Acute Pancreatitis

Pancreatitis Overview

• 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

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

Classification Systems for Acute Pancreatitis

Revised Atlanta Classification

•  The Revised Atlanta Classification provides a structured framework for assessing the severity of acute pancreatitis by distinguishing between early and late phases of the disease. The severity is classified as follows:
• Mild Acute Pancreatitis:
  • No organ failure.
  • Absence of local or systemic complications.
  • Typically resolves within the first week.
• Moderately Severe Acute Pancreatitis:
  • Presence of transient organ failure (resolves within 48 hours).
  • Local complications or exacerbation of pre-existing comorbidities.
• 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

• This classification evaluates the extent of pancreatic inflammation and the presence of fluid collections or necrosis, using contrast-enhanced computed tomography (CT):
• 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

Gallstones

• Account for 40–50% of cases in developed countries.
• Obstruction of the bile duct increases pancreatic ductal pressure, causing enzyme activation and acinar injury.
• Microlithiasis is implicated in many "idiopathic" cases.

Alcohol use

• Contributes to 25–35% of cases globally.
• 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.

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

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.

Postoperative ischaemia

• Abdominal or cardiopulmonary bypass surgeries can result in gland ischaemia, leading to pancreatitis.

Drug-Induced Pancreatitis

• Rare, accounting for ~2% of cases.
• Drugs definitively linked include azathioprine, sulfonamides, valproic acid, and oestrogens.
• Mechanism likely idiosyncratic or dose-related toxicity.

Infections

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

Genetic and Structural Causes

• Hereditary pancreatitis: related to PRSS1 and SPINK1 mutations, often manifests in childhood or adolescence.
• Pancreas divisum: a common anatomical variant, controversial as a direct cause.
• Congenital malformations: such as annular pancreas, leading to ductal obstruction.

Other Causes

• Autoimmune pancreatitis: associated with IgG4-related systemic disease; presents with diffuse pancreatic enlargement and strictures.
• Hypercalcaemia: due to hyperparathyroidism or excessive vitamin D intake.
• Trauma: including penetrating or blunt abdominal trauma.

Rare and Controversial Causes

• Toxins: such as scorpion stings (e.g., Tityus trinitatis) and organophosphate poisoning.
• Tumours: pancreatic or ampullary malignancies causing ductal obstruction.
• Vasculitis: including 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., tumour 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 oedema, necrosis, and haemorrhage.

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

Oedematous pancreatitis

• Characterised by peripancreatic fat necrosis and parenchymal oedema.

Necrotising pancreatitis

• Involves widespread pancreatic necrosis with haemorrhage 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.
• Gallstones account for 50% of cases, alcohol 25%, and other factors 25%.

United States

• Incidence rates are 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, partly due to increased metabolic syndrome and hypertriglyceridaemia.

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.
• Alcoholic pancreatitis predominates in the United States.

Age-Related Demographics

• Median age varies by aetiology:
  • 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:
  • In males, alcohol is the leading cause.
  • In 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%.
• Mortality rises 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

Diarrhoea

• May accompany the primary symptoms.

Dyspnoea

• In severe cases, dyspnoea may result from diaphragmatic splinting, pleural effusions, or acute respiratory distress syndrome (ARDS).

Patterns Based on Aetiology

Gallstone-associated pancreatitis

• Pain has a rapid onset, is more acute, and is well localised.

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

Vital signs

• Fever (up to 76%) and tachycardia (65%) are frequent.
• Hypotension may indicate severe fluid depletion or shock.

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.

Jaundice

• Seen in 28% of patients, often due to biliary obstruction or pancreatic head oedema.

Respiratory Findings

Dyspnoea

• Present in 10% of cases, caused by diaphragmatic irritation, pleural effusion, or acute respiratory distress syndrome (ARDS).
• Tachypnoea and basilar rales, particularly in the left lung, may be noted.

Pleural effusion

• Often localised to the left side; detected by reduced air entry and dullness to percussion.

Signs of Severe Disease

Hemodynamic instability

• Hypotension, pallor, diaphoresis, and listlessness.
• Requires immediate resuscitation.

Rare findings

• Cullen’s sign: Periumbilical ecchymosis indicating hemoperitoneum.
• Grey-Turner’s sign: Flank discolouration due to retroperitoneal bleeding.
• Purtscher retinopathy: Retinal ischaemic 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

Chvostek’s sign

• Facial muscle spasm triggered by tapping the facial nerve, indicating hypocalcaemia.
• Sensitivity and specificity are limited.

Panniculitis

• Tender red nodules due to subcutaneous fat necrosis, often on distal extremities.

Correlating Findings with Aetiology

Alcoholic pancreatitis

• Hepatomegaly, indicative of chronic alcohol use.

Hyperlipidaemic pancreatitis

• Xanthomas.

Mumps-associated pancreatitis

• Parotid swelling.

Laboratory Investigations

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).

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.

Full Blood Count (FBC)

• Leukocytosis with a left shift is common.
• Elevated hematocrit (>44%) suggests hemoconcentration and correlates with severe disease.

C-Reactive Protein (CRP)

• A marker of systemic inflammation.
• Levels >150 mg/L at 48 hours predict severe pancreatitis.

Serum Calcium

• Hypocalcemia may result from fat saponification in severe disease.
• Hypercalcemia can indicate an underlying etiology such as hyperparathyroidism.

Serum Triglycerides

• Levels >11.3 mmol/L are diagnostic for hypertriglyceridemia-induced pancreatitis.
• Measurement is essential when alcohol or gallstones are not apparent causes.

Blood Urea Nitrogen (BUN) and Creatinine

• Elevated levels indicate dehydration and correlate with disease severity.

Additional Tests

• IgG4 Levels: Assess for autoimmune pancreatitis.
• Arterial Blood Gas (ABG): Detects hypoxemia or acid-base imbalances.

Imaging Investigations

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.

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.

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.

Endoscopic Ultrasound (EUS)

• Highly sensitive for detecting microlithiasis and subtle pancreatic lesions.
• Indicated in idiopathic pancreatitis after negative initial workup.

Chest X-ray (CXR)

• Evaluates pleural effusion, atelectasis, or elevated hemidiaphragm in severe cases.

Abdominal Radiography

• Limited role but may show:
  • Sentinel loop or colon cutoff sign.
  • Calcifications indicative of chronic pancreatitis.

Advanced Diagnostic Tools

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.

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.

Genetic Testing

• Useful in recurrent or idiopathic pancreatitis.
• Common mutations: PRSS1, SPINK1, CFTR.

Practical Considerations

• 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

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.

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.

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.

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.

Mesenteric Ischemia

• Symptoms: Severe abdominal pain disproportionate to physical findings; history of vascular disease.
• Investigations: Elevated lactate; CT angiography confirms diagnosis.

Viral Gastroenteritis

• Symptoms: Diffuse abdominal discomfort, nausea, vomiting, diarrhea.
• Investigations: Stool studies; normal pancreatic enzyme levels.

Systemic Causes

Myocardial Infarction

• Symptoms: Retrosternal pain radiating to the jaw or arm, diaphoresis, dyspnea.
• Investigations: Elevated cardiac enzymes (troponins), ECG changes; normal lipase.

Aortic Dissection

• Symptoms: Tearing abdominal pain radiating to the back, hypotension, unequal pulses.
• Investigations: CT angiography or transesophageal echocardiography.

Acute Hepatitis

• Symptoms: Right upper quadrant pain, jaundice, anorexia.
• Investigations: Elevated ALT/AST >1000 IU/L; normal amylase and lipase.

Diabetic Ketoacidosis

• Symptoms: Abdominal pain, nausea, dehydration, fruity breath odor.
• Investigations: Hyperglycemia, elevated ketones, metabolic acidosis.

Rare Differentials

Intestinal Obstruction

• Symptoms: Distension, vomiting, constipation.
• Investigations: X-ray or CT shows dilated bowel loops, air-fluid levels.

Basilar Pneumonia

• Symptoms: Pleuritic chest pain, fever, productive cough.
• Investigations: Chest X-ray confirms infiltrates.

Oesophageal Spasm

• Symptoms: Dysphagia, retrosternal pain.
• Investigations: Barium swallow or manometry.

Initial Supportive Treatment

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.

Pain Management

• Use NSAIDs or opioids (e.g., morphine or fentanyl) for effective pain control.
• Regularly reassess pain levels and adjust treatment accordingly.

Oxygen Therapy

• Administer supplemental oxygen for hypoxemia.
• Severe cases with PaO₂ <60 mmHg may require intensive care and ventilatory support.

Electrolyte Monitoring

• Monitor calcium, magnesium, sodium, and potassium levels closely.
• Correct hypocalcemia and magnesium deficiency, particularly in severe cases.

Nutrition

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.

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.

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

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.

Alcohol-related Pancreatitis

• Initiate support for alcohol cessation during hospitalisation.

Management of Local Complications

Sterile Pancreatic Necrosis

• Managed conservatively without prophylactic antibiotics.

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.

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

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.

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

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).

Modified CT Severity Index (CTSI)

• Combines imaging findings (extent of necrosis and inflammation) to predict severity and guide treatment.

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

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.

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

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.

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.

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.

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

Chronic Pancreatitis

• Develops in 8%–16% of patients with recurrent acute episodes.
• Characterised by glucose intolerance, pancreatic insufficiency, and calcifications.

Enteric Fistulas

• Rarely occurs due to inflammation involving the duodenum or colon.

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.

Pseudocyst Formation

• Encapsulated fluid collections forming after 4 weeks.
• Asymptomatic pseudocysts are often monitored, while symptomatic cases may require drainage.

Infections

Sepsis

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

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

Hemorrhagic Pancreatitis

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

Disseminated Intravascular Coagulation (DIC)

• Triggered by systemic inflammation and pancreatic enzymes entering circulation.

Vascular Complications

Splenic or Mesenteric Venous Thrombosis

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

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