Internal Medicine

Acute Pancreatitis

Acute inflammation of pancreatic parenchyma caused by destructive effects of pancreatic enzymes and resulting in acinar cell injury.

Acute inflammation of pancreatic parenchyma caused by destructive effects of pancreatic enzymes and resulting in acinar cell injury.

  • 3% of all abdominal pains
  • M/C pancreatic disorder in children
  • Reversible process (chronic pancreatitis causes irreversible damage)
  • Acute recurrent pancreatitis: ≥ 2 separate episodes of acute pancreatitis with interim return to baseline.


Injury to acinar cells and impairment of secretion of zymogen granules or damage to duct epithelium and delaying of enzymatic secretion:


  • Idiopathic
  • Gallstones (50-75% cases) (M/C cause in adults)
  • Ethanol (25% cases)
  • Trauma (blunt trauma, bicycle handle injury in children)
  • Steroids
  • Mumps, Malnutrition
  • Autoimmune pancreatitis, Abdominal trauma, Ampullary tumour
  • Scorpion
  • Hyperparathyroidism, Hypercalcemia, Hereditary (40% risk of pancreatic cancer)
  • ERCP (Endoscopic retrograde cholangiopancreatography) (1-3%)
    EUS-FNA (Endoscopic Ultrasound-Guided Fine-Needle Aspiration)
  • Drugs: Corticosteroids, azathioprine, asparaginase, valproic acid, thiazides, oestrogens
Pathophysiology of severe acute pancreatitis
Pathophysiology of severe acute pancreatitis: The local injury induces the release of TNF-α and IL-1. Both cytokines produce further pancreatic injury and amplify the inflammatory response by inducing the release of other inflammatory mediators, which cause distant organ injury. This abnormal inflammatory response is responsible for the mortality seen during the early phase of acute pancreatitis. | Themes, U. (2016). Exocrine Pancreas. Retrieved 31 July 2022, from
Acute pancreatitis pathogenesis
The Calgary Guide |


  • Epigastric abdominal pain radiating to the back ((40%-70% cases, can last several hours to days)
  • Nausea & vomiting (90% cases, can last for several days)
  • Abdominal pain
Acute pancreatitis pathogenesis
The Calgary Guide |

Physical examination:

  • Tripod position/doubled-over position (relief of sitting or bending forwards, worsens on eating)
  • Patient looks ill: Profound shock, toxicity & confusion
  • Tachypnoea, tachycardia, hypotension
  • Normal/subnormal temperature
    • Acute swinging pyrexia suggests cholangitis
  • Hypocalcemia (used up by fat necrosis)
  • Cullen’s sign: Bruising around periumbilical region (belly button)
  • Grey Turner’s sign: Ecchymoses/bruising along flank, between hips & ribs
    • Indicate severe disease (acute haemorrhagic pancreatitis)
  • Abdominal guarding
  • Fox sign: Bruising around inguinal region
  • Abdominal distension: With ascites + shifting dullness
  • Pleural effusion (10-20%)


Local complications:

Most common complications following AP include acute peri-pancreatic fluid collection, pancreatic pseudocyst, acute necrotic collections, and walled off necrosis.
Interstitial edematous pancreatitis (~80%)Necrotizing pancreatitis (~20%)
No wall (<4 weeks)Acute peripancreatic fluid collection (APFC)Acute necrotic collection (ANC)
Wall present (>4 weeks)Pancreatic pseudocystWalled-off necrosis (WON)

Peripancreatic complications:

  • Thrombosis of splanchnic venous circulation (24% cases):
    • M/C in splenic vein >> portal and/or superior mesenteric veins
    • Can lead to development of gastric varices leading to gastrointestinal bleeding.
  • Pseudoaneurysm: Sudden gastrointestinal bleeding, drop in hemoglobin and worsening abdominal pain
  • Abdominal compartment syndrome: Secondary to tissue edema from aggressive fluid resuscitation, peripancreatic inflammation, and ascites

Systemic complications:

Any patient with AP is at an increased risk for exacerbation of underlying conditions including cardiac, lung, hepatic, and nephrogenic disease.
Complications of acute pancreatitis
Acute pancreatitis complication
(2021) What is the BISAP score?. Retrieved March 05, 2021, from


Diagnostic criteria:

2 of 3 required:
  1. Acute epigastric pain often radiating to the back
  2. ↑ Serum amylase/lipase (more specific) to upper limit of normal
  3. Characteristic imaging findings

Serum tests:

  • Amylase (initially tested): ↑ x3-4 times by 6-12 hours, peaks at 48 hours, remains elevated up to 4 days
  • Lipase (GOLD STANDARD, M/specific): ↑ by 4-8 hours, peaks at 24-48 hours, remains elevated 8-14 days longer than amylase
  • Trypsin (↑ earlier than amylase)
  • AST/LDH (↑ suggestive of tissue necrosis)
  • Polymorphonuclear leukocyte elastase
  • Hypo/hyperglycemia (endocrine insufficiency)
  • Liver function test (LFT):
    • ALP, bilirubin (↑ obstruction)

Complete blood count (CBC):

  • TC: Leucocytosis
  • Hb: ↑ (hemoconcentration) or ↓ (haemorrhage)


Initial diagnosis

Abdominal radiography:

Non-specific signs seen
  • Sentinel loop sign
  • Colon cutoff sign
  • Gasless abdomen

Contrast-enhanced CT (CECT):

GOLD STANDARD investigation
  • Inflammation, necrosis
  • Peripancreatic heterogenous collections (fat necrosis)
  • Renal halo sign (due to extension of peri-pancreatic inflammation into the pararenal space into para-renal fat)
    • Common on left side
  • Pseudocysts
Axial CT in a patient with acute exudative pancreatitis
Axial CT in a patient with acute exudative pancreatitis showing extensive fluid collections surrounding the pancreas. | By Hellerhoff – Own work, CC BY-SA 3.0,

Differential diagnosis:

Acute GI related abdominal pain


Revised Atlanta Classification (2013):

Divides AP into interstitial edematous or necrotizing pancreatitis, distinguish early and late phase pancreatitis, and emphasizes the importance of SIRS and multiorgan failure
Acute Pancreatitis: Revised Atlanta Classification and the Role of Cross-Sectional Imaging
Acute Pancreatitis: Revised Atlanta Classification and the Role of Cross-Sectional Imaging. AJR 2015 | International Consensus. Gut. (2020) Pancreatitis classification – Rad Clarity. Retrieved November 14, 2020, from

Acute Physiology and Chronic Health Evaluation (APACHE) II scoring system

Originally developed for patients in the intensive care unit (ICU) and utilizes 12 variables in order to help calculate a score that can be used upon admission, 24 h, and 48 h. This allows the advantage of the score being recalculated throughout the patient’s stay allowing for appropriate adjustments and interventions.

Determinant-Based Classification (DBC):

For severity of AP based on the factors called “determinants” which are both local and systemic.

Modified Glasgow (Imrie) prediction score:

Glasgow Imrie criteira for acute pancreatitis

Bedside Index of Severity in Acute Pancreatitis (BISAP) Score

Mortality based prognostic tool for physi-cians to use within the first 24 h of admission. The scoring system takes into account 5 variables: Blood urea nitrogen (BUN) > 25 mg/dL, impaired mental status, SIRS, age greater than 60, or the presence of a pleural effusion.

Ranson criteria:

Takes into account 11 variables: 5 of which are measured at admission while 6 of these are measured 48 h after admissio
Ranson's criteria & BISAP score

Computed tomography severity index (CTSI):

Based on a combination of peri-pancreatic inflammation, phlegmon, and degree of pancreatic necrosis seen on initial CT scan of the abdomen within one week of AP. This study was developed to grade the severity of pancreatitis (Balthazar score) and establish a correlated mortality rate. Best scoring system

Modified Marshal score:

Persistent organ failure is now defined by a Modified Marshal Score
Modified Marshall score


The cornerstones in the management of AP include aggressive early intravenous hydration, appropriate nutrition, necessary interventions, and pain management.

A flowchart encompassing the patient’s journey from diagnosis of acute pancreatitis through to further investigation and definitive management
A flowchart encompassing the patient’s journey from diagnosis of acute pancreatitis through to further investigation and definitive management. | CBD, common bile duct; CT, computed tomography; ERCP, endoscopic retrograde cholangiopancreatography; EUS, endoscopic ultrasound; HIDA, fatty meal hepatobiliary iminodiacetic acid scan; LFT, liver function test; MRCP, magnetic resonance cholangiopancreatography; TUS, transabdominal ultrasound. | Shah, A. P., Mourad, M. M., & Bramhall, S. R. (2018). Acute pancreatitis: current perspectives on diagnosis and management. Journal of Inflammation Research, 11, 77–85.

Fluid resuscitation:

Normal Saline and Ringer’s Lactate are equally efficacious in the management of AP


Initiating early oral feedings (within 24 h) in patients with mild AP.

Pain management:

Uncontrolled pain can lead to hemodynamic instability leading to worse outcomes.
  • Opioids (first-line for pain medication)


Indicated in infected pancreatitis or infected necrosis if patient fails to improve after 1 week.
  • Good pancreatic necrosis penetration: Carbapenems, quinolones, and metronidazole

Endoscopic intervention:

Indicated in patients with AP who have concurrent cholangitis or biliary obstruction.
  • ERCP


Presence of gallstones in the gallbladder or biliary tree, infected necrosis preferably for more than 4 wk after antibiotics if stable, and necrosectomy in symptomatic patients are common indications for surgical management
  • Cholecystectomy: All patients with mild AP related to gallstones
    • Early surgical intervention in biliary pancreatitis drastically reduces mortality and gallstones related complications


Indicated in hemorrhagic complications


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