Thyroid storm

Introduction:

This condition is also known as thyrotoxic crisis caused by hypermetabolic state induced by excessive secretion and release of thyroid hormones in individuals with thyrotoxicosis. In children this could be the initial presentation of thyrotoxicosis. This is more so in neonates.

Clinical manifestations:

1. Marked hypermetabolism
2. Excessive adrenergic response
3. Hyperpyrexia (reliable finding)
4. Flushing / sweating / tachycardia /atrial fibrillations / elevated pulse pressure / cardiac failure
5. CNS symptoms include – agitation / psychosis / restlessness / delirium / coma.
6. GI symptoms include – diarrhoea / jaundice
7. Hypertension may be present. * Normal blood pressure doesn't rule out thyroid strom.
8. Elderly patients may manifest atypical symptoms like (apathetic thryoid strom).
9. Heat intolerance

Diagnosis is primarly made on clinical grounds, as no specific lab test is going to clinch the diagnosis.


Triggering factors include:

1. Thyroid surgery
2. Radio active iodine therapy
3. Pregnancy / during delivery
4. Acute iodine load
5. Trauma
6. Acute infection
7. Drug reaction
8. Trauma
9. Myocardial infarction (rare)
10. Graves disease

Incidence:

It is 5 times more common in women than in men.
It is more common in prepeubertal children.
Common in children born to mothers with Graves disease.
More common in adolescents.

Pathophysiology:

Thyroid crisis is the most extreme state of thyrotoxicosis. It should be considered to be a decompensated state of thyroid hormone. Studies have shown that there is no clear evidence that increased secretion of thyroid hormones lead to thyroid strom. Increased levels of catecholamines and increased sensitivity of catecholamine receptors have been suggested to play a role. Decreased binding to thyroid binding globulin can also play a vital role as this would lead to a relative increase in the risk of increasing levels of serum T3 and T4.

Management:

All patients with suspected thyroid strom should be managed only in an ICU setup.

Treatment should be considered to be a triangular one.

Iv life line is to be started.
Dextrose is to be administered because of the increasing biological demand for glucose.
Serum electrolytes should be estimated and abnormalities if any should be corrected.
Cardiac arrythmias if present should be treated aggressively.
Hyperthermia can be managed by ice packs / acetaminophen 15 mg/kg orally.
Propranalol should be administered to block sympathomimetic effects of thyroxine.
Anti thyroid medications are to be administered. High dose of propyl thiouracil is preferred because it blocks peripheral conversion of T4 to T3. Hepatic parameters should be monitored while administering propylthiouracil.
Administration of Lugol's iodine will help by blocking the release of thyroid hormones. Lugol's iodinee is preferred.
Glucocorticoids are also administered in order to reduce peripheral conversion of T4 to T3.
Plasma pheresis can be resorted to in cases of accidental / suicidal ingestion of large doses of thyroxine.
Underlying cause should be looked for and treated.

Theories explaining thyroid strom:

1. These patientts have relatively high levels of thryoid hormones than normal controls. This may not be the case always.
2. Adrenergic receptor activation theory. Sympathetic nerves are supposed to innervate thyroid gland. Increased sympathetic stimulation causes an increase in thyroid hormone synthesis and secretion. This increase in thyroid hormone levels increase the density of beta receptors.
3. Excess hormones could be liberated when the gland is manipulated during surgery.
4. Rapid reduction in the levels of thyroid binding globulin levels cause increased levels of thyroid hormones
5. Alterations in tissue tolerance to thyroid hormones.


Differential diagnosis:

1. Anxiety disorder
2. Cardiac failure
3. Hypertension
4. Hyperthyroidism
5. Phaeochromocytoma
6. Atrial tachycardia / fibrillation