Acute Pancreatitis

Definition

Acute pancreatitis is an acute inflammatory condition of the pancreas that can involve surrounding peripancreatic tissues and, in severe cases, lead to a systemic inflammatory response and multi-organ failure (1, 2). The diagnosis requires at least two of the following three criteria: (i) characteristic acute onset of persistent, severe, epigastric abdominal pain often radiating to the back; (ii) serum lipase or amylase activity at least three times greater than the upper limit of normal; and (iii) characteristic findings on contrast-enhanced computed tomography (CT), magnetic resonance imaging (MRI), or transabdominal ultrasonography (3).

Epidemiology

Limited recent data exists on the precise incidence and prevalence of acute pancreatitis in Malaysia. A 2002 study from a single centre in Ipoh noted a significant over-representation of patients of Indian ethnicity (56.4%) compared to their population distribution, followed by Malays (28.6%) and Chinese (14.3%). In this cohort, alcohol was the predominant etiology, particularly among Indian males, while gallstones were more common in females (4). Another earlier study from 1995 in Kelantan reported a different pattern, with a female predominance and idiopathic pancreatitis being most common, suggesting significant regional variation (5). [Specific, up-to-date national prevalence data for Malaysia was not found in the latest National Health and Morbidity Survey reports; the available data is over two decades old and may not reflect current trends, thus it should be interpreted with caution].

Globally, the incidence of acute pancreatitis is estimated to be between 34 and 45 per 100,000 people per year, with gallstones and alcohol consumption being the leading causes, accounting for 70-80% of cases (1, 6).

Pathophysiology

The core mechanism of acute pancreatitis involves the inappropriate, premature activation of digestive proenzymes within pancreatic acinar cells, leading to autodigestion of the gland. The process typically begins with an inciting event, such as an obstructing gallstone in the ampulla of Vater or the toxic effects of alcohol, which disrupts cellular processes and triggers the conversion of trypsinogen to its active form, trypsin (7).

This initial activation of trypsin sets off a cascade, activating other enzymes like elastase and phospholipase A2. This enzymatic activity leads to local tissue injury, causing interstitial edema, fat necrosis, and hemorrhage (7, 8). The resulting inflammation stimulates the release of a surge of pro-inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6) into the systemic circulation. This can lead to a Systemic Inflammatory Response Syndrome (SIRS), increased vascular permeability, third-space fluid loss, and potentially, the development of acute respiratory distress syndrome (ARDS), acute kidney injury, and multi-organ dysfunction syndrome (MODS) in severe cases (8).

Clinical Presentation

Patients typically present with a classic history of acute, severe, and persistent epigastric pain that may radiate to the back. The onset is often sudden, and the pain is commonly described as "boring" or "stabbing."

• Diagnostic Clues: The diagnosis is strongly suggested by the combination of characteristic epigastric pain and a serum lipase or amylase level >3 times the upper limit of normal (3).

• Common Symptoms (>50%):

  • Severe epigastric pain (~95%) (2)

  • Nausea and vomiting (2)

  • Abdominal tenderness (2)

• Less Common Symptoms (10-50%):

  • Fever and tachycardia (2)

  • Jaundice (may suggest a biliary cause) (2)

  • Dyspnoea (can be due to pain, pleural effusion, or ARDS) (8)

• ⚠️ Red Flag Signs & Symptoms:

  • Hypotension and shock

  • Altered mental status or confusion (impaired Glasgow Coma Scale)

  • Oliguria or anuria

  • Respiratory distress (SpO2 <94% on room air)

  • Peritonism (guarding, rebound tenderness)

  • Cullen's sign (periumbilical bruising) and Grey Turner's sign (flank bruising) are rare signs of retroperitoneal hemorrhage in severe necrotizing pancreatitis.

Complications

Complications can be categorized as local or systemic and are more common in severe disease.

• Local Complications:

  • Acute Peripancreatic Fluid Collection (APFC) (8)

  • Pancreatic Pseudocyst (an encapsulated collection of fluid, usually occurring >4 weeks after onset) (8)

  • Acute Necrotic Collection (ANC) (8)

  • Walled-Off Necrosis (WON) (an encapsulated collection of necrotic debris) (8)

  • Infected Pancreatic Necrosis (a life-threatening development) (8)

  • Gastric outlet obstruction, splenic or portal vein thrombosis (2).

• Systemic Complications:

  • Cardiovascular: Hypovolemic shock (8).

  • Pulmonary: Pleural effusions, atelectasis, Acute Respiratory Distress Syndrome (ARDS) (8).

  • Renal: Acute Kidney Injury (AKI) (8).

  • Metabolic: Hypocalcemia, hyperglycemia (2).

  • Hematological: Disseminated Intravascular Coagulation (DIC) (2).

Prognosis

The majority of patients (~80%) have mild, self-limiting acute pancreatitis with a mortality rate of <1%. However, about 20% of patients develop moderately severe or severe pancreatitis, which is associated with organ failure and/or local complications (1, 6). Severe acute pancreatitis carries a substantial mortality rate, which can be as high as 15-30%, especially in cases of infected necrosis or persistent multi-organ failure (6, 8). Prognostic scoring systems like the Bedside Index of Severity in Acute Pancreatitis (BISAP) or the APACHE II score can help risk-stratify patients on admission (3).

Differential Diagnosis

• Perforated Peptic Ulcer: This is a key differential due to the sudden onset of severe epigastric pain. However, it is often distinguished by the presence of peritonism and free air under the diaphragm on an erect chest X-ray, whereas serum lipase/amylase levels are typically normal or only mildly elevated (2).

• Acute Cholecystitis: Consider this diagnosis due to the shared features of upper abdominal pain and nausea. However, the pain in cholecystitis is typically localized to the right upper quadrant, may radiate to the right shoulder, and is associated with a positive Murphy's sign. While liver enzymes might be elevated, pancreatic enzymes are usually not significantly raised unless there is concurrent pancreatitis (9).

• Myocardial Infarction (Inferior Wall): This must be considered as it can present with epigastric pain and nausea. An urgent ECG is crucial for differentiation, as it will show characteristic ST-segment changes. Cardiac troponin levels will also be elevated, which is critical for ruling out a cardiac cause for the symptoms (2).

• Acute Mesenteric Ischemia: This is a critical differential, especially in older patients with vascular risk factors, due to the characteristically severe pain that is often out of proportion to clinical findings on examination. It is distinguished by a rapidly worsening clinical picture, metabolic acidosis with high lactate, and requires urgent CT angiography for diagnosis (2).

Investigations

Immediate & Bedside Tests

These are STAT orders to assess severity and rule out life-threatening differentials.

• Bedside ECG: This is mandatory to immediately rule out an inferior myocardial infarction presenting as epigastric pain (the action), which is a critical differential requiring a completely different management pathway (the rationale).

• Fingerstick Blood Sugar: Essential for rapidly detecting hyperglycemia, which can be a systemic complication of pancreatitis, or hypoglycemia in alcoholic patients (the action), allowing for immediate correction to prevent metabolic derangement (the rationale).

Diagnostic Workup

• First-Line Investigations:

  • Serum Lipase and/or Amylase: A level >3 times the upper limit of normal is a core diagnostic criterion (the action). Lipase is preferred due to its higher specificity and longer half-life, making it more reliable, especially in late presentations or alcohol-induced pancreatitis (the rationale) (3).

  • Full Blood Count: Essential to assess for leukocytosis, indicating inflammation or infection, and to establish a baseline hematocrit (the action). A rising hematocrit is a marker of hemoconcentration and predicts severe disease, guiding fluid resuscitation needs (the rationale) (3).

  • Renal Profile & Electrolytes (Urea, Creatinine, Electrolytes): Crucial for assessing for acute kidney injury and electrolyte disturbances like hypocalcemia (the action), which are common systemic complications that require immediate correction (the rationale) (2).

  • Liver Function Tests: Mandatory to evaluate for a potential biliary etiology (the action), as elevated ALT, AST, and bilirubin strongly suggest gallstone pancreatitis and may necessitate earlier intervention like ERCP if cholangitis is present (the rationale) (3).

  • Abdominal Ultrasound (Right Upper Quadrant): This is the primary imaging modality to identify gallstones as the cause (the action), which is critical as it will guide the decision for cholecystectomy to prevent recurrence (the rationale) (3).

• Gold Standard: The diagnosis is typically clinical and biochemical. Imaging confirms the diagnosis and assesses for complications. A Contrast-Enhanced Computed Tomography (CECT) of the abdomen is considered the gold standard for staging severity but is not usually required for initial diagnosis. It is best performed 72-96 hours after symptom onset, as it provides the most comprehensive assessment of pancreatic necrosis and peripancreatic collections (the rationale), which is vital for prognosis and planning interventions in patients who fail to improve or deteriorate (the action) (10).

Monitoring & Staging

• C-Reactive Protein (CRP): Serial CRP measurement after 48 hours is a widely available and cost-effective tool to monitor disease severity (the action), as levels >150 mg/L are associated with severe pancreatitis and help in prognostic assessment (the rationale) (3).

• Arterial Blood Gas (ABG): Performed in patients with respiratory distress or signs of shock to assess for hypoxemia and metabolic acidosis (the action), which are hallmarks of severe disease and impending organ failure requiring ICU care (the rationale) (8).

Management

Management Principles

The management of acute pancreatitis focuses on early aggressive fluid resuscitation, adequate pain control, early identification and management of complications, and providing appropriate nutritional support (3).

Acute Stabilisation (The First Hour)

• Airway/Breathing: Administer high-flow oxygen via a non-rebreather mask to maintain SpO2 >94% (the action), which is crucial to prevent tissue hypoxia driven by the systemic inflammatory response and increased metabolic demand (the rationale).

• Circulation: Secure two large-bore IV cannulas (e.g., 16G or 18G) and commence aggressive intravenous fluid resuscitation (the action) to correct hypovolemia from third-spacing and restore end-organ perfusion, which is key to preventing pancreatic necrosis and organ failure (the rationale) (3, 11).

  • Fluid Choice: Lactated Ringer's solution is generally preferred over Normal Saline as it may reduce the incidence of SIRS (11).

  • Initial Rate: An initial bolus followed by a goal-directed approach is recommended. While specific rates vary, a common starting point is 5-10 mL/kg/hour, adjusted based on clinical response (e.g., heart rate, blood pressure, urine output) (3, 11).

• Disability/Exposure: Assess Glasgow Coma Scale (GCS) and check blood glucose. Treat severe pain promptly.

Definitive Therapy

There is no specific curative therapy for the pancreatic inflammation itself. Management is supportive and aimed at preventing progression and treating the underlying cause.

• First-Line Treatment (Gallstone Pancreatitis): For patients with biliary pancreatitis, an early cholecystectomy during the same hospital admission is recommended to prevent recurrence (3). If there is concurrent acute cholangitis, an urgent ERCP (within 24 hours) is indicated for biliary drainage (3).

• First-Line Treatment (Alcohol-Induced Pancreatitis): The cornerstone of management is complete alcohol cessation and counseling (3).

• Hypertriglyceridemia-Induced Pancreatitis: Management may involve insulin infusion and/or plasmapheresis to rapidly lower triglyceride levels (2).

• Antibiotics: Prophylactic antibiotics are not recommended for sterile pancreatitis, regardless of severity (mild or severe necrotizing) (3). Antibiotics should only be used for treating a confirmed or highly suspected infection, such as infected necrosis, cholangitis, or bacteremia (3).

Supportive & Symptomatic Care

• Pain Control: Adequate analgesia is critical. Opioids are safe and effective.

  • Fentanyl: IV boluses of 25-50 mcg every 1-2 hours as needed or via Patient-Controlled Analgesia (PCA) are effective (12, 13). Dosage should be individualized.

  • Morphine: Can be used as an alternative, typically IV 2-4 mg every 2-4 hours as needed (14).

• Nutritional Support:

  • Mild Pancreatitis: Patients can resume an oral diet (low-fat, solid) as soon as pain is improving and nausea/vomiting has resolved. There is no need to wait for lipase to normalize (3).

  • Moderately Severe/Severe Pancreatitis: If unable to tolerate oral intake within 48-72 hours, enteral nutrition is strongly preferred over parenteral nutrition. A nasogastric tube is usually sufficient; a nasojejunal tube is not typically required (3). This is crucial to maintain gut integrity, prevent bacterial translocation, and reduce infectious complications (the rationale).

• Antiemetics: Administer as needed (e.g., IV Metoclopramide 10mg TDS) to manage nausea and vomiting.

Key Nursing & Monitoring Instructions

• Strict hourly input/output charting to guide fluid resuscitation.

• Monitor vital signs (HR, BP, RR, SpO2, Temp) at least 4-hourly, or hourly if unstable.

• Inform medical staff immediately if urine output is <0.5mL/kg/hr.

• Inform medical staff if systolic BP drops below 90 mmHg or heart rate exceeds 120 bpm.

• Monitor for any signs of respiratory distress or worsening abdominal pain.

Long-Term Plan & Patient Education

• Arrange for cholecystectomy for all patients with gallstone pancreatitis, ideally before discharge.

• Provide counseling on complete alcohol abstinence for those with alcohol-induced pancreatitis.

• Educate the patient and family on the warning signs of recurrence (severe abdominal pain) and the importance of seeking immediate medical attention.

• Address other etiologies such as hypertriglyceridemia with appropriate lipid-lowering therapy and dietary advice.

When to Escalate

Call Your Senior (MO/Specialist) if:

• The patient meets criteria for severe pancreatitis (e.g., BISAP score ≥3, persistent organ failure).

• Hemodynamic instability (hypotension, tachycardia) not responding to initial fluid resuscitation.

• Signs of organ dysfunction develop (rising creatinine, worsening hypoxemia, altered GCS).

• Urine output remains <0.5mL/kg/hr despite adequate fluids.

• There is any diagnostic uncertainty.

Referral Criteria:

• Refer to the Intensive Care Unit (ICU)/High Dependency Unit (HDU) for any patient with persistent (>48 hours) organ failure or signs of shock or severe respiratory distress.

• Refer to the Gastroenterology/Surgical team for consideration of ERCP in suspected choledocholithiasis or for management of local complications like infected necrosis.

• Refer to Interventional Radiology for percutaneous drainage of symptomatic pseudocysts or infected collections.

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References

(1) Lankisch, P. G., Apte, M., & Banks, P. A. (2015). Acute pancreatitis. The Lancet, 386(9988), 85–96. https://doi.org/10.1016/S0140-6736(14)60649-8

(2) Greenberg, J. A., Hsu, J., Bawazeer, M., et al. (2016). Clinical practice guideline: management of acute pancreatitis. Canadian Journal of Surgery, 59(2), 128–140. https://doi.org/10.1503/cjs.015015

(3) Crockett, S. D., Wani, S., Gardner, T. B., Falck-Ytter, Y., & Barkun, A. N. (2018). American Gastroenterological Association Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology, 154(4), 1096–1101. https://doi.org/10.1053/j.gastro.2018.01.032

(4) Navaratnam, P., & Parasakthi, N. (2002). Acute pancreatitis in a multi-ethnic population. Singapore Medical Journal, 43(6), 288-291. http://www.smj.org.sg/sites/default/files/4306/4306a2.pdf

(5) Kudva, Y. C., & Rajendran, V. M. (1995). Acute pancreatitis in north-eastern peninsular Malaysia: an unusual demographic and aetiological pattern. Singapore Medical Journal, 36(4), 371–374. https://pubmed.ncbi.nlm.nih.gov/8919148/

(6) IAP/APA evidence-based guidelines for the management of acute pancreatitis. (2013). Pancreatology, 13(4 Suppl 2), e1–e15. https://doi.org/10.1016/j.pan.2013.07.063

(7) Sah, R. P., Dawra, R. K., & Saluja, A. K. (2013). New insights into the pathogenesis of pancreatitis. Current opinion in gastroenterology, 29(5), 523–530. https://doi.org/10.1097/MOG.0b013e328363e399

(8) Baron, T. H., DiMaio, C. J., Wang, A. Y., & Morgan, K. A. (2020). Acute Pancreatitis. In UpToDate. Retrieved July 6, 2025, from https://www.uptodate.com/contents/management-of-acute-pancreatitis

(9) Indar, A. A., & Beckingham, I. J. (2002). Acute cholecystitis. BMJ, 325(7365), 639–643. https://doi.org/10.1136/bmj.325.7365.639

(10) Balthazar, E. J. (2002). Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology, 223(3), 603–620. https://doi.org/10.1148/radiol.2233010680

(11) de-Madaria, E., Buxbaum, J. L., Maisonneuve, P., et al. (2022). Aggressive or Moderate Fluid Resuscitation in Acute Pancreatitis. New England Journal of Medicine, 387(11), 989–1000. https://doi.org/10.1056/NEJMoa2202884

(12) Ministry of Health Malaysia. (n.d.). Fentanyl Citrate 50mcg/ml Injection. Formulari Ubat KKM (FUKKM). Retrieved July 6, 2025, from https://pharmacy.moh.gov.my/en/apps/fukkm

(13) StatPearls. (2024). Fentanyl. StatPearls Publishing. Retrieved July 6, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK459275/

(14) Drugs.com. (2025). Morphine Dosage. Retrieved July 6, 2025, from https://www.drugs.com/dosage/morphine.html