6.4 Hepatic, Pancreatic & Nutritional Disorders

Hepatic, Pancreatic & Nutritional Disorders

The liver, pancreas, and nutritional status are deeply interconnected: hepatic failure disrupts metabolism and clotting, pancreatic inflammation is often self-digestive and rapidly severe, and malnutrition compounds every other critical illness by impairing wound healing and immune function.

Cirrhosis and Portal Hypertension

Cirrhosis is irreversible scarring of the liver from chronic injury (alcohol use, viral hepatitis, metabolic-associated liver disease, autoimmune disease). Scarring raises resistance to portal blood flow, causing portal hypertension, which drives the classic complications progressive care nurses manage: esophageal and gastric varices (dilated collateral vessels at risk of catastrophic rupture), ascites (fluid shifting into the peritoneal cavity, managed with sodium restriction, diuretics such as spironolactone plus furosemide, and therapeutic paracentesis), and hepatic encephalopathy from impaired ammonia clearance. Cirrhotic patients also develop coagulopathy because the liver produces most clotting factors, so an elevated INR and thrombocytopenia — the latter from splenic sequestration secondary to portal hypertension — are expected findings, not incidental abnormalities.

Cirrhosis severity and short-term prognosis are commonly quantified with the Child-Pugh score, which assigns points across five clinical and laboratory findings:

Total scores of 5-6 points define Class A (best prognosis), 7-9 points define Class B, and 10-15 points define Class C (decompensated, highest short-term mortality risk) — a classification progressive care nurses use to anticipate which patients are most likely to develop variceal bleeding, refractory ascites, or hepatorenal syndrome during the admission.

Hepatitis, whether viral, alcoholic, autoimmune, or drug-induced, causes hepatocellular injury with elevated transaminases (AST/ALT), jaundice, and, in severe cases, progression to acute liver failure with coagulopathy and encephalopathy developing over days to weeks.

Two complications deserve special vigilance in cirrhotic patients. Spontaneous bacterial peritonitis (SBP) is an infection of ascitic fluid without an obvious surgical source, presenting with fever, abdominal pain, or unexplained clinical decline (sometimes subtly, as worsening encephalopathy); diagnosis requires paracentesis with fluid analysis showing an elevated absolute neutrophil count, and treatment is prompt IV antibiotics. Nursing care after a therapeutic paracentesis includes monitoring the puncture site for leakage, watching for hypotension from rapid fluid shifts, and administering albumin when large volumes are removed to prevent post-paracentesis circulatory dysfunction. Hepatorenal syndrome is a form of functional kidney failure that develops in advanced cirrhosis with portal hypertension, in the absence of other identifiable causes of kidney injury, and signals a poor prognosis without liver transplantation. Because these patients often already have low albumin and a fragile fluid balance, both diuretic dosing and IV fluid administration require careful titration to avoid tipping the patient into either worsening ascites or intravascular volume depletion that further stresses renal perfusion.

Pancreatitis

Acute pancreatitis is most commonly caused by gallstones or alcohol use, and results from premature activation of pancreatic enzymes that begin digesting the pancreas itself. Lipase is the more specific and reliable diagnostic marker; amylase rises and falls faster and is less specific, but both are typically included in the initial workup. Diagnosis generally requires two of three criteria: characteristic epigastric pain radiating to the back, lipase or amylase greater than three times normal, and confirmatory imaging.

Severity is assessed clinically and with scoring tools such as Ranson's criteria or BISAP, watching for complications including pancreatic necrosis, pseudocyst formation, and third-spacing of massive fluid volumes into the retroperitoneum, which can produce hypovolemic shock even without external fluid loss. Management centers on aggressive early fluid resuscitation, pain control, and early enteral nutrition once tolerated — current evidence favors early enteral feeding over prolonged bowel rest, since it maintains gut mucosal integrity and reduces infectious complications compared with withholding nutrition or defaulting to parenteral feeding.

Malnutrition and Failure to Thrive

Critically ill patients are frequently malnourished on admission or become malnourished during a prolonged stay, from increased metabolic demand, malabsorption, or inadequate intake. Failure to thrive and malabsorption syndromes impair wound healing, immune response, and muscle mass, including respiratory muscle strength, which can prolong ventilator weaning. Nutritional screening and early involvement of a dietitian are standard progressive care practice, and low prealbumin or albumin trends — recognizing both are affected by inflammation, not just nutrition — support ongoing monitoring. Prealbumin has a shorter half-life (about two days) than albumin (about three weeks), which makes it more useful for tracking short-term nutritional response, though acute inflammation depresses both regardless of intake.

Enteral and Parenteral Nutrition

The guiding principle is "if the gut works, use it" — enteral nutrition is preferred over parenteral whenever the GI tract is functional, because it preserves gut mucosal integrity, supports immune function, and carries a much lower infection risk than central-line-delivered total parenteral nutrition (TPN). Enteral feeding tube placement should be confirmed by x-ray before initial use, and gastric residual volumes and abdominal exam are monitored to detect intolerance. TPN is reserved for patients with a non-functional gut (bowel obstruction, ischemic bowel, severe ileus) and requires dedicated central line access, strict glucose monitoring, and infection-control vigilance.

Any patient who has been severely malnourished and starts aggressive nutritional repletion, enteral or parenteral, is at risk for refeeding syndrome: as the body shifts back to carbohydrate metabolism, insulin release drives phosphate, potassium, and magnesium intracellularly, producing dangerous hypophosphatemia, hypokalemia, and hypomagnesemia that can trigger cardiac arrhythmias and respiratory failure. Prevention requires starting nutrition slowly, replacing electrolytes proactively, and monitoring levels closely during the first several days of refeeding.