Thyroid Crisis in the Maxillofacial Trauma Patient



Thyroid Crisis in the Maxillofacial Trauma Patient




Journal of Oral and Maxillofacial Surgery, 2014-11-01, Volume 72, Issue 11, Pages 2148.e1-2148.e7, Copyright © 2014 American Association of Oral and Maxillofacial Surgeons


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.


Case Report

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.

Computed tomography scan, axial cut, bony window, showing right globe exophthalmos ( asterisk ).
Figure 1
Computed tomography scan, axial cut, bony window, showing right globe exophthalmos (
asterisk ).

Computed tomography scan, axial cut, bony window, showing a fracture to the right zygomatic arch ( arrow ) and an air fluid level in the right maxillary sinus ( asterisk ).
Figure 2
Computed tomography scan, axial cut, bony window, showing a fracture to the right zygomatic arch (
arrow ) and an air fluid level in the right maxillary sinus (
asterisk ).

Computed tomography scan, axial cut, bony window, showing displacement of the zygomaticomaxillary complex into the right maxillary sinus ( arrow ).
Figure 3
Computed tomography scan, axial cut, bony window, showing displacement of the zygomaticomaxillary complex into the right maxillary sinus (
arrow ).

Computed tomography scan, coronal cut, bony window, showing lateral rotation of the right zygomaticomaxillary complex ( arrow ).
Figure 4
Computed tomography scan, coronal cut, bony window, showing lateral rotation of the right zygomaticomaxillary complex (
arrow ).

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.

Table 1
Burch and Wartofsky System for Stratifying Patients in Thyroid Crisis
Adapted from Burch and Wartofsky.
Body System Manifestations Score Our Patient's Score
Thermoregulatory (°C)
37.2-37.7 5
37.8-38.2 10
38.3-38.8 15 X
38.9-39.9 20
39.4-39.9 25
>40 30
Tachycardia (beats/minute)
99-109 5
110-119 10
120-129 15 X
130-139 20
>140 25
Congestive heart failure
None 0
Mild (pedal edema) 5
Moderate (bilateral rales) 10 X
Severe (pulmonary edema) 15
Atrial fibrillation
None 0 X
Present 10
Precipitant present
None 0
Present 10 X
Gastric and hepatic
None 0
Moderate (nausea, vomiting, diarrhea, gastric pain) 10 X
Severe (unexplained jaundice) 20
Central nervous system
None 0
Mild (agitation) 10
Moderate (delirium, psychosis, extreme lethargy) 20 X
Severe (seizure, coma) 30
Interpretation
Thyroid storm highly likely >45 X
Thyroid storm looming 25-44
Thyroid storm unlikely <25
Patient total 80

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


Epidemiology

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.


Pathophysiology

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.


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Thyroid Crisis in the Maxillofacial Trauma Patient Robert J. Weinstock DDS , Tashorn Lewis DDS , Jared Miller DDS and Earl I. Clarkson DDS Journal of Oral and Maxillofacial Surgery, 2014-11-01, Volume 72, Issue 11, Pages 2148.e1-2148.e7, Copyright © 2014 American Association of Oral and Maxillofacial Surgeons 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. Case Report 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. Figure 1 Computed tomography scan, axial cut, bony window, showing right globe exophthalmos ( asterisk ). Figure 2 Computed tomography scan, axial cut, bony window, showing a fracture to the right zygomatic arch ( arrow ) and an air fluid level in the right maxillary sinus ( asterisk ). Figure 3 Computed tomography scan, axial cut, bony window, showing displacement of the zygomaticomaxillary complex into the right maxillary sinus ( arrow ). Figure 4 Computed tomography scan, coronal cut, bony window, showing lateral rotation of the right zygomaticomaxillary complex ( arrow ). 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. Table 1 Burch and Wartofsky System for Stratifying Patients in Thyroid Crisis Adapted from Burch and Wartofsky. Body System Manifestations Score Our Patient's Score Thermoregulatory (°C) 37.2-37.7 5 37.8-38.2 10 38.3-38.8 15 X 38.9-39.9 20 39.4-39.9 25 >40 30 Tachycardia (beats/minute) 99-109 5 110-119 10 120-129 15 X 130-139 20 >140 25 Congestive heart failure None 0 Mild (pedal edema) 5 Moderate (bilateral rales) 10 X Severe (pulmonary edema) 15 Atrial fibrillation None 0 X Present 10 Precipitant present None 0 Present 10 X Gastric and hepatic None 0 Moderate (nausea, vomiting, diarrhea, gastric pain) 10 X Severe (unexplained jaundice) 20 Central nervous system None 0 Mild (agitation) 10 Moderate (delirium, psychosis, extreme lethargy) 20 X Severe (seizure, coma) 30 Interpretation Thyroid storm highly likely >45 X Thyroid storm looming 25-44 Thyroid storm unlikely <25 Patient total 80 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 Epidemiology 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. Pathophysiology 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. Thyroid Crisis Thyroid crisis is a clinical diagnosis based on the physical examination findings. In thyroid crisis, an abrupt exacerbation of hyperthyroidism will occur caused by the sudden release of excessive thyroid hormones into the circulation. Thyroid crisis does not usually present as an abrupt exacerbation of thyrotoxicosis; it can sometimes be difficult to differentiate these 2 conditions. Thyroid crisis has 4 major elements: hyperthermia, tachycardia, disorientation, and a precipitating factor. The hyperthermia of thyroid crisis manifests as a core body temperature greater than 101.3°F and is often accompanied by profuse sweating. Electrolyte disturbances can result from substantial fluid losses. The tachycardia of thyroid crisis will typically manifest as a heart rate greater than 140 beats/minute. Such patients also will be at risk of developing dysrhythmias such as atrial fibrillation. Central nervous system impairment can begin as confusion and agitation and progress to seizures and, eventually, coma. Thyroid crisis typically will have had a triggering event such as infection, surgery, trauma, iodine-containing contrast, certain medications, and, rarely, such as in the present patient, minor trauma. The clinical features of thyroid crisis can present gradually. When suspicion of thyroid crisis arises, the Burch and Wartofsky scoring system can be helpful in determining the likelihood that a patient is actually in crisis ( Table 1 ). Management of Thyroid Crisis When strong clinical evidence is present that a patient is in thyroid crisis, the patient should be treated in the intensive care unit. The management of thyroid crisis has 3 objectives: reducing the active thyroid hormone pool, reducing thyroid hormone synthesis, and controlling the sequelae of thyroid crisis (tachycardia, hypertension, hyperpyrexia, and so forth). A summary of the management of thyroid crisis is listed in Table 2 . Table 2 Summary of the Management of Thyroid Crisis Reduction of thyroid hormone secretion 1. Administer iodine-containing medications (eg, Lugol's solution, radiologic contrast agents) Inhibit triiodothyronine to thyroxine conversion 1. Intravenous corticosteroids 2. Radiologic contrast agents 3. Plasmapheresis Inhibit synthesis of thyroid hormones 1. Methimazole 2. Propylthiouracil Supportive care 1. Transfer patient to monitored setting (intensive care unit) 2. Provide acetaminophen and cooling beds for fever 3. Administer β-blockers for tachycardia and hypertension 4. Initiate isotonic fluid replacement for electrolyte imbalance Immediate reduction of thyroid hormone secretion can be achieved with administration of iodides. Iodine-containing contrast agents such as iopanate or ipodate can also be used to achieve this effect. Lugol's solution and potassium iodide are additional drugs with proven efficacy in reducing thyroid hormone secretion. Lithium can be used in patients allergic to iodine to reduce thyroid hormone secretion. Blocking the conversion of T4 to T3 can reduce the thyroid hormone pool. Iodine-containing contrast mediums can be used for this purpose; however, the more common practice has been administration of intravenous corticosteroids. Determining treatment efficacy can be achieved by monitoring of serum free T3 and reverse T3. Reverse T3 will tend to increase with therapy. Plasmapheresis is a last resort to block T4 to T3 conversion, but plasmapheresis is only capable of extracting small amounts (about 20%) of T4 and T3 from the circulation. The final strategy for managing thyroid crisis is inhibiting synthesis of T3 and T4. Methimazole and propylthiouracil are commonly used medications for this purpose. The most important part of managing thyroid crisis is mitigating the sequelae, such as hypertension, tachycardia, electrolyte disturbances, and hyperpyrexia. The hypertension and tachycardia of thyroid crisis can be managed with β-blocking drugs such as propranolol. The electrolyte disturbances can be significant, often requiring 3 to 5 L of isotonic fluid replacement. Hyperpyrexia can best be managed with acetaminophen. Nonsteroidal anti-inflammatory drugs should not be used, because they inhibit thyroid-binding proteins and can increase the amount of circulating thyroid hormones. Additional measures to reduce the core body temperature have included malignant hyperthermia cooling blankets and placing chilled saline bags around the patient. In conclusion, thyroid crisis is a rare life-threatening emergency associated with uncontrolled hyperthyroidism. Early recognition and intervention are critical for reducing the morbidity and mortality from this condition. In our case report, the likely trigger that launched the patient into thyroid crisis was the trauma that had occurred 2 weeks earlier. This emphasizes that thyrotoxicosis and thyroid crisis do not necessarily occur as an abrupt exacerbation of hyperthyroidism. With the findings from our case report, the healthcare provider is reminded that clinical suspicion and a low threshold for intervention are the keys to patient survival. References 1. Nayak B., Burman K.: Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am 2006; 35: pp. 663. 2. Burger A.G., Philippe J.: Thyroid emergencies. Baillieres Clin Endocrinol Metab 1992; 6: pp. 77. 3. Delikoukos S., Mantzos F.: Thyroid storm induced by trauma due to spear-fishing gun trident impaction in the neck. BMJ Case Rep 2009; 2009: 4. Delikoukos S., Mantzos F.: Thyroid storm induced by blunt thyroid gland trauma. Am Surg 2007; 73: pp. 1247. 5. Hagiwara A., Murata A., Matsuda T., et. al.: Thyroid storm after blunt thyroid injury: A case report. J Trauma 2007; 63: pp. E85. 6. Sabnis G.R., Karnik N.D., Chavan S.A., et. al.: Trauma precipitating thyroid storm. J Assoc Physicians India 2011; 59: pp. 117. 7. Vora N.M., Fedok F., Stack B.C.: Report of a rare case of trauma-induced thyroid storm. Ear Nose Throat J 2002; 81: pp. 570. 8. Yoshida D.: Thyroid storm precipitated by trauma. J Emerg Med 1996; 14: pp. 697. 9. Chiha M., Samarasinghe S.: Thyroid storm: An updated review. J Intensive Care Med 2013 Aug 5; Epub 10. Langley R., Burch R.: Perioperative management of the thyrotoxic patient. Endocrinol Metab Clin North Am 2003; 32: pp. 519. 11. Wartofsky L.: Thyrotoxic storm.Braverman L.Utiger R.Werner & Ingbar's the Thyroid (ed 9).2005.Williams & WilkinsPhiladelphia, PA:pp. 651-657. 12. Dillmann W.H.: Thyroid storm. Curr Ther Endocrinol Metab 1997; 6: pp. 81. 13. Akamizu T., Satoh T., Isozaki O., et. al.: Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid 2012; 22: pp. 661. 14. Jameson J.L., Weetman A.P.: Disorders of the thyroid gland.Fauci A.S.Braunwald E.Kasper S.L. et. al.Harrison's Principles of Internal Medicine.2008.McGraw-Hill ProfessionalNew York, NY:pp. 2224-2246. 15. Ross D.S.: Treatment of toxic adenoma and toxic multinodular goiter.Bascow D.S.UpToDate.2013.UpToDateWaltham, MA: 16. Waltman P.A., Brewer J.M., Lobert S.: Thyroid storm during pregnancy: A medical emergency. Crit Care Nurse 2004; 24: pp. 74. 17. Burch H.B., Wartofsky L.: Life-threatening thyrotoxicosis: Thyroid storm. Endocrinol Metab Clin North Am 1993; 22: pp. 263. 18. Sarlis N., Gourgiotis L.: Thyroid emergencies. Rev Endocr Metab Disord 2003; 4: pp. 129.

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