The initial approach to the patient with altered sensorium is covered in Chapter 36. Upon completion of the initial priorities and screening for the more common sources of altered sensorium the possibility of myxedema should always be considered. The clinical stigmata of generalized slowing across all organ systems are readily assessed without the need for advanced testing modalities. A careful history from family or friends as well as review of the patient's prescriptions, if available, may yield valuable clues to the diagnosis. Obviously specific history of thyroid disorder is pivotal and one should bear in mind that history of hypo- or hyperthyroidism suggests the diagnosis in the appropriate clinical context. A patient who is undergoing radioablative or pharmacologic therapy for hyperthyroidism is as much at risk as the patient who neglects to take their thyroid supplementation in the presence of diagnosed hypothyroidism. Further historical screening should focus on complaints of fatigue, cold intolerance, and especially somnolence.1,2 The presence of an acute superimposed illness over baseline hypothyroidism can precipitate an acute crisis particularly when the diagnosis of hypothyroidism was previously undiscovered or underreplaced.1,2 In addition to altered sensorium the expected physical examination findings include bradycardia and hypothermia along with hyporeflexia.1,2 The classical skin and hair changes of the disease are further supportive as is any evidence of surgical thyroidectomy. A depressed EtCO2 in the setting of normal minute ventilation may be a clue to the hypometabolic state.3
The management of myxedema focuses on the acute replacement of the deficient steroids. If practical, blood can be drawn and saved for later analysis of the TSH, free T4, and cortisol levels preceding treatment. The dose of T4 varies in the literature with no large-scale RCTs to convincingly support one dose over another but there is general agreement on a dose between 200 and 400 µg IV acutely.4,5 It should also be remembered that the possibility of concomitant adrenal insufficiency exists and until that entity is excluded there must be concurrent supplementation of glucocorticoid.4–6 A dose of 100mg hydrocortisone IV or 4mg dexamethasone IV is sufficient in this setting.6,7 Apart from the aforementioned disease-specific therapy, standard treatment with large-volume isotonic crystalloid and vasopressors is appropriate for hemodynamic support.
The diagnosis of severe thyrotoxicosis is a clinical one and often requires the exclusion of many other more common entities. Thyroid storm may develop in a patient with long-standing hyperthyroidism or may be the initial presentation of the disease.2,8 Consistent with other endocrine emergencies the presence of significant physiologic stressors can precipitate a storm.9,10 Infection, trauma, iodine exposure, and thyroid surgery are all well described to have the potential to precipitate a crisis.12 It should be noted that amiodarone exposure may be the inciting iodine source.12 In general, it is the sympathomimetic properties of thyroid hormone excess that will be the most dramatic findings leading to the diagnosis. Tachycardia and hypertension leading later to hypotension as rate-related cardiomyopathy ensues is a typical progression.8,9 Hyperpyrexia with warm and moist skin are often present.10,11 Mental status changes favor agitation and psychosis but may conversely also present as coma.10,11 The presence of hyperreflexia, tremor, goiter, and ophthalmopathy concurrently are strongly consistent with the diagnosis.8–10,11
Standard therapeutic regimens focus on controlling the adrenergic activity followed by disruption of hormone synthesis, release, and peripheral conversion. Not having the depth of pharmacologic options prehospitally that are present in the ED it would be reasonable to focus on β-blockade and glucocorticoid supplementation followed by thionamide and iodine treatment upon arrival at the receiving facility.10,11 Propranolol 0.5 to 1mg over 10 minutes and esmolol 250 to 500 µg/kg loading dose followed by an infusion at one-fifth that dose per minute are established protocols for this purpose.8–10,11 The balance of the management is supportive.