Throid Storm

INTRODUCTION
• Thyroid Storm (Accelerated Hyperthyroidism) is an extreme accentuation of

thyrotoxicosis.
• It is usually occur in association with Graves disease but sometimes with toxic
multinodular goiter in the elderly patient.
• It is a life threatening emergency with mortality rate as high as (10-75%)
despite treatment.
• The serum thyroid hormone levels in crisis are not appreciably greater than
those in severe uncomplicated thyrotoxicosis, but the patient can no longer
adapt to the metabolic stress.
PRESENTATION
Thyroid storm is usually of abrupt onset and occurs in patients in whom

preexisting thyrotoxicosis has been treated incompletely or has not been
treated at all.
PRECIPITATING EVENTS
CLINICAL FEATURES
• The clinical picture is one of severe hypermetabolism or exaggeration of
thyrotoxicosis.
PHYSICAL FINDINGS-
• may reveal goiter
• ophthalmopathy (in the presence of Graves' disease),
• lid lag
• hand tremor
• warm and moist skin.
• Jaundice
• Pedal edema and engorged neck veins
• Fever is almost invariable and may be severe upto 104 to 106°F.
Cardiovascular signs and symptoms-
• Marked tachycardia of sinus or ectopic origin.
• Arrhythmias most commonly ATRIAL FIBRILLATION.
• Basal rales suggestive of pulmonary edema.
• Hypotension
Neurological symptoms-
• Delirium
• Psychosis
• Tremors
• Apathy
• Stupor
• Coma
Gastrointestinal symptoms-
Nausea
Vomitting
Jaundice
Diarrhoea
DIAGNOSIS
• This clinical picture in a patient with a history of preexisting

thyrotoxicosis or with goiter or exophthalmos or both is sufficient to
establish the diagnosis, and emergency treatment should not await
laboratory confirmation.
CLINICAL SCORE USED TO HELP CONFIRM THE DIAGNOSIS-
TREATMENT OF THYROID STORM
• Treatment aims to correct both the severe thyrotoxicosis and the

precipitating illness and to provide general support.
• The patient thought to have thyroid storm should be monitored in a

medical intensive care unit during the initial phases of therapy.
BASIC TREATMENT PRINCIPLES-
The therapy should be directed towards-
• Supportive care- airway, fluid status and cardiovascular support.
• Combat the hyperpyrexia
• Treating the precipitating cause
• Medical therapy
PRINCIPLES OF MEDICAL THERAPY
• Antagonize the increased sensitivity to adrenergic stimulation

mediated by severe thyrotoxicosis.
• Inhibit de novo hormone synthesis.
• Inhibit release of new hormone.
• Reduce peripheral conversion of T4 to T3.

MEDICATIONS-
ANTITHYROID DRUGS-
• Propylthiouracil(PTU) – up to 400 mg every 4-6 hours are given by

mouth, by stomach tube, or, if necessary, per rectum.
• PTU is preferable to methimazole because it has the additional action

of inhibiting the peripheral as well as the thyroidal generation of T3
from T4 by the type 1 iodothyronine deiodinase.
• Methimazole-
• Given as 20 mg orally every four to six hours.
• May be preferred for severe, but not life-threatening,
hyperthyroidism because methimazole has a longer duration of action
and, after weeks of treatment, results in more rapid normalization of
serum T3 compared with PTU and because methimazole is less
hepatotoxic.
IODINE-
• Administered either as SSKI (three drops twice daily) or the

equivalent as Lugol solution (10 drops twice daily), acutely retards the
release of preformed hormone from the thyroid gland.
• Theoretically, PTU is administered before iodine to inhibit the

synthesis of additional thyroid hormone from the administered
iodine.
DRUGS TO BLOCK EXCESSIVE SYMPATHETIC ACTIVITY
• BETA BLOCKERS-
• In the absence of cardiac insufficiency or asthma a β-adrenergic blocking

agent should be given to ameliorate the hyperadrenergic state.
• Propranolol- given at a dose of 40 to 80 mg orally every 6 hours, it also

reduces the peripheral conversion of T4 to T3.
• A very short-acting β-adrenergic blocker such as labetalol or esmolol may

be safer if propranolol can not be given.
• CALCIUM CHANNEL BLOCKERS-
• If β-adrenergic blocking agents are contraindicated, a calcium channel
blocker (diltiazem) may be used to slow the heart rate.
CORTICOSTEROIDS
• Dexamethasone as 8 mg orally once daily or hydrocortisone as 150

mg every 8 hours as should be given.
• These acts by supporting the response to stress, inhibiting both the

release of hormone from the gland and possibly the peripheral
generation of T3 from T4.
MEDICATIONS SUMMARY
• BETA BLOCKER to control the symptoms and signs induced by increased

adrenergic tone.
• THIONAMIDE to block new hormone synthesis.
• IODINE SOLUTION to block the release of thyroid hormone.
• GLUCOCORTICOIDS to reduce T4-to-T3 conversion, promote vasomotor

stability, and possibly treat an associated relative adrenal insufficiency.

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INTRODUCTION

• Thyroid Storm (Accelerated Hyperthyroidism) is an extreme accentuation of

Thyroid storm is usually of abrupt onset and occurs in patients in whom

• This clinical picture in a patient with a history of preexisting

• Treatment aims to correct both the severe thyrotoxicosis and the

• The patient thought to have thyroid storm should be monitored in a

• Supportive care- airway, fluid status and cardiovascular support.

• Combat the hyperpyrexia

• Treating the precipitating cause

• Antagonize the increased sensitivity to adrenergic stimulation

• Inhibit de novo hormone synthesis.

• Inhibit release of new hormone.

• Reduce peripheral conversion of T4 to T3.

• Propylthiouracil(PTU) – up to 400 mg every 4-6 hours are given by

• PTU is preferable to methimazole because it has the additional action

• Administered either as SSKI (three drops twice daily) or the

• Theoretically, PTU is administered before iodine to inhibit the

• In the absence of cardiac insufficiency or asthma a β-adrenergic blocking

• Propranolol- given at a dose of 40 to 80 mg orally every 6 hours, it also

• A very short-acting β-adrenergic blocker such as labetalol or esmolol may

• Dexamethasone as 8 mg orally once daily or hydrocortisone as 150

• These acts by supporting the response to stress, inhibiting both the

• BETA BLOCKER to control the symptoms and signs induced by increased

• THIONAMIDE to block new hormone synthesis.

• IODINE SOLUTION to block the release of thyroid hormone.

• GLUCOCORTICOIDS to reduce T4-to-T3 conversion, promote vasomotor

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