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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 2  |  Issue : 2  |  Page : 41-45

Postoperative Myxedema Coma: A Rare Presentation of Hypothyroidism


Department of Anesthesiology and Perioperative Medicine, Medical College of Georgia at Augusta University, Augusta, GA, USA

Date of Submission31-Jul-2020
Date of Acceptance29-Aug-2020
Date of Web Publication31-Dec-2020

Correspondence Address:
Dr. Mafdy N Basta
Department of Anesthesiology and Perioperative Medicine, Medical College of Georgia at Augusta University, 1120 15th Street, Augusta, GA 30912
USA
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DOI: 10.4103/jtccm.jtccm_13_20

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  Abstract 


Myxedema coma is a rare life-threatening form of severe hypothyroidism with physiological decompensation. It occurs as a result of long-standing, undiagnosed, or undertreated hypothyroidism and is usually precipitated by an acute event similar to infection, cerebrovascular accident, myocardial infarction, trauma, cold exposure, surgery, or drug therapy. Patients with myxedema coma are generally severely ill with hypothermia and depressed mental status. It is a medical emergency with a high mortality rate. If the diagnosis is suspected, immediate management is necessary before confirming the diagnosis. Patients with myxedema coma should be treated in an intensive care unit with continuous cardiac monitoring. Initial steps in management include airway management, thyroid hormone replacement, glucocorticoid therapy, and supportive measures. Fortunately, it is now a rare presentation of hypothyroidism, likely due to earlier diagnosis as a result of the widespread availability of thyroid-stimulating hormone assays. The following presentation is a case of postoperative myxedema coma that was successfully managed with multidisciplinary effort. The patient has had a complete recovery.

Keywords: Hydrocortisone, hypothermia, hypothyroidism, levothyroxine, liothyronine, myxedema coma, thyroid-stimulating hormone


How to cite this article:
Basta MN. Postoperative Myxedema Coma: A Rare Presentation of Hypothyroidism. J Transl Crit Care Med 2020;2:41-5

How to cite this URL:
Basta MN. Postoperative Myxedema Coma: A Rare Presentation of Hypothyroidism. J Transl Crit Care Med [serial online] 2020 [cited 2021 Nov 30];2:41-5. Available from: http://www.tccmjournal.com/text.asp?2020/2/2/41/305788




  Introduction Top


Myxedema coma is a rare life-threatening form of severe hypothyroidism that occurs most commonly in older women as a result of long-standing, undiagnosed, or undertreated hypothyroidism. It is usually precipitated by an acute event similar to infection, cerebrovascular accident, myocardial infarction, trauma, cold exposure, surgery, or drug therapy. It is a medical emergency with a high mortality rate. Patients with myxedema coma are generally severely ill with depressed mental status. If the diagnosis is suspected, immediate management is necessary before confirming the diagnosis. Patients with myxedema coma should be treated in an intensive care unit. The mortality rate remains high despite treatment. Older age, cardiac complications, reduced consciousness, need for mechanical ventilation, persistent hypothermia, and sepsis are predictive of high mortality rate. This paper describes a case of postoperative myxedema coma in a female patient that occurred as a result of medication noncompliance, and illustrates the multidisciplinary management implemented. The patient had a complete recovery.


  Case Report Top


The patient is a 61-year-old Caucasian female that underwent abdominoperineal resection of rectal carcinoma. Her past medical history was significant for the recent completion of neoadjuvant chemo/radiotherapy in anticipation of the scheduled resection of the rectal cancer. She has undergone a diverting colostomy 4 months prior, and the perioperative course was uneventful. The review of the patient's records revealed a diagnosis of hypothyroidism among the problem list. However, no prescribed thyroxine was noticed under her medications list. No thyroid function tests were obtained before the scheduled (or prior) surgery. No documentation of the preoperative anesthesia clinic visit was present before her scheduled surgery. The patient was evaluated by the anesthesia personnel on the day of surgery. The review of the preanesthesia evaluation indicated a normal physical examination and vital signs. A comment on the prior recent uneventful anesthesia and the anesthesia plan for the scheduled procedure were documented. No specific concern was raised at the evaluation.

After an uneventful surgical procedure, the patient was recovered at the postanesthesia care unit (PACU) and later admitted to the surgery ward for postoperative management.

On postoperative day 1, the patient was found by the nursing staff to be hypotensive and lethargic. The patient was assessed by the surgical team and the relevant laboratory values were reviewed. Vital signs recorded immediately before PACU discharge, the evening of postoperative day 0, and on postoperative day 1 are presented in [Table 1]. Relevant laboratory values including an arterial blood gas on room air, on postoperative day 1 are presented in [Table 2].
Table 1: Vital signs at the postanesthesia care unit through postoperative day #1

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Table 2: Laboratory values on postoperative day #1

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The patient's hypotension was initially attributed to hypovolemia and she was administered a total of 2 L of sodium chloride 0.9% over 4 h but without any noticeable improvement of her hemodynamics. On further questioning, the patient stated that she was previously prescribed thyroxine for hypothyroidism, but she has not been taking it over the past several months. Serum thyroid-stimulating hormone (TSH) level was ordered by the primary team on postoperative day 1 when the possibility of hypothyroidism was entertained due to medication noncompliance. TSH level was 104 mcIU/mL (reference range 0.4–4.7 mcIU/mL). No levothyroxine (T4) or liothyronine (T3) levels were obtained. Medical record review revealed that the patient was administered 75 μg intravenous (IV) thyroxine on postoperative day 1 following the TSH result. The surgical team requested transferring the patient to the surgical intensive care unit (SICU) for further management.

On evaluation by the intensive care team, the patient was noted to be obtunded and lethargic and her speech was slurred and incomprehensible. The patient was hypotensive (blood pressure [BP] 84/58 mmHg) and bradycardic (heart rate [HR] 52/min). Her respiratory rate was 10/min and her oral temperature (Temp) was 35.4°C.

In light of significantly elevated TSH level, along with mental status changes and hypothermia, myxedema coma was suspected and the patient was transferred to the SICU for further management. An endocrine consult was placed.

Serum sample for the patient's TSH, free T4, T3, and cortisol levels was collected before the administration of a loading dose of 400 μg of IV thyroxine to be followed by 100 μg IV daily. Concurrently, hydrocortisone 100 mg IV every 8 h was ordered to be administered. T3 administration was entertained but advised against by endocrinology due to concerns for high risk of side effects (e.g., dysrhythmia and coronary ischemia) in this patient. Empiric broad-spectrum antibiotics were started after blood and urine cultures were collected.

The patient was passively rewarmed with blankets. Sodium chloride 0.9% IV was ordered to be infused as maintenance IV fluid; her hemodynamics were supported in the interim with dopamine and norepinephrine, titrated to mean BP ≥65 mmHg. The patient was monitored invasively using arterial and central venous catheters.

Her thyroid hormone levels and random cortisol, drawn upon SICU admission (POD # 2) and before loading with IV T4, are presented in [Table 3].
Table 3: Thyroid function tests during the hospital course

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The patient's mental status started to improve 12–24 h after starting IV T4. Her repeat TSH continued to decrementally decrease and her free T4 continued to incrementally increase [Table 3] after several days of treatment with IV thyroxine. In the interim, her hemodynamics improved significantly and she was successfully weaned off the vasoactive medications. The empiric antibiotics were discontinued after the cultures remained negative for 48–72 h.

Testing for adrenal insufficiency was performed using the cosyntropin stimulation test after hydrocortisone was held for 24 h. Her early morning cortisol level was 11 μg/dL and following administration of 250 μg of cosyntropin IV, the cortisol level 1 h later was 26 μg/dL. The test was interpreted as negative for adrenal insufficiency. Her hydrocortisone was successfully tapered off. The patient was transferred to the surgery ward and started on oral thyroxine 112 μg daily. She was discharged home a few days later and instructed to follow-up with the endocrinology clinic as scheduled. The patient was counseled before discharge regarding the utmost importance of compliance with all prescribed medications, including thyroxine.


  Discussion Top


Myxedema coma is a rare life-threatening form of severe hypothyroidism with physiological decompensation.[1] It occurs as a result of long-standing, undiagnosed, or undertreated hypothyroidism and is usually precipitated by an acute event such as infection, myocardial infarction, cerebrovascular accident, cold exposure, trauma, or surgery.[2] Patients with myxedema coma are generally severely ill with hypothermia and depressed mental status. It is a medical emergency with a high mortality rate.[3] Older women are most often affected.[4] It can result from any of the causes of hypothyroidism, most commonly chronic autoimmune thyroiditis. It has been reported in secondary hypothyroidism, lithium-induced hypothyroidism,[5] and amiodarone-induced hypothyroidism.[6]

The hallmarks of myxedema coma are decreased mental status and hypothermia. Hypotension, bradycardia, hyponatremia, hypoglycemia, and hypoventilation can also be present.[7] Despite the term myxedema coma, most patients do not present in coma, but rather manifest variable degrees of confusion, lethargy, and obtundation.[4] Untreated, patients will progress to coma.

Hypothermia, due to the decrease in thermogenesis that accompanies the decrease in metabolism, is frequently present. Hyponatremia, secondary to inappropriate excess vasopressin secretion and impaired water excretion, is common and may contribute to the decrease in mental status.[8] Concomitant adrenal insufficiency in some patients could also contribute to hyponatremia.

Hypoventilation, primarily from central depression of ventilatory drive with decreased responsiveness to hypoxia and hypercapnia, could be present.[9] Other contributing factors to hypoventilation include respiratory muscle weakness, mechanical obstruction by a large tongue, and obesity hypoventilation syndrome.

Cardiovascular manifestations include bradycardia, diastolic hypertension, and narrow pulse pressure. Severe cases can be associated with decreased myocardial contractility, myocardial depression, hypotension, arrhythmias, and pericardial effusion.[10] Congestive heart failure is rarely seen in the absence of preexisting cardiac disease.

Gastrointestinal manifestations include malabsorption, gastric atony, impaired peristalsis, paralytic ileus, and megacolon. A higher risk of gastrointestinal bleeding caused by coagulopathy related to an acquired von Willebrand syndrome[11] has been reported. Hypoglycemia, due to decreased gluconeogenesis and concurrent adrenal insufficiency, is not uncommon.

Chronic autoimmune thyroiditis, the most common cause of hypothyroidism, could coexist with other autoimmune endocrine disorders. In polyglandular autoimmune syndrome type 2, primary adrenal insufficiency occurs in addition to type 1 diabetes mellitus and autoimmune thyroiditis.[12]

The thyroid-adrenal interactions include suppression of TSH production by high cortisol level, decreased conversion of T4 to T3 by cortisol, and cortisol-induced increased resistance to thyroid hormones. On the other hand, thyroid hormone levels may alter the secretion and metabolism of cortisol; low thyroid hormone levels decrease cortisol secretion and metabolism by the adrenals.[13],[14] The clinical features of myxedema coma are summarized in [Table 4].
Table 4: Clinical features of myxedema coma

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The diagnosis of myxedema coma should be considered in any patient with coma or depressed mental status who also has hypothermia, hyponatremia, and/or hypercapnia.[4] Important clues to the possible presence of myxedema coma in a poorly responsive patient are the presence of a thyroidectomy scar or a history of radioiodine therapy or hypothyroidism.

If the diagnosis is suspected, a blood sample should be drawn before treatment for the measurement of TSH, free T4, and cortisol. The serum T4 concentration is usually very low. The serum TSH concentration may be high, indicating primary hypothyroidism, or it may be low, normal, or slightly high, indicating secondary hypothyroidism. Most patients with myxedema coma have primary hypothyroidism. Patients may have concomitant adrenal insufficiency. Ideally, cortisol should be measured before and after cosyntropin administration.

Myxedema coma is an endocrine emergency that should be managed aggressively as the mortality rate remains high, ranging from 30% to 50%. If the diagnosis is suspected, immediate management is necessary before confirming the diagnosis. Treatment consists of thyroid hormone, glucocorticoids (until the possibility of coexisting adrenal insufficiency has been excluded), supportive measures, and appropriate management of any coexisting infection.

The ideal mode of therapy and doses of thyroid hormone therapy in myxedema coma remain controversial due to the rarity of the condition and lack of clinical trials. Some clinicians favor the administration of T4, whereas others prefer a combination of T4 and T3. The American Thyroid Association recommends combination therapy with T4 and T3.[15] Combined therapy is preferable to either hormone alone. Both are given IV, when available, as a slow bolus because gastrointestinal absorption may be impaired.[15]

A typical regimen consists of an initial dose of 200–400 μg T4 IV, followed by daily IV doses of 50–100 μg until the patient can take T4 orally. The lower end of the dosing range is preferred in older patients and in those at risk for cardiac complications (myocardial infarction and arrhythmia). T3 is given IV at the same time; the initial dose is 5–20 μg, followed by 2.5–10 μg every 8 h, with lower doses chosen for older patients and those with coexisting cardiovascular disease. T3 is continued until there is clinical improvement and the patient is stable.[15]

Therapy should be monitored by every other day measurement of serum free T4 and T3 and doses adjusted accordingly. Clinical and biochemical improvement is typically evident within a week. Once there is improvement (regained consciousness, improved mental status, and improved pulmonary and cardiac function), the patient can be treated with oral T4 alone.[16]

Until the possibility of coexisting adrenal insufficiency has been excluded, the patient must be treated with glucocorticoids in stress doses (e.g., hydrocortisone given IV, 100 mg every 8 h). The other rationale for the treatment with corticosteroids is the potential risk of precipitating acute adrenal insufficiency caused by the accelerated metabolism of cortisol that follows T4 therapy.[3] The dose can be tapered off after adrenal insufficiency is ruled out with a cosyntropin stimulation test.[17]

An alternative to hydrocortisone is dexamethasone at a dose of 2–4 mg every 12 h. Dexamethasone has the advantage of not affecting the serum cortisol concentration and can be used immediately without affecting the results of the cosyntropin stimulation test, which can be performed at any time. If the test is normal, corticosteroids can be stopped without tapering.

Supportive measures include treatment in an intensive care unit, mechanical ventilation if necessary, judicious administration of IV fluids including electrolytes and glucose, correction of hypothermia, and treatment of any underlying infection.

Hypotonic fluids should be avoided in hyponatremic patients to prevent a further reduction in the plasma sodium concentration. Severe hypotension that does not respond to fluids should be treated with a vasopressor drug until the T4 has had time to act. Empiric administration of antibiotics should be considered until appropriate cultures are proven negative.

The mortality rate remains high, up to 30%–50%, despite treatment.[18] Older age, cardiac complications, reduced consciousness, need for mechanical ventilation, persistent hypothermia, and sepsis are predictive of high mortality rate.[18] Some patients could have a complete recovery.[19]


  Conclusion Top


Myxedema coma, though rare, is a medical emergency with a high mortality rate. If the diagnosis is suspected, immediate management is necessary before confirming the diagnosis. Patients with myxedema coma should be treated in an intensive care unit with continuous cardiac monitoring. Initial steps in management include airway management, thyroid hormone replacement, glucocorticoid therapy, and supportive measures. Older age, cardiac complications, reduced consciousness, need for mechanical ventilation, persistent hypothermia, and sepsis are predictive of a high mortality rate. Some patients could have a complete recovery.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal the identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Nicoloff JT, LoPresti JS. Myxedema coma. A form of decompensated hypothyroidism. Endocrinol Metab Clin North Am 1993;22:279-90.  Back to cited text no. 1
    
2.
Yafit D, Carmel-Neiderman NN, Levy N, Abergel A, Niv A, Yanko-Arzi R, et al. Postoperative myxedema coma in patients undergoing major surgery: Case series. Auris Nasus Larynx 2019;46:605-8.  Back to cited text no. 2
    
3.
Klubo-Gwiezdzinska J, Wartofsky L. Thyroid emergencies. Med Clin North Am 2012;96:385-403.  Back to cited text no. 3
    
4.
Kwaku MP, Burman KD. Myxedema coma. J Intensive Care Med 2007;22:224-31.  Back to cited text no. 4
    
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Waldman SA, Park D. Myxedema coma associated with lithium therapy. Am J Med 1989;87:355-6.  Back to cited text no. 5
    
6.
Hawatmeh A, Thawabi M, Abuarqoub A, Shamoon F. Amiodarone induced myxedema coma: Two case reports and literature review. Heart Lung 2018;47:429-31.  Back to cited text no. 6
    
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Ono Y, Ono S, Yasunaga H, Matsui H, Fushimi K, Tanaka Y. Clinical characteristics and outcomes of myxedema coma: Analysis of a national inpatient database in Japan. J Epidemiol 2017;27:117-22.  Back to cited text no. 7
    
8.
Iwasaki Y, Oiso Y, Yamauchi K, Takatsuki K, Kondo K, Hasegawa H, et al. Osmoregulation of plasma vasopressin in myxedema. J Clin Endocrinol Metab 1990;70:534-9.  Back to cited text no. 8
    
9.
Zwillich CW, Pierson DJ, Hofeldt FD, Lufkin EG, Weil JV. Ventilatory control in myxedema and hypothyroidism. N Engl J Med 1975;292:662-5.  Back to cited text no. 9
    
10.
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. 10
    
11.
Manfredi E, van Zaane B, Gerdes VE, Brandjes DP, Squizzato A. Hypothyroidism and acquired von Willebrand's syndrome: A systematic review. Haemophilia 2008;14:423-33.  Back to cited text no. 11
    
12.
Dittmar M, Kahaly GJ. Polyglandular autoimmune syndromes: Immunogenetics and long-term follow-up. J Clin Endocrinol Metab 2003;88:2983-92.  Back to cited text no. 12
    
13.
Samuels MH. Effects of variations in physiological cortisol levels on thyrotropin secretion in subjects with adrenal insufficiency: A clinical research center study. J Clin Endocrinol Metab 2000;85:1388-93.  Back to cited text no. 13
    
14.
Tsigos C, Chrousos GP. Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. J Psychosom Res 2002;53:865-71.  Back to cited text no. 14
    
15.
Jonklaas J, Bianco AC, Bauer AJ, Burman KD, Cappola AR, Celi FS, et al. Guidelines for the treatment of hypothyroidism: Prepared by the American thyroid association task force on thyroid hormone replacement. Thyroid 2014;24:1670-751.  Back to cited text no. 15
    
16.
Arlot S, Debussche X, Lalau JD, Mesmacque A, Tolani M, Quichaud J, et al. Myxoedema coma: Response of thyroid hormones with oral and intravenous high-dose L-thyroxine treatment. Intensive Care Med 1991;17:16-8.  Back to cited text no. 16
    
17.
Bigos ST, Ridgway EC, Kourides IA, Maloof F. Spectrum of pituitary alterations with mild and severe thyroid impairment. J Clin Endocrinol Metab 1978;46:317-25.  Back to cited text no. 17
    
18.
Beynon J, Akhtar S, Kearney T. Predictors of outcome in myxoedema coma. Crit Care 2008;12:111.  Back to cited text no. 18
    
19.
Salomo LH, Laursen AH, Reiter N, Feldt-Rasmussen U. Myxoedema coma: An almost forgotten, yet still existing cause of multiorgan failure. BMJ Case Rep 2014; 2014: bcr2013203223.  Back to cited text no. 19
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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