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A cute renal failure Dr. Abdul- Monim Batiha Assistant Professor Critical Care Nursing Philadelphia university. At the end of this lecture the student’s will be able to:. Define a cute hepatic failure, fulmennant hepatic failure. List Causes of fulminant hepatic failure(FHF): The ABCs
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Fulminant hepatic failure refers to the rapid development of severe acute liver injury with impaired synthetic function and encephalopathy in a person who previously had a normal liver or had well-compensated liver disease.
The development of encephalopathy within eight weeks of the onset of symptoms in a patient with a previously healthy liver .
Exocrine: bile is secreted by the liver and contains cholesterol, bile salts and waste products such as bilirubin. Bile salts aid in the digestion of fats. Accumulation of bile salts resulting in hypercholesterolemia, steatorrhea, fate soluble vitamine deficiencies, and purities(due to build up of bile salts in the skin).
Synthesis: Liver makes almost all plasma proteins, therefore, hepatic failure leads to albumin and coagulation factor deficiencies.
Acute hepatic failure is characterized by loss of greater than 90% of hepatocytes ; consequently , loss of excretory , exocrine , synthetic and metabolic functions.
The cause of hepatic encephalopathy is thought to be related to the accumulation of toxic agents absorbed from the intestinal tract . These substances accumulate because the liver has lost the ability to metabolized and detoxify these substances. Elevated serum ammonia, a byproduct of protein and amio acid metabolism , is one of the suspected neurotoxins.
3.Elevated testosterone levels causing of amenorrhea, or menstrual irregularity in women, whereas elevated estrogen levels are responsible testicular atrophy, and gynecomastia in men and for pectoral and axillary alopecia and palmer erythemia in both sexes. Elevated corisol precipitate moon faces , weight gain. Hyperaldesteronism predisposes the patient to fluid and electrolyte imbalance leading to generalized edema, and ascites.
6. Peripheral edema as the fluid moves from the intravascular to the interstitial spaces, secondary to hypoproteinemia
9. Altered levels of consciousness, ranging from irritability and confusion to stupor, somnolence, and coma
II- Management of metabolic and fluid and electrolyte disturbances:
Restriction of Na and fluids to limit genelized edema and ascities. Na should be restricted to between 500 to 2000 mg/day, while fluid are restricted to 500 to 1500ml/day based on severity of ascities.
Gastric lavage with normal saline through NGT will control bleeding, remove toxins, blood clots, and old blood from the stomach.
X.Additional medical interventions, depending on the patient’s condition, may include:
3. Assess for ascites, edema, jaundice, bleeding, asterixis, presence or absence of reflexes.
D. Risk for Impaired Skin Integrity related to malnutrition, deposition of bile salts, peripheral edema, decreased activity
- Cardiac gallop
- pulmonary carckles
- shortness of breath
-jugular vein distention
- peripheral edema
4. Assist patient in turn cough deep breath, and use incentive spirometry q2h.
4. Provide mouth care if the patient has bleeding gums or fetor hepaticus.
6- patients with fatty stools (steatorrhea) should receive water soluble forms of fat soluble vitamins A, D, E and K.
4- irritant soaps and use of adhesive tape are avoided to prevent trauma to the skin. Lotion may be soothing to irritant skin, measures are taken to minimized the patient scratching of the skin.
4. Maintain close follow-up for laboratory testing and evaluation by health care provider.