What are the chances?

The approach to clinical conundrums by an expert clinician is revealed through the presentation of an actual patient’s case in an approach typical of a morning report. Similarly to patient care, sequential pieces of information are provided to the clinician, who is unfamiliar with the case. The focus is on the thought processes of both the clinical team caring for the patient and the discussant. The bolded text represents the patient’s case. Each paragraph that follows represents the discussant’s thoughts.

Two weeks after undergoing a below-knee amputation (BKA) and 10 days after being discharged to a skilled nursing facility (SNF), an 87-year-old man returned to the emergency department (ED) for evaluation of somnolence and altered mental state. In the ED, he was disoriented and unable to provide a detailed history.

The differential diagnosis for acute confusion and altered consciousness is broad. Initial possibilities include toxic-metabolic abnormalities, medication side effects, and infections. Urinary tract infection, pneumonia, and surgical-site infection should be assessed for first, as they are common causes of postoperative altered mentation. Next to be considered are subclinical seizure, ischemic stroke, and infectious encephalitis or meningitis, along with hemorrhagic stroke and subdural hematoma.

During initial assessment, the clinician should ascertain baseline mental state, the timeline of the change in mental status, recent medication changes, history of substance abuse, and concern about any recent trauma, such as a fall. Performing the physical examination, the clinician should assess vital signs and then focus on identifying localizing neurologic deficits.

First steps in the work-up include a complete metabolic panel, complete blood cell count, urinalysis with culture, and a urine toxicology screen. If the patient has a “toxic” appearance, blood cultures should be obtained. An electrocardiogram should be used to screen for drug toxicity or evidence of cardiac ischemia. If laboratory test results do not reveal an obvious infectious or metabolic cause, a noncontrast computed tomography (CT) of the head should be obtained. In terms of early interventions, a low glucose level should be treated with thiamine and then glucose, and naloxone should be given if there is any suspicion of narcotic overdose.

More history was obtained from the patient’s records. The BKA was performed to address a nonhealing transmetatarsal amputation. Two months earlier, the transmetatarsal amputation had been performed as treatment for a diabetic forefoot ulcer with chronic osteomyelitis. The patient’s post-BKA course was uncomplicated. He was started on intravenous (IV) ertapenem on postoperative day 1, and on postoperative day 4 was discharged to the SNF to complete a 6-week course of antibiotics for osteomyelitis. Past medical history included paroxysmal atrial fibrillation, coronary artery disease, congestive heart failure (ejection fraction 40%), and type 2 diabetes mellitus. Medications given at the SNF were oxycodone, acetaminophen, cholecalciferol, melatonin, digoxin, ondansetron, furosemide, gabapentin, correctional insulin, tamsulosin, senna, docusate, warfarin, and metoprolol. While there, the patient’s family expressed concern about his diminishing “mental ability.” They reported he had been fully alert and oriented on arrival at the SNF, and living independently with his wife before the BKA. Then, a week before the ED presentation, he started becoming more somnolent and forgetful. The gabapentin and oxycodone dosages were reduced to minimize their sedative effects, but he showed no improvement. At the SNF, a somnolence work-up was not performed.

Several of the patient’s medications can contribute to altered mental state. Ertapenem can cause seizures as well as profound mental status changes, though these are more likely in the setting of poor renal function. The mental status changes were noticed about a week into the patient’s course of antibiotics, which suggests a possible temporal correlation with the initiation of ertapenem. An electroencephalogram is required to diagnose nonconvulsive seizure activity. Narcotic overdose should still be considered, despite the recent reduction in oxycodone dosage. Digoxin toxicity, though less likely when the dose is stable and there are no changes in renal function, can cause a confused state. Concurrent use of furosemide could potentiate the toxic effects of digoxin.

Non-medication-related concerns include hypoglycemia, hyperglycemia, and, given his history of atrial fibrillation, cardioembolic stroke. Although generalized confusion is not a common manifestation of stroke, a thalamic stroke can alter mental state but be easily missed if not specifically considered. Additional lab work-up should include a digoxin level and, since he is taking warfarin, a prothrombin time/international normalized ratio (PT/INR). If the initial laboratory studies and head CT do not explain the altered mental state, magnetic resonance imaging (MRI) of the brain should be performed to further assess for stroke.

On physical examination in the ED, the patient was resting comfortably with eyes closed, and arousing to voice. He obeyed commands and participated in the examination. His Glasgow Coma Scale score was 13; temperature, 36.8°C, heart rate, 80 beats per minute; respiratory rate, 16 breaths per minute; blood pressure, 90/57 mm Hg; and 100% peripheral capillary oxygen saturation while breathing ambient air. He appeared well developed. His heart rhythm was irregularly irregular, without murmurs, rubs, or gallops. Respiratory and abdominal examination findings were normal. The left BKA incision was well approximated, with no drainage, dehiscence, fluctuance, or erythema. On neurologic examination, the patient was intermittently oriented only to self. Pupils were equal, round, and reactive to light; extraocular movements were intact; face was symmetric; tongue was midline; sensation on face was equal bilaterally; and shoulder shrug was intact. Strength was 5/5 and symmetric in the elbow and hip and 5/5 in the right knee and ankle (not tested on left because of BKA). Deep tendon reflexes were 3+ and symmetrical at the biceps, brachioradialis, and triceps tendons and 3+ in the right patellar and Achilles tendons. Sensation was intact and symmetrical in the upper and lower extremities. The patient’s speech was slow and slurred, and his answers were unrelated to the questions being asked.

The patient’s mental state is best described as lethargic. As he is only intermittently oriented, he meets the criteria for delirium. He is not obtunded or comatose, and his pupils are at least reactive, not pinpoint, so narcotic overdose is less likely. Thalamic stroke remains in the differential diagnosis; despite the seemingly symmetrical sensation examination, hemisensory deficits cannot be definitively ruled out given the patient’s mental state. A rare entity such as carcinomatosis meningitis or another diffuse, infiltrative neoplastic process could be causing his condition. However, because focal deficits other than abnormal speech and diffuse hyperreflexia are absent, toxic, infectious, or metabolic causes are more likely than structural abnormalities. Still possible is a medication toxicity, such as ertapenem toxicity or, less likely, digoxin toxicity. In terms of infectious possibilities, urinary tract infection could certainly present in this fashion, especially if the patient had a somewhat low neurologic reserve at baseline, and hypotension could be secondary to sepsis. Encephalitis or meningitis remains in the differential diagnosis, though the patient appears nontoxic, and therefore a bacterial etiology is very unlikely.