Liver disease and complications

Liver items ask which failing job is killing the client right now: clotting and varices, ammonia and the brain, or fluid in the belly crowding the lungs. Active upper GI bleed sequences also live in GI bleeding and obstruction. This chapter owns the cirrhosis complication map around them.

What cirrhosis breaks

A scarred liver cannot clear toxins, make clotting factors, or keep portal blood flowing easily. Portal hypertension backs blood into esophageal and gastric varices and pushes fluid into the abdomen as ascites. Lost synthetic function means easy bruising and prolonged bleeding. Failed detox means ammonia rises and the brain slows. Low albumin worsens fluid shift. Name which failure is in front of you before you pick a first action.

Bedside baseline for any advanced liver client: fall risk, bleeding precautions, daily weights, and a neuro check that catches subtle confusion early. Small insults tip compensated cirrhosis into failure: infection, a GI bleed, constipation that keeps ammonia in the gut, dehydration, or sedating drugs that mask mentation. The distractor is treating sleepy as rest when it is early encephalopathy, or scrubbing fragile skin until it bleeds.

Varices: the bleed that rewrites the shift

Varices are thin-walled veins under high pressure. Vomiting bright red blood or coffee-ground material with tachycardia and hypotension is the same upper-bleed emergency as elsewhere (airway, oxygen as needed, large-bore access, volume support, NPO, notify), but the cirrhotic client may crash faster and tolerate less volume overload. Coagulopathy and thrombocytopenia make every invasive move riskier.

1. Hematemesis with unstable vitals: emergency bleed pathway now.
2. Known varices: no blind NG. Follow ordered endoscopy, banding, or drug pathway.
3. Avoid straining and rough-food teaching when varices are active as ordered.
4. After a bleed, watch for encephalopathy. Blood in the gut is a classic ammonia load.

Why blind NG is dangerous: the tube can lacerate fragile variceal veins and convert a smoldering risk into exsanguination. If decompression is needed, it follows a deliberate order and plan, not habit. Beta-blocker or vasoactive pathways appear in some stems as ordered prevention or acute adjuncts. Nursing owns recognition, NPO, access, and escalation.

Ascites and breathing

Ascites is portal pressure plus low oncotic pull dumping fluid into the peritoneum. The abdomen swells, the diaphragm rises, and breathing shortens. Nursing moves are measurement and gentle unloading: sodium restriction as ordered, diuretics carefully (often spironolactone with or without a loop agent as ordered), daily weights and girth, elevate the head of the bed for work of breathing, and prepare for paracentesis when ordered.

After large-volume paracentesis, fluid shifts can drop blood pressure. Albumin replacement, when ordered, is about supporting intravascular volume, not a protein party. Spontaneous bacterial peritonitis can look like worsening ascites plus fever, abdominal pain, or encephalopathy. Escalate rather than blaming diet alone.

• Sudden weight jump or tighter belly: assess breathing and notify.
• After paracentesis: vitals, puncture site, and volume status.
• Upright positioning helps the diaphragm when the belly is tight.

Hepatic encephalopathy and lactulose

When the liver cannot clear ammonia and related toxins, neurons misfire. Early cues are sleep inversion, mild confusion, personality change, and handwriting change. Later you see asterixis (liver flap), marked confusion, and coma. Fetor hepaticus (musty breath) signals advanced failure. Constipation, GI bleeding, infection, dehydration, and excess dietary protein load are classic triggers because they raise the ammonia burden.

Lactulose: mechanism and hold rules

Lactulose acidifies the gut and promotes stools that carry ammonia out as ammonium. The goal is soft, frequent stools as ordered, not watery collapse. If the client has severe diarrhea, dehydration, or hypokalemia, hold and notify per protocol rather than pushing more until clean. Hypokalemia itself can worsen encephalopathy, so chasing diarrhea without electrolyte attention fails the stem.

Protein teaching is nuanced on exams. During active encephalopathy, follow the ordered restriction or modified intake. When stable, adequate protein for healing returns under dietitian guidance. Antibiotics that reduce gut ammonia-producing bacteria appear in some stems as ordered adjuncts. The wrong answer is a high-protein celebration tray for a confused client to build strength, or benzodiazepines for sleep that hide declining LOC.

Jaundice, itch, and daily teaching

Bilirubin backs up when the liver cannot conjugate or drain bile. Skin and sclera yellow, urine darkens (conjugated bilirubin in urine), stools lighten when bile does not reach the gut, and bile salts itch. Cool baths, mild soap, trimmed nails, loose clothing, and ordered antipruritics beat hot showers that worsen itch. Scratching open skin invites infection the cirrhotic client cannot afford.

• Alcohol cessation and infection avoidance keep the next tip into failure from starting.
• Many drugs are hepatically cleared. Review the med list rather than adding sedatives casually.
• Bleeding precautions: soft toothbrush, electric razor, careful IV and IM decisions per policy.
• Pancreatitis and surgical GI recovery stay in the GI-bleed chapter when those stems appear.

Teaching that sticks is practical: how to weigh daily at home, which foods hide sodium, when to call for black stools or confusion, and why lactulose continues even after the client feels clearer. Shame-based alcohol lectures without a safety plan do not replace clear complication teaching.

Priority map