Hypothyroidism and Myxedema Coma Clinical Presentation

The symptoms characteristic of hypothyroidism are numerous yet often vague and subtle, especially in early stages of the disease. Note the following:

• Lethargy

• Generalized weakness

• Brittle or thinning hair

• Menstrual irregularity

• Menorrhagia

• Forgetfulness

• Fullness in throat

• Deep, husky voice secondary to mucopolysaccharide infiltration of the vocal cords

• Cold intolerance

• Weight gain/difficulty losing weight

• Muscle/joint pain or weakness

• Inability to concentrate

• Headaches

• Constipation

• Emotional lability

• Depression

• Blurred vision

• Dry hair

Potential physical examination findings include the following:

• Pseudomyotonic reflexes - Prolonged relaxation phase, usually at least twice as long as the contraction phase

• Hypothermia (especially in myxedema coma)

• Skin changes - Dry, cool, coarse, and thickened with a yellowish appearance

• Subcutaneous tissues - Nonpitting, waxy, dry edema secondary to accumulation of polysaccharides

• Loss of axillary and pubic hair

• Pallor

• Loss of outer one third of eyebrows

• Abdominal distention

• Goiter

• Unsteady gait/ataxia

• Pericardial effusion

• Dull facial expression

• Coarsening or huskiness of voice

• Periorbital edema

• Bradycardia, narrow pulse pressure

• Macroglossia

• Thyroidectomy scar - In patients with altered mental status, suggests myxedema coma as a potential cause

A Swedish study, by Mourtzinis et al, found the rates of hypothyroidism and hyperthyroidism in patients with atrial fibrillation to be 5.9% and 2.3%, respectively, compared with 3.7% and 0.8%, respectively, in controls. ^[8]

The most common etiology of hypothyroidism worldwide is iodine deficiency as associated with endemic goiter. Conversely, a study among Chinese patients also demonstrated a significant increase in overt hypothyroidism in those with an excessive intake of iodine. ^[9] Within the United States and developed nations, the major causes of hypothyroidism are autoimmune destruction of the thyroid gland (eg, Hashimoto thyroiditis) and iatrogenic secondary to the treatment of Graves disease (surgical or radioactive iodine ablation of the thyroid gland). Primary hypothyroidism (dysfunction of the thyroid gland) accounts for up to 90-95% of cases. Secondary hypothyroidism (dysfunction of the pituitary or hypothalamus) accounts for most of the remainder of cases. ED management rarely requires distinguishing between primary and secondary origins.

Primary causes include autoimmune, idiopathic, postoperative, and congenital etiologies; radiation; radioiodine therapy; iodine deficiency; metabolic disorders; and medications (eg, lithium, amiodarone, phenytoin, carbamazepine, iodides). Furthermore, those with underlying autoimmune thyroiditis are susceptible to disease progression while taking these medications. Antineoplastic agents are also recognized to cause thyroid dysfunction in 20-50% of patients. Since symptoms of hypothyroidism may be vague and attributed to adverse effects of medication, it may be appropriate to monitor thyroid function regularly during treatment. ^[10]

A retrospective study by Spiegel et al indicated that small-for-gestational-age infants are at increased risk for childhood hypothyroidism, with an adjusted odds ratio of 3.2. ^[11]

Secondary causes include pituitary and hypothalamic disorders such as trauma, neoplasm, irradiation, and infiltrative diseases including sarcoidosis or amyloidosis.

In a patient with underlying hypothyroidism, inciting factors responsible for developing myxedema coma are numerous and include infection, trauma, cold exposure, or medications such as sedatives and anesthetics.