Pankreatitis Akut

01Pathophysiology

The central mechanism of acute pancreatitis is premature activation of trypsinogen to trypsin within pancreatic acinar cells. Under normal physiology, trypsinogen remains inactive until it reaches the duodenum, where enterokinase cleaves it into its active form. When this activation occurs prematurely inside the pancreas, trypsin initiates a cascade by activating other zymogens, including elastase, phospholipase A2, and kallikrein. The result is enzymatic autodigestion of the pancreatic parenchyma, leading to edema, vascular injury, hemorrhage, and cell necrosis.
Gallstones cause pancreatitis by transiently or persistently impacting at the ampulla of Vater. This obstruction raises ductal pressure and allows reflux of bile into the pancreatic duct, triggering premature enzyme activation. This is why you will see a vignette describing an obese, middle-aged woman with sudden epigastric pain after a fatty meal, paired with elevated lipase and gallstones on ultrasound.
Alcohol injures the pancreas through a different route. Ethanol is directly toxic to acinar cells, promotes premature intracellular enzyme activation, increases the protein content of pancreatic secretions causing ducite plugging, and raises sphincter of Oddi tone. The typical vignette describes a male patient with a long history of heavy drinking who presents with recurrent bouts of epigastric pain.
Hypertriglyceridemia (levels exceeding 1000 mg/dL) is the third most common cause. Free fatty acids released from excessive triglyceride hydrolysis by pancreatic lipase are directly toxic to acinar cells and the capillary endothelium. This is a commonly tested scenario: a patient with poorly controlled diabetes or familial hyperlipidemia who develops pancreatitis with a "milky" or lipemic serum and a falsely normal or low amylase (lipemia interferes with the assay).
The local inflammatory response can escalate to a systemic inflammatory response syndrome (SIRS), which in turn may progress to multiorgan failure, acute respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC). This progression from local autodigestion to systemic inflammation explains why patients with severe pancreatitis may develop pulmonary infiltrates, renal failure, and shock, all driven by cytokine-mediated endothelial damage.

02Classification and Clinical Manifestation

The Revised Atlanta Classification (2012) is the standard framework for categorizing severity and complications. Severity is graded by the presence and duration of organ failure.

Local complications are classified by morphology and timing:

The distinction between a pseudocyst and walled-off necrosis is heavily tested. A pseudocyst is a fluid-only collection without solid components, while walled-off necrosis contains both fluid and solid necrotic debris. Both develop after 4 weeks and have encapsulating walls, but their contents differ entirely, and this dictates management.

03Diagnostic Workup

Serum lipase is the single most important laboratory test and the best initial step for any vignette suggesting pancreatitis. It is both more sensitive and more organ-selective than amylase for pancreatic injury. A level more than three times the upper limit of normal, combined with characteristic abdominal pain, is sufficient to establish the diagnosis without imaging.
Do not order a CT scan on admission for every patient with pancreatitis. This is a common trap. CT with IV contrast is indicated only when the diagnosis is in doubt, when the patient fails to improve after 48 to 72 hours of appropriate therapy, or when you need to evaluate for complications such as necrosis, abscess, or pseudocyst. Early CT (within the first 48 to 72 hours) can actually underestimate the extent of necrosis because the full inflammatory cascade has not yet declared itself on imaging.
Right upper quadrant ultrasound should be performed in every patient with a first episode of acute pancreatitis to look for gallstones. This is a "never miss" step. Even if the patient has a clear history of heavy alcohol use, gallstones must be excluded because the management changes dramatically: gallstone pancreatitis requires cholecystectomy.
MRCP or endoscopic ultrasound is ordered when you have intermediate suspicion for a common bile duct stone (mildly dilated duct, moderately elevated liver enzymes) but the patient does not meet criteria for urgent ERCP. If the patient has frank cholangitis (Charcot triad: fever, jaundice, right upper quadrant pain) or a clearly obstructed common bile duct, skip straight to ERCP within 24 hours because this is both diagnostic and therapeutic.
For severity scoring, the BISAP score (BUN > 25, Impaired mental status, SIRS, Age > 60, Pleural effusion) is the most practical bedside tool because it can be calculated within the first 24 hours using readily available data. Ranson criteria require 48 hours for full calculation, which limits its early utility.

04Management and Treatment

Aggressive IV fluid resuscitation is the cornerstone of early management and the tested "next best step" in almost every pancreatitis vignette. Lactated Ringer solution is preferred over normal saline because it has been shown to reduce SIRS and inflammatory markers. The initial rate of 250 to 500 mL/hour should be titrated based on urine output, heart rate, blood pressure, and hematocrit. The goal is to prevent pancreatic hypoperfusion, which worsens necrosis.
Pain control with IV opioids is essential. The old teaching that morphine is contraindicated because it causes sphincter of Oddi spasm is no longer supported by current evidence, and morphine can be used. However, many vignettes still favor hydromorphone or fentanyl as first-line choices.
Early oral refeeding is a paradigm shift from the traditional "NPO until pain resolves" approach. Current guidelines recommend starting a low-fat solid diet within 24 hours of admission as long as the patient is not vomiting and pain is decreasing. Prolonged fasting increases gut mucosal atrophy and the risk of bacterial translocation, which can seed pancreatic necrosis. If the patient cannot tolerate oral feeding, enteral nutrition via nasojejunal tube is the next step, not total parenteral nutrition (TPN). TPN increases infection risk and should only be used when the enteral route is entirely impossible.
For gallstone pancreatitis, cholecystectomy during the index admission is the standard for mild cases. Delaying surgery leads to a high rate of recurrent biliary events. In severe or necrotizing gallstone pancreatitis, cholecystectomy is postponed until clinical improvement, typically 6 to 8 weeks later. If cholangitis coexists with gallstone pancreatitis, the next best step is ERCP within 24 hours, not cholecystectomy. The sequence matters: ERCP first to relieve the obstruction, then cholecystectomy later.
For necrotizing pancreatitis, the approach depends on whether the necrosis is sterile or infected. Sterile necrosis is managed conservatively with supportive care. Infected necrosis (suspected when there is clinical deterioration after initial improvement, persistent fever, rising white cell count, or gas bubbles within the necrotic collection on CT) requires antibiotics and intervention. The step-up approach is the current standard: start with percutaneous catheter drainage or endoscopic transmural drainage, then escalate to minimally invasive video-assisted retroperitoneal debridement (VARD) only if drainage alone is insufficient. Open surgical necrosectomy is a last resort. Intervention should ideally be delayed to beyond 4 weeks so that the acute necrotic collection matures into walled-off necrosis, which has a defined capsule that makes drainage and debridement safer and more effective.
Prophylactic antibiotics are not indicated in acute pancreatitis, even if necrosis is present on imaging. This is a high-yield "do not do" that appears frequently. Antibiotics are started only when infection is confirmed or strongly suspected.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most common mistake students make with acute pancreatitis is ordering a CT scan as the initial diagnostic step. The diagnosis is clinical and biochemical: characteristic pain plus lipase more than three times the upper limit of normal is sufficient. CT is reserved for diagnostic uncertainty or failure to improve, and ordering it too early (before 48 to 72 hours) underestimates the true extent of necrosis.
The second major trap involves amylase reliability. Students often anchor on amylase as the diagnostic marker and fail to recognize that amylase can be falsely normal in two important scenarios: hypertriglyceridemic pancreatitis (lipemia interferes with the assay) and alcohol-induced pancreatitis with a chronically damaged gland that produces less amylase. Lipase is always the preferred test.
Another frequently tested pitfall is the management of gallstone pancreatitis with concurrent cholangitis. The next best step is ERCP within 24 hours, not cholecystectomy. Students who jump to cholecystectomy are selecting a correct intervention at the wrong time. The obstruction must be relieved first.
Students also lose points by recommending prophylactic antibiotics for sterile necrosis. The presence of necrosis on CT does not by itself warrant antibiotics. The trigger for antibiotic therapy is evidence of infection: clinical deterioration, persistent fevers, or gas bubbles within the necrotic collection on imaging.
Finally, the old teaching that morphine is contraindicated because of sphincter of Oddi spasm continues to appear as a distractor answer. Current guidelines no longer support this contraindication, and morphine is an acceptable analgesic in acute pancreatitis.
The core competency being tested across pancreatitis questions is the ability to correctly sequence diagnostic and therapeutic steps: lipase first (not CT), ultrasound to evaluate etiology, early fluids and feeding, ERCP before cholecystectomy when cholangitis is present, and delayed intervention for necrosis. Recognizing the right action at the right time point is what separates correct from incorrect answers.