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Liver Cirrhosis

Liver cirrhosis is a chronic disease marked by the replacement of normal liver tissue with fibrosis, disrupting liver function. The main types include alcoholic cirrhosis, postnecrotic cirrhosis, and biliary cirrhosis, each with distinct causes and symptoms. Complications can include ascites, hepatic encephalopathy, and esophageal varices, requiring specific medical management and nursing interventions to address symptoms and prevent further complications.

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0% found this document useful (0 votes)
20 views5 pages

Liver Cirrhosis

Liver cirrhosis is a chronic disease marked by the replacement of normal liver tissue with fibrosis, disrupting liver function. The main types include alcoholic cirrhosis, postnecrotic cirrhosis, and biliary cirrhosis, each with distinct causes and symptoms. Complications can include ascites, hepatic encephalopathy, and esophageal varices, requiring specific medical management and nursing interventions to address symptoms and prevent further complications.

Uploaded by

jessie marietan
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd

LIVER CIRRHOSIS

●​ a chronic, degenerative disease characterized by


replacement of normal liver tissue with diffuse fibrosis that
disrupts the structure and function of the liver

TYPES
A.​ Alcoholic Cirrhosis ( Laennec’s Cirrhosis)
○​ Most common type of liver cirrhosis
○​ Caused by chronic alcoholism

B.​ Postnecrotic cirrhosis


○​ Late result of a previous bout of acute viral hepatitis ASSESSMENT: Clinical manifestations

C.​ Biliary cirrhosis S/Sx (Early)


○​ Resulted from chronic biliary obstruction and ●​ anorexia, nausea, indigestion
infection ●​ aching or heaviness in right upper quadrant
○​ Least common type ●​ weakness & fatigue

PREDISPOSING/PRECIPITATING FACTORS S/Sx (Late)


●​ Malnutrition ●​ abnormal liver function tests: ​
●​ Effects of alcohol abuse ○​ ↑ bilirubin (N=0-0.9mg/dl)
●​ Chronic impairment of bile excretion – biliary obstruction in ○​ AST (N=4.8-19U/L)
the liver and common bile duct (gallbladder stones) ○​ ALT (N= 2.4-17U/L)
●​ Necrosis from hepatotoxins or viral hepatitis ○​ Serum alkaline phosphatase (N=30-40U/L)
●​ Congestive heart failure ○​ Ammonia (plasma) (N= 15-45umol/L)
●​ intermittent jaundice, pruritus
PATHOPHYSIOLOGY ●​ edema, ascites, prominent abdominal wall veins
●​ liver cell damage result in inflammation & hepatomegaly ●​ Ecchymosis, bleeding tendencies
●​ attempts at regeneration eventually result to fibrosis and a ●​ anemia
small nodular liver ●​ Infection
●​ hepatic function is slowly impaired ●​ Gynecomastia, testicular atrophy
●​ obstruction of venous channels blocks hepatic blood flow ●​ Neurologic changes
and cause portal hypertension
Assist with Paracentesis
Complications of Liver Cirrhosis ●​ have the client void before the procedure
1.​ Ascites ●​ high –fowlers position during the procedure
●​ abnormal intraperitoneal accumulation of watery fluid ●​ monitor pt. for hypovolemia & electrolyte imbalance
containing small amounts of protein ●​ observe puncture wound for leakage & signs of infection
●​ Due to
○​ ↑ intravascular colloidal pressure 2.​ Hepatic Encephalopathy
●​ cerebral dysfunction assoc. with severe liver disease
○​ ↑ capillary hydrostatic pressure
●​ inability of the liver to metabolize substances that can be
○​ Na and H2O retention
toxic to the brain such as ammonia, which is produced by
○​ Failure of the liver to metabolize aldosterone
the breakdown of protein in the intestinal tract

S/Sx
●​ abdominal enlargement, wt.
●​ fatigue
●​ abdominal discomfort, respiratory difficulty

Med. Mgt. (depending on severity of ascites)


✔Na+ & fluid restriction (500-1000 ml/day)
✔diuretic therapy (furosemide/ spironolactone)
✔Paracentesis – for diagnosis or when fluid volume compromise
comfort & breathing

Nursing Interventions to ↓ ascites & increase/promote comfort


✔ maintain on bed rest
✔ fluid & Na restriction
✔ monitor I/O, daily wt.
✔ measure abd. girth every shift
✔ Maintain high-Fowlers for max. respiration
✔ support abdomen with pillows
✔ administer diuretics, salt-poor albumin IV as ordered
-​ monitor for signs of CHF, pulmonary edema, dehydration,
electrolyte imbalance, hypersensitivity reaction
Encephalopathy 3.​ Esophageal Varices
S/Sx ●​ distention of the smaller blood vessels of the esophagus as a
●​ Asterixis - flapping hand tremors (early sign) result of portal hypertension – due to obstruction of venous
●​ LOC – lethargy progressing to coma circulation w/in the damaged liver
●​ mental status, confusion, disorientation ●​ the ↑ portal venous pressure causes blood to be forced into
●​ dullness, slurred speech these vessels – become tortuous and fragile
●​ behavioral changes, lack of interest in grooming/ appearance ●​ blood vessels become prone to injury by mechanical trauma
●​ twitching, muscular incoordination, tremors from ingestion of coarse food and acid pepsin erosion which
●​ Fetor hepaticus may result in bleeding
●​ elevated serum ammonia level ●​ bleeding may also occur as a result of coughing, vomiting,
sneezing, straining at stool or any physical exertion that
Hepatic Encephalopathy abdominal venous pressure
Interventions:
a.​ ↓ ammonia production S/Sx:
●​ ↓ dietary protein to 20-40 g/day, maintain adequate calories ▪ ●​ upper GI bleeding (hematemesis) - melena
●​ ↓ ammonia formation in the intestine – give laxative, enema ●​ massive hemorrhage
as ordered and Neomycin - ↓ bacterial ammonia production ●​ signs/symptoms of hypovolemic shock

b.​ Protect pt. from injury Med. Mgt.


●​ side rails up ✔ find the source of bleeding – esophagoscopy, angiography
●​ turning to side ✔ control bleeding
●​ assess mental status, LOC a.​ Gastric lavage, administration of antacid via NGT
●​ proper positioning (semi-Fowler’s) b.​ Surgical bypass procedures (splenorenal shunt)
●​ prevent aspiration c.​ Variceal band ligation (esophageal variceal ligation (EVL)
d.​ Endoscopic sclerotherapy or injection sclerotherapy
c.​Prevent further episodes of encephalopathy e.​ Balloon tamponade
●​ low protein diet ●​ insertion of Sengstaken–Blakemore tube with
●​ prescribed medications gastric and esophageal balloon that are inflated to
●​ avoid constipation ( to ammonia production by bacteria in stop bleeding
the GIT)
●​ early signs of encephalopathy (restlessness, slurred speech,
dec. attention span)
POSSIBLE NURSING DIAGNOSES
●​ Activity intolerance R/T fatigue, lethargy, and malaise
●​ Imbalanced nutrition R/T abdominal distention and
discomfort, and anorexia
●​ Impaired skin integrity R/T pruritus from jaundice and
edema
●​ High risk for injury R/T altered clotting mechanisms and
altered LOC
●​ Disturbed body image R/T changes in appearance, sexual
dysfunction, and role function
●​ Chronic pain R/T enlarged tender liver and ascites
●​ Fluid volume excess R/T ascites and edema formation
●​ Ineffective breathing pattern R/T restriction of thoracic
excursion secondary to ascites and abdominal distention

NURSING INTERVENTIONS
1.​ Reduce metabolic demands on the liver
●​ provide bed rest
●​ eliminate ingestion of toxic substances to the liver: sedatives
opiates, alcohol, acetaminophen
●​ ↓ activities

2.​ Provide adequate nutrition & hydration


●​ Low – protein, high-carbohydrate, high calorie, sodium-
restricted diet
●​ multiple vitamin therapy
●​ restrict fluids & sodium if there is edema or ascites
●​ provide mouth care before meals
●​ monitor I/O, daily wt.

3.​ Prevent infection


●​ encourage good personal hygiene
●​ reverse isolation
●​ assess for signs of infection esp. urinary
●​ encourage deep breathing/position changes
4.​ Protect pt. from bleeding
●​ monitor urine, stool, gums, skin for signs of bleeding/
bruising
●​ avoid injections, apply pressure to venipuncture sites for at
least 5 mins.
●​ Monitor prothrombin time, bleeding time
●​ Teach pt. to use soft toothbrush, avoid constipation
●​ Prevent scratching from pruritus, proper skin care
●​ Administer Vit. K as ordered

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