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Biomedical subjects

Steven A Sahn

Publications and source records attributed to Steven A Sahn.

At least 19 recordsLinked to original sources
PubMed2007

Characteristics of trapped lung: pleural fluid analysis, manometry, and air-contrast chest CT.

STUDY OBJECTIVES: To review the pleural fluid characteristics, pleural manometry, and radiographic data of patients who received a diagnosis of trapped lung in our pleural diseases service. DESIGN: Retrospective case series. METHODS: The procedure records of 247 consecutive patients who underwent pleural manometry at the Medical University of South Carolina between October 2002 and November 2005 were reviewed. Eleven patients in whom a diagnostic pneumothorax was introduced were identified. Manometry data, radiographic findings, pleural fluid analysis, final clinical diagnosis, and information regarding the initial pleural insult were retrieved from the medical record. RESULTS: All 11 patients had a clinical diagnosis of trapped lung. The causes of trapped lung were attributed to coronary artery bypass graft surgery, uremia, thoracic radiation, pericardiotomy, spontaneous bacterial pleuritis and repeated thoracentesis, and complicated parapneumonic effusion. Mean pleural fluid pH was 7.30, pleural fluid lactate dehydrogenase (LDH) was 124 IU/L, and pleural fluid total protein was 2.9 g/dL. Pleural fluid was paucicellular with mononuclear cell predominance. Pleural space elastance was increased in all cases and ranged from 19 to 149 cm H(2)O/L of pleural fluid removed. All demonstrated abnormal visceral pleural thickness on air-contrast chest CT. CONCLUSIONS: Trapped lung is a clinical entity characterized by the presence of a restrictive visceral pleural peel that was first described in 1967. The pleural fluid is paucicellular, LDH is low, and protein may be in the exudative range. The elevated total pleural fluid protein may be related to factors other than active pleural inflammation or malignancy and does not exclude the diagnosis.

Clinical Protocols↗
PubMed2006

Pleural effusions of extravascular origin.

Most pleural effusions are caused by hydrostatic and oncotic pressure imbalance, inflammation or infection, or abnormalities in lymphatic drainage. A select number of effusions are caused by fluid of extravascular origin. Some of these effusions result from complications of treatment, whereas others are a ramification of the underlying disease. The incidence, pathogenesis, clinical presentation, chest radiographic manifestations, pleural fluid analysis, diagnosis, and management are discussed.

Catheterization, Central Venous↗
PubMed2006

Staphylococcal superantigens of the enterotoxin gene cluster (egc) for treatment of stage IIIb non-small cell lung cancer with pleural effusion.

There has been renewed interest in the superantigens as antitumor agents with the discovery of a group of bacterial superantigens known as the enterotoxin gene cluster (egc staphylococcal enterotoxins [SEs]). This article discusses the mechanisms by which egc SEs induce tumor killing and pleurodesis. The application of SE homolog and nucleic acid compositions as vaccines and for treatment of established tumors is reviewed. Finally, the use of native SEs ex vivo-intratumorally and intravesicularly administered superantigens against established tumors-is described and the interrelation between superantigen therapy and chemoradiotherapy.

Animals↗
PubMed2006

Pleural disease in lymphangioleiomyomatosis.

Pleural disease is a common complication of lymphangioleiomyomatosis (LAM). The incidence and recurrence rates of secondary spontaneous pneumothorax in LAM are the highest among chronic pulmonary disorders. Most patients have at least one pneumothorax before LAM is diagnosed, and pneumothorax is often the sentinel event that leads to the diagnosis. Although early, definitive treatment for recurrent pneumothorax by pleurodesis is recommended, the failure rate for chemical and surgical approaches is high. Chylothorax occurs owing to obstruction of lymphatics by proliferating smooth muscle cells and often requires pleurodesis to control expanding and recurrent effusions. Because of the rarity of the LAM, few data exist on whether the occurrence of pleural complications in LAM accelerates functional decline or portends a worse prognosis.

Age of Onset↗
PubMed2006

The spectrum of pleural effusions after coronary artery bypass grafting surgery.

Pleural effusions are common after coronary artery bypass grafting (CABG) surgery and can be categorized by time intervals: perioperative (within the first week), early (within 1 month), late (2-12 months), or persistent (after 6 months). The perioperative effusions are usually attributable to diaphragm dysfunction or internal mammary artery harvesting and are typically self-limited. Early effusions are usually attributable to postcardiac injury syndrome and may require corticosteroid treatment. Although late effusions can have multiple causes, persistent effusions are attributable to trapped lung and often require decortication. Diagnostic thoracentesis should be performed for patients with large symptomatic pleural effusions or fever after CABG surgery. The range of management includes observation, therapeutic thoracentesis, corticosteroids, or decortication depending on the cause and course of the effusion.

Coronary Artery Bypass↗
PubMed2006

Pleural fluid and peripheral eosinophilia from hemothorax: hypothesis of the pathogenesis of EPE in hemothorax and pneumothorax.

Blood and air in the pleural space are the most common conditions associated with an eosinophilic pleural effusion. The recruitment of eosinophils is dependent upon stimulation by cytokines, specifically interleukin (IL)-3, IL-5, granulocyte-monocyte cell stimulating factor (GM-CSF), and RANTES (regulated upon activation, normal t-cell expressed and secreted), that cause eosinophil proliferation in the bone marrow, movement into the circulation, and adhesion and migration across endothelial barriers into tissues. There are several possible mechanisms that can explain eosinophilic pleural effusions. We report a case of an eosinophilic pleural effusion after spontaneous hemothorax that illustrates the course of pleural fluid and blood eosinophilia in following hemothorax and describe the different pathophysiology of eosinophil trafficking in the pleural space and serum following hemothorax and pneumothorax.

Adult↗
PubMed2006

Colonoscopy-associated pneumothorax: a case of tension pneumothorax and review of the literature.

A 64-year-old woman presented with severe abdominal pain and was found to have a large fecolith in the sigmoid colon with resulting bowel obstruction. During a therapeutic colonoscopy, she developed severe shortness of breath and hypoxia, and was found to have a tension pneumothorax. We review the potential mechanisms by which pneumothorax may occur following colonoscopy. In addition, the eight previously published cases are reviewed. Pneumothorax, with or without pneumomediastinum, can occur through a variety of mechanisms following colonoscopy. Although rarely reported, this may represent an underappreciated complication and should be fully investigated in the appropriate setting. Colonoscopy, an exceedingly common procedure, will continue to increase with the aging population. As a result, tension pneumothorax can have a profound effect on the patient outcome and therefore physicians, both gastroenterologists and pulmonologists, should be aware of all the potential problems with this procedure.

Colonoscopy↗
PubMed2006

Patient perspectives on management of pneumothorax in lymphangioleiomyomatosis.

STUDY OBJECTIVES: The American College of Chest Physicians Delphi Consensus Statement on management of spontaneous pneumothorax recommended pleurodesis after the first secondary spontaneous pneumothorax to prevent recurrence, and evaluation of patients' perspectives regarding pneumothorax treatment was identified as a future research priority. Patients with lymphangioleiomyomatosis (LAM) are an ideal population for performing these studies, since pneumothorax occurs and recurs more commonly in LAM than in any other chronic pulmonary disorder. STUDY DESIGN AND PARTICIPANTS: A 23-item questionnaire evaluating opinions of pneumothorax treatment was distributed to 615 patients in the LAM Foundation patient database, with a response rate of 52%. RESULTS: Of respondents, 69% (216 of 314 patients) reported a history of radiographically documented pneumothorax, and 181 patients (84%) reported at least one pleurodesis procedure. Neither a history of pneumothorax nor surgical management of pneumothorax affected reported oxygen use or perception of overall lung function, yet 41% thought that their pneumothorax had contributed to a decline in lung function. Few patients (12%) worried frequently about a pneumothorax developing, but one third made lifestyle modifications due to fear of pneumothorax. Extensive pain associated with chest tube placement and inadequate pain management throughout treatment for pneumothorax were frequent concerns. Only 25% of respondents thought that pleurodesis was appropriate for a first pneumothorax, while 60% favored pleurodesis for a second pneumothorax. Despite the apparent reluctance to undergo pleurodesis, most patients agreed that pleurodesis helps prevent pneumothorax recurrence. One third of patients believed that their physicians did not consider their preferences regarding pneumothorax management. CONCLUSIONS: LAM patients and physicians may have different views about the significance of pneumothorax, in that most patients appear to favor a conservative initial approach to pneumothorax management. In conjunction with appropriate pain management, a better understanding of patients' perspectives will facilitate cooperative decision making and may ultimately improve clinical outcomes in LAM related to pneumothorax.

Chest Tubes↗
PubMed2006

Management of pneumothorax in lymphangioleiomyomatosis: effects on recurrence and lung transplantation complications.

STUDY OBJECTIVES: Pneumothorax is a common complication of lymphangioleiomyomatosis (LAM), and the optimal approach to its treatment and prevention is unknown. Chemical or surgical pleurodesis are often required to prevent recurrence. However, their efficacy in LAM is unclear, and whether they contribute to perioperative complications during lung transplantation is uncertain. SETTING: The LAM Foundation database of registered patients. DESIGN: A questionnaire was sent to all registered patients who had at least one pneumothorax to determine rates and patterns of recurrence and efficacy of interventions. A second questionnaire was sent to registered LAM patients who received a lung transplant. PATIENTS OR PARTICIPANTS: Of 395 registered patients, 260 patients (66%) reported at least one pneumothorax during their lifetime, 193 of whom (74%) completed the questionnaire. Of the 85 lung transplant patients who were sent a separate questionnaire, 80 patients (94%) responded. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Of the 193 respondents to the pneumothorax questionnaire, data on 676 episodes of pneumothorax were collected. Eighty-two percent (158 of 193 patients) had their first pneumothorax prior to a diagnosis of LAM. One hundred forty patients (73%) had at least one additional pneumothorax, either an ipsilateral recurrence (99 of 140 patients, 71%) or a contralateral pneumothorax (104 of 140 patients, 74%). Recurrence rates were 66% after conservative therapy, 27% after chemical pleurodesis, and 32% after surgery. In patients who had undergone lung transplantation, prior chemical or surgical pleurodesis was performed in 45 of 80 patients (56%). Fourteen of 80 patients (18%) reported pleural-related postoperative bleeding, 13 of whom (93%) had prior pleurodesis. CONCLUSIONS: Chemical pleurodesis or surgery are equally effective and better than conservative therapy in preventing recurrence of pneumothorax in LAM. Due to the high recurrence rate, either procedure should be considered for the initial pneumothorax in these patients. However, both contribute to increased perioperative bleeding following lung transplantation, with no effect on length of hospital stay.

Adolescent↗
PubMed2006

Pleural effusions in a series of 181 outpatients with sarcoidosis.

OBJECTIVES: Pleural effusion (PE) is considered to be a rare manifestation of pulmonary sarcoidosis. We performed thoracic ultrasonography prospectively in consecutive outpatients with sarcoidosis to determine the frequency of PEs caused by sarcoidosis and to define their pleural fluid characteristics. DESIGN: Consecutive outpatients aged >/= 18 years with biopsy-proven sarcoidosis underwent ultrasonography. SETTING: University hospital, outpatient sarcoidosis clinic. RESULTS: One hundred eighty-one outpatients were enrolled into the study. The subjects were predominately African-American and female. Most were between 30 and 60 years of age. The Scadding radiograph stages were fairly evenly distributed across all five stages (0 through 4). Five (2.8%) of 181 patients were found to have pleural fluid. Two patients had a unilateral left-sided PE, and three patients had bilateral PEs. Pleural fluid analysis (PFA) was performed in four patients. The PFA showed a lymphocyte-predominant exudate using protein criterion in only two patients, which is consistent with sarcoidosis-related PE; one patient underwent pleural biopsy, which was consistent with the diagnosis of sarcoidosis. A sarcoidosis-related PE was seen in 1 of 9 patients (11.1%) who had an exacerbation of pulmonary sarcoidosis compared to 1 of 172 patients (0.6%) who did not have an exacerbation (p < 0.4). CONCLUSION: PEs are rare in outpatients with sarcoidosis, even when a sensitive technique, such as ultrasonography, is used. The frequency of PEs was 2.8% (5 of 181 patients) with only 2 of the 181 PEs (1.1%) caused by sarcoid pleural involvement. PE in patients with sarcoidosis should not be assumed to be related to sarcoidosis. Discordance between levels of pleural fluid total protein and lactate dehydrogenase may be a characteristic finding in patients with sarcoid PE. An exacerbation of pulmonary sarcoidosis was not an independent risk factor for the development of sarcoid-related PE.

Adult↗
PubMed2006

Pathophysiology of pneumothorax following ultrasound-guided thoracentesis.

STUDY OBJECTIVES: Pneumothorax following ultrasound-guided thoracentesis is rare. Our goal was to explain the mechanisms of pneumothorax following ultrasound-guided thoracentesis in a setting where pleural manometry is routinely used. METHODS: We reviewed the patient records and procedure reports of 401 patients who underwent ultrasound-guided thoracentesis. When manometry was performed, pleural space elastance was determined. A model assuming dependence of the pleural space elastic properties on respiratory system elastic properties was used to isolate cases with presumed normal pleural space elastance. Elastance outside mean +/- SD x 2 of the isolated sample was considered abnormal. Four radiographic criteria of unexpandable lung were used: visceral pleural peel, lobar atelectasis, basilar pneumothorax, and pneumothorax with ipsilateral shift. RESULTS: There were 102 diagnostic thoracenteses, 192 therapeutic thoracenteses with pleural manometry, and 73 therapeutic thoracenteses without manometry. There was one pneumothorax that occurred from lung puncture and eight unintentional pneumothoraces, all of which showed radiographic evidence of unexpandable lung. Four of eight unintentional pneumothoraces had abnormal elastance; none had excessively negative pleural pressure (< -25 cm H(2)O). CONCLUSIONS: Unintentional pneumothoraces cannot be prevented by monitoring for symptoms or excessively negative pressure. These pneumothoraces were drainage related rather than due to penetrating lung trauma or external air introduction. We speculate that unintentional pneumothoraces are caused by transient, parenchymal-pleural fistulae caused by nonuniform stress distribution over the visceral pleura that develop during large-volume drainage if the lung cannot conform to the shape of the thoracic cavity in some patients with unexpandable lung. These fistulae appear to be pressure dependent, and the resulting pneumothoraces rarely require treatment. Drainage-related pneumothorax is an unavoidable complication of ultrasound-guided thoracentesis and appears to account for the vast majority of pneumothoraces occurring in a procedure service.

Biomechanical Phenomena↗
PubMed2006

Effect of thoracentesis on respiratory mechanics and gas exchange in the patient receiving mechanical ventilation.

BACKGROUND: This study reports the effect of thoracentesis on respiratory mechanics and gas exchange in patients receiving mechanical ventilation. STUDY DESIGN: Prospective. SETTING: University hospital. PATIENTS: Eight patient receiving mechanical ventilation with unilateral (n = 7) or bilateral (n = 1) large pleural effusions. INTERVENTION: Therapeutic thoracentesis (n = 9). MEASUREMENTS: Resistances of the respiratory system measured with the constant inspiratory flow interrupter method measuring peak pressure and plateau pressure, effective static compliance of the respiratory system (Cst,rs), work performed by the ventilator (Wv), arterial blood gases, mixed exhaled Pco2, and pleural liquid pressure (Pliq). RESULTS: Thoracentesis resulted in a significant decrease in Wv and Pliq. Thoracentesis had no significant effect on dynamic compliance of the respiratory system; Cst,rs; effective interrupter resistance of the respiratory system, or its subcomponents, ohmic resistance of the respiratory system and additional (non-ohmic) resistance of the respiratory system; or intrinsic positive end-expiratory pressure (PEEPi). Indices of gas exchange were not significantly changed by thoracentesis. CONCLUSIONS: Thoracentesis in patients receiving mechanical ventilatory support results in significant reductions of Pliq and Wv. These changes were not accompanied by significant changes of resistance or compliance or by significant changes in gas exchange immediately after thoracentesis. The reduction of Wv after thoracentesis in patients receiving mechanical ventilation is not accompanied by predictable changes in inspiratory resistance and static compliance measured with routine clinical methods. The benefit of thoracentesis may be most pronounced in patients with high levels of PEEPi.

Adult↗
PubMed2004

Drug-induced pleural disease.

Drug-induced pleural disease is uncommon and less known to clinicians than drug-induced parenchymal lung disease. Pleural reactions from drugs manifest as pleural effusions, pleural thickening, or pleuritic chest pain, and may occur in the absence of parenchymal infiltrates. The clinician should be cognizant of the possibility of a drug-induced pleural reaction. A detailed drug history, temporal relationship between symptom onset and initiation of therapy, and pleural fluid eosinophilia should raise the suspicion of a drug-related process. We suspect that as new drugs are marketed in the United States, the number of drugs that result in pleuropulmonary toxicity will continue to increase. Moreover, if the cause of an exudative pleural effusion is not clinically obvious after pleural fluid analysis, drug therapy withdrawal should be a consideration if clinically appropriate before initiating an extensive diagnostic evaluation that may entail unnecessary economic burden and discomfort for the patient.

Anti-Infective Agents, Urinary↗
PubMed2004

Eucalyptus as a specific irritant causing vocal cord dysfunction.

BACKGROUND: Vocal cord dysfunction (VCD) is a well-recognized clinical entity that frequently mimics asthma and is characterized by inappropriate adduction of the vocal cords during inspiration. The pathogenesis of VCD has not yet been defined. The only previous report suggested that respiratory irritants may trigger paradoxical motion of the vocal cords. OBJECTIVE: To report the case of a 46-year-old woman with VCD precipitated by eucalyptus exposure. METHODS: A masked flexible fiberoptic nasolaryngoscopy was performed to confirm whether VCD occurred with eucalyptus and not with other known respiratory irritants. The patient underwent inhalation challenges consisting of water, ammonia, pine oil, and a combination of eucalyptus (dried leaves) and ammonia. Two independent observers before patient challenge could not identify eucalyptus. RESULTS: Vocal cord dysfunction occurred within minutes of exposure to eucalyptus. This is the first report to prospectively document that a specific irritant, eucalyptus, can precipitate VCD. Negative skin prick test results, total IgE level, and negative IgE eucalyptus-specific antibodies support a nonimmunologic mechanism. CONCLUSIONS: A new pathogenic mechanism for this clinical entity is supported by our observations. Furthermore, a nonimmunologic mechanism in which respiratory irritants may induce VCD is suspected. Future studies to elucidate this mechanism need to be performed in individuals with irritant-specific VCD.

Alveolitis, Extrinsic Allergic↗
PubMed2004

Causes and management of pleural fibrosis.

The development of pleural fibrosis follows severe pleural space inflammation which is typically associated with an exudative pleural effusion. The response of the mesothelial cell to injury and its ability, along with the basement membrane, to maintain its integrity, is vital in determining whether there is normal healing or pleural fibrosis. The formation of a fibrinous intrapleural matrix is critical to the development of pleural fibrosis. This matrix is the result of disordered fibrin turnover, whereby fibrin formation is up-regulated and fibrin dissolution is down-regulated. Cytokines, such as TGF-beta and TNF-alpha, facilitate the fibrin matrix formation. A complete understanding of the pathogenesis of pleural fibrosis and why abnormal pleural space remodeling occurs in some and not in others, remains unknown. Clinically significant pleural fibrosis requires involvement of the visceral pleura. Isolated parietal pleural fibrosis, as with asbestos pleural plaques, does not cause restriction or respiratory impairment. The causes of visceral pleural fibrosis include asbestos-associated diffuse pleural thickening, coronary bypass graft surgery, pleural infection (including tuberculous pleurisy), drug-induced pleuritis, rheumatoid pleurisy, uraemic pleurisy, and haemothorax. Systemic and intrapleural corticosteroids administered during the initial presentation of rheumatoid pleurisy in small series may decrease the incidence of pleural fibrosis. Several randomised control trials using corticosteroids in tuberculous pleurisy have not shown efficacy in reducing residual pleural fibrosis. Decortication is effective in treating symptomatic patients regardless of the cause of pleural fibrosis as long as chronicity has been documented and significant underlying parenchymal disease has been excluded.

Asbestosis↗
PubMed2004

Intrapleural staphylococcal superantigen induces resolution of malignant pleural effusions and a survival benefit in non-small cell lung cancer.

BACKGROUND: Malignant pleural effusion (MPE) may occur in up to 50% of patients with non-small cell lung cancer (NSCLC). The majority of these patients have a poor performance status and a dismal prognosis, with survival duration ranging from 2 to 3 months. Since these patients are typically symptomatic from their MPE, prompt treatment is required. Patients with symptomatic MPE from NSCLC and poor performance scores (Eastern Cooperative Oncology Group [ECOG] score >/= 2, Karnofsky performance status [KPS] score < 50) are generally not offered systemic chemotherapy. Treatment is palliative and includes intrapleural catheter drainage or chemical pleurodesis with talc, doxycycline, or bleomycin. None of the latter modalities prolong survival. OBJECTIVE: Our goal was to investigate the toxicity and therapeutic effect of a new therapeutic agent, Staphylococcus aureus superantigen (SSAg), a powerful T-cell stimulant administered intrapleurally to unselected, consecutive patients with MPE from NSCLC (stage IIIb with pleural effusion) and a poor performance status. By providing direct access of the SSAg to the bronchial and mediastinal lymphatics, we predicted that intrapleural administration of SSAg would induce resolution of MPE and prolong survival in this population with advanced NSCLC and a limited prognosis. METHODS: Fourteen consecutive, unselected patients with MPE from NSCLC and a median pretreatment KPS score of 40 (range, 10 to 60) received pleural instillation of SSAg, 100 to 400 pg, once or twice weekly (mean, 3.7 +/- 1.3 treatments [+/- SD]) until the pleural effusions resolved. They were evaluated for drug toxicity, resolution, duration of MPE, and survival. RESULTS: Other than mild fever (maximum grade 2), toxicity of SSAg treatment was trivial and notably devoid of respiratory distress or hypotension. Eleven patients had a complete response (CR), and 3 patients had a partial response of their MPE. In 12 patients, the response endured for > 90 days, with a median time to recurrence of 5 months (range, 3 to 23 months). The median survival for the SSAg-treated group was 7.9 months (range, 2 to 36 months; 95% confidence interval [CI], 5.9 to 11.4 months), compared to a median survival of 2.5 months (range, 0.1 to 57 months; 95% CI, 1.3 to 3.4 months) for 18 consecutive, unselected patients with MPE from NSCLC (stage IIIb) treated with talc poudrage (p = 0.044). Survival duration of all 14 SSAg-treated cases and 13 talc-poudrage-treated patients with comparable pretreatment KPS (range, 10 to 60; median, 40 and 30, respectively), and distribution (p = 0.5) was 7.9 months (95% CI, 5.9 to 11.4 months) and 2.0 months (95% CI, 0.4 to 2.9 months), respectively (p = 0.0023). Nine of 14 patients treated with SSAg survived > 6 months, 4 patients survived > 9 months, and 3 patients survived > 350 days. One of the patients in the CR group has survived 36 months. None of the 13 talc-treated patients survived > 6 months. INTERPRETATION: In 14 unselected, consecutive patients with MPE from NSCLC and poor pretreatment performance (median KPS of 40), the intrapleural administration of SSAg was efficacious in resolving the MPE without any clinically important adverse effects. SSAg-treated patients with a median KPS of 40 (range, 10 to 60) had a median survival that exceeded that with talc poudrage, and was comparable to current systemic chemotherapy used in patients with KPS >/= 70 status. SSAg treatment is simple to perform, minimally invasive, and does not require hospital time. It may be an attractive alternative to existing palliative modalities for stage IIIb patients with MPE and poor performance who are not candidates for systemic chemotherapy.

Aged↗
PubMed2004

Pleural manometry: technique and clinical implications.

INTRODUCTION: Pleural manometry during large-volume thoracentesis can prevent the development of excessively negative pleural pressures, which have been associated with re-expansion pulmonary edema; can diagnose an unexpandable lung; and can predict pleurodesis success. We currently perform pleural manometry simultaneously with both a vertical-column water manometer with an interposed resistive element, and a hemodynamic transducer connected to a standard physiologic system. We present the technique as well as the advantages and disadvantages of both systems in measuring pleural liquid pressures. TECHNIQUE: A flexible thoracentesis catheter is inserted in the most dependent portion of the pleural effusion. The water manometer consists of two lengths of IV tubing connected through a 22-gauge needle inserted into an injection terminal. The system is connected to the zeroing port of the pressure transducer, and both are carefully purged of air. The electronic system is zeroed at the level the thoracentesis catheter is introduced into the patient. Measurements are performed initially and after each 250 mL of fluid that is withdrawn. ACCURACY OF THE WATER MANOMETER: Forty consecutive patients who underwent therapeutic thoracentesis had pressure measurements. Pleural fluid removed ranged from 50 to 4,200 mL (mean, 1,445 mL). A total of 291 pressure measurements were acquired and analyzed. Mean pleural liquid pressure obtained by the water manometer had a strong positive correlation with the values obtained by a standard physiologic system (r = 0.97, p < 0.001). CONCLUSION: An overdamped water manometer is a valid method to measure mean pleural liquid pressure. Coughing invalidates pressure measurements with the water manometer; however, with the electronic method, periods of quiet breathing can be identified, allowing for the measurement of pleural pressure.

Adult↗