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Myxoedema coma (or myxoedema crisis) is a severe and potentially fatal form of decompensated hypothyroidism with an underlying cause. A low index of suspicion and a search for triggering factors should be the first step in dealing with the condition at an early stage. Myxoedema coma should be suspected in patients who present with hypothermia, altered mental status, and coma, even if hypothyroidism has not previously been recognized. The symptoms of hypothyroidism decompensation may mistakenly be attributed to its precipitating factors, which may include sepsis, cardiac failure, myocardial infarction, cerebrovascular accident, anaesthetic, sedatives, antidepressant medications, or metabolic and electrolyte abnormalities. Here, we present a case of myxoedema coma with two major underlying precipitating causes: septic shock and diabetic ketoacidosis.
Keywords: DKA, Hypothyroidism, Myxedema Coma, Septic Shock
Myxoedema coma is a severe and life-threatening form of decompensated hypothyroidism with an underlying precipitating factor. It can present with altered mental status, hypothermia, bradycardia, respiratory failure, and hyponatremia. Mortality rates may be as high as 25–60%, even with the best possible treatment [1-3].
A low index of suspicion and a search for precipitating factors should be the initial step in dealing with myxoedema coma at an early stage [4]. Triggers may include poor medication compliance, thyroidectomy, acute events (including infection and cardiac infection among other stresses), and medical treatments that cause loss of thyroid homeostasis [5]. The mainstay of treatment includes hydrocortisone, intravenous liothyronine, levothyroxine, electrolyte correction, supportive therapies, and treating any underlying precipitant such as infection, surgery, or trauma [1,6]. Suspected myxoedema coma cases should receive intravenous hydrocortisone while awaiting laboratory results, as any delay can be life-threatening. The condition should ideally be managed in the intensive care unit (ICU) with pulmonary and cardiovascular support [7,8]. Here we report a case of myxoedema coma presenting with two main underlying precipitating factors: septic shock and diabetic ketoacidosis (DKA).
The patient was a 42-year-old male with a history of Down syndrome, epilepsy, and type 1 diabetes mellitus (T1DM). One year prior, he had required a 28-day admission to the ICU where he received treatment for pneumonia, ultimately recovering without complications. In the current admission, he was transferred from a primary hospital to the emergency department (ED) on October 18, 2023 having been intubated for septic shock secondary to pneumonia and DKA. Prior to his transfer, the patient had experienced three days of fever, cough, sore throat, decreased level of consciousness, and loss of appetite. Upon arrival at the Emergency Department, the patient was intubated for mechanical ventilation using a 7.5 mm endotracheal tube (ETT) positioned at a depth of 22 cm. Ventilation was provided in the assist-control volume control (AC/VC) mode, with the following parameters: fraction of inspired oxygen (FiO2) 100%, tidal volume (Vt) 480 mL, positive end-expiratory pressure (PEEP) 8 cmH2O, and a respiratory rate of 20 breaths per minute. Oxygen saturation (SpO2) was recorded at 92%, and bilateral inspiratory crackles were noted. The patient was afebrile, with a blood pressure of 118/80 mm Hg, heart rate of 126 beats per minute, and random blood glucose level of 581 mg/dl. Venous cannulae (20 gauge) were secured, and the patient received ongoing sedation with fentanyl (100 mcg per hour) as well as norepinephrine (30 mcg per hour). He was following a protocol for the treatment of DKA, involving regular doses of insulin (7 IU), as well as potassium chloride at a dose of 15 meq in 500 ml fluid, administered intravenously at a rate of 250 ml per hour. Additionally, he had an indwelling urinary catheter (size F12 silicone), connected to a collection bag. However, despite this setup, only minimal urinary output was observed.
Management in the Emergency Department: The patient was connected to a cardiac monitor and a bolus of 1000 ml normal saline was administered. Intravenous medications were also administered, including a single dose of 5 mg midazolam followed by a continuous infusion at 5 mg per hour, and an increase in fentanyl infusion to 200 mcg per hour. Hydrocortisone 50 mg and meropenem 1000 mg were also administered. A right femoral central venous catheter (size 7) was inserted at a depth of 20 cm; vasopressin infusion was initiated at a rate of 0.04 IU per minute; and a 65-cm nasogastric tube (size F14) was inserted and confirmed via auscultation to be patent and intact. A urinary output of 200 ml was noted, which was amber in colour. Chest X-ray revealed bilateral infiltrations, while urine dipstick analysis showed significant levels of protein, glucose, ketones, and blood. Table 1 illustrates the patient’s venous blood gases along with the chemistry panel. The patient was admitted for DKA and septic shock secondary to pneumonia and showed no
As his TSH levels dropped, the patient started to stabilize vitally, regained consciousness, and was extubated. Another important tool in the management of severe hypothyroidism is glucocorticoids [15,16], due to the risk of adrenal insufficiency that accompanies this condition. In our case, a dose of hydrocortisone was given in the ED. In summary, myxoedema can easily be misdiagnosed, especially when symptoms are masked by other critical conditions ― in the case of our patient, septic shock complicated by DKA. Thus, suspicion should be raised even where there is no known history of hypothyroidism. While the mortality of myxoedema remains high, early recognition and treatment can play a major role in improving patient outcomes.
Myxedema coma should be suspected in patients presenting with hypothermia, altered mental status, and coma, even where there is no history of hypothyroidism, and particularly in those at greater risk for the condition, such as, in our case, people with Down syndrome. Many factors can trigger myxedema, including cold exposure, sepsis, DKA, and cardiogenic shock. Those at high risk should be investigated, given that mortality is high even with the appropriate management.