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Hyperthyroidism, thyroid storm, and Graves disease

Hyperthyroidism, thyroid storm, and Graves disease are conditions of excess thyroid hormone. The elevated level of thyroid hormones can result in clinical manifestations ranging from mild to severely toxic with resultant morbidity and mortality for affected patients.

Hyperthyroidism

Hyperthyroidism presents as a constellation of symptoms due to elevated levels of circulating thyroid hormones. Because of the many actions of thyroid hormone on various organ systems in the body, the spectrum of clinical signs produced by the condition is broad. The presenting symptoms can be subtle and nonspecific, making hyperthyroidism difficult to diagnose in its early stages without the aid of laboratory data.

The term hyperthyroidism refers to inappropriately elevated thyroid function. Though often used interchangeably, the term thyrotoxicosis, which is an excessive amount of circulating thyroid normal thyroid function, such as in instances of inappropriate exogenous thyroid hormone or excessive release of stored hormone from an inflamed thyroid gland.

Graves disease

Graves disease (diffuse toxic goiter), the most common form of overt hyperthyroidism, is an autoimmune condition in which autoantibodies are directed against the thyroid-stimulating hormone (TSH) receptor. As a result, the thyroid gland is inappropriately stimulated with ensuing gland enlargement and increase of thyroid hormone production. Risk factors for Graves disease include family history of hyperthyroidism or various other autoimmune disorders, high iodine intake, stress, use of sex steroids, and smoking. The disease is classically characterized by the triad of goiter, exophthalmos, and pretibial myxedema.

Thyroid storm

Thyroid storm is a rare and potentially fatal complication of hyperthyroidism. It typically occurs in patients with untreated or partially treated thyrotoxicosis who experience a precipitating event such as surgery, infection, or trauma. Thyroid storm must be recognized and treated on clinical grounds alone, as laboratory confirmation often cannot be obtained in a timely manner. Patients typically appear markedly hypermetabolic with high fevers, tachycardia, nausea and vomiting, tremulousness, agitation, and psychosis. Late in the progression of disease patients may become stuporous or comatose with hypotension.

Pathophysiology:In healthy patients, the hypothalamus produces thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary gland to secrete thyroid-stimulating hormone (TSH); this in turn triggers the thyroid gland to release thyroid hormone.

Thyroid hormone concentration is regulated by negative feedback by circulating free hormone primarily on the anterior pituitary gland and to a lesser extent on the hypothalamus. The secretion of TRH is also partially regulated by higher cortical centers.

The thyroid gland produces the prohormone thyroxine (T4), which is deiodinated primarily by the liver and kidneys to its active form, triiodothyronine (T3). The thyroid gland also produces a small amount of T3 directly. T4 and T3 exist in 2 forms: a free, unbound portion that is biologically active and a portion that is protein bound to thyroid-binding globulin (TBG). Despite consisting of less than 0.5% of total circulating hormone, free or unbound T4 and T3 levels best correlate with the patient's clinical status.



History: The clinical presentation of hyperthyroidism ranges from an array of nonspecific historical features to an acute life-threatening event. Historical features common to hyperthyroidism and thyroid storm are numerous and represent a hypermetabolic state with increased beta-adrenergic activity.

  • Weight loss
    • Patients typically report an average loss of approximately 15% of their prior weight.
    • Basal metabolic rate is increased with a stimulation of lipolysis and lipogenesis.
  • Palpitations
  • Chest pain - Often occurs in the absence of cardiovascular disease
  • Psychosis
  • Menstrual irregularity
  • Disorientation
  • Tremor
  • Nervousness, anxiety, or emotional lability
  • Heat intolerance
  • Increased perspiration
  • Fatigue
  • Weakness - Typically affects proximal muscle groups
  • Edema
  • Dyspnea
  • Frequent bowel movements

Physical:

  • Fever
  • Tachycardia (often out of proportion to the fever)
  • Diaphoresis (often profuse)
  • Dehydration secondary to GI losses and diaphoresis
  • Warm, moist skin
  • Widened pulse pressure
  • Congestive heart failure (may be a high output failure)
  • Thyromegaly
    • Nontender, diffuse enlargement in Graves disease
    • Tender, diffusely enlarged gland in thyroiditis
    • Thyroid nodules, either single or multinodular goiter
  • Exophthalmos
  • Shock
  • Atrial fibrillation
    • Typically in elderly patients
    • May be refractory to attempted rate control with digitalis
    • Converts after antithyroid therapy in 20-50% of patients
  • Myopathy
  • Thyroid bruit - Relatively specific for thyrotoxicosis
  • Fine, resting tremor

Causes: Hyperthyroidism results from numerous etiologies, including autoimmune, drug-induced, infectious, idiopathic, iatrogenic, and malignancy.

  • Autoimmune
    • Graves disease
    • Chronic thyroiditis (Hashimoto thyroiditis) - Although the primary cause of hypothyroidism, the disease process occasionally presents initially with thyrotoxicosis
    • Subacute thyroiditis (de Quervain thyroiditis) - Diffuse, painful inflammation of the thyroid producing a transient state leakage of stored hormone
    • Postpartum thyroiditis - Presents similarly to subacute thyroiditis 2-6 months postpartum but typically painless with mild symptoms
  • Drug-induced
    • Iodine-induced - Occurs after administration of either supplemental iodine to those with prior iodine deficiency or pharmacologic doses of iodine (contrast media, medications) in those with underlying nodular goiter
    • Amiodarone - Its high iodine content is primarily responsible for producing a hyperthyroid state, though the medication may itself induce autoimmune thyroid disease.
  • Infectious
    • Suppurative thyroiditis - Often bacterial, results in a painful gland commonly in those with underlying thyroid disease or in immunocompromised individuals
    • Postviral thyroiditis
  • Idiopathic
    • Toxic multinodular goiter - The second most common cause of hyperthyroidism, characterized by functionally autonomous nodules, typically after age 50 years
  • Iatrogenic
    • Thyrotoxicosis factitia - A psychiatric condition in which high quantities of exogenous thyroid hormone are consumed
    • Surgery - Now uncommon secondary to preventative measures, manipulation of the thyroid gland during thyroidectomy historically caused a flood of hormone release, often resulting in highly toxic blood levels
  • Malignancy
    • Toxic adenoma - A single, hyperfunctioning nodule within a normally functioning thyroid gland commonly among patients in their 30s and 40s
    • Thyrotropin-producing pituitary tumors
    • Struma ovarii - Ovarian teratoma with ectopic thyroid tissue
  • Thyroid storm can be triggered by many different events, classically in patients with underlying Graves disease or toxic multinodular goiter.
    • Infection
    • Surgery
    • Cardiovascular events
    • Toxemia of pregnancy
    • Diabetic ketoacidosis, hyperosmolar coma, and insulin-induced hypoglycemia
    • Thyroidectomy
    • Discontinuation of antithyroid medication
    • Radioactive iodine
    • Vigorous palpation of the thyroid gland in hyperthyroid patients

Emergency Department Care:

  • Do not delay treatment once thyroid storm is suspected.
  • Patients with severe thyrotoxicosis must be placed on a cardiac monitor. The patient should be intubated if profoundly altered. Supplemental oxygen may be required. Aggressive fluid resuscitation may be indicated.
  • Fevers are treated with cooling measures and antipyretics. However, aspirin should be avoided to prevent decreased protein binding and subsequent increases in free T3 and T4 levels. Only in the setting of subacute thyroiditis is aspirin indicated.
  • Aggressive hydration of up to 3-5 L/d of crystalloid compensates for potentially profound GI and insensible losses.

  • Appropriate electrolyte replacement should be directed by laboratory values.
  • Atrial fibrillation due to thyroid storm may be refractory to rate control, and conversion to sinus rhythm may be impossible until after antithyroid therapy has been initiated.
  • Intravenous glucocorticoids are indicated if adrenal insufficiency is suspected. Large doses of dexamethasone (2 mg q6h) inhibit hormone production and decrease peripheral conversion from T4 to T3.
  • Antithyroid medications such as propylthiouracil (PTU) and methimazole (MMI) oppose synthesis of T4 by inhibiting the organification of tyrosine residues.
    • PTU also inhibits the conversion of T4 to active T3.
    • Clinical effects may be seen as soon as 1 hour after administration. Both agents are administered orally or via a nasogastric tube.
    • PTU and MMI inhibit the synthesis of new thyroid hormone but are ineffective in blocking the release of preformed thyroid hormone. Iodide administration serves this purpose well; however, it should be delayed until 1 hour after the loading dose of antithyroid medication to prevent the utilization of iodine in the synthesis of new thyroid hormone. Lithium may be used as an alternative in those with iodine allergy.
  • Beta-adrenergic blocking agents are the mainstays of symptomatic therapy for thyrotoxicosis. Propranolol has been used with the greatest success due to the additional benefit of inhibition of peripheral conversion of T4 to T3.

Date: 2015-01-12; view: 1039


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