Acute pancreatitis is an acute inflammatory process of the pancreas arising from premature activation of digestive enzymes (primarily trypsinogen → trypsin) within the acinar cells, causing autodigestion, local inflammation, and systemic responses.
Key diagnostic criterion: Lipase >3× Upper Limit of Normal (ULN) — preferred over amylase due to higher sensitivity/specificity. Amylase rises faster but normalises in 24–72 h; lipase remains elevated for 7–14 days.
📊Revised Atlanta Classification (2012)
MILD
No organ failure
No local/systemic complications
Resolves within 1 week
Mortality <1%
MODERATELY SEVERE
Transient organ failure (<48 h) OR
Local complications OR
Exacerbation of co-morbidity
Mortality ~8%
SEVERE
Persistent organ failure (>48 h)
Single or multi-organ failure
ICU admission required
Mortality 30–50%
Organ failure defined by Marshall Score ≥2 in any of: Respiratory (PaO₂/FiO₂), Cardiovascular (systolic BP), or Renal (serum creatinine).
🧪Aetiology — GET SMASHED Mnemonic
GET SMASHED — Common Causes of Acute Pancreatitis
GGallstones — 40% (most common overall; highest in GCC)
EEthanol (alcohol) — 30% (lower in GCC Muslim-majority populations)
~15–20% remain idiopathic after full investigation. Consider occult microlithiasis, sphincter of Oddi dysfunction, or genetic mutations (PRSS1, SPINK1, CFTR).
🩺Clinical Presentation
Symptoms
Severe epigastric pain — constant, boring in nature
Both indicate severe haemorrhagic pancreatitis (appear 24–72 h)
Epigastric tenderness ± guarding
Tachycardia, hypotension (severe cases)
Jaundice (if CBD obstruction by gallstone)
Fox's sign — inguinal/groin bruising (rare)
Cullen's & Grey Turner's signs: Retroperitoneal blood tracking to the anterior abdominal wall (Cullen) or flanks (Grey Turner). Present in <3% of cases but strongly associated with haemorrhagic necrotising pancreatitis and poor prognosis.
📷Diagnosis & CT Severity Index (CTSI)
Investigation
Finding / Threshold
Clinical Significance
Serum Lipase
>3× ULN (preferred)
Peak at 24 h; elevated 7–14 days
Serum Amylase
>3× ULN
Less specific; normalises 24–72 h
FBC
WBC >12 × 10⁹/L; haematocrit >44%
Haemoconcentration → pancreatic necrosis risk
CRP
>150 mg/L at 48 h
Best marker for necrosis at 48 h
LFTs / Bilirubin
ALT >150 IU/L (3× ULN)
Suggests gallstone aetiology
Serum Calcium
Hypocalcaemia
Saponification; poor prognosis
Ultrasound
First-line imaging
Gallstones, CBD dilation
CECT Abdomen
After 48–72 h if severe
Necrosis, fluid collections (CTSI)
CTSI Scoring (Balthazar + Necrosis)
Grade A (0 pts) — Normal pancreas
Grade B (1 pt) — Focal/diffuse enlargement
Grade C (2 pts) — Peripancreatic fat stranding
Grade D (3 pts) — Single fluid collection
Grade E (4 pts) — ≥2 collections / gas
Necrosis 0% = 0 pts
Necrosis <30% = 2 pts
Necrosis 30–50% = 4 pts
Necrosis >50% = 6 pts
CTSI Interpretation
0–3: Mild — low morbidity/mortality
4–6: Moderate — increased complications
7–10: Severe — high morbidity (~17%), mortality (~3%)
CTSI should be performed after 48–72 h for accurate assessment of necrosis extent.
BISAP Severity Score Calculator
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📋BISAP Score — Full Reference
Score
Risk Category
Mortality
Action
0–1
Low risk
<1%
Ward-based care; monitor closely
2
Moderate risk
~2%
HDU consideration; senior review
3–5
High risk
≥15–20%
ICU admission; multidisciplinary team
BISAP score ≥3 on admission should prompt immediate escalation of care, senior gastroenterology/surgical review, and ICU referral.
🏆Glasgow-Imrie Score (within 48 hours)
Score ≥3 at 48 h = Severe acute pancreatitis. Each factor scores 1 point:
Factor
Threshold
Pathophysiology
Age
>55 years
Reduced physiological reserve
WBC
>15 × 10⁹/L
Systemic inflammation
Glucose
>10 mmol/L (non-diabetic)
Stress hyperglycaemia; islet destruction
BUN (Urea)
>16 mmol/L
Dehydration / renal impairment
LDH
>600 IU/L
Tissue necrosis
Albumin
<32 g/L
Capillary leak, malnutrition
Calcium
<2.0 mmol/L
Saponification in fat necrosis
PaO₂
<8 kPa (60 mmHg)
ARDS / respiratory failure
Memory Aid: PAWBUCAG
PPaO₂ <8 kPa
AAge >55
WWBC >15
BBUN/Urea >16 mmol/L
UUrea (same)
CCalcium <2.0 mmol/L
AAlbumin <32 g/L
GGlucose >10 mmol/L
🏥APACHE II in ICU Setting
Acute Physiology And Chronic Health Evaluation II — used for ICU severity assessment. APACHE II ≥8 indicates severe pancreatitis.
12 acute physiological variables + age + chronic health points
Score 0–71; higher = greater severity and predicted mortality
Reassessed every 24 h in ICU — trends more important than single values
APACHE II >8 on admission: predict severe course; arrange ICU
APACHE II >13: mortality risk approximately 20–30%
🔴Marshall Organ Failure Score
System
Parameter
Score 0
Score 1
Score 2
Score 3
Score 4
Respiratory
PaO₂/FiO₂
≥400
301–400
201–300
101–200
≤100
Cardiovascular
Systolic BP (mmHg)
≥90
<90 (fluid responsive)
—
<90 (pH<7.3)
<90 (pH<7.2)
Renal
Creatinine (µmol/L)
≤134
134–169
170–310
311–439
>439
Score ≥2 in any organ system = organ failure. Persistent organ failure (>48 h) = Severe Acute Pancreatitis per Revised Atlanta Classification.
🔬Local Complications (Atlanta 2012)
Early (<4 weeks)
Acute Peripancreatic Fluid Collection (APFC) — without necrosis; often resolves spontaneously
Acute Necrotic Collection (ANC) — contains necrosis; high infection risk
Late (>4 weeks)
Pseudocyst — encapsulated fluid without necrosis; drain if symptomatic
Lactated Ringer's (Hartmann's) is preferred over Normal Saline — WATERFALL trial (2022) demonstrated reduced SIRS rates and improved outcomes. Normal saline associated with hyperchloraemic acidosis.
Protocol
Initial bolus: 500 mL Hartmann's over 20–30 min if haemodynamically unstable
Maintenance rate: 250–500 mL/hour for first 12–24 hours
Target: Urine output ≥0.5 mL/kg/hr (monitor via urinary catheter)
Reassess every 4–6 hours — haematocrit, BUN, urine output, HR, BP
Haematocrit >44% on admission → increased pancreatic necrosis risk
Early enteral feeding (within 24–48 hours) is preferred over TPN — preserves gut mucosal integrity, reduces bacterial translocation, reduces infections, and lowers costs.
Nasogastric (NG) may be tolerated in mild-moderate cases
Start at 20–30 mL/hr, increase to target rate over 24–48 h
Elemental/semi-elemental formula preferred in severe cases
Reduces gut permeability, bacterial translocation
Reduces infectious complications vs TPN
TPN — Indications
Enteral feeding not tolerated after 48–72 h attempts
Prolonged ileus preventing enteral access
Enterocutaneous fistula
Abdominal compartment syndrome
Higher infection risk — strict line care protocol required
Risk of line sepsis, metabolic complications
Nil by mouth (NBM) is only maintained briefly for pain control/vomiting in the first 24 h. Early oral feeding should be attempted as soon as tolerated in mild pancreatitis.
💊Pain Management
IV Morphine: 2.5–5 mg IV every 4–6 h — effective, titrate to pain score
IV Patient-Controlled Analgesia (PCA): morphine or fentanyl
Epidural analgesia: for severe, refractory pain — also improves splanchnic perfusion
NSAIDs — use with caution (renal impairment risk in dehydrated patients)
Paracetamol IV for adjunct analgesia
Avoid pethidine (meperidine) — accumulation of toxic metabolite norpethidine
Thoracic epidural anaesthesia (TEA) at T6–T10 provides superior analgesia and has evidence of improving pancreatic microcirculation in severe acute pancreatitis.
Insulin infusion if glucose >10 mmol/L (GGI protocol)
Twice-daily observations minimum; hourly in ICU
Daily urea, creatinine, electrolytes, FBC, LFTs in first 48 h
CRP at 48 h (necrosis marker)
Interventions
IV access: large-bore IV × 2 or central venous catheter in severe
Anti-emetics: ondansetron 4–8 mg IV, metoclopramide, prochlorperazine
VTE prophylaxis: LMWH (enoxaparin) when not actively bleeding — compression stockings and pneumatic compression
Nasogastric drainage if prolonged ileus/vomiting
NBM initially; reintroduce oral diet when pain subsides
Oral care — frequent mouth care while NBM
Position: semi-recumbent; knee-chest position for comfort
🔬Antibiotics & Other Pharmacological
Prophylactic antibiotics — NOT recommended in sterile necrotising pancreatitis (evidence does not support routine use)
Antibiotics indicated for: infected necrosis (confirmed by FNA or clinical suspicion with CT gas), cholangitis, other infections
Carbapenems (imipenem/meropenem) — good pancreatic penetration for infected necrosis
PPI/H2 antagonist — stress ulcer prophylaxis in ICU patients
ERCP + sphincterotomy: within 24–72 h if gallstone pancreatitis + cholangitis or CBD obstruction
Cholecystectomy: same admission (mild) or within 6 weeks (severe) to prevent recurrence
🦠Infected Pancreatic Necrosis
Step-Up Algorithm for Infected Necrosis ▶
Infected necrosis occurs in ~30–40% of necrotising pancreatitis. Suspect when: fever + SIRS persisting or worsening after 7–10 days + CT shows gas in necrosis (pathognomonic). CT-guided fine needle aspiration (FNA) can confirm if clinical picture unclear.
Step 1 — Antibiotics
Carbapenems: meropenem 1g IV 8-hourly or imipenem-cilastatin
Metronidazole: add for anaerobic coverage if needed
Duration guided by clinical response + CRP trends
Step 2 — Percutaneous Drainage (PCD)
CT or US-guided percutaneous catheter drainage
Preferred first-line drainage approach
Allows stabilisation; avoids early open surgery
Failure = inadequate drainage or clinical deterioration after 72 h
Preferred over surgery if lesion abuts gastric/duodenal wall
Lower morbidity than open surgery; comparable efficacy
Step 4 — Surgical Necrosectomy
Reserved for failure of less invasive approaches
Video-assisted retroperitoneal debridement (VARD)
Open surgical necrosectomy: highest morbidity/mortality
Ideally delayed to ≥4 weeks — allows "walling off" of necrosis
Timing principle: Delay drainage/debridement for ≥4 weeks if clinical condition allows (walled-off necrosis is safer to drain than acute necrotic collection). Early surgery (<2 weeks) carries very high mortality.
🫁ARDS in Acute Pancreatitis
Occurs in ~20% of severe acute pancreatitis
Mechanism: systemic release of phospholipase A2, cytokines → lung injury
Dosing: 25,000–50,000 PhEur units lipase with main meals; 25,000 units with snacks
Take with/immediately before food — essential for efficacy
Fat-soluble vitamin supplementation (A, D, E, K)
Dietary advice: low-fat diet unnecessary with adequate PERT; medium-chain triglycerides if malabsorption persists
📋Chronic Pancreatitis — Overview & Diagnosis
Chronic pancreatitis is a progressive fibro-inflammatory syndrome causing irreversible structural damage, exocrine and endocrine insufficiency, and chronic pain.
Amsterdam Criteria for Diagnosis of Chronic Pancreatitis: Two or more of: (1) Chronic abdominal pain characteristic of pancreatitis; (2) Morphological evidence of chronic pancreatitis on imaging (ductal dilatation ≥3mm, calcifications, atrophy, irregular contour); (3) Exocrine insufficiency (faecal elastase <200 µg/g, or 72-h faecal fat); (4) Endocrine insufficiency (diabetes); (5) Histological evidence of fibrosis.
Titrate dose to symptom control; maximum dose ~80,000 units/meal
Alkaline environment needed — PPI co-prescription if suboptimal response
💉Endocrine Insufficiency — Type 3c Diabetes
Type 3c (Pancreatogenic) Diabetes is distinct from Type 1 and Type 2 DM. It results from destruction of both islet beta cells (insulin) AND alpha cells (glucagon), making it unpredictable and "brittle."
Key Features
Brittle / labile: wide glucose swings; severe hypoglycaemia risk
Hypoglycaemia-prone: absent glucagon counter-regulation; no warning symptoms
Q1. A 45-year-old male presents with severe epigastric pain radiating to the back, nausea, and vomiting. Serum lipase is 1,850 U/L (ULN = 60 U/L). On examination, you note bruising around the umbilicus. Which sign is this, and what does it indicate?
A. Grey Turner's sign — retroperitoneal haemorrhage tracking to the flanks
C. Fox's sign — inguinal bruising from retroperitoneal haemorrhage
D. Murphy's sign — suggestive of acute cholecystitis
Answer: B — Cullen's sign. Periumbilical bruising (Cullen's sign) indicates blood tracking from a retroperitoneal haemorrhage to the anterior abdominal wall. Grey Turner's sign = flank bruising. Both are signs of severe haemorrhagic pancreatitis and indicate a poor prognosis. Lipase >3× ULN (here ~30× ULN) confirms acute pancreatitis.
Q2. You are caring for a patient with severe acute pancreatitis. BISAP score on admission: BUN 30 mg/dL, confused (GCS 13), SIRS criteria met (HR 102, Temp 38.5°C, WBC 14), age 65, bilateral pleural effusions on CXR. What is the BISAP score and appropriate nursing action?
A. BISAP 2 — monitor on general ward with 4-hourly observations
B. BISAP 3 — consider HDU admission and notify registrar
C. BISAP 5 — high risk; escalate immediately to ICU, urgent senior review
D. BISAP 4 — commence antibiotics and continue on surgical ward
Answer: C — BISAP 5. All 5 BISAP criteria are present: BUN >25 mg/dL (✓), Impaired mental status (✓), SIRS (✓), Age >60 (✓), Pleural effusion (✓). Score = 5/5. BISAP ≥3 = high risk ≥15–20% mortality → ICU admission required. This patient needs immediate escalation, aggressive fluid resuscitation (Hartmann's preferred), and multidisciplinary involvement.
Q3. A patient with acute pancreatitis is receiving IV fluid resuscitation. Which intravenous fluid is preferred according to the WATERFALL trial, and what is the primary reason?
A. 0.9% Normal Saline — isotonic and prevents hypokalaemia
B. Lactated Ringer's (Hartmann's solution) — reduces SIRS rates and avoids hyperchloraemic acidosis
C. 5% Dextrose — provides caloric support during NPO status
D. Colloid (albumin 4%) — better volume expansion and preferred in all critical illness
Answer: B — Lactated Ringer's / Hartmann's solution. The WATERFALL trial (2022, NEJM) demonstrated that Lactated Ringer's reduced the rate of moderate or severe pancreatitis and SIRS compared to Normal Saline. Normal saline's high chloride content causes hyperchloraemic acidosis, which worsens outcomes. Target: 500 mL bolus then 250 mL/hr; reassess with urine output (>0.5 mL/kg/hr), HR, and haematocrit targets.
Q4. A 55-year-old woman with chronic pancreatitis due to gallstones is prescribed Creon® 25,000 units. She reports continued steatorrhoea and weight loss despite taking capsules. Which of the following is the most likely reason and correct intervention?
A. The dose is too high — reduce to 10,000 units per meal
B. She should take PERT 30 minutes before meals for best effect
C. She may be taking PERT at wrong timing, crushing capsules, or dose may need titration upward; add PPI if suboptimal response
D. Switch from Creon to TPN — enteral absorption is not possible in chronic pancreatitis
Answer: C. Common causes of suboptimal PERT response: (1) Wrong timing — must take WITH or DURING food, not before/after; (2) Crushing/chewing capsules destroys enteric coating; (3) Insufficient dose — may need to increase to 50,000–75,000 units/meal; (4) Acidic gastric environment inactivating enzymes — add PPI to raise pH ≥4; (5) Concurrent diabetes causing delayed gastric emptying. TPN is not indicated as first-line.
Q5. A patient with necrotising pancreatitis develops fever (39.2°C), persistent SIRS, and CT scan shows gas bubbles within the peripancreatic necrosis at Day 10. What is the most appropriate immediate management?
A. Immediate open surgical necrosectomy to debride infected tissue
B. Continue conservative management and repeat CT in 2 weeks
C. Commence prophylactic antibiotics only and monitor SIRS markers
D. Commence carbapenems (meropenem), consider CT-guided percutaneous drainage, follow step-up approach; delay open surgery if possible
Answer: D — Step-up approach. Gas in necrosis on CT = pathognomonic of infected pancreatic necrosis. The step-up approach: (1) Antibiotics with good pancreatic penetration — carbapenems preferred; (2) Percutaneous drainage if accessible; (3) Endoscopic necrosectomy; (4) Surgical necrosectomy only if above fail. Open surgery at Day 10 carries very high mortality — delay to ≥4 weeks if clinically possible. CT-guided FNA confirms infection if gas not yet visible.
📚Key References & Guidelines
Revised Atlanta Classification of Acute Pancreatitis (Banks et al., 2013) — Gut
ACG Clinical Guideline: Management of Acute Pancreatitis (Tenner et al., 2013)
IAP/APA Evidence-Based Guidelines for the Management of Acute Pancreatitis (2013)
WATERFALL Trial — Lactated Ringer's vs Normal Saline (de-Madaria et al., NEJM 2022)
UEG Evidence-Based Guidelines for Chronic Pancreatitis (Lévy et al., 2017)
ESPEN Guidelines on Clinical Nutrition in Acute Pancreatitis (2020)
DHA Clinical Practice Guidelines — UAE Ministry of Health