Out of the blue! Thyroid crisis.

A 45-year-old male patient with an irregularly irregular rhythm and fast ventricular rate was posted for an emergency laparotomy for hollow viscus perforation. His history was not suggestive of any systemic disorders. An echocardiography revealed left ventricular dysfunction with an ejection fraction of 47% without any valvular or chamber abnormality. Thyromegaly noticed during placement of central venous catheter was suspected to be the etiology for his cardiovascular status and was successfully managed. Thyroid crisis in an undiagnosed case of hyperthyroidism poses a diagnostic and therapeutic challenge. Timely and aggressive management is essential to correct the homeostatic decompensation characteristic of thyroid storm.

INTRODUCTION

Thyroid storm is an acute exacerbation of hyperthyroidism due to a sudden release of thyroid hormones into the systemic circulation and can be triggered by inadequate treatment, severe medical stress induced by infection, surgery or anesthesia. It is characterized by irritability, hyperthermia, tachycardia, rhythm disturbances, dehydration and congestive heart failure. Though rare, with a incidence of 0.2 cases/100,000 population, it carries a high mortality rate of 20–30%.[12] Incidence of thyroid storm is more common 6–18 h postoperatively than in the intra-operative period.[3] We report a case of thyroid storm in a 45-year-old male patient posted for hollow viscus perforation. Our case was unique, as the patient was not a known case of hyperthyroidism and did not give history suggestive of hyperthyroidism in contrast to the previous case reports.

CASE REPORT

A 45-year-old male patient with hollow viscus perforation was scheduled for emergency laparotomy with a history of high-grade fever of 5 days and pain abdomen of 2 day's duration. He was conscious and coherent with an irregularly irregular pulse of 183/min, respiratory rate of 48/min, blood pressure of 130/60 mmHg, temperature of 102°F and oxygen saturation of 93% on room air. A two-dimensional-echo revealed left ventricular (LV) dysfunction with an ejection fraction (EF) of 47%, atrial fibrillation (AF) with fast ventricular rate and no valvular pathology. His history did not specify any systemic disorders. A loading dose of amiodarone, followed by a continuous infusion failed to normalize the rate and rhythm. His routine biochemical investigations, arterial blood gas (ABG) and chest X-ray were within normal limits. (Hb - 11.4 g%, total leucocyte count - 13,400 mm3, blood glucose - 96 mg/dL, serum creatinine - 0.7 mg/dL, pH - 7.41, pCO2-38 mmHg, pO2-69 mmHg, HCO3− - 24.1 mEq/L, Na+ - 143 mmol/L, K+ - 3.3 mmol/L and Ca+2-1.06 mmol/L).

Radial artery was accessed for invasive arterial blood pressure along with standard monitoring and anesthesia was induced with 200 μg of fentanyl and titrated doses of propofol. Endotracheal intubation was facilitated with 0.1 mg/kg of vecuronium bromide and mechanical ventilation commenced with a tidal volume of 8 ml/kg and frequency of 12/min. Sevoflurane 1% in a mixture of oxygen and nitrous oxide was used for anesthetic maintenance. An increase in end-tidal carbon dioxide was managed by increasing the respiratory rate to 21/min and fresh gas flow to 4 L/min.

Thyromegaly noticed during placement of right subcalvian vein cannulation for central venous access led us to suspect thyrotoxicosis precipitated by hollow viscus perforation to be the etiology for the cardiovascular manifestations. A blood sample was sent for analyzing thyroid profile and troponins. The recorded central venous pressure through the right subclavian was 14 mmHg. Intra-operatively the heart rate surged to 220/min, which was treated with aliquots of 1 mg metoprolol repeated thrice with only mild reduction in heart rate to 180/min. AF with fast ventricular rate persisted throughout the intra-operative period. Blood pressure was maintained at around 110/60 mmHg and SpO2 was 100% throughout the surgical procedure [Figure 1]. A volume of 1500 ml of intravenous (IV) fluids were administered with a urine output of 75 ml over an hour.

Figure 1

Intra-operative hemodynamic parameters: Heart rate, oxygen saturation, blood pressure, Central venous pressure and end-tidal carbon dioxide concentration

The patient was electively ventilated in the intensive care unit and started on carbimazole 20 mg per-rectally and 100 mg hydrocortisone IV twice daily. There were postoperative episodes of hypotension due to fast ventricular rate, which could not be reverted with direct current cardioversion of 50 joules. Amiodarone was stopped, and noradrenaline and dobutamine infusions were started to maintain the blood pressure, which were tapered and discontinued on the first postoperative day following which the patient was extubated. Thyroid profile showed a thyroid stimulating hormone (TSH) - 0.005 μIU/ml, T3-2.12 ηg/ml, T4-12.83 μg/dL and free T4-2.70 mg/dL consistent with hyperthyroidism. Troponin I was negative. Carbimazole 20 mg twice daily and digoxin 0.25 mg once daily were administered through the Ryle's tube. Heart rate gradually decreased, and the rhythm reverted back to sinus rhythm by 5th postoperative day and a repeat two-dimensional-echo showed good LV systolic function with an EF of 66%. On enquiry before discharge, the patient did not give any history of thyroid disease or medications for the same. He however admitted to a small swelling in front of the neck for the last 2 years, which did not bother him. He was continued on anti-thyroid medication and had an uneventful course thereafter.

DISCUSSION

Thyroid storm/crisis is an extreme manifestation of thyrotoxicosis due to overproduction of thyroid hormones. There is no arbitrary serum T4 or T3 cut-off that discriminates severe thyrotoxicosis from thyroid storm. It can occur in poorly treated hyperthyroidism or can be the initial manifestation of an undiagnosed case of hyperthyroidism. Early recognition and appropriate management of life-threatening thyroid crisis are crucial to counteract the high morbidity and mortality that accompanies this disorder.

Diagnosis of thyroid crisis is reached based on the clinical features. History of previous thyroid disease gives a clue to the diagnosis. Its diagnosis in an unknown case of hyperthyroidism needs clinical expertise. Once a thyroid crisis is suspected, emergent treatment should be initiated even before the arrival of thyroid functional tests as resorted to in our case. However, suppressed TSH and elevated free T4 levels are essential to confirm the diagnosis. A scoring system was developed by Burch and Wartofsky to assess the degree of dysfunction of thermoregulatory, central nervous, gastrointestinal, and cardiovascular systems in thyrotoxicosis.[4]

Treatment of thyroid storm needs a multi-faceted approach with hydration, cooling, β-receptor antagonists, inotrope support, glucocorticoids and specific anti-thyroid drugs to decrease the synthesis of thyroid hormones and their circulating levels. Propylthiouracil or methimazole are the mainstay of treatment. The mean onset of activity of anti-thyroid drugs is 8 days.[5] Propranolol is the β-blocker of choice to attenuate the extreme adrenergic response. It also decreases the peripheral conversion of T4 to T3 but caution is essential in heart failure and asthma. Asprin should not be used as an anti-pyretic in these patients as it increases the free T4 levels by competing with binding sites on thyroid binding globulin. Glucocorticoids are essential to treat relative adrenal insufficiency, which coexists with thyrotoxicosis and to decrease the peripheral conversion of T4 to T3.[6] Thyroid storm can recur if steroids are withdrawn too rapidly after initial clinical improvement. Hypotension unresponsive to fluids needs judicious administration of vasopressors as these patients are over-responsive to endogenous and exogenous catecholamines.

Thyroid crisis should be distinguished from other hypermetabolic states. Hollow viscus perforation per se causes anxiety, dehydration, tachycardia, hypotension, hyperpyrexia and AF secondary to electrolyte disturbances mimicking the symptoms of thyrotoxic crisis. The absence of exposure to triggering factors, normal pH, O2 and CO2 partial pressures in ABG, absence of masseter spasm, muscle rigidity excludes malignant hyperthermia to be the causative factor for this clinical scenario. Absence of hypertension in association with tachycardia excludes pheochromocytoma to be the etiological factor. This exclusion is essential as β-blockers used to treat thyrotoxicosis can lead to unopposed α induced hypertensive crisis in pheochromocytoma. Valvular heart diseases and electrolyte abnormalities also need to be excluded.

Presence of a thyroid swelling tracked us to suspected thyroid crisis. Detailed history and physical examination should be a part of preanesthetic evaluation. Thyroid storm should always be dealt with in a critical care setup with invasive monitoring to manage cardiac events and large fluid shifts associated with this condition.

CONCLUSION

Thyroid storm unmasked by acute infection can present as life-threatening emergency in an undiagnosed case of hyperthyroidism. Prompt recognition, initiation of immediate and appropriate treatment is the mainstay of management.

AUTHOR'S CONTRIBUTION

Mrunalini Parasa and Bala Kusuma Kumari Chinthakunta anaesthetised the case and did further management. Mrunalini Parasa collected, reviewed the data and prepared the manuscript. Nagendra Nath Vemuri and Mastan Saheb Shaik, analysed the manuscript.