PRATICHI K. GOENKA
HISTORY OF PRESENT ILLNESS
The patient, a 15-year-old boy, was well until 1 week ago. At that time, he developed the acute onset of chest pain accompanied by fever and chills. He described the pain as sharp and intermittent. It was mid-sternal and did not radiate. The pain did not increase with exertion, but was worse while lying supine or with subtle movement. He denied any syncope, shortness of breath, or diaphoresis. He did not have night sweats, cough, or weight loss.
The boy had no significant medical history. He emigrated from Liberia 6 weeks prior to his presentation. He had received bacille Calmette-Guerin immunization 5 years prior and was noted to have a 12 mm induration after tuberculin skin testing (purified protein derivative; PPD) on arrival in the United States.
T 36.8°C; HR 80 bpm; RR 24/min; BP 111/64 mmHg
Weight 25th to 50th percentile
In general, he was a lean boy in no acute distress. His cardiac examination revealed a normal S1 and S2 with a regular rate and rhythm. No cardiac murmur was appreciated. His chest examination demonstrated clear breath sounds bilaterally. His liver edge was minimally palpated just below his right costal margin. The remainder of his physical examination was within normal limits.
The complete blood count revealed a WBC count of 6800 cells/mm3. The hemoglobin was 12.8 gm/dL and the platelet count was 426 000/mm3. Serum electrolytes, blood urea nitrogen, and creatinine were normal. Calcium, albumin, AST, alkaline phosphatase, total bilirubin and prothrombin and partial thromboplastin times were also normal. Lactate dehydrogenase was elevated at 904 U/L. A chest roentgenogram (Figure 14-3A) was initially interpreted as normal.
FIGURE 14-3. A. Chest radiograph. B. Chest CT.
COURSE OF ILLNESS
The patient was then discharged home with ibuprofen for his chest pain. The chest roentgenogram (Figure 14-3A) was reviewed the following day and the interpretation revised. Computed tomography of the chest also revealed significant abnormalities (Figure 14-3B).
DISCUSSION CASE 14-2
Chest pain in an adolescent boy is rarely life-threatening. However, a careful history and physical examination must be undertaken to determine which cases require further investigations.
The majority of cases of chest pain in childhood are classified as idiopathic. Adolescents are more likely to have psychogenic causes for their chest pain than younger children, with this diagnosis being more common in girls. Musculoskeletal causes are quite common, including muscle strain, trauma, and costochondritis. Other common etiologies can include cough, asthma, and pneumonia. Less commonly, chest pain in adolescents is caused by gastroesophageal reflux, pneumothorax, pneumomediastinum, or pleural effusion. In an adolescent with chest pain, it is important to inquire about tobacco, cocaine, and methamphetamine use as these all can be associated with chest pain. In adolescent girls, one should consider pubertal breast development or fibrocystic breast disease, and in boys gynecomastia. Rarely, but importantly, one should consider cardiovascular causes of chest pain including structural diseases (e.g., idiopathic hypertrophic cardiomyopathy), coronary artery disease, myocarditis, pericarditis, and arrhythmias.
The features of this case that warrant further evaluation include the acute onset of chest pain as well as variability with positional changes.
The chest roentgenogram revealed numerous small cystic spaces with increased interstitial and air space opacities in the left upper lobe (Figure 14-3A). The chest CT revealed dense consolidation in the left upper lobe containing cavitary lesions and air bronchograms (Figure 14-3B); an additional focus of consolidation is seen in the left lower lobe. An echocardiogram performed demonstrated a 10 mm circumferential pericardial effusion with nodular areas noted alongside the myocardial surface. Electrocardiogram revealed ST elevation. A repeat PPD demonstrated a 19 mm area of induration. The patient underwent pericardial window placement with pericardial biopsy. Stains of pericardial fluid were negative for acid-fast bacilli but microscopic examination of the pericardial tissue revealed numerous granulomas and acid-fast smear of the tissue demonstrated organisms. Mycobacterium tuberculosis was detected from culture of the pericardial tissue 12 days after inoculation. The diagnosis is tuberculosis complicated by tuberculous pericarditis. He was treated with isoniazid, rifampin, pyrazin-amide, and ethambutol.
Sputum was acid-fast stain and acid-fast culture was negative. His family refused human immunodeficiency virus (HIV) testing. He was ultimately discharged home to complete his treatment under directly observed therapy.
INCIDENCE AND EPIDEMIOLOGY
Mycobacterium tuberculosis infections are the most frequent cause of death worldwide due to a single infectious organism. Approximately one-third of the world’s population has been infected with M. tuberculosis. Generally, infection occurs through inhalation of droplet nuclei and cause pulmonary infections. The HIV epidemic has significantly increased the infection rate worldwide.
Pericarditis may be due to infectious or non-infectious causes (Table 14-5). Pericarditis, an uncommon complication of tuberculosis infection, can be fatal even with proper diagnosis and treatment. Tuberculous pericarditis occurs by extension of an adjacent focus of infection. This may include mediastinal or hilar nodes, lung, spine, or sternum. It occurs less commonly in association with miliary tuberculosis.
TABLE 14-5. Most common causes of pericarditis.
Tuberculous pericarditis is believed to occur in 0.4%-4% of children with tuberculosis. The prevalence of tuberculosis varies among geographic regions. Certainly, its relationship to HIV disease is well known. In many African countries where tuberculosis and HIV are endemic, pericarditis in an HIV-positive patient is tuberculosis until proven otherwise.
The presentation of pericarditis varies depending on the cause. The pain associated with pericarditis is often retrosternal, radiating to the shoulder and neck. The pain is typically worsened by deep breathing, swallowing, and supine positioning. Tuberculosis pericarditis can have both acute and insidious presentations. The most common symptoms include cough, dyspnea, and chest pain, as described earlier. Other associated symptoms may include night sweats, orthopnea, weight loss, and edema. Physical examination may reveal fever, tachycardia, and pericardial rub. Pulsus paradoxus, hepatomegaly, pleural effusions, and muffled heart sounds are often associated with the condition.
The diagnosis of pericarditis is straightforward but establishing M. tuberculosis as the etiologic agent is more challenging.
Tuberculin skin test. A positive skin test increases the suspicion for tuberculosis pericarditis, but a negative skin test does not eliminate the diagnosis.
Chest imaging. Chest radiograph will generally reveal cardiomegaly due to pericarditis and pericardial effusions. Approximately 40% of patients with tuberculous pericarditis will have an associated pleural effusion. Patients with tuberculous pericarditis may also have findings suggestive of pulmonary or miliary tuberculosis.
Electrocardiogram. Electrocardiogram is abnormal in most cases of pericarditis, reflecting pericardial inflammation. ST-segment elevations develop early in the illness. Large pericardial effusions are associated with reduced QRS voltage. Other ECG findings include PR depression or electrical alter-nans if pericardial effusion is also present.
Echocardiogram. Echocardiogram detects associated pericardial effusions and pericardial thickening. Patients with tuberculous pericarditis may have nodular densities along the pericardium.
Pericardiocentesis and pericardial biopsy. Acid-fast stains of pericardial fluid are often negative, however, pericardial fluid cultures are positive for M. tuberculosis in approximately 50% of cases. Polymerase chain reaction testing to detect M. tuberculosis has been attempted but the reliability of this test in pericardial fluid specimens is not clear. Granulomas detected on microscopic examination of pericardial tissue strongly suggest the diagnosis of tuberculous pericarditis. Pericardial tissue is usually acid-fast stain and culture positive and is considered critical to confirming the diagnosis. This will yield the most accurate results if the pericardial tissue is obtained prior to the start of antituberculous therapy.
HIV test. Due to the close association of HIV and tuberculous pericarditis, HIV testing should be performed in all patients diagnosed with tuberculous pericarditis.
If the patient has hemodynamic compromise, pericardiocentesis is indicated. Certainly, in cases of tamponade this is necessary. A second option for drainage is an open surgical procedure, which allows for removal of the pericardial fluid as well as obtaining pericardial tissue for culture and histopathologic study. Controversy does exist as to whether in uncomplicated cases, pericardiocentesis versus open drainage should be the procedure of choice in suspected tuberculous pericarditis. Either way, one must strive to prevent the formation of a constrictive pericarditis.
Antibiotic therapy consists of the same regimens as for pulmonary tuberculosis. Adjuvant corticosteroid therapy appears to decrease the amount of effusion and reaccumulation of pericardial fluid, reducing the need for repeated interventions. Long-term complications of tuberculous pericarditis include constrictive pericarditis.
1. Dooley DP, Carpenter JL, Rademacher S. Adjunctive corticosteroid therapy for tuberculosis: a critical reappraisal of the literature. Clin Infect Dis. 1997;25:872-877.
2. Gewitz MH, Vetter VL. Cardiac emergencies. In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 4th ed. Baltimore, Maryland: Lippincott Williams &Wilkins; 2000:659-700.
3. Haas DW. Mycobacterium tuberculosis. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 5th ed. Philadelphia: Churchill Livingstone; 2000:2576-2604.
4. Starke JR. Tuberculosis. In: McMillan JA, DeAngelis CD, Feigin RD, Warshaw JB, eds. Oski’s Pediatrics: Principles and Practice. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 1999:1026-1039.
5. Trautner BW, Darouiche RO. Tuberculous pericarditis: optimal diagnosis and management. Clin Infect Dis. 2001;33:954-961.