a)    List important clinical features of thyroid storm.                                (30% marks) 
b)    Outline the principles of management of myxoedema coma.                     (70% marks) 


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College answer

  1. List important clinical features of thyroid storm.                                            3 marks
    1. Hyperpyrexia – temperature 40 - 41º C
    2. CVS – sinus tachycardia usually exceeding 140, atrial fibrillation, decompensated CCF, hypotension/shock and in extreme cases cardiac arrest.
    3. CNS – agitation, anxiety, delirium, stupor and coma.         
    4. GI symptoms – diarrhoea, abdominal pain, jaundice
    5. Physical exam may reveal Goiter, opthalmopathy, lid lag, tremors, warm moist skin.
  1. Outline the principles of management of myxoedema coma.                            7 marks
    1. Establish IV access including CVC and collect blood for Investigations including thyroid function tests, BSL, electrolytes etc.
    2. Establish monitoring – arterial BP, ECG, temp, pulse oximetry etc.
    3. Airway – Intubation to protect airway and Mechanical ventilation to normal gas exchange
    4. Fluid + vasopressors as appropriate to a MAP 65-70 mmHg.
    5. Passive rewarming while close monitoring of haemodynamics and temperature.
    6. slow replacement is key. IV T3 and T4 – T3 has greater biologic activity and quicker onset of action. Daily monitoring of T3 and T4 levels to avoid toxicity.
    7. IV hydrocortisone to treat possible coexisting adrenal insufficiency. viii.     IV dextrose to maintain BSL, NG feeding if possible.
    1. Consider IV antibiotic if clinical evidence of infection after collecting appropriate cultures.
    2. Monitor and treat cardiac arrhythmias, coronary ischaemia


Clinical features of thyroid storm:

  1. Goitre: possible airway compromise)
  2. Tachypnoea due to increased CO2 production;
    Increased O2ER (increased metabolic fuel use)
  3. Tachycardia,
    Atrial fibrillation and ventricular arrhythmias
    Heart failure
    Hypertension (early), hypotension (late)
  4. Tremor;
    Agitation, progressing to encephalopathy, coma and seizures.
    There is the phenomenon of "apathetic thyrotoxicosis" which presents with weakness
  5. Low potassium and magnesium (particularly in "apathetic thyrotoxicosis")
    Serum cortisol should be elevated. If it is not, one might consider a relative adrenal insufficiency, and supplement some hydrocortisone.
  6. Rhabdomyolysis may be present; CK may be elevated. This is "thyrotoxic myopathy"
  7. Diarrhoea, nausea and vomiting
    Increased metabolic rate; increased demand for metabolic substrate.
    Nutritional requirements are increased
    Hyperglycaemia may be apparent in the non-diabetic patient
    Jaundice may develop
  8. Leukocytosis; a left shift
  9. Fever: in fact, may go up to 41°C. This is apparently the most characteristic feature.

Management of myxoedema coma

The model answer offered for this section is somewhat surprising, as some of its components - on first assessment - could not possibly score any marks in a question which asks for the principles of management of myxoedema coma. Statements such as "mechanical ventilation to normal gas exchange" and "consider IV antibiotic if clinical evidence of infection after collecting appropriate cultures" not only violate the rules of grammar but do nothing to support one's impression that the writer was an expert on extreme hypothyroidism. But, as these generic supportive strategies are offered by the college in their model answer template, one must assume that they expected them to also appear in the candidate's written responses, and so they are offered as a post-script in the management strategy here.


  • Replace thyroid hormone - preferably IV
    • loading dose is 300-400μcg
    • a rising body temperature and normalising cardiovascular parameters alert you to the success of your management strategy
  • Replace corticosteroids - there is usually a concomitant adrenal insufficiency. One would use a "stress dose".
  • Correct the sodium: this is usually a hypervolemic hyponatremia which resembles that of CCF (in fact, it is because of exactly the same mechanism: poor cardiovascular performance leads to ADH and aldosterone driven retention of water and sodium, with a resulting hypervolemic hyponatremia. Because the patient is usually obtunded, one is obliged to correct a particularly low sodium with hypertonic saline, being careful not to demyelinate the CNS.
  • Good solid supportive management:
    • Establish an airway if this is needed
    • Maintain normoxia and normocapnea with the ventilator
    • Maintain normotension to support organ system perfusion, with a catecholamine infusion
    • Correct the Na+ deficit - consider using water restriction alone.
    • Correct hypoglycaemia
    • Correct hypothermia with warming blanket



Summers, V. K. "Myxoedema coma." British medical journal 2.4832 (1953): 366.

Wartofsky, Leonard. "Myxedema coma." Endocrinology and metabolism clinics of North America 35.4 (2006): 687-698.

Mathew, Vivek, et al. "Myxedema coma: a new look into an old crisis." Journal of thyroid research 2011 (2011).

Lezama, Maybelline V., Nnenna E. Oluigbo, and Jason R. Ouellette. "Myxedema Coma and Thyroid Storm: Diagnosis and Management." Internal Medicine 14.Part 2 (2011): 1.

Chu, Michael, and Terry F. Seltzer. "Myxedema coma induced by ingestion of raw bok choy." New England Journal of Medicine 362.20 (2010): 1945-1946.

Wall, Cristen Rhodes. "Myxedema coma: diagnosis and treatment." American family physician 62.11 (2000).

Bondugulapati, Laxmi, Mohamed Adlan, and Lakdasa Premawardhana. "Thyroid Emergencies." Sri Lanka Journal of Critical Care 2.1 (2011): 1-12.