NURSING MANAGEMENT OF
A PATIENT WITH
HEPATIC COMA
Mrs. Daisy Kuruvilla
HEPATIC COMA
DEFINITION
• Hepatic encephalopathy (HE) is decline in brain function especially altered level of
consciousness as a result of liver failure. In the advanced stages it can result in a coma
called hepatic coma.
• It is the coma induced by severe liver disease.
• A coma occurring in advanced cirrhosis, hepatitis, poisoning, or other liver disease.
RISK FACTORS
• Acute fulminant viral hepatitis
• Toxic hepatitis. caused by exposure to alcohol, chemicals, drugs, or supplements.
• Reye’s syndrome. s primarily seen in children. It causes sudden swelling and
inflammation of the liver and the brain.
CAUSES
• Laennec's cirrhosis (a type of cirrhosis of the liver characterized by a nodular
appearance of the liver surface, associated with alcoholism.)
• acute viral hepatitis
• uremia
PAHTOPHYSIOLOGY
o liver fails to break down toxins properly
o it’s triggered by a buildup of toxins in the bloodstream
( liver removes toxic chemicals such as ammonia from your body. These toxins are left
over when proteins are metabolized or broken down for use by various organs in body.
kidneys change these toxins into safer substances that are then removed through
urination.)
o When liver is damaged, it’s unable to filter out all the toxins.
o Toxins can then build up in your bloodstream and potentially get into your brain.
o Toxic buildup can also damage other organs and nerves.
o Lead to neurogenic manifestations.
Ammonia is produced in the gastrointestinal tract by the bacterial degradation of amines,
amino acids, purines, and urea. Enterocytes also convert glutamine to glutamate and
ammonia by the activity of glutaminase. Normally, ammonia is detoxified in the liver by
conversion to urea by the Krebs-Henseleit cycle. Ammonia is also consumed in the conversion
of glutamate to glutamine, a reaction that depends upon the activity of glutamine synthetase.
glutamate is a nonessential amino acid and glutamine is a conditional amino acid.
WHAT ARE THE DIFFERENT STAGES OF HEPATIC ENCEPHALOPATHY?
Hepatic encephalopathy is divided into stages based on the severity of the symptoms. Common
classification systems include the West Haven Criteria and the Glasgow Coma Scale.
THE FIVE STAGES OF HEPATIC ENCEPHALOPATHY, ACCORDING TO THE
WEST HAVEN CRITERIA, ARE:
STAGE GRADE FEATURES
0 Normal symptoms are minimal.
1 Mild shortened attention span changes tosleep habits, such as hypersomnia
or insomnia, mild confusion, euphoria, anxiety, short attention span,
impaired performance of addition
2 Moderate Minimally disoriented to time and place, lethargic, drowsiness, subtle
personality change, impaired performance of subtraction
3 Severe Somnolence but arousable, marked confusion, gross disorientation
4 Very severe Coma unresponsive to verbal or noxious stimuli
CLINICAL MANIFESTATIONS
• disordered consciousness
• confusion
• Unresponsive to verbal/ noxious stimuli
• the general features of organic psychosis
• a flapping tremor of the outstretched hands
• hypertonicity with flexor plantar response
• fetor hepaticus.
COMPLICATIONS
• haemorrhage
• Infection
• brain herniation
• brain swelling
• multiple organ failure
DIAGNOSIS
• Blood tests : CBC, sodium, potassium, ammonia, ABG analysis, BUN, creatinine
• Imaging test, such as a CT scan or MRI, can check for bleeding in your head or
abnormalities in your brain.
• GCS
• Liver function tests
TREATMENT
1. AIRWAY:
Those with severe encephalopathy (stages 3 and 4) are at risk of obstructing their airway due to
decreased protective reflexes such as the gag reflex. This can lead to respiratory arrest.
Transferring the person to a higher level of nursing care, such as an intensive care unit, is
required and intubation of the airway is often necessary to prevent life-threatening complications
(e.g., aspiration or respiratory failure).
In severe cases that cause difficulty breathing, a ventilator or oxygen mask may be necessary.
2. HYGIENIC AND ELIMINATION NEEDS
3. DIET:
• Placement of a nasogastric tube permits the safe administration of nutrients and
medication.
• A recent consensus statement from the International Society for Hepatic Encephalopathy
and Nitrogen Metabolism recommends that patients with recurrent or persistent hepatic
encephalopathy should consume a diet low in animal protein and rich in vegetable protein
4. LACTULOSE AND LACTITOL
Lactulose and lactitol are disaccharides that are not absorbed from the digestive tract. They are
thought to decrease the generation of ammonia by bacteria, render the ammonia inabsorbable by
converting it to ammonium (NH4
+
) ions, and increase transit of bowel content through the gut.
Doses of 15-30 ml are typically administered three times a day; the result is aimed to be 3–5 soft
stools a day, or (in some settings) a stool pH of <6.0.
5. ANTIBIOTICS
• The antibiotic rifaximin may be recommended in addition to lactulose for those with
recurrent disease.
• The antibiotics neomycin and metronidazole are other antibiotics used to treat hepatic
encephalopathy.
6. L-ORNITHINE AND L-ASPARTATE
• The combination of L-ornithine and L-aspartate (LOLA) lowers the level of ammonia in a
person's blood. LOLA lowers ammonia levels by increasing the generation of urea
through the urea cycle, a metabolic pathway that removes ammonia by turning it into the
neutral substance urea.
7. LIVER TRANSPLANT
PREVENTION
The best way to prevent hepatic encephalopathy is to prevent or manage liver disease. You can
lower your chances of getting liver disease by taking these steps:
• Avoid alcohol or consume it in moderation.
• Avoid high-fat foods.
• Maintain a healthy weight.
• Don’t share contaminated needles.
• To avoid getting viral hepatitis:
• Wash your hands well after using the bathroom or changing a diaper.
• Avoid close contact with people diagnosed with viral hepatitis.
• Get vaccinated against hepatitis A and hepatitis B.
NURSING MANAGEMENT
1. Disturbed consciousness
o Assess level of consciousness
o Monitor for restlessness and agitation
o Monitor handwriting daily; it becomes worse with increasing ammonia levels
o Assess deep tendon reflexes
o Evaluate serum ammonia values daily.
o Monitor for progress/ worsening of impending coma.
o Monitor electrolyte status and intervene as indicated to correct any imbalances.
o Monitor the client closely, and administer a conservative dose of prescribed
sedative or analgesic medication, because liver damage alters drug metabolism.
o Administer a high cleansing enema to reduce ammonia absorption from the GI
tract.
2. Activity intolerance; Self-care deficit; Impaired mobility;
o Use braden scale to assess the risk of bedsore
o Back care
o Skin care
o Do physiotherapy
o train family members to assist client in basic needs
3. Impaired social interaction; Ineffective role performance;
o Closely monitor neurologic status for any changes.
o Assess level of consciousness
o Monitor for restlessness and agitation
o Assess deep tendon reflexes
o Encourage family members to interact with the client frequently
o Support the family members to take up roles performed by the client before
4. Risk for injury
o Provide side rails
o Identify symptoms of seizure
o Maintain skin integrity
5. Imbalanced nutrition;
o Maintain adequate protein intake
o Start on RT feed based on the calorie requirement
6. Impaired verbal communication
o Explain the activities to the client and family members before it is done
7. Risk for aspiration;
o Start on RT feed, not oral feed until gag reflex regains
o Each time check for RT position before feed given
o If aspiration suspected, turn head to one side and do suction
8. Impaired gas exchange;
o Ckeck for signs of impaired circulation
o Administer oxygen
o Chest physiotherapy
o Suctioning
o ABG analysis
9. Impaired tissue integrity
o Use braden scale to assess the risk of bedsore
o Back care
o Skin care
o Do physiotherapy

1. hepatic coma converted

  • 1.
    NURSING MANAGEMENT OF APATIENT WITH HEPATIC COMA Mrs. Daisy Kuruvilla
  • 2.
    HEPATIC COMA DEFINITION • Hepaticencephalopathy (HE) is decline in brain function especially altered level of consciousness as a result of liver failure. In the advanced stages it can result in a coma called hepatic coma. • It is the coma induced by severe liver disease. • A coma occurring in advanced cirrhosis, hepatitis, poisoning, or other liver disease. RISK FACTORS • Acute fulminant viral hepatitis • Toxic hepatitis. caused by exposure to alcohol, chemicals, drugs, or supplements. • Reye’s syndrome. s primarily seen in children. It causes sudden swelling and inflammation of the liver and the brain. CAUSES • Laennec's cirrhosis (a type of cirrhosis of the liver characterized by a nodular appearance of the liver surface, associated with alcoholism.) • acute viral hepatitis • uremia PAHTOPHYSIOLOGY o liver fails to break down toxins properly o it’s triggered by a buildup of toxins in the bloodstream ( liver removes toxic chemicals such as ammonia from your body. These toxins are left over when proteins are metabolized or broken down for use by various organs in body. kidneys change these toxins into safer substances that are then removed through urination.) o When liver is damaged, it’s unable to filter out all the toxins. o Toxins can then build up in your bloodstream and potentially get into your brain. o Toxic buildup can also damage other organs and nerves. o Lead to neurogenic manifestations.
  • 3.
    Ammonia is producedin the gastrointestinal tract by the bacterial degradation of amines, amino acids, purines, and urea. Enterocytes also convert glutamine to glutamate and ammonia by the activity of glutaminase. Normally, ammonia is detoxified in the liver by conversion to urea by the Krebs-Henseleit cycle. Ammonia is also consumed in the conversion of glutamate to glutamine, a reaction that depends upon the activity of glutamine synthetase. glutamate is a nonessential amino acid and glutamine is a conditional amino acid. WHAT ARE THE DIFFERENT STAGES OF HEPATIC ENCEPHALOPATHY? Hepatic encephalopathy is divided into stages based on the severity of the symptoms. Common classification systems include the West Haven Criteria and the Glasgow Coma Scale. THE FIVE STAGES OF HEPATIC ENCEPHALOPATHY, ACCORDING TO THE WEST HAVEN CRITERIA, ARE: STAGE GRADE FEATURES 0 Normal symptoms are minimal. 1 Mild shortened attention span changes tosleep habits, such as hypersomnia or insomnia, mild confusion, euphoria, anxiety, short attention span, impaired performance of addition 2 Moderate Minimally disoriented to time and place, lethargic, drowsiness, subtle personality change, impaired performance of subtraction 3 Severe Somnolence but arousable, marked confusion, gross disorientation 4 Very severe Coma unresponsive to verbal or noxious stimuli CLINICAL MANIFESTATIONS • disordered consciousness • confusion • Unresponsive to verbal/ noxious stimuli • the general features of organic psychosis • a flapping tremor of the outstretched hands • hypertonicity with flexor plantar response • fetor hepaticus.
  • 4.
    COMPLICATIONS • haemorrhage • Infection •brain herniation • brain swelling • multiple organ failure DIAGNOSIS • Blood tests : CBC, sodium, potassium, ammonia, ABG analysis, BUN, creatinine • Imaging test, such as a CT scan or MRI, can check for bleeding in your head or abnormalities in your brain. • GCS • Liver function tests TREATMENT 1. AIRWAY: Those with severe encephalopathy (stages 3 and 4) are at risk of obstructing their airway due to decreased protective reflexes such as the gag reflex. This can lead to respiratory arrest. Transferring the person to a higher level of nursing care, such as an intensive care unit, is required and intubation of the airway is often necessary to prevent life-threatening complications (e.g., aspiration or respiratory failure). In severe cases that cause difficulty breathing, a ventilator or oxygen mask may be necessary. 2. HYGIENIC AND ELIMINATION NEEDS 3. DIET: • Placement of a nasogastric tube permits the safe administration of nutrients and medication. • A recent consensus statement from the International Society for Hepatic Encephalopathy and Nitrogen Metabolism recommends that patients with recurrent or persistent hepatic encephalopathy should consume a diet low in animal protein and rich in vegetable protein 4. LACTULOSE AND LACTITOL Lactulose and lactitol are disaccharides that are not absorbed from the digestive tract. They are thought to decrease the generation of ammonia by bacteria, render the ammonia inabsorbable by converting it to ammonium (NH4 + ) ions, and increase transit of bowel content through the gut. Doses of 15-30 ml are typically administered three times a day; the result is aimed to be 3–5 soft stools a day, or (in some settings) a stool pH of <6.0. 5. ANTIBIOTICS • The antibiotic rifaximin may be recommended in addition to lactulose for those with recurrent disease. • The antibiotics neomycin and metronidazole are other antibiotics used to treat hepatic encephalopathy.
  • 5.
    6. L-ORNITHINE ANDL-ASPARTATE • The combination of L-ornithine and L-aspartate (LOLA) lowers the level of ammonia in a person's blood. LOLA lowers ammonia levels by increasing the generation of urea through the urea cycle, a metabolic pathway that removes ammonia by turning it into the neutral substance urea. 7. LIVER TRANSPLANT PREVENTION The best way to prevent hepatic encephalopathy is to prevent or manage liver disease. You can lower your chances of getting liver disease by taking these steps: • Avoid alcohol or consume it in moderation. • Avoid high-fat foods. • Maintain a healthy weight. • Don’t share contaminated needles. • To avoid getting viral hepatitis: • Wash your hands well after using the bathroom or changing a diaper. • Avoid close contact with people diagnosed with viral hepatitis. • Get vaccinated against hepatitis A and hepatitis B. NURSING MANAGEMENT 1. Disturbed consciousness o Assess level of consciousness o Monitor for restlessness and agitation o Monitor handwriting daily; it becomes worse with increasing ammonia levels o Assess deep tendon reflexes o Evaluate serum ammonia values daily. o Monitor for progress/ worsening of impending coma. o Monitor electrolyte status and intervene as indicated to correct any imbalances. o Monitor the client closely, and administer a conservative dose of prescribed sedative or analgesic medication, because liver damage alters drug metabolism. o Administer a high cleansing enema to reduce ammonia absorption from the GI tract. 2. Activity intolerance; Self-care deficit; Impaired mobility; o Use braden scale to assess the risk of bedsore o Back care o Skin care o Do physiotherapy o train family members to assist client in basic needs 3. Impaired social interaction; Ineffective role performance; o Closely monitor neurologic status for any changes. o Assess level of consciousness o Monitor for restlessness and agitation o Assess deep tendon reflexes o Encourage family members to interact with the client frequently o Support the family members to take up roles performed by the client before
  • 6.
    4. Risk forinjury o Provide side rails o Identify symptoms of seizure o Maintain skin integrity 5. Imbalanced nutrition; o Maintain adequate protein intake o Start on RT feed based on the calorie requirement 6. Impaired verbal communication o Explain the activities to the client and family members before it is done 7. Risk for aspiration; o Start on RT feed, not oral feed until gag reflex regains o Each time check for RT position before feed given o If aspiration suspected, turn head to one side and do suction 8. Impaired gas exchange; o Ckeck for signs of impaired circulation o Administer oxygen o Chest physiotherapy o Suctioning o ABG analysis 9. Impaired tissue integrity o Use braden scale to assess the risk of bedsore o Back care o Skin care o Do physiotherapy