Mrs. R was a 71‐year‐old female admitted to the neurological intensive care unit (NICU) with “the worst headache of her life.” The patient was found to have a left anterior communicating artery aneurysm, for which she was immediately taken to the operating room (OR), where she underwent a craniotomy for clipping of the ruptured aneurysm. Afterward, her neurologic exam waxed and waned from lethargic to obtunded. When lethargic, she was able to follow commands; when obtunded, she was able to move all her extremities in response to pain with nonfocal weakness. Besides her level of consciousness, the only other remarkable aspect of her exam was preexisting exophthalmos, which was due to her known history of hyperthyroidism.
The postoperative course was complicated by a series of events. First the patient developed a non‐ST elevated myocardial infarction (MI) after the surgical procedure. After a week and with satisfactory resolution of the MI, the patient required another surgery for the placement of a ventriculo‐peritoneal shunt (VPS). Mrs. R was being followed by physical therapy staff members for her deconditioned status and by case management staff members for rehabilitation placement. However, during the course of that next week, Mrs. R developed a deep vein thrombosis (DVT) in her left lower extremity, leading to pulmonary emboli. She was not given anticoagulants at that time because of her recent craniotomy and VPS placement. An inferior vena cava filter was placed to minimize risk of further pulmonary embolism.
Over the course of several days after these incidents, Mrs. R's appetite diminished, as did her neurological status. She was lethargic; she had temperatures ranging from 100 °F to 102 °F; and she was tachycardic, with a rate in the low 100s and bursts up to around 150 beats per minute. Her medications included nebulizer treatments, subcutaneous heparin, nimodipine (Nimotop), phenytoin (Dilantin), lansoprazole (Prevacid), metoprolol (Toprol XL), the antithyroid medication methimazole (Tapazole), and labetalol and acetaminophen as needed. Mrs. R was treated with antibiotics and given fluid boluses for her fevers. She was also given labetalol to control the episodes of supraventricular tachycardia (SVT). The patient continued to be treated for possible infection. Despite these efforts, her condition did not improve.
Although fevers and SVT occur frequently in the neurologically impaired patient, they are often a symptom of something other than neurologic causes. A systematic review of the clinical picture and medication list can help determine the cause. First, why did she have a fever? Several aspects of her condition made her predisposed to fevers, including her hemorrhage and DVT, as well as urosepsis from her indwelling urinary catheter. She was also at high risk for aspiration pneumonia. All were reasonable explanations for her fevers.
Next, why did she persist in having episodes of SVT? The day‐shift nurse also noted a murmur not previously documented in the chart. Her recent MI could have contributed to conduction problems, as could dehydration or sepsis. All of these problems were reasonable contributing factors.
What else could contribute to her picture? Mrs. R, with her bulging eyes, displayed symptoms of a marked hyperthyroidism, evidenced by her very low thyroid stimulating hormone (TSH) level on admission. Her antithyroid medication, methimazole, was withheld multiple times because she had trouble swallowing in her lethargic state. The staff also noted that the medication was to be given with meals. A nasogastric tube was not placed for several days, by the wishes of her family, who hoped she would not need it. Since Mrs. R did not eat much, and because the staff was unfamiliar with the importance of this medication, it was given infrequently. Placement of a percutaneous endoscopic gastrotomy (PEG) was delayed because of time constraints in the OR. It was hoped that Mrs. R would recover enough to make the PEG unnecessary; however, it was finally placed. Thus, for almost three weeks, the patient received her thyroid medication only sporadically. After being hospitalized for a month, Mrs. R went into a thyroid storm precipitated by her multiple medical comorbidities.
The thyroid, an endocrine gland found in the anterior neck, is normally not palpable. It regulates the rate of metabolism, growth, and function of other systems through a negative feedback system monitored by levels of thyroxine (T4), triiodothyronine (T3), and calcitonin (Bullock & Henze, 1999). Thyroxine is the predominant hormone, which converts to triiodothyronine in the peripheral system. Calcitonin is essential for decreasing calcium levels in the blood when there is too much circulating calcium (Bullock & Henze). The hypothalamus releases thyrotropin releasing hormone (TRH) to stimulate the pituitary to release thyroid stimulating hormone (TSH). Then, TSH stimulates the thyroid to release thyroxine to regulate the function of the cells in the body (Bullock & Henze). If any one of these mechanisms breaks down, the entire system malfunctions. Thyroxine is critical to metabolism and growth; children with thyroid dysfunction will not grow well or will have impaired brain development. In hyperthyroidism, TSH deficiency can be due to several causes. Recall the complex feedback mechanism: If the hypothalamus is damaged, it may in turn disrupt the pathway of TRH secretion from the pituitary. This disruption will directly affect TSH, which is under the influence of TRH. More commonly, TSH production does not stop, even though its levels are consistently low. The thyroid continues to produce thyroxine because the negative feedback mechanism no longer processes the signal to stop. Disturbances of normal homeostatic mechanisms can happen at any level: in the thyroid, the pituitary, or the peripheral tissues. The excessive release of thyroxine sustains a hypermetabolic state, thereby increasing the heart rate and temperature. Patients tend to sweat profusely, lose weight, and become fatigued from the hypermetabolic state (Bullock & Henze).
The signs and symptoms of hyperthyroidism affect the entire body (Becker et al., 1995). Patients may suffer nervousness, irritability, and agitation. They may experience heat intolerance, sweat profusely, or lose hair. Cardiovascular symptoms frequently seen are tachycardia, palpitations, angina, and a new‐onset heart murmur called the Means‐Lerman “scratch” murmur—a systolic scratchy sound, thought to result from rubbing of the pericardium against the pleura. There may be diarrhea, weight loss, hyperphagia, tongue tremors, and increased thirst. A hand tremor may also be seen, in addition to muscle atrophy, weakness, or paralysis. Neurological symptoms include fever, delirium, stupor, coma, and syncope. Long‐standing hyperthyroidism can also cause osteoporosis.
Common causes of hyperthyroidism are toxic diffuse goiter (Graves disease), toxic adenoma, toxic multinodular goiter, and painful subacute thyroiditis. The most common cause is Graves disease (Franklyn, 1994), an autoimmune illness that creates autoimmune antibodies that directly attack the thyroid, activating the synthesis of thyroid hormone (Lee, 2005). The TSH level is low because the body recognizes the state of impairment but is unable to correct it.
The eyes may also start bulging (a condition called exophthalmos) as a result of an inflammatory process of tissue damage that is mediated by the response of B and T lymphocytes to autoantibodies produced in Graves disease (Yeung, 2005). Depending on the cause of hyperthyroidism, exophthalmos may or may not be present.
Left untreated, thyroid storm is an acute, lifethreatening complication of thyrotoxicosis or poorly managed hyperthyroidism. In its full state, mortality rates of thyroid storm are around 90% (Singhal & Campbell, 2004). Early recognition is essential. Common clinical presentation includes fever, tachycardia, neurologic abnormalities, and hypertension, which is followed by hypotension and shock, two late signs that are usually fatal. Diagnosis is primarily clinical, so it is imperative that hyperthyroidism be carefully monitored. Thyroid storm is a decompensated state of severe hypermetabolism (Singhal & Campbell). Fever changes to hyperpyrexia in thyroid storm, and body temperature can reach 109 °F. Mild to moderate sinus tachycardia can intensify quickly to accelerated tachycardia, hypertension, high‐output heart failure, and arrhythmias. Irritability and restlessness can cause severe agitation, delirium, seizures, and coma. Extremely high metabolism also increases oxygen and energy consumption (Jao, Chen, Lee, & Tai, 2004). Factors known to precipitate thyroid storm are infection, surgery, trauma, radioactive iodine treatment in patients with toxic nodular goiters, pregnancy, anticholinergic and adrenergic drugs, thyroid hormone ingestion, and diabetic ketoacidosis (American Association of Clinical Endocrinologists [AACE], 2002).
Thyroid storm is a clinical diagnosis of exclusion; thus, lab tests will not verify that a person has this condition. If a person has a known history of hyperthyroidism, then TSH, free T4, T3, and a complete blood count should be evaluated. Like the blood count, which may show a mild leukocytosis, liver function tests are also followed and may show nonspecific abnormalities (AACE, 2002). A chest radiograph may show cardiac enlargement due to congestive heart failure, and an electrocardiogram (ECG) may reveal atrial fibrillation or other arrhythmias (AACE, 2002).
Treatment of thyroid storm focuses on symptom control. The basics must be considered: hyperthermia is controlled with ice packs, cooling blankets, and acetaminophen (Franklyn, 1994). Beta‐adrenergic blockers are used to minimize sympathomimetic symptoms and block the adrenergic sites, which are thought to be stimulated by hyperactive catecholamines released by the thyroid hormones (Osman, Gammage, Sheppard, & Franklyn, 2002). These drugs are the mainstay of therapy to control the autonomic effects of thyroid hormone. They also block peripheral conversion of T4 to T3, which is an important component of managing thyroid storm. Giving antithyroid medications blocks production of thyroid hormones and further reduces the peripheral conversion of T4 to T3 (Singhal & Campbell, 2004).
A second line of treatment is the use of the antithyroid medications propylthiouracil (PTU) and methimazole. Propylthiouracil inhibits synthesis of thyroid hormone by decreasing iodine production (which produces T4) and also inhibits peripheral conversion of T4 to T3. Methimazole, another antithyroid medication, works much like PTU, except it does not inhibit peripheral conversion of T4 to T3; however, it is about 10 times more potent. Fewer side effects are associated with methimazole, making it preferable to PTU. Neither drug is available in anything other than oral form (Singhal & Campbell, 2004). Important points to remember with these two drugs are (1) the concurrent use of potassium iodide may cause hypothyroidism, and (2) if either is used with anticoagulation, a bleeding diathesis may result.
These antithyroid medications may be complemented by glucocorticoid steroids, which assist in preventing conversion of T4 to T3. They have been found to significantly reduce mortality rates when used in thyroid storm in conjunction with antithyroid medications (Singhal & Campbell, 2004).
Soon after the nurse noted Mrs. R's “scratch” murmur, the medical team was consulted to evaluate her. After reconstructing the history of the patient's stay in the hospital and the discovery of the TSH levels, the team hypothesized that the clinical picture could be consistent with thyroid storm. Endocrinology staff were immediately consulted. When the endocrinology team came to assess the patient, they concurred with the clinical diagnosis of thyroid storm. Mrs. R was treated with intravenous lopressor (7.5 mg every 6 hr around the clock) and high‐dose dexamethasone (20 mg every 12 hr). Her methimazole was increased to 10 mg three times a day. The nurses were educated on the importance of this drug in preventing thyrotoxicosis. The patient was then transferred to the medicine service for further management.
Mrs R was successfully treated for thyroid storm on the medicine service and returned to the floor, only to suffer from a mucous plug that caused her to stop breathing. She was found unresponsive and pulseless. She was successfully resuscitated and transferred to the medical intensive care unit. A little over 2 weeks later she finally transferred back to the floor. The dexamethasone was discontinued, and the lopressor was switched to the oral equivalent and regulated at 100 mg twice a day. After spending almost 2 months in the hospital, Mrs. R, completely exhausted but alert and oriented to her surroundings, was discharged to a rehabilitation unit.
Thyroid storm is a potentially life‐threatening complication of hyperthyroidism. Astute nursing care is the first line of defense in preventing the devastating results of an uncontrolled storm cascade. Recognition and prevention are the keys to managing thyroid storm. Being familiar with the signs and symptoms of clinical presentation are essential, especially in the neurologically impaired patient, whose symptoms can easily be masked by other conditions and whose subjective complaints can be distorted by an impaired level of consciousness.