Hypothyroidism in the ICU

Severe hypothyroidism comes up often as a differential for various things, but only Question 11 from the second paper of 2002 and Question 14 from the second paper of 2021 address it directly (diagnosis, features, management). The hypothyroidism considered in this chapter lays somewhere between the mild "sick euthyroid" syndrome and frank myxoedema. Myxoedema coma comes up much more often in the exam, and has been allocated to its own chapter.

Causes of hypothyroidism

An excellent article is available, which treats this topic with the detail it deserves. This detail has been distilled and concentrated in this table, to simplify revision:

Features of hypothyrodism

One can summarise these by saying that everything goes slower.

There's yet more findings which are not listed here. What you see here are findings associated with severe hypothyroidism, of the sort that might require hospitalisation. In addition to this, there are features listed in the myxoedema coma chapter, which represent the next level of clinical severity in the spectrum. Thoseinclude ECG changes, cardiogenic shock, and so forth. 

Management of hypothyroidism

Well, one could do no better than to replace the missing hormone. Its not clever, but it is the right solution. In myxoedema coma, one may wish to replace it intravenously. A dose of 50 to 200mcg is usually enough. One traces the efficacy of one's management by observing the decrease in TSH (which should be elevated in "proper" hypothyroidism, and which will fall to normal levels as thyroid function is restored). The addition of corticosteroids into the mix tends to be advocated because until test results are available, one is never sure whether one is dealing with some sort of hypoadrenal syndrome.

The literature for the management of severe hypothyroism and myxoedema coma is somewhat scant on evidence. For example, one of the best articles on this topic is  Ringel (2001), where one could literally go for some pages of excellent practical suggestions without encountering a single supporting reference. Clearly a lot of what we do in the ICU for this condition is based on expert opinion, theoretical physiology and personal experience. With that caveat:

  • Specific management:
    • Replace thyroxine.  One could do no better than to replace the missing hormone. Its not clever, but it is the right solution. In myxoedema coma, one may even wish to replace it intravenously as triiodothyronine, 10mcg three times a day.  The advantage of this is that the patient's level of consciousness will recover faster, as enteric T4 will need to get converted to T3 peripherally first, and that might take some time. A dose of 50 to 200mcg of enteral thyroxine is usually enough for severe hypothyroidism. Huge initial doses, 300-500mcg, are recommnended for myxoedema (and there does not seem to be any benefit in going higher, according to Ridgeway et al, 1972). One traces the efficacy of one's management by observing the decrease in TSH (which should be elevated in "proper" hypothyroidism, and which will fall to normal levels as thyroid function is restored). Also, there should be some resolution of the clinical features, eg. the level of consciousness improving, the hypotension resolving, etc. 
    • Add corticosteroids. Particularly where hypothyroidism is the consequence of some sort of central problem, eg. a pituitary adenoma, a concomitant loss of ACTH secretion should be anticipated, and corticosteroids should be commenced, 
    • Eliminate thyrotoxic substances; eg. think of another antiarrhythmic so you can stop the amiodarone.
    • Treat the underlying condition,  if there is something specific (eg. some autoimmune thyroiditis, or a high pituitary adenoma)
  • Supportive management:
    • Intubation may be required. These people may have an abnormal level of consciousness. Myxoedema coma is the most severe manifestation of hypothyroidism, and it maybe the reason the patient is admitted to the ICU in the first place. However, even without it, hypothyroid patients may require intubation because their threshold for unconsciousness is decreased.
    • Mechanical ventilation may be required as these patients tend to hypoventilate, and may develop hypercapnia or hypoxia due to atelectasis. After a course of ventilation, hypothyroidism may delay weaning because of respiratory muscle weakness, and may be one of the causes of weaning failure.
    • Haemodynamic support with vasopressors and inotropes, of which you should expect to use more than usual. The responses to catecholamine vasopressors will be blunted in hypothyroidism. Initially, tests performed on patients before and after treatment demonstrated no such relationship. However, later publications confirmed that there is indeed a dampening of the response to sympathomimetics, and that this response is by no means uniform. Hypothyroidism results in a decreased expression of adrenergic receptors, and a dysfunction of posterceptor signalling. However, it seems there is usually still enough "spare receptors" around to maintain a normal response to infused catecholamines. A few unlucky patients may be so receptor-depleted that their catecholamine requirements may increase.
    • Avoid QT-prolo
    • Careful sedation, meaning "use less drug". When one is going to administer the anaesthetic for intubation, one would be well advised to down-titrate one's doses, because hypothyroid patients will be more sensitive to anaesthetic agents. There has been several case series of hypothyroid patients who were diagnosed after they reacted badly to routine anaesthesia.
    • Correct electrolyte derangement. Hyponatremia is a common feature. It's usually of a hypervolemic variety, and usually not severe enough to require hypertonic saline. The right answer is usually fluid restriction. 
    • Correct hypoglycaemia. This is the consequence of the adrenal insufficiency which could co-exist with the hypothyroidism.
    • Monitor for bleeding. Severe hypothyroidism seems to promote bleeding by increasing the rate of fibrinolysis. This is in contrast to the increase in fibrinolytic activity which is seen with mild and moderate hypothyroidism. The mechanism for this is poorly understood.


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