A cute renal failure Dr AbdulMonim Batiha Assistant

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 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

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)

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.

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

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.

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.

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.

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

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. Metabolic: Impaired glucose metabolism, glucose synthesis, ketone body synthesis, fatty acid synthesis, drug metabolism, and estrogen metabolism.

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.

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

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.

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.

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

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

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

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.

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.

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

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.

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.

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 1500 ml/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.

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.

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 (H 2) antagonists to reduce the risk of bleeding from stress ulcers.

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.

VII- management of pulmonary disturbances: Elevate the head of bed 45 -90 degree. Treat ascitis. O 2 therapy. Intubation and mechanical ventilation if needed.

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.

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

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

IX- Surgical treatment: 1 - Liver transplantation has become the treatment of choice. An extacorporeal liver assist device has been developed and is being used.

X. Additional medical interventions, depending on the patient’s condition, may include: Hemodialysis, hemofiltration, hemoperfusion, or plasmapheresis. Hemoperfusion consists of the passage of anticoagulated blood through a device, usually a column, that contains adsorbent particles

Complications 1. 2. 3. 4. 5. Acute respiratory failure Infections and sepsis Cardiac dysfunction, hypotension Hepatorenal failure Hemorrhage

Nursing Assessment 1. Obtain history of exposure to drugs, chemicals, or toxins; exposure to infectious hepatitis; and course of illness. 2. Assess respiratory status, breath, level of consciousness, and vital signs.

3. Assess for ascites, edema, jaundice, bleeding, asterixis, presence or absence of reflexes. 4. Assess results of arterial blood gas evaluations, electrolytes, prothrombin time, and hemoglobin and hematocrit determinations.

Nursing Diagnoses A. Fluid Volume Deficit related to hypoproteinemia, peripheral edema, ascites, bleeding. B. Ineffective Breathing Pattern related to anemia and decreased lung expansion from ascites C. Altered Nutrition: Less Than Body Requirements, related to carbohydrate, protein, and fate metabolism disturbances.

D. Risk for Impaired Skin Integrity related to malnutrition, deposition of bile salts, peripheral edema, decreased activity E. Risk for Infection related to altered immune response F. Risk for Injury related to encephalopathy

Nursing Interventions

A. Maintaining Adequate Fluid Volume 1. Monitor vital signs frequently. 2. Weigh patient daily and keep an accurate intake and output record; record frequency and characteristics of stool. 3. Measure and record abdominal girth daily. 4. Assess and record the presence of peripheral edema. 5. Restrict sodium and fluids; replace electrolytes as directed. 6. Administer low-molecular-weight dextran or albumin and diuretics as prescribed

7. Assess for any signs and symptoms of hemorrhage or bleeding. 8. Monitor signs of volume overload: - Cardiac gallop - pulmonary carckles - shortness of breath -jugular vein distention - peripheral edema 9 - Administer diuretics as ordered

B. Improving Respiratory Status 1. Monitor respiratory rate, depth, use of accessory muscles, nasal flaring, and breath sounds. 2. Evaluate results of arterial blood gases and hemoglobin and hematocrit evaluations. 3. Elevate head of the bed to lower diaphragm and decrease respiratory effort.

4. Assist patient in turn cough deep breath, and use incentive spirometry q 2 h. 5. Administer oxygen therapy as directed. To oxygenate the damage cells and prevent further cell destruction. 6. provide chest percussion with postural drainage if indicated q 4 h.

C. Improving Nutritional Status 1. Consult a nutrition specialist to help evaluate nutritional status and needs. 2. Encourage the patient to eat in a sitting position to decrease abdominal tenderness and feeling of fullness. 3. Provide small, frequent meals or dietary supplements to conserve the patient’s energy.

4. Provide mouth care if the patient has bleeding gums or fetor hepaticus. 5. Restrict sodium intake and protein based on ammonia levels and symptoms of encephalopathy. If the patient shows of impeding advancing coma, a low-protein diet should be given temporarily. Too much high protein food such as meats may produce portal systemic encephalopathy(PSE), and too little may cause negative nitrogen balance and wasting

6 - patients with fatty stools (steatorrhea) should receive water soluble forms of fat soluble vitamins A, D, E and K. 7 -patient preferences are considered. 8 -folic acid and iron are prescribed to prevent anemia. 9 -A high caloric intake should be maintained, and supplementary vitamins and minerals should be provided ( e. g. , oral potassium, if the serum potassium is low and if renal function is normal) 10. Provide enteral and parenteral feedings as needed.

D. Maintaining Skin Integrity 1 - Inspect skin for any alteration in integrity. 2 - carful skin care is provided because of the presence of subcutaneous edema, the immobility of the patient, jaundice, and increased susceptibility to skin breakdown and infection. 3 -frequent change of position are necessary to prevent pressure ulcer.

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. 5. Keep the patient’s fingernails short to prevent scratching from pruritus. 6. Administer medications as prescribed for pruritus. 7. Assess for signs of bleeding from broken areas on the skin. 8. Avoid trauma and friction to the skin.

E. Preventing Infection 1. Be alert for signs of infection, such as fever, cloudy urine, abnormal breath sounds. 2. Use good hand washing and aseptic technique when caring for any break in the skin or mucous membranes. 3. Restrict visits with anyone who may have an infection. 4. Encourage the patient to try and not scratch itching skin.

F. Preventing Injury 1. Maintain close observation, side rails, and nurse call system. 2. Assist with ambulation as needed and avoid obstructions to prevent falls. 3. Have well-lit room and frequently reorient patient. 4. Observe for subtle changes in behavior (such as unkempt appearance), worsening of sample of handwriting, and change in sleeping pattern to detect worsening encephalopathy.

Patient Education/ Health Maintenance 1. Teach patient and family to notify health care provider of increased abdominal discomfort, bleeding, increased edema or ascites, hallucinations, or lapses in consciousness. 2. Instruct to avoid activities that increase the risk of bleeding: scratching, falling, forceful nose blowing, aggressive tooth brushing, use of straight-edged razor. 3. Advise on limiting activities when fatigued and use of frequent rest periods.

4. Maintain close follow-up for laboratory testing and evaluation by health care provider. . Prepare patient/significant others for procedures such as paracentesis or laboratory studies. • Teach patient and family information regarding sodium, protein, and fluid restrictions. Give written materials. • Teach signs and symptoms of progressing hepatic failure (e. g. , change in mentation, skin coloration, ascites). • Teach signs and symptoms of occult bleeding and respiratory infection. • Teach home medication regimen. • Teach comfort measures

Evaluation A. Blood pressure stable, urine output adequate B. Respirations unlabored C. Tolerating 3 to 4 small feedings a day D. Skin intact without abrasions E. No fever or signs of infection F. No falls