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Year : 2015  |  Volume : 59  |  Issue : 5  |  Page : 315-317  

Myxoedema coma in adults: Experience from a tertiary referral hospital intensive care unit

1 Intensive Care Unit, Columbia Asia Referral Hospital, Yeshwantpur, Bengaluru, Karnataka, India
2 Department of Medicine (Endocrinology), Columbia Asia Referral Hospital, Yeshwantpur, Bengaluru, Karnataka, India

Date of Web Publication12-May-2015

Correspondence Address:
Dr. Pradeep Rangappa
ICU, Columbia Asia Referral Hospital, Yeshwantpur, Malleswaram West, Bengaluru - 560 055, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-5049.156889

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How to cite this article:
Murthy TA, Rangappa P, Jacob I, Janakiraman R, Rao K. Myxoedema coma in adults: Experience from a tertiary referral hospital intensive care unit. Indian J Anaesth 2015;59:315-7

How to cite this URL:
Murthy TA, Rangappa P, Jacob I, Janakiraman R, Rao K. Myxoedema coma in adults: Experience from a tertiary referral hospital intensive care unit. Indian J Anaesth [serial online] 2015 [cited 2021 Mar 4];59:315-7. Available from: https://www.ijaweb.org/text.asp?2015/59/5/315/156889

   Introduction Top

Myxoedema coma is an uncommon, life-threatening form of long-standing, neglected hypothyroidism. [1] It is 3-10 times more common in women. [2] It commonly occurs in elderly with a peak incidence in the seventh decade. [3] We considered persistent surface body temperature of less than 96°F (>3 readings in spite of rewarming efforts) as hypothermia (considering the tropical climate in India. [4] Most common precipitants include exposure to cold, infection, drugs, haemorrhage, hypoxia, hypercapnia, hypoglycaemia, sepsis, and adrenal insufficiency. [3] We report a retrospective analysis of six cases in our intensive care unit (ICU).

   Case Reports Top

Our first patient was a 75-year-old male with a history of being bed ridden for 2 weeks, developing bed sores and was brought to emergency room (ER). He underwent debridement surgery, was shifted to ICU for further care. He was noted to have hyponatremia and on investigation, revealed the previously undiagnosed hypothyroidism. As his Glasgow Coma Scale (GCS) score remained persistently low, he underwent computed tomography scan of the brain, which showed pituitary macroadenoma. He was treated conservatively and discharged home. Second patient was a 65-year-old lady, who presented with a history of weakness, altered sensorium and abdominal pain of one-day duration. After investigations, a diagnosis of urosepsis with septic shock was made. She was noted to have hyponatremia and investigation revealed hypothyroidism. She went into multi-organ failure and eventually succumbed. Third patient was an 89-year-old male, known case of hypothyroidism, chronic obstructive pulmonary disease, type II diabetes mellitus (DM) and hypertension, presenting with history of fever, breathing difficulty and altered sensorium since one day. He had persistently low GCS and hyponatremia, which on investigation revealed hypothyroidism. He was treated conservatively and was discharged home. Fourth patient was a 78-year-old lady, known case of DM and hypothyroidism, presenting with a history of bilateral lower limb swelling, fever, abdominal pain for 1 day and unresponsiveness since 4 h. She was diagnosed as a case of urosepsis, cellulitis and acute pancreatitis. Thyroid function was sub-normal. She was treated accordingly but eventually she succumbed. Fifth patient was a 68-year-old lady, known diabetic, hypertensive and hypothyroid with a history of swelling of lower limbs, facial puffiness for 2 weeks and altered sensorium for 2 days. Diagnosed as community-acquired pneumonia with sepsis, she developed multi-organ failure and died eventually. Sixth patient was a 96-year-old lady, known hypertensive, with fracture femur operated one week earlier, presenting with history of disorientation (3 days), bowel incontinence and anuria (1 day). Investigations revealed urinary tract infection. She had hyponatremia with subnormal thyroid function. She went into multi-organ failure and did not survive [Table 1].
Table 1: Clinical details of individual patients with myxoedema coma

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   Discussion Top

Myxoedema coma is a rare, life-threatening form of hypothyroidism with physiological decompensation. [1] Data from the western world indicate an incidence of about 0.22/million/year. However, there is scarcity of epidemiological data from tropical countries like India. [4]

The computerised data and case records of patients admitted between January 2009 and August 2013 to our ICU were reviewed. Those who fulfilled our diagnostic criteria formulated in conjunction with diagnostic criteria followed by the Indiana University School of Medicine, Indianapolis were selected [Table 2]. [5] Demographic information, clinical manifestations, investigations, treatments and outcomes were noted. Microsoft Excel sheet was used to get the statistical variables.
Table 2: Diagnostic criteria for Myxoedema Coma

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Our 4 years database depicted an incidence of 1.3 cases per 1000 ICU admissions. Low intracellular T3 causes hypothermia and suppression of cardiac activity. [4] In this decompensated state, cardiogenic shock may not respond to vasopressors without concomitant thyroid hormone replacement. Hence, thyroid hormone replacement is an integral and indispensable part of treatment. [6] The possible precipitating factor is infection and septicaemia. [4]

We found six patients with a confirmed diagnosis of myxoedema coma. Retrospective inclusion was based on clinical features, laboratory findings, high index of suspicion, and treatment response. All our patients were neglected elderly people, with a symptom duration of about 10 days. Male to female ratio was 1:2 suggesting it was twice as common in females than males. Other co-morbidities were present in 84%, and all of them had positive cultures, electrocardiogram changes and hyponatremia with mental obtundation requiring invasive ventilation. Survival was about 33.3%. All female patients succumbed suggesting a higher severity in females. Sepsis was the most common precipitating factor, and 33% (2 out of 6) had defaulted on thyroid supplements. Thyroid stimulating hormone (TSH) had no role either in prognostication or diagnosis.

Up to 61% of the patients had defaulted on thyroxine supplements as per literature whereas we found about 33%. [7] Dutta et al. found 39% with undetected hypothyroidism. In our 6 patients, incidence of undetected hypothyroidism was 66.6% (4/6). Reinhardt and Mann report hypoxaemia in 80%, hypercapnia in 80%, hypercapnia in 54%, and hypothermia with a temperature less than 94°F in 88% of all the patients with myxoedema crisis. [8]

All of our patients were neglected elderly with infective insult and undetected/untreated hypothyroidism. High TSH values did not aid in prognostication (50% of our patients had TSH levels within the normal range) [Table 1]. Normal thyroid hormone levels may reflect the deviation from a higher pre-morbid set-point highlighting importance of careful clinical evaluation in patients with disparate clinical findings. [3] Low admission GCS (<8) requiring airway protection and anaemia was seen in all. Average time to diagnosis was 3 days on par with those reported. [9] Case reports of myxoedema coma as post-operative complication are scanty. [10] The mortality rate of 100% amongst our female patients suggested more severity in them. We could not conclude whether intravenous thyroxine is absolutely indispensable as it is commercially unavailable in this country, and all our patients were treated with an oral formulation. An incidence of 50%, of nosocomial infections suggested diminished immune response. We found some case reports of pituitary adenomas secreting TSH causing secondary hypothyroidism and eventually myxoedema coma. [11]

   Conclusion Top

Myxoedema coma is a diagnosis of exclusion requiring a high index of suspicion as there is no definitive single tool to diagnose it. There is a need to develop universal objective diagnostic criteria. Further studies are required with larger cohorts for evidence-based and protocolised management.

   Acknowledgements Top

Ipe Jacob, Intensive Care Unit, Columbia Asia Referral Hospital, Yeshwantpur, Bengaluru.

   References Top

Wall CR. Myxedema coma: Diagnosis and treatment. Am Fam Physician 2000;62:2485-90.  Back to cited text no. 1
Rodríguez I, Fluiters E, Pérez-Méndez LF, Luna R, Páramo C, García-Mayor RV. Factors associated with mortality of patients with myxoedema coma: Prospective study in 11 cases treated in a single institution. J Endocrinol 2004;180:347-50.  Back to cited text no. 2
Mallipedhi A, Vali H, Okosieme O. Myxedema coma in a patient with subclinical hypothyroidism. Thyroid 2011;21:87-9.  Back to cited text no. 3
Mathew V, Misgar RA, Ghosh S, Mukhopadhyay P, Roychowdhury P, Pandit K, et al. Myxedema coma: A new look into an old crisis. J Thyroid Res 2011;2011:493462.  Back to cited text no. 4
Chiong YV, Mariash CN. Development of an objective tool for the diagnosis of myxedema coma. Endocrinology Review. Indianapolis: Indiana University School of Medicine; 2011. p. 24-6.  Back to cited text no. 5
Gardner DG, Shoback D, editor. Endocrine Emergencies. Greenspan's Basic and Clinical Endocrinology. 8 th ed. New York: McGraw-Hill; 2007.  Back to cited text no. 6
Dutta P, Bhansali A, Masoodi SR, Bhadada S, Sharma N, Rajput R. Predictors of outcome in myxoedema coma: A study from a tertiary care centre. Crit Care 2008;12:R1.  Back to cited text no. 7
Reinhardt W, Mann K. Incidence, clinical picture and treatment of hypothyroid coma. Results of a survey. Med Klin (Munich) 1997;92:521-4.  Back to cited text no. 8
Pereira VG, Haron ES, Lima-Neto N, Medeiros-Neto GA. Management of myxedema coma: Report on three successfully treated cases with nasogastric or intravenous administration of triiodothyronine. J Endocrinol Invest 1982;5:331-4.  Back to cited text no. 9
Ragaller M, Quintel M, Bender HJ, Albrecht DM. Myxedema coma as a rare postoperative complication. Anaesthesist 1993;42:179-83.  Back to cited text no. 10
Khandelwal D, Jyotsna VP. Myxedema coma. Thyroid 2011;8:21-3.  Back to cited text no. 11


  [Table 1], [Table 2]


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