Abstract
Objective:
Our objective is to present a case of thyroid abscess complicated by thyroid storm secondary to intravenous drug use. Cases of thyroid abscess causing thyrotoxicosis are rare. This is the first report of thyroid abscess from intrathyroidal injection of illicit drugs resulting in thyroid storm.
Methods:
We used biochemical evaluation, computed tomography (CT), and ultrasound to assess the thyroid abscess. Treatment included antithyroid drugs, steroids, antibiotics, and surgical drainage.
Results:
A 28-year-old female presented with neck pain and fever after injecting heroin into her neck. CT showed bilateral thyroid abscesses measuring 3.0 cm on the left and 2.0 cm on the right. Thyroid-stimulating hormone (TSH) was 0.40 mIU/L (reference range is 0.34 to 5.60 mIU/L). She left against medical advice, then returned with worsening symptoms. CT showed multiloculated, bilateral thyroid abscess measuring 8.6 cm on the left and 5.3 cm on the right. She suffered a cardiac arrest and was resuscitated. Her white blood cell count was 25.9 × 103 cells/mL, TSH <0.01 mIU/L, free thyroxine was 4.25 ng/dL (reference range is 0.89 to 1.76 ng/dL), triiodothyronine was 96 ng/dL (reference range is 70 to 204 ng/dL), and thyroid-stimulating immunoglobulin was <89% (reference range is <140%). She had fever, tachycardia, heart failure, and elevated bilirubin confirming a diagnosis of thyroid storm by Japan Thyroid Association criteria and Burch-Wartofsky score. She was treated with propylthiouracil, hydrocortisone, and antibiotics. Two days later her TSH was <0.005 mIU/L, free thyroxine was 3.06 ng/dL, and triiodothyronine was 62.0 ng/dL. Ultrasound showed enlarged, heterogeneous thyroid with loculated fluid collections. Following surgical abscess drainage, her thyroid function normalized and progressed to hypothyroidism.
Conclusion:
We conclude that thyroid abscess can be a life-threatening complication of intravenous drug use as it can precipitate thyroid storm. Along with surgical drainage of the abscess, successful management includes antithyroid drugs, antibiotics, and steroids to control thyrotoxicosis, infection, and inflammation.
INTRODUCTION
Thyroid abscess is a rare disorder of the thyroid (1). It develops as a progression from acute suppurative thyroiditis, which is an infection in the thyroid gland (2,3). Acute suppurative thyroiditis accounts for just 0.1 to 0.7% of thyroid diseases and as of 2006, there were <500 thyroid abscess cases reported (2,4). Thyroid abscess can be life-threatening, making it crucial to identify cases early (2,5). The mortality rate for acute suppurative thyroiditis can be >12% without appropriate treatment (6).
The thyroid is considered resistant to infection due to its dense vascularity, lymphatic drainage, thyroid capsule, high iodine content, and presence of hydrogen peroxide as a substrate for thyroid hormone synthesis (2,7). Thus, thyroid abscess usually occurs in the presence of risk factors such as an immunocompromised state or congenital abnormalities of thyroid development (6,7). However, despite multiple protective mechanisms, direct puncture of the normal thyroid gland in a healthy individual can lead to acute suppurative thyroiditis and thyroid abscess (2).
We describe a case of thyroid abscess as a direct result of intravenous drug use (IVDU) which was complicated by thyroid storm. The patient injected heroin directly into her neck and, although there are reports of direct inoculation of bacteria during needle aspiration biopsy causing thyroid abscess (7), there are no reported cases of thyroid abscess from direct IVDU into the thyroid. There is 1 case reported in the literature of thyroid abscess causing thyroid storm (8). However, that patient had a 7-year history of Graves disease (GD) previously treated with thiamazole. He had discontinued thiamazole and had chronic diarrhea with weight loss of 20 kg in the preceding 6 months with positive thyroid-stimulating hormone (TSH) receptor antibody. This suggested that his underlying GD was contributing to thyroid storm and the abscess was possibly the precipitating factor.
Our patient met the diagnostic criteria for thyroid storm based on Burch-Wartofsky score (9) and by the Japan Thyroid Association criteria for thyroid storm (10). The criteria were primarily met based on the presence of cardiac and hepatic manifestations. As our patient was transferred across multiple hospitals for escalation of care from community settings to university hospitals, the reference ranges for thyroid hormone assays and liver function tests varied slightly across settings. The varying reference ranges are listed throughout the manuscript.
CASE REPORT
A 28-year-old female with a history of IVDU and chronic hepatitis C virus presented to the emergency department with neck pain, fever, chills, and odynophagia. She had injected heroin into the right side of her neck 10 days prior. She had tachycardia, scleral icterus, right neck ecchymosis, and a firm, enlarged, nontender thyroid. Laboratory workup was significant for white blood cell count of 16.3 × 103 cells/mL (reference range is 4.0 to 11.0 × 103 cells/mL), TSH of 0.40 mIU/L (reference range is 0.34 to 5.60 mIU/L), alanine aminotransferase of 240 U/L (reference range is 0 to 33 U/L), aspartate aminotransferase of 60 U/L (reference range is 0 to 30 U/L), and alkaline phosphatase of 228 U/L (reference range is 35 to 125 U/L).
Computed tomography (CT) of the neck with contrast showed early signs of bilateral abscess measuring 3.0 cm on the left and 2.0 cm on the right with heterogeneous enhancement in the remainder of the thyroid concerning for thyroiditis. She was started on vancomycin and piperacillin/tazobactam. Hepatitis A antibody IgM and hepatitis C virus antibody were reactive with low hepatitis C viral load of <15 IU/mL (reference range is 15 to 100,000,000 IU/mL). Bedside laryngoscopy was unremarkable. Her blood cultures were positive for methicillin-resistant Staphylococcus aureus and urine culture showed Escherichia coli. However, she left against medical advice without antibiotics.
The patient returned 9 days later with worsening neck swelling and pain. Her TSH was <0.01 mIU/L and free thyroxine (T4) was 4.25 ng/dL (reference range is 0.89 to 1.76 ng/dL) (Table 1). CT of the neck showed significant interval progression with multiloculated thyroid abscess involving bilateral thyroid lobes measuring 8.6 cm on the left and 5.3 cm on the right with mass effect on the trachea, esophagus, supraglottic larynx, and hypopharynx (Fig. 1). She then suffered a ventricular fibrillation cardiac arrest, was intubated, and was resuscitated with epinephrine and defibrillation. She was afebrile with sinus tachycardia to 163 beats per minute and hypotension requiring vasopressors.
Table 1.
Laboratory Analyses During Hospitalization
| First hospitalization | Second hospitalization | ||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Patient left AMA | PTU, HC, and antibiotics started | PTU stopped, I&D of thyroid abscess | HC stopped | Oral LT4 at 50 μg daily started | |||||||||
| Hospital day | −9 | −8 | 0 | 0 | 2 | 2 | 3 | 4 | 4 | 5 | 6 | 7 | 9 |
| TSH (mIU/L, reference range is 0.400–4.500 mIU/L)* | 0.400 | <0.010 | 0.010 | <0.005 | 0.007 | 0.006 | <0.005 | 0.010 | 0.062 | 1.200 | |||
| Free T4 (ng/dL, reference range is 0.89–1.76 ng/dL) | 4.25 | 4.40 | 3.06 | 2.48 | 2.15 | 1.68 | 1.30 | 0.97 | 0.92 | 0.58 | |||
| T3 (ng/dL, reference range is 60.00–181.00 ng/dL) | 96.00 | 57.60 | 62.00 | 56.90 | 60.70 | 44.40 | 36.30 | 33.10 | 32.10 | ||||
| Total T4 (μg/dL, reference range is 5.5–11.0 μg/dL) | 15.5 | ||||||||||||
| Thyroglobulin (ng/mL, reference range is 0.1–36.8 ng/mL) | 186.8 | 34.8 | |||||||||||
| Thyroglobulin antibody (IU/mL, reference range is 0–4.0 IU/mL) | <1 | ||||||||||||
| Thyroid-stimulating immunoglobulin (reference range is <140% baseline) | <89 | ||||||||||||
| Thyroid microsomal antibody (reference range is <1:100) | <1:100 | ||||||||||||
Abbreviations: AMA = against medical advice; HC = intravenous hydrocortisone; I&D = incision and drainage; LT4 = levothyroxine; PTU = propylthiouracil; T3 = triiodothyronine; T4 = thyroxine; TSH = thyroid-stimulating hormone.
*The reference ranges listed for TSH, free T4, and T3 correspond to the laboratory assays from the patient's final hospital stay as her hospital course took place in multiple institutions.
Fig. 1.

Computed tomography with contrast showing a multiloculated thyroid abscess of bilateral thyroid lobes. The abscess measures 8.6 cm on the left and 5.3 cm on the right with mass effect on the trachea, esophagus, supraglottic larynx, and hypopharynx. The panels include (A) cross-sectional, (B) coronal, and (C) sagittal sections.
She was restarted on vancomycin and piperacillin/tazobactam and treated with intravenous amiodarone for 2 days. Laboratory workup showed white blood cells were 25.9 × 103 cells/mL, lactate was 2.4 mmol/L (reference range is 0.5 to 2.2 mmol/L), TSH was <0.01 mIU/L, free T4 was 4.4 ng/dL (reference range is 0.7 to 2.0 ng/dL), thyroglobulin was 186.8 ng/mL (reference range is 0.1 to 36.8 ng/mL), and her erythrocyte sedimentation rate was 128 mm/hour (reference range is 0 to 20 mm/hour). Her condition was concerning for thyroid abscess causing a destructive thyroiditis. Her Burch-Wartofsky score was highly suggestive of thyroid storm at 60 points (9).
She was given propylthiouracil (PTU) at 500 mg then 250 mg every 4 hours and intravenous hydrocortisone at 300 mg then 100 mg every 8 hours. Beta blockade was not used due to hypotension. Neck ultrasound showed diffusely enlarged and heterogeneous loculated fluid collections without intrinsic or peripheral vascularity (Fig. 2). The right lobe measured 6.3 cm × 3.0 cm × 2.5 cm, and the left lobe measured 7.6 cm × 5.2 cm × 4.1 cm. Bedside needle aspiration of the thyroid drained 12 mL of purulent fluid.
Fig. 2.

Thyroid ultrasound on hospital day 2 shows an enlarged, heterogeneous thyroid with multiple loculated fluid collections in (A) sagittal and (B) transverse views of the right lobe and (C) sagittal and (D) transverse views of the left lobe.
On hospital day 2 her TSH was <0.05 mIU/L, free T4 was 3.06 ng/dL (reference range is 0.89 to 1.76 ng/dL), triiodothyronine (T3) was 57.60 ng/dL (reference range is 60 to 181 ng/dL). Thyroid-stimulating immunoglobulin and thyroid microsomal antibody were negative. Transthoracic echocardiography showed an ejection fraction of 20%. She developed marked elevation of liver function tests, with direct bilirubin at 5.5 mg/dL (reference range is 0.0 to 0.6 mg/dL), aspartate aminotransferase of 2,881 U/L (reference range is 15 to 37 U/L), alanine aminotransferase 906 U/L (reference range is 16 to 61 U/L), and alkaline phosphatase of 172 U/L (reference range is 45 to 117 U/L).
With this presentation of tachycardia, heart failure, and elevated bilirubin she met diagnostic criteria for thyroid storm based on the presence of thyrotoxicosis and a combination of 2 of the following: fever, tachycardia, heart failure, or gastrointestinal or hepatic manifestations (10). PTU was discontinued in the setting of transaminitis due to shock liver secondary to ventricular fibrillation arrest. She underwent incision and drainage of the abscess with removal of 100 mL of frank pus. On postoperative day 2, free T4 normalized at 1.68 ng/dL. Operating room cultures were positive for methicillin-resistant S. aureus. By postoperative day 6, her thyroid function trended towards hypothyroidism with TSH at 1.2 mIU/L (reference range is 0.4 to 4.5 mIU/L), free T4 at 0.58 ng/dL (reference range is 0.89 to 1.76 ng/dL), and T3 at 32.10 ng/dL (Fig. 3). The patient was discharged on levothyroxine at 50 μg daily with endocrinology follow up.
Fig. 3.

Thyroid function tests trended over the hospital course with notable events including medication initiation and discontinuation times. AMA = against medical advice; HC = intravenous hydrocortisone; I&D = incision and drainage; LT4 = levothyroxine; PTU = propylthiouracil.
DISCUSSION
Thyroid storm is most commonly due to GD, while toxic multinodular goiter and toxic adenoma are less frequent causes (11). In most situations, thyroid storm occurs in the context of a superimposed insult with an underlying predisposition to thyrotoxicosis (11). However, in this case, thyroid storm occurred in a patient with previously normal thyroid function and negative thyroid-stimulating immunoglobulin, making GD less likely.
To the best of our knowledge this is the first report of thyroid storm occurring as a complication of thyroid abscess due to intrathyroid injection of illicit drugs with no underlying cause for hyperthyroidism. The patient suffered a ventricular fibrillation arrest precipitated by thyrotoxicosis and met criteria for thyroid storm based on cardiac and hepatic manifestations of heart failure, tachycardia, and bilirubinemia (9,10). She was managed with high-dose steroids and PTU along with antibiotics, incision and drainage, and supportive treatment.
The rationale for her treatment was that PTU would facilitate control of thyrotoxicosis by inhibiting new hormone production, reducing thyroglobulin synthesis, and inhibiting the peripheral conversion of T4 to T3 (12,13). High-dose hydrocortisone was used to decrease conversion of T4 to T3 and improve vasomotor stability (12). In addition, glucocorticoids would treat potentially associated limited adrenal reserve and have been shown to improve outcomes in thyroid storm (14,15). Since iodine works by blocking release of thyroid hormones, it was less likely to be effective in thyrotoxicosis due to destruction of thyroid follicles. Thus, thyroid storm due to thyroid abscess can be successfully managed with multimodal antithyroid therapeutic options, surgical drainage, and supportive measures. Partial or total thyroidectomy may be required in cases where the abscess persists, progresses, or for extensive disease that cannot be controlled with surgical drainage (2).
Only a few cases of thyroid abscess following IVDU have been reported (6,16,17). In a previous report, a patient developed thyroid abscess following bacteremia due to a left forearm abscess from IVDU (7). She had a preexisting multinodular goiter but no thyrotoxicosis at baseline (6). It has been postulated that patients with preexisting multi-nodular goiter may have an impaired antioxidant defense mechanism which increases risk of thyroid infection (6). After developing thyroid abscess, that patient became only mildly thyrotoxic with TSH at 0.02 U/mL, free T4 at 3.89 ng/dL, and free T3 at 5.1 pg/mL (6). She was managed with antibiotics, incision and drainage, propranolol, and naproxen. Another risk factor for development of thyroid abscess is a persistent pyriform sinus fistula (2).
Per the Japan Thyroid Association criteria for thyroid storm (10), thyroid storm is diagnosed based on different combinations of clinical manifestations. About 76% of patients with thyroid storm had more than 3 manifestations consistent with multiorgan failure and the most common association, which was seen in 15% of patients, was the simultaneous presence of central nervous system symptoms, fever, tachycardia, and gastrointestinal or hepatic manifestations. A multimodal approach with antithyroid drugs, iodide, steroids, beta blockers, and antipyretics should be used to treat thyrotoxicosis (10).
On ultrasound, thyroid abscesses appear as heterogeneous areas with a superimposed anechoic or hypoechoic mass where the abscess begins (18,19). The echotexture varies depending on degree of hemorrhage or internal debris (18,19). They tend to have peripheral hypervascularity with less internal vascular flow (18,19). In contrast, subacute thyroiditis, which is the most common cause of painful thyroiditis, appears as a diffusely heterogeneous thyroid with low vascularity (2). CT of the neck can demarcate the abscess and demonstrate evidence of compression and extension into surrounding structures (2).
Our case was unusual as our patient with thyroid abscess presented in thyroid storm, while thyroid function tends to remain normal in more than two-thirds of patients with thyroid abscess (2,7). Acute suppurative thyroiditis causes thyrotoxicosis in only 5 to 10% of cases (6). Transient or permanent hypothyroidism may occur due to thyroid destruction by the disease process or due to therapeutic interventions such as surgical drainage (2). Our patient developed hypothyroidism acutely after incision and drainage, but it remains to be seen if this will be permanent.
CONCLUSION
We conclude that thyroid abscess resulting in thyroid storm is a rare complication of IVDU. Thyroid function usually remains normal in thyroid abscess, but rarely thyroid storm can occur. A high index of suspicion in patients presenting with neck pain and swelling, and a multimodal therapeutic approach can achieve successful outcomes in this life-threatening endocrine complication of IVDU.
Abbreviations
- CT
computed tomography
- GD
Graves disease
- IVDU
intravenous drug use
- PTU
propylthiouracil
- T3
triiodothyronine
- T4
thyroxine
- TSH
thyroid-stimulating hormone
Footnotes
DISCLOSURE
The authors have no multiplicity of interest to disclose.
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