Thyroid crisis, also known as thyroid storm, is a rare complication of thyrotoxicosis that results in a hypermetabolic and hyperadrenergic state. This condition requires prompt recognition and treatment because the mortality from thyroid crisis approaches 30%. Thyrotoxicosis alone will usually not progress to thyroid crisis. Thyroid crisis will typically be precipitated by some concomitant event such as infection, iodine-containing contrast agents, medications such as amiodarone, pregnancy, or surgery. Trauma is a rare precipitator of thyroid crisis. Several published studies have reported thyroid crisis resulting from blunt or penetrating neck trauma. Significant systemic trauma, such as motor vehicle accidents, has also been reported to precipitate thyroid crisis. It is very unusual for minor trauma to precipitate thyroid crisis. In the present study, we report the case of a patient who had incurred relatively minor maxillofacial trauma and developed thyroid crisis 2 weeks after the initial trauma.
Thyroid crisis, also known as thyroid storm, is a rare complication of thyrotoxicosis that results in a hypermetabolic and hyperadrenergic state. This condition requires prompt recognition and treatment because the mortality from thyroid crisis approaches 30%. Thyrotoxicosis alone will usually not progress to thyroid crisis. Thyroid crisis is typically precipitated by some concomitant event such as infection, iodine-containing contrast agents, medications such as amiodarone, pregnancy, and surgery. Trauma is a rare precipitator of thyroid crisis. Several published studies have reported thyroid crisis resulting from blunt or penetrating neck trauma. Significant systemic trauma, such as motor vehicle accidents, has also been reported to precipitate thyroid crisis. It is very unusual for minor trauma to precipitate thyroid crisis. In the present study, we report the case of a patient who had incurred relatively minor maxillofacial trauma and developed thyroid crisis 2 weeks after the initial trauma.
A 46-year-old male patient presented to the emergency department at Woodhull Medical Center (Brooklyn, NY) after an interpersonal altercation in which blunt trauma had been sustained to the right side of his face. The patient's chief complaint was right facial pain, right facial numbness, and right facial swelling. His medical history was significant for uncontrolled hyperthyroidism, polysubstance abuse (marijuana, cocaine, and other opioid use), hypertension, and mild intermittent asthma. The only reported home medication was methimazole (Tapazole, King Pharmaceuticals, Pfizer, Bristol, TN; Northyx, Cedar Pharmaceuticals, Shreveport, LA) 10 mg. The baseline vital signs in the emergency department were as follows: blood pressure, 140/90 mm Hg, pulse 80 beats/minute, respirations 15 breaths/minute, and temperature 98.5°F. The head and neck physical examination findings were significant for right facial swelling, tenderness over the zygoma, trismus (20 mm maximal interincisal opening), and hypoesthesia of the right infraorbital nerve. The neck examination findings were negative for signs of hyperthyroidism such as goiter. Mild right exophthalmos was present, without any disruption of the vision ( Fig 1 ). A facial bone noncontrast-enhanced computed tomography scan confirmed the presence of a depressed right zygomaticomaxillary complex fracture ( Figs 2-4 ). An ophthalmology consultation was obtained to evaluate the extent of the ocular injury.
The patient was evaluated by the ophthalmology service. Tonometry was performed and revealed an intraocular pressure of 17 mm Hg in the right eye and 15 mm Hg in the left eye (range 12 to 22 mm Hg). Exophthalmometry was performed and revealed 22 mm in the right eye and 17 mm in the left eye. The extraocular movements were not restricted, albeit he experienced pain with an upward gaze. The ophthalmology service concluded that he had possible right inferior rectus muscle inflammation, proptosis of the right eye likely due to retrobulbar inflammation, and no optic nerve or retinal trauma. No ocular contraindications were found against surgical repair of the fractures.
The patient was under police custody at the time and was too edematous from his acute injures for the extent of the deformity from the trauma to be accurately assessed. The patient was discharged with naproxen 500 mg twice daily to allow for reduction of the swelling and advised to return for follow-up in 10 days for, if necessary, surgical repair of the fractures.
The patient returned 2 weeks later to the outpatient oral and maxillofacial surgery clinic complaining of unresolved facial asymmetry, persistent trismus, and moderate pain in his right face. The clinical examination revealed right infraorbital nerve hypoesthesia, malar depression, and trismus (maximal interincisal opening 30 mm). The findings from the remainder of the head, neck, and systemic examination were unremarkable. The patient was admitted to the oral and maxillofacial surgery service for preoperative optimization and open reduction internal fixation of the right zygomaticomaxillary complex fractures ( Fig 1 ).
The preoperative workup included laboratory studies for the complete blood count, metabolic panels, prothrombin time, activated partial thromboplastin time, and international normalized ratio, with all results within normal limits. A thyroid panel was also performed, with abnormal findings. The thyroid-stimulating hormone level (TSH) was 0.008 MIU/mL (normal range 0.5 to 4.8), thyroxine (T4) level was more than 30 μg/dL (normal range 4.5 to 11), and total triiodothyronine (T3) was 338.4 ng/dL (normal range 60 to 180). Internal medicine and endocrinology consultations were requested.
In the evening of hospital day 1, the patient developed signs and symptoms suggestive of decompensating thyrotoxicosis. The patient complained of nausea and subsequently had 2 episodes of bilious vomitus followed by an episode of hemorrhagic vomitus within 1 hour. After the emesis, the patient was noted to be lethargic, diaphoretic, and tachycardic. The patient's vital signs were as follows: blood pressure of 167/98 mm Hg, respiratory rate of 22 breaths/minute, heart rate of 109 beats/minute, and temperature of 99.5°F. On chest auscultation, the presence of rales was suggestive of pulmonary edema or congestive heart failure. Thyrotoxicosis with impending thyroid crisis was diagnosed, with a Burch and Wartofsky score of 80 ( Table 1 ). The patient was transferred to the medical intensive care unit (MICU), where his condition continued to deteriorate. The tachycardia and lethargy worsened (pulse 124 beats/minute, blood pressure 154/95 mm Hg, and temperature 101.3°F), and acute respiratory distress ensued (34 respirations/minute, oxygen saturation 90%). He was subsequently intubated and sedated.
|Body System Manifestations||Score||Our Patient's Score|
|Congestive heart failure|
|Mild (pedal edema)||5|
|Moderate (bilateral rales)||10||X|
|Severe (pulmonary edema)||15|
|Gastric and hepatic|
|Moderate (nausea, vomiting, diarrhea, gastric pain)||10||X|
|Severe (unexplained jaundice)||20|
|Central nervous system|
|Moderate (delirium, psychosis, extreme lethargy)||20||X|
|Severe (seizure, coma)||30|
|Thyroid storm highly likely||>45||X|
|Thyroid storm looming||25-44|
|Thyroid storm unlikely||<25|
The elements of thyroid storm were managed supportively and individually. Propranolol (60 mg) was administered for the tachycardia. Propylthiouracil (300 mg) and hydrocortisone (50 mg) were administered to reduce the circulating pool of thyroid hormone. On MICU day 2, transthoracic echocardiography revealed severe left ventricular hypertrophy and pulmonary hypertension. He was appropriately treated with diuretics and supportive systemic care, and his clinical status improved. On MICU day 5, he was successfully extubated. He returned to the medical floor and was subsequently discharged home. Surgical intervention was postponed indefinitely because the potential risks outweighed the benefits.
Review of Thyroid Crisis
Thyroid disorders can be divided into hyperthyroidism and hypothyroidism. Our report focused on hyperthyroidism. “Thyrotoxicosis” and “hyperthyroidism” are 2 terms often used interchangeably and erroneously. To define these terms accurately, “thyrotoxicosis” is a state of excessive circulating thyroid hormone and “hyperthyroidism” is a disorder in which the thyroid gland produces excessive amounts of thyroid hormone. Thus, hyperthyroidism is one of several possible causes of thyrotoxicosis.
Hyperthyroidism occurs more frequently than hypothyroidism, with a 4:1 ratio. Women are 3 times more likely than men to develop hypothyroidism and 10 times more likely to develop hyperthyroidism. As such, thyrotoxicosis and thyroid crisis both occur more frequently in women. Up to 10% of patients hospitalized for thyrotoxicosis could develop thyroid crisis. As previously mentioned, patients in thyroid crisis are critically ill, with mortality rates approaching 30%. Even when acute recognition and aggressive management is performed in a timely manner, the prognosis for these patients has been guarded. The causes of death have included congestive heart failure, systemic organ failure, sepsis, and disseminated intravascular coagulation.
The true incidence of thyroid crisis has been poorly defined in published studies. The incidence of thyroid crisis in hospitalized thyrotoxic patients has been previously reported as 1 to 2%. A recent Japanese study sought to clarify the epidemiology of thyroid crisis during a 5-year period. Akamizu et al reported a thyroid crisis incidence of 0.22% (0.2 person/100,000 Japanese population annually). However, they had not used the Burch and Wartofsky scoring system (discussed in subsequent paragraphs). Instead, they combined a diagnosis of thyrotoxicosis with specific elements of thyroid crisis, such as hepatic manifestations or tachycardia. Therefore, the actual incidence of thyroid crisis might be even lower than the 0.22% reported in their study.
The thyroid gland is an endocrine gland responsible for synthesis of hormones regulating growth, development, and metabolism. The thyroid hormones are T3 and T4. Both T3 and T4 are metabolically active; however, T3 is far more potent. The production of thyroid hormone is regulated by TSH released from the anterior pituitary gland. TSH production, in turn, is regulated by thyrotropin-releasing hormone, which is released by the hypothalamus. The 3 glands involved in thyroid hormone synthesis and release belong to an autoregulating negative feedback loop referred to as the hypothalamic–pituitary–thyroid axis. Any disruption in this feedback loop will result in loss of regulation of thyroid hormone synthesis and release.
Central to the pathophysiology of hyperthyroidism is the overabundance of the circulating pool of T3 and T4. Although a variety of conditions can manifest from either primary causes (an intrinsic thyroid disorder) or secondary causes (a thyroid disorder caused by pathologic features in a different endocrine gland, such as the hypothalamus or pituitary gland), Grave's disease has been the initiating factor in approximately 60 to 80% of cases.
In Grave's disease, autoantibodies continually mimic the function of TSH at the thyrotropin receptor on the thyroid gland. The resulting unregulated release of thyroid hormones into the systemic circulation has been termed “thyrotoxicosis” and is responsible for the clinical manifestations of the disease. Thyroid crisis is the decompensated form of thyrotoxicosis.
After Grave's disease, the next most common cause of hyperthyroidism is toxic multinodular goiter (TMNG). TMNG is a condition characterized by the presence of multiple foci of hyperfunctioning thyroid tissue. Often the outcome of an iodine-deficient diet in developing countries, TMNG produces T3 and T4 independent of stimulation from TSH. A toxic adenoma of the thyroid is the single-nodule variant of TMNG and is slightly less common.
Secondarily, hyperthyroidism can be caused by adenomas of the anterior pituitary, where TSH is normally secreted. Anterior pituitary adenomas will continue to function without regard to the negative feedback of high levels of circulating thyroid hormone, disrupting the homeostasis maintained by the hypothalamic–pituitary–thyroid axis.
Many patients who develop thyroid crisis will have undiagnosed hyperthyroidism ; thus, prevention will often be impossible for this cohort. A comprehensive history and physical examination might identify patients with undiagnosed hyperthyroidism and prevent the development of thyroid crisis. One of the clinical signs of hyperthyroidism is the presence of a goiter—a diffuse enlargement of the thyroid gland—alerting the physician to a possible problem. Additional signs of hyperthyroidism include dermopathy, acropachy, hypertension with widened pulse pressures, atrial fibrillation, ileus, exophthalmos, Duroziez's sign of the ulnar artery, and hyperventilation. On a review of symptoms, patients with hyperthyroidism might complain of heat intolerance, feeling warm, decreased weight, increased appetite, fatigue, and moist, warm skin.