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Thyroid crisis

Up Cortisol deficiency Diabetes insipidus Diabetes Myxoedema Thyroid crisis


Thyroid crisis

- life threatening clinical extreme of hyperthyroidism
- F>M
- mortality 10-20% with treatment
- FT3 and FT4 correlate poorly with severity of condition: condition is essentially an inability of end-organs to modulate their response to excess thyroid hormone

Aetiology

- usually occurs in patients with poorly controlled or unrecognized hyperthyroidism
- precipitated by intercurrent illness, in particular:

  • infection
  • trauma
  • surgery
  • uncontrolled DM
  • labour
  • eclampsia

- other precipitants include excessive palpation of thyroid, incomplete pre-op preparation, inadequate peri-operative dose of beta blockers, use of radio-iodine in unprepared patients, drugs such as iodides in patients with impaired autoregulation, haloperidol, massive overdose of thyroid hormone

Clinical features

Exacerbation of features of hyperthyroidism
- hyperpyrexia. May be extreme (>41oC) and is generally considered essential to diagnosis. Skin usually moist and warm
- confusion, fits, coma, muscle weakness. Very common. Features of UMN lesions have been described as has rhabdomyolysis and sudden onset of thyrotoxic periodic paralysis
- arrhythmias, cardiac failure. Decreasing pulse rate and BP with the development of shock are associated with poor prognosis
- vomiting, diarrhoea. Occasionally jaundice: associated with poor prognosis
- hypercalaemia relatively common (15%) but rarely a problem in itself
- rarely apathetic hyperthyroidism (usually elderly patients) may present in crisis with features of profound exhaustion, tachycardia, hyporeflexia, severe myopathy, marked weight loss and hypotension

Differential diagnosis

- malignant hyperpyrexia
- sepsis

Treatment

  1. treat underlying cause
  2. decrease thyroid hormone concentrations
  3. reduce peripheral action of thyroid hormones
  4. supportive therapy

Treatment to reduce thyroid hormone concentrations

- iodine: in large doses inhibits release of thyroid hormones. Generally given > 1 h after PTU/carbimazole/methimazole, as otherwise, it may lead to an increase in thyroid hormone synthesis. Use Lugol's iodine (16 mg bd PO), potassium iodide (50 mg bd PO) or sodium iodide (0.5 mg bd IVI). Iodine containing contrast media may specifically ameliorate cardiac effects of thyroxine, are potent blockers of peripheral conversion of T4 and may block peripheral thyroid hormone receptors (iopanoic acid 1-3 g daily or sodium ipodate 0.5 mg/day). ? drugs of choice. Lithium carbonate (300 mg qds titrated to a serum lithium level of 0.7-1.4 mmol/l) is an alternative in patients who are allergic to iodine. Has similar action in blocking thyroid hormone release

- propylthiouracil (inhibits conversion of T4 to T3 as well as blocking iodination of tyrosine and hence secretion of T4). PO/NG 1 g loading followed by 200-300 mg 4-6 hrly. GI absorption impaired or unreliable in thyroid crisis but there is no parenteral formulation. Rapid onset of action. Alternatives are methimazole and carbimazole (metabolized to methimazole). Methimazole may be absorbed more slowly than PTU but is longer acting. Does not affect peripheral conversion of T4. Transient leucopenia common with antithyroid drugs (20%) but agranulocytosis is rare

Treatment to reduce peripheral action of thyroid hormones

- beta blockade: IV propranolol - titrate against heart rate using increments of 0.5 mg to a total of 10 mg. Give further doses 4-6 hrly. Drug of choice: inhibits peripheral conversion of T4 to T3. Tachycardia, fever, hyperkinesis, tremor, proximal myopathy, periodic paralysis, bulbar palsy and hypercalcaemia respond. Beta1 selective agents do not inhibit T4 to T3 conversion as effectively but may be preferred in patients with reactive airways or heart failure. Esmolol useful because of short half-life

- although b blockers are of benefit in thyroid storm precipitated by high catecholamine concentrations associated with surgery it is not clear if thyroid storm due to other causes is as responsive to b blockade

- diltiazem, reserpine and guanethidine should be considered in patients in whom beta blockade is contraindicated

-contrast media may block peripheral thyroid hormone receptor

- glucocorticoids, PTU, oral contrast media, amiodarone block peripheral conversion of T4 to T3

Action
Blocks:

PTU

Methimazole

Lithium carbonate

Potassium iodide

Oral contrast media

Thyroid iodide uptake

 

 

++

 

 

T4 synthesis

+++

+++

 

 

+

T4 release

 

 

++

+++

+

T4® T3

+++

 

 

 

+++

Thyroid hormone receptor

 

 

 

 

+

Supportive therapy

- glucose for nutrition.
- steroids: hydrocortisone 300 mg loading followed by 100 mg tds. Relative hypoadrenalism occurs as a result of increased metabolism of corticosteroids
- sedation
- NG suction
- vitamins (especially thiamine).
- active cooling. Chlorpromazine 25-50 mg 4-6 hrly to prevent shivering
- fluid replacement. Patients tend to be fluid depleted because of increased insensible loss, diarrhoea and vomiting and decreased ADH secretion
- cooling should be attempted before specific therapy is given for congestive cardiac failure. However judicious use of inotropes and diuretics may be necessary
- clearance of many drugs is increased and a shortening of dose intervals may be necessary. (Dose intervals will have to be increased again once thyroid storm is controlled). Anti-coagulants and adrenergic drugs are exceptions.
- avoid salicylates and frusemide both of which cause abrupt increases in free thyroid hormones
- anecdotal reports of successful treatment of cases unresponsive to conventional treatment with plasma exchange and charcoal haemoperfusion.

Prevention

- postpone operation if possible. If not, take measures outlined above before operation rather than after development of symptoms.

Further reading

Weiss RE, Refetoff S. Thyroid disesase. In Hall JB, Schmidt GA, Wood LH (eds). Principles of Critical Care, 2nd ed., 1998. McGraw-Hill, New York. pp 1205-19.


© Charles Gomersall November 1999

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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