Fulminant hepatic failure (FHF)

Function of liver Def. of fulminant hepatic failure: Acute sever impairment of Diagnostic test: V-management of hematological changes:
• Detoxification : liver filters 1 liter of blood each minute and liver function associated with progressive mental changes in pt 1. Prolonged prothrombin time, decreased platelet • Administration of blood products: in patient
eliminates the multitude of toxins
had liver disease for less than 8 weeks 2. Elevated ammonia, amino acid with active bleeding, backed RBCs are
• Stores essential vitamins (like vitamins A, B, D, and K), minerals
(like iron and copper), and glucose (in the form of glycogen Causes of fulminant hepatic failure: ABCs 3. Hypoglycemia or hyperglycemia administered to treat a low Hb or Htc .
• Plays a key role in carbohydrate metabolism, by converting • A Acetaminophen, hepatitis A, autoimmune hepatitis 4. Dilutional hyponatremia or hypernatremia, • Infusion of fresh-frozen plasma to provide blood
glucose to glycogen. Glycogen is stored as fat in the body . • B Hepatitis B hypokalemia, hypocalcemia, and Hypomagnesemia. clotting factors, and platelet administration
• Converts vitamins, minerals, and amino acids into their • C Cryptogenic ,hepatitis C 5. CBC: thrombocytopenia, anemia. corrects thrombocytopenia.
biologically active forms For example, the liver activates B • D Hepatitis D, drugs (acetamenophine, and salicylate) 6. bile pigment: increased total bilirubin, and direct. • Pancreatic enzymes, if diarrhea and steatorrhea
vitamins; converts beta carotene to bio-available vitamin A
• E Esoteric causes - Wilson's disease, Budd-Chiari syndrome 7. Liver ultrasound establish patency and flow in are present, to permit better tolerance of diet.
• Helps to regulate blood sugar levels
• Regulates protein metabolism. (hepatic vein thrombosis) hepatic vein, artery, and portal vein, it excludes the • Gastric lavage with normal saline through NGT
• Immunity : liver produces some immune factors (such as • F Fatty Infiltration - acute fatty liver of pregnancy. presence of tumor ,establish presence of ascites. will control bleeding, remove toxins, blood clots,
fibrinogen) that help body fight off infection . • Wilson's disease rare inherited disorder that causes copper to 8. Liver biopsy shows cell necrosis, injury, fatty liver. and old blood from the stomach.
• Hormonal balance The liver converts the thyroid hormone accumulate in liver, brain and vital organs. Most people with 9. CT may show brain edema in FHF , brain herniation. • Supplemental vitamins (A, B complex, C, and K)
thyroxin (T4) into its more active form (T3) Wilson's disease diagnosed between ages of 5 and 35, but can and folate.
• Digestion and fat regulation: liver is responsible for the
affect younger and older people, as well. Copper plays key Medical management: • Antacids and histamine-2 (H2) antagonists to
production of bile that aids in the digestion of fats and fat-
soluble vitamins role in development of healthy nerves, bones, collagen and I-Correction of precipitating causes — reduce the risk of bleeding from stress ulcers.
Def. of Acute Liver Failure: is loss of liver function that skin pigment melanin. Normally, copper is absorbed from The first step is the identification and correction of
occurs rapidly — in days or weeks — usually in a person food, and excess is excreted through a substance produced in precipitating causes. Careful evaluation should be VI- Management of cardiovascular system
who has no preexisting liver disease. It's most commonly liver (bile). performed to determine the presence of any of the disturbances:
caused by a hepatitis virus or drugs, such as • Budd-Chiari syndrome is condition in which hepatic veins following: • hemodynamic monitoring including pulse , BP,
acetaminophen (veins that drain liver) are blocked or narrowed by clot . This • Hypovolemia and CVP Central venous pressure
blockage causes blood to back up into the liver, and as a • Gastrointestinal bleeding • As mention before, fluid administration using
Def. of cirrhosis: progressive disease of the liver result, the liver grows larger • Hypokalemia and/or metabolic alkalosis colloids, or crystolloids that increase the oncotic
Extensive parenchymal cell degeneration, Pathophysiology of fulminant hepatic failure • Hypoxia pressure.
Hepatic failure is accompanied by: • Sedatives or tranquilizers • Vitamin K administration.
Destruction of parenchymal cells It is irreversible Execratory : failure to excrete bilirubin resulting in • Hypoglycemia
end stage of many different hepatic injuries, hyperbilirubinemia (hemoglobin breackdown product=bilirubin). VII- management of pulmonary disturbances:
including steatohepatitis (i.e., “fatty liver”), the Clinical Manifestations fulminant hepatic failure II- Management of hepatic encephalopathy: • Elevate the head of bed 45-90 degree.
metal storage diseases, alcoholic liver disease, 1. Malaise, anorexia, nausea, vomiting, fatigue and clay color 1. Oral or rectal administration of lactulose to • Treat ascitis.
and toxic hepatitis . stool due to obstructive jaundice. minimize formation of ammonia and other • O2 therapy.
causes of liver cirrhosis 2. Jaundice, especially mucous membranes nitrogenous by-products in bowel. • Intubation and mechanical ventilation if
Cell necrosis occurs destroyed liver cells are replaced by 3. Elevated testosterone levels causing of amenorrhea, or 2. Rectal administration of neomycin to suppress needed.
scar tissue-(Normal architecture becomes nodular) menstrual irregularity in women, whereas elevated estrogen urea-splitting enteric bacteria in bowel and VIII-management of cerebral edema in FHF:
Four types of cirrhosis: levels are responsible testicular atrophy, and gynecomastia in decrease ammonia formation. • Mannitol (Osmitrol) IV for management of
1. Alcoholic (Laennec’s) cirrhosis men and for pectoral and axillary alopecia and palmer 3. Restriction of dietary protein and sodium while cerebral edema when indicated.
2. Post necrotic cirrhosis erythemia in both sexes. Elevated cortisol precipitate moon maintaining adequate caloric intake with diet or • Elevate the head of bed 20-30 degree, with the
3. Biliary cirrhosis faces , weight gain. Hyperaldesteronism predisposes the hypertonic dextrose solutions. head in the midline position.
4. Cardiac cirrhosis patient to fluid and electrolyte imbalance leading to • Avoidance of sedative that impaired accurate
1- Alcoholic (Laennec’s) Cirrhosis generalized edema, and ascites. III- Management of metabolic and fluid and patient assessment.
• Associated with alcohol abuse 4. Pruritus caused by bile salts deposited on skin electrolyte disturbances: • Hyperventilation that reduce cerebral blood
• Preceded by theoretically reversible fatty infiltration 5. Carbohydrate, fate, and protein metabolism abnormalities: • Monitoring blood gloucouse level, administration of flow.
of the liver cells manifestation of hypoglysemia, hypercholesterolemia, as bolus IV dextrose 50%, IV of 10% glucose • Provision in quiet room.
• Widespread scar formation Steatorrhea and diarrhea due to decreased fat absorption, infusion, or as parenteral nutrition. • Managing hyperthermia by cooling methods and
2- Cardiac Cirrhosis fate soluble vitamins deficiency. • Low-molecular-weight albumin followed by a compresses.
Results from longstanding severe right-sided heart failure 6. Peripheral edema as the fluid moves from the intravascular to potassium-sparing diuretic (spironolactone) to VIII- management of skin disturbances.
3- Post necrotic Cirrhosis the interstitial spaces, secondary to hypoproteinemia enhance fluid shift from interstitial back to 1-Cholestyramine (Questran) to promote fecal
• Complication of toxic or viral hepatitis 7. Ascites from hypoproteinemia and/or portal hypertension intravascular spaces. excretion of bile salts to decrease itching.
• Accounts for 20% of the cases of cirrhosis 8. Easy bruising, overt bleeding due to clotting deficiency • Abdominal paracentensis in case of ascites. IX- Surgical treatment:
• Broad bands of scar tissue form within the liver 9. Altered levels of consciousness, ranging from irritability and • Restriction of Na and fluids to limit genelized
1- Liver transplantation has become the treatment
4- Biliary Cirrhosis confusion to stupor, somnolence, and coma edema and ascities. Na should be restricted to
of choice. An extacorporeal liver assist device has
• Associated with chronic biliary obstruction and 10.Change in deep tendon reflexes—initially hyperactive; between 500 to 2000 mg/day, while fluid are
been developed and is being used.
infection become flaccid restricted to 500 to 1500ml/day based on severity
• Accounts for 15% of all cases of cirrhosis. Biliary 11.Fetor hepaticus—breath odor of acetone of ascities.
X.Additional medical interventions, depending on
cirrhosis represents the end result of continuous, 12.Portal systemic encephalopathy, also known as hepatic coma • Colloid and crystalloid administration: blood
the patient’s condition, may include:
ongoing inflammation of the bile ducts . Persistent or hepatic encephalopathy, can occur in conjunction with products, albumin, or crystalloid may be given to
• Hemodialysis, hemoperfusion, or
biliary obstruction results in inflammation and scarring cerebral edema correct serum oncotic pressure and thus preventing
plasmapheresis.
of the liver . The consequence is diffuse and 13.Cerebral edema is often the cause of death due to brain stem edema and ascitis.
• Hemoperfusion consists of the passage of
widespread fibrosis with regenerative nodule herniation or respiratory arrest
anticoagulated blood through a device, usually a
formation , with the complications of portal column, that contains adsorbent particles
hypertension described earlier.
 Complications Nursing Interventions C. Improving Nutritional Status E. Preventing Infection
A. Maintaining Adequate Fluid Volume 1. Consult a nutrition specialist to help • Be alert for signs of infection, such as
1. Acute respiratory failure 1.Monitor vital signs frequently. evaluate nutritional status and needs. fever, cloudy urine, abnormal breath
2. Infections and sepsis 2.Weigh patient daily and keep an accurate 2. Encourage the patient to eat in a sitting sounds.
intake and output record; record frequency position to decrease abdominal • Use good hand washing and aseptic
3. Cardiac dysfunction, hypotension and characteristics of stool. tenderness and feeling of fullness. technique when caring for any break in
4. Hepatorenal failure 3.Measure and record abdominal girth daily. 3. Provide small, frequent meals or dietary the skin or mucous membranes.
4.Assess and record the presence of supplements to conserve the patient’s • Restrict visits with anyone who may have
5. Hemorrhage peripheral edema. energy. an infection.
5.Restrict sodium and fluids; replace 4. Provide mouth care if the patient has • Encourage the patient to try and not
Nursing Assessment
electrolytes as directed. bleeding gums or fetor hepaticus. scratch itching skin.
1. Obtain history of exposure to drugs,
6.Administer low-molecular-weight dextran or 5. Restrict sodium intake and protein based F. Preventing Injury
chemicals, or toxins; exposure to
albumin and diuretics as prescribed on ammonia levels and symptoms of 1. Maintain close observation, side rails, and
infectious hepatitis; and course of illness.
7. Assess for any signs and symptoms of encephalopathy. If the patient shows of nurse call system.
2. Assess respiratory status, breath, level of
hemorrhage or bleeding. impeding advancing coma, a low-protein 2. Assist with ambulation as needed and
consciousness, and vital signs.
8.Monitor signs of volume overload: diet should be given temporarily. Too avoid obstructions to prevent falls.
3. Assess for ascites, edema, jaundice,
- Cardiac gallop much high protein food such as meats 3. Have well-lit room and frequently reorient
bleeding, asterixis, presence or absence
- pulmonary carckles may produce portal systemic patient.
of reflexes.
- shortness of breath encephalopathy(PSE), and too little may 4. Observe for subtle changes in behavior
4. Assess results of arterial blood gas
-jugular vein distention cause negative nitrogen balance and (such as unkempt appearance),
evaluations, electrolytes, prothrombin
- peripheral edema wasting worsening of sample of handwriting, and
time, and hemoglobin and hematocrit
9- Administer diuretics as ordered 6. patients with fatty stools (steatorrhea) change in sleeping pattern to detect
determinations.
should receive water soluble forms of fat worsening encephalopathy.
Nursing Diagnoses
B. Improving Respiratory Status soluble vitamins A, D, E and K.
A. Fluid Volume Deficit related to
1. Monitor respiratory rate, depth, use of 7. patient preferences are considered. Patient Education/Health Maintenance
hypoproteinemia, peripheral edema,
accessory muscles, nasal flaring, and 8. 8-folic acid and iron are prescribed to  Teach patient and family to notify health
ascites, bleeding.
breath sounds. prevent anemia. care provider of increased abdominal
B. Ineffective Breathing Pattern related to
2. Evaluate results of arterial blood gases 9. high caloric intake should be maintained, discomfort, bleeding, increased edema
anemia and decreased lung expansion
and hemoglobin and hematocrit and supplementary vitamins and minerals or ascites, hallucinations, or lapses in
from ascites
evaluations. should be provided ( e.g., oral potassium, consciousness.
C. Altered Nutrition: Less Than Body
3. Elevate head of the bed to lower if the serum potassium is low and if renal  Instruct to avoid activities that increase
Requirements, related to carbohydrate,
diaphragm and decrease respiratory function is normal) the risk of bleeding: scratching, falling,
protein, and fate metabolism
effort. 10. Provide enteral and parenteral feedings forceful nose blowing, aggressive tooth
disturbances.
4. Assist patient in turn cough deep breath, as needed. brushing, use of straight-edged razor.
D. Risk for Impaired Skin Integrity related to
and use incentive spirometry q2h. D. Maintaining Skin Integrity  Advise on limiting activities when
malnutrition, deposition of bile salts,
5. Administer oxygen therapy as directed. 1. Inspect skin for any alteration in integrity. fatigued and use of frequent rest
peripheral edema, decreased activity
To oxygenate the damage cells and 2. carful skin care is provided because of periods.
E. Risk for Infection related to altered
prevent further cell destruction. the presence of subcutaneous edema,  Maintain close follow-up for laboratory
immune response
6. provide chest percussion with postural the immobility of the patient, jaundice, testing and evaluation by health care
F. Risk for Injury related to encephalopathy
drainage if indicated q4h. and increased susceptibility to skin provider.
breakdown and infection.  Prepare patient/significant others for
Evaluation Complications of fulminant hepatic 3. frequent change of position are necessary procedures such as paracentesis or
A. Blood pressure stable, urine output failure to prevent pressure ulcer. laboratory studies.
4. irritant soaps and use of adhesive tape  Teach patient and family information
adequate 1. Acute respiratory failure are avoided to prevent trauma to the skin. regarding sodium, protein, and fluid
Lotion may be soothing to irritant skin, restrictions. Give written materials.
B. Respirations unlabored 2. Infections and sepsis measures are taken to minimized the  Teach signs and symptoms of
C. Tolerating 3 to 4 small feedings a patient scratching of the skin. progressing hepatic failure (e.g.,
3. Cardiac dysfunction, hypotension 5. Keep the patient’s fingernails short to change in mental status, skin
day prevent scratching from pruritus. coloration, ascites).
6. Administer medications as prescribed for  Teach signs and symptoms of occult
D. Skin intact without abrasions 4. Hepatorenal failure pruritus. bleeding and respiratory infection.
7. Assess for signs of bleeding from broken  Teach home medication regimen.
E. No fever or signs of infection 5. Hemorrhage areas on the skin.  Teach comfort measures
F. No falls 8. Avoid trauma and friction to the skin.