THE WESTERN JOURNAL OF MEDICINE
o
DECEMBER 1 ggo
o
153
*
myoglobin dissociation is slower than COHb due to its increased affinity for myoglobin, a "rebound effect" with a delayed return of symptoms can occur.7 Carbon monoxide poisoning does not cause dyspnea or tachypnea until it causes hypoxemia from circulatory dysfunction or lactic acidosis from tissue hypoxia. At low levels, chronic cardiopulmonary problems, for example, angina and chronic obstructive pulmonary disease, may be exacerbated because cardiac myoglobin binds with great affinity and rapidly reduces myocardial oxygen reserve. With acute exposure, blood levels correlate with symptoms and signs but do not reflect tissue CO levels. Arterial blood gas levels are used to determine the degree of carbon monoxide intoxication and treatment.8 9 With levels less than 0.10 (10%), patients are usually asymptomatic. As the COHb concentration increases above 0.20 (20%), headache, dizziness, confusion, and nausea may develop. Chest pain due to myocardial ischemia may occur, as can cardiac arrhythmias. Coma and seizures due to cerebral edema are common with concentrations of greater than 0.40 (40%), and death is likely with more than 0.60 (60%).1°-12 The differential diagnosis includes viral illnesses, food poisoning, depression, transient ischemic attacks, coronary artery disease, arrhythmias, and functional illnesses, among others. The most common misdiagnosis is a "flulike" syndrome.9 The mainstay of therapy is supplemental oxygen and monitoring for cardiac arrhythmias. The goal of oxygen therapy is to improve the oxygen content of the blood by maximizing the fraction dissolved in plasma (Pao2)."3 The advantage of hyperbaric oxygen therapy is a more rapid reduction in COHb levels. Disadvantages of this treatment modality include few available treatment centers and the requirement for patient transport. Patients with severe neurologic or cardiovascular symptoms or very high COHb concentrations would benefit from hyperbaric oxygen, but it is these very sick patients for whom transport is most hazardous.
Once treatment begins, oxygen therapy and observation must continue long enough to rule out delayed sequelae as the carboxymyoglobin unloads. The initial presentation of our patients was consistent with gastroenteritis, for which they were given intravenous hydration and other supportive measures. We initially did not consider inhaled toxins. Once an adequate history, which included indoor cooking, and after arterial blood gas results were obtained, they were placed on 100% oxygen therapy with a complete resolution of the symptoms. They were discharged to a safe environment within three hours of the correct diagnosis. This case illustrates the importance of always considering CO poisoning when two or more patients are similarly or simultaneously sick. The diagnosis must be excluded by a directed history and physical examination. If suspicion remains, COHb testing should be done and oxygen therapy should be started empirically while results are pending. If CO poisoning is confirmed, the source must be identified and recommendations for correction or avoidance made. REFERENCES
1. Heimbach DM, Waeckerle JF: Inhalation injuries. Ann Emerg Med 1988; 17:1316-1320 2. Meredith T, Vale A: Carbon monoxide poisoning. Br Med J 1988; 296:7779 3. Myers RA, Linberg SE, Cowley RA: Carbon monoxide poisoning: The injury and its treatment. JACEP 1979 1979; 8:479-484 4. Goldbaum LR, Orellano T, Dergal E: Mechanism of the toxic action of carbon monoxide. Ann Clin Lab Sci 1976; 6:372-376
6
657
5. Petersen JE, Stewart RD: Absorption and elimination of carbon monoxide by inactive young men. Arch Environ Health 1970; 21:165-171 6. Coburn RF: Carbon monoxide body stores. Ann NY Acad Sci 1970; 174: 117. Anderson GK: Treatment of carbon monoxide poisoning with hyperbaric oxygen. Milit Med 1978; 143:538-541 8. Van Hoesen KB, Camporesi EM, Moon RE, Hage ML, Piantadosi CA: Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning? A case report and literature review. JAMA 1989; 261:10391043 9. Dolan MC: Carbon monoxide poisoning. Can Med Assoc J 1985; 133:392398 10. Larkin J, Brahos G, Moylan J: Treatment of carbon monoxide poisoning: Prognostic factors. J Trauma 1976; 16:111-115 11. Peters WJ: Inhalation injury caused by the products of combustion. Can Med Assoc J 1981; 125:249-252 12. Guy CR, Salhany JM, Eliot RS: Disorders of hemoglobin-oxygen release in ischemic heart disease. Am Heart J 1971; 82:824-832 13. Crocker PJ: Carbon monoxide poisoning, the clinical entity and its treatment: A review. Milit Med 1984; 149:257-263
Primary Tuberculous Thyroid Abscess Mimicking Carcinoma Diagnosed by Fine Needle Aspiration Biopsy MARIA LEISA C. MAGBOO, MD ORLO H. CLARK, MD San Francisco, Califomia
TUBERCULOSIS AFFECTING the thyroid gland is a rare condition. Exact figures for the incidence of tuberculosis of the thyroid are unavailable. The infection may present first in the thyroid gland or appear secondary to a tuberculous process elsewhere in the body. Barnes and Weatherstone noted that 7% of cases of miliary tuberculosis involve the thyroid gland.' The gland can also become involved with focal caseating tuberculosis, which can be blood-borne,23 or by direct extension from the larynx and cervical lymph nodes. The pathologic forms include multiple thyroidal granulomata, goiter with caseation, cold abscess, chronic fibrosing thyroiditis, and, least common, acute abscess.4 Patients present with a thyroid nodule,5 abscess,4 thyroiditis,6 or findings suggesting carcinoma7 of the thyroid gland. A tuberculous abscess of the thyroid gland as the sole manifestation of tuberculosis is even more uncommon. Swelling of the neck is the most consistent sign and dysphagia the most common complaint.3 The diagnosis of a tubercular abscess is rarely made clinically. In the case reported here, the clinical presentation suggested an undifferentiated thyroid cancer or granulomatous disease of the thyroid. Fine needle aspiration biopsy revealed milky fluid, and subsequent cultures confirmed the diagnosis preoperatively.
Report of a Case The patient, a 61-year-old, asymptomatic, married white woman, was referred to the University of California, San Francisco, Medical Center because of a right neck mass of 1/2 months' duration, clinically suggestive of anaplastic (Magboo MLC, Clark OH: Primary tuberculous thyroid abscess mimicking carcinoma diagnosed by fine needle aspiration biopsy. West J Med 1990 Dec; 153:657-659) From the Metabolic Research Unit (Dr Magboo), and the Department of Surgery (Dr Clark), University of California, San Francisco, School of Medicine, and the Department of Surgery, Veterans Administration Medical Center, San Francisco (Dr Clark). Dr Magboo is a fellow in endocrinology and metabolism. Supported in part by the Medical Research Service of the Veterans Adminis-
tration.
Reprint requests to Orlo H. Clark, MD, Surgical Faculty Practice, Ambulatory Care Center, 400 Parnassus Ave, Rm 680A, San Francisco, CA 94143.
ALERTS, NOTICES, AND CASE REPORTS
658
ALERTS,
658
ABBREVIATIONS USED IN TEXT
AIDS = acquired immunodeficiency syndrome HIV = human immunodeficiency virus
carcinoma of the thyroid. She
was on
thyroxine replace-
ment therapy following a subtotal thyroidectomy in 1958
for Graves' disease. She had otherwise been in excellent health but was upset because the referring surgeon thought by physical examination that she had an invasive thyroid cancer. On physical examination she was anxious but had a normal blood pressure (130/70 mm of mercury), pulse rate (72 beats per minute and regular), and temperature (37.6°C). She had a large, nontender, hard mass in the right lobe of the thyroid gland that was relatively fixed to the adjacent structures. There was no adjacent lymphadenopathy or overlying erythema. Laboratory test findings included a thyroxine radioimmunoassay of 75 nmol per liter (5.8 /Ag per dl [normal, 64 to 132]), free thyroxine index 4.9 (normal, 6.5 to 12), and thyroid-stimulating hormone 0.29 units per liter (normal, 0.4 to 4.8). A complete blood count included a hemoglobin of 139 grams per liter (13.9 grams per dl), hematocrit 0.41 (40.9%), and leukocyte count 7.7 x 109 per liter (7,700 per
Figure 1.-A 7.5-MHz ultrasonographic scan (longitudinal view) shows a 3.0by 2.8- by 1.6-cm mass in the right lobe af the thyroid gland. Note the hypoechoic nature of the tuberculous abscess with internal echoes.
Figure 2.-A photomicrograph of a tissue specimen from the right lobe of the thyroid gland shows acute inflammatory cells, amorphous debris, and multinucleated giant cells (original magnification x 100).
NOTICES,
AND
CASE
REPORTS
idl). The sedimentation rate was 9 mm per hour. Liver func-
tion test results and serum electrolyte levels were normal. Chest radiography was normal. A urine culture was negative for acid-fast bacilli. Ultrasonography of her neck revealed a 3.0- by 2.8- by 1.6-cm mass in the right lobe of the thyroid gland compressing the internal jugular vein (Figure 1). No thyroid gland was noted on the left side. An aspiration biopsy revealed 3 ml of milky white, odorless opalescent material. On cytologic examination there were no tumor cells and the direct smear was negative for bacteria. A month later, culture of the aspirated fluid grew Mycobacterium tuberculosis. A month after the aspiration biopsy, the patient had redness and an enlarging, nontender 5- by 3-cm mass in the right thyroid. Fine needle aspiration smears again revealed acid-fast bacilli. The patient was taken to surgery because of the abscess and presumed secondary infection, with erythema and an enlarging thyroid mass, and because of the possibility of an underlying malignant lesion. She underwent incision and drainage of a thyroid abscess with excision of necrotic muscle and part of the right lobe of the thyroid gland. During the operation there was dense brawny induration seen in the subcutaneous tissues extending almost to the skin on the right side of the neck. The muscles and the underlying portion of the thyroid gland were partially destroyed and were necrotic and hemorrhagic. All tissues were matted together so that it was difficult to identify the planes between the sternocleidomastoid muscle and the sternohyoid and sternothyroid muscles. Histologic examination showed granulomatous inflammation with multinucleated giant cells (Figure 2). A direct smear using a Kinyoun stain was positive for polymorphonuclear cells and a few acid-fast bacilli. M tuberculosis grew in the culture. The patient had an unremarkable postoperative course. She was treated with isoniazid, 300 mg per day, and rifampin, 600 mg per day, and has been well without any signs or symptoms of localized or systemic tuberculosis. She has a monogamous relationship and says she does not abuse drugs nor has she had a blood transfusion during the previous ten years.
Discussion Bruns in 1893 was the first to make the clinical diagnosis of tuberculosis of the thyroid gland in a living patient.8 The first report of a tuberculous abscess of the thyroid gland was in 1894.9 There were several reviews of this subject in the literature before 1945.2.3.10 Our patient's previous thyroid condition and surgical therapy may have been important. Altemeier in 1950 reported that half of the patients with suppurative thyroiditis also had adenomatous goiters, and in these patients the infection was localized rather than diffuse.1 In 1965 Goldfarb and co-workers reported the 28th case of a tuberculous thyroid abscess and considered it the first case of tuberculous thyroiditis proved by smears and cultures.12 Since then, single cases of tuberculous abscess ofthe thyroid gland have been reported in the Englishlanguage literature.4713-16 Confusion with thyroid cancer,67 acute staphylococcal infection,1s and subacute thyroiditis16 is common. The definitive diagnosis of tuberculosis of the thyroid gland is made by demonstrating the presence of tubercle bacilli either by histologic examination, bacterial culture, or animal inoculation. Berger and associates identified 19 cases of thyroiditis due to M tuberculosis and one case each due to Mycobacterium chelonei and Mycobacterium intracellulare.17 They noted that most of the previously diagnosed
THE WESTERN JOURNAL OF MEDICINE * DECEMBER 1990 *
153 * 6
cases were based solely on the findings of lymphocytic infiltration or granulomata that may accompany other conditions like thyroidal sarcoidosis, granulomatous syphilis, parenchymatous giant cell granulomas, Hashimoto's thyroiditis, carcinoma, and simple invagination of thyroid epithelial rests. Most of the proven cases of tuberculous involvement of the thyroid gland have been diagnosed either postoperatively or at autopsy. Of 1,200 thyroidectomies in 1926, 5 cases of tuberculous involvement were recorded by Coller and Huggins,'8 whereas 1 among 1,225 was reported by Keynes and Camb in 1918.'9 Of 20,758 tissue specimens examined at the Mayo Clinic between 1920 and 1931, only 21 showed tuberculosis of the thyroid gland.8 In 1952 Levitt and colleagues found 2 cases of tuberculous involvement of the thyroid among 2,114 partial thyroidectomies.20 Only 2 cases of tuberculosis of the thyroid were found in 74,393 thyroid specimens at an Italian center between 1941 and 1970.1
Making the diagnosis of primary tuberculosis of the thyroid is difficult, but this disorder should be considered in any patient who appears to have an invasive or undifferentiated thyroid cancer. The only initial complaint of our patient was the nodular mass in the thyroid, which was the only site clinically affected by tuberculosis. Cytologic examination of aspirate confirmed the diagnosis. Extrapulmonary tuberculosis is increasing in frequency in patients with human immunodeficiency virus (HIV)-induced immunosuppression. Patients with tuberculosis and the acquired immunodeficiency syndrome (AIDS) have high rates of extrapulmonary disease ranging from 45% to 75%.2 Patients with HIV infection are therefore more likely to have tuberculosis of the thyroid or at other extrapulmonary sites. Our patient was questioned about extramarital relationships, blood transfusions, or injections but denied any such factors for AIDS. She refused HIV testing. To our knowledge, this is the first case of primary thyroid tuberculosis presenting as a cold abscess in which the preoperative diagnosis was made by fine needle aspiration biopsy. This procedure made the diagnosis of malignancy unlikely, and tuberculosis was proved by smears and cultures. The use of fine needle aspiration has been popular in Sweden since the early 1950s.22 It is the most accurate and cost-effective screening technique for thyroid nodules,2324 with an accuracy of the cytologic analyses ranging from 50% to 90%.25 Until recently, however, some physicians in the United States have been reluctant to adopt fine needle aspiration biopsy as the initial diagnostic step in the evaluation of nodular goiter.24
659
Whenever infection is suspected as the cause of a thyroid nodule, fine needle aspiration biopsy is recommended and cytologic examination, as well as smear and culture for bacterial and fungal infection, should be done. This rapid, simple, and safe office procedure may reveal a surprising origin for a thyroid nodule. With the knowledge of tuberculosis in the thyroid gland, operative treatment can be avoided in most patients. REFERENCES 1. Barnes P, Weatherstone R: Tuberculosis of the thyroid. Br J Dis Chest 1979; 73:187-191 2. Klassen KP, Curtis GM: Tuberculous abscess of the thyroid gland. Surgery 1945; 17:552-559 3. Postlethwait RW, Berg P Jr: Tuberculous abscess of the thyroid gland. Arch Surg 1944; 48:429-437 4. Johnson AG, Philipps ME, Thomas RJS: Acute tuberculous abscess of the thyroid gland. Br J Surg 1973; 60:668-669 5. Jaffe RH: Tubercle like structures in human goiter. Arch Surg 1930; 21:717-728 6. Laohapand T, Ratanarapee S, Chantarakul N, Vitavasiri A: Tuberculous thyroiditis: A case report. J Med Assoc Thai 1981; 64:256-260 7. Crompton GK, Cameron SJ: Tuberculosis of the thyroid gland mimicking carcinoma. Tubercle 1969; 50:61-64 8. Bruns P, cited by Rankin FW, Graham AS: Tuberculosis of the thyroid gland. Ann Surg 1932; 96:625-648 9. Rodgers BM, Wolfe W, Detmer DE: Atypical mycobacterial infection of the thyroid gland. J Pediatr Surg 1975; 10:827-829 10. Lindsay LM, Mead CI: Tuberculosis of the thyroid gland with report of a case in a child aged three. Can Med Assoc J 1934; 30:373-377 11. Altemeier WA: Acute pyogenic thyroiditis. Arch Surg 1950; 61:76-85 12. Goldfarb H, Schifrin D, Graig FA: Thyroiditis caused by tuberculous abscess of the thyroid gland. Am J Med 1965; 38:825-828 13. Viranuvatti V, Viseshakul B, Chainuvat T, Chaovanapreecha K, Bhodhisuwan W, Chandrcharoensin C: Dysphagia due to tuberculosis of thyroid: A case report. J Med Assoc Thai 1980; 63:291-295 14. Kukreja HK, Sharma ML: Primary tuberculosis of thyroid gland. Indian J Surg 1982; 44:190-192 15. Cheah OSH: Tuberculosis of the thyroid gland: A case report. Med J Malays 1987; 42:127-128 16. Sachs MK, Dickenson G, Amazon K: Tuberculous adenitis of the thyroid mimicking subacute thyroiditis. Am J Med 1988; 85:573-575 17. Berger SA, Zonszein J, Villamena P, Mittman N: Infectious diseases of the thyroid gland. Rev Infect Dis 1983; 5:108-122 18. Coller FA, Huggins CB: Tuberculosis of the thyroid gland. Ann Surg 1926; 84:804-820 19. Keynes G, Camb MD: Tuberculosis of the thyroid gland. Lancet 1938; 2: 1357-1358 20. Levitt T: The status of lymphadenoid goitre, Hashimoto's and Reidels' diseases. Ann R Coll Surg 1952; 10:369-404 21. Theuer CP: Tuberculosis in patients with human immunodeficiency virus infection-Review of current concepts. West J Med 1989; 150:700-704 22. Soderstrom N: Aspiration biopsy puncture of goiter for aspiration biopsy. Acta Med Scand 1952; 144:237-244 23. Miller JM, Hamburger JI, Kini SR: The impact of needle biopsy on the pre-operative diagnosis of thyroid nodules. Henry Ford Hosp Med J 1980;
28:145-148 24. Tsung JS: Fine needle aspiration biopsy of thyroid nodules. Indiana Med 1988; 81:701-705 25. Rojeski MT, Gharib H: Nodular thyroid disease. N Engl J Med 1985; 313:428-436
o
DECEMBER 1 ggo
o
153
*
myoglobin dissociation is slower than COHb due to its increased affinity for myoglobin, a "rebound effect" with a delayed return of symptoms can occur.7 Carbon monoxide poisoning does not cause dyspnea or tachypnea until it causes hypoxemia from circulatory dysfunction or lactic acidosis from tissue hypoxia. At low levels, chronic cardiopulmonary problems, for example, angina and chronic obstructive pulmonary disease, may be exacerbated because cardiac myoglobin binds with great affinity and rapidly reduces myocardial oxygen reserve. With acute exposure, blood levels correlate with symptoms and signs but do not reflect tissue CO levels. Arterial blood gas levels are used to determine the degree of carbon monoxide intoxication and treatment.8 9 With levels less than 0.10 (10%), patients are usually asymptomatic. As the COHb concentration increases above 0.20 (20%), headache, dizziness, confusion, and nausea may develop. Chest pain due to myocardial ischemia may occur, as can cardiac arrhythmias. Coma and seizures due to cerebral edema are common with concentrations of greater than 0.40 (40%), and death is likely with more than 0.60 (60%).1°-12 The differential diagnosis includes viral illnesses, food poisoning, depression, transient ischemic attacks, coronary artery disease, arrhythmias, and functional illnesses, among others. The most common misdiagnosis is a "flulike" syndrome.9 The mainstay of therapy is supplemental oxygen and monitoring for cardiac arrhythmias. The goal of oxygen therapy is to improve the oxygen content of the blood by maximizing the fraction dissolved in plasma (Pao2)."3 The advantage of hyperbaric oxygen therapy is a more rapid reduction in COHb levels. Disadvantages of this treatment modality include few available treatment centers and the requirement for patient transport. Patients with severe neurologic or cardiovascular symptoms or very high COHb concentrations would benefit from hyperbaric oxygen, but it is these very sick patients for whom transport is most hazardous.
Once treatment begins, oxygen therapy and observation must continue long enough to rule out delayed sequelae as the carboxymyoglobin unloads. The initial presentation of our patients was consistent with gastroenteritis, for which they were given intravenous hydration and other supportive measures. We initially did not consider inhaled toxins. Once an adequate history, which included indoor cooking, and after arterial blood gas results were obtained, they were placed on 100% oxygen therapy with a complete resolution of the symptoms. They were discharged to a safe environment within three hours of the correct diagnosis. This case illustrates the importance of always considering CO poisoning when two or more patients are similarly or simultaneously sick. The diagnosis must be excluded by a directed history and physical examination. If suspicion remains, COHb testing should be done and oxygen therapy should be started empirically while results are pending. If CO poisoning is confirmed, the source must be identified and recommendations for correction or avoidance made. REFERENCES
1. Heimbach DM, Waeckerle JF: Inhalation injuries. Ann Emerg Med 1988; 17:1316-1320 2. Meredith T, Vale A: Carbon monoxide poisoning. Br Med J 1988; 296:7779 3. Myers RA, Linberg SE, Cowley RA: Carbon monoxide poisoning: The injury and its treatment. JACEP 1979 1979; 8:479-484 4. Goldbaum LR, Orellano T, Dergal E: Mechanism of the toxic action of carbon monoxide. Ann Clin Lab Sci 1976; 6:372-376
6
657
5. Petersen JE, Stewart RD: Absorption and elimination of carbon monoxide by inactive young men. Arch Environ Health 1970; 21:165-171 6. Coburn RF: Carbon monoxide body stores. Ann NY Acad Sci 1970; 174: 117. Anderson GK: Treatment of carbon monoxide poisoning with hyperbaric oxygen. Milit Med 1978; 143:538-541 8. Van Hoesen KB, Camporesi EM, Moon RE, Hage ML, Piantadosi CA: Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning? A case report and literature review. JAMA 1989; 261:10391043 9. Dolan MC: Carbon monoxide poisoning. Can Med Assoc J 1985; 133:392398 10. Larkin J, Brahos G, Moylan J: Treatment of carbon monoxide poisoning: Prognostic factors. J Trauma 1976; 16:111-115 11. Peters WJ: Inhalation injury caused by the products of combustion. Can Med Assoc J 1981; 125:249-252 12. Guy CR, Salhany JM, Eliot RS: Disorders of hemoglobin-oxygen release in ischemic heart disease. Am Heart J 1971; 82:824-832 13. Crocker PJ: Carbon monoxide poisoning, the clinical entity and its treatment: A review. Milit Med 1984; 149:257-263
Primary Tuberculous Thyroid Abscess Mimicking Carcinoma Diagnosed by Fine Needle Aspiration Biopsy MARIA LEISA C. MAGBOO, MD ORLO H. CLARK, MD San Francisco, Califomia
TUBERCULOSIS AFFECTING the thyroid gland is a rare condition. Exact figures for the incidence of tuberculosis of the thyroid are unavailable. The infection may present first in the thyroid gland or appear secondary to a tuberculous process elsewhere in the body. Barnes and Weatherstone noted that 7% of cases of miliary tuberculosis involve the thyroid gland.' The gland can also become involved with focal caseating tuberculosis, which can be blood-borne,23 or by direct extension from the larynx and cervical lymph nodes. The pathologic forms include multiple thyroidal granulomata, goiter with caseation, cold abscess, chronic fibrosing thyroiditis, and, least common, acute abscess.4 Patients present with a thyroid nodule,5 abscess,4 thyroiditis,6 or findings suggesting carcinoma7 of the thyroid gland. A tuberculous abscess of the thyroid gland as the sole manifestation of tuberculosis is even more uncommon. Swelling of the neck is the most consistent sign and dysphagia the most common complaint.3 The diagnosis of a tubercular abscess is rarely made clinically. In the case reported here, the clinical presentation suggested an undifferentiated thyroid cancer or granulomatous disease of the thyroid. Fine needle aspiration biopsy revealed milky fluid, and subsequent cultures confirmed the diagnosis preoperatively.
Report of a Case The patient, a 61-year-old, asymptomatic, married white woman, was referred to the University of California, San Francisco, Medical Center because of a right neck mass of 1/2 months' duration, clinically suggestive of anaplastic (Magboo MLC, Clark OH: Primary tuberculous thyroid abscess mimicking carcinoma diagnosed by fine needle aspiration biopsy. West J Med 1990 Dec; 153:657-659) From the Metabolic Research Unit (Dr Magboo), and the Department of Surgery (Dr Clark), University of California, San Francisco, School of Medicine, and the Department of Surgery, Veterans Administration Medical Center, San Francisco (Dr Clark). Dr Magboo is a fellow in endocrinology and metabolism. Supported in part by the Medical Research Service of the Veterans Adminis-
tration.
Reprint requests to Orlo H. Clark, MD, Surgical Faculty Practice, Ambulatory Care Center, 400 Parnassus Ave, Rm 680A, San Francisco, CA 94143.
ALERTS, NOTICES, AND CASE REPORTS
658
ALERTS,
658
ABBREVIATIONS USED IN TEXT
AIDS = acquired immunodeficiency syndrome HIV = human immunodeficiency virus
carcinoma of the thyroid. She
was on
thyroxine replace-
ment therapy following a subtotal thyroidectomy in 1958
for Graves' disease. She had otherwise been in excellent health but was upset because the referring surgeon thought by physical examination that she had an invasive thyroid cancer. On physical examination she was anxious but had a normal blood pressure (130/70 mm of mercury), pulse rate (72 beats per minute and regular), and temperature (37.6°C). She had a large, nontender, hard mass in the right lobe of the thyroid gland that was relatively fixed to the adjacent structures. There was no adjacent lymphadenopathy or overlying erythema. Laboratory test findings included a thyroxine radioimmunoassay of 75 nmol per liter (5.8 /Ag per dl [normal, 64 to 132]), free thyroxine index 4.9 (normal, 6.5 to 12), and thyroid-stimulating hormone 0.29 units per liter (normal, 0.4 to 4.8). A complete blood count included a hemoglobin of 139 grams per liter (13.9 grams per dl), hematocrit 0.41 (40.9%), and leukocyte count 7.7 x 109 per liter (7,700 per
Figure 1.-A 7.5-MHz ultrasonographic scan (longitudinal view) shows a 3.0by 2.8- by 1.6-cm mass in the right lobe af the thyroid gland. Note the hypoechoic nature of the tuberculous abscess with internal echoes.
Figure 2.-A photomicrograph of a tissue specimen from the right lobe of the thyroid gland shows acute inflammatory cells, amorphous debris, and multinucleated giant cells (original magnification x 100).
NOTICES,
AND
CASE
REPORTS
idl). The sedimentation rate was 9 mm per hour. Liver func-
tion test results and serum electrolyte levels were normal. Chest radiography was normal. A urine culture was negative for acid-fast bacilli. Ultrasonography of her neck revealed a 3.0- by 2.8- by 1.6-cm mass in the right lobe of the thyroid gland compressing the internal jugular vein (Figure 1). No thyroid gland was noted on the left side. An aspiration biopsy revealed 3 ml of milky white, odorless opalescent material. On cytologic examination there were no tumor cells and the direct smear was negative for bacteria. A month later, culture of the aspirated fluid grew Mycobacterium tuberculosis. A month after the aspiration biopsy, the patient had redness and an enlarging, nontender 5- by 3-cm mass in the right thyroid. Fine needle aspiration smears again revealed acid-fast bacilli. The patient was taken to surgery because of the abscess and presumed secondary infection, with erythema and an enlarging thyroid mass, and because of the possibility of an underlying malignant lesion. She underwent incision and drainage of a thyroid abscess with excision of necrotic muscle and part of the right lobe of the thyroid gland. During the operation there was dense brawny induration seen in the subcutaneous tissues extending almost to the skin on the right side of the neck. The muscles and the underlying portion of the thyroid gland were partially destroyed and were necrotic and hemorrhagic. All tissues were matted together so that it was difficult to identify the planes between the sternocleidomastoid muscle and the sternohyoid and sternothyroid muscles. Histologic examination showed granulomatous inflammation with multinucleated giant cells (Figure 2). A direct smear using a Kinyoun stain was positive for polymorphonuclear cells and a few acid-fast bacilli. M tuberculosis grew in the culture. The patient had an unremarkable postoperative course. She was treated with isoniazid, 300 mg per day, and rifampin, 600 mg per day, and has been well without any signs or symptoms of localized or systemic tuberculosis. She has a monogamous relationship and says she does not abuse drugs nor has she had a blood transfusion during the previous ten years.
Discussion Bruns in 1893 was the first to make the clinical diagnosis of tuberculosis of the thyroid gland in a living patient.8 The first report of a tuberculous abscess of the thyroid gland was in 1894.9 There were several reviews of this subject in the literature before 1945.2.3.10 Our patient's previous thyroid condition and surgical therapy may have been important. Altemeier in 1950 reported that half of the patients with suppurative thyroiditis also had adenomatous goiters, and in these patients the infection was localized rather than diffuse.1 In 1965 Goldfarb and co-workers reported the 28th case of a tuberculous thyroid abscess and considered it the first case of tuberculous thyroiditis proved by smears and cultures.12 Since then, single cases of tuberculous abscess ofthe thyroid gland have been reported in the Englishlanguage literature.4713-16 Confusion with thyroid cancer,67 acute staphylococcal infection,1s and subacute thyroiditis16 is common. The definitive diagnosis of tuberculosis of the thyroid gland is made by demonstrating the presence of tubercle bacilli either by histologic examination, bacterial culture, or animal inoculation. Berger and associates identified 19 cases of thyroiditis due to M tuberculosis and one case each due to Mycobacterium chelonei and Mycobacterium intracellulare.17 They noted that most of the previously diagnosed
THE WESTERN JOURNAL OF MEDICINE * DECEMBER 1990 *
153 * 6
cases were based solely on the findings of lymphocytic infiltration or granulomata that may accompany other conditions like thyroidal sarcoidosis, granulomatous syphilis, parenchymatous giant cell granulomas, Hashimoto's thyroiditis, carcinoma, and simple invagination of thyroid epithelial rests. Most of the proven cases of tuberculous involvement of the thyroid gland have been diagnosed either postoperatively or at autopsy. Of 1,200 thyroidectomies in 1926, 5 cases of tuberculous involvement were recorded by Coller and Huggins,'8 whereas 1 among 1,225 was reported by Keynes and Camb in 1918.'9 Of 20,758 tissue specimens examined at the Mayo Clinic between 1920 and 1931, only 21 showed tuberculosis of the thyroid gland.8 In 1952 Levitt and colleagues found 2 cases of tuberculous involvement of the thyroid among 2,114 partial thyroidectomies.20 Only 2 cases of tuberculosis of the thyroid were found in 74,393 thyroid specimens at an Italian center between 1941 and 1970.1
Making the diagnosis of primary tuberculosis of the thyroid is difficult, but this disorder should be considered in any patient who appears to have an invasive or undifferentiated thyroid cancer. The only initial complaint of our patient was the nodular mass in the thyroid, which was the only site clinically affected by tuberculosis. Cytologic examination of aspirate confirmed the diagnosis. Extrapulmonary tuberculosis is increasing in frequency in patients with human immunodeficiency virus (HIV)-induced immunosuppression. Patients with tuberculosis and the acquired immunodeficiency syndrome (AIDS) have high rates of extrapulmonary disease ranging from 45% to 75%.2 Patients with HIV infection are therefore more likely to have tuberculosis of the thyroid or at other extrapulmonary sites. Our patient was questioned about extramarital relationships, blood transfusions, or injections but denied any such factors for AIDS. She refused HIV testing. To our knowledge, this is the first case of primary thyroid tuberculosis presenting as a cold abscess in which the preoperative diagnosis was made by fine needle aspiration biopsy. This procedure made the diagnosis of malignancy unlikely, and tuberculosis was proved by smears and cultures. The use of fine needle aspiration has been popular in Sweden since the early 1950s.22 It is the most accurate and cost-effective screening technique for thyroid nodules,2324 with an accuracy of the cytologic analyses ranging from 50% to 90%.25 Until recently, however, some physicians in the United States have been reluctant to adopt fine needle aspiration biopsy as the initial diagnostic step in the evaluation of nodular goiter.24
659
Whenever infection is suspected as the cause of a thyroid nodule, fine needle aspiration biopsy is recommended and cytologic examination, as well as smear and culture for bacterial and fungal infection, should be done. This rapid, simple, and safe office procedure may reveal a surprising origin for a thyroid nodule. With the knowledge of tuberculosis in the thyroid gland, operative treatment can be avoided in most patients. REFERENCES 1. Barnes P, Weatherstone R: Tuberculosis of the thyroid. Br J Dis Chest 1979; 73:187-191 2. Klassen KP, Curtis GM: Tuberculous abscess of the thyroid gland. Surgery 1945; 17:552-559 3. Postlethwait RW, Berg P Jr: Tuberculous abscess of the thyroid gland. Arch Surg 1944; 48:429-437 4. Johnson AG, Philipps ME, Thomas RJS: Acute tuberculous abscess of the thyroid gland. Br J Surg 1973; 60:668-669 5. Jaffe RH: Tubercle like structures in human goiter. Arch Surg 1930; 21:717-728 6. Laohapand T, Ratanarapee S, Chantarakul N, Vitavasiri A: Tuberculous thyroiditis: A case report. J Med Assoc Thai 1981; 64:256-260 7. Crompton GK, Cameron SJ: Tuberculosis of the thyroid gland mimicking carcinoma. Tubercle 1969; 50:61-64 8. Bruns P, cited by Rankin FW, Graham AS: Tuberculosis of the thyroid gland. Ann Surg 1932; 96:625-648 9. Rodgers BM, Wolfe W, Detmer DE: Atypical mycobacterial infection of the thyroid gland. J Pediatr Surg 1975; 10:827-829 10. Lindsay LM, Mead CI: Tuberculosis of the thyroid gland with report of a case in a child aged three. Can Med Assoc J 1934; 30:373-377 11. Altemeier WA: Acute pyogenic thyroiditis. Arch Surg 1950; 61:76-85 12. Goldfarb H, Schifrin D, Graig FA: Thyroiditis caused by tuberculous abscess of the thyroid gland. Am J Med 1965; 38:825-828 13. Viranuvatti V, Viseshakul B, Chainuvat T, Chaovanapreecha K, Bhodhisuwan W, Chandrcharoensin C: Dysphagia due to tuberculosis of thyroid: A case report. J Med Assoc Thai 1980; 63:291-295 14. Kukreja HK, Sharma ML: Primary tuberculosis of thyroid gland. Indian J Surg 1982; 44:190-192 15. Cheah OSH: Tuberculosis of the thyroid gland: A case report. Med J Malays 1987; 42:127-128 16. Sachs MK, Dickenson G, Amazon K: Tuberculous adenitis of the thyroid mimicking subacute thyroiditis. Am J Med 1988; 85:573-575 17. Berger SA, Zonszein J, Villamena P, Mittman N: Infectious diseases of the thyroid gland. Rev Infect Dis 1983; 5:108-122 18. Coller FA, Huggins CB: Tuberculosis of the thyroid gland. Ann Surg 1926; 84:804-820 19. Keynes G, Camb MD: Tuberculosis of the thyroid gland. Lancet 1938; 2: 1357-1358 20. Levitt T: The status of lymphadenoid goitre, Hashimoto's and Reidels' diseases. Ann R Coll Surg 1952; 10:369-404 21. Theuer CP: Tuberculosis in patients with human immunodeficiency virus infection-Review of current concepts. West J Med 1989; 150:700-704 22. Soderstrom N: Aspiration biopsy puncture of goiter for aspiration biopsy. Acta Med Scand 1952; 144:237-244 23. Miller JM, Hamburger JI, Kini SR: The impact of needle biopsy on the pre-operative diagnosis of thyroid nodules. Henry Ford Hosp Med J 1980;
28:145-148 24. Tsung JS: Fine needle aspiration biopsy of thyroid nodules. Indiana Med 1988; 81:701-705 25. Rojeski MT, Gharib H: Nodular thyroid disease. N Engl J Med 1985; 313:428-436
