pt•rcent, much closer to the APACHE Ill rate of 88.1 pen·ent than the value presented. This error in research was probably inadvertent, hut is Jwverthelt•ss misleading.
Danid Ten•s, M.D., Critical Care Division, Baystate Medical Center, Springfield, Massachusetts; and Stanll'Y l..i.'llu:shorc, Ph.D., Dt'1Hirlllwnt of Biostanvtics and Epidl'tniology, University of Massachusetts, Amherst REFERENCES
Knaus \VA, \Vagnt·r DP, Draper EA. Zimmerman JE, Bergner M, Bastos PC, et al. The APACHE Ill prognostic system: risk prediction ofhospitalmortality for critically ill hospitalized adults. Chest 1991; 100:1619-36 2 Lemeshow S, Teres D, Avnmin JS, GageR\\~ Refining intensive care unit oulme prediction hy using changing probabilities of mortality. Crit Care Mt•d 198R; 16:470-77 FIGURE 1. A T2-weighted image (relaxation time, 1,400 ms; echo time, 100 ms) shows an intermediate-intensity mass t'mtaining some low-intensity spots. Intensity of fat tissue is high, and fat can he easily distinguished from tumor.
To the Editor: We agn•e. We used a figure from Table 6 of the artide by Lemeshow et al, which was fr a restricted set of patients. The t"rrect overall classification from the study was 84.9 percent, achieved with the patients from a single hospital as t"mpared with a mrrect classification of 8R.1 percent \\ith APACHE Ill on a 40hospital data base. We emphasize, however, that because of the bias inherent in trying to t"mpare t"rrect classification rates across data files that have varying baseline outt.,me rates, we prefer receiver operating characteristie (ROC) areas. For the specific issue of predicting hospital death rates. ROC areas are even more useli.JI, since the mnventional thn•shold of a 0.50 risk of death used in the above t~>rrect classification caleulations is arbitrary. The APACHE Ill system achieved a 0.90 ROC area. \Ve also would like to take this opportunity to mrrect one error in our APACHE Ill article. The st•x ratio was reversed. The t1>rrect distribution of sex across !Cll admissions is 55.2 pt•rcent male and 44.8 pereent female. Sex has no relationship with outmme and is not used in any APACHE onlt1>me predictions.
William A. Knaus, M.D., ICU Research, Gt:orgt• \'Hsclelike figures, moneytic keratinization, and intercellular bridges were also noted. An MR imaging study of the chest (Fig 1) was obtained with a 0.5-T supermnducting system (SMT 50, Simazu, Kyoto, Japan).
1920
Batra P. Hermann C, Mulder D. Mediastinal imaging in myasthenia gravis: mrrelation of chest radiology, CT, M R, and surgical findings. AJR 1986; 148:515-19 2 Molina PL, Siegel MJ, Glazer HS. Thymic masses on MR imaging. AJR 1990; 155:495-500 3 Dimario FJ, Lisak RP, Kostein MJ, Bnx>ks JJ. Myasthenia gravis and primary squamous cell carcinoma of the thymus: a case reJX>rt. Neurology 198R; 38:580-82 4 Shimosato Y, Kumeya T, Nagai K, Suemasu K. Squamous cell carcinoma of the thymus: an analysis of eight cases. Am J Surg Pathol1977; 1:109-21
Reexpansion Pulmonary Edema To the Editor: We read with great interest the article by Matsuura and t1>lleagues,1 which appeared in the December 1991 issue of Chest. In re1x>rting their experience with reexpansion pulmonary edema in a Communications to the Editor
large series of patients treated for spontaneous pneumothorax, they focus on the clinical aspects, but also list the possible mechanisms of reexpansion pulmonary edema, including increased pulmonary microvascular permeability (PMVP). The direct measurement of PMVP in man remains impossible, but a double-isotope scintigraphic method that provides a noninvasive index of PMVP has been developed. 2 This method can be used to generate parametric images of the lung fields, so that regional differences in PMVP can be studied? Using this technique, we have been able to demonstrate increased PMVP in the reexpanded lobe or segment in the majority of patients in whom a large pneumothorax has been drained.' These changes are also detected after drainage of large pleural effusions and after reexpansion of collapsed lung by laser bronchoscopic resection of occlusive endobronchial tumor. 5 At present, only supportive therapy can be offered once reexpansion pulmonary edema has developed, but it is hoped that further insights into the pathophysiologic mechanisms may lead to more specific treatments.
Simon W Davies, M.A., M.R.C.P., james W Bailey, D.C.R., D.R.l., lbul Wilkinson, M.R.C.P., Robin M. Rudd, M.D., F.R.C.P., London Chest Hospital,
London, England
REFERENCES
2 3 4
5
Matsuura Y, Nomimura T, Murakami H, Matsushima T, Kakehashi M, Kajihara H. Clinical analysis of reexpansion pulmonary edema. Chest 1991; 100:1562-66 Basran GS, Byrne AJ, Hardy JG. A noninvasive technique for monitoring lung vascular permeability in man. Nucl Med Commun 1985; 3:3-10 Keegan J, Bailey J, Wilkinson P, Davies S, Rudd R. Pulmonary microvascular permeability using double isotope scintigraphy. Nucl Med Commun 1989; 10:871-78 Wilkinson PW, Davies SW, Keegan J, Bailey J, Rudd R. Changes in pulmonary microvascular permeability accompanying re-expansion pulmonary oedema: evidence from dual isotope scintigraphy. Thor.uc 1990; 45:456-59 Davies SW, George J, Bailey J, Goldsmith SR, Keegan J, Rudd R. Increased microvascular permeability in lungs re-expanded by endoscopic laser treatment [abstract]. Am Rev Respir Dis 1990; I41(suppl):A293
To the Editor: We were pleased to learn that Dr Davies and his colleagues had read our article on reexpansion pulmonary edema (REPE). Although REPE is clinically a very important matter, the mechanism of its occurrence has remained unexplained. We have not had the means to inspect the mechanism in detail because, as Dr Davies and his colleagues point out, the direct measurement of pulmonary microvascular permeability (PMVP) in man remains impossible. On the basis of the results of a retrospective study of clinical cases of REPE, we postulated that age-related changes in the lung may afford some degree of protection against the development of REPE. Dr Davies and his colleagues found that PMVP increased in the reexpanded lobe or segment and proposed that increased PMVP causes REPE. These findings are very interesting and important, although they do not explain why REPE occasionally occurs in the contralateral lung. I think that our findings and the findings of Dr Davies do not clash substantially, because we did not study the mechanism of occurrence of REPE but postulated that age-related changes in the lung may afford some degree of protection against the development of REPE. I should like to ask Dr Davies and his colleagues whether there is a difference in PMVP according to age.
I agree with Davies et al that further insights into the physiologic mechanisms may lead to more specific treatments against REPE.
Yuichiro Matsuura, M.D., First Department of Surgery, Hiroshima University School of Medicine, Hiroshima City, japan
Pulmonary Toxicity Following Exposure to Methylene Chloride and Its Combustion Product, Phosgene To the Editor: The stripper strikes again! As we reported• in the March 1992 issue of Chest, chemical paint removers containing methylene chloride are widely used in domestic and industrial settings where exposure to a heat source with conversion to phosgene is possible. We have now cared for an additional patient with nearly identical problems. A 37-year-old man presented to the emergency room with complaints of shortness of breath associated with chest discomfort. His past medical history was unremarkable, and he was not a smoker. He had been using a paint remover consisting of80 percent methylene chloride two days before coming to the emergency room. He had been refinishing a piece of furniture in a poorly ventilated garage heated with a kerosene heater. The emergency room evaluation included a chest x-ray film, which revealed extensive bilateral alveolar and interstitial infiltrates. Initial arterial blood gas analysis on room air revealed the following values: pH, 7.39; Pco2 , 41 mm Hg; Po 2 , 50 mm Hg. The carbon monoxide level was 2.5 percent. The patient was treated with oxygen, and his symptoms improved during the next 48 to 72 h. A repeat x-ray film obtained three days later revealed marked but not complete resolution of the previously noted infiltrates. Oximetry at that time revealed 96 percent hemoglobin saturation on room air. At the time of discharge, the patient had a residual cough. Ten days later he was asymptomatic, and a chest x-ray film was normal. This presentation of another patient soon after our previous report suggests that this problem occurs more frequently than we had previously suggested and may well be underreported. This certainly seems to be true in a suburban setting, where home furniture refinishing by nonprofessionals is epidemic due to current economic conditions. We would like to again emphasize the need for complete medical evaluation following toxic exposures and for observation of the patient for a prolonged interval of time because of the potential for delayed clinical problems. We would also like to stress the need to carefully read warning labels when using paint removers containing methylene chloride and to avoid exposure to heat or open flame because of the added risk of phosgene production. Lethal concentrations have been reported within 5 to 10 min under test conditions. 2
Richard W Snyder, M.D., F.C.C.P., HenryS. Mishel, M.D., F.C.C.P., and G. Chris Christensen Ill, D.Q, F.C.C.P., Abington, Pennsylvania
REFERENCES 1 Snyder Rw, Mishel HS, Christensen GC III. Pulmonary toxicity following exposure to methylene chloride and its combustion product, phosgene. Chest 1992; 101:860-61 2 Gerritsen WB, Buschmann CH. Phosgene poisoning caused by the use of chemical paint removers containing methylene chloride in ill-ventilated rooms heated by kerosene stoves. Br J Ind Med 1960; 17:187-89 CHEST I 102 I 6 I DECEMBER, 1992
1921
Danid Ten•s, M.D., Critical Care Division, Baystate Medical Center, Springfield, Massachusetts; and Stanll'Y l..i.'llu:shorc, Ph.D., Dt'1Hirlllwnt of Biostanvtics and Epidl'tniology, University of Massachusetts, Amherst REFERENCES
Knaus \VA, \Vagnt·r DP, Draper EA. Zimmerman JE, Bergner M, Bastos PC, et al. The APACHE Ill prognostic system: risk prediction ofhospitalmortality for critically ill hospitalized adults. Chest 1991; 100:1619-36 2 Lemeshow S, Teres D, Avnmin JS, GageR\\~ Refining intensive care unit oulme prediction hy using changing probabilities of mortality. Crit Care Mt•d 198R; 16:470-77 FIGURE 1. A T2-weighted image (relaxation time, 1,400 ms; echo time, 100 ms) shows an intermediate-intensity mass t'mtaining some low-intensity spots. Intensity of fat tissue is high, and fat can he easily distinguished from tumor.
To the Editor: We agn•e. We used a figure from Table 6 of the artide by Lemeshow et al, which was fr a restricted set of patients. The t"rrect overall classification from the study was 84.9 percent, achieved with the patients from a single hospital as t"mpared with a mrrect classification of 8R.1 percent \\ith APACHE Ill on a 40hospital data base. We emphasize, however, that because of the bias inherent in trying to t"mpare t"rrect classification rates across data files that have varying baseline outt.,me rates, we prefer receiver operating characteristie (ROC) areas. For the specific issue of predicting hospital death rates. ROC areas are even more useli.JI, since the mnventional thn•shold of a 0.50 risk of death used in the above t~>rrect classification caleulations is arbitrary. The APACHE Ill system achieved a 0.90 ROC area. \Ve also would like to take this opportunity to mrrect one error in our APACHE Ill article. The st•x ratio was reversed. The t1>rrect distribution of sex across !Cll admissions is 55.2 pt•rcent male and 44.8 pereent female. Sex has no relationship with outmme and is not used in any APACHE onlt1>me predictions.
William A. Knaus, M.D., ICU Research, Gt:orgt• \'Hsclelike figures, moneytic keratinization, and intercellular bridges were also noted. An MR imaging study of the chest (Fig 1) was obtained with a 0.5-T supermnducting system (SMT 50, Simazu, Kyoto, Japan).
1920
Batra P. Hermann C, Mulder D. Mediastinal imaging in myasthenia gravis: mrrelation of chest radiology, CT, M R, and surgical findings. AJR 1986; 148:515-19 2 Molina PL, Siegel MJ, Glazer HS. Thymic masses on MR imaging. AJR 1990; 155:495-500 3 Dimario FJ, Lisak RP, Kostein MJ, Bnx>ks JJ. Myasthenia gravis and primary squamous cell carcinoma of the thymus: a case reJX>rt. Neurology 198R; 38:580-82 4 Shimosato Y, Kumeya T, Nagai K, Suemasu K. Squamous cell carcinoma of the thymus: an analysis of eight cases. Am J Surg Pathol1977; 1:109-21
Reexpansion Pulmonary Edema To the Editor: We read with great interest the article by Matsuura and t1>lleagues,1 which appeared in the December 1991 issue of Chest. In re1x>rting their experience with reexpansion pulmonary edema in a Communications to the Editor
large series of patients treated for spontaneous pneumothorax, they focus on the clinical aspects, but also list the possible mechanisms of reexpansion pulmonary edema, including increased pulmonary microvascular permeability (PMVP). The direct measurement of PMVP in man remains impossible, but a double-isotope scintigraphic method that provides a noninvasive index of PMVP has been developed. 2 This method can be used to generate parametric images of the lung fields, so that regional differences in PMVP can be studied? Using this technique, we have been able to demonstrate increased PMVP in the reexpanded lobe or segment in the majority of patients in whom a large pneumothorax has been drained.' These changes are also detected after drainage of large pleural effusions and after reexpansion of collapsed lung by laser bronchoscopic resection of occlusive endobronchial tumor. 5 At present, only supportive therapy can be offered once reexpansion pulmonary edema has developed, but it is hoped that further insights into the pathophysiologic mechanisms may lead to more specific treatments.
Simon W Davies, M.A., M.R.C.P., james W Bailey, D.C.R., D.R.l., lbul Wilkinson, M.R.C.P., Robin M. Rudd, M.D., F.R.C.P., London Chest Hospital,
London, England
REFERENCES
2 3 4
5
Matsuura Y, Nomimura T, Murakami H, Matsushima T, Kakehashi M, Kajihara H. Clinical analysis of reexpansion pulmonary edema. Chest 1991; 100:1562-66 Basran GS, Byrne AJ, Hardy JG. A noninvasive technique for monitoring lung vascular permeability in man. Nucl Med Commun 1985; 3:3-10 Keegan J, Bailey J, Wilkinson P, Davies S, Rudd R. Pulmonary microvascular permeability using double isotope scintigraphy. Nucl Med Commun 1989; 10:871-78 Wilkinson PW, Davies SW, Keegan J, Bailey J, Rudd R. Changes in pulmonary microvascular permeability accompanying re-expansion pulmonary oedema: evidence from dual isotope scintigraphy. Thor.uc 1990; 45:456-59 Davies SW, George J, Bailey J, Goldsmith SR, Keegan J, Rudd R. Increased microvascular permeability in lungs re-expanded by endoscopic laser treatment [abstract]. Am Rev Respir Dis 1990; I41(suppl):A293
To the Editor: We were pleased to learn that Dr Davies and his colleagues had read our article on reexpansion pulmonary edema (REPE). Although REPE is clinically a very important matter, the mechanism of its occurrence has remained unexplained. We have not had the means to inspect the mechanism in detail because, as Dr Davies and his colleagues point out, the direct measurement of pulmonary microvascular permeability (PMVP) in man remains impossible. On the basis of the results of a retrospective study of clinical cases of REPE, we postulated that age-related changes in the lung may afford some degree of protection against the development of REPE. Dr Davies and his colleagues found that PMVP increased in the reexpanded lobe or segment and proposed that increased PMVP causes REPE. These findings are very interesting and important, although they do not explain why REPE occasionally occurs in the contralateral lung. I think that our findings and the findings of Dr Davies do not clash substantially, because we did not study the mechanism of occurrence of REPE but postulated that age-related changes in the lung may afford some degree of protection against the development of REPE. I should like to ask Dr Davies and his colleagues whether there is a difference in PMVP according to age.
I agree with Davies et al that further insights into the physiologic mechanisms may lead to more specific treatments against REPE.
Yuichiro Matsuura, M.D., First Department of Surgery, Hiroshima University School of Medicine, Hiroshima City, japan
Pulmonary Toxicity Following Exposure to Methylene Chloride and Its Combustion Product, Phosgene To the Editor: The stripper strikes again! As we reported• in the March 1992 issue of Chest, chemical paint removers containing methylene chloride are widely used in domestic and industrial settings where exposure to a heat source with conversion to phosgene is possible. We have now cared for an additional patient with nearly identical problems. A 37-year-old man presented to the emergency room with complaints of shortness of breath associated with chest discomfort. His past medical history was unremarkable, and he was not a smoker. He had been using a paint remover consisting of80 percent methylene chloride two days before coming to the emergency room. He had been refinishing a piece of furniture in a poorly ventilated garage heated with a kerosene heater. The emergency room evaluation included a chest x-ray film, which revealed extensive bilateral alveolar and interstitial infiltrates. Initial arterial blood gas analysis on room air revealed the following values: pH, 7.39; Pco2 , 41 mm Hg; Po 2 , 50 mm Hg. The carbon monoxide level was 2.5 percent. The patient was treated with oxygen, and his symptoms improved during the next 48 to 72 h. A repeat x-ray film obtained three days later revealed marked but not complete resolution of the previously noted infiltrates. Oximetry at that time revealed 96 percent hemoglobin saturation on room air. At the time of discharge, the patient had a residual cough. Ten days later he was asymptomatic, and a chest x-ray film was normal. This presentation of another patient soon after our previous report suggests that this problem occurs more frequently than we had previously suggested and may well be underreported. This certainly seems to be true in a suburban setting, where home furniture refinishing by nonprofessionals is epidemic due to current economic conditions. We would like to again emphasize the need for complete medical evaluation following toxic exposures and for observation of the patient for a prolonged interval of time because of the potential for delayed clinical problems. We would also like to stress the need to carefully read warning labels when using paint removers containing methylene chloride and to avoid exposure to heat or open flame because of the added risk of phosgene production. Lethal concentrations have been reported within 5 to 10 min under test conditions. 2
Richard W Snyder, M.D., F.C.C.P., HenryS. Mishel, M.D., F.C.C.P., and G. Chris Christensen Ill, D.Q, F.C.C.P., Abington, Pennsylvania
REFERENCES 1 Snyder Rw, Mishel HS, Christensen GC III. Pulmonary toxicity following exposure to methylene chloride and its combustion product, phosgene. Chest 1992; 101:860-61 2 Gerritsen WB, Buschmann CH. Phosgene poisoning caused by the use of chemical paint removers containing methylene chloride in ill-ventilated rooms heated by kerosene stoves. Br J Ind Med 1960; 17:187-89 CHEST I 102 I 6 I DECEMBER, 1992
1921
