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Sun Feb 24 20:25:40 GMT 2008

Karim, I put a few abstracts here - it appears large TV and no PEEP causes injury the lung like you mentioned.
Also, in a trauma patient it is difficult to limit i.v.fluids like we anesthesiologists normally do in a schedule pneumonectomies. It would be no surprise that trauma pneumonectomies have a high incidence of postpneumonectomy pulmonary edema.   

I cannot find any confirmation there is normally any pulmonary hypertension proven to exist after pneumonectomies, I never had a PA catheter in with one of those. Even so, the pulmon. HTN if it comes from the pulmonary vessels would be protective of pulmonary edema. It would have to be transmitted from high filling pressures from the left heart to cause pulmonary edema, for which however there is no reason: so I don't thing hemodynamics has much to do with it, unless there are both "too much" cardiac output through the remaining lung with secondarily somewhat increased PA pressures with a normal wedge. In that case NO would be the way to go together with betablockade and general measures to decrease peripheral O2 demand.

All else regards lung injury from overdistention - why would that lead to pulmonary edema and not to other type of acute lung injury ? Unless there is associated lung injury with the edema.
Don't understand it really.

The following is the popular PRO/CON duo of papers on this issue:
http://www.anesthesia-analgesia.org/cgi/content/full/103/2/268
http://www.anesth-analg.net/cgi/content/full/103/2/271

Intraoperative Tidal Volume as a Risk Factor for Respiratory Failure after Pneumonectomy
Anesthesiology - Volume 105, Issue 1 (July 2006)  -  Copyright © 2006 American Society of Anesthesiologists, Inc.  -  About This Journal  

Clinical Investigations
Intraoperative Tidal Volume as a Risk Factor for Respiratory Failure after Pneumonectomy

Evans R. Fernández-Pérez, M.D.*,* 
Mark T. Keegan, M.B.M.R.C.P.I.‡ 
Daniel R. Brown, M.D., Ph.D.‡ 
Rolf D. Hubmayr, M.D.‡ 
Ognjen Gajic, M.D., M.Sc.§ 

*  Fellow in Critical Care Medicine, Division of Critical Care Medicine 
‡  Assistant Professor of Anesthesiology, Division of Anesthesia and Critical Care Medicine 
‡  Professor of Medicine and Physiology 
§  Assistant Professor of Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic College of Medicine 

* Address correspondence to Dr. Fernández-Pérez: OL 2-115, Old Marian Hall, Saint Mary’s Hospital, Mayo Clinic, Rochester, Minnesota 55905.

E-mail address:  fernandez.evans at mayo.edu

Manuscript received  November  11,   2005 , accepted  February  23,   2006
Intraoperative mechanical ventilation with large tidal volumes is associated with postpneumonectomy respiratory failure.

This article is accompanied by an Editorial View. Please see: Slinger PD: Postpneumonectomy pulmonary edema: Good news, bad news. Anesthesiology 2006; 105:2–5.Received from the Mayo Clinic College of Medicine, Rochester, Minnesota. Supported in part by a grant from the Mayo Foundation, Rochester, Minnesota (Dr. Fernández-Pérez and Dr. Brown) and grant No. K23 HL78743-01A1 from the National Institutes of Health, National Heart, Lung and Blood Institute, Bethesda, Maryland (Dr. Gajic). An abstract of this study was presented at the American College of Chest Physicians Annual Conference, Montréal, Québec, Canada, October 29–November 3, 2005.Individual article reprints may be purchased through the Journal Web site, www.anesthesiology.org.

PII S0003-3022(06)60673-3

 Background: 
Respiratory failure is a leading cause of postoperative morbidity and mortality in patients undergoing pneumonectomy. The authors hypothesized that intraoperative mechanical ventilation with large tidal volumes (VTs) would be associated with increased risk of postpneumonectomy respiratory failure.
Methods: 
Patients undergoing elective pneumonectomy at the authors’ institution from January 1999 to January 2003 were studied. The authors collected data on demographics, relevant comorbidities, neoadjuvant therapy, pulmonary function tests, site and type of operation, duration of surgery, intraoperative ventilator settings, and intraoperative fluid administration. The primary outcome measure was postoperative respiratory failure, defined as the need for continuation of mechanical ventilation for greater than 48 h postoperatively or the need for reinstitution of mechanical ventilation after extubation.
Results: 
Of 170 pneumonectomy patients who met inclusion criteria, 30 (18%) developed postoperative respiratory failure. Causes of postoperative respiratory failure were acute lung injury in 50% (n = 15), cardiogenic pulmonary edema in 17% (n = 5), pneumonia in 23% (n = 7), bronchopleural fistula in 7% (n = 2), and pulmonary thromboembolism in 3% (n = 1). Patients who developed respiratory failure were ventilated with larger intraoperative VT than those who did not (median, 8.3 vs. 6.7 ml/kg predicted body weight; P < 0.001). In a multivariate regression analysis, larger intraoperative VT (odds ratio, 1.56 for each ml/kg increase; 95% confidence interval, 1.12–2.23) was associated with development of postoperative respiratory failure. The interaction between larger VT and fluid administration was also statistically significant (odds ratio, 1.36; 95% confidence interval, 1.05–1.97).
Conclusion: 
Mechanical ventilation with large intraoperative VT is associated with increased risk of postpneumonectomy respiratory failure.
Postpneumonectomy Pulmonary Edema: Good News, Bad News
Anesthesiology - Volume 105, Issue 1 (July 2006)  -  Copyright © 2006 American Society of Anesthesiologists, Inc.  -  About This Journal  

Editorial Views
Postpneumonectomy Pulmonary Edema: Good News, Bad News

Peter D. Slinger, M.D. 

Department of Anesthesia, University of Toronto, Toronto General Hospital, Toronto, Ontario, Canada 

E-mail address:  peter.slinger at uhn.on.ca

Manuscript accepted  February  14,   2006

This Editorial View is accompanied by the following article: Fernández-Pérez ER, Keegan MT, Brown DR, Hubmayr RD, Gajic O: Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy. Anesthesiology 2006; 105:14–8.The author is not supported by, nor maintains any financial interest in, any commercial activity that may be associated with the topic of this article.

PII S0003-3022(06)60669-1

IN this issue of Anesthesiology, Drs. Fernández-Pérez et al.[1] present a retrospective analysis of perioperative risk factors related to the development of respiratory failure necessitating mechanical ventilatory assistance beyond 48 h after pneumonectomy. Of 170 pneumonectomy patients studied during a 4-yr period at one institution, 30 developed postoperative respiratory failure. Half (15) of these respiratory failure cases were due to complications common to all major intrathoracic (and many nonthoracic) surgeries such as cardiogenic pulmonary edema, pneumonia, and pulmonary emboli. The other 15 cases (9% of pneumonectomies) were due to acute lung injury (ALI). This latter 9% represent a dreaded complication both for anesthesiologists and thoracic surgeons because this “postpneumonectomy pulmonary edema,”[1] unrelated to other identifiable etiologies of respiratory failure, has a case-fatality rate of more than 50% in most reports.[2] The most
 significant perioperative factor that Fernández-Pérez et al. found to be associated with postpneumonectomy respiratory failure was larger intraoperative tidal volumes (median 8.3 ml/kg predicted body weight in failure patients vs. 6.7 ml/kg in nonfailure pneumonectomy controls). The other significant factor was larger amounts of intraoperative fluids administered (median 2.2 l for cases vs. 1.3 l for controls). Patients who developed respiratory failure had a higher 60-day mortality than controls (23% vs. 4%) and a longer hospital stay (22 vs. 6 days).
Before we conclude that large tidal volumes and intravenous fluids contribute to postpneumonectomy pulmonary edema, there are some caveats that we must place on the analysis and that the authors largely acknowledge. In their retrospective analysis, the authors were not able to get clear data on the exact tidal volumes or duration of one-lung ventilation. They could only document the largest intraoperative tidal volume; this could represent one- or two-lung ventilation. However, because it has been a common clinical practice to use the same tidal volume for one- and two-lung ventilation,[3] I believe these data are probably valid. Also, the authors do not provide a between-subgroup comparison of the associations with tidal volume and fluids for the ALI versus the non-ALI respiratory failure cases. It seems plausible that tidal volumes might impact ALI but would not have an effect on non-ALI cases, whereas fluids could impact both cardiogenic and
 noncardiogenic pulmonary edema.
The original description of postpneumonectomy pulmonary edema as a specific entity seems to have been in a series of 10 cases published in 1984 by Zeldin et al.[4] After retrospective comparison with controls, they identified three significant risk factors: right pneumonectomy (9 of 10 cases), increased perioperative intravenous fluids, and increased postoperative urine output. Zeldin et al. further demonstrated their thesis that this was an anesthetic complication caused by overhydration by producing postpneumonectomy pulmonary edema in a dog model with fluid overload. In their recommendations, they wrote, “… the most important thing that we can do in terms of recognizing this problem is to watch our anesthetists as they start loading the patient up with fluid.” In the 20+ yr since the article of Zeldin et al. was published, there have been at least a dozen similar case-series reviews of this topic, with varied conclusions about the role of fluid
 administration as a cause of this complication. Also, a variety of other associated and potentially causative factors have been proposed, such as the administration of fresh frozen plasma, mediastinal lymphatic damage,[5] serum cytokines, and oxygen toxicity.[6] 
The largest study of postpneumonectomy pulmonary edema was by Turnage and Lunn.[7] In a retrospective survey of 806 pneumonectomies published in 1993 (from the same institution as Fernández-Pérez et al.), they found 21 cases (2.5%) of postpneumonectomy pulmonary edema, one of the lowest incidences reported of this complication. They found no differences in any measure of perioperative fluid balance between postpneumonectomy pulmonary edema cases (mean positive fluid balance at 24 h = 10 ml/kg) versus uncomplicated pneumonectomy controls (24-h positive balance = 13 ml/kg). However, the routine practice at their institution was rigorous fluid restriction, compared with many other reports where the 24-h fluid balance often exceeds 20 ml/kg.[8] This suggests that by limiting fluids the incidence of postpneumonectomy, ALI can be decreased but not eliminated.
Traditional teaching has been to use large tidal volumes, 10–12 ml/kg, during one-lung ventilation to prevent atelectasis in the dependent lung and to avoid hypoxemia.[3] However, the incidence of hypoxemia during one-lung ventilation has declined from 20–25% in the 1970s[9] to less than 1% currently.[10] This decrease can be attributed to several advances in thoracic anesthesia, including the use of fiberoptic bronchoscopy for positioning double-lumen endobronchial tubes and bronchial blockers and the use of newer volatile anesthetics[11] (isoflurane, sevoflurane, desflurane) that cause less inhibition of hypoxic pulmonary vasoconstriction and less shunt during one-lung ventilation than older volatile agents.[12] Before this study of Fernández-Pérez et al., several other reports have also suggested that the use of large tidal volumes and pressures during one-lung ventilation may contribute to post–lung resection ALI. Van der Werff et al.[13]
 found ALI, diagnosed radiographically, in 42% of pneumonectomy patients who were ventilated with peak airway pressures greater than 40 cm H2O. Licker et al.[14] found that the most significant predictor of ALI was the product of the airway pressure and the duration of one-lung ventilation. Also, bronchial lavage levels of some inflammatory markers were higher after one-lung ventilation with 10 ml/kg tidal volumes versus 5 ml/kg.[15] 
Central to our current understanding of postpneumonectomy ALI is the appreciation that the patients develop a low-pressure, high-protein-content pulmonary edema, which indicates an endothelial injury.[7] It has been demonstrated that the nonoperated lung develops a capillary-leak injury after a pneumonectomy but not a lobectomy.[16] There is no single mechanism that can fully explain ALI after lung resection, and its etiology is likely multifactorial; it may represent one end of a spectrum of lung injury that occurs with all pulmonary resections and is proportional to the amount of lung tissue resected. Changes in plasma makers of oxidative damage after pulmonary resection were found to be largest in pneumonectomy patients, less in lobectomy, and not significant in wedge resection or abdominal surgery.[17] 
Understanding that lung endothelial injury occurs after major lung resection supports management principles similar to other conditions associated with ALI and acute respiratory distress syndrome.[18] As a general principle, it seems that the lung is least injured when a pattern of ventilation as close as possible to normal spontaneous ventilation can be followed: fraction of inspired oxygen as low as acceptable, variable tidal volumes, beginning inspiration at functional residual capacity, and avoiding atelectasis[19] with frequent recruitment maneuvers.[20] Studies in acute respiratory distress syndrome demonstrate that ALI is exacerbated by the use of large tidal volumes and that lung-protective ventilation strategies with low tidal volumes and positive end-expiratory pressure are less injurious.[21] The most important factor in the etiology of ventilator-induced lung injury is the end-inspiratory lung volume.[22] Many patients, particularly those
 with emphysema, develop auto–positive end-expiratory pressure during one-lung ventilation,[23] thus beginning inspiration at a lung volume above functional residual capacity. It is conceivable that routine use of large tidal volumes (10–12 ml/kg) during one-lung ventilation in such patients produces end-inspiratory lung volumes close to levels that contribute to ALI, particularly in the smaller left lung.
Based on our current appreciation of post–lung resection ALI, several management principles for pneumonectomy (and potential pneumonectomy) patients seem evident. Overinflation of the nonoperated (ventilated) lung should be avoided using lung-protective ventilation (tidal volumes 5–6 ml/kg), adding positive end-expiratory pressure to those patients without auto–positive end-expiratory pressure and limiting plateau and peak inspiratory pressures to less than 25 cm H2O and less than 35 cm H2O, respectively.[24] Minimizing pulmonary capillary pressures by avoiding overhydration for patients undergoing pneumonectomy is reasonable, while acknowledging that not all increases in pulmonary artery pressures perioperatively are due to intravascular volume replacement. Other factors, such as hypercapnia, hypoxemia, and pain, can all increase pulmonary pressures and must be treated.
It should be appreciated that not all hyperinflation of the residual lung occurs in the operating room. Overexpansion of the remaining lung after pneumonectomy may occur postoperatively either with or without a chest drain in place. This prolonged hyperinflation during the period of increased endothelial permeability may be one of the major causes of postpneumonectomy pulmonary edema. There is currently no consensus among thoracic surgeons on the best method to manage the postpneumonectomy chest cavity. There are at least four methods: chest closure without a chest drain, attachment of a chest drain to underwater seal, repeated unclamping of a chest drain, and use of a balanced chest drainage system to maintain the mediastinum in a neutral position.[25] Use of a balanced chest drainage system has been suggested to contribute to a marked decline in postpneumonectomy pulmonary edema in one center.[26] A sheep study (University of Western Australia, Perth,
 Australia) found a significant reduction in postpneumonectomy pulmonary edema with the use of a balanced chest drainage system compared with no drain or the other methods of chest drain management (personal communication, John M. Alvarez, M.B., B.S., F.R.A.C.S., Clinical Associate Professor, Department of Cardiothoracic Surgery, January 2006).
In summary, there is good news and bad news about postpneumonectomy ALI. The good news is that as the etiology begins to become clearer and we understand that there is a postresection lung endothelial injury, we can begin to use ventilation strategies that have been shown to improve survival in patients with other forms of ALI. Also good news is that we, as anesthesiologists, do not cause the injury with intravenous fluids (we can make it worse, but we do not cause it). And also good news is that the mortality of postpneumonectomy pulmonary edema seems to be decreasing. Fernández-Pérez et al. found that greater than 75% of patients survived. This compares to less than 50% survival in previous reports. However, this may be more related to better intensive care of established cases than to anesthetic management.[27] 
The bad news is that the incidence of postpneumonectomy pulmonary edema does not seem to be decreasing. The incidence in the current study is 9%, compared with an incidence of less than 3% at the same institution 10 yr ago.[7] This could be due heightened awareness and more aggressive treatment. Also, few anesthesiologists have yet adopted lung-protective ventilation in thoracic anesthesia, so it may be too early to expect an improvement. Also bad news is that fluid restriction does seem to be indicated for anesthetic management of pneumonectomy patients. This complicates perioperative management in patients who often receive thoracic epidural analgesia and tend to be hypotensive. And finally, bad news is that much of the etiology of post–lung resection ALI may be related to the extent of the surgical resection and the postoperative chest drain management and thus may be out of the control of the anesthesiologist.

Extravascular lung water after pneumonectomy and one-lung ventilation in sheep
Critical Care Medicine - Volume 35, Issue 6 (June 2007)  -  Copyright © 2007 Lippincott Williams & Wilkins  -  About This Journal  

Laboratory Investigations
Extravascular lung water after pneumonectomy and one-lung ventilation in sheep

Vsevolod V. Kuzkov, MD, PhD 
Evgeny V. Suborov, MD 
Mikhail Y. Kirov, MD, PhD 
Vladimir N. Kuklin, MD, PhD 
Mehrdad Sobhkhez, MSci 
Solveig Johnsen, MD 
Kristine Waerhaug, MD 
Lars J. Bjertnaes, MD, PhD 

From the Department of Anesthesiology, Institute of Clinical Medicine, University of Tromsø, Tromsø, Norway (VVK, EVS, MYK, VNK, MS, SJ, KW, LJB); and the Department of Anesthesiology and Intensive Care Medicine, Northern State Medical University, Arkhangelsk, Russian Federation (VVK, EVS, MYK) 

Presented, in part, at the 28th Scandinavian Congress of Anesthesiologists, Reykjavik, Iceland, July 2005; at the Norwegian Anesthesiological Society, Tromsø, Norway, October 2005; and at the Euroanesthesia Congress 2006, Madrid, Spain, June 2006.Dr. Kirov is a member of the medical advisory board of Pulsion Medical Systems. The other authors have not disclosed any potential conflicts of interest.Supported, in part, by Helse Nord, Norway (project 4001.721.477); the Research Council of Norway; Pulsion Medical Systems, Germany; and departmental funds of the Department of Anesthesiology, University Hospital of North Norway.For information regarding this article, E-mail: vkuzkov at atnet.ru; v_kuzkov at mail.ru

PII S0090-3493(07)60358-7

 Objective: 
To compare the single thermodilution and the thermal-dye dilution techniques with postmortem gravimetry for assessment of changes in extravascular lung water after pneumonectomy and to explore the evolution of edema after injurious ventilation of the left lung.
Design: 
Experimental study.
Setting: 
University laboratory.
Subjects: 
A total of 30 sheep weighing 35.6 ± 4.6 kg. The study included two parts: a pneumonectomy study (n = 18) and an injurious ventilation study (n = 12).
Methods: 
Sheep were anesthetized and mechanically ventilated with an Fio2 of 0.5, tidal volume of 6 mL/kg, and positive end-expiratory pressure of 2 cm H2O. In the pneumonectomy study, sheep were assigned to right-sided pneumonectomy (n = 7), left-sided pneumonectomy (n = 7), or lateral thoracotomy only (sham operation, n = 4). In the injurious ventilation study, right-sided pneumonectomy was followed by ventilation with a tidal volume of 12 mL/kg and positive end-expiratory pressure of 0 cm H2O (n = 6) or by ventilation with a tidal volume of 6 mL/kg and positive end-expiratory pressure of 2 cm H2O for 4 hrs (n = 6). Volumetric variables, including extravascular lung water index (EVLWI), were measured with single thermodilution (STD; EVLWISTD) and thermal-dye dilution (TDD; EVLWITDD) techniques. We monitored pulmonary hemodynamics and respiratory variables. After the sheep were killed, EVLWI was determined for each lung by gravimetry (EVLWIG).
Results: 
In total, the study yielded strong correlations of EVLWISTD and EVLWITDD with EVLWIG (n = 30; r = .83 and .94, respectively; p < .0001). After pneumonectomy, both the left- and the right-sided pneumonectomy groups displayed significant decreases in EVLWISTD and EVLWITDD. The injuriously ventilated sheep demonstrated significant increases in EVLWI that were detected by both techniques. The mean biases (±2 sd) compared with EVLWIG were 3.0 ± 2.6 mL/kg for EVLWISTD and 0.4 ± 1.6 mL/kg for EVLWITDD.
Conclusions: 
After pneumonectomy and injurious ventilation of the left lung, TDD and STD displayed changes in extravascular lung water with acceptable accuracy when compared with postmortem gravimetry. Ventilator-induced lung injury seems to be a crucial mechanism of pulmonary edema after pneumonectomy.

Association of High Tidal Volume with Postpneumonectomy Failure
Anesthesiology - Volume 106, Issue 4 (April 2007)  -  Copyright © 2007 American Society of Anesthesiologists, Inc.  -  About This Journal  

Correspondence
Association of High Tidal Volume with Postpneumonectomy Failure

Steve Neustein, M.D. 

Mount Sinai Medical Center, New York, New York 

E-mail address:  steve.neustein at msnyuhealth.org

Manuscript accepted  November  15,   2006

PII S0003-3022(07)60141-4

To the Editor:— 
I read with interest the article titled “Intraoperative Tidal Volume as a Risk Factor for Respiratory Failure after Pneumonectomy” by Fernández-Pérez et al.[1] This is an important article because the traditional approach to one-lung ventilation has been to deliver 10–12 ml/kg tidal volume.[2] As the authors pointed out, two previous studies reported that high intraoperative airway pressures during one-lung ventilation were associated with postoperative acute lung injury. [3] , [4] The study by Fernández-Pérez et al.[1] showed that larger tidal volumes were associated with a higher risk of postoperative respiratory failure. However, the largest tidal volume recorded on the chart was used in the analysis. This would most likely have been during two-lung ventilation, even if the tidal volume had been reduced during one-lung ventilation. If the tidal volume is not adjusted when initiating one-lung ventilation, the airway pressure will increase due
 to reduced compliance. It is possible that the ventilator will not deliver the full tidal volume, and then the largest recorded tidal volume would be the two-lung tidal volume. Data were missing in more than 20% of the cases in this study, but it may still have been useful to examine what data were available, because this is the critical time period, and apparently there still would have been more than 100 cases to analyze. It would be important to follow up this study with either a prospective, randomized study using different tidal volumes during one-lung ventilation or even a retrospective study in which the tidal volumes can be definitely correlated with one-lung ventilation.
The authors stated that their most interesting finding was the association of both large tidal volume and greater fluid administration with postoperative respiratory failure. This makes sense in that the larger fluid administration can lead to pulmonary edema, once there is a capillary leak from a ventilator-induced injury. The authors hypothesized that the larger tidal volumes might have led to hypotension, which “forced” the anesthesiologists to administer more fluid. Although it is possible that resulting hypotension could have been treated with fluid, an alternative would have been infusion of a vasoconstrictor, such as phenylephrine. A more likely possibility is simply that the anesthesiologist who does not limit the tidal volumes or airway pressures during one-lung ventilation is less likely to be vigilant in limiting fluid administration. I do not understand, based on their data, how the authors concluded that even brief exposure to such
 ventilator settings could cause the postoperative complications.

REFERENCES:

1  Fernández-Pérez ER, Keegan MT, Brown D, Hubmayr RD, Gajic O:  Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy.   Anesthesiology 105. 14-18.2006;   Full Text 
2  Brodsky JB, Fitzmaurice B:  Modern anesthetic techniques for thoracic operations.   World J Surg 25. 162-166.2001;   Abstract 
3  Licker M, de Perrot M, Spiliopoulos A, Robert J, Diaper J, Chevalley C, Tschopp JM:  Risk factors for acute lung injury after thoracic surgery for lung cancer.   Anesth Analg 97. 1558-1565.2003;   Full Text 
4  van der Werff YD, van der Houwen HK, Heijmans PJ, Duurkens VA, Leusink HA, van Heesewijk HP, de Boer A:  Postpneumonectomy pulmonary edema: A retrospective analysis of incidence and possible risk factors.   Chest 111. 1278-1284.1997;   Full Text 

Ivan Hronek MD 
SFMC, Los Angeles
cell: 310 487-3288
ivanhronek at yahoo.com
http://health.groups.yahoo.com/group/Anesthideas/
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----- Original Message ----
From: "Hardcastle, Tim, Dr <tch at sun.ac.za>" <tch at sun.ac.za>
To: "Trauma & Critical Care mailing list" <trauma-list at trauma.org>
Sent: Monday, February 11, 2008 9:03:29 PM
Subject: RE: Post pneumonectomy pulmonary oedema

Karim

Post-operative fluid redistribution and rapid onset fulminant pulmonary oedema. His extubation may have been too early - the positive pressure controls the fluid shifts and once it is removed he starts to leak into the alveoli; slowly drowning in his own third space fluid, given that his right heart will be maximally strained the first 48 hours post-pneumonectomy. Happended to the last patient we did one of these on - ours was blunt trauma. The reported literature survival of pneumonectomy for trauma, specifically in the damage control context is BAD.

Better luck next time.

Tim (yes - I'm back at last!)
Dr T C Hardcastle
M.B.,Ch.B.(Stell); M.Med(Chir); FCS(SA)
Senior Surgeon / Senior Lecturer: Surgery (Trauma and ICU)
ATLS  instructor and DSTC Cape Town Course Director
Intern program Coordinator: Surgery
M.Med (Emergency Medicine) Executive Committee member
Clinical Head (Director): Diana Princess of Wales Trauma Unit
Division of Surgery (General) Room 4064
Department of Surgical Sciences
Tygerberg Hospital / University of Stellenbosch
PO Box 19063
Tygerberg 7505
Western Cape
South Africa
e-mail: tch at sun.ac.za
Cell: +27824681615
Office: +27219389281 or 4911 pager 0302

-----Original Message-----
From: trauma-list-bounces at trauma.org
[mailto:trauma-list-bounces at trauma.org]On Behalf Of Karim Brohi
Sent: Tuesday, February 12, 2008 5:31 AM
To: 'Trauma &amp; Critical Care mailing list'
Subject: Post pneumonectomy pulmonary oedema

Recently had a fit adult admitted following penetrating injury to the right
chest with injury of the lower lobe of the lung extending to the hilum with
associated extra-pericardial pulmonary vein laceration.  Had a right
pneumonectomy as very coagulopathic with oversew of the pulmonary vein. 

Initially did well, extubated at 24 hours, comfortable, haemoserous drainage
from chest tubes. 12 hours later after a couple of transient dips in
saturation developed acute pulmonary oedema, froth coming up the ET tube,
and died within minutes.  

Any ideas?

Karim

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