Hypotension in a Patient With Progressive Neurological Decline

Case Study

A rapid response was called for a patient because of new-onset hypothermia and hypotension. Upon the rapid response team’s arrival, the patient was noted to be a 78-year-old female with a known history of hypertension treated with amlodipine and osteoporosis. She was admitted earlier in the day as a direct admission from the clinic for failure to thrive. Her daughter had found her unable to care for herself at home because of progressive fatigue, lethargy, somnolence, and dyspnea on exertion. She had also been unsteady on her feet and had had a few near falls.

Vital Signs

Temperature: 93.7 °F, rectal
Blood Pressure: 80/62 mmHg
Heart Rate: 48 beats per min (bpm), sinus bradycardia on telemetry ( Fig. 58.1 )

Fig. 58.1

Telemetry strip showing sinus bradycardia with a heart rate of 48 bpm.
Respiratory Rate: 8 breaths per min
Pulse Oximetry: 97% on room air

Focused Physical Examination

A quick exam revealed a somnolent older woman in no apparent distress. She was opening her eyes only to painful stimuli and was responding in a garbled voice. Her responses were incomprehensible. She could move all limbs spontaneously but could not follow simple commands. Cardiac and pulmonary exams were unremarkable. The abdomen was benign.

Interventions

A cardiac monitor and pacer pads were attached to the patient’s chest. A 1 L bolus of normal saline was ordered stat. Point-of-care glucose level was checked and noted to be 65 mg/dL. Then, 25 g of 50% IV dextrose was administered, which improved the blood glucose but had no effect on the patient’s mental status. Stat complete blood count (CBC), comprehensive metabolic panel (CMP), arterial blood gas (ABG), and lactate were obtained, which came back unremarkable except for mild hyponatremia of 131. Blood cultures were drawn, and broad-spectrum antibiotics were initiated. A review of labs from admission showed a thyroid-stimulating hormone (TSH) of 125 mIU/L. Free T4 was undetectable. The patient was given 100 mg IV hydrocortisone. Stat consult was called to endocrinology, who recommended 200 mcg IV levothyroxine which was initiated. Given worsening altered mentation, there was a concern for the protection of the airway. The patient was intubated and transferred to the intensive care unit for further care.

Final Diagnosis

Myxedema coma.

Myxedema Coma

The thyroid hormone is one of the primary regulators of metabolism in the human body. The thyroid hormone production is regulated by a negative feedback loop in the hypothalamic-pituitary-thyroid (HPT) axis. Reduction in circulating levels of thyroid hormone or increase in the body’s demand for thyroid hormone leads to a fall in blood levels, which then leads to increased production of thyrotropin-releasing hormone from the hypothalamus, which in turn stimulates the production of TSH from the pituitary gland, which leads to increased production of T4 and T3 ( Fig. 58.2 ). The reverse occurs when there is excess thyroid hormone (T4 and T3) in the blood.

Myxedema coma is a severe, life-threatening endocrinopathy caused by a severe deficiency of thyroid hormone. The mortality rate approaches 30%-50%. The dysfunction of thyroid hormone production can occur at any level of the HPT axis. It is usually seen in patients with uncontrolled hypothyroidism when they face a precipitating event. See Table 58.1 for classification of hypothyroidism.

Table 58.1

Classification of hypothyroidism

	Primary hypothyroidism	Central hypothyroidism
	Primary hypothyroidism	Secondary	Tertiary
Mechanism	Defect at the level of the thyroid gland	Defect at the level of the pituitary gland	Defect at the level of the hypothalamus
Examples	Hashimoto thyroiditis	Pituitary macroadenoma	Stroke affecting hypothalamus
Lab features	Increased thyrotropin-releasing hormone (TRH), thyroid-stimulating hormone (TSH) Decreased T4, T3	Increased TRH Decreased TSH, T4, T3	Decreased TRH, TSH, T4, T3