Thyrotoxic Storm Following Thyroidectomy Medication
- Author: Peter F Czako, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA more...
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
These agents block thyroid hormone synthesis.
Thiourea agent that blocks production of thyroid hormones. In addition, inhibits peripheral deiodination of T4 to T3. Preferred over MMI in thyroid storm.
Active moiety of parent compound carbimazole. Blocks incorporation of iodine into thyroglobulin within 1 h of ingestion.
Methimazole was initially thought to be associated with neonatal aplasia cutis (ie, defect in the neonatal scalp) and was thought to be more likely to cross the placenta than PTU. However, recent studies by Wing et al concluded that PTU and MMI are equally effective and safe in the treatment of hyperthyroidism in pregnancy.
Used in patients intolerant to iodine; impairs thyroid hormone release.
Inhibits thyroid hormone secretion. Contains 8 mg of iodide per drop. May be mixed with juice or water for intake.
Iodide treatment is reserved for the treatment of thyroid storm. It is also used for 10-14 d prior to surgical procedure, including thyroidectomy. Can be used with Graves thyrotoxicosis but exacerbates thyrotoxicosis from toxic multinodular goiter and toxic adenoma.
Sodium ipodate (Oragrafin)
One of the most effective inhibitors of deiodinase, which converts T4 to the more biologically active T3. Reduction in conversion of T4 to T3 can greatly reduce T3 levels and thyrotoxic symptoms.
These agents reduce iodine uptake and antibody titers of thyroid-stimulating antibodies with stabilization of the vascular bed.
Has many pharmacologic benefits but significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, and inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6, IL-2, IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down granulocyte aggregates and improves pulmonary microcirculation. Has inhibitory effect on conversion of T4 to T3.
Adverse effects include hyperglycemia, hypertension, weight loss, GI bleeding or perforation synthesis, cerebral palsy, adrenal suppression, and death. Most of the adverse effects of corticosteroids are dose dependent or duration dependent.
Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining property of hydrocortisone.
Patients can be switched from an IV to PO regimen in a 1:1 ratio.
Elicits anti-inflammatory properties and causes profound and varied metabolic effects. Modifies the body's immune response to diverse stimuli.
Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties.
Inhibits action of endogenous pyrogens on heat-regulating centers; reduces fever by a direct action on the hypothalamic heat-regulating centers, which, in turn, increases the dissipation of body heat via sweating and vasodilation.
These agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.
DOC to counter peripheral action of thyroid hormone; blocks beta-adrenergic receptors; prevents conversion of T4 to T3.
Ultra–short-acting agent that selectively blocks beta1-receptors with little or no effect on beta2-receptor types. Particularly useful in patients with elevated arterial pressure, especially if surgery is planned. Shown to reduce episodes of chest pain and clinical cardiac events compared with placebo. Used successfully in thyrotoxicosis and thyroid storm. Can be discontinued abruptly if necessary.
Useful in patients at risk for experiencing complications from beta-blockade; particularly those with reactive airway disease, mild-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.
These agents reduce blood pressure.
For use in patients with congestive cardiac failure, bronchospasm, or history of asthma.
For use in patients with congestive cardiac failure, bronchospasm, or history of asthma; successful treatment has been documented in cases of thyroid storm resistant to large doses of propranolol.
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|Uncomplicated Thyrotoxicosis||Thyroid Storm|
|1. Heat intolerance, diaphoresis||1. Hyperpyrexia, temperature in excess of 106o C, dehydration|
|2. Sinus tachycardia, heart rate 100-140||2. Heart rate faster than 140 beats/min, hypotension, atrial dysrhythmias, congestive heart failure|
|3. Diarrhea, increased appetite with loss of weight||3. Nausea, vomiting, severe diarrhea, abdominal pain, hepatocellular dysfunction-jaundice|
|4. Anxiety, restlessness||4. Confusion, agitation, delirium, frank psychosis, seizures, stupor or coma|