DEFINITION OF THE COMPLAINT
Chest pain is a relatively common complaint in children with a frequency of 0.6% of pediatric emergency room visits. It occurs equally in boys and girls with a median age at presentation of 12 years. The most common causes of chest pain in children are generally benign but this complaint causes much anxiety among parents and patients due to concern for a cardiac etiology (Table 14-1).
TABLE 14-1. Common causes of chest pain in children.
In understanding the multiple causes for chest pain, one must consider the various innervation patterns that occur throughout the chest. Musculoskeletal pain is transmitted via intercostal nerves while the vagus nerve innervates the large bronchi and trachea. Pain fibers from the parietal pleura travel via intercostal nerves while the visceral pleura lacks pain fibers. Peripheral diaphragmatic disease is transmitted through intercostal fibers, and therefore can cause referred pain in the chest wall. This is in contrast to the central diaphragm, innervated by the phrenic nerve, which results in pain referred to the shoulder. The pericardium has multiple innervations including the phrenic, vagal, and recurrent laryngeal nerves, as well as the esophageal plexus. Thus, pericardial disease can present with diverse sensations and can be difficult to diagnose. Finally, cardiac pain itself transmits via the thoracic sympathetic chain and other cardiac nerves. Chest pain, therefore, is a very general term that can describe a variety of symptoms and etiologies. Only by a very careful history and physical examination can one accurately determine the cause of the patient’s discomfort.
COMPLAINT BY CAUSE AND FREQUENCY
Causes of chest pain in children can be separated by age (Table 14-2) or etiology (Table 14-3). Chest pain is classified as idiopathic in 20%-61% of cases. In terms of organic etiology, 7%-69% of cases are determined to be musculoskeletal, 13%-24% of cases are respiratory (including asthma), less than 10% of cases are psychogenic and gastrointestinal in origin, and cardiac causes are found in 5% of cases or less. Children younger than 12 years of age are more likely to have a cardiac or respiratory etiology, whereas children older than 12 years of age will more often have psychogenic causes for their chest pain. In one study, most children presented with pain duration of less than 24 hours. However, children with a nonorganic cause are more likely to have pain lasting over 6 months.
TABLE 14-2. Causes of chest pain in childhood by age.
TABLE 14-3. Causes of chest pain in childhood by etiology.
A complete history and physical examination will often reveal the diagnosis in a patient with chest pain. It is essential to have the patient describe the pain in detail: time of onset, duration, frequency, intensity, location, radiation, precipitating, and relieving factors. The patient’s activity at the time of diagnosis can often provide valuable information. The following questions may provide clues to the diagnosis:
• Is the chest pain associated with exertion, syncope, or palpitations?
—Chest pain associated with exertion, syncope, or palpitations is more concerning for cardiopulmonary disease and warrants further investigation. Chest pain with exertion may indicate exercise-induced asthma. Hypertrophic cardiomyopathy and aortic stenosis should always be considered in children presenting with chest pain on exertion. In children with anomalous coronary arteries, there may be insufficient coronary blood flow during exercise, causing symptoms to manifest at this time. In some cases, syncope may also occur. Palpitations may indicate an underlying arrhythmia such as supraventricular tachycardia or ventricular tachycardia.
• How is the pain characterized?
—Pain that is worse on inspiration or coughing but is poorly localized may indicate pleural or pulmonary pathology, whereas similar pain that is well localized and elicited on palpation is usually related to a chest wall etiology. Cardiac pain may be described as squeezing or pressure-like in quality, and may radiate to the left arm or neck. Midsternal pain may come from the esophagus, particularly if it worsens when supine. Kehr sign, or acute pain felt in the shoulder, may represent blood in the peritoneal cavity. Finally, psychogenic pain may be nonspecific in location and vague in quality.
• Is there a family history of sudden death?
—Hypertrophic cardiomyopathy is inherited in an autosomal dominant fashion, so there may be a family history of sudden death. These patients may have a murmur that is augmented with standing or a Valsalva maneuver. Furthermore, their chest pain may be most severe with exercise. In congenital hyperlipidemia, patients may present at a young age with myocardial infarction and have a family history of sudden death.
• Is the pain relieved with changes in position?
—Patients with pericarditis often have stabbing precordial pain that worsens while lying down and improves with sitting and leaning forward. These patients are often febrile, have a friction rub that is best heard while the patient leans forward, and may also have distant heart sounds, jugular venous distension, and pulsus paradoxus.
• Is there a history of precipitating trauma?
—In the trauma patient, tachycardia and hypotension may be secondary to a hemothorax or other vascular injury. In patients with poor perfusion and decreased cardiac output, one should consider myocardial contusion, tension pneumothorax, and cardiac tamponade.
• Is there a prior history of cardiorespiratory disease?
—Patients with a history of asthma, cystic fibrosis, and connective tissue disorders have an increased risk of pneumothorax and pneumomediastinum.
• Can the pain be reproduced on physical examination?
—Musculoskeletal pain generally can be elicited by palpation of the chest wall. Costochondritis, most commonly seen in teenage girls, is associated with palpable pain over the costal cartilage. Muscle strain, which may result from cough or new/vigorous physical activity, will generally have palpable pain over the affected muscle.
• Does the child have fever?
—Fever is a nonspecific sign that may be present with pneumonia, pericarditis, myocarditis, endocarditis, or pleurodynia (most often caused by infection with coxsackievirus B).
• Is the child taking any medications?
—Oral contraceptives increase the risk of pulmonary embolism. Steroids and nonsteroidal antiinflammatory medications increase the risk for gastritis. Iron, tetracyclines, and nonsteroidal antiinflammatory agents among others may cause pill esophagitis.
• Does the pain relate to meals?
—Chest pain from gastroesophageal reflux commonly occurs after meals.
• Have there been any recent stressors in the patient’s life?
—Psychogenic chest pain may occur in patients with recent major stressful events in their lives. These patients often have multiple somatic complaints in addition to chest pain. A family history of depression or a somatization disorder increases the likelihood that a child will develop psychogenic pain.
• Does the pain wake the child from sleep?
—Children who awake from sleep secondary to chest pain are more likely to have an organic etiology.
• Is there a history of substance use or abuse?
—Tobacco use may be associated with a chronic cough and chest pain. Cocaine and methamphetamine abuse may lead to coronary artery vaso-spasm and ischemic chest pain.
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2. Thull-Freedman J. Evaluation of chest pain in the pediatric patient. Med Clin North Am. 2010;94(2):327-347.
3. Tunnessen WW. Chest pain. In: Tunnessen WW, Roberts KB, eds. Signs and Symptoms in Pediatrics. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 1999:361-369.
4. Kocis KC. Chest pain in pediatrics. Pediatr Clin North Am. 1999;46(2):189-203.
5. Lin CH, Lin WC, Ho YJ, Chang JS. Children with chest pain visiting the emergency department. Pediatr Neonatol. 2008;49(2):26-29.
HISTORY OF PRESENT ILLNESS
The patient is a 17-year-old boy who was in good health until 3 days prior to his admission. At that time, he fell while playing basketball and noted some pain in his right thigh. He also complained of shortness of breath and chest discomfort when lying flat. He denied fever, rash, joint pains, and cough.
Bilateral inguinal hernia repairs were performed in infancy, but he has no history of other hospitalizations. He was not taking any medications. A paternal uncle required a renal transplant at 43 years of age for an unknown diagnosis. A maternal grandmother has systemic lupus erythematosus.
T 37.2°C; HR 92 bpm; RR 20/min; BP 151/66 mmHg; SpO2 100% in room air
Weight 50th percentile; Height 75th percentile
Initial examination revealed a teenage boy who was awake and alert and in no respiratory distress. A rash was distributed across his nose and cheeks. The rash consisted of erythematous patches with keratotic scaling (Figure 14-1). His chest examination demonstrated decreased breath sounds at the right base. No wheezes or rales were noted. His cardiac examination was significant for slightly diminished heart sounds but no murmurs or rubs. His right thigh was swollen with a circumference 6 cm greater than the left thigh. He also had swelling of his right calf, which was 2 cm greater than the left calf. Flexion of the right knee was limited and there was mild calf pain with dorsiflexion of the right foot. The remainder of his physical examination was normal.
FIGURE 14-1. Rash on the face.
Laboratory analysis revealed a peripheral blood count with 6000 WBCs/mm3 with 79% segmented neutrophils and 14% lymphocytes. Hemoglobin was 12.9 g/dL and the platelet count was 156 000/mm3. An erythrocyte sedimentation rate was elevated at 101 mm/h. Prothrombin and partial thromboplastin times were 13.6 and 31.9 seconds, respectively. Urinalysis revealed large blood and 3+ protein. A Doppler ultrasound of the right lower extremity revealed a thrombus extending from the superficial femoral vein to the calf vein.
COURSE OF ILLNESS
The patient was admitted and treated with intravenous heparin at 20 units/kg/h for his deep vein thrombosis (DVT) and with furosemide for his hypertension. A chest roentgenogram in conjunction with further laboratory work suggested an underlying condition that predisposed to this presentation (Figure 14-2).
FIGURE 14-2. Chest radiograph.
Chest pain in children and adolescents is rarely life-threatening. The majority of cases of chest pain in these age groups are classified as idiopathic. Among adolescents, the most common nonidiopathic etiologies include psychogenic, cough, asthma, pneumonia, and musculoskeletal pain. Less common etiologies include trauma, drug use or abuse, gastroesophageal reflux, and pneumothorax. Cardiac etiologies are exceedingly uncommon, but should be considered in certain clinical situations, such as patients with syncope and exertional or positional symptoms.
This patient has many physical and laboratory findings that warrant further evaluation. The two most worrisome findings include his chest pain when supine and his deep venous thrombosis. Shortness of breath and chest pain that worsens while lying supine suggests possible pericardial disease. The development of deep venous thrombosis in an otherwise healthy adolescent is extremely uncommon. In this situation one should suspect underlying hypercoagulable disorders. Finally, this DVT in conjunction with shortness of breath and chest pain suggest a pulmonary embolus as a possible diagnosis.
The chest roentgenogram revealed blunting of the right costophrenic angle, suggesting a small right pleural effusion, and cardiomegaly (Figure 14-1). An echocardiogram demonstrated a small-to-moderate-sized pericardial effusion that accounted for the finding of cardiomegaly on the chest radiograph. A ventilation-perfusion (VQ) scan suggested a low probability of pulmonary embolus.
As his hospitalization progressed, his hemoglobin dropped acutely to 10.3 g/dL and Coombs positive warm antibodies were demonstrated. A 24-hour urine collection demonstrated 8.5 g protein/day. Antinuclear antibody titer was elevated at 1:1280 and complement C3 and C4 were decreased. Autoantibody studies were positive including anti-Smith, anti-RNP, anti-SSA, anti-SSB, anti-SCL 70, and anti-JO 30. As part of his hypercoagulable work up, he was found to have anticardiolipin antibodies and antiphospholipid antibodies.
These laboratory values along with his clinical picture, including the rash, suggested the underlying diagnosis of systemic lupus erythematosus (SLE). He was treated with prednisone for his nephritis. After a period of time, his anticoagulation was changed to low-molecular weight heparin and he was discharged home on the tenth day of hospitalization.
INCIDENCE AND EPIDEMIOLOGY
SLE is a multisystemic autoimmune disorder that can present in children and adolescents. Determining the incidence of SLE in children is difficult with minimal data. However, national registries in Canada and Finland have suggested a mean annual incidence of 0.36/100 000 and 0.37/100 000, respectively. Studies in the United States have suggested an annual incidence of 0.53-0.60/100 000.
SLE rarely develops before the age of 5, and most commonly has its onset during adolescence. Girls are more commonly affected than boys with a ratio of approximately 5:1. There is a suggestion of a higher incidence in African-Americans followed by Hispanic children/adolescents.
SLE has a quite variable presentation, with children often having more severe presentations than adults. The most common presenting signs and symptoms overall include fever, arthralgias or arthritis, rashes, lymphadenopathy, hepatosplenomegaly, malaise, and weight loss. However, almost all organ systems have the potential for involvement.
Constitutional symptoms are common at diagnosis and with disease flares. Cutaneous findings may include the classic butterfly rash, discoid rash, or even mucosal ulcerations. Arthralgias and arthritis as well as aseptic necrosis of the femoral head may occur. Classic cardiac findings may include pericarditis, pericardial effusions, myocarditis, and Libman-Sacks endocarditis. Pulmonary manifestations occur in approximately 50% of patients. Both pleural and parenchymal involvement can occur with pleuritis and pneumonitis most often seen. Neurologic findings include seizures, psychosis, cerebrovascular accidents, peripheral neuropathies, and pseudotumor cerebri. Ocular findings includes papilledema and retinopathy. From a hematologic standpoint, patients with SLE are at a higher risk for the development of the antiphospholipid syndrome placing them at high risk of thromboembolic events. Finally, renal disease is also common with the development of glomerulonephritis, nephrotic syndrome and hypertension. These renal manifestations are probably the major prognostic factors in patients with SLE.
With such a variable presentation, attempts have been made to provide criteria for the diagnosis of SLE. The American College of Rheumatology updated the criteria for the diagnosis of SLE in 1997 (Table 14-4).
TABLE 14-4. American College of Rheumatology diagnostic criteria for systemic lupus erythematosus. 4
*Diagnostic for systemic lupus erythematosus if four or more criteria are present
In general, patients with a minimum of 4 of the 11 criteria are diagnosed with SLE. The criteria can present serially or simultaneously and during any interval of observation. In childhood, this has a sensitivity of 96% and a specificity of 100%.
Acute-phase reactants. Most acute-phase reactants will be elevated in lupus exacerbations, including erythrocyte sedimentation rate, serum ferritin levels, and a hypergammaglobulinemia.
Hematologic studies. Approximately 50% of children with SLE will have anemia of chronic disease.
Other findings include an acute hemolytic anemia, leukopenia and thrombocytopenia. As mentioned previously, a high proportion of SLE patients will have a hypercoagulable state with the presence of antiphospholipid antibodies.
Autoantibodies. The majority of SLE patients will have detectable antinuclear antibodies. Those antinuclear antibodies that can be seen in SLE include anti-dsDNA, anti-DNP, anti-Ro (SS/A), anti-La (SS/B), anti-Sm and anti-histone antibodies. Various other autoantibodies include antierythrocyte, antilymphocytotoxic, antitissue specific, antiphospholipid antibodies as well as rheumatoid factors. In terms of diagnosis, antibodies against dsDNA are considered pathognomonic of SLE.
Complement levels. Decreased complement levels are particular indicators of active disease in SLE. One can measure either complement components C3 and C4 or total hemolytic complement, as measured by CH50 (ability of a test sample to hemolyze 50% of antibody coated erythrocytes).
Urinalysis. The most common abnormality on a urinalysis in SLE is proteinuria. Hematuria and RBC casts also occur. Further tests to evaluate for lupus nephritis include creatinine clearance, glomerular filtration rate studies, renal ultrasonography, and biopsy.
There is no standard protocol to treat patients with SLE, as each child has a variable presentation. The primary goal is to prevent exacerbations, rather than treat each flare episodically. Certain recommendations are universal including the need to avoid exposure to excessive sunlight.
A variety of pharmacologic agents are available to treat symptoms of SLE. Nonsteroidal antiinflammatory agents are typically used for the treatment of musculoskeletal complaints. Patients with anticardiolipin antibodies often receive low-dose aspirin to decrease the risk of thromboembolisms. Hydroxychloroquine can be very effective in conjunction with glucocorticoids to minimize disease exacerbations. However, these agents may not always be effective in controlling the disease and other immunosuppressive agents such as azathioprine, cyclophosphamide, and methotrexate may be needed.
1. Hiraki LT, Benseler SM, Tyrrell PN, Hebert D, Harvey E, Silverman ED. Clinical and laboratory characteristics and long-term outcomes of pediatric systemic lupus erythematosus: a longitudinal study. J Pediatr. 2008;152:550-556.
2. Lawrence EC. Systemic lupus erythematosus and the lung. In: Lahita RG, ed. Systemic Lupus Erythematosus. New York: Academic Press; 1987:691-708.
3. Petty RE, Cassidy JT. Systemic lupus erythematosus. In: Cassidy JT, Petty RE, eds. Textbook of Pediatric Rheumatology. 4th ed. Philadelphia: WB Saunders, 2001:396-438.
4. Tucker LB. Caring for the adolescent with systemic lupus erythematosus. Adol Med: State of the Art Reviews. 1998;9:59-67.
5. Tan EM, Cohen AS, Fries JF, Masi AT, McShane DJ, Rothfield NF, et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum. 1982;25:1271-1277.
6. Hochberg MC. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus [letter]. Arthritis Rheum. 1997;40:1725.
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.
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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.
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HISTORY OF PRESENT ILLNESS
The patient is a 20-year-old boy with a history of spina bifida. Six days prior to admission he reported fatigue and was unable to leave his house. During the next few days, he developed a fever, sore throat, and myalgias. Two days prior to admission, he noted increasing shortness of breath which was worse while lying supine. He described a “pounding” discomfort in his chest.
The boy was born at full term and found to have a meningomyelocele at birth. His spinal defect was at L3 and he underwent surgical correction when he was 4 days old. A ventriculoperitoneal (VP) shunt was placed in the first weeks of life. He has required several shunt revisions due to obstruction. The last revision was 6 years ago. He also has a history of bilateral club feet. Four months prior to admission he was diagnosed with pelvic osteomyelitis related to extension of a gluteal ulcer. He was treated with surgical debridement and 3 months of intravenous antibiotics.
He is able to walk with a brace and has a mild intellectual disability. At the time of presentation, he was not taking any medication. He had a tattoo drawn on his arm 2 weeks prior. There is a family history of asthma in his mother, and his father died at age 40 of a myocardial infarction.
T 41.3°C; HR 138 bpm; RR 20/min; BP 113/80 mmHg; Oxygen saturation, 98% in room air
In general, he was an obese young boy in moderate respiratory distress. His oropharyngeal examination revealed an exudative pharyngitis. His cardiac examination revealed a normal S1 and S2 without murmur, rub, or gallop. His physical examination was otherwise unremarkable.
The complete blood count revealed a WBC count of 13 500 cells/mm3 with 42% segmented neutrophils, 26% lymphocytes, 18% atypical lymphocytes, and 1% monocytes. The hemoglobin was 11.3 gm/dL, and his platelets were 133 000/mm3. Electrolytes, blood urea nitrogen, and glucose were within normal limits. A serum creatinine was slightly elevated at 1.1 mg/dL. Total bilirubin was elevated at 4.0 mg/dL with an unconjugated fraction of 2.3 mg/dL. Aspartate aminotransferase and alanine amino-transferase were 246 U/L and 130 U/L, respectively. Erythrocyte sedimentation rate was mildly elevated at 44 mm/h. A chest roentgenogram revealed normal heart size and no pulmonary infiltrates.
COURSE OF ILLNESS
Prior to his arrival at the hospital, the patient was administered adenosine twice for tachycardia with heart rate above 160 bpm. This did not have any significant effect. On arrival in the emergency department, his chest pain resolved and his electrocardiogram abnormalities resolved. An echocardiogram demonstrated a shortening fraction of 28% and no wall motion abnormalities.
The boy was evaluated for a possible myocardial infarction, given his family history. His cardiac enzymes remained normal. He developed bilious emesis believed to be secondary to his hepatitis. He had a repeat electrocardiogram (Figure 14-4) and echocardiogram on arrival in the intensive care unit. The electrocardiogram suggested a diagnostic category and the specific cause was suggested by the initial laboratory testing and confirmed later by serologic testing.
FIGURE 14-4. Electrocardiogram.