Abstract
Hypothyroidism is a common disease with nonspecific clinical symptoms depending on the severity and the age of onset. Myxedema is a rare and life-threatening subset of hypothyroidism that can manifest in patients facing a secondary insult, including surgery, trauma, and infection. We present a case of severe hypothyroidism associated with pericardial effusion and cardiac tamponade, requiring emergent pericardiocentesis and subsequent pericardial window. We review the definition, physiology, clinical signs, and diagnosis. We also recapitulate the anesthesia complications related to hypothyroidism, with emphasis on prevention and treatment.
Keywords
hypothyroidism, myxedema coma, thyroxine, triiodothyronine, Hashimoto’s autoimmune thyroiditis
Case Synopsis
A 53-year-old woman with a long history of hypothyroidism and tobacco abuse presents to the emergency department with generalized weakness, lethargy, mild shortness of breath, edema of her lower extremities, constipation, and slow speech. She admits to stopping her thyroid replacement 2 years ago. Her current medication list includes only Flonase and Metamucil. Her physical examination is significant for hypothermia, lethargy, bradylalia, dry mucosa, brittle and coarse hair, distant heart tones, bradycardia, decreased breath sounds bilaterally, a distended but nontender abdomen, and bilateral lower extremity nonpitting edema. The laboratory results are notable for mild anemia (hemoglobin 9.4 g/dL), leukocytosis (white blood cell count 17.2 × 10 9 /L), and hypokalemia (3.1 mM). The patient is profoundly hypothyroid with a thyroid-stimulating hormone (TSH) level of 120 mU/L (normal value 0.4–4.0 mU/L) and free T 4 of 0.08 ng/dL (normal value 0.46–0.76 ng/dL). Chest, abdomen, and pelvic computed tomography images reveal a large pericardial effusion, small right pleural effusion, and marked ascites. The endocrinology consultant immediately starts the patient on intravenous (IV) levothyroxine, liothyronine, and hydrocortisone. The patient also requires a dopamine infusion secondary to persistent bradycardia and hemodynamic instability.
Because there were mild signs of early tamponade, a needle pericardiocentesis was completed, followed 3 days later by a pericardial window for the large recurrent pericardial effusion. The induction of anesthesia for the pericardial window was performed using a combination of glycopyrrolate 0.4 mg, hydrocortisone 100 mg, etomidate 20 mg, fentanyl 50 μg, and succinylcholine 120 mg. The initial intubation attempt was unsuccessful with a 7.5 endotracheal tube (ETT), probably due to the airway edema and mucosal swelling. Therefore a 6.5 ETT was passed into the trachea. An appropriate depth of anesthesia was achieved with only 0.4 minimum alveolar concentration (MAC) isoflurane, low-dose fentanyl, and intermittent cisatracurium. Her anesthetic course was significant for hypothermia and bradycardia. Thus the patient also required a total of 50 mg of IV ephedrine to maintain an appropriate heart rate. The trachea was extubated at the end of the procedure after a prolonged emergence. Levothyroxine was continued throughout her hospitalization, and hydrocortisone was gradually tapered over 2 weeks. The pericardial drain was maintained for 3 days during her intensive care unit stay. The patient was discharged from the hospital to a long-term care facility 14 days after admission.
Acknowledgment
The authors wish to thank Dr. Pam Roberts for her contribution to the previous edition of this chapter.
Problem Analysis
Definition and Physiology
Hypothyroidism is a common disease characterized by hypoactive thyroid function with decreased production and secretion of thyroid hormones. Myxedema is a life-threatening form of hypothyroidism manifested by decreased level of consciousness, leading to stupor or coma. Myxedema coma develops in chronic hypothyroid or untreated hypothyroid patients who face a secondary insult (infection, trauma, surgery, cold exposure, or even certain medications).
The thyroid gland normally secretes 80% thyroxine (T 4 ) and 20% triiodothyronine (T 3 ), the most active form of the thyroid hormones. T 4 and T 3 of thyroidal origin are synthesized by iodination and coupling of tyrosyl and thyroglobulin, and subsequently stored in the colloidal space. The majority of T 3 (80%) is actually synthesized by extrathyroidal conversion in organs such as the liver, kidney, and brain by deiodination of T 4 . Some of the circulating T 4 is also converted to the inactive reverse-T 3 (rT 3 ). T 3 and T 4 are bound to serum proteins (thyroxin-binding globulin and transthyretin) in the plasma; only free T 3 and T 4 are available for uptake in the target tissues.
The thyroid-stimulating hormone (TSH) or thyrotropin is a pituitary hormone that stimulates biosynthesis and release of T 4 and T 3 . The TSH secretion is regulated by T 3 and T 4 levels via a negative feedback mechanism. Hydrocortisone also inhibits the secretion of TSH. The TSH secretion is pulsatile, with the highest TSH level in the late evening. The thyrotropin-releasing hormone (TRH) is produced by the hypothalamus and stimulates the release of TSH.
The systemic activity of thyroid hormone is mediated via the nucleic receptors at the cellular level of many target tissues. Thyroid hormone also has an important role in neural and somatic development during fetal life and infancy. Thyroid hormone actions target almost all tissues and have important effects during adult life. They increase the basic metabolic rate; regulate protein, fat, and carbohydrate metabolism; stimulate bone growth; potentiate neural maturation; and increase sensitivity to catecholamine. The clinical effects include increased cardiac output and heart rate, ventilation rate, elevated basal metabolic rate, stimulated brain development and cognitive function, and increased global catabolism.
Recognition
Clinical Signs and Diagnosis
The clinical manifestations of hypothyroidism are nonspecific depending on the severity and the age of onset. Common symptoms include fatigue and weakness, weight gain, cognitive dysfunction, depression, dyspnea on exertion, cold intolerance, hoarseness, myalgia, dry skin, hair loss, constipation, infertility, and menstrual irregularities. Laboratory changes may reveal macrocytic anemia, hyponatremia, hypoglycemia, hyperlipidemia, and increased creatine kinase. Pericardial fluid, pleural effusion, and anasarca may become evident. The physical examination commonly reveals goiter, slow speech, delayed relaxation of tendon reflexes, bradycardia, diastolic hypertension, depressed spontaneous ventilation, and upper airway edema and possible obstruction. Other findings include severely attenuated response to hypoxemia and hypercarbia, depressed inotropy and chronotropy, increased vascular resistance, and intravascular volume depletion. The electrocardiogram may reveal sinus bradycardia, small-voltage QRS complexes, prolonged Q-T intervals, isoelectric T-wave changes, or even supraventricular tachycardia.
If hypothyroidism is suspected, the first test to be performed is TSH. If the TSH level is increased, the TSH test is repeated along with T 4 . High TSH and low free T 4 characterize primary hypothyroidism ( Table 12.1 ). Serum concentrations of thyroid peroxidase antibodies are elevated in patients with chronic autoimmune hypothyroidism. If TSH is high with a normal level of free T 4 , the diagnosis is subclinical hypothyroidism. Therapy for such situations requires expert consultation to avoid complications. A TSH-secreting pituitary adenoma may also manifest with increased TSH and normal or high free T 4 .
| Assessment | TSH | Free T 4 | Free T 3 |
|---|---|---|---|
| Primary hypothyroidism | High | Low | Low |
| Subclinical hypothyroidism | High | Normal | Normal |
| Central hypothyroidism | Low or normal | Low or normal | Low or normal |
| Nonthyroidal illness | Low | Low | Low |
| Resistance to thyroid hormones | High | Low or normal | Low or normal |
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