HISTORY OF PRESENT ILLNESS
The patient is a 17-year-old boy who presented with left-sided chest pain. He was well until 8 days prior to presentation when he developed left axillary and shoulder pain. The pain was worse with inspiration. He denied fever, nausea, vomiting, or diarrhea. He reported rhinorrhea and a dry cough 2 weeks prior. He had mild shortness of breath with exercise. He had no history of trauma.
The boy had a history of depression with no history of suicide attempts. He denied a history of asthma or other chronic illnesses. His family and social histories are noncontributory. He denied any drug use, but did admit to having smoked cigarettes in the past.
T 36.6°C; HR 108 bpm; RR 18-20/min; BP 120/60 mmHg; SpO2 95% in room air
Weight 50th percentile-75%; Height 75th-90th percentile
In general, he was in no acute respiratory distress. His chest examination revealed no chest wall deformity and was nontender to palpation. Breath sounds were decreased at the bases, left greater than right. No wheezes or rales were appreciated. His cardiac examination revealed normal S1 and S2 with no murmurs, rubs, or gallops heard. The remainder of his physical examination was normal.
A complete blood count revealed a WBC count of 5600 cells/mm3 with 55% segmented neutrophils, 31% lymphocytes, 11% monocytes, and 3% eosinophils. Electrolytes were normal.
COURSE OF ILLNESS
A chest roentgenogram was considered diagnostic (Figure 14-5).
FIGURE 14-5. A. Chest radiograph. B. Chest radiograph close-up.
DISCUSSION CASE 14-4
The differential diagnosis for chest pain in this adolescent boy should focus on the acute nature of his pain. In general, the most common etiologies for chest pain in the adolescent age group include psychogenic, cough, asthma, musculoskeletal pain, and pneumonia. These causes most often produce a subacute and subtle type of chest pain.
Thus, the acute onset of chest pain in this boy should focus on the differential diagnosis of a number of other causes. Certainly, tobacco use or the abuse of cocaine or methamphetamine may cause the acute onset of chest pain secondary to vaso-spasm of the coronary arteries. Pneumothorax or pneumomediastinum commonly present with the acute onset of chest pain. Some abdominal processes, such as pancreatitis or cholecystitis, may present with acute chest pain. Cardiovascular causes are less common but are life-threatening. With acute chest pain, one should consider coronary artery disease, arrhythmias, structural cardiac defects, and infections.
A chest roentgenogram revealed a left pneumothorax (Figure 14-5). The diagnosis is left spontaneous pneumothorax.
INCIDENCE, EPIDEMIOLOGY, AND PATHOPHYSIOLOGY
Pneumothoraces are divided into three groups: spontaneous, traumatic, and iatrogenic. Within spontaneous pneumothoraces, one can have either a primary or secondary event. A primary spontaneous pneumothorax occurs when there is no underlying lung disease and a secondary spontaneous pneumothorax occurs in patients with underlying lung pathology.
The incidence of primary spontaneous pneumothorax ranges between 7.4 and 18 cases per 100 000 men and between 1.2 and 6 cases per 100 000 women. It is most common in tall, lean boys between 10 and 30 years of age. Cigarette smoking increases the risk of developing a primary spontaneous pneumothorax in a dose-dependent fashion.
Secondary spontaneous pneumothoraces occur in patients with underlying lung disease. The major causes include airway disease (e.g., cystic fibrosis), infection (e.g., pneumocystis carinii pneumonia), interstitial lung disease, connective-tissue disease, malignancy, and thoracic endometriosis. The incidence of secondary spontaneous pneumothorax is 6.3 cases per 100 000 men and 2 cases per 100 000 women. Secondary spontaneous pneumothoraces have a later peak incidence at 60-65 years of age.
Subpleural bullae are seen in 76%-100% of children who are taken to video-assisted thoracoscopic surgery. There is some speculation as to the mechanism of bullae formation. It is likely that elastic fibers are degraded in the lung, which ultimately leads to an imbalance in the protease/antiprotease system and the development of bullae. A pneumothorax then develops as alveolar pressure increases with air subsequently leaking into the interstitium.
Traumatic pneumothoraces occur secondary to blunt, crush, or penetrating trauma to the chest, as a result of mechanical ventilation, or by injury from a diagnostic or therapeutic procedure.
Primary spontaneous pneumothorax usually develops while the patient is at rest. Patients describe pleuritic ipsilateral chest pain and dyspnea. With a small pneumothorax, the physical examination may be completely normal. Tachycardia may be noted. In patients with a large pneumothorax, one may see poor chest wall movement, a hyperresonant chest, and decreased breath sounds on the side with the pneumothorax. Tachycardia and hypotension indicate that the patient has developed tension physiology and requires emergent intervention.
With a large pneumothorax, the patient develops a decreased vital capacity and an increased alveolar-arterial oxygen gradient. In patients with primary spontaneous pneumothoraces, their underlying lung function is normal and, therefore, they do not develop hypercapnia. In contrast, patients with secondary spontaneous pneumothoraces by definition have underlying lung disease and are more likely to develop hypercapnia.
Chest roentgenogram. A posterior-anterior chest roentgenogram reveals the presence of a pneumothorax. Small apical pneumothoraces may be difficult to detect in this fashion, and on occasion an expiratory roentgenogram will be necessary.
Chest computed tomography (CT). A chest CT may be necessary to differentiate a bulla from a pneumothorax.
A variety of treatment options exist when managing a pneumothorax. They range from observation, simple aspiration with a catheter, chest tube insertion, pleurodesis, thoracoscopy with video-assisted thoracoscopic surgery, and thoracotomy.
Patients with small primary spontaneous pneumothoraces may be observed without intervention if there is no respiratory distress. They may be treated with supplemental oxygen to hasten the reabsorption of air. With supplemental oxygen, the air is reabsorbed at a rate of 2% per day. With larger primary spontaneous pneumothoraces, needle aspiration or chest tube insertion are required. Secondary spontaneous pneumothoraces generally require intervention as patients are usually ill due to their underlying lung disease.
The main debate with spontaneous pneumothoraces is the ability to prevent recurrences. With a primary spontaneous pneumothorax, the recurrence rate is around 30% and most will recur 6 months to 2 years after the initial event. Smoking and younger age are risk factors for recurrent disease. The recurrence rate with secondary spontaneous pneumothoraces is similar at 39%-47%.
The general consensus is to recommend preventative therapy after the second ipsilateral pneumothorax. However, patients who participate in risky activities such as scuba diving and flying should be considered for intervention after their first spontaneous pneumothorax. Options for recurrence prevention include the instillation of sclerosing agents through a chest tube and mechanical pleurodesis. With video-assisted thoracoscopic procedures, blebs can also be identified and oversewn.
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