Acute Pancreatitis Advanced Nursing Guide

Acute Pancreatitis Overview

Acute pancreatitis is inflammation of the pancreas, ranging from mild self-limiting disease to severe, life-threatening necrotising pancreatitis with multi-organ failure. Mortality in severe disease reaches 20–30%.

Common Causes — GET SMASHED

Mnemonic	Cause
G	Gallstones (35–40% — most common in GCC women)
E	Ethanol/alcohol (30% in Western countries; lower in GCC due to alcohol restrictions)
T	Trauma (blunt abdominal trauma)
S	Steroids
M	Mumps (and other viral infections)
A	Autoimmune (IgG4-related)
S	Scorpion sting (rare; Trinidad, Middle East)
H	Hyperlipidaemia (hypertriglyceridaemia >1000 mg/dL), Hypercalcaemia
E	ERCP (post-procedural)
D	Drugs (azathioprine, furosemide, tetracyclines, valproate, GLP-1 agonists)

In GCC: Gallstone pancreatitis is the most common cause — high-fat diets, obesity and high gallstone prevalence in GCC females. Hypertriglyceridaemia pancreatitis is increasing with metabolic syndrome epidemic.

Revised Atlanta Classification

Severity	Criteria	Mortality
Mild	No organ failure, no local/systemic complications	<1%
Moderately severe	Transient organ failure (<48 hrs) and/or local complications	8%
Severe	Persistent organ failure (>48 hrs) — respiratory, renal or cardiovascular	36–50%

Severity Scoring

Ranson Criteria

Assessed at admission (5 criteria) and at 48 hours (6 criteria). Score ≥3 = severe pancreatitis.

At Admission	At 48 Hours
Age >55 years	Haematocrit drop >10%
WBC >16 × 10⁹/L	Urea rise >1.8 mmol/L
Blood glucose >11.1 mmol/L (non-diabetic)	Calcium <2.0 mmol/L
AST >250 U/L	PaO₂ <8 kPa
LDH >350 U/L	Base deficit >4 mmol/L
	Fluid sequestration >6 L

Score <3 = mild (1% mortality). Score 3–4 = 15% mortality. Score 5–6 = 40% mortality. Score >6 = 100% mortality.

BISAP Score (Bedside Index for Severity in AP)

Criterion	Points
BUN >25 mg/dL (urea >8.9 mmol/L)	1
Impaired mental status (GCS <15)	1
SIRS criteria ≥2	1
Age >60 years	1
Pleural effusion on imaging	1

Score ≥3 → high mortality risk; ICU admission warranted.

CT Severity Index (Balthazar Score)

CT Grade	Description	Points
A	Normal pancreas	0
B	Pancreatic oedema	1
C	Peripancreatic inflammatory change	2
D	Single fluid collection	3
E	Multiple fluid collections or gas in/near pancreas	4

+ Necrosis score (0–4 points based on % pancreatic necrosis). CTSI = grade + necrosis. Score ≥7 = 17× higher morbidity and mortality.

Treatment

Fluid Resuscitation — Most Critical Intervention

Aggressive early fluid resuscitation is the most important treatment in acute pancreatitis. Reduces pancreatic necrosis by maintaining microvascular perfusion.

First-line fluid: Lactated Ringer's (Hartmann's) — superior to 0.9% NaCl; reduces SIRS response; avoid in hypercalcaemia
Rate: 250–500 mL/hr initial bolus, then 250 mL/hr for first 12–24 hrs; titrate to response
Target markers: Urine output ≥0.5 mL/kg/hr, HR <100, MAP 65–85 mmHg, BUN falling, haematocrit 35–44%
Warning: Avoid over-resuscitation — abdominal compartment syndrome worsens outcomes
Monitoring: Hourly urine output (IDC in severe cases), BGL every 4 hrs, electrolytes 12-hourly

Pain Management

IV opioid analgesia — morphine or hydromorphone via PCA; adequate pain control is a priority
Historical teaching that morphine caused sphincter of Oddi spasm and worsened pancreatitis — NOT evidence-based; morphine is safe and effective
Paracetamol IV as baseline adjunct
Avoid NSAIDs — risk of GI haemorrhage and renal compromise in shocked patients
Document pain scores hourly; titrate analgesia accordingly

Complications

Complication	Timing	Management
Pancreatic necrosis	Days 3–7	Majority managed conservatively; infected necrosis → step-up approach (antibiotics → endoscopic drainage → surgical necrosectomy)
Pancreatic pseudocyst	Weeks–months	<6 cm: conservative; >6 cm or symptomatic: endoscopic or surgical drainage
ARDS	Days 1–4	Lung-protective ventilation, prone positioning if refractory
Acute kidney injury	Early	Aggressive hydration, avoid nephrotoxins, renal replacement therapy if severe
Hypocalcaemia	Days 2–5	IV calcium gluconate; monitor ECG for prolonged QT
Hyperglycaemia	Throughout	Insulin infusion; target BGL 6–10 mmol/L in ICU
Coagulopathy/DIC	Severe cases	FFP, cryoprecipitate, platelets per TEG/ROTEM

Nutritional Support

Paradigm shift: Early enteral nutrition (within 24–48 hrs) is now recommended over traditional "nil by mouth" approach. Enteral feeding maintains gut barrier, reduces bacterial translocation and improves outcomes.

Feeding Strategy

Severity	Route	Timing
Mild AP	Oral diet — soft, low-fat as soon as tolerated	Resume oral feeding within 24–48 hrs if pain improving
Moderate-severe AP	Nasojejunal (NJ) tube feeding preferred; NG acceptable if NJ not available	Start within 24–48 hrs of admission
Severe AP with ileus	Parenteral nutrition (TPN) as bridge if enteral not tolerated within 72 hrs	TPN if EN failed after 5–7 days

Nasojejunal vs nasogastric: NJ tube bypasses stomach and pancreatic stimulation — preferred. NG acceptable if NJ not available as studies show equivalent outcomes in most cases. Confirm NJ position by X-ray.

Nursing Enteral Feeding Considerations

Gastric residual volume (GRV) monitoring: hold feed if GRV >500 mL; document and escalate
Anti-emetics: ondansetron, metoclopramide for nausea during feeding
Feed rate: start at 20–25 mL/hr; titrate up to target every 4–6 hrs if tolerated
Oral care: continuous oral hygiene despite NBM / nasogastric feeding
Blood glucose: monitor 4-hourly; adjust insulin sliding scale

GCC-Specific Context

Acute Pancreatitis in GCC

Hypertriglyceridaemia pancreatitis: Markedly increased in GCC due to metabolic syndrome, type 2 diabetes, obesity and high-fat diet. TG >1000 mg/dL causes direct pancreatic toxic injury. Management includes insulin infusion (activates lipoprotein lipase), heparin, and plasmapheresis in refractory cases. Fibrates and omega-3 fatty acids for secondary prevention
Gallstone pancreatitis in GCC women: High-parity GCC women have elevated gallstone risk — gallstones are the most common pancreatitis cause in GCC females. ERCP with sphincterotomy and cholecystectomy within same admission
Ramadan fasting and re-feeding: Sudden high-fat iftars after prolonged fasting may precipitate gallstone sludge and biliary pancreatitis — seasonal clustering reported in GCC EDs during Ramadan
GLP-1 agonists: Increasingly prescribed for diabetes/obesity in GCC (semaglutide, liraglutide) — class-associated pancreatitis risk; monitor serum amylase/lipase in symptomatic patients on GLP-1 agents

Exam Tips

Ranson score ≥3 = severe. Know the 11 Ranson criteria (5 at admission + 6 at 48 hrs)
Most common cause in GCC: gallstones
First-line fluid: Lactated Ringer's (Hartmann's) — superior to 0.9% NaCl
Early enteral nutrition within 24–48 hrs — NOT prolonged NBM
Hypocalcaemia in pancreatitis = calcium saponification in fat necrosis (fat necrosis consumes calcium)
Infected necrosis = antibiotics (imipenem/meropenem); do NOT routinely give prophylactic antibiotics in sterile necrosis
Morphine is SAFE for pain in pancreatitis — old teaching was incorrect

Exam MCQs — DHA / SCFHS / QCHP

Q1. A patient with acute pancreatitis has serum calcium of 1.7 mmol/L. What is the MOST LIKELY pathophysiological mechanism?

A) Hyperparathyroidism causing calcium depletion B) Calcium saponification in areas of peripancreatic fat necrosis C) Renal calcium wasting from acute tubular necrosis D) Inadequate calcium intake during the NBM period

✅ B — Hypocalcaemia in acute pancreatitis results from calcium saponification — liberated free fatty acids from fat necrosis bind calcium ions, sequestering them as calcium soaps in necrotic fat tissue. This is a marker of severe disease and a Ranson criterion at 48 hours (Ca <2.0 mmol/L).

Q2. A patient with severe acute pancreatitis is to be started on nutritional support. What is the PREFERRED route based on current evidence?

A) Total parenteral nutrition (TPN) — pancreas must rest completely B) Nil by mouth for 7–10 days then gradual oral reintroduction C) Early enteral nutrition via nasojejunal tube within 24–48 hours D) Clear fluids orally from day 1 regardless of severity

✅ C — Current evidence (ESPEN, ACG guidelines) strongly recommends early enteral nutrition via nasojejunal tube within 24–48 hours. Enteral nutrition maintains gut mucosal integrity, prevents bacterial translocation from the gut to the pancreatic necrosis, and is superior to TPN. "Rest the pancreas" with prolonged NBM is an outdated concept.

Q3. A patient with acute pancreatitis has the following on admission: age 62, WBC 18 × 10⁹/L, blood glucose 13 mmol/L (non-diabetic), AST 310 U/L, LDH 380 U/L. At 48 hours: Hct dropped 12%, BUN risen 2.1 mmol/L, Ca 1.85 mmol/L, PaO₂ 7.2 kPa. What is the Ranson score?

A) 3 B) 6 C) 8 D) 9

✅ D — 9 (All 5 admission criteria: age >55, WBC >16, glucose >11.1, AST >250, LDH >350 = 5 points. Plus 48-hr: Hct drop >10% + BUN rise >1.8 + Ca <2.0 + PaO₂ <8 kPa = 4 more points = 9 total). Score >6 predicted nearly 100% mortality historically. Patient requires ICU admission.

Q4. A patient with acute pancreatitis develops fever, worsening abdominal pain and rising WBC 5 days into admission. CT shows gas within a pancreatic necrotic collection. What does this finding indicate and what is the treatment?

A) Expected resolution — gas is from normal digestive processes B) Pancreatic pseudocyst — schedule elective endoscopic drainage C) Infected pancreatic necrosis — requires antibiotics (carbapenem) and step-up drainage intervention D) ARDS developing — start lung-protective ventilation

✅ C — Gas within a pancreatic necrotic collection = infected pancreatic necrosis (pathognomonic). This is a life-threatening complication requiring: IV carbapenem antibiotics (imipenem or meropenem — good pancreatic penetration), CT/endoscopic guided drainage (step-up approach: percutaneous → endoscopic → surgical necrosectomy if needed). Mortality is high without intervention.

🫀 Acute Pancreatitis — Advanced