Liver Cirrhosis Flashcards
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Is the end-stage of liver dz
Is characterized by extensive degeneration & destruction of liver cells
Results in the replacement of liver tissue by fibrosis (scar tissue) & regenerative nodules that occur from the liver’s attempt to repair itself
Cirrhosis
- Usually happens after decades of chronic liver dz
- Cirrhosis combined w/chronic liver dz ranks as 8th leading cause of death in the US
- Is twice as common in men compared to women
- Most common causes in US are chronic hepatitis C & alcohol-induced liver dz
- Chronic hepatitis combined w/alcohol ingestion has a synergistic effect in accelerating liver damage
- Approx 20% w/chronic Hep C & 10-20% w/chronic Hep B will develop cirrhosis
Other causes
> Extreme dieting, malabsorption, obesity
> Environmental factors
> Genetic predisposition
[Photo] - cirrhosis that developed 2° alcoholism
Characteristic diffuse nodularity of the surface is d/t the combo of regeneration & scarring of the liver
___ cirrhosis
Results from long-standing severe right-sided HF
> Causes venous congestion, parenchymal damage, necrosis of liver cells, & fibrosis over time
! Treatment towards managing underlying HF
Cardiac (cirrhosis)
___ cirrhosis
Includes primary biliary cirrhosis (PBC) & primary sclerosing cholangitis (PSC)
Biliary (cirrhosis)
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This is a chronic inflammatory condition affecting the liver & bile ducts that’s frequently found in men
Primary sclerosing cholangitis (PSC)
Clinical Manifestations
- Relatively few sx’s in early stage dz
- Fatigue & enlarged liver may be early sx’s
- Blood tests may be normal - compensated cirrhosis
Late Manifestations
- Result from liver failure & portal HTN
> Jaundice, peripheral edema, ascites
Other
> Skin lesions, hematologic disorders, endocrine disturbances, & peripheral neuropathies
- In adv stages, liver becomes small & nodular
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This condition results from decreased ability to conjugate & excrete bilirubin into the small intestines
Jaundice
Jaundice
- Overgrowth of connective tissue in liver compresses bile ducts
> Leads to obstruction
> Inc in bilirubin in vascular system
- May be minimal or severe, depending on ° liver damage
- Skin lesions
> D/t inc in circulating estrogen caused by inability of liver to metabolize steroid hormones
> Spider angiomas (telangiectasia or spider nevi)
> Palmar erythema
- Hematologic disorders
> Thrombocytopenia
Leukopenia
Anemia
Coagulation disorders
Thrombocytopenia, leukopenia, & anemia are thought to be caused by the splenomegaly that results from backup of blood from the portal vein into the spleen (__ __)
portal hypertension
Anemia can result from inadequate RBC production & survival, poor diet, poor absorption of folic acid, & bleeding from varices
Coagulation problems result from liver’s inability to produce PT & other factors essential for blood clotting
> Bleeding tendencies incl epistaxis, purpura, petechiae, easy bruising, gingival bleeding, & heavy menstrual bleeding
Endocrine disorders
- 2° to dec metabolism of hormones
- Gynecomastia, loss of axillary & pubic hair, testicular atrophy, impotence, & loss of libido (men) [d/t inc estrogen lvls]
- Amenorrhea or vaginal bleeding
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Hyperaldosteronism in both sexes
> If the liver fails to metabolize aldosterone adequately; subseq sodium & water retention & K loss
___ ___
Is a common finding in alcoholic cirrhosis & is probably d/t a dietary deficiency of thiamine, folic acid, & cobalamin
Usually results in sensory & motor sx’s, but sensory sx’s may predominate
Peripheral neuropathy
Patients who are cirrhotic but who have no obvious complications are considered to have ___ cirrhosis
compensated (cirrhosis)
Those who have 1 or more complications of their liver dz have ___ cirrhosis
decompensated (cirrhosis)
Major complications of cirrhosis
! Portal HTN w/resultant esophageal and/or gastric varices
! Peripheral edema & abd ascites
! Hepatic encephalopathy (mental status changes, incl coma)
! Hepatorenal syndrome (a late complication of cirrhosis aff kidneys & manifested by oliguria, elevated BUN & creatinine, & inc urine osmolarity)
___ ___
- Increased venous pressure in portal circulation
- Splenomegaly
- Large collateral veins
- Ascites
- Gastric & esophageal varices
Portal hypertension
Esophageal varices [80%]
> A complex of tortuous, enlarged veins @ lower end of the esophagus
Gastric varices [make up 20% of all varices]
> Located in upper portion of stomach
Both are very fragile, bleed easily
> Ruptured are the most life-threatening complication of cirrhosis & are a med emergency
Peripheral edema
↓ colloidal oncotic pressure from impaired liver synthesis of albumin
↑ portacaval pressure from portal HTN
Occurs as lower extremities [ankle]/presacral edema
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Is the accumulation of serous fluid in the peritoneal or abdominal cavity
> Several mechanisms lead to this
Ascites
Mechanisms
> Portal hypertension
- causes proteins to shift from blood vessels into lymph space
- when lymphatic system unable to carry off excess proteins & water, they leak into peritoneal cavity
- osmotic pressure of proteins pulls add’l fluid into peritoneal cavity
> Hypoalbuminemia
- d/t liver’s dec ability to make albumin
- results in dec colloidal oncotic pressure
> Hyperaldosteronism
- happens when aldosterone is metabolized by damaged hepatocytes
- inc lvl of aldosterone causes inc Na reabsorption by renal tubules
- retention of Na combined w/an inc in ADH in blood, leads to add’l water retention
- b/c edema formation, there’s dec intravascular volume & subs dec renal blood flow & glomerular filtration
Mechanisms of Ascites - Pathophysiology Map
- Abd distention; weight gain
- Eversion of umbilicus
- Abd striae w/distended abd wall veins
- Sx’s of dehydration (dry tongue & skin; sunken eyeballs; muscle weakness)
- Dec u/o
- Hypokalemia d/t hyperaldosteronism & diuretic therapy
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Is a bacterial infection of the ascites fluid; occurs in 15-25% of hospitalized pts w/cirrhosis & ascites; particularly common >variceal hemorrhage
> E. coli causative
Spontaneous bacterial peritonitis (SBP)
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Is a neuropsychiatric manifestation of liver dz
- Neurotoxic effects of ammonia
- Abn neurotransmission
- Astrocyte swelling
- Inflammatory cytokines
Hepatic encephalopathy
- Liver unable to convert inc ammonia
- Ammonia crosses blood-brain barrier
- Changes in neurologic & mental responsiveness
- Impaired consciousness and/or inappropriate behavior
- Sleep disturbances, trouble concentrating, coma
- Grading system of stages 0-4, 4 being most advanced (textbook has stages 1-4, p. 1157)
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Flapping tremors most common in arms & hands
Asterixis
- Impairment in writing
> Difficulty in moving pen left to right
> ___ (difficulty to construct simple figures)
> Hyperventilation, hypothermia, tongue fasciculations, & grimacing/grasping reflexes
apraxia
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Is a musty, sweet odor of the pt’s breath
Odor is from the accumulation of digestive byproducts that the liver is unable to degrade
Fetor hepaticus
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- Is a type of renal failure w/azotemia, oliguria, & intractable ascites
- No structural abnormality of kidneys
- Portal HTN → vasodilation → renal vasoconstriction
- Treat w/liver transplantation
Hepatorenal syndrome
- In the pt w/cirrhosis, this typically follows diuretic therapy, GI hemorrhage, or paracentesis
Pathophysiology of Cirrhosis
Systemic clinical manifestations of liver cirrhosis
Diagnostic Studies
- Liver enzyme tests
> Alkaline phosphatase, AST, ALT, GGT are initially elevated b/c release from inflamed liver cells
> In end-stage dz, AST & ALT lvls may be normal d/t death & loss of hepatocytes
↓ serum total protein & albumin levels
↑ serum bilirubin & globulin levels
- Prolonged prothrombin time
- Dec cholesterol levels
- US elastography (Fibroscan) [to quantify the ° of liver fibrosis]
- Liver biopsy
- Diff analysis of ascitic fluid
Interprofessional Care
- Rest
- Admin of B-complex vitamins
- Avoidance of alcohol
- Minimization or avoidance of asa, acetaminophen, & NSAIDs
- Ascites
- Sodium restriction (based on ° of ascites)
> 2 g/day
> Severe = 250-500 mg/day - Albumin (infusion to maintain intravascular volume & adequate u/o by inc plasma colloid oncotic pressure)
- Diuretics
- Tolvaptan (Samsca)
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Is an effective diuretic, even in pts w/severe ascites
Is also an antagonist of aldosterone & is K-sparing
spironolactone (Aldactone)
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This is a high-potency loop diuretic that’s freq used in combo w/a K-sparing drug
furosemide (Lasix)
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A vasopressin-receptor antagonist, often seen in pts w/cirrhosis
Causes an inc in water excretion, resulting in an inc in serum Na conc
Tolvaptan (Samsca)
- Paracentesis
- Transjugular intrahepatic portosystemic shunt (TIPS)
> Is used to alleviate ascites that doesn’t respond to diuretics
- Peritoneovenous shunt
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This is a surgical procedure that provides continuous reinfusion of ascitic fluid into the venous system
Peritoneovenous shunt
Its use has almost been eliminated b/c high rate of complications
Esophageal & gastric varices - Prevent bleeding/hemorrhage
- Avoid alcohol, asa, NSAIDs
- Screen for presence w/upper endoscopy (EGD)
- Nonselective β-blocker
- nadolol (Corgard)
- propranolol (Inderal)
> Reduces incidence of hemorrhage by dec high portal pressure, which dec risk for rupture
- If bleeding occurs, stabilize pt, manage airway, provide IV therapy, & blood products
Drug therapy
> octreotide [Sandostatin] (somatostatin analog)
> Vasopressin [VP]
Endoscopic therapy
> Band ligation
> Sclerotherapy
- IV admin of octreotide or VP produces vasoconstriction of the splanchnic arterial bed, dec portal blood flow, & dec portal HTN
- Now, octreotide is more widely used in this setting b/c of its limited side effect profile when compared w/VP
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Involves injection of a sclerosing solution into the swollen veins through an injection needle that’s placed through the endoscope
Sclerotherapy
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Is placement of a small rubber band (elastic O-ring) around the base of the varix (enlarged vein)
Endoscopic variceal ligation (EVL or “banding”)
Balloon tamponade
> Controls the hemorrhage by mechanical compression of varices
Sengstaken-Blakemore tube
> Minnesota tube
Linton-Nachlas tube
Sengstaken-Blakemore tube
- Tube inserted into esophagus & stomach; 3 lumens
SAFETY ALERT
- Label each lumen to avoid confusion
- Secure the tube to prevent movement of the tube which could result in occlusion of the airway
- Deflate balloons for 5 min every 8 to 12 hrs per institutional policy to prevent tissue necrosis
Supportive measures for acute bleed
- Fresh frozen plasma & packed RBCs
- Vitamin K (Aquamephyton [phytonadione])
- Antibiotics (prevent bacterial infection)
- Proton pump inhibitors (pantoprazole [Protonix])
- Lactulose (Cephulac) & rifaximin (Xifaxan)
- Prevent hepatic encephalopathy from breakdown of blood & release of ammonia in intestine
Long-term management
- Nonselective β-adrenergic blockers
- Repeated band ligation
- Portosystemic shunts
Shunting procedures
- Used more after 2nd major bleeding episode
- Nonsurgical: TIPS [transjugular intrahepatic portosystemic shunt]
- Surgical: portacaval & distal splenorenal shunt
Currently, the surgical shunts most commonly used are the portacaval & distal splenorenal shunt
Total portal diversion after TIPS
- A catheter is placed in the jugular vein & then threaded through the superior & inferior vena cava to the hepatic vein
- Wall of hepatic vein is punctured, & the catheter is directed to the portal vein
- Stents are positioned along the passageway, overlapping in liver tissue & extending into both veins
- This reduces portal venous pressure & decompresses the varices, thus controlling bleeding
! TIPS does not interfere w/a future liver transplantation
! Is contraindicated in pts w/severe hepatic encephalopathy, hepatocellular carcinoma, severe hepatorenal syndrome, & portal vein thrombosis
Portacaval shunt
Portal vein is anastomosed to the IVC, diverting blood from the portal vein to the systemic circulation
Distal splenorenal shunt
Splenic vein is anastomosed to the renal vein
Portal venous flow remains intact, & esophageal varices are selectively decompressed
Spleen conducts blood from the high-pressure esophageal & gastric varices to the low-pressure renal vein
Interprofessional Care - Hepatic encephalopathy
- Reduce ammonia formation
- Lactulose (Cephulac), which traps ammonia in gut
- Rifaximin (Xifaxan) antibiotic
- Prevent constipation
- Treatment of precipitating cause
- Lowering dietary protein intake
- Preventing & controlling GI bleeding
- Remove blood from GI tract
Drug therapy
- Not specific for cirrhosis
- Used to treat symptoms & complications of advanced liver dz
Diet for patients w/o complications
- High in calories (3000 cal/day)
- ↑ carbohydrate
- Moderate to low fat
- Protein restriction rarely justified
> For many pts, malnutrition is a more serious clinical problem than hepatic encephalopathy
- Protein supplements for protein-calorie malnutrition
- Low-sodium diet for pt w/ascites & edema
- Seasonings to make food more palatable
- Collaborate w/a dietician
Past Health History
- Hepatitis
- NASH
- Chronic biliary obstruction & infection
- Severe right-sided HF
Rx’s
- Adverse rxn’s
- Anticoagulants, asa, NSAIDs, acetaminophen
Health perception-health management
- Chronic alcoholism
- Weakness, fatigue
Nutritional-metabolic
- anorexia, wt loss
- Dyspepsia
- N/V
- Gingival bleeding
Elimination
- dark urine
- dec u/o
- light-colored or black stools
- flatulence
- change in bowel habits
- dry, yellow skin
- bruising
Cognitive-perceptual
- dull, RUQ or epigastric pain
- numbness, tingling of extremities
- pruritus
Sexuality-reproductive
- impotence
- amenorrhea
General
- fever, cachexia, wasting of extremities
Integumentary
- icteric sclera, jaundice
- petechiae, ecchymoses
- spider angiomas, palmar erythema
- alopecia, loss of axillary & pubic hair
- peripheral edema
Respiratory
- shallow, rapid respirations
- epistaxis
Gastrointestinal
- abd distention, ascites
- distended abd wall veins
- palpable liver & spleen
- foul breath
- hematemesis; black, tarry stools
- hemorrhoids
Neurologic
- altered mentation, asterixis
Reproductive
- gynecomastia & testicular atrophy (men)
- impotence (men)
- loss of libido (men/women)
- amenorrhea or heavy menstrual bleeding (women)
Possible diagnostic findings
- anemia, thrombocytopenia, leukopenia
- ↓ serum albumin & K levels
- Abn LFT’s
- ↑ INR, ammonia, & bilirubin levels
- Abn find on abd US or MRI
Nursing Diagnoses (for the pt w/cirrhosis)
- Imbalanced nutrition: less than body requirements
- Impaired skin integrity
- Excess fluid volume
- Ineffective health management
- Dysfunctional family processes
Overall Goals (for the pt w/cirrhosis)
- Have relief of discomfort
- Have minimal to no complications (ascites, esophageal varices, hepatic encephalopathy)
- Return to as normal a lifestyle as possible
Health Promotion
- Reduce or eliminate risk factors
- Treat alcoholism
- Maintain adequate nutrition
- Identify & treat acute hepatitis
- Bariatric surgery for morbidly obese (reduces incidence of NAFLD)
Acute Care
Rest needs
> Prevent complications
> Modify schedule
Nutritional needs
> Oral hygiene
> Between-meal nourishment
> Food preferences
> Explanation of dietary restrictions
Assess for jaundice
Measures to relieve pruritus
- Cholestyramine or hydroxyzine
- Baking soda or Alpha Keri baths
- Lotions, soft or old linen
- Temperature control
- Short nails; rub w/knuckles
Monitor color of urine & stools
- when jaundice is present, the urine is often dark brown & the stool is gray or tan
- Accurate I&O recording
- Daily wt measurement
- Extremities measurement
- Abd girth measurement
Acute Care - Paracentesis
- Pt voids immediately before
- When done, place in high-Fowler’s position or sitting on side of bed
- Monitor for hypovolemia & electrolyte imbalances
- Monitor BP & HR
- Monitor dressing for bleeding/leakage of ascitic fluid
Acute Care - Relief of dyspnea
- semi- or high Fowler’s position
Skin care
- special mattress
- turning schedule, @ least q2h
- ROM exercises
- C&DB exercises
- Elevate lower extremities/scrotum [edema]
! Dyspnea is a freq problem for the pt w/severe ascites & can lead to pleural effusions
Monitor for F&E disturbances
- Hypokalemia
- Water excess (hyponatremia)
- Observe for bleeding disorders
- Assess pt’s response to altered body image
> Supportive listening
Acute Care - Bleeding varices
- Close observation for signs of bleeding
- Balloon tamponade care
> Explanation of procedure
> Check for patency
> Position of balloon verified by x-ray
Acute Care - Bleeding varices
- Close observation for signs of bleeding
- Balloon tamponade care
> Explanation of procedure
> Check for patency
> Position of balloon verified by x-ray
! Monitor for complications (i.e., aspiration, pneumonia)
- Scissors @ bedside
- Semi-Fowler’s position
- Oral/nasal care
Acute Care - Hepatic encephalopathy
- Maintain safe environment
- Assess carefully; sustain life
! Reduce ammonia formation
! At risk for falls d/t confusion
- Level of responsiveness
- Sensory & motor abnormalities
- F&E imbalances
- Acid-base imbalances
- Effects of treatment measures
- Perform neurologic assessment every 2 hrs
- Prevent falls & injuries
- Minimize constipation (reduce ammonia production)
- Encourage fluids (if not contraindicated)
- Control factors known to precipitate encephalopathy
> GI bleeding
> Constipation (d/t dehydration, opioid rx’s)
Supportive measures
* Proper diet
* Rest
* Avoidance of hepatotoxic OTC rx’s [acetaminophen in high doses]
* Abstinence from alcohol
Caring attitude always
- Community support programs (AA)
- Sx’s of complications
- When to seek medical attention
- Written instructions w/adequate explanations for pt/family
- Referral to community or home health RN
Evaluation - Expected Outcomes
✓ Maintain food & fluid intake adequate to meet nutritional needs
✓ Maintain skin integrity w/relief of edema & pruritus
✓ Experience normalization of fluid balance as a result of medical & nursing interventions
✓ Acknowledge & get treatment for a substance abuse problem
