3. • The liver is located in the upper right-hand portion of the abdominal
cavity, beneath the diaphragm, and on top of the stomach, right
kidney, and intestines.
• Shaped like a cone, the liver is a dark reddish-brown organ that
weighs about 3 pounds.
4. Functions of the liver
• Production of bile, which helps carry away waste and break down fats
in the small intestine during digestion
• Production of certain proteins for blood plasma
• Production of cholesterol and special proteins to help carry fats
through the body
• Conversion of excess glucose into glycogen for storage (glycogen can
later be converted back to glucose for energy) and to balance and
make glucose as needed
• Regulation of blood levels of amino acids, which form the building
blocks of proteins
5. • Processing of hemoglobin for use of its iron content (the liver stores
iron)
• Conversion of poisonous ammonia to urea (urea is an end product of
protein metabolism and is excreted in the urine)
• Clearing the blood of drugs and other poisonous substances
• Regulating blood clotting
• Resisting infections by making immune factors and removing bacteria
from the bloodstream
• Clearance of bilirubin, also from red blood cells.
6. introduction
• Liver failure is a life threatening condition that demands urgent medical care.
Most often, liver failure happens gradually, over many years. It’s the final stage of
many liver disease. But a rarer condition known as acute liver failure happens
rapidly and can be difficult to detect at first. Liver failure happens when large
parts of the liver become damaged beyond repair and the liver cant work
anymore.
• There are 2 types of liver failure. Acute and chronic liver failure. Acute liver
failure is also known as fulminant hepatic failure.
7. DEFINITION
• Fulminant hepatic failure is the acute impairment of liver function
associated with severe Progressive mental changes in patients who
have had liver disease for less than 8 weeks
8. INCIDENCE:
• In developed country incidence is 10 cases per million people per
year
• It accounts for 6 of all deaths due to liver disease
• It is more common in women then in men, and more common in
white people than in other faces
9. ETIOLOGY:
• IDIOPATHIC: in 40-50% cases.
• INFECTIVE›
• VIRAL CAUSES.
• Hepatitis a,b,c,d & e
• high risk of fulminant hepatic failure occurs in combined infections with the hepatitis B
virus (HBV) and hepatitis D.
• EBV.
• Adenovirus-
• Enterovirus .
• Cmv.
• Parvovirus B19
• Herpes simplex .
• Varicella zoster
11. • DRUGS:
• Acetaminophen overdose is the most common etiology of acute
hepatic failure in children andadolescents
• Isoniazid
• Sodium valproate.
• Phenytoin
• Salicylates
• Halothane
• Exposure to carbon tetrachloride, Amanita phalloides mushroom,
herbal medication, methanol.
14. Pathophysiology
▸ Hepatic failure is accompanied by:
‣ Execratory failure to excrete bilirubin resulting in hyperbilirubinemia (hemoglobin
breakdown 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, fat soluble vitamin
deficiencies, and purities(due to build up of bile salts in the skin).
15. • 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.
16. • 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.
17. 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 amenorrhea, or menstrual irregularity in
women, whereas elevated estrogen levels are responsible for testicular atrophy,
and gynecomastia in men and for pectoral and axillary alopecia and palmer
erythemia in both sexes.
18. • Elevated cortisol 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.Carbohydrate, fate, and protein metabolism abnormalities: manifestation of
hypoglysemia, hypercholesterolemia, Steatorrhea and diarrhea due to decreased
fat absorption, fate soluble vitamins deficiency.
19. • 6. Peripheral edema as the fluid moves from the intravascular to the
interstitial spaces, secondary to hypo proteinemia
• 7. Ascites from hypo proteinemia 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
20. • 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 respiratory arrest
21. 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.
22. • 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
• Liver biopsy shows liver cell necrosis, injury, or fatty liver.
• CT may show brain edema in FHF and brain herniation.
23. 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
24. • 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.
25. II- Management of metabolic and fluid and electrolyte disturbances
• Monitoring blood glucose level, administration of as bolus IV dextrose, or as
parenteral nutrition.
• Low-molecular-weight albumin followed by a potassium-sparing diuretic
(spironolactone) to enhance fluid shift from interstitial space to intravascular
spaces.
• Abdominal paracentensis in case of ascites.
26. • Restriction of Na and fluids to limit generalized edema and ascites. Na
should be restricted,
• fluid are restricted to 500 to 1500ml/day based on severity of ascites.
• Colloid and crystalloid administration: blood products, albumin, or
crystalloid may begiven to correct serum oncotic pressure and thus
preventing edema and ascites.
27. • 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.
28. • 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, K) and folate.
• Antacids and histamine-2 (H2) antagonists to reduce the risk of
bleeding from stress ulcers.
29. • 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.
30. • VII-management of pulmonary disturbances:
▸ Elevate the head of bed 45-90 degree.
▸ Treat ascitis.
‣ 02 therapy.
‣ Intubation and mechanical ventilation needed.
31. • 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.
32. • IX- management of skin disturbances.
▸1-Cholestyramine (Questran) to promote fecal excretion of bile salts
to decrease itching.
34. • liver dialysis
• liver dialysis with an albumin-containing dialysate, and biologic liver
support devices that involve perfusion of the patient's blood through
a cartridge containing liver cell lines or porcine hepatocytes can
remove some toxins, improve serum biochemical abnormalities.
36. 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.
37. 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.
38. 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
40. • 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
6. Administer low-molecular-weight dextran or albumin and diuretics
as prescribed
41. 7. Assess for any signs and symptoms of hemorrhage or bleeding.
8.Monitor signs of volume overload:-
-Cardiac gallop
- pulmonary crackles
- shortness of breath
- jugular vein distention
- peripheral edema
9. Administer diuretics as ordered
42. • 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.
43. • 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 .
44. • 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.
45. 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.
46. • 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.
47. • 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
48. • 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.
49. • 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.
50. • 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, worsening of sample of
handwriting, and change in sleeping pattern to detect worsening
encephalopathy.
51. PATIENT EDUCATION
• 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.
52. • 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.
53. 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
