Transcript Fulminant hepatic failure

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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
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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.
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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.
 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, BuddChiari syndrome (hepatic vein thrombosis)
 F Fatty Infiltration - acute fatty liver of
pregnancy.
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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.
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Hepatic failure is accompanied by:
Execratory : failure to excrete bilirubin
resulting in hyperbilirubinemia (hemoglobin
breackdown product=bilirubin).
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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).
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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.
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Acute hepatic failure is characterized by loss
of greater than 90% of hepatocytes ;
consequently , loss of excretory , exocrine ,
synthetic and metabolic functions.
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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.
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1.Malaise, anorexia, nausea, vomiting, fatigue
and clay color stool due to obstructive
jaundice.
2. Jaundice, especially mucous membranes
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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.
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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.
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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
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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
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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
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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.
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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.
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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
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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.
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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.
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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.
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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.
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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.
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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.
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VII- management of pulmonary disturbances:
Elevate the head of bed 45-90 degree.
Treat ascitis.
O2 therapy.
Intubation and mechanical ventilation if
needed.
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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.
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Hyperventilation that reduce cerebral blood
flow.
Provision in quiet room.
Managing hyperthermia by cooling methods
and compresses.
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VIII- management of skin disturbances.
1-Cholestyramine (Questran) to promote
fecal excretion of bile salts to decrease
itching.
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IX- Surgical treatment:
1- Liver transplantation has become the
treatment of choice. An extacorporeal liver
assist device has been developed and is being
used.
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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
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Acute respiratory failure
Infections and sepsis
Cardiac dysfunction, hypotension
Hepatorenal failure
Hemorrhage
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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.
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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.
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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.
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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
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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
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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
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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.
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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.
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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.
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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
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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.
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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.
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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.
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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.
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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.
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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.
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4. Maintain close follow-up for laboratory testing
and evaluation by health care provider.
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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
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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