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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review, three aspects of pleural disease are discussed. Although it was thought for many years that the origin of pleural fluid was the capillaries in the parietal or visceral pleura, recent evidence suggests that in many cases the origin of pleural fluid is the interstitial space of the lung. The interstitial space of the lung appears to be the source of the pleural fluid in patients who have congestive heart failure, parapneumonic effusions, pulmonary embolism, and lung transplants. The Hantavirus pulmonary syndrome is characterized by rapidly progressive, noncardiogenic pulmonary edema in relatively young, previously healthy individuals. The mortality rate with this syndrome is approximately 60%, and at autopsy most patients have large pleural effusions. Patients after lung transplantation frequently have profuse drainage from their chest tubes because most of the fluid that enters the lung must exit through the pleural space. The incidence of pleural effusion is very high in patients who have a complication of their lung transplantation, but the pleural fluid findings in patients after lung transplantation have not been well studied. Similarly, virtually all patients who undergo liver transplantation have a right-sided pleural effusion. The effusion usually reaches its maximum size around the third postoperative day. If the effusion increases in size after this time, serious complications should be suspected. The approach to pleural diseases has been altered with the advent of videothoracoscopy. Videothoracoscopy should be considered in patients who have undiagnosed pleural effusions and are not improving; in patients who have had recurrent pneumothorax, or a spontaneous pneumothorax with a persistent airleak or unexpanded lung; or in patients who have a traumatic hemothorax with clotted blood.
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PMID:Diseases of the pleura. 936 70

A 21-year-old man; complaining of left chest pain and dyspnea, was admitted to our hospital with a diagnosis of spontaneous pneumothorax. Though chest X-ray on admission did not show hemothorax, chest drainage revealed intrapleural bleeding. As chest X-ray on the following day showed evident fluid level, emergency operation was carried out with a diagnosis of spontaneous hemopneumothorax. Bleeding point was a ruptured vessel between parietal pleura and bulla in apex of lung. The bulla was resected following hemostasis. After improvement of complicating postoperative re-expansive pulmonary edema, the patient was discharged on the 18th postoperative day. On treatment of spontaneous hemopneumothorax, existence of such a case as ours should be taken into account.
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PMID:[A case of spontaneous hemopneumothorax occurred after thoracic drainage]. 978 30

Acute ipsilateral or bilateral pulmonary oedema following lung re-expansion after pleurocentesis or treatment of pneumothorax is an unusual clinical phenomenon that may have serious consequences. It usually occurs when the chronically collapsed lung is rapidly re-expanded. There are, however, no reported cases of this complication following one-lung ventilation used to facilitate surgery. A report of the occurrence of unilateral re-expansion oedema in a young female undergoing scoliosis correction is described.
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PMID:Re-expansion pulmonary oedema following one-lung ventilation--a case report. 1056 74

With the advent of smaller biphasic transvenous implantable cardioverter defibrillators (ICDs) and the experience gained over the years, it is now feasible for electrophysiologists to implant them safely in the abdominal or pectoral area without surgical assistance. Throughout the years, general anesthesia has been used as the standard technique of anesthesia for these procedures. However, use of local anesthesia combined with deep sedation only for defibrillation threshold (DFT) testing might further facilitate and simplify these procedures. The purpose of this study was to test the feasibility of using local anesthesia and compare it with the standard technique of general anesthesia, during implantation of transvenous ICDs performed by an electrophysiologist in the electrophysiology laboratory. For over 4 years in the electrophysiology laboratory, we have implanted transvenous ICDs in 90 consecutive patients (84 men and 6 women, aged 58 +/- 15 years). Early on, general anesthesia was used (n = 40, group I), but in recent series (n = 50, group II) local anesthesia was combined with deep sedation for DFT testing. Patients had coronary (n = 58) or valvular (n = 4) disease, cardiomyopathy (n = 25) or no organic disease (n = 3), a mean left ventricular ejection fraction of 35%, and presented with ventricular tachycardia (n = 72) or fibrillation (n = 16), or syncope (n = 2). One-lead ICD systems were used in 74 patients, two-lead systems in 10 patients, and an AVICD in 6 patients. ICDs were implanted in abdominal (n = 17, all in group I) or more recently in pectoral (n = 73) pockets. The DFT averaged 9.7 +/- 3.6 J and 10.2 +/- 3.6 J in the two groups, respectively (P = NS) and there were no differences in pace-sense thresholds. The total procedural duration was shorter (2.1 +/- 0.5 hours) in group II (all pectoral implants) compared with 23 pectoral implants of group I (2.9 +/- 0.5 hours) (P < 0.0001). Biphasic devices were used in all patients and active shell devices in 67 patients; no patient needed a subcutaneous patch. There were six complications (7%), four in group I and two in group II: one pulmonary edema and one respiratory insufficiency that delayed extubation for 3 hours in a patient with prior lung resection, both probably related to general anesthesia, one lead insulation break that required reoperation on day 3, two pocket hematomas, and one pneumothorax. There was one postoperative arrhythmic death at 48 hours in group I. No infections occurred. Patients were discharged at a mean time of 3 days. All devices functioned well at predischarge testing. Thus, it is feasible to use local anesthesia for current ICD implants to expedite the procedure and avoid general anesthesia related cost and possible complications.
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PMID:Electrophysiologist-implanted transvenous cardioverter defibrillators using local versus general anesthesia. 1066 58

A 21-year-old male with bilateral pneumothorax underwent thoracoscopic bullaectomy in the lateral decubitus position. General anesthesia was induced using thiopental 250 mg and suxamethonium 80 mg and maintained using the combination of the thoracic-epidural anesthesia with assisted spontaneous respiration. He was intubated with a tube equipped with mobile bronchial cuff. On the left bullaectomy, two lung ventilation (TLV) was applied and its course was uneventful. On the right, one lung ventilation (OLV) was done. Fifty minutes after the start of OLV of the left lung, percutaneous arterial hemoglobin saturation (SpO2) declined to 60% with PaO2 36 mmHg. Then, under super imposed HFJV (high frequency jet ventilation) added to manual assisted ventilation through the bronchial brocker, SpO2 increased rapidly to 100%. Postoperative chest X-p showed signs of re-expansion pulmonary edema (RPE) in the dependent, left lung. PaO2 after 25 minutes of hypoxic episode increased to 339.2 mmHg. About 2 hours later he was extubated uneventfully. We conclude that superimposed HFJV is very beneficial for treatment of the RPE of the dependent lung during OLV applied for thoracoscopic operation with bilateral pneumothorax.
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PMID:[A case of anesthetic management for re-expansion pulmonary edema of the dependent lung saved by superimposed HFJV during one lung ventilation for the thoracoscopic operation associated with bilateral pneumothorax]. 1088 44

A 15-year-old patient has been admitted to the intensive care unit for severe respiratory distress syndrome that developed as a result of pneumonia. Interstitial lung edema was confirmed by computer-aided tomography. It was successfully treated by positive pressure ventilation (PPV). Although PEEP did not exceed 7 cm H2O, PPV was complicated by interstitial emphysema, pneumomediastinum, and bilateral pneumothorax as a result of barotrauma. Pulmonary artery pressure (PAP) and pulmonary capillary wedge pressure (PCWP) were monitored. High PCWP values were inconsistent with the diagnosis of acute respiratory distress syndrome. The authors suggest that high PCWP was caused by high intraalveolar pressure, pneumomediastinum, and venule constriction in the hypoxic sites of the lung.
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PMID:[A case of respiratory distress syndrome complicated by the development of interstitial emphysema and pneumomediastinum]. 1090 Jul 27

Re-expansion pulmonary edema (RPE) is an uncommon complication of sudden reinflation of a lung collapsed by pneumothorax or pleural effusion. We present a case of bilateral pulmonary edema following unilateral drainage of a pleural effusion in a young child with non-Hodgkin's lymphoma.
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PMID:Bilateral re-expansion pulmonary edema in a child: a reminder. 1093 4

Reexpansion pulmonary edema is a well-described complication of treatment for pleural effusion and pneumothorax. It is very rarely described in association with anesthesia and video-assisted thoracoscopic surgery. The etiology is unclear but several mechanisms have been proposed. We report a case of reexpansion pulmonary edema after video-assisted thoracoscopic surgery treated successfully with continuous positive airway pressure.
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PMID:Reexpansion pulmonary edema after VATS successfully treated with continuous positive airway pressure. 1096 4

Barotrauma is well known to be a relatively common complication of high-frequency jet ventilation (HFJV); however, the occurrence of reexpansion pulmonary edema (REPE) is extremely rare. We report herein a case of REPE caused by difficulties encountered with anesthesia using HFJV during video-assisted thoracic surgery (VATS) for a spontaneous pneumothorax. We believe the rapid increase in pressure in the lung after degassing for VATS resulted in REPE as well as typical barotrauma.
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PMID:Reexpansion pulmonary edema due to high-frequency jet ventilation: report of a case. 1119 44

Ipsilateral pulmonary edema may occur in a lung that has been rapidly reinflated after a period of collapse. The syndrome of re-expansion pulmonary edema is associated with variable degrees of hypotension and hypoxemia. In its extreme form, it may result in cardiac arrest and death. The initial cause of uninflated pulmonary parenchyma described with re-expansion pulmonary edema has typically been either a large undrained pleural effusion or a pneumothorax. The authors describe a patient in whom re-expansion pulmonary edema developed when inadvertent puncture of large emphysematous bullae released previously atelectatic lung.
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PMID:Re-expansion pulmonary edema following puncture of a giant bulla. 1121 67


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