Acute Pancreatitis Clinical Overview
I. The "On-Call" Snapshot
Clinical Significance in Malaysia: This is a common and serious cause of severe abdominal pain presenting to your Emergency Department. It's often linked to gallstones or alcohol. Your initial management in the first 48 hours is critical and directly impacts patient outcomes.
High-Yield Definition: Acute pancreatitis is an acute inflammatory condition of the pancreas that can trigger a systemic inflammatory response, potentially leading to multi-organ failure.
Clinical One-Liner: Simply put, the pancreas starts digesting itself, causing excruciating central abdominal pain that bores through to the back.
II. Etiology & Risk Factors
Etiology: The two main culprits in Malaysia are gallstones (obstructing the common channel) and heavy alcohol consumption. Together, they account for over 70% of cases. A helpful mnemonic for other causes is "I GET SMASHED".
Risk Factors:
Modifiable:
Heavy alcohol consumption
Hypertriglyceridemia (>11.3 mmol/L)
Obesity (associated with worse outcomes)
Smoking
Certain medications (e.g., thiazides, azathioprine)
Non-modifiable:
Cholelithiasis (gallstones)
Post-ERCP procedure
Abdominal trauma
Autoimmune conditions (e.g., IgG4-related disease)
Anatomical variants (e.g., pancreas divisum)
III. Quick Pathophysiology
The core problem is the premature activation of digestive enzymes, particularly trypsin, inside the pancreas instead of in the gut. This leads to autodigestion of pancreatic and surrounding fatty tissue. This process triggers a massive local and then systemic inflammatory response (SIRS). This inflammation makes blood vessels leaky, causing massive fluid shifts from the circulation into the retroperitoneal space ("third-spacing"), leading to hypovolemia and shock.
IV. Clinical Assessment
Red Flags & Immediate Actions:
Hypotension (SBP <90 mmHg) or Tachycardia (HR >130 bpm): Alert your senior immediately. Secure two large-bore IV cannulas and start an aggressive fluid bolus with crystalloids (e.g., Hartmann's solution).
Hypoxia (SpO2 <94% on room air): Sit the patient up, apply high-flow oxygen, and get an arterial blood gas (ABG) to check for ARDS.
Oliguria (<0.5 mL/kg/hr) or Altered Mental Status: These are signs of organ failure. The patient likely needs HDU/ICU level care.
History:
Common (>50%): Severe, constant epigastric pain boring to the back, often with nausea and vomiting.
Less Common (10-50%): Dyspnea (from pleural effusion/ARDS), history of biliary colic, or a recent alcohol binge.
Pertinent Negatives: Ask about a history of peptic ulcer disease or NSAID use to help rule out a perforation.
Physical Examination:
General: Patient will look unwell, diaphoretic, tachycardic, and tachypneic.
Abdomen: Marked epigastric tenderness is classic. Guarding and reduced bowel sounds (ileus) are common.
Rare Signs (indicate severe necrotizing disease):
Cullen's sign: Periumbilical bruising.
Grey Turner's sign: Flank bruising.
Clinical Pearl: The pain is typically so severe that patients are restless and can't find a comfortable position. They often find some relief by leaning forward.
V. Diagnostic Workflow
Differential Diagnosis:
Perforated Peptic Ulcer:
Points For: Sudden, severe epigastric pain.
Points Against: Pain is often peritonitic from the start. May have a history of H. pylori or NSAID use.
How to Differentiate: Erect chest X-ray will show free air under the diaphragm.
Acute Cholecystitis/Cholangitis:
Points For: RUQ pain, vomiting, possible gallstone history.
Points Against: Pain is typically localized to the RUQ. Cholangitis presents with fever and jaundice (Charcot's triad).
How to Differentiate: Ultrasound abdomen will show a thickened gallbladder wall or dilated bile ducts.
Inferior Myocardial Infarction:
Points For: Can present with epigastric pain and vomiting.
Points Against: Pain is more likely crushing/pressure-like, with radiation to the arm or jaw.
How to Differentiate: An ECG is mandatory to rule this out.
Investigations Plan:
Bedside / Initial (First 15 Mins):
ECG: To exclude an inferior MI.
Blood Glucose: Hyperglycemia can occur due to stress and endocrine dysfunction.
First-Line Labs & Imaging:
Serum Lipase: The most specific test. A level >3 times the upper limit of normal is diagnostic.
Full Blood Count: Raised white cell count (inflammation) and a rising hematocrit (hemoconcentration) are poor prognostic signs.
Renal Profile: To check for acute kidney injury (AKI).
Liver Function Test: Elevated ALT/ALP points towards a gallstone etiology.
CRP: Get a baseline. A level >150 mg/L at 48 hours suggests severe pancreatitis is developing.
Ultrasound Abdomen: Crucial initial imaging to look for gallstones as the cause.
Confirmatory / Gold Standard:
Contrast-Enhanced CT (CECT) Abdomen: This is not for initial diagnosis. It's done after 48-72 hours if the patient isn't improving, to look for complications like necrosis.
VI. Staging & Severity Assessment
We use the Modified Atlanta Classification, which is determined after the first 48 hours.
Mild: No organ failure, no complications. Most patients fall into this group.
Moderately Severe: Transient organ failure (resolves in <48 hrs) OR local complications (e.g., fluid collections).
Severe: Persistent organ failure (>48 hrs). These patients belong in HDU/ICU.
To predict severity on admission, we use scoring systems like the Modified Glasgow Score. A score of 3 or more suggests a severe attack and warrants early senior review and consideration for higher-level care.
VII. Management Plan
Immediate Stabilisation (The ABCDE Plan):
A/B: Give high-flow oxygen to keep sats >94%.
C: This is the most important step. Aggressive IV fluid resuscitation with a balanced crystalloid like Hartmann's solution. A typical starting rate is 5-10 mL/kg/hour. You must monitor the response (urine output, HR, BP).
D/E:
Analgesia: Start with IV Tramadol. If pain is uncontrolled, escalate to IV Morphine.
Keep Nil By Mouth (NBM) initially.
Catheterise to accurately monitor urine output, which is a key marker of adequate resuscitation.
Definitive Treatment (The Ward Round Plan):
Fluid Management: Continue aggressive hydration for the first 24-48 hours. This is the cornerstone of preventing progression to severe disease.
Nutrition:
Mild: Once the pain and nausea resolve, you can start a low-fat oral diet. There's no need to wait for lipase to normalise.
Severe: If unable to eat by day 3-5, early enteral nutrition via a nasojejunal (NJ) tube is preferred over TPN. It protects the gut barrier and reduces septic complications.
Treating the Cause:
Gallstone Pancreatitis: If there is evidence of ongoing obstruction (cholangitis or persistent jaundice), the patient will need an urgent ERCP. All patients with gallstone pancreatitis should have a cholecystectomy, preferably during the same admission.
Antibiotics: Do not give prophylactic antibiotics. They are only indicated for confirmed infected necrosis, not for preventing it.
VIII. Complications
Immediate (First week):
SIRS & Organ Failure (ARDS, AKI, Shock): Management: Supportive care in HDU/ICU.
Short-Term (Weeks):
Acute Pancreatic Fluid Collections: Management: Most resolve on their own.
Pancreatic Necrosis (Sterile or Infected): Management: Infected necrosis is a life-threatening condition requiring IV antibiotics and drainage (endoscopic or surgical).
Long-Term (Months):
Pancreatic Pseudocyst: Management: Requires drainage only if large, symptomatic, or complicated.
Chronic Pancreatitis and Diabetes: Can be long-term sequelae after severe episodes.
IX. Prognosis
Mortality: Less than 1% for mild pancreatitis. This can rise to over 20-30% for severe disease with infected necrosis.
Key Prognostic Factors:
Persistent organ failure at 48 hours.
The extent of necrosis seen on a CECT scan.
The development of infected necrosis.
X. How to Present to Your Senior
"Dr, for your review. This is Mr. Tan, a 50-year-old man with a history of gallstones, who presented with severe epigastric pain. His lipase is over 4000. On assessment, he is tachycardic at 120 and his blood pressure is 90/50. My diagnosis is severe acute pancreatitis secondary to gallstones, with hypovolemic shock. I've sent off the initial bloods, started aggressive fluid resuscitation with Hartmann's, given IV morphine, and kept him nil by mouth. I am concerned about his poor haemodynamics and would like to discuss admitting him to HDU."
XI. Summary & Further Reading
Top 3 Takeaways:
The diagnosis requires 2 of 3 criteria: characteristic pain, lipase >3x normal, or imaging findings.
Aggressive IV fluid resuscitation in the first 24-48 hours is the single most important intervention.
Find and treat the underlying cause (especially gallstones). Do not use prophylactic antibiotics.
Key Resources:
UpToDate: Search for "Management of acute pancreatitis".
Amboss: Search for "Acute Pancreatitis".
Key Guideline: IAP/APA evidence-based guidelines on the management of acute pancreatitis. Pancreatology 2013.
