Cirrhosis/liver failure complication

  1. Complications
    • Portal HTN
    • Esophageal varices
    • infection
    • edema
    • ascites
    • hepatic encephalpathy
    • hepatarenal syndrome
  2. Portal Htn
    • Persistent elev BP in the portal venous system
    • due to incr resistance to/obstruction of blood flow into the liver
    • - compression & destruction of liver and portal circulation
    • backs up in the GI, esophagus, spleen, rectum
  3. Portal HTN
    collateral vessels develop
    • to relieve pressure
    • reduce increased plasma volume
    • return of blood to right atrium
    • Other organs become congested:
    • - spleen
    • - GI
    • for collateral vessels: helps to bypass congestion, thin wall, help to bring blood flow to the heart
  4. Portal HTN
    • development of collateral vessels
    • ascites
    • splenomagly
    • varices
    • hepatic encephalopathy
  5. Collateral vessels
    • often asymptomatic until bleed
    • develops due to incr pressure in the portal system (vein)
    • lower esophagus, anterior abd wall, peritoneum, rectum
    • - **varicosites**- esophageal, gastric varices, caput medusae, hemorrhoids
    • - weak, fragile, thin walled vessels can rupture under pressure or with external irritation
  6. Collateral Vessels
    Most life threatening complications
    • 30-50% die within 6 wk of 1st esophageal bleed
    • can have massive bleed
    • hemorrhagic shock- decr perfusion-- end organ damage
    • - hypovolemic shock
    • - review past info on hypovolemic shock
  7. Varices
    • dilated tortuous veins
    • - esophageal: lower end of the esophagus
    • - Gastric: upper portion of the stomach
    • Rupture and bleed in response to ulceration/irritation
    • - alcohol ingestion, swallowing of rough/coarse foods, acid reflux, vomiting, passage of NGT, meds, incr abd pressure, cough
  8. Varices
    the patient may present with melena, hematemesis, slow oozing or massive,sudden exsanguination (bleed out)
  9. Varices
    • bleeding
    • increase risk of hepatic encephalopathy- worst if bleed. bc of breaking down protein RBC- hemoglobin is protein
  10. Ascites
    • accumulation of serous fluid in peritoneal space
    • -peritoneal membranes
    • elevated pressure in portal vein- incr hydrostatic pressure- fluid shifts
  11. Ascites 2
    • hypoalbuminemia worsens this- cause dec colloidal oncotoc pressure
    • excess aldosterone
    • - steroid/hormone liver can't metabolize all our hormones
  12. Ascites 3
    • intravascular hypovolemia
    • decre blood flow to kidneys
    • stimulates renin and RAAS
    • further adds to fluid retention
    • fluid ends up in peritoneum
  13. Ascites S&S
    • Abdominal distention
    • wt gain
    • abdominal striae
    • signs of hypovolemia
    • hypokalemia (aldosterone)- bc we have extra aldosterone it kicks out K
    • pushes other organs- SOB, bowel changes
    • increa risk of infection
  14. Infection
    • blood does not reach the Kupffer cells (plays a role w/the immune system- blood can't get to it) due to portal HTN/collateral circulation
    • Leukopenia due to splenomagaly
    • spontaneous bacterial peritonitis
    • - bacteremia due to translocation of intestinal flora (usually gram negative)
    • - usually asymptomatic
    • - leading cause of hepatorenal syndrome
    • (think the bowel leaks bacteria out, infection is in the peritoneal space)
    • usual peritoneal has 5-15ml in it...with ascites u can pull liters.
  15. Edema
    • decr oncotic pressure (albumin)
    • incre hydrostatic pressure
    • over production of aldosterone
    • seen: ankle and sacral area- can be generalized
    • usuall occurs with ascites
  16. Hepatic Encephalopathy
    normal ammonia working
    • cause not known fully
    • known to be due in part to inability to metabolize ammonia (NH3)
    • NH3 normally produced in the GI tract when protein broken down by bacteria
    • NH3 normally travels to the liver to be converted to urea, then sent to kidney for excretion
  17. Hepatic Encephalopathy
    • with cirrhosis, liver does not clear NH3 well
    • - shunted blood is not cleared at all
    • large amts of NH3 stay in circulation
    • crosses blood-brain-barrier, toxic
    • CNS depressant
  18. What incr Hepatic encephalopathy
    • NH3 accumulation may incr w/factors:
    • GI bleeding
    • high protein diet
    • constipation
    • infection
    • dehydration
  19. hepatic encephalopathy
    • onset can be insidious and suble or can be acute secondary to large bleed
    • grading tool 0-4
    • - west haven criteria
    • - changes in LOC, cognitive fx, behaviors
  20. HE
    • range: sleep distrubances, lethargy to deeply comatose (person can wake when arouse but goes right back to sleep)
    • earliest symptoms:
    • - minor mental statuses changes- personality changes, irritability, agitation, lack of awareness (safety)
    • - motor disturbances
    • also: impairment in memory, attention and concentration, computation, impaired responses
  21. HE
    later s/s
    • slow/slurred speech becoming incomprehensible
    • impaired judgement, inapproriate behavior
    • inc confusion
    • inc drowsiness, difficult to awaken
    • abnormal reflexes
  22. HE
    advancing towards comatose
    • Asterixis (liver flap)- when u extend hands and it starts flapping up and down
    • constructional apraxia, significant changes in handwriting (not able to copy shapes)
    • fetor hepaticus- musty sweet odor (breath) d/t byproduct of ammonia
  23. Hepatorenal syndrome
    • poor prognosis indicator
    • mult changes from liver failure lead to renal failure
    • - portal htn, liver decompensation and decr circulating blood volume (not being profused)
    • significant ascites
    • tx- liver transplant
Card Set
Cirrhosis/liver failure complication