8.2 Pancreatitis, Acute Abdomen, Bowel Ischemia & Nutrition
Key Takeaways
- Acute pancreatitis is diagnosed by 2 of 3: characteristic epigastric pain radiating to the back, lipase (or amylase) >3x the upper limit of normal, and imaging; lipase is more specific and stays elevated longer.
- Ranson criteria (5 on admission, 6 at 48 hours) and revised Atlanta severity predict outcome; massive third-spacing drives hypovolemic shock and ARDS, requiring aggressive isotonic fluids, ideally lactated Ringer's.
- Acute mesenteric ischemia causes pain out of proportion to exam with lactic acidosis; free air under the diaphragm signals perforation and peritonitis, both surgical emergencies.
- Abdominal compartment syndrome is sustained intra-abdominal pressure >20 mmHg (measured by bladder pressure) with new organ dysfunction; refractory cases need decompressive laparotomy.
- Early enteral nutrition within 24-48 hours is preferred over parenteral; keep the head of bed at 30-45 degrees to limit aspiration, and advance slowly to prevent refeeding syndrome.
Acute Pancreatitis
Acute pancreatitis is inflammation from premature intrapancreatic enzyme activation causing autodigestion. The CCRN diagnostic rule requires 2 of 3: (1) characteristic epigastric pain radiating to the back, (2) lipase or amylase >3x the upper limit of normal, and (3) confirmatory imaging (CT/MRI/ultrasound). Lipase is preferred—more sensitive and specific than amylase and it stays elevated longer. Enzyme magnitude does not predict severity. Gallstones and alcohol are the leading causes; others include hypertriglyceridemia (>1000 mg/dL), hypercalcemia, post-ERCP, and drugs.
Severity Scoring and Third-Spacing
Severity is stratified with Ranson criteria (5 measured on admission, 6 at 48 hours), APACHE II, BISAP, and the revised Atlanta classification (mild; moderately severe; severe = persistent organ failure >48 hours). More Ranson points equal higher mortality.
| Ranson – On Admission | Ranson – Within 48 Hours |
|---|---|
| Age >55 years | Hematocrit fall >10% |
| WBC >16,000/mm3 | BUN rise >5 mg/dL |
| Glucose >200 mg/dL | Serum calcium <8 mg/dL |
| AST >250 units/L | PaO2 <60 mmHg |
| LDH >350 units/L | Base deficit >4 mEq/L; fluid sequestration >6 L |
The dominant early danger is third-spacing: systemic inflammation and capillary leak sequester liters of fluid, producing hypovolemic and distributive shock, ARDS, and acute kidney injury. Management is aggressive isotonic fluid resuscitation (lactated Ringer's preferred), analgesia, and close respiratory/hemodynamic monitoring. Feed early enterally; prophylactic antibiotics are not routine and are reserved for infected necrosis. Complications include necrotizing pancreatitis, infected necrosis, pseudocyst, hypocalcemia (fat saponification), hyperglycemia, pleural effusion, and abdominal compartment syndrome.
Acute Abdomen and Perforation
An acute abdomen is sudden severe abdominal pain requiring urgent evaluation for a surgical cause. Hollow viscus perforation—from a perforated peptic ulcer, diverticulitis, obstruction, or ischemic bowel—spills luminal contents and produces peritonitis: a rigid, board-like abdomen, rebound tenderness, guarding, and absent bowel sounds. The tested imaging sign is free air under the diaphragm on an upright chest film. Perforation is a surgical emergency; management is fluid resuscitation, broad-spectrum antibiotics, and operative repair, with rapid progression to septic shock if delayed.
Mesenteric and Bowel Ischemia
Acute mesenteric ischemia is compromised intestinal perfusion and carries very high mortality. The hallmark is pain out of proportion to physical exam—severe pain with a deceptively benign belly early on. Causes: SMA embolism (often atrial fibrillation), SMA thrombosis, nonocclusive low-flow states (shock, high-dose vasopressors), and mesenteric venous thrombosis. Laboratory clues are elevated lactate and metabolic acidosis; CT angiography is diagnostic. As bowel infarcts, peritonitis and hemodynamic collapse follow. Treatment: resuscitation, anticoagulation, and surgical revascularization or resection of dead bowel.
Abdominal Compartment Syndrome
Intra-abdominal hypertension (IAH) is sustained intra-abdominal pressure (IAP) >=12 mmHg. Abdominal compartment syndrome (ACS) is sustained IAP >20 mmHg with new organ dysfunction. IAP is measured indirectly via bladder (intravesical) pressure: instill ~25 mL sterile saline into the Foley, transduce at end-expiration, supine, zeroed at the midaxillary line/symphysis pubis.
Rising pressure compresses the vena cava and diaphragm, causing decreased venous return and cardiac output, oliguria/AKI, rising peak airway pressures, and reduced organ perfusion. Non-operative measures come first—sedation/analgesia, nasogastric and rectal decompression, paracentesis for ascites, avoiding over-resuscitation, and neuromuscular blockade—but refractory ACS requires decompressive laparotomy.
Critical-Care Nutrition
Nutrition is a graded CCRN competency. Enteral nutrition (EN) is preferred over parenteral because it maintains gut mucosal integrity, reduces bacterial translocation and infection, and costs less—"if the gut works, use it." Start early enteral feeding within 24-48 hours once the patient is hemodynamically stable (hold or use caution during escalating vasopressors/shock). Use post-pyloric placement for high aspiration risk or gastric intolerance.
Aspiration is the chief EN hazard: keep the head of bed elevated 30-45 degrees, verify tube placement, and treat intolerance with prokinetics. Current guidance does not require routine gastric residual volume checks, and feeding need not be held for residuals below ~500 mL without other intolerance. Total parenteral nutrition (TPN) is reserved for a nonfunctioning gut—bowel obstruction, mesenteric ischemia, high-output fistula—or when EN cannot meet needs. Advance calories gradually in malnourished patients to prevent refeeding syndrome, marked by falling phosphate, potassium, and magnesium as insulin drives them intracellularly; replace electrolytes aggressively, especially phosphate.
Feeding Targets and Ileus vs. Obstruction
General ICU energy targets are roughly 25-30 kcal/kg/day with 1.2-2.0 g/kg/day protein; critically ill and burn/trauma patients need the higher protein range. Trophic (low-rate) feeding is acceptable early in ARDS and does not worsen outcomes versus full feeding in the first week. Distinguish paralytic ileus (absent bowel sounds, gas throughout including colon, from opioids, electrolyte derangement, or a post-op state) from mechanical obstruction (colicky pain, distension, air-fluid levels, a transition point). Ileus is managed by removing offending drugs, correcting potassium and magnesium, and bowel rest; obstruction may need decompression or surgery. Ogilvie syndrome (acute colonic pseudo-obstruction) can respond to neostigmine under monitoring.
Putting It Together: A Worked Scenario
A post-operative patient with a distended abdomen has an intra-abdominal (bladder) pressure of 22 mmHg, urine output dropping to 10 mL/hr, and peak airway pressures climbing. Recognize abdominal compartment syndrome: the priority is to lower IAP—decompress the stomach, drain ascites, deepen sedation, and consider neuromuscular blockade; if organ failure persists, prepare for decompressive laparotomy. Adding fluid would worsen the compartment, and blaming the ventilator would delay lifesaving decompression. This sequence—recognize the pattern, relieve the pressure, escalate to surgery—captures how the CCRN tests GI critical care.
A patient with severe epigastric pain radiating to the back has a lipase greater than three times the upper limit of normal. Which finding at 48 hours by the Ranson criteria signals a WORSE prognosis?
A ventilated patient after massive fluid resuscitation has a bladder (intra-abdominal) pressure of 24 mmHg, new oliguria, and rising peak airway pressures. This picture is BEST described and managed as:
A hemodynamically stable ICU patient with a functioning gastrointestinal tract requires nutrition support. Which approach reflects best practice?