Review Question - QID 213876

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Hepatic Encephalopathy Introduction Pathogenesis QID: 213876 (M1.OMB.20.1)

QID 213876 (Type "213876" in App Search)

A 55-year-old woman is admitted into the hospital for progression of breast cancer. During her hospital stay, she is found to be more lethargic, appears depressed, and is less interactive with her family. There were no recent medication changes, and she has not had fevers during her hospital stay. Her medical history is significant for stage IV breast cancer complicated by metastasis to her brain and bones. She also has a history of hypertension and hyperlipidemia. On neurologic examination, the patient is awake but is not interactive. She becomes somnolent during the examination. She is oriented to self but not place or date. She has poor attention and concentration and is able to follow simple commands. She moves all four of her extremities against gravity but shows poor effort to engage in motor confrontational testing. She withdraws to noxious stimuli in all her extremities. When her arms are outstretched, she is noted to have asterixis. An electroencephalogram is performed which demonstrates diffuse cerebral slowing and triphasic waves. Laboratory studies are shown below:

Hemoglobin: 14 g/dL
Hematocrit: 41%
Leukocyte count: 8,500/mm^3 with normal differential
Platelet count: 220,000/mm^3

Serum:
Na+: 141 mEq/L
Cl-: 98 mEq/L
K+: 3.8 mEq/L
HCO3-: 24 mEq/L
BUN: 29 mg/dL
Glucose: 140 mg/dL
Creatinine: 1.1 mg/dL

Which of the following is the most likely cause of her poor mental status?

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Depression

13%

34/271

Infection

8/271

Liver disease

61%

166/271

Seizure

20/271

Stroke

10%

28/271

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This patient is presenting with altered mental status, asterixis, transaminitis, and hyperammonemia, in the context of metastatic breast cancer. This patient has liver disease (likely metastasis) leading to her altered mental status.

Hepatic encephalopathy describes an alteration in cerebral function secondary to impaired liver function or portosystemic shunting. In liver impairment, the liver is unable to metabolize ammonia into urea. In portosystemic shunting, the ammonia-rich blood bypasses the liver and eventually reaches the brain. The mechanism by which altered cerebral function occurs is not fully clear; however, it is believed to be due to the toxic effects of hyperammonemia in cerebral function. As ammonia crosses the blood-brain barrier, it gets converted to glutamine within astrocytes via glutamine synthetase, leading to cerebral edema. Glutamine also leads to increased reactive oxygen species within astrocytes, and ammonia itself alters neurotransmitter function. Patients typically present with confusion, behavior change, lethargy, somnolence, and even coma.

Incorrect Answers:
Answer 1: Depression can make patients less interactive; however, they typically are not confused and somnolent. Also, one would not expect to see triphasic waves and asterixis in depression.

Answer 2: Infection can result in altered mental status as it can cause encephalitis or meningitis; however, this patient does not have an elevated white blood cell count and is found to have a notable transaminitis and hyperammonemia.

Answer 4: Seizure can result in altered mental status; however, the patient’s altered mental status has been sustained and progressively worsening, without evidence of limb shaking or gaze-deviation. Also, the patient’s electroencephalogram demonstrates triphasic waves, which is seen in patients with toxic and metabolic illness.

Answer 5: Stroke can result in altered mental status; however, the patient would have focal deficits such as limb and facial weakness.

Bullet Summary:
Hepatic encephalopathy results from hyperammonemia and leads to altered mental status with asterixis.

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