A cute renal failure Dr. Abdul-Monim Batiha Assistant Professor Critical Care Nursing Philadelphia university - PowerPoint PPT Presentation


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A cute renal failure Dr. Abdul-Monim Batiha Assistant Professor Critical Care Nursing Philadelphia university


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 ... – PowerPoint PPT presentation

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Title: A cute renal failure Dr. Abdul-Monim Batiha Assistant Professor Critical Care Nursing Philadelphia university

A cute renal failure Dr. Abdul-Monim
BatihaAssistant ProfessorCritical Care
NursingPhiladelphia university
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At the end of this lecture the students will be
able to
  • Define a cute hepatic failure, fulmennant hepatic
  • 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

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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
  • 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
  • B Hepatitis B
  • C Cryptogenic ,hepatitis C
  • D Hepatitis D, drugs (acetamenophine, and
  • E Esoteric causes - Wilson's disease, Budd-Chiari
    syndrome (hepatic vein thrombosis)
  • F Fatty Infiltration - acute fatty liver of
  • pregnancy.

  • Glucose Metabolism
  • Ammonia Conversion
  • Protein Metabolism(albumin, alpha and beta
    globulins, blood clotting factors, specific
    transport proteins, and most of the plasma
  • Fat Metabolism
  • Vitamin and Iron Storage
  • Drug Metabolism
  • Bile Formation
  • Bilirubin Excretion
  • Inactivation of estrogen, aldosterone, and

  • Hepatic failure is accompanied by
  • Execratory failure to excrete bilirubin
    resulting in hyperbilirubinemia (hemoglobin
    breackdown productbilirubin).

  • 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

  • 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

  • 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
  • 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
  • 8. Easy bruising, overt bleeding due to clotting

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

  • 11. Fetor hepaticusbreath 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
  • 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

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

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 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.

  • 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 (H2) antagonists to
    reduce the risk of bleeding from stress ulcers.

  • VI- Management of cardiovascular system
  • 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.
  • O2 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

  • 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 patients 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

  • 1. Acute respiratory failure
  • 2. Infections and sepsis
  • 3. Cardiac dysfunction, hypotension
  • 4. Hepatorenal failure
  • 5. 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,
  • 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
  • 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
  • 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
  • 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 q2h.
  • 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 q4h.

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 patients 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

  • 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
  • 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

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 patients fingernails short to
    prevent scratching from pruritus.
  • 6. Administer medications as prescribed for
  • 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
  • 3. Restrict visits with anyone who may have an
  • 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
  • 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
  • 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

  • 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
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