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      Delayed recovery from anaesthesia secondary to undiagnosed myxoedema coma: a case report


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            Delayed emergence from anaesthesia presents with significant cardio-respiratory complications. (1) Its causes are multifactorial, and can include incorrect drug dosing, prolonged neuromuscular blockade (NMB) and endocrine disorders such as severe hypothyroidism, metabolic derangements such as hypoglycaemia and severe hyperglycaemia, hypernatremia, hypoxia, hypercapnia, uraemia, and neurological issues. (1) We report a rare case of an elderly female patient with delayed emergence due to myxoedema coma, following an uneventful laparotomy for a perforated duodenal ulcer.

            CASE REPORT

            History and examination

            A 72-year-old Caucasian female with a body mass index (BMI) of 20.8 kg/m2 and no comorbid conditions, presented with an acute abdomen for an emergency exploratory laparotomy. Surgeons diagnosed a perforated hollow viscus. She had no history of chronic medication use. There was no significant previous surgical history. She was fully conscious and alert, with a blood pressure (BP) of 140/70 mmHg, a heart rate (HR) of 40 beats per minute (bpm), oxygen saturation (SaO2) of 97% and a respiratory rate (RR) of 10 breaths per minute. Despite the bradycardia, the patient had no paroxysmal nocturnal dyspnoea, orthopnoea, or decreased effort tolerance. Her respiratory examination was unremarkable. Guarding and epigastric tenderness were present on abdominal examination.

            An electrocardiogram (ECG) showed a sinus bradycardia with premature ventricular contractions. The preoperative laboratory workup revealed a raised c-reactive protein (CRP) of 190 mg/dl with normal haemoglobin (Hb):13.1g/dL and platelets: 376.x109/L. Renal function tests, Pro-B- Type Natriuretic Peptide (proBNP) and an arterial blood gas (ABG) were not done preoperatively.

            Induction of anaesthesia

            A rapid sequence induction was performed with fentanyl 100 µg, propofol 70 mg and suxamethonium 75 mg, following placement of standard vitals monitoring. A size 7.0 mm endotracheal tube (ETT) was utilized. The patient was mechanically ventilated on a volume-controlled ventilation (VCV) mode at a fraction of inspired oxygen (FiO2) of 0.4, a tidal volume of 350 ml, a RR of 12 and positive end expiratory pressure (PEEP) of 8. An ABG showed a pH of 7.314, sodium (Na): 137 mmol/L, potassium (K): 4.0 mmol/L, chloride (Cl): 106 mmol/L, lactate: 0.9 mmol/L, base excess: -1.2 mmol/L, HCO3: 22.5 mmol/L (Table 1). Five minutes post induction, the patient made spontaneous respiratory efforts and received a further 100 µg of fentanyl and 20 mg of rocuronium. One gram of cefazolin was given for antibiotic prophylaxis. Anaesthesia was maintained with sevoflurane at a concentration of 1.5 – 2.0%. Morphine 4 mg and paracetamol 1 g were administered for postoperative pain. The patient was haemodynamically stable, and core body temperature ranged between 36.5 and 37 ºC.

            Table 1:

            Laboratory data

            Laboratory dataValueNormal range
            Sodium137 mmol/L(135 – 146) mmol/L
            Potassium4.0 mmol/L(3.5 – 5.0) mmol/L
            Chloride106 mmol/L(98 – 107) mmol/L
            Calcium1.25 mmol/L(1.15-1.3) mmol/L
            Glucose6.0 mmol/L
            Bicarbonate22.5 mmol/L(21 – 32) mmol/L
            Thyroid Stimulating Hormone (TSH)49.87 mIU/L (0.5 – 5.0) mIU/L
            Free T4 11.9 µg/dL(6 – 12) µg/dL
            Haemoglobin (Hb)13.1 g/dL(13 – 18) g/dL
            Base Excess-1.2 mmol/L
            Lactate0.9 mmol/L(0.5-1.0) mmol/L
            CRP190 mg/L
            Intraoperative events

            The laparotomy, which lasted 55 minutes, revealed a perforated duodenal ulcer with minimal contamination, and was repaired with a Graham's patch. Neostigmine 2.5 mg and glycopyrrolate 0.4 mg was administered for reversal of NMB. Following NMB reversal, the patient started breathing spontaneously, was opening eyes to verbal commands, had an adequate head lift and a strong hand grip and was thus extubated. Five minutes post extubation, signs suggestive of incomplete reversal of NMB were evidenced by a drop in SaO2, below 90%, and an inability to raise the head or protrude the tongue, a weak hand grip and a declining level of consciousness. The airway was supported by bag mask ventilation (BMV) with 100% oxygen, a laryngeal mask airway (LMA) was inserted and SaO2 stabilized. A peripheral nerve stimulator showed train of four (TOF) twitches of 2/4. Sedation was administered, and the patient reintubated and ventilated. Regular reassessments with a nerve stimulator over the next 30 minutes showed cycles of improved and incomplete NMB recovery with a 3/4 TOF twitch count.

            A 12 lead ECG done at that time showed no abnormalities, and all ABG parameters were normal, including glucose, sodium, calcium, potassium, and lactate. Pupils were equal and reactive to light. The intensive care unit (ICU) agreed to admit the patient postoperatively pending bed availability.

            After three and a half hours of continuous monitoring in theatre, the patient started obeying commands, moving all four limbs, and generating adequate tidal volumes spontaneously. A TOF twitch count was 4/4 at a ratio of 90%. Extubation was attempted and further monitoring was done in theatre for 20 minutes. Oxygen saturation was maintained between 94 and 99% and she was transported to the post anaesthesia care unit (PACU). On arrival in PACU, the patient desaturated to a SaO2 of 40% and had muscle weakness. She was reintubated and mechanically ventilated. A central venous catheter and an arterial line were inserted, and the patient was transferred to ICU, after having spent eight hours and 20 minutes in theatre.

            In ICU, a blood work-up was done. Thyroid function tests (TFT) revealed an elevated thyroid stimulating hormone (TSH) level of 49.87 mIU/L (normal range: 0.5 – 5.0 mIU/L) and a T4 level of 11.9 µg/dL (normal range: 6 -12 µg/dL). A diagnosis of myxoedema coma was made and managed accordingly. Twenty-four hours post admission, the patient became haemodynamically unstable, requiring inotropic support. An infusion of adrenaline 0.2 µg/kg/min was initiated. A 12 lead ECG revealed an ST segment elevated myocardial infarction (STEMI), and a cardiologist consult was sought. The cardiologists managed the patient conservatively and no cardiac catheterization was performed. The patient demised 72 hours later.


            Myxoedema coma is a rare life-threatening endocrine emergency that occurs as a complication of hypothyroidism, secondary to a precipitating event which results in exhaustion of compensatory responses. (2) The incidence is quoted as 0.22 events per million per year (1), with hypothyroidism occuring fourfold more often in female than male patients in age groups above 60 years. (3) Precipitants can include burns, carbon dioxide retention, gastrointestinal haemorrhage, hypoglycaemia, hypothermia, infections, beta blockers, trauma and stress related to anaesthesia and surgery. (2) In our case, the patient reported no prior diagnosis or treatment of hypothyroidism, however possible precipitants include anaesthetic and surgical stress; other intraoperative parameters such as electrolytes, glucose levels and temperature were normal. Multiple failed attempts at extubation can be attributed to acute hypoventilation episodes, and deterioration of this patient's mentation is a cardinal sign of this diagnosis. (2)

            There is lack of globally validated scoring criteria for the diagnosis of myxoedema coma owing to the rarity of this condition. Chiong et. al (4) however, developed an objective tool for its diagnosis. It consists of six criteria:

            • Glasgow Coma Scale GCS: 0-10 (4 points), 11-13 (3 points), 14 (2 points) and 15 (0 points)

            • TSH >30 (2 points), and 15-30 (1 point)

            • T4 below normal (1 point)

            • Hypothermia (temperature < 35.56 ºC) (1 point)

            • Bradycardia (HR <60) (1 point)

            • Precipitating illness present (1 point)

            A score of ≥7 is suggestive of myxoedema coma, 5-7 makes the diagnosis likely and <5 suggests an unlikely diagnosis. (4) Despite the limited number of participants in the development of this scoring tool, the overall model showed statistical significance in diagnosing patients with myxoedema coma. Our patient scored 8, which was highly suggestive of the diagnosis.

            Hypothyroid patients are hyperresponsive to central nervous system depressants. Vascular and respiratory reflexes are depressed leading to hypotension and delayed recovery of spontaneous ventilation, (5) as occurred in our patient. The haemodynamic instability which led to the requirement of inotropic support eventually occurred in ICU and complicated into a STEMI. A complex relationship exists between thyroid diseases and cardiovascular function. Cardiac catheterization was not performed on this patient, thus the state of her coronary anatomy and function is not known. Thyroid dysfunction is, however, known to trigger coronary spasm which could have contributed to the STEMI. (5)

            Mortality secondary to myxoedema coma, is described to be between 25 – 52%. (6) A large, retrospective observational study by Ono et. al, (6) reported an overall in-hospital mortality of 29.5%. The literature has shown that in severe disease, patients are more likely to require and receive higher doses of steroids, cardiovascular and mechanical ventilation support. The use of catecholamine and higher age are significant predictors of in-hospital mortality. (6)


            There are a variety of factors that can cause and contribute to delayed awakening following surgery. They are broadly classified into patient related factors, anaesthetic drugs, including the use of several pharmacological agents, surgical factors, and metabolic and electrolyte derangements. Myxoedema coma is one such metabolic complication that occurs in severely hypothyroid patients. It is uncommon but life-threatening. A differential diagnosis was employed in this case and obvious causes such as inadequate muscle relaxant reversal, electrolyte imbalances, hypothermia, and hypoglycaemia, were properly excluded by the clinicians. The bradyarrhythmia noted prior to surgery, was probably the only clinical sign the patient presented with. It was evident that her surgery was an emergency, and further probing revealed a haemodynamically stable patient. The clinical deterioration in the immediate postoperative period and the change of haemodynamics in ICU necessitated further clinical investigations. The highly elevated TSH level, the cardiac event and the hypotension pointed towards the eventual diagnosis of myxoedema coma. This was not a clear case of severe hypothyroidism; however, one needs to consider hypothyroidism in the differential diagnosis of delayed emergence from anaesthesia.


            1. ShailajaS, GurumurthyT, ShettyK, HarshavardhanK, VargheseN. Myxedema coma - a cause for delayed recovery from anaesthesia. J Evol Med Dent Sci. 2013; 2(4):360–3.

            2. WallCR. Myxedema coma: diagnosis and treatment. Am Fam Physician 2000; 62(11):2485–90.

            3. MunirA. Myxedema Coma. J Ayub Med Coll Abbottabad. 2018; 30(1):119–20.

            4. ChiongYV, BammerlinE, MariashCN. Development of an objective tool for the diagnosis of myxedema coma. Transl Res. 2015; 166(3):233–43.

            5. BraitehN, SenyondoGD, RahmanMF, ChaudhryR, KashouH. An Unusual Presentation of ST Elevation Myocardial Infarction Complicated with Cardiogenic Shock Due to Myxedema Coma: A Case Report. Am J Case Rep. 2021; 22:e929573–1.

            6. OnoY, OnoS, YasunagaH, MatsuiH, FushimiK, TanakaY. Clinical characteristics and outcomes of myxedema coma: Analysis of a national inpatient database in Japan. J Epidemiol. 2017; 27(3):117–22.


            Author and article information

            Wits Journal of Clinical Medicine
            Wits University Press (5th Floor University Corner, Braamfontein, 2050, Johannesburg, South Africa )
            : 3
            : 3
            : 219-222
            [1] Department of Anaesthesiology, School of Clinical Medicine, Faculty of Heath Sciences University of the Witwatersrand, Johannesburg, South Africa
            Author notes
            [* ] Correspondence to: Hlamatsi J. Moutlana, hlamatsi@ 123456yahoo.com

            Distributed under the terms of the Creative Commons Attribution Noncommercial NoDerivatives License https://creativecommons.org/licenses/by-nc-nd/4.0/, which permits noncommercial use and distribution in any medium, provided the original author(s) and source are credited, and the original work is not modified.

            Case Report

            General medicine,Medicine,Internal medicine


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