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<< Identifying And Treating Thyroid Storm And Myxedema Coma In The Emergency Department

ED Evaluation

Initial Approach

When the patient arrives at the ED, the emergency clinician's initial efforts should focus on respiratory and cardiovascular stabilization. Concomitant with the initial assessment, start cardiac monitoring, begin continuous pulse oximetry, determine blood glucose levels and core temperature, and establish intravenous access. Patients presenting with an altered level of consciousness may require emergent, definitive airway control. Hypotensive patients warrant initial treatment with an isotonic intravenous solution before beginning vasopressors. Hypothermic patients need gentle external rewarming, unless core temperatures are critically low. Consider chemical restraint for the extremely agitated, combative patient. Strainingagainst physical restraints can worsen hyperthermia, rhabdomyolysis, and dehydration in hyperthyroidism. Sudden cardiovascular collapse may result. Investigate and intervene in conditions such as systemic infections, acute myocardial infarction, trauma, stroke, intoxication, and other sources of physiologic stress that may exacerbate hypo- and hyperthyroidism.

Important Historical Questions (From Patient, Medics, Witnesses, Family, And Other People)

Patients with thyrotoxicosis report hyperadrenergic symptoms that include palpitations, nervousness, agitation, and tremor. A focused review of systems may reveal a history of weight loss, dyspnea, fever, agitation, anxiety, restlessness, proximal myopathy, menstrual irregularity, and heat intolerance. Considered together, these common symptoms point to a diagnosis of underlying hyperthyroidism. Include a thorough past medical history, including questions about recent medication changes, recent anesthesia, infectious prodromes, radiologic imaging that required an oral or intravenous iodinated contrast agent, and thyroid manipulation. (See Table 4.)



Patients in a hypothyroid state may present with diverse complaints. Hypothyroidism mimics a number of common disease processes presenting to the ED. A lack of thyroid hormone results in a depressed metabolic state, and many of the most common patient complaints reflect this. Patients with hypothyroidism may report fatigue, weight gain, cold intolerance, constipation, dry skin, paresthesia, hair loss, voice change, constipation, menstrual irregularity often with amenorrhea, and depression. (See Table 5.) It is important to elicit a medication history with special attention to recent changes. Some medications known for exacerbation of hypothyroidism include phenothiazines, phenobarbital, narcotics, anesthetics, benzodiazepines, lithium, phenytoin, and rifampin. As with thyroid storm, in ferreting out the presence of myxedema coma, some of the most important historical facts to elicit are recent precipitants, such as exposure to cold, infection, major life stress, and trauma.



Important Physical Findings

The physical examination should target essential concerns. The patient with profound thyrotoxicosis classically presents febrile, tachycardic, and tremulous. In a retrospective review of 58 patients newly diagnosed with thyrotoxicosis who were not clinically decompensated, weakness (50%), weight loss (40%), and palpitations (35%) were the most common clinical characteristics reported.19,20

A hyperdynamic cardiovascular state manifests with a persistent resting tachycardia, widened pulse pressure resulting in a bounding pulse, and a normal to elevated blood pressure. Atrial fibrillation is the second most common dysrhythmia following sinus tachycardia in thyrotoxicosis. The reported incidence of atrial fibrillation in acute thyrotoxicosis varies from 5% to 15.5%. A retrospective review of thyroid function test result abnormalities reported that approximately 5% of all admitted patients with new onset atrial fibrillation or flutter had either subclinical or overt hyperthyroidism.21 Atrial fibrillation with rapid ventricular response decreases the time of ventricular diastole. This allows less filling time for the ventricles, leading to high output heart failure.

A patient's age plays a significant role in the clinical signs likely to be present. In a prospective cohort study of 152 patients, tachycardia, fatigue, and weight loss were found in more than 50% of older patients (mean age 80.2 years), whereas only anorexia (32%) and atrial fibrillation (35%) were found significantly more frequently in younger patients.22 Another prospective study, with 880  patients, identified weight loss and atrial fibrillation as the most common clinical findings of hyperthyroidism in patients older than 50 years.23 Goiters were significantly more likely to be present in younger patients (94%; mean age 37.4 years) than older patients (50%). The clinical signs of hyperactive reflexes, increased sweating, heat intolerance, tremor, nervousness, polydipsia, and increased appetite were found significantly less frequently in older patients. Older patients had significantly fewer clinical signs then younger patients did. As compared with older controls, the clinical signs of apathy, tachycardia, and weight loss were highly associated with thyrotoxicosis in non-geriatric patients.22

Patients with thyrotoxicosis are typically nervous and anxious. There may be a fine tremor at rest and movement. Behavioral changes may be profound and present as paranoia, although acute affective disorders such as depression and mania are reportedly more common.24 Increased CO2 production secondary to the rise in basal metabolic rate causes tachypnea. Proximal muscle weakness in the pelvic girdle and shoulder muscles may be evident if there has been a history of untreated hyperthyroidism. Significant muscle atrophy and loss of 40% of muscle strength may be evident, especially in the larger proximal muscles.25 Profound muscle weakness may affect the muscles of respiration, and this, in combination with the tachypnea, predisposes patients to acute respiratory failure. Rarely, an entity described as hypokalemic periodic paralysis, which is found commonly in Asian men, results in muscle stiffness, cramps, weakness, and flaccid paralysis.26 Significant weight loss may precede thyroid storm, with 25% to 50% of patients reporting more than 40 pounds (18.14 kg) weight loss in the preceding months.27,28 Burch et al devised a clinical scoring system to differentiate thyroid storm, "impending thyroid storm," and uncomplicated thyrotoxicosis, although it is unclear whether it has been validated.29,30 Ultimately, however, the distinction between thyroid storm and severe but "compensated" thyroid storm complicated by other serious disease is immaterial in the ED. Treatment should be initiated as soon as the diagnosis is suspected because of the high mortality rate related to thyroid storm.

Severe hypothyroidism presents typically with skin changes, hypothermia, pseudomyotonic deep tendon reflexes, and depressed mental function. As mentioned earlier, coma is rare even in profound life-threatening hypothyroidism. However, the critical life-threatening signs associated with profound hypothyroidism include respiratory insufficiency, hypotension, hypothermia, and coma. Look for a thyroidectomy scar as a marker of hypothyroidism.

Although blood pressure changes range from low to elevated, 50% of those with myxedema coma are hypotensive and have systolic pressures less than 100 mm Hg.31

Pleura- and pericardial effusions, though rare,may be present. These effusions tend to accumulate slowly and are unlikely to produce clinically significant cardiovascular effects.32,33 A nonpitting edema, termed myxedema, secondary to chronic hypothyroidism, may be present and is especially noticeable in the face, hands and pretibial region. A husky, deep voice may be present and has been attributed to mucopolysaccharide infiltration of the vocal cords, a mechanism similar to nonpitting edema that is present in other areas of the body due to chronic hypothyroidism.34 A preceding weight gain of 7 to 8 pounds (3.2-3.6 kg) is common as is a history of menorrhagia with irregular menses stemming from chronic hypothyroidism.35

The depressed metabolic state resulting from a lack of thyroid hormone affects all the major organ systems. Pseudomyotonic deep tendon reflexes are almost universally present. The relaxation phase is classically twice as long as the contraction phase and may best be elicited with the Achilles reflex. Parathesia, especially a mononeuropathy involving the median nerve, is present in about 50% of cases.36-39 Reduced intestinal motility results in constipation and abdominal distention, potentially even mimicking an acute abdomen.

Hypothermia in myxedema coma is so common that an elevated temperature suggests an underlying infection. A core body temperature of less than 35.50C (95.90F) is found in 80% of severely hypothyroid comatose patients, with reported temperatures as low as 24C (75.2F).40,41 Neurological changes may be accompanied by seizures, ataxia, positive Romberg's sign, slowed speech, short-term memory loss, intention tremors, nystagmus, and poor coordination. These changes may be secondary to increased muscle tone and prolonged muscle contraction, as opposed to any primary cerebellar cause. There is 1 case report of a patient presenting with status epilepticus due to myxedema.42 A depressed central respiratory drive response to hypoxia and hypercapnia secondary to the metabolic derangements related to hypothyroidism, in concert with a depressed mental status, necessitates emergent airway management.43

Most patients with thyroid storm and myxedema coma are significantly hypovolemic. Hypovolemia can be a result of decreased oral intake due to an underlying illness or injury. The progression toward altered mental status with myxedema coma results in decreased oral intake. The hypermetabolic state in thyroid storm causes increased insensible fluid loss. 

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Last Modified: 04/26/2017
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