1 / 72

At the end of this lecture the student’s will be able to:

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

jamalia-mcmillan
Download Presentation

At the end of this lecture the student’s will be able to:

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. A cute renal failure Dr. Abdul-MonimBatihaAssistant ProfessorCritical Care NursingPhiladelphia university

  2. 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 • Identify Pathophysiology of FHF • Enomerate Diagnostic tests and studies for FHF. • Identify medical managements for FHF • List complications of FHF • Discuss nursing care plane for FHF

  3. A cute hepatic failure • Hepatic failure results when the liver is unable to perform its function. • Hepatic failure may occur acutely as a result of massive hepatocellular, or be chronic process with recurring hepatocyte injury, regeneration, and progressive fibrosis(cirrhosis)

  4. Fulminanthepatic failure 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.

  5. Several definitions of the time course for which liver failure should be considered fulminant have been proposed:

  6. The development of encephalopathy within eight weeks of the onset of symptoms in a patient with a previously healthy liver . • The appearance of encephalopathy within two weeks of developing jaundice, even in a patient with previous underlying liver dysfunction.

  7. Causes of fulminant hepatic failure: The ABCs • A Acetaminophen, hepatitis A, autoimmune hepatitis • B Hepatitis B • C Cryptogenic ,hepatitis C • D Hepatitis D, drugs (acetamenophine, and salicylate) • E Esoteric causes - Wilson's disease, Budd-Chiari syndrome (hepatic vein thrombosis) • F Fatty Infiltration - acute fatty liver of pregnancy.

  8. FUNCTIONS OF THE LIVER • Glucose Metabolism • Ammonia Conversion • Protein Metabolism(albumin, alpha and beta globulins, blood clotting factors, specific transport proteins, and most of the plasma lipoproteins.) • Fat Metabolism • Vitamin and Iron Storage • Drug Metabolism • Bile Formation • Bilirubin Excretion • Inactivation of estrogen, aldosterone, and cortisol.

  9. Pathophysiology : • Hepatic failure is accompanied by: • Execratory : failure to excrete bilirubin resulting in hyperbilirubinemia (hemoglobin breackdown product=bilirubin).

  10. 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).

  11. Synthesis: Liver makes almost all plasma proteins, therefore, hepatic failure leads to albumin and coagulation factor deficiencies. • Metabolic: Impaired glucose metabolism, glucose synthesis, ketone body synthesis, fatty acid synthesis, drug metabolism, and estrogen metabolism.

  12. Acute hepatic failure is characterized by loss of greater than 90% of hepatocytes ; consequently , loss of excretory , exocrine , synthetic and metabolic functions.

  13. 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.

  14. Clinical Manifestations • 1.Malaise, anorexia, nausea, vomiting, fatigue and clay color stool due to obstructive jaundice. • 2. Jaundice, especially mucous membranes

  15. 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.

  16. 4. Pruritus caused by bile salts deposited on skin • 5.Charbohydrate, fate, and protein metabolism abnormalities: manifestation of hypoglysemia, hypercholesterolemia, Steatorrhea and diarrhea due to decreased fat absorption, fate soluble vitamins deficiency.

  17. 6. Peripheral edema as the fluid moves from the intravascular to the interstitial spaces, secondary to hypoproteinemia • 7. Ascites from hypoproteinemia and/or portal hypertension • 8. Easy bruising, overt bleeding due to clotting deficiency

  18. 9. Altered levels of consciousness, ranging from irritability and confusion to stupor, somnolence, and coma • 10. Change in deep tendon reflexes—initially hyperactive; become flaccid

  19. 11. Fetor hepaticus—breath odor of acetone • 12. Portal systemic encephalopathy, also known as hepatic coma or hepatic encephalopathy, can occur in conjunction with cerebral edema • 13. Cerebral edema is often the cause of death due to brain stem herniation or respiratory arrest

  20. Diagnostic test: • 1. Prolonged prothrombin time, decreased platelet count • 2. Elevated ammonia, amino acid • 3. Hypoglycemia or hyperglycemia • 4. Dilutional hyponatremia or hypernatremia, hypokalemia, hypocalcemia, and Hypomagnesemia. • 5. CBC: thrombocytopenia, anemia. • 6. bile pigment: increased total bilirubin, and direct.

  21. Diagnostic studies: • 1-Liver ultrasound establish patency and flow in hepatic vein, artery, and portal vein, it excludes the presence of tumor and establish the presence of ascites. • 2-Liver biopsy shows liver cell necrosis, injury, or fatty liver. • 3-CT may show brain edema in FHF and brain herniation.

  22. Medical management: • I-Correction of precipitating causes — • The first step is the identification and correction of precipitating causes. Careful evaluation should be performed to determine the presence of any of the following: • Hypovolemia • Gastrointestinal bleeding • Hypokalemia and/or metabolic alkalosis • Hypoxia • Sedatives or tranquilizers • Hypoglycemia

  23. II- Management of hepatic encephalopathy: • 1.Oral or rectal administration of lactulose to minimize formation of ammonia and other nitrogenous by-products in the bowel. • 2. Rectal administration of neomycin to suppress urea-splitting enteric bacteria in the bowel and decrease ammonia formation. • 3. Restriction of dietary protein and sodium while maintaining adequate caloric intake with diet or hypertonic dextrose solutions.

  24. II- Management of metabolic and fluid and electrolyte disturbances: • Monitoring blood gloucouse level, administration of as bolus IV dextrose 50%, IV of 10% glucose infusion, or as parenteral nutrition. • Low-molecular-weight albumin followed by a potassium-sparing diuretic (spironolactone) to enhance fluid shift from interstitial back to intravascular spaces. • Abdominal paracentensis in case of ascites.

  25. 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. • Colloid and crystalloid administration: blood products, albumin, or crystalloid may be given to correct serum oncotic pressure and thus preventing edema and ascitis.

  26. V-management of hematological changes: • Administration of blood products: in patient with active bleeding, backed RBCs are administered to treat a low Hb or Htc . • Infusion of fresh-frozen plasma to provide blood clotting factors, and platelet administration corrects thrombocytopenia. • Pancreatic enzymes, if diarrhea and steatorrhea are present, to permit better tolerance of diet.

  27. Gastric lavage with normal saline through NGT will control bleeding, remove toxins, blood clots, and old blood from the stomach. • Supplemental vitamins (A, B complex, C, and K) and folate. • Antacids and histamine-2 (H2) antagonists to reduce the risk of bleeding from stress ulcers.

  28. VI- Management of cardiovascular system disturbances: • hemodynamic monitoring including pulse , BP, CVP, PAWP, and cardiac index. • As mention before, fluid administration using colloids, or crystolloids that increase the oncotic pressure. • K administration.

  29. VII- management of pulmonary disturbances: • Elevate the head of bed 45-90 degree. • Treat ascitis. • O2 therapy. • Intubation and mechanical ventilation if needed.

  30. VIII-management of cerebral edema in FHF: • Mannitol (Osmitrol) IV for management of cerebral edema when indicated. • Elevate the head of bed 20-30 degree, with the head in the midline position. • Avoidance of sedative that impaired accurate patient assessment.

  31. Hyperventilation that reduce cerebral blood flow. • Provision in quiet room. • Managing hyperthermia by cooling methods and compresses.

  32. VIII- management of skin disturbances. • 1-Cholestyramine (Questran) to promote fecal excretion of bile salts to decrease itching.

More Related