol Crystals: Mucin and biliary proteins enhance the crystallisation process.
  
  

Complications

• Gangrenous Cholecystitis: Persistent ischemia can lead to necrosis and perforation.
• Emphysematous Cholecystitis: Infection with gas-producing bacteria such as Clostridium perfringens can result in gas accumulation within the gallbladder wall, increasing the risk of rupture.

Mechanisms of Disease Development

• Cystic Duct Obstruction: The primary cause of acute cholecystitis is obstruction of the cystic duct, usually by gallstones, leading to bile stasis and inflammation.
• Acalculous Cholecystitis: This occurs in a smaller percentage of cases and is attributed to ischemia, biliary stasis, or direct bacterial invasion, often in critically ill patients.
  
  

Gallbladder Inflammation and Injury

1. Bile Stasis and Increased Pressure:
   • When the cystic duct is obstructed, bile cannot drain, resulting in increased intraluminal pressure and mucosal injury.
2. Prostaglandin-Mediated Inflammation:
   • Mechanical irritation from gallstones stimulates the release of prostaglandins (PGI2, PGE2), promoting vascular dilation, fluid accumulation, and neutrophil infiltration.
   • These inflammatory changes cause gallbladder wall thickening, pain, and tenderness.
3. Ischemic Injury and Necrosis:
   • As the gallbladder becomes distended, blood supply to the tissue is compromised, leading to ischemia and, in severe cases, necrosis or perforation.
4. Bacterial Superinfection:
   • Although not always present initially, secondary bacterial infection may occur, involving common organisms such as Escherichia coli, Klebsiella, Enterococcus, and Bacteroides fragilis.
   • In some cases, no bacterial growth is detected, indicating that infection is a consequence rather than the primary cause of inflammation.
     
     

Pathogenesis of Acalculous Cholecystitis

• Biliary Stasis and Sludge Formation:
  • Common in critically ill patients, this occurs due to impaired gallbladder motility, often secondary to systemic illness, prolonged fasting, or total parenteral nutrition.
  • Retained concentrated bile is highly toxic to the gallbladder mucosa, leading to inflammation.
• Hypoperfusion and Ischemia:
  • Hypotension, sepsis, or trauma may reduce gallbladder blood flow, leading to ischemic necrosis.
  • Endotoxins can further impair gallbladder contraction by inhibiting cholecystokinin (CCK)-mediated responses.
    
    

Disease Progression and Complications

• Potential Outcomes:
  1. Some cases resolve spontaneously if the impacted stone dislodges, restoring cystic duct patency.
  2. Persistent obstruction, however, leads to further complications.
• Severe Complications:
  1. Gangrenous Cholecystitis: Persistent ischemia results in tissue necrosis and a high risk of perforation.
  2. Emphysematous Cholecystitis: Gas-forming bacteria (Clostridium perfringens) cause intramural gas accumulation, increasing the risk of rupture.
  3. Pericholecystic Abscess: Inflammatory spread leads to abscess formation around the gallbladder.
  4. Mirizzi’s Syndrome: An impacted gallstone compresses the common bile duct, leading to jaundice.
     
     

Classification of Acute Cholecystitis

1. Calculous Cholecystitis (90-95%):
   • Caused by gallstone obstruction of the cystic duct.
2. Acalculous Cholecystitis (5-10%):
   • Occurs in critically ill patients due to ischemia or bile stasis.
     
     

Pathological Stages

1. Oedematous Stage (2-4 days):
   • Mucosal inflammation with subserosal edema.
2. Necrotising Stage (3-5 days):
   • Vascular compromise leads to hemorrhagic necrosis, though without full-thickness wall involvement.
3. Suppurative Stage (7-10 days):
   • Bacterial invasion results in intra-wall abscesses and pericholecystic collections.
4. Chronic Cholecystitis:
   • Recurrent inflammation leads to fibrosis and gallbladder dysfunction.
5. Emphysematous Cholecystitis:
   • Characterised by gas formation in the gallbladder wall due to anaerobic bacterial infection, frequently seen in diabetics.

Prevalence and Incidence

• Acute cholecystitis follows the epidemiological pattern of gallstone disease, its most common cause.
• Gallstone Disease: Affects approximately 10-20% of adults, though only a portion develop symptoms. Among those with asymptomatic gallstones, 1-2% become symptomatic annually.
• Acute Cholecystitis: Develops in about 10% of individuals with symptomatic gallstones.
• Surgical Interventions: Cholecystectomy is one of the most frequently performed major surgical procedures, with hundreds of thousands of operations occurring annually.
  
  

Age Distribution

• The incidence of cholecystitis increases with age, particularly after the fourth decade of life.
• Elderly populations have a greater prevalence, with a notable increase among older men, possibly related to hormonal changes, including shifts in androgen-to-estrogen ratios.
  
  

Sex Differences

• Women are 2-3 times more likely to develop gallstones and acute cholecystitis than men.
• Hormonal factors, particularly estrogen and progesterone, contribute to gallbladder stasis and gallstone formation.
• Pregnancy-Related Risk: Elevated progesterone levels during pregnancy impair gallbladder motility, predisposing women to gallstone formation and acute cholecystitis.
• Acalculous Cholecystitis: While gallstone-related cholecystitis is more common in women, acalculous cholecystitis occurs more frequently in elderly men.
  
  

Ethnic and Geographic Variations

• Higher Prevalence: Scandinavian populations, Native American groups (particularly Pima Indians), and Hispanic individuals have higher rates of gallstone disease and cholecystitis.
• Lower Prevalence: Individuals from sub-Saharan Africa and Asia have lower incidences.
• In the U.S., gallbladder disease is more common among White populations compared to Black populations.
  
  

Acalculous Cholecystitis

• Accounts for 5-14% of acute cholecystitis cases.
• More frequently observed in critically ill patients, particularly those in intensive care settings, burn units, or post-trauma care.
• Risk factors include total parenteral nutrition (TPN), prolonged fasting, sepsis, and major surgical interventions.

Acute Cholecystitis

• Primary Symptom: Right upper quadrant (RUQ) abdominal pain is the most common presenting complaint. The pain often begins in the epigastric region and migrates to the RUQ.
• Pain Characteristics:
  • Typically severe and constant, lasting several hours.
  • May radiate to the right shoulder or back.
  • Unlike biliary colic, which resolves within a few hours, acute cholecystitis pain persists beyond six hours.
• Associated Symptoms:
  • Nausea and vomiting are frequent.
  • Fever may be present due to inflammation or secondary bacterial infection.
  • Some patients describe a history of biliary colic before the onset of acute symptoms.
• Acalculous Cholecystitis:
  • More commonly seen in critically ill patients.
  • Patients may lack a prior history of gallstones or biliary colic.
  • Fever and signs of sepsis may be the primary presenting features.
    
    

Chronic Cholecystitis

• Presentation:
  • Recurrent episodes of RUQ pain with postprandial discomfort, bloating, and nausea.
  • Food intolerances, particularly to greasy or spicy foods, are common.
  • Patients often report increased belching or gas.
• Pain Characteristics:
  • Less intense than in acute cholecystitis but can be persistent over months or years.
  • Sometimes mistaken for other gastrointestinal conditions like reflux or peptic ulcer disease.
• Progression:
  • Recurrent episodes may lead to fibrosis and loss of gallbladder function, increasing the risk of complications such as gallstone pancreatitis or choledocholithiasis.
    
    

Risk Factors and Predisposing Conditions

• Gallstones:
  • Present in 90% of cases of acute cholecystitis.
  • Previous biliary colic increases the risk of developing acute cholecystitis.
• Severe Illness:
  • Critically ill patients may develop gallbladder dysmotility or ischemia, leading to acalculous cholecystitis.
• Metabolic and Drug-Related Factors:
  • Ceftriaxone: Can precipitate with calcium, forming biliary sludge.
  • Ciclosporin: Decreases bile acid secretion, increasing the risk of bile stasis and stone formation.
• Other Conditions Increasing Risk:
  • Diabetes mellitus.
  • Prolonged fasting or total parenteral nutrition.
  • Severe trauma, burns, or systemic vasculitis.
  • Atherosclerotic disease and acute renal failure.
  • HIV-related cholangiopathy, often associated with opportunistic infections like cytomegalovirus and Cryptosporidium.
    
    

Additional Symptoms to Elicit

• Fever and Chills:
  • Suggests secondary infection or developing complications such as empyema or perforation.
• Jaundice:
  • Occurs in about 10% of cases.
  • Can result from direct compression of the biliary tree by an inflamed or distended gallbladder.
• Gastrointestinal Symptoms:
  • Anorexia is commonly reported.
  • Vomiting may occur, particularly if there is an obstructing gallstone.
• Referred Pain:
  • Pain may extend to the right scapular or interscapular area.
    
    

General Findings

• Fever and Tachycardia:
  • Suggests systemic inflammation or secondary bacterial infection.
  • More common in moderate-to-severe cases.
• Signs of Peritoneal Irritation:
  • Right upper quadrant (RUQ) tenderness is the most consistent finding.
  • Guarding and rebound tenderness may be present in cases of advanced inflammation or perforation.
    
    

Murphy’s Sign

• Definition: An inspiratory pause due to pain when palpating the RUQ during deep inspiration.
• Sensitivity and Specificity:
  • Reported sensitivity ranges from 20% to 97%.
  • More reliable when assessed via ultrasound (sonographic Murphy’s sign), which has a higher predictive value for acute cholecystitis.
• Limitations:
  • Less reliable in elderly patients.
  • Can be absent in gangrenous cholecystitis or in patients with altered pain perception due to diabetes or neuropathy.
    
    

Palpable Gallbladder and Mass

• Gallbladder Enlargement:
  • A palpable, tender gallbladder is found in 30-40% of cases.
  • Suggests significant bile stasis and possible obstruction.
• Pericholecystic Abscess or Local Perforation:
  • May present as a localised RUQ mass.
  • Requires imaging for further evaluation.
    
    

Jaundice and Biliary Obstruction

• Jaundice (Present in ~15% of Cases):
  • Mild jaundice with a serum bilirubin <60 μmol/L can result from inflammation or compression of the bile duct.
  • Higher bilirubin levels may indicate choledocholithiasis or Mirizzi’s syndrome.
• Differentiation:
  • If bilirubin >60 μmol/L, further imaging is warranted to assess for common bile duct obstruction.
    
    

Atypical Presentations

• Elderly Patients:
  • May present without fever or localised tenderness.
  • Symptoms may be vague, including generalised weakness or confusion.
  • Higher risk of rapid progression to complicated cholecystitis.
• Diabetic Patients:
  • Higher likelihood of developing emphysematous cholecystitis, which can present with subcutaneous emphysema in the RUQ.
• Acalculous Cholecystitis:
  • Frequently occurs in critically ill patients.
  • Can present with sepsis without localised pain.
  • Associated with prolonged fasting, total parenteral nutrition, and major surgery.
    
    

First-Line Investigations

1. Abdominal Ultrasound (Preferred Initial Imaging)
   • First-line imaging due to high sensitivity for detecting gallstones and acute cholecystitis.
   • Key findings:
     • Pericholecystic fluid
     • Gallbladder distension
     • Wall thickening (>3 mm)
     • Presence of gallstones
     • Sonographic Murphy’s sign (pain elicited when the ultrasound probe is placed over the gallbladder, though this may be absent in gangrenous cholecystitis).
2. Liver Function Tests (LFTs)
   • Elevated bilirubin suggests bile duct obstruction or acute focal cholestasis.
   • Increased levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT) may indicate associated cholestasis.
3. Full Blood Count (FBC)
   • Leukocytosis with a left shift suggests infection or inflammation.
   • Significant elevation may indicate severe cholecystitis or sepsis.
4. C-Reactive Protein (CRP)
   • Elevated CRP is a marker of inflammation or infection.
   • Higher levels may indicate more severe disease or potential complications.
5. Bilirubin
   • Moderate elevation suggests gallbladder inflammation affecting adjacent liver tissue.
   • Significant elevation (>60 µmol/L) may indicate obstruction of the common bile duct.
     
     

Investigations to Consider

1. Magnetic Resonance Cholangiopancreatography (MRCP)
   • Indicated when ultrasound does not detect bile duct stones but there is bile duct dilation or abnormal LFTs.
   • Findings in acute cholecystitis:
     • Gallbladder wall thickening (≥4 mm)
     • Gallbladder enlargement (long axis ≥8 cm, short axis ≥4 cm)
     • Presence of gallstones or retained debris
     • Fluid accumulation around the gallbladder
     • Linear shadows in the surrounding fatty tissue.
   • More cost-effective than endoscopic retrograde cholangiopancreatography (ERCP) for diagnosing bile duct stones.
2. Endoscopic Ultrasound (EUS)
   • Considered if MRCP does not confirm bile duct stones.
   • Higher sensitivity for detecting distal common bile duct stones.
   • Can be combined with ERCP for therapeutic intervention.
3. Computed Tomography (CT)
   • Used when ultrasound is inconclusive or if emphysematous cholecystitis, gallbladder perforation, or sepsis is suspected.
   • Key findings:
     • Gallbladder wall thickening (>4 mm)
     • Pericholecystic fluid
     • Intramural gas (suggestive of emphysematous cholecystitis)
     • Abscess formation.
4. Hepatobiliary Iminodiacetic Acid (HIDA) Scan
   • Highly sensitive for detecting cystic duct obstruction.
   • Used when ultrasound is inconclusive or when acalculous cholecystitis is suspected.
   • Findings:
     • Non-visualization of the gallbladder due to cystic duct obstruction.
5. Serum Amylase and Lipase
   • Ordered to exclude acute pancreatitis in patients with upper abdominal pain.
   • Lipase is preferred over amylase due to prolonged elevation (up to 14 days vs. 5 days for amylase).
   • Levels >3 times the upper normal range confirm acute pancreatitis
6. Blood Cultures
   • Recommended for patients with moderate to severe cholecystitis.
   • Useful in identifying bacteremia in patients with sepsis.

Gastrointestinal Causes

1. Acute Cholangitis
   • Symptoms: Charcot’s triad—fever, jaundice, and RUQ pain (Reynolds’ pentad includes hypotension and confusion in severe cases).
   • Investigations:
     • Elevated bilirubin and alkaline phosphatase (suggesting bile duct obstruction).
     • Magnetic resonance cholangiopancreatography (MRCP) or endoscopic ultrasound (EUS): Identifies intraductal stones and purulent bile stasis.
     • Blood cultures: Identify bacterial infection in sepsis-related cases.
2. Biliary Colic
   • Symptoms: Colicky RUQ pain lasting minutes to hours, often following fatty meals.
   • Investigations:
     • Normal inflammatory markers (no leukocytosis or elevated CRP).
     • Ultrasound: Gallstones present without gallbladder wall thickening or pericholecystic fluid.
3. Chronic Cholecystitis
   • Symptoms: Recurrent episodes of postprandial RUQ pain, nausea, bloating.
   • Investigations:
     • Ultrasound: Gallbladder wall thickening, mucosal atrophy, and gallstones.
     • Histopathology (if gallbladder is removed): Fibrosis and chronic inflammation.
4. Peptic Ulcer Disease
   • Symptoms: Epigastric pain, burning sensation relieved by food or antacids, nocturnal pain.
   • Investigations:
     • Endoscopy: Identifies gastric or duodenal ulcers.
     • Helicobacter pylori testing: Urea breath test or stool antigen test.
5. Acute Pancreatitis
   • Symptoms: Severe epigastric or periumbilical pain radiating to the back, nausea, vomiting.
   • Investigations:
     • Serum amylase or lipase: Elevated (>3 times normal).
     • CT abdomen: Pancreatic inflammation, peripancreatic fluid collections.
6. Gastroesophageal Reflux Disease (GERD)
   • Symptoms: Heartburn, acid regurgitation, symptoms worsened by lying down.
   • Investigations:
     • Endoscopy: May show esophagitis.
     • Therapeutic trial with proton pump inhibitors (PPI): Symptom relief supports GERD.
       
       

Hepatobiliary and Vascular Causes

1. Hepatic Abscess
   • Symptoms: RUQ pain, fever, hepatomegaly.
   • Investigations:
     • CT or MRI: Hypodense liver lesion with rim enhancement.
     • Blood cultures: May be positive for bacterial or amoebic infection.
2. Mesenteric Ischemia
   • Symptoms: Severe, diffuse abdominal pain, often disproportionate to examination findings.
   • Investigations:
     • CT angiography: Identifies vascular occlusion or ischemic changes.
     • Lactate levels: Elevated in advanced cases.
       
       

Other Abdominal and Systemic Conditions

1. Appendicitis
   • Symptoms: Pain migrating from the periumbilical region to the right iliac fossa.
   • Investigations:
     • CT scan: Enlarged appendix with wall thickening, hyperenhancement.
     • Ultrasound (in children/pregnant patients): Thickened, non-compressible appendix.
2. Sickle Cell Crisis
   • Symptoms: Acute pain episodes, possibly in the RUQ, unrelated to gallstones.
   • Investigations:
     • Peripheral blood smear: Presence of sickle cells.
     • Hemoglobin electrophoresis: Confirms sickle cell disease.
3. Right Lower Lobe Pneumonia
   • Symptoms: Fever, cough, pleuritic chest pain that may mimic RUQ pain.
   • Investigations:
     • Chest X-ray: Consolidation in the right lower lobe.
     • Blood cultures: In cases of pneumonia-associated sepsis.
4. Acute Coronary Syndrome (ACS)
   • Symptoms: Central or epigastric chest pain, radiation to the left arm or jaw.
   • Investigations:
     • ECG: ST-segment elevation, T-wave inversions.
     • Cardiac enzymes: Elevated troponin in myocardial infarction.
       
       

Initial Management

• Intravenous Fluids: Essential for maintaining perfusion, particularly in patients with dehydration, sepsis, or hemodynamic instability. Balanced crystalloids (e.g., Ringer’s lactate) are preferred to avoid hyperchloremic acidosis.
• Analgesia: Pain control should be initiated early to prevent respiratory compromise and reduce stress-related tachycardia.
  • First-line: Paracetamol or NSAIDs (e.g., diclofenac, ibuprofen).
  • Second-line: Opioids (e.g., morphine) if NSAIDs are ineffective; however, opioids should be used cautiously as they may increase sphincter of Oddi tone.
• Nil by Mouth (NPO) Status: Recommended to reduce gallbladder stimulation and prepare for possible surgery.
• Early Warning Score Monitoring: Systems such as the National Early Warning Score (NEWS2) should be used to assess patient deterioration, particularly in those at risk of sepsis.
  
  

Sepsis and Organ Dysfunction

• Sepsis Management:
  • Broad-spectrum intravenous antibiotics should be started immediately in suspected cases of sepsis.
  • Close monitoring of lactate levels and blood pressure to assess for septic shock.
  • Transfer to intensive care if organ dysfunction develops.
• Organ Support:
  • Respiratory support if signs of respiratory distress.
  • Vasopressors (e.g., norepinephrine) for refractory hypotension despite fluid resuscitation.
    
    

Antibiotic Therapy

• First-line options:
  • Piperacillin-tazobactam (4.5 g IV every 8 hours) – broad-spectrum coverage including anaerobes.
  • Ampicillin-sulbactam (3 g IV every 6 hours) – alternative if penicillin-sensitive organisms are suspected.
• For life-threatening infections:
  • Meropenem (1 g IV every 8 hours) or Imipenem-cilastatin (500 mg IV every 6 hours) – used in critically ill patients with suspected multidrug-resistant pathogens.
• For beta-lactam allergy:
  • Ciprofloxacin + Metronidazole or Levofloxacin + Metronidazole.
    
    

• Adjust regimen based on blood and bile culture results.
• De-escalation to oral antibiotics once stable, typically continued for 7-10 days to prevent antimicrobial resistance.
  
  

Surgical Management

• Gold-standard treatment for acute cholecystitis.
• Early LC (within 72 hours) is preferred over delayed surgery, as it reduces hospital stays, complications, and conversion rates to open surgery.
• If local expertise is unavailable, transfer to a specialist hepatobiliary unit.
  
  

• Considered when:
  • Severe peritonitis or gangrenous cholecystitis is present.
  • Significant adhesions or fibrosis make laparoscopic dissection challenging.
  • Bile duct injury risk is high due to unclear anatomy.

Alternative and Adjunctive Interventions

• Indicated for patients unfit for surgery due to severe comorbidities.
• Provides temporary drainage and symptom relief.
• Follow-up:
  • If clinical improvement occurs, consider elective cholecystectomy after 6-8 weeks.
  • If symptoms persist or worsen, repeat imaging to rule out abscess formation or ongoing bile leakage.
    
    

• Suitable for patients in whom both surgery and PC are contraindicated.
• Requires specialised expertise and is typically performed in high-volume centers.
• Can be achieved through endoscopic ultrasound (EUS)-guided transmural drainage.
  
  

Management of Complications

• Definition: Pus accumulation within the gallbladder, leading to high risk of perforation and sepsis.
• Management:
  • Percutaneous cholecystostomy as first-line treatment.
  • Early cholecystectomy once the patient stabilises.

• Definition: Ischemic necrosis of the gallbladder wall due to severe inflammation.
• Risk Factors:
  • Elderly patients (>60 years)
  • Diabetes mellitus
  • Prolonged inflammation (>48-72 hours)
• Management:
  • Urgent laparoscopic cholecystectomy to prevent perforation.
  • Conversion to open surgery may be required if there is extensive necrosis.
    
    

Gallbladder Perforation

• Incidence: Occurs in up to 10% of cases, particularly when treatment is delayed.
• Clinical Clues:
  • Sudden pain relief followed by signs of peritonitis.
• Management:
  • Percutaneous drainage or immediate laparoscopic cholecystectomy depending on perforation severity.
    
    

• Definition: Infection of the biliary tree, commonly due to bile duct obstruction.
• Clinical Features:
  • Charcot’s triad: Fever, jaundice, RUQ pain.
  • Reynolds’ pentad: Above triad + hypotension + altered mental status (severe cases).
• Management:
  • Urgent ERCP to relieve obstruction.
  • Antibiotics and fluid resuscitation.
    
    

Postoperative and Long-Term Care

• Simple analgesia (paracetamol, NSAIDs) is usually sufficient.
• Opioids only for severe pain.
  
  

• No absolute dietary restrictions after cholecystectomy.
• Fatty foods may initially cause mild diarrhea or bloating but generally resolve over time.
  
  

• Monitor for jaundice or bile duct obstruction.
• Address any post-cholecystectomy syndrome (bloating, pain, or indigestion).
  
  

Overall Prognosis

• Uncomplicated acute cholecystitis has a favorable prognosis, with most patients recovering within 1 to 4 days following appropriate treatment.
• The mortality rate for mild calculous cholecystitis is low when managed with early intervention, particularly laparoscopic cholecystectomy.
• 25-30% of patients experience complications or require emergency surgery due to disease progression.
• Complicated acute cholecystitis has a significantly worse prognosis, especially if left untreated.
  • Perforation occurs in 10-15% of cases and increases mortality.
  • Gangrene and emphysematous cholecystitis contribute to high morbidity.
  • Sepsis and organ failure can further elevate the mortality risk.
    
    

Acalculous Cholecystitis Prognosis

• This condition carries a far higher mortality rate than calculous cholecystitis due to its association with critical illness.
• Mortality ranges from 10% to 50%, often due to delayed diagnosis and the presence of underlying systemic disease.
• In critically ill patients with perforation or gangrene, mortality can rise to 50-60%.
  
  

Mortality and Risk Factors

• Overall mortality for calculous cholecystitis: ~4%.
• Acalculous cholecystitis mortality: 10-50%, due to high rates of sepsis and organ failure.
• Gallbladder perforation increases mortality risk to 30%.
• Severe inflammation requiring ICU admission significantly worsens outcomes.
  
  

Complications Affecting Prognosis

1. Bile Duct Injury
   • Iatrogenic bile duct injury remains a serious complication of cholecystectomy, with risk increasing in the setting of acute inflammation.
   • Patients with moderate cholecystitis have double the risk of bile duct injury compared to those without active inflammation.
   • In severe cholecystitis, the risk is more than eightfold.
   • The use of intraoperative cholangiography reduces bile duct injury risk by approximately 50%.
2. Gallbladder Empyema
   • Bacterial overgrowth in an obstructed gallbladder can lead to purulent infection.
   • Patients often develop high fever, leukocytosis, and systemic toxicity.
   • Conversion from laparoscopic to open cholecystectomy is frequently required for surgical management.
3. Gallstone Ileus
   • Occurs when a large gallstone erodes through the gallbladder wall, creating a fistula to the gastrointestinal tract.
   • The stone may become impacted in the terminal ileum or pylorus, causing mechanical obstruction.
   • Requires emergency surgical intervention, often an enterotomy with stone extraction.
4. Emphysematous Cholecystitis
   • A rare but severe form of cholecystitis, occurring in approximately 1% of cases.
   • Caused by gas-forming bacteria (Clostridium perfringens, Escherichia coli, Klebsiella).
   • More common in diabetics and elderly males.
   • High risk of gangrene and perforation, requiring emergency cholecystectomy.
5. Acute Pancreatitis
   • Gallstone migration can obstruct the pancreatic duct, leading to pancreatitis.
   • Severe cases may result in multi-organ dysfunction requiring ICU admission.
6. Sepsis and Multi-Organ Failure
   • Untreated cholecystitis can lead to ascending cholangitis, with a high risk of septic shock.
   • Early antibiotic therapy and biliary drainage are critical to improving survival rates.
     
     

Long-Term Prognosis and Preventative Strategies

• Elective Cholecystectomy:
  • Prevents recurrence of biliary colic and acute cholecystitis.
  • Reduces the risk of emergency surgery and complications.
  • Recommended for patients with symptomatic gallstones.
• Post-Cholecystectomy Outcomes:
  • Most patients fully recover after laparoscopic cholecystectomy.
  • Some may develop post-cholecystectomy syndrome, presenting with bloating, mild diarrhea, or upper abdominal discomfort, usually resolving over time.
• Follow-Up and Surveillance:
  • Monitor for signs of jaundice, indicating possible bile duct obstruction.
  • Assess liver function postoperatively to ensure resolution of inflammation and obstruction.
  • Address any persistent gastrointestinal symptoms, particularly in patients who undergo emergency surgery or have had bile duct manipulation.
    
    

Infectious and Inflammatory Complications

1. Suppurative Cholecystitis
   • Progresses from acute cholecystitis when bacterial overgrowth and inflammation cause pus formation within the gallbladder wall.
   • Hallmarks include thickened gallbladder walls, intra-wall abscesses, and necrosis.
   • If untreated, it may result in perforation and pericholecystic abscess formation.
   • Requires urgent cholecystectomy or percutaneous drainage if the patient is not fit for surgery.
2. Gallbladder Empyema
   • Characterised by pus accumulation within the gallbladder due to ongoing bacterial infection.
   • Presents with high fever, systemic toxicity, and leukocytosis.
   • Percutaneous cholecystostomy may be needed for temporary relief in high-risk surgical patients.
3. Emphysematous Cholecystitis
   • A rare but severe form of infection caused by gas-forming bacteria (Clostridium perfringens, Escherichia coli, Klebsiella).
   • More common in elderly, diabetic, and immunocompromised patients.
   • High risk of gangrene and perforation, necessitating emergency cholecystectomy.
     
     

Biliary and Gastrointestinal Complications

1. Bile Duct Injury (Post-Surgical)
   • A known risk of cholecystectomy, particularly in cases of severe inflammation and difficult anatomy.
   • Can lead to biliary leakage, strictures, and obstruction.
   • Managed by endoscopic stenting, percutaneous transhepatic dilation, or surgical repair.
   • The risk of injury is significantly reduced by intraoperative cholangiography.
2. Gallstone Ileus
   • Occurs when a large gallstone erodes through the gallbladder wall, creating a fistula between the biliary and intestinal tracts.
   • The stone enters the intestine, leading to mechanical obstruction, often at the terminal ileum.
   • Patients present with abdominal pain, nausea, and signs of bowel obstruction.
   • Treatment involves surgical enterotomy for stone removal, followed by cholecystectomy 4 to 6 weeks later.
3. Cholecystoenteric Fistula
   • An abnormal connection between the gallbladder and nearby organs, most commonly the duodenum or colon.
   • Can cause spontaneous decompression of the gallbladder, temporarily relieving symptoms.
   • May lead to bile reflux gastritis or gallstone migration.
   • Definitive cholecystectomy is typically required.
4. Bile Leak and Biloma
   • Occurs when bile leaks into the peritoneal cavity, forming a localised collection.
   • Can result from spontaneous perforation, traumatic injury, or surgical complications.
   • Managed with percutaneous drainage or ERCP with stent placement.
     
     

Severe and Systemic Complications

1. Sepsis and Multi-Organ Failure
   • Untreated cholecystitis can progress to ascending cholangitis, leading to septic shock.
   • Broad-spectrum antibiotics, fluid resuscitation, and biliary drainage (via ERCP) are critical for survival.
2. Hepatic and Small Bowel Injury
   • Iatrogenic liver or bowel injury can occur during complicated cholecystectomies, particularly in cases with severe adhesions or inflammation.
   • May require laparoscopic or open repair.
3. Postoperative Bleeding
   • Can result from vascular injury, particularly cystic artery bleeding during surgery.
   • Managed by endovascular embolisation or surgical hemostasis.
     
     

Management Strategies for Complications

• Early Diagnosis and Surgical Intervention:
  • Timely laparoscopic cholecystectomy reduces the risk of complications.
  • Delaying surgery beyond 72 hours increases the likelihood of gallbladder gangrene, perforation, and sepsis.
• Alternative Drainage Options:
  • Percutaneous cholecystostomy for high-risk surgical patients.
  • Endoscopic ultrasound-guided gallbladder drainage in specialised centers.
• Preventing Bile Duct Injury:
  • Intraoperative cholangiography significantly lowers the risk.
  • Referral to hepatobiliary specialists for difficult cases.
    
    

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