What are the chances?

The patient’s hyperreflexia may be an important clue. Although the strength of his reflexes at baseline is unknown, seizures can cause transiently increased reflexes as well as a confused, lethargic mental state. Reflexes can also be increased by a drug overdose that has caused serotonin syndrome. Of the patient’s medications, only ondansetron can cause this reaction. Hyperthyroidism can cause brisk reflexes and confusion, though more typically it causes agitated confusion. A thyroid-stimulating hormone level should be added to the initial laboratory panel.

A complete blood count revealed white blood cell count 11.86 K/uL with neutrophilic predominance and immature granulocytes, hemoglobin 11.5 g/dL, and platelet count 323 K/uL. Serum sodium was 141 mEq/L, potassium 4.2 mEq/L, chloride 103 mEq/L, bicarbonate 30 mEq/L, creatinine 1.14 mg/dL (prior baseline of 0.8-1.0 mg/dL), blood urea nitrogen 26 mg/dL, blood glucose 159 mg/dL, and calcium 9.1 mg/dL. His digoxin level was 1.3 ng/mL (reference range 0.5-1.9 mg/mL) and troponin was undetectable. INR was 2.7 and partial thromboplastin time (PTT) 60 seconds. Vitamin B₁₂ level was 674 pg/mL (reference range >180). A urinalysis had 1+ hyaline casts and was negative for nitrites, leukocyte esterase, blood, and bacteria. An ECG revealed atrial fibrillation with a ventricular rate of 80 beats per minute. A chest radiograph showed clear lung fields. A CT of the head without IV contrast had no evidence of an acute intracranial abnormality. In the ED, 1 liter of IV normal saline was given and blood pressure improved to 127/72 mm Hg.

The head CT does not show intracranial bleeding, and, though it is reassuring that INR is in the therapeutic range, ischemic stroke must remain in the differential diagnosis. Sepsis is less likely given that the criteria for systemic inflammatory response syndrome are not met, and hypotension was rapidly corrected with administration of IV fluids. Urinary tract infection was ruled out with the negative urinalysis. Subclinical seizures remain possible, as does medication-related or other toxicity. A medication overdose, intentional or otherwise, should also be considered.

The patient was admitted to the hospital. On reassessment by the inpatient team, he was oriented only to self, frequently falling asleep, and not recalling earlier conversations when aroused. His speech remained slurred and difficult to understand. Neurologic examination findings were unchanged since the ED examination. On additional cerebellar examination, he had dysmetria with finger-to-nose testing bilaterally and dysdiadochokinesia (impaired rapid alternating movements) of the left hand.

His handedness is not mentioned; the dysdiadochokinesia of the left hand may reflect the patient’s being right-handed, or may signify a focal cerebellar lesion. The cerebellum is also implicated by the bilateral dysmetria. Persistent somnolence in the absence of CT findings suggests a metabolic or infectious process. Metabolic processes that can cause bilateral cerebellar ataxia and somnolence include overdose of a drug or medication. Use of alcohol or a medication such as phenytoin, valproic acid, or a benzodiazepine can cause the symptoms in this case, but was not reported by the family, and there was no documentation of it in the SNF records. Wernicke encephalopathy is rare and is not well supported by the patient’s presentation but should be considered, as it can be easily treated with thiamine. Meningoencephalitis affecting the cerebellum remains possible, but infection is less likely. Both electroencephalogram and brain MRI should be performed, with a specific interest in possible cerebellar lesions. If the MRI is unremarkable, a lumbar puncture should be performed to assess opening pressure and investigate for infectious etiologies.

MRI of the brain showed age-related volume loss and nonspecific white matter disease without acute changes. Lack of a clear explanation for the neurologic findings led to suspicion of a medication side effect. Ertapenem was stopped on admission because it has been reported to rarely cause altered mental status. IV moxifloxacin was started for the osteomyelitis. Over the next 2 days, symptoms began resolving; within 24 hours of ertapenem discontinuation, the patient was awake, alert, and talkative. On examination, he remained dysarthric but was no longer dysmetric. Within 48 hours, the dysarthria was completely resolved, and he was returned to the SNF to complete a course of IV moxifloxacin.

Among elderly patients presenting to the ED, altered mental status is a common complaint, accounting for 10% to 30% of visits.¹ Medications are a common cause of altered mental status among the elderly and are responsible for 40% of delirium cases.¹ The risk of adverse drug events (ADEs) rises with the number of medications prescribed.^1-3 Among patients older than 60 years, the incidence of polypharmacy (defined as taking >5 prescription medications) increased from roughly 20% in 1999 to 40% in 2012.^4,5 The most common ADEs in the ambulatory setting (25%) are central nervous system (CNS) symptoms, including dizziness, sleep disturbances, and mood changes.⁶ A medication effect should be suspected in any elderly patient presenting with altered mental state.