Hepatic Coma Nursing Management

 HEPATIC COMA

Hepatic coma, one of the dreaded complications of liver disease, occurs with profound liver failure and results from the accumulation of ammonia and other identified toxic metabolites in the blood.

Ammonia accumulates because damaged liver cells fail to detoxify and convert to urea the ammonia that is constantly entering the bloodstream as a result of its absorption from the GIT and its liberation from kidney and muscle cells.]

[Normally, NH, produced by protein Breakdown in the bowel in metabolized to urea in the liver.]

Causes

• Precise Etiology - unknown
• As a result of chronic hepatic disease.

Pathophysiology

Chronic hepatic disease
⬇
Damaged hepatic cells
⬇
Fails to detoxify NH3 and convert it to urea
⬇
NH, directly enters systemic circulation [absorption from GIT and its liberation from kidney and muscle cells] muscle
⬇
NH, carried to brain
⬇
Increased NH, concentration in blood.
⬇
Brain dysfunction and damage
⬇
Hep. encephalopathy and hep. coma

Clinical Manifestations

Patient will be

(1) slightly confused, alterations in mood
(2) He becomes untidy and experiences altered sleep patterns [sleeps during the day and restlessness and insomnia at night]. As coma progresses he may be
(3) difficult to awaken
(4) Asterixis or flapping tremor of the hands.
(5) Occasionally fetor hepaticus, à characteristic breath odor like Freshly mowed grass, acetone or old urine.
(6) More advanced stages gross disturbances of consciousness and patient will be completely disoriented with respect to time and place. Later he lapses into frank coma and may have convulsions.

Diagnostic Investigations

1. Clinical features
2. Serum ammonia levels in venous and arterial samples are elevated.
3. Electroencephalography - shows generalized slowing and an increase in amplitude of brain waves.

Medical Management

1. Treatment eliminates NH, from GIT
2. Administration of neomycin to suppress bacterial flora (preventing them from converting amino acids into ammonia),
3. Sorbitol-induced catharsis to produce osmotic diarrhea.
4. Continuous aspiration of blood from the stomach.
5. Reduction of dietarý protein intake
6. To reduce ammonia absorption from the GIT, a high cleaning enema may be prescribed. Lactulose (Cephulac) is given to reduce blood ammonia which promotes the excretion of ammonia in the stool. [Bacterial enzyme in colon change lactulose to lactic acid, thereby rendering the colon too acidic for bacterial growth. The resulting increase in free H prevents diffusion of NH, through the mucosa, lactulose promotes conversion of systemically absorbable NH, to ammonium, which is poorly absorbed and can be excreted]. Maintain a fluid and electrolyte balance.

Nursing Management

1. Frequently assess and record patient's level of consciousness. Orient him to place and time. Keep a daily record of patient's handwriting to monitor progression of neurologic involvement.
2. Promote rest, comfort and a quiet atmosphere. Discourage stressful exercise.
3. Monitor I/O and fluid and e balance. Check weight and abdominal girth daily.
4. Monitor patient's serum ammonia level [for signs of
5. improvement]. Administer medication as ordered. Watch for side effects.
6. Provide low-protein diet, with CHO supplying most of the calories. Provide good mouth care, As ordered, provide parenteral nutrition to the semicomatose or comatose patient.
7. Use safety measures to protect patient from injury. Avoid physical restraints.
8. Don't give sedation (semicomatose or comatose patient)
9. Deepen the coma. Protect patient's eyes from corneal injury by using artificial tears or eye patches.
10. Provide emotional support to patient's family.