Спонтанный пневмоторакс


Re: Спонтанный пневмоторакс

Сообщение vash61 » 06 май 2012, 17:02

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Re: Спонтанный пневмоторакс

Сообщение слава » 06 май 2012, 17:09

Учитывая тот факт точ при первичном СП в большинстве случаев вообще вы не обнаруживаете изменений то КТ превращается в один из способо относительно честного метода зарабатывания денег или просто их отъема если это касается только пациента.
Даже если вы работаете с раздельной интубацией (мы не работаем, наши анестезиологи считают это излишеством) если буллы не видны вы всегда можете попросить анестезиолога порадобать обоими легкими.

PS: расскажите пожалуйста - что такое буллезная болезнь. У нас еще в отделении пишут буллезная дистрофия.
Ответы мне конечно дают, после которых я понимаю что интеграция с медициной остальных 70% Земли будет не возможна еще много лет.
Что расти с какого-то момента
мы перестаем — большая жалость:
мне, возможно, два лишь сантиметра
до благоразумия осталось.
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Re: Спонтанный пневмоторакс

Сообщение Ибрагимова » 06 май 2012, 17:16

скажите, а вы выполняли КТ ОГК при первом эпизоде? или у вас есть статьи может с данными о том что при первом эпизоде при КТ не визуализируются буллы? мне интересно было бы посмотреть? желательно что-нибудь из серьёзной литературы и публикаций. и на счёт буллёзной болезни - мне кажется я писала буллёзная эмфизема - это верная трактовка диагноза.
ухожу в Нирвану...
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Re: Спонтанный пневмоторакс

Сообщение vash61 » 06 май 2012, 17:32

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Re: Спонтанный пневмоторакс

Сообщение слава » 06 май 2012, 18:23

Что расти с какого-то момента
мы перестаем — большая жалость:
мне, возможно, два лишь сантиметра
до благоразумия осталось.
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Re: Спонтанный пневмоторакс

Сообщение Ибрагимова » 06 май 2012, 18:26

у нас используется ХОБЛ :-): за ссылку спасибо. обязательно просмотрю
ухожу в Нирвану...
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Re: Спонтанный пневмоторакс

Сообщение слава » 06 май 2012, 18:33

тоесть клинический диагноз у вас - ХОБЛ, малый СП справа, например?
Что расти с какого-то момента
мы перестаем — большая жалость:
мне, возможно, два лишь сантиметра
до благоразумия осталось.
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Re: Спонтанный пневмоторакс

Сообщение Ибрагимова » 06 май 2012, 19:31

ХОБЛ: буллёзная эмфизема лёгких (с преимущественным пораженинем....). Спонтанный пневмоторакс с...
На счёт необходимости КТ при первичном спонтанном пневмотораксе инфо: Primary spontaneous pneumothorax in adults

Author
Richard W Light, MD Section Editor
Steven A Sahn, MD Deputy Editor
Helen Hollingsworth, MD



Last literature review version 17.3: September 2009 | This topic last updated: July 9, 2009 (More)


INTRODUCTION — A primary spontaneous pneumothorax (PSP) is a pneumothorax that occurs without a precipitating event in a person who does not have known lung disease. In actuality, most individuals with PSP have unrecognized lung disease, with the pneumothorax resulting from rupture of a subpleural bleb [1-5] .

In this topic review, the incidence, pathogenesis, presentation, and management of PSP are discussed. Secondary spontaneous pneumothorax, which occurs as a complication of underlying lung disease, is reviewed in detail elsewhere. (See "Secondary spontaneous pneumothorax in adults").

INCIDENCE — The incidence of primary spontaneous pneumothorax (PSP) in men varies geographically, from 7.4 per 100,000 population per year in the United States to 37 per 100,000 population per year in the United Kingdom. The incidence is substantially less in women than in men, ranging from 1.2 per 100,000 population per year in the United States to 15.4 per 100,000 population per year in the United Kingdom [6] . The reason for these differences is unknown.

Estimates of the incidence of recurrent PSP range from 25 percent to more than 50 percent, with most recurrences occurring within the first year [6] . As an example, a study of 153 patients with PSP found a recurrence rate of 54 percent [7] . Female gender, tall stature, low body weight, and failure to stop smoking have been associated with an increased risk of recurrence [7,8] .

RISK FACTORS — Factors that have been proposed or shown to predispose patients to primary spontaneous pneumothorax (PSP) include smoking, family history, Marfan syndrome, homocystinuria, and thoracic endometriosis.

Smoking — Cigarette smoking is a significant risk factor for primary spontaneous pneumothorax (PSP), probably due to consequences of airway inflammation. As an example, in an analysis of four studies that included 505 patients with PSP, 461 of the patients (91 percent) were smokers [6] . Furthermore, the risk of PSP was directly related to the amount of cigarette smoking. Compared to nonsmokers, the relative risk of PSP in men was seven times higher in light smokers (one to 12 cigarettes per day), 21 times higher in moderate smokers (13 to 22 cigarettes per day), and 102 times higher in heavy smokers (>22 cigarettes per day). For women, the relative risk was 4, 14, and 68 times higher in light, moderate, and heavy smokers, respectively [9] .

Respiratory bronchiolitis, a form of airway inflammation associated with cigarette smoking, may contribute to the development and recurrence of PSP. In a study of 115 patients with PSP who underwent video-assisted thoracoscopic surgery (VATS), pneumothorax recurrence rates were higher in patients with extensive rather than nonextensive respiratory bronchiolitis for both nonoperative and postoperative pneumothorax (p < .004 and .001, respectively) [10] .

Family history — Reports have been published describing the clustering of PSP in certain families [11-17] . Autosomal dominant, autosomal recessive, polygenic, and X-linked recessive inheritance mechanisms have all been proposed [12-14] . The autosomal dominant Birt-Hogg-Dube syndrome, which predisposes patients to benign skin tumors and renal cancer, is associated with an increased incidence of PSP [15,16,18] . In one study of 198 patients with this syndrome, 48 patients (24 percent) had a history of pneumothorax [18] . The presence of lung cysts was associated with pneumothorax, as well as lung cyst volume, diameter, and number.

The gene responsible for this familial cancer syndrome (called FLCN) has been mapped to chromosome 17p11.2 [15,16] . FLCN and its associated protein, folliculin, appear to have important tumor suppression function. However, other mutations of FLCN have been associated with spontaneous pneumothorax and bullous lung disease in the absence of the oncologic manifestations of Birt-Hogg-Dube syndrome [11,17] . In one Finnish family with an extensive history of PSP, a novel mutation was associated with autosomal dominant inheritance of bullous lung lesions in all carriers (100 percent penetrance) [11] .

Genetic testing is available for the Birt-Hogg-Dube syndrome [19] . Periodic screening for renal tumors is recommended in affected patients. (See "Epidemiology; pathology; and pathogenesis of renal cell carcinoma", section on Risk factors).

Other — PSP also occurs with increased frequency in patients with Marfan syndrome and homocystinuria. In addition, catamenial pneumothorax may result from thoracic endometriosis, and should be considered in women presenting with PSP temporally related to menstruation [20,21] . (See "Thoracic endometriosis").

CLINICAL PRESENTATION — Primary spontaneous pneumothorax (PSP) usually occurs when the patient is at rest [22] . Patients are typically in their early 20s, with PSP being rare after age 40. Patients usually complain of the sudden onset of dyspnea and pleuritic chest pain. The severity of the symptoms is primarily related to the volume of air in the pleural space, with dyspnea being more prominent if the pneumothorax is large.

Characteristic physical findings when a large pneumothorax is present include decreased chest excursion on the affected side, diminished breath sounds, and hyperresonant percussion. Subcutaneous emphysema may be present. Evidence of labored breathing and hemodynamic compromise (eg, tachycardia, hypotension) suggests a possible tension pneumothorax, which necessitates emergency decompression.

Hypoxemia is common because collapsed and poorly ventilated portions of lung continue to receive significant perfusion. In contrast, hypercapnia is unusual because underlying lung function is relatively normal and adequate alveolar ventilation can be maintained by the contralateral lung [1] . Acute respiratory alkalosis may exist if pain, anxiety, and/or hypoxemia are substantial.

Imaging — The presence of a pneumothorax is established by demonstrating a white visceral pleural line on the chest radiograph. The visceral pleural line defines the interface of the lung and pleural air; it is either straight or convex towards the chest wall (show radiograph 1). In most cases, no pulmonary vessels are visible beyond the visceral pleural edge. Inspiratory and expiratory films have equal sensitivity in detecting pneumothoraces; thus, a standard inspiratory chest radiograph is sufficient in most cases [23] . (See "Imaging of pneumothorax").

The underlying lung parenchyma should be examined for the presence of underlying lung disease that would suggest a secondary spontaneous pneumothorax. (See "Secondary spontaneous pneumothorax in adults").

Tension pneumothorax may develop in approximately 1 to 2 percent of PSP [24] . However, the sensitivity and specificity of the plain chest radiograph for detection of tension are unclear. Contralateral shift of the trachea and mediastinum is a typical finding in spontaneous pneumothorax and not necessarily suggestive of tension. Conversely, patients may have clinical evidence of tension (eg, tachycardia, hypotension, dyspnea) in the absence of "typical" radiographic findings. (See "Imaging of pneumothorax", section on Tension pneumothorax).

CT scanning is generally not necessary unless abnormalities are noted on the plain chest radiograph that require further evaluation, or aberrant chest tube placement is suspected [25] .

DIAGNOSIS — The diagnosis of primary spontaneous pneumothorax (PSP) is established by detection of a visceral pleural line on the chest radiograph of a patient without underlying lung disease. (See "Imaging" above).

The differential diagnosis includes the causes of spontaneous pneumothorax in patients who have underlying lung disease that has not yet been diagnosed (eg, catamenial pneumothorax, chronic obstructive lung disease, interstitial lung disease, lung cancer, lymphangioleiomyomatosis). When managing patients with a persistent air leak or recurrent spontaneous pneumothorax, a CT scan should be considered as well as a lung biopsy at the time of thoracoscopy. The diseases associated with secondary spontaneous pneumothorax are discussed in more detail separately. (See "Secondary spontaneous pneumothorax in adults", section on Etiologies).

TREATMENT OPTIONS — Initial management is directed at removing air from the pleural space, with subsequent management directed at preventing recurrence. In the discussion that follows, we expand upon published clinical consensus statements [25,26] . These consensus statements were derived using the Delphi method, a process of collecting data from the opinions of published experts using several rounds of questionnaires [27] .

Initial management — Initial treatment options for primary spontaneous pneumothorax (PSP) include observation, supplemental oxygen, needle aspiration of intrapleural air, chest tube insertion (ie, tube thoracostomy), and thoracoscopy. The choice of procedure depends on patient characteristics and clinical circumstances: Patients who are clinically stable and having their first PSP can be administered supplemental oxygen and observed if their pneumothorax is small (? 2 to 3 cm between the lung and chest wall on a chest radiograph) [28] . Patients who are clinically stable and having their first PSP should undergo needle aspiration if their pneumothorax is large (>3 cm rim of air on chest radiograph), or if they are symptomatic with chest pain or dyspnea. Patients who fail aspiration should have a chest tube inserted (ie, tube thoracostomy) and thoracoscopy should be considered during the same hospitalization. Chemical pleurodesis through the chest tube should be performed, if the air leak persists and thoracoscopy is not readily available. Patients who are clinically stable with either a recurrent PSP or a concomitant hemothorax (ie, a hemopneumothorax), should undergo thoracoscopy after chest tube insertion. If thoracoscopy is not readily available, chemical pleurodesis through the chest tube may be performed after drainage of the pleural space. Clinically unstable patients should undergo chest tube insertion. Decompression of the pleural space can be performed by advancing a standard 14 gauge intravenous catheter into the pleural space at the junction of the midclavicular line and the second or third intercostal space, if the chest tube insertion is delayed.

Supplemental oxygen — Observation should last six hours, after which reliable patients with ready access to emergency medical services can be discharged home if a repeat chest radiograph excludes progression of the pneumothorax. While the patient is hospitalized, supplemental oxygen should be administered to facilitate resorption of the pleural air.

The importance of supplemental oxygen should not be underestimated. Air in the pleural space is reabsorbed when the communication between the alveoli and the pleural space (ie, the air leak) closes. The rate of resorption can be markedly increased if supplemental oxygen is administered [29] . As an example, a normal rate of resorption is approximately 1.25 percent of the volume of the hemithorax per 24 hours [6] . However, the rate of resorption increases six-fold if humidified 100 percent oxygen is administered in an animal model [30] .

Aspiration — Aspiration is most easily accomplished with a commercially available thoracentesis kit. An 18-gauge needle with an 8 to 9 French (Fr) catheter is inserted into the pleural space, the catheter is threaded deeper into the pleural space, and then the needle is withdrawn. Air is manually withdrawn through the indwelling catheter until no more can be aspirated. It is assumed that there is a persistent air leak if there is still no resistance after four liters of air has been aspirated and the lung has not expanded. Thoracoscopy should be performed if this occurs. Alternatively, a chest tube should be inserted if thoracoscopy is not readily available.

Two equally acceptable approaches exist once no further air can be aspirated: A closed stopcock can be attached and the indwelling catheter secured to the chest wall. A chest radiograph should be obtained four hours later and, if adequate lung expansion has occurred, the catheter can be removed. Following an additional two hours of observation, another chest radiograph should be performed. The patient can be discharged if the lung remains expanded on this chest radiograph [31] . The catheter can be left in place and attached to a Heimlich (ie, one-way) valve. The patient can then be discharged with follow up within two days [26] .

One of the advantages of aspiration over tube thoracostomy is that the patient need not be hospitalized, whether the catheter is removed after the aspiration or left attached to the Heimlich valve.

Based on evidence from several studies, we prefer to manage most hemodynamically-stable patients initially with aspiration, rather than tube thoracostomy [25,32-35] . As examples: In a meta-analysis of three randomized, controlled trials (194 patients) that compared aspiration versus tube thoracostomy, aspiration resulted in shorter hospitalizations and similar clinical outcomes at one week and one year [32] . In a randomized trial, 137 patients who had a first episode of PSP were assigned to receive manual aspiration or tube thoracostomy [33] . The groups had similar rates of immediate (62 versus 68 percent) and one-week success (89 versus 88 percent); however, aspiration was associated with a shorter hospital stay (1.8 versus 4 days).

Thoracoscopy — Video-assisted thoracoscopy (VATS) is effective in the treatment of spontaneous pneumothorax [5,36-38] . With this procedure, pleurodesis is created by pleural abrasion or a partial parietal pleurectomy; when necessary, an endoscopic stapler can be used to resect bullae, as reported in several uncontrolled observational studies [39-42] .

Tube thoracostomy — Most patients with PSP can be managed successfully with a small chest tube (? 22 Fr) or chest catheter (? 14 Fr) [43] . The chest tube can be connected to a water seal device, with or without suction and left in position until the pneumothorax resolves. We suggest that suction be applied to the chest tube if the pneumothorax fails to resolve.

Once the air leak has resolved, the lung has expanded, and the pleural air has been removed, the chest tube can be removed in a sequential fashion. Specifically, we advocate that the chest tube be clamped twelve hours after the last evidence of an air leak and that a chest radiograph be performed 24 hours after the last evidence of an air leak. The chest tube can be removed if the pneumothorax has not reaccumulated.

We advocate a more aggressive approach if the lung has not expanded fully or an air leak persists after three days: For patients whose lung is at least 90 percent expanded but who have a persistent air leak, the simplest alternative is to attach a Heimlich valve to the chest tube and send the patient home. For patients who have a persistent air leak and whose lung is less than 90 percent expanded, the preferred procedure is VATS.

Recurrence prevention — We suggest that all patients with recurrent PSP should undergo an intervention to prevent future recurrences once the acute air leak has resolved, the lung has expanded, and the pleural air has been removed. In addition, we suggest that patients experiencing their first PSP should have a preventive intervention if they require VATS or tube thoracostomy as part of their initial management, or have a vocation in which recurrence of the pneumothorax is dangerous to the patient or others (eg, airplane pilot or deep sea diver). Options for preventing recurrence include pleurodesis via VATS, chemical pleurodesis via tube thoracostomy, and thoracotomy.

VATS pleurodesis — Video-assisted thoracoscopic surgery (VATS) is not only effective in the treatment of spontaneous pneumothorax as described above, but also in the prevention of recurrent pneumothorax [5,36-42,44-47] . The rate of recurrent pneumothorax is less than 5 percent after VATS with bleb/bullae resection and pleurodesis. Several techniques have been recommended to induce pleural symphysis including parietal pleurectomy, intrapleural instillation of talc or a tetracycline derivative, laser abrasion of the parietal pleura, and pleural abrasion with dry gauze. We prefer mechanical pleurodesis using pleural abrasion with dry gauze, since it is both simple and effective.

Chemical pleurodesis — In patients who are unable or unwilling to undergo VATS, intrapleural injection of a chemical irritant (most commonly a tetracycline derivative or talc) is another alternative [25] . We prefer to use the tetracycline derivative, doxycycline, for the reasons that follow, although many experts prefer talc.

Chemical pleurodesis with tetracycline decreases the recurrence rate for pneumothorax to 16 to 25 percent. In an unblinded trial of 229 patients with PSP, who were randomly assigned to either undergo or not undergo chemical pleurodesis using tetracycline; tetracycline decreased the rate of recurrent spontaneous pneumothorax (25 versus 41 percent, respectively) [48] . In a series of 390 patients, the pneumothorax recurrence rate was 16 percent with intrapleural tetracycline [49] . Respiratory failure due to an apparent allergic reaction to doxycycline intrapleural instillation has been reported [50] . (See "Chemical pleurodesis").

Talc slurry administered via chest tube can also be used to treat PSP [45,51,52] . Pneumothorax recurrence rates vary between 5 and 8 percent. However, controversy exists whether talc should be used as the sclerosant agent in young, otherwise healthy individuals because of safety reasons and fear for long-term complications. Intrapleural injection of talc for malignant pleural effusions has been associated with the development of the acute respiratory distress syndrome (ARDS) in 1 to 2 percent of patients [53] . Additionally, in one patient, extensive pleural thickening with calcifications developed [54] . On the other hand, several studies support the safety of talc pleurodesis for prevention of recurrent pneumothorax [45,55,56] . (See "Talc pleurodesis").

For patients with recurrent PSP, who have a chest tube in place and are not candidates for VATS pleurodesis, we prefer doxycycline for pleurodesis because we believe that its effectiveness is comparable to talc and it has not been associated with the development of ARDS. We suggest using doxycycline (500 mg dissolved in a total volume of 50 mL of normal saline) administered via the chest tube. Intrapleural doxycycline can be very painful; as a result, patients should be premedicated with analgesics (eg, opiates) and, possibly, anxiolytics (eg, midazolam). Some experts also use intrapleural lidocaine 25 mL (250 mg) of a 1 percent solution; however, intrapleural lidocaine alone is ineffective for pain control.

Thoracotomy — The indications for open thoracotomy are the same as those for VATS. Thoracoscopy has essentially replaced open thoracotomy in the management of spontaneous pneumothorax in many medical centers for two main reasons: hospitalization is shorter and postoperative pain is less [57,58] . Thoracotomy is presently recommended only if thoracoscopy is unavailable or has failed. During thoracotomy, apical pleural blebs are oversewn and the pleura is scarified.

Smoking cessation — The strong association between smoking and an initial PSP suggests that smoking cessation may help prevent recurrent pneumothoraces; this benefit has been confirmed by at least one retrospective study [7] . (See "Patterns of tobacco use and benefits of smoking cessation").

SUMMARY AND RECOMMENDATIONS A primary spontaneous pneumothorax (PSP) is a pneumothorax that occurs without a precipitating event in a person who does not have known lung disease. In actuality, most individuals with PSP have unrecognized lung disease, with the pneumothorax resulting from rupture of a subpleural bleb (See "Introduction" above). The incidence is increased in men, smokers, and patients with a family history of PSP. Recurrence is estimated to occur in 25 to 54 percent of patients (See "Incidence" above and see "Risk factors" above). PSP usually occurs when the patient is at rest and manifests as acute dyspnea and pleuritic chest pain. The peak age is in the early 20s (See "Clinical presentation" above).

Early management We suggest supplemental oxygen and observation if the patient is clinically stable and the pneumothorax is small (ie, the distance between the lung and the chest wall is ? 3 cm on a chest radiograph), rather than aspiration, chest tube insertion, or video-assisted thoracoscopy (VATS) (Grade 2C). Observation should last six hours, after which the patient can be discharged home, if a repeat chest radiograph excludes progression of the pneumothorax and the patient has access to emergency medical services. (See "Initial management" above and see "Supplemental oxygen" above). We recommend pleural aspiration as initial therapy if the patient is clinically stable and the pneumothorax is large, rather than supplemental oxygen with observation, chest tube insertion, or VATS (Grade 1A). This recommendation is based on the observation that the success of pleural aspiration is sufficiently high to warrant its trial before progressing to options that, although more likely to succeed, are also more likely to have adverse effects. A chest tube should be inserted if aspiration fails and VATS should be considered during the same hospitalization based upon the high success rate of VATS, both short- and long-term. Chemical pleurodesis should be performed through the chest tube if VATS is not readily available. (See "Initial management" above and see "Aspiration" above). We suggest that patients who are clinically stable with a recurrent PSP undergo VATS after chest tube insertion (Grade 2B). This is based upon both the short-term success rate of VATS and our belief that all patients with recurrent PSP should undergo a preventive intervention, which can be accomplished at the same time by VATS. Chemical pleurodesis should be performed through the chest tube if VATS is not readily available. (See "Initial management" above). Clinically unstable patients should undergo chest tube insertion. Decompression performed by advancing a standard 14 gauge intravenous catheter into the pleural space at the junction of the midclavicular line and the second or third intercostal space can be performed as a bridge, if the chest tube insertion is delayed. The chest tube can be connected to a water seal device, with or without suction. We suggest that suction be applied to the chest tube if the pneumothorax fails to resolve (Grade 2C). (See "Initial management" above and see "Tube thoracostomy" above). Patients who require mechanical ventilation or who may have a large air leak should be managed with a 24 to 28 French (Fr) chest tube, rather than a smaller chest tube. All other patients who require chest tube insertion can be managed with a 16 to 22 Fr chest tube or a ? 14 Fr chest catheter, instead of a larger chest tube. (See "Tube thoracostomy" above). For patients being managed with a chest tube whose lung is at least 90 percent expanded but who have an air leak that persists longer than three days, we suggest that the chest tube be attached to a Heimlich valve and the patient discharged home, rather than ongoing management with a chest tube (Grade 2C) (See "Tube thoracostomy" above). For patients being managed with a chest tube who have a persistent air leak and whose lung is less than 90 percent expanded, we suggest VATS, rather than ongoing management with a chest tube (Grade 2B). (See "Tube thoracostomy" above).

Preventing recurrence We suggest a preventive intervention for patients experiencing their first PSP if they are undergoing VATS or tube thoracostomy as part of their initial management, or have a vocation in which recurrence of the pneumothorax is dangerous to the patient or others (eg, airplane pilot or deep sea diver) (Grade 2B). Otherwise, we prefer to forego preventive interventions until a patient experiences recurrent PSP. (See "Recurrence prevention" above). Once it has been determined that a preventive procedure is required, we recommend VATS with pleurodesis, rather than tube thoracostomy with chemical pleurodesis (Grade 1B). This procedure reduces the recurrence rate to less than 5 percent. (See "VATS pleurodesis" above). For patients who are not operative candidates or who refuse VATS, we recommend tube thoracostomy with chemical pleurodesis, rather than tube thoracostomy drainage alone, once it has been determined that a preventive intervention is indicated (Grade 1A). This procedure reduces the recurrence rate to less than 25 percent. (See "Chemical pleurodesis" above).


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Zbar, B, Alvord, WG, Glenn, G, et al. Risk of renal and colonic neoplasms and spontaneous pneumothorax in the Birt-Hogg-Dube syndrome. Cancer Epidemiol Biomarkers Prev 2002; 11:393. Graham, RB, Nolasco, M, Peterlin, B, Garcia, CK. Nonsense mutations in folliculin presenting as isolated familial spontaneous pneumothorax in adults. Am J Respir Crit Care Med 2005; 172:39. Toro, JR, Pautler, SE, Stewart, L, et al. Lung cysts, spontaneous pneumothorax, and genetic associations in 89 families with Birt-Hogg-Dube syndrome. Am J Respir Crit Care Med 2007; 175:1044. Nickerson, ML, Warren, MB, Toro, JR, et al. Mutations in a novel gene lead to kidney tumors, lung wall defects, and benign tumors of the hair follicle in patients with the Birt-Hogg-Dube syndrome. Cancer Cell 2002; 2:157. Johnson, MM. Catamenial pneumothorax and other thoracic manifestations of endometriosis. Clin Chest Med 2004; 25:311. Joseph, J, Sahn, SA. Thoracic endometriosis syndrome: New observations from an analysis of 110 cases. Am J Med 1996; 100:164. Bense, L, Wiman, LG, Hedenstierna G. Onset of symptoms in spontaneous pneumothorax: correlations to physical activity. Eur J Respir Dis 1987; 71:181. Seow, A, Kazerooni, EA, Cascade, PN, et al. Comparison of upright inspiratory and expiratory chest radiographs for detecting pneumothoraces. AJR 1996; 166:313. Noppen, M, De Keukeleire, T. Pneumothorax. Respiration 2008; 76:121. Henry, M, Arnold, T, Harvey, J. BTS guidelines for the management of spontaneous pneumothorax. Thorax 2003; 58 Suppl 2:II39. Baumann, MH, Strange, C, Heffner, JE, et al. Management of spontaneous pneumothorax: an American College of Chest Physicians Delphi consensus statement. Chest 2001; 119:590. Dalkey, NC, Helmer, O. An experimental application of the Delphi method to the use of experts. Publication no. RM-727-PR, Rand Corp, Santa Monica, CA 1962. Kelly, AM, Kerr, D, Clooney, M. Outcomes of emergency department patients treated for primary spontaneous pneumothorax. Chest 2008; 134:1033. Northfield, TC. Oxygen therapy for spontaneous pneumothorax. Br Med J 1971; 4:86. Chernick, V, Avery, ME. Spontaneous alveolar rupture at birth. Pediatrics 1963; 32:816. Vallee, P, Sullivan, M, Richardson, H, et al. Sequential treatment of a simple pneumothorax. Ann Emerg Med 1988; 17:936. Devanand, A, Koh, MS, Ong, TH, et al. Simple aspiration versus chest-tube insertion in the management of primary spontaneous pneumothorax: a systematic review. Respir Med 2004; 98:579. Ayed, AK, Chandrasekaran, C, Sukumar, M. Aspiration versus tube drainage in primary spontaneous pneumothorax: a randomised study. Eur Respir J 2006; 27:477. Wakai, A, O'Sullivan, RG, McCabe, G. Simple aspiration versus intercostal tube drainage for primary spontaneous pneumothorax in adults. Cochrane Database Syst Rev 2007; :CD004479. Noppen, M, Alexander, P, Driesen, P, et al. Manual aspiration versus chest tube drainage in first episodes of primary spontaneous pneumothorax: a multicenter, prospective, randomized pilot study. Am J Respir Crit Care Med 2002; 165:1240. Sawada, S, Watanabe, Y, Moriyama, S. Video-assisted thoracoscopic surgery for primary spontaneous pneumothorax: evaluation of indications and long-term outcome compared with conservative treatment and open thoracotomy. Chest 2005; 127:2226. Ayed, AK, Al-Din, HJ. The results of thoracoscopic surgery for primary spontaneous pneumothorax. Chest 2000; 118:235. Freixinet, JL, Canalis, E, Julia, G, et al. Axillary thoracotomy versus videothoracoscopy for the treatment of primary spontaneous pneumothorax. Ann Thorac Surg 2004; 78:417. Inderbitzi, RGC, Leiser, A, Furrer, M, Althaus, U. Three years experience in video-assisted thoracic surgery (VATS) for spontaneous pneumothorax. J Thorac Cardiovasc Surg 1994; 107:1410. Cardillo, G, Facciolo, F, Giunti, R, et al. Videothoracoscopic treatment of primary spontaneous pneumothorax: a 6-year experience. Ann Thorac Surg 2000; 69:357. Hatz, RA, Kaps, MF, Meimarakis, G, et al. Long-term results after video-assisted thoracoscopic surgery for first-time and recurrent spontaneous pneumothorax. Ann Thorac Surg 2000; 70:253. Lang-Lazdunski, L, de Kerangal, X, Pons, F, Jancovici, R. Primary spontaneous pneumothorax: one-stage treatment by bilateral videothoracoscopy. Ann Thorac Surg 2000; 70:412. Minami, H, Saka, H, Senda, K, et al. Small caliber catheter drainage for spontaneous pneumothorax. Am J Med Sci 1992; 304:345. Janssen, JP, van Mourik, J, Cuesta Valentin, M, et al. Treatment of patients with spontaneous pneumothorax during videothoracoscopy. Eur Respir J 1994; 7:1281. Gyorik, S, Erni, S, Studler, U, et al. Long-term follow-up of thoracoscopic talc pleurodesis for primary spontaneous pneumothorax. Eur Respir J 2007; 29:757. Nathan, DP, Taylor, NE, Low, DW, et al. Thoracoscopic total parietal pleurectomy for primary spontaneous pneumothorax. Ann Thorac Surg 2008; 85:1825. Rena, O, Massera, F, Papalia, E, et al. Surgical pleurodesis for Vanderschueren's stage III primary spontaneous pneumothorax. Eur Respir J 2008; 31:837. Light, RW, O'Hara, VS, Moritz, TE, et al. Intrapleural tetracycline for the prevention of recurrent spontaneous pneumothorax. JAMA 1990; 264:2224. Olsen, PS, Andersen, HO. Long-term results after tetracycline pleurodesis in spontaneous pneumothorax. Ann Thorac Surg 1992; 53:1015. DiBardino, DJ, Vanatta, JM, Fagan, SP, Awad, SS. Acute respiratory failure after pleurodesis with doxycycline. Ann Thorac Surg 2002; 74:257. Almind, M, Lange, P, Viskum, K. Spontaneous pneumothorax: Comparison of simple drainage, talc pleurodesis, and tetracycline pleurodesis. Thorax 1989; 44:627. Tschopp, JM, Boutin, C, Astoul, P, et al. Talcage by medical thoracoscopy for primary spontaneous pneumothorax is more cost-effective than drainage: a randomised study. Eur Respir J 2002; 20:1003. Light, RW. Talc should not be used for pleurodesis. Am J Respir Crit Care Med 2000; 162:2024. Lange, P, Mortensen, J, Groth, S. Lung function 22-35 years after treatment of idiopathic spontaneous pneumothorax with talc poudrage or simple drainage. Thorax 1988; 43:559. Cardillo, G, Carleo, F, Carbone, L, et al. Long-term lung function following videothoracoscopic talc poudrage for primary spontaneous recurrent pneumothorax. Eur J Cardiothorac Surg 2007; 31:802. Hunt, I, Barber, B, Southon, R, Treasure, T. Is talc pleurodesis safe for young patients following primary spontaneous pneumothorax?. Interact Cardiovasc Thorac Surg 2007; 6:117. Hazelrigg, SR, Landreneau, RJ, Mack, M, et al. Thoracoscopic stapled resection for spontaneous pneumothorax. J Thorac Cardiovasc Surg 1993; 105:389. Urschel, JD. Thoracoscopic treatment of spontaneous pneumothorax. A review. J Cardiovasc Surg (Torino)
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Re: Спонтанный пневмоторакс

Сообщение слава » 06 май 2012, 19:39

эта статья у меня есть. Там в принципе то что я вам и говорил - КТ рутинно при СП не показано.
Что расти с какого-то момента
мы перестаем — большая жалость:
мне, возможно, два лишь сантиметра
до благоразумия осталось.
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Re: Спонтанный пневмоторакс

Сообщение Ибрагимова » 06 май 2012, 19:50

и ещё про необходимость КТ:Secondary spontaneous pneumothorax in adults

Author
Richard W Light, MD Section Editor
Steven A Sahn, MD Deputy Editor
Helen Hollingsworth, MD



Last literature review version 17.3: September 2009 | This topic last updated: January 5, 2009 (More)


INTRODUCTION — A secondary spontaneous pneumothorax (SSP) is defined as a pneumothorax that occurs as a complication of underlying lung disease [1,2] . In contrast, primary spontaneous pneumothorax occurs without a precipitating event in the absence of clinical lung disease. In this topic review, we discuss the causes, clinical manifestations, diagnosis, and management of secondary spontaneous pneumothorax. Primary spontaneous pneumothorax and catamenial pneumothorax are discussed in detail elsewhere. (See "Primary spontaneous pneumothorax in adults" and see "Thoracic endometriosis").

ETIOLOGIES — Nearly every lung disease can be complicated by secondary spontaneous pneumothorax (SSP), although it is most commonly associated with chronic obstructive pulmonary disease, Pneumocystis jirovecii infection, cystic fibrosis, and tuberculosis [1] .

Other less common causes include ankylosing spondylitis, asthma, histiocytosis X, idiopathic pulmonary fibrosis, lymphangioleiomyomatosis, lung cancer, Marfan syndrome, necrotizing pneumonia, rheumatoid arthritis, and sarcoidosis [3] . (See "Clinical manifestations of ankylosing spondylitis in adults" and see "Langerhans cell histiocytosis (histiocytosis X, eosinophilic granuloma)" and see "Pulmonary lymphangioleiomyomatosis" and see "The Marfan syndrome" and see "Overview of lung disease associated with rheumatoid arthritis" and see "Clinical manifestations and diagnosis of sarcoidosis").

Chronic obstructive pulmonary disease — Chronic obstructive pulmonary disease (COPD) is the most common cause of SSP, with nearly 70 percent of SSP attributed to COPD [4] . Rupture of apical blebs is the usual cause.

Severity of COPD correlates with the likelihood of developing SSP. As an example, more than 30 percent of patients with SSP due to COPD have a forced expiratory volume in one second (FEV1) less than one liter and an FEV1 to forced vital capacity (FEV1/FVC) ratio less than 40 percent [5] .

Pneumocystis jirovecii — Among patients with acquired immunodeficiency syndrome (AIDS) who develop SSP, greater than 80 percent have current or previous P. jirovecii pneumonia (PCP) [6,7] . Reciprocally, up to 30 percent of patients with Pneumocystis pneumonia will develop SSP [8] . The risk of SSP is greatest among patients with prior PCP who are taking pentamidine prophylaxis, but develop recurrent Pneumocystis pneumonia despite the prophylaxis [6] . Rupture of large subpleural cysts caused by subpleural necrosis is the cause of most SSP in this patient population .

The occurrence of SSP due to PCP has a poor prognosis. In the past, in-hospital mortality exceeded 25 percent and the median survival was about three months [8] . More recent data are lacking. Recurrent ipsilateral or contralateral pneumothorax is common. In one series of 20 patients, 13 patients had a recurrent ipsilateral pneumothorax and 13 patients had a contralateral pneumothorax [9] .

Cystic fibrosis — SSP is relatively common in cystic fibrosis (CF). Approximately 6 percent of all patients with CF will have an episode of SSP, which increases to 16 to 20 percent among those patients who survive to age 18 [10,11] . CF-related SSP is usually due to rupture of apical subpleural cysts.

The risk of pneumothorax is inversely related to the forced expiratory volume in one second (FEV1). In one report, nearly half of all patients with CF who had an FEV1 less than 20 percent of predicted experienced at least one SSP [10] . Other factors associated with an increased risk of pneumothorax included infection with Pseudomonas aeruginosa, Burkholderia cepacia complex, or Aspergillus species, as well as a prior episode of massive hemoptysis.

Tuberculosis — SSP occurs in 1 to 3 percent of patients hospitalized with pulmonary tuberculosis [12] . The pneumothorax is due to rupture of a tuberculous cavity into the pleural space.

PRESENTATION — Most patients with secondary spontaneous pneumothorax (SSP) complain of dyspnea and chest pain on the same side as the pneumothorax [13] . Symptoms due to SSP are generally more severe than those associated with primary spontaneous pneumothorax, presumably because patients with SSP have less pulmonary reserve due to underlying lung disease and, thus, any impairment of pulmonary function has a more noticeable effect.

Characteristic physical findings when a large pneumothorax is present include decreased chest excursion on the affected side, diminished breath sounds, and hyperresonant percussion. Subcutaneous emphysema may be present.

Arterial blood gases are frequently abnormal. In one study, the arterial PO2 was below 55 mmHg in 17 percent of patients and below 45 mmHg in 4 percent, while the arterial PCO2 exceeded 50 mmHg in 16 percent and exceeded 60 mmHg in 4 percent [5] .

Persistent air leaks are more common and tend to persist longer when due to SSP, compared to primary spontaneous pneumothorax [14] .

DIAGNOSIS — The diagnosis of secondary spontaneous pneumothorax (SSP) is established by detection of a visceral pleural line on the chest radiograph of a patient with underlying lung disease. The visceral pleural line defines the interface of the lung and pleural air. (See "Imaging of pneumothorax").

The diagnosis of a pneumothorax can be challenging in patients with severe emphysema: The pleural line may be difficult to visualize because the lung appears hyperlucent, resulting in minimal difference in the radiodensity of the lung and the pneumothorax. A pneumothorax may be difficult to distinguish from a large, thin-walled, air-containing bulla. In general, the pleural line associated with a pneumothorax is convex relative to the lateral chest wall, whereas the pleural line associated with a large bulla is usually concave relative to the lateral chest wall. The two conditions can be easily differentiated by computed tomography of the chest [15] .

TREATMENT — All patients with secondary spontaneous pneumothorax (SSP) should be hospitalized because their diminished pulmonary reserve due to underlying lung disease increases their risk for an adverse outcome. Initial management is directed at removing air from the pleural space, with subsequent management directed at preventing recurrence. In the discussion that follows, we expand upon published clinical consensus statements [16,17] .

Initial management — Initial management is dictated by the severity of the patient's symptoms and the size of the pneumothorax [16] . Patients who are clinically stable and have a small pneumothorax (? 2 cm between the lung and chest wall on a chest radiograph) can be observed. In contrast, patients who are clinically stable but have a large pneumothorax should have a chest tube placed (ie, tube thoracostomy). Clinically unstable patients should have a chest tube placed regardless of the size of the pneumothorax. (See "Tube thoracostomy").

Tube thoracostomy is preferred over needle aspiration because it is more likely to be successful. In one trial, 28 patients with SSP were randomly assigned to receive tube thoracostomy and 33 patients to receive needle aspiration [18] . The tube thoracostomy group was more likely to have their pleural air completely evacuated than the needle aspiration group (93 versus 67 percent). However, patients who have a small pneumothorax and are minimally breathless may be managed with simple aspiration and observation in the hospital for 24 hours [16] .

Tube thoracostomy leads to lung expansion and cessation of the air leak within seven days in about 80 percent of patients with SSP [19,20] . Patients who are clinically unstable or who require mechanical ventilation and, therefore, are at increased risk for a large air leak, should be managed with a 24 to 28 French (Fr) chest tube. A smaller chest tube (eg, 16 Fr to 22 Fr) is preferred for most other patients. Small chest catheters (eg, ? 14 Fr) are acceptable in certain circumstances (eg, very small pneumothoraces, strong patient preferences), but should be considered on a case by case basis.

The chest tube should be connected to a water seal device with or without suction. Failure of the pneumothorax to resolve should prompt the initiation of suction if it was not initially applied. A Heimlich valve can also be used, although a water seal device is preferable.

In general, the chest tube should remain in place until a procedure is performed to prevent recurrent SSP. However, patients who decline preventive interventions can have their chest tube clamped twelve hours after the last evidence of an air leak. A chest radiograph should be performed 24 hours after the last evidence of an air leak and, if the pneumothorax has not recurred, the chest tube can be removed.

Prolonged air leaks — A more aggressive approach should be considered if the lung has not expanded or if an air leak persists after three days of tube thoracostomy. This is a common problem among patients with SSP due to current or prior Pneumocystis pneumonia because their subpleural cysts are large and associated with necrotic lung. As an example, a report of 20 patients described a median duration of tube thoracostomy of 20 days, with eventual success in only four patients [6] .

For patients who have a persistent air leak and whose lung is less than 90 percent expanded, the preferred procedure is video assisted thoracoscopy (VATS), which has a lower morbidity and mortality than open thoracotomy [21,22] . The optimal technique to perform with VATS is uncertain. Most surgeons recommend stapling of the blebs, since recurrence rates are substantially higher if the blebs are not over sewn [23,24] . In contrast, one study reported success in 11 out of 12 patients using VATS-directed insufflation of talc without direct treatment of the air leak [25] .

For stable patients whose lung is at least 90 percent expanded but who have a persistent air leak, an alternative approach is to attach a Heimlich valve to the chest tube and send the patient home [26] . The advantage of this regimen is that it allows the patient to go home rapidly with essentially no morbidity.

Preventing recurrence — Once the air leak has resolved, the lung re-expanded, and pleural air removed, we advocate intervention to prevent recurrence in all patients treated for an initial SSP. This belief is based on our observation that recurrent SSP is both common and frequently life-threatening. As an example, one study reported a 50 percent likelihood of recurrent SSP over three years among patients who were treated for SSP due to COPD, but who did not have an intervention to prevent recurrence [5] .

VATS with stapling of blebs followed by obliteration of the pleural space reduces the recurrence rate to less than 5 percent and, thus, is the preferred intervention in most patients [8] . Several methods are available for obliteration of the pleural space including apical pleurectomy [27] , intrapleural insufflation of talc [28] , Nd-YAG laser abrasion of the parietal pleura [29] , and pleural abrasion with dry gauze [30] . We prefer mechanical pleurodesis, using pleural abrasion with gauze, since it is effective and simple to perform.

Chemical pleurodesis administered via the chest tube reduces the recurrence rate from 50 percent to approximately 25 percent [5] . Although not as effective as the VATS technique described above, it may be useful in patients who are not operative candidates or who refuse VATS. It is performed by instilling a sclerosant into the pleural space. Although the choice of a sclerosant is controversial, we prefer doxycycline because we believe it is the safest option [31-33] . The recommended dose of doxycycline is 500 mg. Technical aspects of chemical pleurodesis are discussed in detail elsewhere. (See "Chemical pleurodesis").

Pleurodesis with an inflammation producing agent should be avoided if the patient is a candidate for lung transplantation, since it increases the risk of excessive bleeding during transplantation [34] . Instead, VATS-directed apical pleurodesis should be performed.

SUMMARY AND RECOMMENDATIONS A secondary spontaneous pneumothorax (SSP) is a pneumothorax that occurs as a complication of underlying lung disease. (See "Introduction" above). Nearly every lung disease can be complicated by SSP, although it is most commonly associated with chronic obstructive pulmonary disease, Pneumocystis jirovecii infection, cystic fibrosis, and tuberculosis. (See "Etiologies" above). SSP is more dangerous than primary spontaneous pneumothorax because patients with SSP generally have less functional reserve and, thus, any impairment of pulmonary function has a more noticeable effect. Most patients complain of dyspnea and chest pain on the same side as the pneumothorax. (See "Presentation" above). The diagnosis of SSP is established by detection of a visceral pleural line on the chest radiograph of a patient with underlying lung disease. (See "Diagnosis" above).

Initial management We suggest hospitalization of all patients with SSP (Grade 2B). (See "Treatment" above). We suggest observation, rather than chest tube insertion, if the patient is clinically stable and the pneumothorax is small (ie, the distance between the lung and the chest wall is ? 2 cm on a chest radiograph) (Grade 2C). We suggest simple aspiration, rather than observation, for patients who have a small pneumothorax and are minimally breathless (Grade 2C). (See "Initial management" aboveSee "Initial management" above). We suggest insertion of a chest tube, rather than observation, if the patient is clinically stable and the pneumothorax is large (Grade 2B). (See "Initial management" aboveSee "Initial management" above). We recommend insertion of a chest tube, rather than observation or simple aspiration, in all clinically unstable patients, regardless of the size of the pneumothorax (Grade 1B). (See "Initial management" aboveSee "Initial management" above). We believe that patients who are clinically unstable, who require mechanical ventilation, or who may have a large air leak should be managed with a 24 to 28 French (Fr) chest tube. Alternatively, a 16 to 22 Fr chest tube should be sufficient in clinically stable, nonventilated patients who require a chest tube. (See "Initial management" aboveSee "Initial management" above). We suggest that the chest tube should be connected to a water seal device, rather than a Heimlich valve (Grade 2C). Suction may or may not be applied to the chest tube initially, but should be applied if the pneumothorax fails to resolve. (See "Initial management" aboveSee "Initial management" above). For patients who have an air leak that persists for more than three days, we suggest video assisted thoracoscopy (VATS), rather than ongoing management with a chest tube (Grade 2B). (See "Prolonged air leaks" above).

Preventing recurrence We recommend that patients undergo a preventive intervention after their initial SSP, rather than waiting until a second SSP occurs (Grade 1B). This recommendation reflects our recognition that SSP will recur in approximately 50 percent of patients who do not undergo a preventive intervention and that these patients are at risk for adverse sequelae due to recurrent SSP. (See "Preventing recurrence" aboveSee "Preventing recurrence" above). We recommend VATS with stapling of blebs and pleural abrasion as the preventive intervention, rather than chemical pleurodesis via the chest tube (Grade 1B). This procedure reduces the recurrence rate to less than 5 percent. (See "Preventing recurrence" aboveSee "Preventing recurrence" above). For patients who are not operative candidates or who refuse VATS, we recommend chemical pleurodesis via the chest tube, rather than forgoing an intervention (Grade 1B). This procedure reduces the recurrence rate to 25 percent. (See "Preventing recurrence" aboveSee "Preventing recurrence" above).


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Re: Спонтанный пневмоторакс

Сообщение Ибрагимова » 06 май 2012, 19:51

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Re: Спонтанный пневмоторакс

Сообщение слава » 06 май 2012, 19:56

CT scanning is generally not necessary unless abnormalities are noted on the plain chest radiograph that require further evaluation, or aberrant chest tube placement is suspected [25]
Что расти с какого-то момента
мы перестаем — большая жалость:
мне, возможно, два лишь сантиметра
до благоразумия осталось.
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Re: Спонтанный пневмоторакс

Сообщение Ибрагимова » 06 май 2012, 20:30

The differential diagnosis includes the causes of spontaneous pneumothorax in patients who have underlying lung disease that has not yet been diagnosed (eg, catamenial pneumothorax, chronic obstructive lung disease, interstitial lung disease, lung cancer, lymphangioleiomyomatosis). When managing patients with a persistent air leak or recurrent spontaneous pneumothorax, a CT scan should be considered as well as a lung biopsy at the time of thoracoscopy. Если я правильно перевожу - то КТ неоходимо для выявления причины и дифдиагностики.
ухожу в Нирвану...
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Re: Спонтанный пневмоторакс

Сообщение mansur_jagudin » 06 май 2012, 21:22

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Re: Спонтанный пневмоторакс

Сообщение Pomor » 07 май 2012, 02:06

Вопрос для Ибрагимовой: если легкое не расправляется 4-5 дней,оно не становится "регидным"? Нас раньше учили так. Возможно все поменялось. (Торакальной хирургией занимаюсь редко.)
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