Ann Thorac Surg 2005;80:714-716
© 2005 The Society of Thoracic Surgeons
Case report
Severe Hypothyroidism After Coronary Artery Bypass Grafting
Apurba Kumar Sarma, MCh
a
,
*
,
Murali Krishna, MS
a
,
Jayakumar Karunakaran, MCh
a
,
Praveen Kumar Neema, MD
b
,
Kurur Sankaran Neelakandhan, MCh
a
a Department of Cardiovascular and Thoracic Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
b Department of Anesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
Accepted for publication January 28, 2004.
* Address reprint requests to Dr Sarma, Department of Cardiovascular and Thoracic Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India 695 011 (Email: aks{at}sctimst.ac.in).
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Abstract
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A 56-year-old man with unstable angina underwent urgent coronary artery bypass grafting. The patient required reintubation and prolonged ventilation because of persistent drowsiness and hypotension. The patient was weaned off the ventilator and extubated; however, he remained drowsy and lethargic. Neurologic examination, electroencephalogram, and computed tomography scan of the brain did not show any organic cause of his depressed neurologic status. His metabolic profile revealed severe hypothyroidism. The patient responded well to oral thyroxine. We report the unusual manner in which hypothyroidism presented in the patient. A high index of suspicion is required to diagnose and treat this complication.
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Introduction
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The clinical features of hypothyroidism include depressed mental status, bradycardia, hypothermia, ileus, pericardial effusion without tamponade, and hypotension. The disease is sometimes associated with diabetes mellitus and adrenal insufficiency. These patients are unusually susceptible and sensitive to anesthetic agents like opioids and muscle relaxants. Although severe hypothyroidism after cardiac operations is rare, this entity should be considered in patients showing depressed cardiac and neurologic status because cardiac surgery under cardiopulmonary bypass (CPB) can aggravate hypothyroidism, and the resulting complications are reversible with thyroid hormone replacement therapy.
A 56-year-old man with history of old anterior and inferior wall myocardial infarction, hypertension, diabetes mellitus, and hypercholesterolemia was admitted with unstable angina. Transthoracic echocardiography (TTE) showed moderate left ventricular dysfunction with an ejection fraction of 37%. His coronary angiography showed diffusely diseased coronary vessels. He was scheduled for urgent coronary artery bypass grafting (CABG) on CPB. His preoperative medication included isosorbide dinitrate, atorvastatin, metoprolol, and aspirin. General physical examination was unremarkable. Laboratory test results were within normal limits. Three-vessel CABG was performed under CPB.
Postoperatively, the patient was hemodynamically stable with minimal inotropic support. His trachea was extubated after 18 hours of ventilation. At the time of extubation, he was mildly drowsy; this was attributed to sedative and analgesic agents used during surgery and the postoperative period. Nine hours after extubation, he was reintubated and ventilated because of persistent drowsiness with sluggish response to various stimuli and hypotension. He also needed an increase in inotropic supports. He was weaned off the ventilator and extubated after 63 hours of ventilatory support. He remained drowsy and lethargic, however, and did not tolerate weaning off inotropic agents and he required enteral alimentation through a nasogastric tube. Routine laboratory results were within normal limits. The TTE showed poor biventricular contractility. Computed tomography scan of brain and electroencephalogram failed to pinpoint the exact cause for the neurologic deterioration.
A thyroid function test done at this juncture revealed severe hypothyroidism: triiodothyronine (T3), 52 ng/dL (normal, 80 to 200 ng/dL); thyroxine (T4), 4 µg/dL (normal, 5 to 13 µg/dL); and thyroid-stimulating hormone (TSH), 12 mIU/L (normal, 0.3 to 5 mIU/L). The patient was started on oral Eltroxin (thyroxine sodium IP; Glaxosmithkline Pharmaceuticals, Nashik, India) 0.15 mg daily through a nasogastric tube. Three days after starting therapy, his neurologic and general condition improved, and he was able to take nutrition by mouth. Inotropic support could also be tapered off. His nutritional status gradually improved, and he was discharged from hospital 1 month after surgery on a regimen of oral Eltroxin 0.1 mg daily. Follow-up after 2 weeks and later at 3 months revealed a normal thyroid function test: T3 to 100 ng/dL, T4 to 9 µg/dL, and TSH to 1.0 mIU/L.
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Comment
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Central nervous system dysfunction after cardiac operations performed under CPB is known and is usually attributed to the effects of CPB on the brain. Thus, when a patient has complications related to the central nervous system, other causes are generally not considered. Diabetic acidosis, nonacidotic hyperosmolar hyperglycemia, drug interaction, endocrine disorders like hypothyroidism, hyperthyroidism, adrenal insufficiency, and residual anesthetic effect are other causes of drowsiness. An exaggerated effect of opioids and muscle relaxants is known in the presence of hypothyroidism. It is conceivable that in our patient the drowsiness could be because of opioids used during anesthesia and the postoperative period, but his drowsiness and lethargy persisted until he received thyroid replacement therapy.
The management strategy in patients having coronary artery disease and hypothyroidism includes institution of thyroid hormone replacement therapy and myocardial revascularization. Hormone replacement therapy is known to improve cardiac function because of reduction in peripheral vascular resistance and improvement in myocardial performance. Patients with preexisting angina pectoris should be evaluated for correctable lesions of coronary arteries and treated appropriately before levothyroxine is administered [1]. The authors [1] consider this approach safer than the institution of replacement therapy before treatment of coronary artery disease.
Despite mild degrees of hypothyroidism demonstrated by the thyroid function test, clinical myxedema during perioperative period is uncommon [2]. Our patient did not show any clinical feature suggestive of hypothyroidism; hence, no thyroid function test was done preoperatively. In our patient, depression of thyroid function after CPB was so severe that he required prolonged ventilation, inotropic supports, and institution of thyroid hormone replacement therapy. It is of special interest that some patients with severe biochemical hypothyroidism have only mild clinical signs, whereas others with minor biochemical changes can have quite severe clinical manifestations [3]. Contrary to the usual belief, only 50% patients have hypothermia as a feature of hypothyroidism [3]. The potential causes of decreased thyroid hormone levels during and after CPB are varied and include hypothermia, reduced peripheral conversion of T4 to T3, hemodilution, nonpulsatile blood flow, the suppressive effect of cytokines and tumor necrosis factor on thyroid function, iodine skin preparations, and cortisol-induced effects on TSH secretion [4]. Evaluation of the impact of cardiac surgery and CPB on thyroid hormone levels has yielded conflicting results. Taggart and associates [5] have documented a decrease in total T3, free T3, T4, and an increase in TSH levels after completion of CPB and during the first 24 to 48 hours after surgery, whereas Gotzche and associates [6] have found no change in TSH and increased free T3 and T4 levels. The impact of these changes on cardiac performance is conflicting. Novitzky and associates [7] suggest an improvement in myocardial function with intravenous T3 administration after CPB, whereas one randomized trial has found no benefit with intravenous T3 administration after CPB [8].
Dependence on inotropic agents after uneventful CABG is unusual. Coexisting generalized endocrine disorder is a possibility, and that should be investigated in patients in whom weaning of inotropic support is difficult. Although the diagnosis of hypothyroidism was delayed in this patient, he responded to oral thyroid hormone supplementation. A high index of suspicion is required to diagnose hypothyroidism in patients having unexplained cardiac and neurologic dysfunction. This report should raise awareness of the possible consequences of untreated hypothyroidism, and the potential impact of CPB on thyroid homeostasis.
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References
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- Larsen PR, Davies TF. Hypothyroidism and thyroiditisIn: Larsen PR, Kronenberg MH, Melmed S, Polonsky KS, editors. Williams textbook of endocrinology. Philadelphia: WB Saunders; 2003. pp. 423-455.
- O’Connor CJ, March R, Tuman KJ. Severe myxedema after cardiopulmonary bypass Anesth Analg 2003;96:62-64.[Abstract/Free Full Text]
- Zulewski H, Muller B, Exer P, Miserez AR, Staub JJ. Estimation of tissue hypothyroidism by a new clinical scoreevaluation of patients with various grades of hypothyroidism and controls. J Clin Endocrinol Metab 1997;82:771-776.[Abstract/Free Full Text]
- Bettendorf M, Schmidt KG, Tieffenbacher U, et al. Transient secondary hypothyroidism in children after cardiac surgery Pediatr Res 1997;41:375-379.[Medline]
- Taggart DP, Fraser W, Gray CE, et al. The effects of systemic intraoperative hypothermia on the acute phase and endocrine responses after cardiac surgery J Thorac Cardiovasc Surg 1992;40:74-78.
- Gotzche LS, Weeke J. Changes in plasma free thyroid hormones during cardiopulmonary bypass do not indicate triiodothyronine substitution J Thorac Cardiovasc Surg 1992;104:273-277.[Abstract]
- Novitzky D, Cooper DKC, Barton CI, et al. Triiodothyronine as an inotropic agent after open-heart surgery J Thorac Cardiovasc Surg 1989;98:972-978.[Abstract]
- Bennett Guerrero E, Jimenez JL, White WD, et al. Cardiovascular effects of intravenous triiodothyronine in patients undergoing coronary artery bypass graft surgeryA randomized double blind placebo controlled trial. JAMA 1996;275:687-692.[Abstract/Free Full Text]
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Abstract
Introduction
