Confused, cold, and lethargic

CASE Confused and cold

Ms. K, age 48, is brought to the emergency department (ED) by her husband because she has become increasingly lethargic over the past 2 weeks and cannot attend to activities of daily living. She is incontinent of stool and poorly responsive.

Ms. K’s husband reports that lethargy culminated in his wife sleeping 30 continuous hours. She has a history of a ruptured cerebral arteriovenous malformation (AVM) complicated by a secondary infarct 7 years ago, with residual symptoms of frontal lobe syndrome. Until 2 weeks ago, however, she was in her usual state of health.

Symptoms have included depression, mood lability, impulsivity, disinhibition, poor focus, and apathy. An outpatient psychiatrist has managed these symptoms with antidepressants and atypical antipsychotics.

When Ms. K arrives in the ED, she is taking citalopram, 30 mg/d, and paliperidone,
6 mg/d. Her psychiatrist started paliperidone 2 months ago, increasing the dosage to 6 mg/d 6 weeks before presentation because of worsening mood lability, disinhibition, and paranoia regarding her caregivers. Her husband denies any other medication changes or exposure to environmental toxins.

In the ED, Ms. K is confused and oriented only to person. Vital signs are: pulse 46 bpm; blood pressure, 66/51 mm Hg; respirations, 12/min; and temperature, 29.9ºC (85.8ºF) via bladder probe.

The authors’ observations

Hypothermia is core body temperature <35ºC (95ºF).¹ It often is caused by exposure to low ambient temperature (Table 1),¹ but Ms. K’s husband denied that she had been exposed to cold. Because of Ms. K’s neurologic history, stroke was high on the differential diagnosis, but physical examination did not reveal evidence of focal dysfunction and was significant only for altered mental status.

Ms. K had no posturing, rigidity, negativism, or excessive motor activity that would suggest catatonia. Before she became lethargic, her husband had not noted any deterioration of mood, although she did exhibit other behavioral changes that prompted her outpatient psychiatrist to increase the dosage of paliperidone. Although Ms. K began experiencing persecutory delusions—she believed that her caregivers were trying to harm her—she and her family denied perceptual disturbances. On examination, she did not appear responsive to auditory or visual hallucinations.

Frontal lobe syndrome is defined as a set of changes in the cognitive, behavioral, or emotional domains, often leading to disturbed affect, alteration of attention, aphasia, perseveration, disinhibition, and personality changes.² These symptoms are not specific to lesions in the frontal lobes but can arise from lesions anywhere in the frontal-striatal-thalamic circuit.³ Causes include traumatic brain injury, neurodegenerative disorders, cerebrovascular disease, tumors, and aging.² Recommended treatment incorporates psychosocial interventions with drug treatment to target specific symptoms. Medications reported to be effective include typical and atypical antipsychotics to target aggression and agitation; benzodiazepines to reduce arousal; antidepressants for mood symptoms, dopamine agonists (eg, bromocriptine) to decrease apathy, and mood stabilizers to target mood lability.⁴

Before her AVM rupture, review of Ms. K’s psychiatric history revealed no psychiatric symptoms or impaired functioning. When hospitalized for the AVM repair, she was started on sertraline. She began seeing a psychiatrist 2 years later because of increased agitation and behavioral disturbances, and aripiprazole was added. Persistent agitation prompted a trial of divalproex sodium, which was discontinued because of slurred speech and increased distractibility. Aripiprazole was tapered and replaced with paliperidone because of poor response. Citalopram was initiated 1 year before she presented to the ED.

EVALUATION Hypothermia

Laboratory tests reveal multiple abnormalities, including thrombocytopenia (platelet level, 53 ×10³/μL), altered coagulation (partial thromboplastin time, 55.6 s), elevated levels of hepatic transaminases (aspartate aminotransferase, 168 U/L; alanine aminotransferase, 357 U/L), and increased alkaline phosphatase (206 U/L). Other mild metabolic disturbances include: sodium, 149 mEq/L; CO₂, 33 mEq/L; and blood urea nitrogen, 24 mg/dL.

These laboratory values are consistent with complications of hypothermia.¹

ECG reveals sinus bradycardia (40 bpm) and Osborn waves (additional deflection at the end of the QRS complex), which are seen often in hypothermia.¹ Head CT and brain MRI show chronic changes after Ms. K’s right temporoparietal AVM rupture, but no acute abnormality. Urinalysis, blood cultures, and chest radiographs are negative for infection. Urine toxicology screen is negative. Results of thyroid function tests and pituitary hormones studies are significant only for hyperprolactinemia of 155.7 ng/mL, a known adverse effect of antipsychotics.⁵