Acute Pancreatitis

• Acute Pancreatitis: Characterised by reversible inflammation, often resolving without significant long-term damage.
• Chronic Pancreatitis: A progressive disease involving recurrent inflammation, leading to irreversible glandular damage and functional loss.
  
  

Pathophysiological Subtypes 

1. Interstitial Oedematous Acute Pancreatitis:
   • Involves localised or diffuse inflammation without tissue necrosis.
2. Necrotising Acute Pancreatitis:
   • Characterised by necrosis of pancreatic or peripancreatic tissue, with potential for secondary infection.
     
     

Classification Systems for Acute Pancreatitis

1. Mild Acute Pancreatitis:
   • No organ failure.
   • Absence of local or systemic complications.
   • Typically resolves within the first week.
2. Moderately Severe Acute Pancreatitis:
   • Presence of transient organ failure (resolves within 48 hours).
   • Local complications or exacerbation of pre-existing comorbidities.
3. Severe Acute Pancreatitis:
   • Persistent organ failure (>48 hours), involving one or more organs.
   • Common local complications include:
     • Peripancreatic fluid collections.
     • Pancreatic and peripancreatic necrosis (sterile or infected).
     • Pseudocysts.
     • Walled-off necrosis (sterile or infected).
       
       

Balthazar Radiological Classification

• Grade A: Normal pancreas.
• Grade B: Focal or diffuse gland enlargement with small intrapancreatic fluid collections.
• Grade C: Presence of peripancreatic inflammatory changes and <30% gland necrosis.
• Grade D: A single extrapancreatic fluid collection and 30–50% gland necrosis.
• Grade E: Extensive extrapancreatic fluid collection, pancreatic abscess, and >50% gland necrosis.
  
  

Overview

• Approximately 10–30% of cases are idiopathic, though many of these are later attributed to microlithiasis or biliary sludge.
  
  

Common Causes

1. Gallstones:
   • Account for 40–50% of cases in developed countries.
   • Mechanism: Obstruction of the bile duct increases pancreatic ductal pressure, causing enzyme activation and acinar injury.
   • Microlithiasis is implicated in many "idiopathic" cases.
2. Alcohol Use:
   • Contributes to 25–35% of cases globally.
   • Mechanisms:
     • Increases pancreatic duct permeability.
     • Promotes protein plug formation, leading to ductal obstruction.
     • Triggers intracellular enzyme activation.
   • Typically develops after 5–15 years of heavy drinking but can also occur with acute binge drinking.
3. Hypertriglyceridemia:
   • Serum triglyceride levels >1000 mg/dL are strongly associated.
   • More common in Type I and Type V hyperlipidemia.
   • Likely mediated by toxic free fatty acids from triglyceride breakdown.
     
     

Post-Procedural Causes

1. Endoscopic Retrograde Cholangiopancreatography (ERCP):
   • Risk: 1–5%, influenced by procedural factors like operator expertise and sphincter of Oddi dysfunction.
   • Prevention: Aggressive IV hydration and rectal indomethacin.
2. Postoperative Ischemia:
   • Abdominal or cardiopulmonary bypass surgeries can result in gland ischemia, leading to pancreatitis.
     
     

Drug-Induced Pancreatitis

• Rare, accounting for ~2% of cases.
• Drugs definitively linked include:
  • Azathioprine, sulfonamides, valproic acid, and estrogens.
• Mechanism: Likely idiosyncratic or dose-related toxicity.
  
  

Infections

1. Viral:
   • Mumps, cytomegalovirus (CMV), Epstein-Barr virus (EBV), and hepatitis viruses.
2. Bacterial:
   • Mycoplasma pneumoniae, Mycobacterium tuberculosis, and Salmonella.
3. Parasitic:
   • Ascaris lumbricoides and Clonorchis sinensis.
     
     

Genetic and Structural Causes

1. Hereditary Pancreatitis:
   • Related to PRSS1 and SPINK1 mutations.
   • Often manifests in childhood or adolescence.
2. Pancreas Divisum:
   • A common anatomical variant, controversial as a direct cause of pancreatitis.
3. Congenital Malformations:
   • Annular pancreas leading to ductal obstruction.
     
     

Other Causes

• Autoimmune Pancreatitis:
  • Associated with IgG4-related systemic disease.
  • Presents with diffuse pancreatic enlargement and strictures.
• Hypercalcemia:
  • Results from conditions like hyperparathyroidism or excessive vitamin D intake.
• Trauma:
  • Penetrating or blunt abdominal trauma.
    
    

Rare and Controversial Causes

• Toxins:
  • Scorpion stings (e.g., Tityus trinitatis) and organophosphate poisoning.
• Tumors:
  • Pancreatic or ampullary malignancies causing ductal obstruction.
• Vasculitis:
  • Polyarteritis nodosa and systemic lupus erythematosus (SLE).
    
    

Normal Pancreatic Function

• The pancreas, located in the upper posterior abdomen, is responsible for:
  • Endocrine Function: Insulin production.
  • Exocrine Function: Secretion of digestive enzymes for carbohydrate, fat, and protein metabolism.
• About 80% of the pancreatic mass supports exocrine functions, which include:
  • Synthesis of digestive enzymes within acinar cells.
  • Packaging of enzymes into zymogen granules.
  • Release into the pancreatic duct for delivery to the small intestine.
    
    

Enzyme Activation

• Digestive enzymes, produced as inactive zymogens, are activated in the duodenum:
  • Enterokinase activates trypsinogen into trypsin at the brush border.
  • Trypsin then activates other zymogens to their functional forms.
• Feedback mechanisms prevent excessive enzyme activation:
  • Elevated trypsin levels suppress secretion through reduced cholecystokinin (CCK) and secretin.
    
    

Protective Mechanisms

• Zymogen granules are stored in an acidic, low-calcium environment to prevent premature activation.
• Enzymes are co-packaged with protease inhibitors.
• Disruption of these mechanisms can lead to intracellular enzyme activation, initiating acute pancreatitis.

Pathogenesis of Acute Pancreatitis

• Initiating Factors:
  • Gallstones, alcohol use, drugs, or trauma disrupt cellular homeostasis, causing acinar cell injury.
  • Impaired zymogen secretion or ductal cell injury can delay enzymatic excretion, leading to accumulation and activation.
• Intracellular Events:
  • Lysosomal and zymogen granule fusion facilitates premature trypsin activation.
  • Activated trypsin initiates a cascade, activating other digestive enzymes within the pancreas.
  • This enzymatic activity leads to tissue autodigestion.
    
    

Inflammatory Cascade

• Acinar cell injury triggers the release of inflammatory mediators, including:
  • Cytokines (e.g., tumor necrosis factor-alpha, interleukins-6 and -8).
  • Chemotactic factors that recruit neutrophils and macrophages.
  • Neutrophil activation exacerbates inflammation through respiratory burst and protease release.
• Consequences include:
  • Increased vascular permeability.
  • Pancreatic edema, necrosis, and hemorrhage.
    
    

Systemic Effects

• Severe cases can progress to systemic inflammatory response syndrome (SIRS), characterised by:
  • Gut barrier dysfunction and bacterial translocation leading to sepsis.
  • Multi-organ dysfunction syndrome (MODS), including renal failure, acute respiratory distress syndrome (ARDS), and cardiovascular collapse.
    
    

Progression

1. Oedematous Pancreatitis:
   • Characterised by peripancreatic fat necrosis and parenchymal edema.
2. Necrotising Pancreatitis:
   • Involves widespread pancreatic necrosis with hemorrhage and gland dysfunction.
   • Complications include pseudocyst formation (encapsulation by granulation tissue) or abscess development (bacterial infection of necrotic tissue).
     
     

Genetic Contributions

• Mutations in genes such as PRSS1, CFTR, and SPINK1 predispose individuals to recurrent acute pancreatitis and progression to chronic pancreatitis.
• These genetic factors disrupt the balance between zymogen activation and inhibition.
  
  

Global Incidence

• The incidence of acute pancreatitis worldwide ranges from 4.5 to 80 per 100,000 individuals annually, influenced by variations in diagnostic criteria, geographic factors, and changing trends over time.
• In the UK, the incidence is approximately 56 per 100,000 people annually, with gallstones accounting for 50% of cases, alcohol 25%, and other factors 25%.
  
  

United States

• Incidence rates: 40–50 cases per 100,000 adults annually.
• Hospitalisations:
  • 1998: 183,000 admissions.
  • 2007: 220,000 admissions to non-federal hospitals.
  • 2009: 275,000 total hospitalisations for acute pancreatitis.
• A rising trend in incidence has been observed over the past decades, attributed partly to increased metabolic syndrome and hypertriglyceridemia.
  
  

International Trends

• The highest incidences are reported in the United States and Finland (up to 73.4 per 100,000 population).
• In Europe and Hong Kong, gallstone pancreatitis is more common, while alcoholic pancreatitis predominates in the United States.
  
  

Age-Related Demographics

• Median age varies by etiology:
  • Alcohol-related: 39 years.
  • Biliary tract-related: 69 years.
  • Trauma-related: 66 years.
  • Drug-induced: 42 years.
  • ERCP-related: 58 years.
  • AIDS-related: 31 years.
• Hospitalisation rates increase with age, especially among those aged 35–75 years.
  
  

Sex-Related Demographics

• Overall male predominance:
  • Males: Alcohol is the leading cause.
  • Females: Biliary tract disease predominates.
• Idiopathic pancreatitis shows no sex predilection.
  
  

Race-Related Demographics

• Hospitalisation rates for acute pancreatitis are three times higher in Black individuals compared to White populations.
• Black males aged 35–64 years have a tenfold higher risk than other groups.
  
  

Mortality

• The overall mortality rate is approximately 5%, rising to 25% in severe cases.
• Advances in early diagnosis and management have contributed to declining mortality rates despite the rising incidence.
  
  

Cardinal Symptoms

• Abdominal Pain:
  • The most common symptom, described as dull, boring, and steady.
  • Typically sudden in onset and intensifies until becoming a constant ache.
  • Often localised in the epigastric region but may radiate to the back or, less commonly, the left or right side.
  • Pain is exacerbated by movement and partially relieved by sitting up or bending forward.
  • Intensity and location of pain are not necessarily indicative of disease severity.
  • A small subset of patients, including postoperative individuals and those with metabolic causes, may present without abdominal pain but exhibit unexplained hypotension or organ dysfunction.
• Nausea and Vomiting:
  • Occurs in 70–80% of cases.
  • May persist for hours and lead to dehydration and electrolyte imbalances.
• Anorexia:
  • Commonly secondary to nausea, pain, and general malaise.
    
    

Additional Features

• Diarrhea may accompany the primary symptoms.
• In severe cases, dyspnea may result from diaphragmatic splinting, pleural effusions, or acute respiratory distress syndrome (ARDS).
  
  

Patterns Based on Aetiology

1. Gallstone-Associated Pancreatitis:
   • Pain has a rapid onset, is more acute, and is well localised.
2. Alcohol-Induced Pancreatitis:
   • Pain develops more gradually, is dull, and often generalised in the epigastrium.
     
     

Associated Historical Features

• Operative/Invasive Procedures:
  • Recent ERCP or abdominal surgery is a recognised cause.
• Alcohol Use:
  • Heavy alcohol use (≥5 years) or binge drinking significantly increases risk.
• Smoking:
  • Identified as a modifiable risk factor.
• Family History:
  • Rare genetic predispositions like hereditary pancreatitis should be considered when common causes are excluded.
    
    

Common Physical Findings

1. Vital Signs:
   • Fever (up to 76%) and tachycardia (65%) are frequent.
   • Hypotension may indicate severe fluid depletion or shock.
2. Abdominal Examination:
   • Epigastric tenderness is common, with or without guarding.
   • Distention is often present, accompanied by diminished or absent bowel sounds due to ileus.
   • Pain is localised to the upper abdomen and may radiate to the back.
3. Jaundice:
   • Seen in 28% of patients, often due to biliary obstruction or pancreatic head oedema.

Respiratory Findings

1. Dyspnoea:
   • Present in 10% of cases, caused by diaphragmatic irritation, pleural effusion, or acute respiratory distress syndrome (ARDS).
   • Tachypnea and basilar rales, particularly in the left lung, may be noted.
2. Pleural Effusion:
   • Often localised to the left side; detected by reduced air entry and dullness to percussion.
     
     

Signs of Severe Disease

1. Hemodynamic Instability:
   • Hypotension, pallor, diaphoresis, and listlessness.
   • Requires immediate resuscitation.
2. Rare Findings:
   • Cullen’s Sign: Periumbilical ecchymosis indicating hemoperitoneum.
   • Grey-Turner’s Sign: Flank discoloration due to retroperitoneal bleeding.
   • Purtscher Retinopathy: Retinal ischemic injury, potentially leading to visual loss.
   • Erythematous Skin Nodules: Subcutaneous fat necrosis, typically on extensor surfaces.
   • Polyarthritis: Associated with fat necrosis or autoimmune responses.

Uncommon and Specific Signs

1. Chvostek’s Sign:
   • Facial muscle spasm triggered by tapping the facial nerve, indicating hypocalcemia.
   • Sensitivity and specificity are limited.
2. Panniculitis:
   • Tender red nodules due to subcutaneous fat necrosis, often on distal extremities.
     
     

Correlating Findings with Aetiology

1. Alcoholic Pancreatitis:
   • Hepatomegaly, indicative of chronic alcohol use.
2. Hyperlipidemic Pancreatitis:
   • Xanthomas.
3. Mumps-Associated Pancreatitis:
   • Parotid swelling.
     
     

Laboratory Investigations

1. Serum Lipase and Amylase:
   • Lipase is the preferred marker due to its higher specificity and longer elevation (up to 14 days) compared to amylase (3–5 days).
   • Levels ≥3 times the upper limit of normal confirm pancreatitis in appropriate clinical settings.
   • Sensitivity:
     • Lipase: 82–100%.
     • Amylase: 67–83%.
   • Limitations:
     • False negatives can occur in alcohol-related or hypertriglyceridemia-induced pancreatitis.
     • Elevated levels may also be seen in other conditions (e.g., renal failure, salivary gland disease, perforated ulcer).
2. Liver Function Tests (LFTs):
   • Elevated alanine aminotransferase (ALT) >3 times the upper limit of normal suggests gallstone pancreatitis.
   • Additional markers include elevated bilirubin, alkaline phosphatase, and aspartate aminotransferase (AST), indicating possible biliary involvement.
3. Full Blood Count (FBC):
   • Leukocytosis with a left shift is common.
   • Elevated hematocrit (>44%) suggests hemoconcentration and correlates with severe disease.
4. C-Reactive Protein (CRP):
   • A marker of systemic inflammation.
   • Levels >150 mg/L at 48 hours predict severe pancreatitis.
5. Serum Calcium:
   • Hypocalcemia may result from fat saponification in severe disease.
   • Hypercalcemia can indicate an underlying etiology such as hyperparathyroidism.
6. Serum Triglycerides:
   • Levels >11.3 mmol/L are diagnostic for hypertriglyceridemia-induced pancreatitis.
   • Measurement is essential when alcohol or gallstones are not apparent causes.
7. Blood Urea Nitrogen (BUN) and Creatinine:
   • Elevated levels indicate dehydration and correlate with disease severity.
8. Additional Tests:
   • IgG4 Levels: Assess for autoimmune pancreatitis.
   • Arterial Blood Gas (ABG): Detects hypoxemia or acid-base imbalances.
     
     

Imaging Investigations

1. Ultrasound:
   • First-line imaging for evaluating gallstones or bile duct dilation.
   • Sensitivity for gallstones: 62–95%.
   • Limitations:
     • May be obscured by bowel gas during acute episodes.
     • Poor sensitivity for detecting necrosis or peripancreatic collections.
2. Contrast-Enhanced Computed Tomography (CECT):
   • Indicated for:
     • Diagnostic uncertainty.
     • Suspected complications like necrosis or abscess formation.
     • Lack of clinical improvement after 48–72 hours.
   • Findings:
     • Pancreatic enlargement, necrosis, or fluid collections.
     • Peripancreatic fat stranding and gas suggestive of infection.
3. Magnetic Resonance Cholangiopancreatography (MRCP):
   • Non-invasive imaging for biliary and pancreatic ducts.
   • Preferred for detecting choledocholithiasis in patients with contraindications to contrast or ERCP.
   • Superior to CECT for identifying small stones (<3 mm) and ductal strictures.
4. Endoscopic Ultrasound (EUS):
   • Highly sensitive for detecting microlithiasis and subtle pancreatic lesions.
   • Indicated in idiopathic pancreatitis after negative initial workup.
5. Chest X-ray (CXR):
   • Evaluates pleural effusion, atelectasis, or elevated hemidiaphragm in severe cases.
6. Abdominal Radiography:
   • Limited role but may show:
     • Sentinel loop or colon cutoff sign.
     • Calcifications indicative of chronic pancreatitis.
       
       

Advanced Diagnostic Tools

1. Endoscopic Retrograde Cholangiopancreatography (ERCP):
   • Reserved for therapeutic interventions such as stone extraction or sphincterotomy.
   • Indicated in:
     • Persistent biliary obstruction.
     • Worsening jaundice or cholangitis despite supportive care.
2. Emerging Biomarkers:
   • Urinary Trypsinogen-2: Rapid diagnostic tool with sensitivity and specificity comparable to lipase.
   • Interleukin-6 and Interleukin-8: Potential markers for severe disease.
3. Genetic Testing:
   • Useful in recurrent or idiopathic pancreatitis.
   • Common mutations: PRSS1, SPINK1, CFTR.
     
     

Practical Considerations

• Imaging timing:
  • Avoid early CT scans unless diagnosis is uncertain.
  • Delayed imaging (72–96 hours) is more effective for assessing severity and necrosis.
• Combine MRCP and EUS for detailed evaluation in idiopathic cases.
• Reassess clinical status frequently to determine the need for additional diagnostic interventions.
  
  

Gastrointestinal Causes

1. Peptic Ulcer Disease:
   • Symptoms: Longstanding epigastric pain, often relieved by antacids or proton pump inhibitors, does not radiate to the back.
   • Investigations: Endoscopy reveals ulcers or erythema; normal or slightly elevated amylase and lipase.
2. Perforated Viscus:
   • Symptoms: Sudden severe abdominal pain, generalised tenderness, and signs of peritonitis.
   • Investigations: Free air on upright abdominal X-ray; normal or mildly elevated pancreatic enzymes.
3. Cholecystitis:
   • Symptoms: Right upper quadrant pain post-fatty meal, nausea, vomiting, fever, positive Murphy’s sign.
   • Investigations: Ultrasound shows gallbladder wall thickening, stones, and pericholecystic fluid; normal or mildly elevated lipase.
4. Choledocholithiasis and Cholangitis:
   • Symptoms: Right upper quadrant pain, jaundice, fever (Charcot’s triad in cholangitis).
   • Investigations: Elevated liver enzymes, bilirubin; ultrasound or MRCP confirms ductal stones.
5. Mesenteric Ischemia:
   • Symptoms: Severe abdominal pain disproportionate to physical findings; history of vascular disease.
   • Investigations: Elevated lactate; CT angiography confirms diagnosis.
6. Viral Gastroenteritis:
   • Symptoms: Diffuse abdominal discomfort, nausea, vomiting, diarrhea.
   • Investigations: Stool studies; normal pancreatic enzyme levels.
     
     

Systemic Causes

1. Myocardial Infarction:
   • Symptoms: Retrosternal pain radiating to the jaw or arm, diaphoresis, dyspnea.
   • Investigations: Elevated cardiac enzymes (troponins), ECG changes; normal lipase.
2. Aortic Dissection:
   • Symptoms: Tearing abdominal pain radiating to the back, hypotension, unequal pulses.
   • Investigations: CT angiography or transesophageal echocardiography.
3. Acute Hepatitis:
   • Symptoms: Right upper quadrant pain, jaundice, anorexia.
   • Investigations: Elevated ALT/AST >1000 IU/L; normal amylase and lipase.
4. Diabetic Ketoacidosis:
   • Symptoms: Abdominal pain, nausea, dehydration, fruity breath odor.
   • Investigations: Hyperglycemia, elevated ketones, metabolic acidosis.
     
     

Rare Differentials

1. Intestinal Obstruction:
   • Symptoms: Distension, vomiting, constipation.
   • Investigations: X-ray or CT shows dilated bowel loops, air-fluid levels.
2. Basilar Pneumonia:
   • Symptoms: Pleuritic chest pain, fever, productive cough.
   • Investigations: Chest X-ray confirms infiltrates.
3. Oesophageal Spasm:
   • Symptoms: Dysphagia, retrosternal pain.
   • Investigations: Barium swallow or manometry.
     
     

Initial Supportive Treatment

1. Fluid Resuscitation:
   • Administer early, goal-directed intravenous crystalloid fluids to reduce the risk of organ failure and mortality.
   • Preferred fluids include Ringer’s lactate, which may have anti-inflammatory properties. Normal saline can also be used depending on clinical judgment.
   • Monitor resuscitation effectiveness via:
     • Heart rate <120 bpm.
     • Mean arterial pressure 65–85 mmHg.
     • Urinary output >0.5–1 mL/kg/hour.
     • Haematocrit maintained at 35%–44%.
   • Avoid excessive hydration to minimise risks such as fluid overload and abdominal compartment syndrome.
2. Pain Management:
   • Use NSAIDs or opioids (e.g., morphine or fentanyl) for effective pain control.
   • Regularly reassess pain levels and adjust treatment accordingly.
3. Oxygen Therapy:
   • Administer supplemental oxygen for hypoxemia.
   • Severe cases with PaO2 <60 mmHg may require intensive care and ventilatory support.
4. Electrolyte Monitoring:
   • Monitor calcium, magnesium, sodium, and potassium levels closely.
   • Correct hypocalcemia and magnesium deficiency, particularly in severe cases.
     
     

Nutrition

1. Early Oral Feeding:
   • Resume oral intake within 24 hours as tolerated.
   • Use a low-fat, soft or solid diet instead of prolonged "nil by mouth" practices.
2. Enteral Feeding:
   • Begin nasojejunal or nasogastric tube feeding within 72 hours if oral intake is not feasible.
   • Enteral nutrition is associated with reduced risks of infections and pancreatic necrosis.
3. Parenteral Nutrition:
   • Reserved for patients unable to tolerate enteral feeding.
   • Use cautiously, as it is associated with higher risks of complications.
     
     

Antibiotic Prophylaxis

• Avoid routine prophylactic antibiotics in all cases, including severe disease or sterile necrosis, as there is no supporting evidence.
• Administer antibiotics only if infection (pancreatic or extra-pancreatic) is proven or strongly suspected.
• Treat suspected infections (e.g., pneumonia, cholangitis, sepsis) empirically with intravenous antibiotics. Discontinue if cultures are negative and no infection source is identified.
• Extra-pancreatic infections are common in the early phase and contribute significantly to mortality.
  
  

Treatment of Underlying Causes

1. Gallstone Pancreatitis:
   • Perform ERCP within 24 hours for patients with concurrent cholangitis.
   • Schedule cholecystectomy during the same admission for mild cases or delay surgery by 6 weeks for severe disease.
2. Alcohol-related Pancreatitis:
   • Initiate support for alcohol cessation during hospitalisation.
     
     

Management of Local Complications

1. Sterile Pancreatic Necrosis:
   • Managed conservatively without prophylactic antibiotics.
2. Infected Necrosis:
   • Suspect based on fever, elevated inflammatory markers, or imaging findings.
   • Initiate antibiotics with good pancreatic penetration, such as imipenem or ciprofloxacin.
   • Utilise a step-up approach, starting with percutaneous or endoscopic drainage. Proceed to necrosectomy only if drainage fails.
3. Pseudocysts:
   • Symptomatic pseudocysts may require drainage; asymptomatic cases are managed conservatively.
     
     

Treatment Setting and ICU Transfer

• Immediate ICU transfer is required for patients with organ failure or any of the following criteria:
  • Heart rate <40 bpm or >150 bpm.
  • Systolic blood pressure <80 mmHg or mean arterial pressure <60 mmHg.
  • Respiratory rate >35 breaths/min.
  • Severe electrolyte imbalances (e.g., sodium <110 or >170 mmol/L, potassium <2 or >7 mmol/L).
  • pH <7.1 or >7.7.
  • Serum glucose >44.4 mmol/L.
  • Serum calcium >3.75 mmol/L.
  • Anuria or coma.
    
    

Overview of Prognosis

• The majority of acute pancreatitis cases (~80%) present as mild, with patients recovering within 3–7 days under conservative management. 
• Mortality in mild cases is less than 2%, whereas it rises dramatically in severe acute pancreatitis to 25–30%. Most deaths in the early phase (<2 weeks) result from systemic inflammatory response syndrome (SIRS) and multi-organ failure. 
• In the late phase (>2 weeks), mortality is predominantly associated with local complications such as infected necrosis or pancreatic abscesses.

Mortality and Severity

• Mild Cases: No organ failure or systemic complications; typically resolves within a week.
• Severe Cases: Persistent organ failure (>48 hours) has a mortality rate of up to 30%.
• Mortality patterns:
  • Early (<2 weeks): Predominantly due to multi-organ failure caused by SIRS.
  • Late (>2 weeks): Primarily linked to local complications such as infected pancreatic necrosis or pseudocysts.
    
    

Risk Factors Influencing Prognosis

1. Aetiology:
   • Alcoholic pancreatitis is associated with recurrent episodes and a higher chance of progression to chronic pancreatitis.
   • Gallstone-related pancreatitis may require cholecystectomy to prevent recurrence.
2. Patient Factors:
   • Advanced age, obesity (BMI >30), and comorbidities such as type 2 diabetes mellitus increase severity and mortality risks.
   • Nonalcoholic fatty liver disease and persistent hypertriglyceridemia worsen outcomes.
     
     

Scoring Systems for Prognosis

1. Bedside Index for Severity in Acute Pancreatitis (BISAP):
   • Includes parameters like blood urea nitrogen (BUN), impaired mental status, SIRS, age >60, and pleural effusion.
   • Higher scores correlate with increased mortality risk (e.g., BISAP 3–5 has >15% mortality).
2. Modified CT Severity Index (CTSI):
   • Combines imaging findings (extent of necrosis and inflammation) to predict severity and guide treatment.
3. APACHE II and Glasgow-Imrie Scores:
   • Historically used but less practical due to complexity and the need for 48-hour data.
     
     

Long-Term Outcomes

• Resolution: Most patients with mild cases recover without residual effects on pancreatic function.
• Chronic Disease Progression: Chronic pancreatitis develops in approximately 10–15% of cases, especially in patients with recurrent episodes.
• Diabetes Mellitus: Acute pancreatitis increases the risk of developing type 2 diabetes, particularly in cases involving pancreatic necrosis.
  
  

Complications Impacting Prognosis

1. Local Complications:
   • Pancreatic necrosis: Associated with a significant increase in morbidity and mortality, particularly if infected.
   • Pseudocysts and abscesses: May necessitate drainage or surgical intervention.
2. Systemic Complications:
   • Acute respiratory distress syndrome (ARDS) and renal failure are common causes of early mortality.
     
     

Lifestyle and Preventive Measures

• Lifestyle Modifications:
  • Alcohol cessation and smoking avoidance reduce recurrence and long-term complications.
  • Management of hypertriglyceridemia and obesity are critical.
• Preventive Interventions:
  • Timely cholecystectomy for gallstone-related cases.
  • Appropriate management of diabetes and comorbid conditions.
    
    

Short-term Complications

1. Acute Renal Failure
   • Occurs in severe cases, often linked to hypovolemia, circulating toxins, or inflammatory mediators.
   • Associated with a poor prognosis, particularly in patients with multi-organ failure.
2. Pancreatic Abscess
   • Results from secondary bacterial contamination of necrotic tissue.
   • Patients typically present 2-4 weeks after onset with fever and clinical deterioration.
   • Diagnostic imaging shows gas-containing ring-enhanced fluid collections.
   • Requires drainage (surgical or percutaneous) and broad-spectrum antibiotics targeting common pathogens.
3. Abdominal Compartment Syndrome (ACS)
   • Defined by intra-abdominal pressure >20 mmHg with new organ failure.
   • Commonly linked to over-aggressive fluid resuscitation.
   • Treatment includes decompressive laparotomy or fluid drainage.
4. Acute Respiratory Distress Syndrome (ARDS)
   • Mediated by inflammatory cytokines damaging the alveolocapillary barrier.
   • Presents with hypoxemia, bilateral infiltrates, and low PaO₂:FiO₂ ratios.
   • May require mechanical ventilation in severe cases.
     
     

Long-term and Chronic Complications

1. Chronic Pancreatitis
   • Develops in 8%-16% of patients with recurrent acute episodes.
   • Characterised by glucose intolerance, pancreatic insufficiency, and calcifications.
2. Enteric Fistulas
   • Rarely occurs due to inflammation involving the duodenum or colon.
3. Pancreatic Ascites and Pleural Effusion
   • High amylase concentrations in fluid suggest pancreatic duct disruption or pseudocyst leakage.
   • Management is variable and may include medical or surgical interventions.
4. Pseudocyst Formation
   • Encapsulated fluid collections forming after 4 weeks.
   • Asymptomatic pseudocysts are often monitored, while symptomatic cases may require drainage.
     
     

Infections

1. Sepsis
   • Caused by translocation of gut bacteria into systemic circulation.
   • Common pathogens include Gram-negative bacteria, requiring empirical antibiotic therapy upon suspicion.
2. Infected Pancreatic Necrosis

• Affects up to one-third of patients with necrotising pancreatitis.
• Indicators include gas on imaging, fever, and systemic signs of infection.
• Delayed intervention (e.g., necrosectomy) is preferred unless clinical deterioration mandates earlier action.
  
  

Hemorrhagic Complications

1. Hemorrhagic Pancreatitis

• Results from vascular erosion or ruptured pseudoaneurysms.
• Requires rapid identification and surgical or radiological intervention.

• Triggered by systemic inflammation and pancreatic enzymes entering circulation.
  
  

Vascular Complications

1. Splenic or Mesenteric Venous Thrombosis

• Associated with peripancreatic inflammation.
• Anticoagulation is considered if thrombosis threatens vital organ perfusion.
  
  

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