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Prompt recognition of thyrotoxicosis and aggressive treatment of the associated manifestations are essential. Critical care nurses who have an understanding of this life-threatening condition can quickly intervene to improve patients’ outcomes. In this article, I describe thyroid physiology, discuss the clinical manifestations and treatment of acute thyrotoxicosis, and present a case study of a patient with thyrotoxicosis who was admitted to the critical care unit because of acute congestive heart failure.
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THYROID PHYSIOLOGY |
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).3 The lobes are joined by a small band of tissue called the isthmus. Normally not visible on inspection, the thyroid gland can be palpated during swallowing when it is upwardly displaced. Thyroid tissue is highly vascular and is composed of follicular cells that synthesize and secrete 2 major hormones: thyroxine (T4) and triiodothyronine (T3). These hormones are sometimes collectively referred to as thyroid hormone.2,4 T3 and T4 affect all cells within the body except those in the brain, spleen, testes, and uterus.
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). The initiating hormone, thyrotropin-releasing hormone, is synthesized and stored in the hypothalamus. Thyrotropin-releasing hormone circulates to the anterior part of the pituitary gland, where it stimulates the release of thyroid-stimulating hormone (TSH). TSH binds to receptor sites located on the thyroid gland, which produces, secretes, and stores T3 and T4. Stimulation by TSH results in an immediate release of stored thyroid hormones into the circulation. Serum levels of T3 and T4 increase as T3 binds to cell receptors. Concurrent effects include an increase in the uptake and oxidation of iodine, an increase in the synthesis of T3 and T4, and an increase in the synthesis and secretion of prostaglandins.2,4,5
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Mechanism of Action
The thyroid gland normally produces 90% T4 and 10% T3. In the body tissues, T4 is converted to T3, which has the greatest systemic metabolic effects (Table 1). Thyroid hormones are involved in glucose oxidation, which increases metabolic rate, consumption of oxygen by tissues, and production of body heat. Upon binding to its receptor, T3 initiates a series of biochemical and physiological responses that affect all systems, including the cardiovascular, respiratory, gastrointestinal, and neuromuscular.2,5
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THYROTOXICOSIS |
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Although thyroid storm is rare, early diagnosis and vigorous therapy can prevent a fatal outcome. Mortality rates of hospitalized patients in thyroid storm are 20% to 50%.1,7,8 Critical care nurses must recognize the hypermetabolic state and ensure that aggressive and supportive treatment is not delayed.
Etiology
Thyrotoxicosis may be due to true hyperthyroidism, in which synthesis and release of hormones from the thyroid gland are increased. Graves’ disease is the most common cause of true hyperthyroidism, accounting for 60% to 90% of all cases. Other causes include a hyperfunctioning thyroid nodule, excessive ingestion of exogenous thyroid hormones, pituitary tumors, pituitary gland abnormalities, and thyroiditis.8–11 A thyrotoxic crisis or thyroid storm may develop precipitously in patients with hyperthyroidism who have had surgery, have experienced trauma, have an infection, are in the postpartum period, or have had antithyroid medication withdrawn.1,2,7
The precipitating event should be determined after the patient’s condition has been stabilized and the hypermetabolic state has been arrested. Critical care nurses must use their assessment skills and clinical judgment to ensure that treatment is not postponed while the precipitating event is determined. Moreover, treatment should not be delayed while waiting for the results of thyroid function tests.
Clinical Manifestations
Patients with thyrotoxicosis have a myriad of clinical features related to increased cellular functioning. Easily recognized characteristics include marked weight loss (>15% of body mass index; index calculated as weight in kilograms divided by the square of height in meters), anxious demeanor, excitable state, fixed stare, and fine tremors of the hands and tongue.1,8–11 Exophthalmos and goiter are commonly associated with hyperthyroidism but are not always present in acute thyrotoxicosis.
Understanding major organ responses to excessive circulating levels of thyroid hormones and recognizing a decompensating hypermetabolic state will help in developing an appropriate plan of care. Aggressive management of acute thyrotoxicosis, including continuous monitoring, can prevent deterioration to thyroid storm.
Cardiovascular Manifestations.
Cardiovascular manifestations of thyrotoxicosis are due to the direct effect of thyroxine on the myocardium, alterations in systemic vascular resistance, and increased sensitivity to endogenous catecholamines.1,5,7–11 Thyroid hormones increase calcium and sodium transport in cardiac muscle, causing a lowered atrial excitation threshold, an increase in sinoatrial node firing, and a shortened refractory period. These changes are compounded by a decrease in systemic vascular resistance and enhanced sympathetic activity.1,10
Tachycardia greater than 140 beats per minute is a common finding, as is atrial fibrillation and various degrees of ventricular dysfunction. The hemodynamic profile in acute thyrotoxicosis includes increased stroke volume, increased oxygen consumption, increased left ventricular stroke work index, and a reduction in peripheral vascular resistance. A patient with failing compensatory mechanisms or heart disease is at risk for high-output heart failure, the clinical hallmark of thyrocardiac disease.5,10
In high-output heart failure, metabolic acidosis is imminent because of the body’s demand for oxygen, so cardiac output is greatly increased. However, despite the elevated cardiac output, the body’s metabolic needs are still not met. Patients in high-output heart failure often have a widened pulse pressure, with elevated systolic pressure. If high-output heart failure is allowed to progress untreated, moderate to severe pulmonary edema develops, indicating marked cardiac and respiratory decompensation.2
Respiratory Manifestations.
In hypermetabolic states, the respiratory system is affected because of the need for greater oxygen supply and utilization. As a result, an increase in carbon dioxide production also occurs. Tachypnea and dyspnea on exertion are common abnormalities that occur because of a decrease in cardiac contractile reserve in patients with thyrotoxicosis. Weakness of the respiratory and skeletal muscles also occurs and places patients at risk for respiratory failure due to muscle fatigue. Consequently, critical care nurses must be diligent in assessing patients for indications of a decompensating respiratory state. Other abnormalities that contribute to respiratory compromise include decreased lung compliance, an engorged pulmonary capillary bed, and high-output ventricular failure.2
Patients in high-output heart failure are also at risk for acute respiratory failure because of the accumulation of fluid in the pulmonary capillary beds and alveoli. Pulmonary congestion further decreases gas exchange and impairs ventricular functioning.8,10 Acute pulmonary edema, a common sequela of untreated heart failure, must be recognized early and managed aggressively.
Gastrointestinal Manifestations.
Gastrointestinal manifestations in thyrotoxicosis are due to accelerated intestinal transport and decreased absorption. Nausea, vomiting, and diarrhea are typical findings and may mimic those of an acute abdominal emergency. Abdominal pain may be the chief symptom in patients with acute thyrotoxicosis. A history of weight loss despite hyperphagia is common because of the need for increased energy requirements. In addition, elevations in transaminase levels and hepatotoxic effects may result in clinical jaundice.1,2,10,11
Neuromuscular Manifestations.
Alterations in the levels of thyroid hormones have a profound effect on the neuromuscular system. Sympathomimetic effects result in changes in mental status that range from rapid mentation, agitation, restlessness, and confusion to delirium, obtundation, and coma if the effects are allowed to progress untreated. Electroencephalograms reveal an increase in alpha-wave activity that can be attributed to increased metabolic activity.2 Hyperreactivity may occur in response to physical and emotional stimuli. A fine motor tremor is present when the hands are outstretched, and patients have fatigue and muscle weakness. Deep tendon reflexes in patients with thyrotoxicosis are brisk, with a shortened relaxation phase.1,7
Myopathy occurs in more than 50% of patients with thyrotoxicosis and most commonly affects the proximal muscle groups of the shoulders and pelvic girdle. Shoulder weakness, difficulty in going from a sitting to a standing position, and generalized weakness and fatigability are common.2
Integumentary Manifestations.
The integument plays a fundamental role in thermoregulation. The skin contains only 
-adrenergic receptors, which are regulated by the sympathetic nervous system. Heat loss is regulated by varying blood flow through the skin in conjunction with the evaporative loss of heat through sweating. In thyrotoxicosis, rapid metabolism causes increased dermal blood flow.2,4
Patients with thyrotoxicosis are heat intolerant and have warm moist skin that is silky and smooth to touch. Increased diaphoresis and hot flushes are common because of the increased blood flow associated with hyper-metabolism. Alopecia and nail friability with separation of the nail from the proximal part of the nail bed are also common findings.1,10
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TREATMENT |
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Specific therapy must be aimed at supporting vital functions, blocking hormone synthesis and release, inhibiting the peripheral conversion of T4 to T3, and ameliorating the effects of the hypermetabolic state. Supportive therapy includes ensuring adequate ventilation and oxygenation, suppressing the heightened response to catecholamines, monitoring for and controlling cardiac dysrhythmias, and administering intravenous fluids to replace sensible and insensible losses of fluid. If vomiting and diarrhea occur, careful attention to electrolyte replacement is necessary. Intravenous fluids should include glucose if hypoglycemia occurs and vitamins, because patients are catabolic. Hyperglycemia may also occur because of the stimulatory effect of T3 on gluconeogensis and glycogenolysis.2,6 Therefore, glucose monitoring should be included in the plan of care.
Medications
Critical care nurses must be knowledgeable about the medications that are necessary to meet the goals of therapy for thyrotoxicosis. This knowledge includes understanding how the various drugs work, how they are metabolized, the individual dosage parameters, precautions for use, and the nursing implications (Table 3).
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Glucocorticoids such as dexamethasone may be given when a patient is thought to have a relative deficiency of steroids. An increased stress response, which often occurs in acute thyrotoxicosis, depletes endogenous cortisol stores even in patients without adrenal insufficiency. Glucocorticoids also inhibit conversion of T4 to T3 in peripheral tissues and have an additive effect when given with propylthiouracil.1,7–9
Blockade of Thyroid Hormones.
Because the amount of hormones stored in the thyroid gland is generally great enough to last several weeks, release of the hormones must be suppressed by administering potassium iodide. Iodide preparations are rapid acting and have a short duration. They maintain and increase the levels of protein-bound thyroid hormones, thereby decreasing the levels of the free, active forms. Iodide preparations should not be given sooner than 1 hour after the administration of antithyroid drugs because if given too soon, the iodide may be used by the body to synthesize more T4, thus paradoxically increasing the toxic state.1,7,9–11 Usually, Lugol solution or a saturated solution of potassium iodide is given orally. Ipodate (Oragrafin) and iopanoic acid (Telepaque), radiographic contrast materials, have also been used to block release of thyroid hormones. Lithium carbonate, a more toxic inhibitor of thyroid hormones has been used in patients who are allergic to iodide. Lithium carbonate must also be given orally or via a gastric tube.
Antagonism of Peripheral Effects of Thyroid Hormones.
Although plasma catecholamine levels are normal in thyrotoxicosis, increased adrenergic activity is a prominent feature, and patients have a heightened sympathetic response.7–9,11 As a result, patients are anxious, tachycardic, and diaphoretic and have tremors. Patients may also report heat intolerance and have tachypnea. Critical care nurses must do frequent assessments and be alert for alterations in cardiac rhythm and for indications of respiratory decompensation due to muscle fatigue and acid-base imbalance.
ß-Adrenergic blockade is the treatment of choice for reducing adrenergic-like signs and symptoms in patients with thyrotoxicosis. Propanolol is the drug of choice to counteract the peripheral effects of increased levels of thyroid hormones because it antagonizes the effects of catecholamines that act on ß-adrenergic receptors. Propanolol is most effective in reducing the cardiovascular manifestations of thyrotoxicosis. Propanolol and similar ß-adrenergic blockers (ie, metoprolol and acebutolol) are metabolized by the liver. Because hepatic blood flow is increased in thyrotoxicosis, higher doses may be required to achieve desired results. Propanolol should not be used in patients with bronchospastic pulmonary disease and/or a history of congestive heart failure.7–9 Agents that deplete catecholamines such as reserpine have been used when propanolol alone is not effective. Guanethidine has also been used; however, its delayed onset of action makes it less useful than other medications in the critical care setting.1,7
Treatment of High-Output Heart Failure.
Acute high-output heart failure is primarily due to impaired myocardial contractility and is aggravated by atrial dysrhythmias. Conventional measures to treat heart failure include use of antiarrhythmic agents, digoxin, and diuretics.7,8 Definitive therapy for heart failure induced by thyrotoxicosis is reestablishment of euthyroidism or a normal thyroid state. Because the metabolism and clearance of medications can be markedly increased during the hypermetabolic state, increased dosages may be necessary to achieve desired results.
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DIAGNOSTIC STUDIES |
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Serum levels of thyroid hormones are elevated in most cases of thyrotoxicosis.5,9 Radioimmunoassay techniques allow accurate measurement of plasma levels of circulating hormones. However, no one single laboratory test is 100% accurate for diagnosing all types of thyroid disease. With a combination of 2 or more tests, even the slightest abnormality in thyroid function can usually be detected.
For diagnosis of true hyperthyroidism, the American Thyroid Association ad hoc committee on thyroid treatment guidelines recommends measurement of levels of free T4, which are elevated in hyperthyroidism, and TSH levels, which are suppressed in hyperthyroidism.9 Pituitary secretion of TSH is determined by plasma levels of thyroid hormones; elevated levels cause the pituitary gland to cease production of TSH. Therefore, when T4 levels are elevated in a patient with hyperthyroidism and the TSH level is not suppressed, pituitary involvement must be considered. The most common reason for these findings is a pituitary adenoma.
Once hyperthyroidism is confirmed, additional tests may be needed, depending on the clinical situation. These may include measurement of plasma levels of T3 and thyroid autoantibodies and a radioactive iodine uptake test.9,10 Because the thyroid gland normally takes up iodine to make thyroid hormones, the test is a useful measurement to determine how much iodine is captured by the gland. The test is often essential for treatment decisions once a patient’s condition is stabilized.
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CONCLUSIONS |
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