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11. PNEUMOTHORAX 11. PNEUMOTHORAX PLEURAL DISEASES SERIES 08 PLEURAL DISEASES SERIES 08 BY WIDIRAHARDJO BY WIDIRAHARDJO
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11. PNEUMOTHORAX

PLEURAL DISEASES SERIES 08 BY WIDIRAHARDJO

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Pneumothorax is air in the pleural space. Pneumothoraces can be divided into: 1. Spontaneous pneumothoraces, which occur without antecedent trauma or other obvious cause, divided into primary and secondary spontaneous pneumothoraces. 2. Traumatic pneumothoraces, which occur from direct or indirect trauma to the chest. A subcategory of traumatic pneumothotax is iatrogenic pneumothorax.

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PRIMARY SPONTANEOUS PNEUMOTHORAX Incidence In the United States, 7.4/100,000/year for men and 1.2/100,000/year for women. In the United Kingdom, the incidence in males and females aged 15 to 34 was 37.0 and 15.4/100,000/year, respectively. Etiologic Factors Results from rupture of subpleural blebs that are usually located in the apices of the lung. The pathogenesis of these subpleural blebs is probably related to airway inflammation by cigarette smoking.

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Spontaneous pneumothoraces were more likely to develop following days when there are broad swings in the atmospheric pressure, thunderstorms, loud music. Usually in taller and thinner man. There is a familial tendency for the development of primary spontaneous pneumothorax, inheritance was either autosomal dominant with incomplete penetrance or X-linked recessive, also patients with human leukocyte antigen (HLA) haplotype A2, B40.

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There is a very high prevalence of bronchial abnormalities in nonsmoking patients with spontaneous pneumothorax, such as: - Disproportionate bronchial anatomy (smaller than normal dimensions and deviating anatomic arrangements of the airways at various locations), - Accessory bronchus, - Missing bronchus.

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Clinical Manifestations The peak age for the occurrence of a primary spontaneous pneumothorax is the early 20s. The main symptoms are an acute onset and localized chest pain and dyspnea. Horner's syndrome has been reported as a rare complication and is thought to be due to traction on the sympathetic ganglion produced by shift of the mediastinum. Usually develops while the patient is at rest.

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Changes on Physical Examination Vital signs usually normal, with the exception of a moderate tachycardia. A tension pneumothorax should be suspected if the pulse rate exceeds 140 or if hypotension, cyanosis, or electromechanical dissociation is present.

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The chest reveals the side with pneumothorax is larger than the contralateral side and moves less during the respiratory cycle. Tactile fremitus is absent. The percussion note is hyperresonant. The breath sounds are absent or reduced on the affected side. The trachea may be shifted toward the contralateral side. The lower edge of the liver may be shifted inferiorly.

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Electrocardiographic Changes In patients with spontaneous left pneumothorax: - Rightward shift of the frontal QRS axis. - Diminution of precordial R voltage. - Decrease in QRS amplitude. - Precordial T-wave inversion. In patients with right-sided pneumothorax: - Prominent R-wave voltage in lead V2 with loss of S-wave voltage. - Reversible reduced QRS voltage. - Marked PR-segment elevation in the inferior leads with reciprocal PR-segment depression in aVR. - Pronounced STsegment elevation in II, III, aVF, and V4-6.

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Diagnosis In a young, thin, tall man, the diagnosis is usually suggested by the clinical history and physical examination. The diagnosis is established by demonstrating a pleural line on the chest radiograph. Chest CT scans are not routinely indicated since there is no close correlation between the presence of subpIeural blebs and the recurrence of pneumothorax.

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Quantitation One should estimate the amount of lung collapse when treating a patient with a pneumothorax. Light index: % pneumothorax (diameter lung)3 = 100 {1 } (diameter hemithorax)3

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The British Thoracic Society's (BTS) guidelines for the management of spontaneous pneumothorax: small pneumothoraces were defined as those in which the rim of air between the pleura and the chest wall was less than I cm, moderate as 1 to 2 cm and large as greater than 2 cm.

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Recurrence Rates The recurrence rate was 54.2%, the recurrence rates were less in men (46%) than in women (71%) and were less in individuals who stopped smoking (40%) than in those who continued smoking (70%). There was no significant relationship between the size of the pneumothorax or the treatment pneumothorax and the recurrence rates.

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Most recurrences occur within the first year. If one could predict which patients are more likely to have a recurrence, those patients could be treated more aggressively at the time of their first pneumothorax. Treatment Therapy have two goals: (a) To rid the pleural space of its air, (b) To decrease of recurrence.

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Several treatments can be used: 1. Supplemental oxygen; 2. Observation; 3. Simple aspiration; 4. Tube thoracostomy with or without the instillation of a sclerosing agent; 5. Medical thoracoscopy with insufflation of talc; 6. Video-assisted thoracoscopy with stapling of blebs, instillation of a sclerosing agent, or pleural abrasion; 7. Open thoracotomy. It should be remembered that a primary spontaneous pneumothorax is mainly a nuisance and is rarely life threatening to the patient.

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Autologous Blood Patch for Persistent Air Leak With this technique, 50 ml, of blood is drawn from a vein and then promptly injected, without anticoagulation, through the chest tube into the pleural space. Air leaks ceased in 78% of patients at 48 hours. There were no recurrences during a follow-up of 12 to 48 months.

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Intrapleural Fibrin Glue for Persistent Air Leak The large amount of diluted fibrin glue might be effective in patients with persistent air leaks. The air leaks ceased within 12 hours of injection. During the follow-up period of 2.5 to 6.5 years, the pneumothorax recurred in 12.5%.

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SECONDARY SPONTANEOUS PNEUMOTHORAX Secondary spontaneous pneumothoraces are more serious than primary spontaneous pneurnothoraces because they decrease the pulmonary function of a patient with already compromised pulmonary function.

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Incidence The incidence is similar to that of primary spontaneous pneumothorax, it was 6.3 and 2.0/100,000/ year for men and women in US. In the United Kingdom, the incidence for males and females above 55 was 32.4 and 10.9/100,000/year.

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Etiologic Factors Most secondary spontaneous pneumothoraces are due to COPD, although almost every lung disease has been reported to be associated with secondary spontaneous pneumothorax, such as: tumor, sarcoidosis, tuberculosis, other pulmonary infections, and miscellaneous.

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Clinical Manifestations The clinical symptoms are more severe. Most patients with secondary spontaneous pneumothorax have dyspnea, which frequently seems out of proportion to the size of the pneumothorax, chest pain and hypotension. A mortality rate was 16%. Causes of death included sudden death before chest tubes could be inserted, respiratory failure within the first 24 hours of treatment, late respiratory failure, and massive gastrointestinal bleeding.

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The physical examination of patients are less helpful, because side-to-side differences may not be apparent. The possibility of a pneumothorax should be considered in any patient with COPD who has increasing shortness of breath, particularly if chest pain is also present.

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Diagnosis The diagnosis is established by the chest radiograph. If there is any doubt as to whether the patient has a pneumothorax or a giant bulla, CT scan should be obtained. It is important to make the distinction between a large bulla and a pneumothorax, because only the pneumothorax should be treated with tube thoracostomy.

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Recurrence Rates The recurrence rates appear higher than those for primary spontaneous pneumothorax. It is about 44%

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Treatment The goals of treatment are to rid the pleural space of air and to decrease the recurrence. The treatment options are usually the same as those for a patient with a primary spontaneous pneumothorax, but differ in the following ways (even if the pneumothorax is small): 1. Initially should be hospitalized and managed by tube thoracostomy.

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2. Aspiration is not recommended because it is less likely to be successful and does nothing to diminish the likelihood of a recurrence. It is recommended that attempts be made to prevent the recurrence of a pneumothorax, by VATS, medical thoracoscopy, mini-thoracotomy, or the instillation of a sclerosant through the chest tube.

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Lung transplantation should be considered if the patient has a disease such as LAM, cystic fibrosis, interstitial pulmonary fibrosis, or COPD. If the lung does not expand within 72 hours or if there is a persistent air leak for more than 3 days, strong consideration should be given to performing VATS or medical thoracoscopy.

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PNEUMOTHORAX SECONDARY TO TUBERCULOSIS All patients with pneumothorax secondary to tuberculosis should be treated with tube thoracostomy. In one older series were treated by observation or repeated pleural aspiration, 64% died. In contrast, patients who treated with chest tubes, 6% died. Once chest tubes are placed, the duration of tube thoracostomy ranged from 5 days to 6 months, with a mean duration of 50 days.

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CATAMENIAL PNEUMOTHORAX A catamenial pneumothorax occurs in conjunction with menstruation and is usually recurrent. The initial pneumothorax usually does not occur until the woman is in her twenties. Classically develop chest pain and sometimes dyspnea within 24 to 48 hours of the onset of the menstrual flow.

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Usually right sided, but left-sided and even bilateral. The pathogenesis of catamenial pneurnothorax is not definitely known, may be the air gained access to the peritoneal cavity during menstruation and then entered the pleural cavity through a diaphragmatic defect, because their initial patient had a diaphragmatic defect, or had diaphragmatic endometriosis.

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The others concluded that the most plausible explanation was leakage of air from the lung owing to subpleural endometrial implants. The medical treatment of catamenial pneumothorax is aimed at treating the endometriosis by suppressing the ectopic endometrium by administering gonadotropin-releasing hormone antagonists. The recurrence rate for patients on hormonal therapy exceeds 50%.

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The surgical treatment for catamenial pneumothorax is thoracoscopy with closure of the diaphragmatic defects, stapling of any blebs in the lung, and pleural abrasion. Thoracotomy with partial pleurectomy and plication of the diaphragm, if thoracoscopy fail or unavailable. Some cases bilateral tubal ligation is recommended.

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IATROGENIC PNEUMOTHORAX The major causes of iatrogenic pneumothorax are: - Transthoracic needle aspiration - Subclavian needle stick - Thoracentesis - Transbronchial biopsy - Pleural biopsy - Positive-pressure ventilation - Supraclavicular needle stick - Nerve block

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At present, the leading cause of iatrogenic pneumothorax is transthoracic needle aspiration of lung masses. The incidence of iatrogenic pneumothorax with this procedure ranged from 19% to 40%. The use of a smaller coaxial needle (#19) in comparison to a larger needle (#18) reduced the incidence of pneumothorax.

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The occurrence of an iatrogenic pneumothorax should be suspected in patients who become more short of breath after a medical or surgical procedure known to be associated with the development of an iatrogenic pneumothorax. The treatment of iatrogenic pneumothorax differs from that of spontaneous pneumothorax in that recurrence is not likely, and, therefore, one need not try to create a pleurodesis.

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TRAUMATIC (NONIATROGENIC) PNEUMOTHORAX Traumatic pneumothorax can result from either penetrating or non penetrating chest trauma. The mechanism of the pneumothorax is from the wound allows air to enter the pleural space directly through the chest wall. In addition, the visceral pleura is frequently penetrated, allowing air to enter the pleural space from the alveoli.

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With nonpenetrating trauma, the ribs may become fractured or dislocated, and the visceral pleura may thereby be lacerated, leading to a pneumothorax. In nonpenetrating trauma, if no associated rib fractures, the mechanism of the pneumothorax is by sudden chest compression, the alveolar pressure increases and this may cause alveolar rupture. Air then enters the interstitial spaces and dissects either toward the visceral pleura or toward the mediastinum to produce mediastinal emphysema.

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Most traumatic pneumothoraces should be treated with tube thoracostomy. The air leak usually ceases within 72 hours.

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TENSION PNEUMOTHORAX A tension pneumothorax is said when the intrapleural pressure exceeds atmospheric pressure throughout expiration and often during inspiration as well. Most tension pneumothoraces occur in patients who are receiving positive pressure ventilation either from mechanical ventilation or during resuscitation.

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In other cases tension pneumothorax develops probably related to some type of one-way valve process in which the valve is open during inspiration and closed during expiration. A one-way valve mechanism must be implicated; otherwise, on expiration, when the pleural pressure is positive with respect to the alveolar pressure, gas would flow from the pleural space into the alveoli, and no positive pressure would develop in the pleural space.

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Tension pneumothorax occasionally evolves from a spontaneous pneumothorax. The clinical status of patients with tension pneumothorax is striking, appears distressed with rapid labored respirations, cyanosis, and usually profuse diaphoresis, hypotension, and marked tachycardia. Arterial blood gases reveal marked hypoxemia and, sometimes, respiratory acidosis. The physical findings are those of any large pneumothorax, but in addition, the involved hemithorax is larger than the contralateral hemithorax with the interspaces widened. The trachea is usually shifted toward the contralateral side.

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Because tension pneumothorax is a medical emergency, the valuable time should not be wasted on radiologic studies because the clinical situation and the physical findings are usually sufficient to establish the diagnosis. The patient should immediately be given a high concentration of supplemental oxygen to combat the hypoxia. Then, the elevated pressure in the pleural space must be eliminated by decompression procedure.

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If a tension pneumothorax is present, preparations should be made for the immediate insertion of a large chest tube.

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BRONCHOPLEURAL AND ALVEOLARPLEURAL FISTULAS When a chest tube is in place, there will be an air leak through the tube if there is communication by bronchopleural fistula between a bronchus and the pleural space, or by alveolar- pleural fistula between the pulmonary parenchyma and the pleural space.

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Classification of Air Leaks It is important to semiquantitate the amount of leak. Cerfolio has developed classification of air leaks by four types: 1. The largest and the most uncommon is the continuous (C) air leak. 2. The second largest type of air leak, which is also uncommon, is an inspiratory (I) air leak.

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3. The third largest type of air leak, which is very common, is an expiratory (E) air leak. 4. The smallest type of air leak is the forced expiratory (FE) air leak. Air leaks begin to resolve or heal, they usually go from an E leak to an FE leak.