This morning we discussed a case of a 60 year old male with end stage liver disease secondary to Hepatitis C who presented with confusion. Dr Panisko guided us through the process of building a differential diagnosis using the patient's past medical history as a starting point. This is a useful method of organizing your approach, especially when faced with a non-specific presentation such as confusion. Another useful acronym for an approach to delirium is DIMS:

D - Drugs, drugs, drugs
I - Infection
M - Metabolic derangement (endocrine, electrolyte)
S - Structural (intra-cranial process, liver/renal/heart failure)

 Inouye SK. Delirium in older persons. N Engl J Med. 2006;354: 1157-1165

Our patient had multiple possible causes for his confusion:

1) Drugs: Drugs are the most common causes of delirium. Common culprits are psychotropic meds (anxiolytics, antipsychotics, dopamine agonists), anticholinergics, analgesics (opioids), corticosteroids, anticonvulsants etc. Our patient was on seroquel, paroxetine and bupropion, all of which may have contributed to his delirium. One must think of serotonin syndrom given this patient's use of an SSRI. The patient however did not fulfill the Hunter criteria for serotonin syndrome, which includes history of ingesting a seritonergic agent and one of:

• Spontaneous clonus
• Inducible clonus PLUS agitation or diaphoresis
• Ocular clonus PLUS agitation or diaphoresis
• Tremor PLUS hyperreflexia
• Hypertonia PLUS temperature above 38ºC PLUS ocular clonus or inducible clonus

2) Hepatic encephalopathy: Our patient had allegedly stopped his lactulose which puts him at risk for developing hepatic encephalopathy. The pathophysiology of this involves increased blood to brain transport of neurotoxins (such as amonia, amino acids) and biochemical alterations in the uptake and function of neurotransmitters. Up to Date has a good review on the pathophysiology of HE.

3) Infection: Patients with cirrhosis have altered immune defenses and are considered immunocompromised individuals. Changes in gut motility and increased translocation of bacteria can result in increased risk of developing SBP and other infections. Early treatment of infection is important in end stage liver disease (Management of bacterial infections in cirrhosis, J Hepatol. 2012;56 Suppl 1:S1-12)

4) Hyponatremia: Patients with cirrhosis are at risk for developing hyponatremia. This is largely secondary to the systemic vasodilation resulting in the activation of the renin-angiotensin system and ADH, thereby decreaseing the kidney's ability to excrete free water. Treatment for hyponatremia in cirrhosis involves fluid restriction and vasopressin receptor antagonists.

Physical Exam




We reviewed the physical exam for ascites. The following is a table from the JAMA Rational Clinical Exam series for ascites:

JAMA. 1992. 267 (19): 2645-2649

Bottom line:
1. Sensitive tests for Ruling OUT ascites:

• Negative history for ankle swelling/increased abdo girth

• Lack of bulging flanks, flank dullness or shifting dullness

2. Specific tests for Ruling IN ascites:

• Positive shifting dullness and fluid wave