An extensive literature search revealed that myxedema psychosis is a rare yet well-established entity.
5 A presentation of myxedema psychosis is often seen in patients with longstanding Hashimoto thyroiditis, after thyroidectomy, or with medication noncompliance.
1,2 Progressively worsening symptoms of hypothyroidism can include fatigue, cold intolerance, decreased concentration, weight gain, hoarse voice, and constipation (
Figure). Severe symptoms can include hypotension, hyponatremia, or hypoglycemia. This myriad of symptoms, if left untreated, can ultimately lead to hallucinations, myxedema psychosis, or myxedema coma.
6 The patient in the current case report not only had myxedema psychosis as his initial and only symptom and an unremarkable medical history, but he had the highest level of TSH noted in the literature for patients presenting with hypothyroid-induced psychosis. Reported levels have ranged from 21.9 mIU/L to 122.2 mIU/L.
1-8
Hypothyroidism can be found in 0.3% to 0.4% of people, and subclinical hypothyroidism in 4.30% to 8.5%.9 Despite the high incidence of hypothyroidism, psychiatric disturbances as a presenting symptom of hypothyroidism are extremely rare, with an unknown incidence.
7,8 Forty percent of patients with hypothyroidism have superimposed signs and symptoms of depression.
1,9 A meta-analysis performed by Howland
9 found that approximately 50% of patients with refractory depression had evidence of subclinical hypothyroidism.
Management of myxedema psychosis is similar to that of myxedema coma, with the ideal therapy remaining controversial, owing to the lack of clinical trials. Treatment in an ICU is recommended, with cardiac monitoring and monitoring for hyponatremia, hypoglycemia, hypoventilation, hypothermia, and hypotension, which can be severe and life threatening in some cases.
6 The American Thyroid Association recommends combination levothyroxine and liothyronine.
10 Intravenous loading doses of 300 to 600 µg of levothyroxine, followed by daily doses of 50 to 100 µg, have been successfully used, with higher doses conferring the possibility of cardiac complications such as myocardial infarction and arrhythmias but without providing any additional benefit.
6,9,12 With decreased conversion of thyroxine to triiodothyronine in patients with severe thyroid hormone abnormalities, replacement with liothyronine with initial 5 to 20 µg, followed by 2.5 to 10 µg every 8 hours, can be given. Symptomatic and clinical improvement is expected to take place over 7 days with continued thyroid hormone replacement medication. Conversion to oral medication should be made as soon as patients are able to tolerate medications by mouth.
Concerns for concomitant primary adrenal insufficiency and increased metabolism of cortisol after sudden correction of thyroid levels should be addressed with steroid replacement. Stress-dose steroids should be administered in any patients with these concerns until further testing with random cortisol or adrenocorticotropic hormone stimulation testing can rule out adrenal insufficiency. Fifty to 100 mg of hydrocortisone every 8 hours or 2 to 4 mg of dexamethasone every 12 hours can be given, with the latter having the advantage of not interfering with the results of a cortisol or adrenocorticotropic hormone stimulation test.
The use of antipsychotics during thyroid replacement therapy remains a controversial issue.
4,13 A review of the literature
13 found that antipsychotics are best reserved for patients who have received thyroid replacement therapy, achieved a euthyroid state, and have not had improvement in their psychosis.
4 In the current case, haloperidol was used for severe agitation before the patient could achieve a euthyroid state.
It is essential to rule out Hashimoto encephalopathy as a cause of psychosis, which can be a common mimicker of myxedema psychosis and is not responsive to thyroid replacement therapy. In the current case, a computed tomographic scan of the patient’s head and an electroencephalograph were negative for intracranial abnormalities, which made myxedema psychosis a more likely diagnosis. Although Hashimoto encephalopathy can present with similar psychiatric disturbances, it is also often accompanied by ataxia, myoclonus, aphasia, tremors, and seizures. Electroencephalogram studies are found to be abnormal in 98% of patients with Hashimoto encephalopathy,
11 which was not seen in the current case. Differentiation of these 2 clinically separate entities is of paramount importance, as the management of Hashimoto encephalopathy requires corticosteroids and does not respond to thyroid hormone replacement therapy. Undiagnosed and untreated myxedema psychosis has a 20% mortality rate.
6
The osteopathic manipulative treatment (OMT)approach to a patient with hypothyroidism is centered around increasing fluid flow and nerve conduction to the thyroid gland. After initial viscerosomatic responses initiated by the thyroid gland, left untreated, the dysfunction perpetuates itself, leading to a vicious cycle of autonomic imbalance. Although directed OMT to the thyroid was not possible in our acutely agitated patient, ideally, treatment should be initiated at the first sign of thyroid abnormalities to maintain homeostasis. Because myxedema psychosis was the presenting symptom, implementation of OMT was not possible. Management should be focused on somatic dysfunctions in the cervical, upper thoracic, and shoulder soft tissue reflected by hypertonicity of the musculature. Myofascial trigger points found at C2, C3, and C4 dermatomes respond well to OMT techniques applied to the sternocleidomastoid (C2-3), trapezius (CN 12, C3-4), and splenius capitus (C4-5) muscles.
14