Thyrotoxicosis is the clinical state associated with excess thyroid hormones and occurs primarily in autoimmune thyroid disease.¹⁾ However, although very rare, it can be caused by trauma. Trauma to the neck may cause thyroid hemorrhage, and an expanding thyroid hematoma can lead to airway compromise, which requires emergency surgical intervention. Moreover, although uncommon, concurrent thyroid dysfunction can occur, leading to thyroid storm.²⁾ Previous cases of blunt trauma to the neck with hemorrhagic complications have mainly involved acute airway management and surgery.^3-6) Most trauma mechanisms described thus far include traffic accidents, falls, sports accidents, and hanging.⁷⁾ Here, we report that a case of transient thyrotoxicosis after horse-induced neck trauma mainly focused on the disease course.

A previously healthy, 60-year-old man who worked at a racetrack presented at the emergency department of our medical center with a head and neck injury caused by a horse kick (Day 1). He complained of facial and neck pain caused by a direct kick by the horse’s hoof. The patient had an alert mental status with a blood pressure of 161/91 mmHg, a heart rate of 57 bpm, peripheral oxygen saturation of 97% in room air, and a temperature of 36.4°C. The following were noted on physical examination; tongue laceration, left ear bleeding, and neck swelling. Neurological deficits were not observed. Computed tomography (CT) of the head and neck revealed a nasal bone fracture and a C6 right transverse process fracture. Hypoattenuation of the right thyroid gland with perihemorrhagic fluid and adjacent soft tissue swelling suggested a right thyroid rupture and hematoma (Fig. 1).

As the patient was hemodynamically stable and showed no neurological deficits, he was admitted to the trauma care department for close monitoring rather than immediate surgery. The patient’s clinical course, including neck pain and swelling, gradually improved during monitoring. On Day 4, neck ultrasonography (US) was performed, revealing a 1.4×0.7× 1.2 cm sized solid hypoechoic lesion with irregular margin in the right lower pole, suggestive of thyroid hematoma (Fig. 2A, B). A hematoma was clinically suspected; however, fine-needle aspiration (FNA) was performed carefully because of the possibility of an underlying high-suspicious thyroid nodule. The pathological examination showed that some macrophages, neutrophils, and lymphocytes were admixed with inflammatory debris without any follicular cells. Considering the possibility of thyroid function abnormalities following a thyroid injury, a thyroid function test (TFT) was performed. The TFT results during the clinical course are shown in Table 1. On Day 4, the TFT demonstrated a suppressed TSH level of 0.01 uIU/mL (reference range, 0.25-4 uIU/mL), a free T4 level of 3.54 ng/dL (reference range, 0.78-1.94 ng/dL) and a free T3 level of 8.71 pg/mL (reference range, 2.2-5.5 pg/mL). TSH-receptor antibody was negative No thyrotoxicosis symptoms or signs were observed. The patient was discharged on Day 6 with nearly complete recovery from neck pain.

No neck tenderness was reported during the first outpatient clinic 3 weeks after initial trauma presentation. TFT showed that TSH was still suppressed (0.01 uIU/mL) but thyrotoxicosis improved compared with those of Day 4. The free T4 and free T3 levels was 1.3 ng/dL and 6.67 pg/mL, respectively (Table 1). Anti-thyroid peroxidase antibody (anti-TPO Ab) and Anti-thyroglobulin antibody (anti-Tg Ab) tests were negative. The follow-up neck US reveals a decrease in size (0.6×1.2×0.75 cm) of the solid hypoechoic lesion with irregular margin (Fig. 2C, D). Compared to the previous US (Fig. 2A, B), the soft tissue swelling in the anterior neck improved. To identify the etiology of persistent subclinical thyrotoxicosis, a thyroid scan (Tc⁹⁹ scintigraphy) was performed at 3 weeks after the neck trauma. The scan showed a mild diffuse enlargement of the thyroid gland with decreased radiotracer uptake in the right lower pole, suggestive of a cold nodule (Fig. 3). TFT 2 months after trauma showed that all parameters (TSH: 0.82 uIU/mL, free T4 level: 0.79 ng/dL, and free T3 level: 3.98 pg/mL) recovered to the reference range (Table 1).

Here we report a case of acute thyrotoxicosis after horse-induced neck trauma mainly focused on thyroid US and changes in TFT. In the present case, the patient had a relatively indolent disease course and was observed without emergent airway protection or surgery. The thyroid hematoma decreased after 3 weeks, and thyrotoxicosis recovered to normal after 2 months.

Thyrotoxicosis after trauma results from the rupture of the thyroid acini and release of thyroid hormones into the bloodstream.⁸⁾ In several cases of trauma-induced thyroid hematoma, thyrotoxicosis occurs regardless of previous thyroid disease or hyperthyroid symptoms during the clinical course, and usually improves with a decreased extent of thyroid hematoma.^5,6,9) Previous reports demonstrated that focal hematoma and diffuse injury of the thyroid gland may cause destructive thyroiditis.^5,7) In this case, given that the area of the hematoma on the thyroid US showed decreased uptake on the thyroid scan, transient thyrotoxicosis likely occurred due to destructive thyroiditis of the focal hematoma. The patient was previously healthy and did not complain about thyrotoxicosis symptoms, including palpitation or tremor even if the free T4 level was as high as 3.54 ng/dL. Examination of thyroid function in patients with neck trauma may be required to identify patients with asymptomatic thyrotoxicosis. Moreover, trauma-induced thyroiditis can involve a triphasic course that starts with temporary thyrotoxicosis and proceeds to hypothyroidism followed by recovery.⁸⁾ Thus, after recovery of normal thyroid function, a follow-up TFT is needed. However, the patient in this case did not visit the next outpatient clinic. Therefore, additional TFT or follow-up autoantibody levels could not be measured. Another important reason for considering thyroid abnormalities in trauma patients is the possibility of a thyroid storm. It is known that patients with hyperthyroidism may be at high risk of developing thyroid storms after trauma.⁸⁾ A previous case report showed that patients with thyroid trauma can experience a thyroid storm even in the absence of underlying hyperthyroidism.¹⁰⁾ Therefore, if symptoms, including tachycardia, fever, or altered consciousness, persist after managing the hypovolemic state or other possible correctable causes in a patient with neck trauma, the possibility of a thyroid storm should be suspected, and TFT evaluation is mandatory.

Trauma to the thyroid gland is treated either surgically or conservatively, according to the degree of thyroid injury. Heizmann et al.¹¹⁾ suggested a classification of blunt thyroid injuries from grade I to IV which is as follows: a small parenchymal laceration is categorized as grade I, a rupture with a parathyroid hematoma or a neck hematoma as grades II and III, and laceration of the surrounding tissue as grade IV. Recently, a modified classification and treatment protocol was released that included dyspnea and increasing hoarseness when deciding whether endotracheal intubation or surgical neck exploration is needed rather than observation and repeat US.³⁾ According to a literature review, nearly half of the 34 cases of thyroid injury were surgically treated.³⁾ It is noteworthy that a delayed onset of symptoms, even later than 24 hours after the initial trauma, has been reported.³⁾ Therefore, at least 24 hours of monitoring is needed even if a patient initially does not have dyspnea or hoarseness. In this case, the patient had a grade II thyroid gland injury; because the hematoma was located adjacent to the right inferior thyroid artery, an arterial injury was also suspected. However, there were no definitive radiological findings, including extravasation of contrast from the artery, and no symptoms of dyspnea or signs of increasing hoarseness. Therefore, the patient was admitted to the trauma care department for close observation considering the delayed onset of airway compression.

Traumatic rupture of the thyroid gland can occur either in a thyroid with a pre-existing underlying pathology or in a normal thyroid gland.⁶⁾ According to a previous literature review, pre-existing pathological alterations in the thyroid gland were found in half of these patients.³⁾ In addition, no correlation was observed between the pre-existence of thyroid lesions and the need for emergency surgical therapy.⁷⁾ It is unknown whether this patient had an underlying thyroid lesion because he had never undergone thyroid US. However, considering that the thyroid lesion was shrinking and FNA revealed inflammatory cells but no follicular cells, it is less likely that this patient had an underlying thyroid nodule. Regardless of whether the hematoma arises from a preexisting underlying pathology or a normal thyroid gland, thyroid US can be a good option to quickly evaluate thyroid rupture and the extent of bleeding.⁵⁾

The strength of this case is that we performed serial follow-up of thyroid function and US scans. Transient thyrotoxicosis improved spontaneously, and free T4 and TSH levels recovered to the normal range after 3 weeks and 2 months, respectively. Decreased size of the hematoma and soft tissue swelling were identified by neck US, performed after 3 weeks; however, there was still decreased radiotracer uptake in the thyroid scan. In addition, the fact that the trigger in our case was a horse kick is unusual, given that vehicle accidents and falls are the most frequent causes of thyroid trauma in Korea.

Trauma is a rare cause of acute thyroiditis. Clinicians should be aware of the possibility of thyroid hematoma and thyrotoxicosis in patients with neck trauma. Neck US is helpful for assessing the initial extent of thyroid hematoma during follow-up. TFT monitoring for at least 2 months is required for patients with initial thyrotoxicosis.