1. Internal medicine L-5 Hepatic Encephalopathy
Prepared by:
Kholod Hamad
MSc clinical pharmacy, BCPS

2. Hepatic Encephalopathy HE
Definition: Hepatic encephalopathy is a brain dysfunction caused by liver insufficiency or portosystemic shunting;
it manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma.

4. Thought to be secondary to the accumulation of nitrogenous substances (mainly NH3) arising from the gut; overall, NH3 serum concentrations do not correlate well with mental status
Other theories are related to the activation of GABA (γ-aminobutyric acid receptors) by endogenous benzodiazepine-like substances, possible zinc deficiency, or altered cerebral metabolism.

5. Management of Hepatic Encephalopathy HE
Treatment a. Assess need for airway support and remove possible precipitating factors. b. Main treatments targeted at reducing the nitrogen load in the gut c. Lactulose d. Antibiotics e. Treat drug induce HE

6. Hepatic Encephalopathy
R.C., a 57-year-old man, was admitted to the hospital because of nausea, vomiting, and abdominal pain. He had a long history of alcohol abuse, with multiple hospital admissions for alcoholic gastritis and alcohol withdrawal. Physical examination revealed a cachectic male patient (weighing 55 kg) with clouded mentation who was not responsive to questions about name and place. Tense ascites and edema were noted, and the liver was percussed at 9 cm below the right costal margin. The spleen was not palpated, and no active bowel sounds were heard.

7. Laboratory results on admission included the following:
BUN, 24 mg/dL SCr, 1.4 mg/dL
Hgb, 9.2 g/dL Hct, 24.1%
AST, 520 IU
Alkaline phosphatase, 218 IU
LDH 305 IU
Total bilirubin, 3.5 mg/dL
PT, 22 seconds (INR 1.8)

8. The patient was placed on diuretic therapy in an attempt to reduce the edema and ascites. Morphine sulfate and prochlorperazine were ordered for his abdominal pain and nausea respectively. Two days after admission, R.C. had an episode of hematemesis. He became mentally confused and at times nonresponsive to verbal command. An NG tube was inserted and coffee-ground material was produced on continuous suctioning. Saline lavage was continued until the aspirate became clear. The next morning, R.C. was still in a confused mental state. He demonstrated prominent asterixis, and fetor hepaticus was noted on his breath

9. Hepatic encephalopathy and upper GI bleeding were added to the problem list.
Questions
What aspects of R.C.’s history are compatible with a diagnosis of hepatic encephalopathy?
What are the drug related problems in Mr. RC?
Outline the therapeutic alternatives for management of Mr. RC encephalopathy?
What is the optimum treatment plan in Mr RC?

10. What monitoring are required for Mr RC?
What counseling is to ensure that Mr RC’s medication is effective and had least side effects?

11. References
Clinical pharmacy & therapeutics, Edi 5, chapter 16 Liver disease. Page 238