Early Description of ARDS

Table I-Expected Costa ofSpontaRe0U8 Pneumothorax in Smolren va Nonmwlren or E%-amoIren Type of cost Inpatient care Men Women Outpatient care Production loss Men Women Total costs

Smokers

Nonsmokers

34,062* 16,590 3,800

3,406* 4,977 608

23,104 8,500 86,056

*In thousands of SEK SEK =Swedish crowns; 100 SEK

related direct costs of medical care thus amount to about SEK 900 million. The total costs of smoking, including those due to Sp, indicate the potential health and economic benefits of giving up smoking. Furthermore, advice given by the general practitioner to his patient to stop smoking is one ofthe least costly health-promoting measures, according to calculations for Great Britain. '2.13

lAszlO Bense, M.D., Ph.D., F.C.C.P.; and Lars COsta Wiman, M.D., Ph.D., F.C.C.P.,

2,301 2,549 13,841

Huddinge University Hospital, Huddinge, Sweden; Stefan ]endteg, B.A., and Bjorn Undgren, Ph.D., Swedish Institute for Medical Economics, Lund, Sweden

=$15 US

At present, the total costs of SP during one year amount to approximately SEK 86 million (Table 1).The direct costs correspond to 63 percent of the total costs, and the indirect costs cover the remaining 37 percent. In order to calculate the corresponding costs in a hypothetic situation in which there are no smokers or exsmokers, we used the percentage of cases of SP attributable to smoking among men and women (90 and 70 percent, respectively), estimated by Bense et aI.e Of the original 2,000 cases, 1,260 cases would then be avoided among men and 420 cases among women: 1,680 cases total (84 percent). With the same assumptions concerning duration of inpatient care, visits to physicians, length of sick leave, and costs as in the first alternative, the total costs of SP not due to smoking were calculated to be nearly SEK 14 million (Table 1). Thus, the total costs (direct costs of care and indirect costs due to productivity losses) would be reduced by approximately SEK 72 million if SP due to smoking could be eliminated. In addition, merely by changing the therapeutic measure, the annual costs in the two situations could be reduced by SEK 11 million and 2 million, respectively. ,. The total health and economic consequences of smoking are considerable. According to Hjalte et al," the smoking-related mortality in Sweden in 1980 implied about 100,000 lost years of life, while the smoking-related morbidity was calculated to lead to approximately 1,000 disability pensions (Table 2). 'Iaken together, this corresponds to approximately 29,000 lost productive work years (ie, indirect costs of about SEK 3.3 billion in 1986 prices). In the same study, it was calculated that tobacco smoking also led to about 450,000 bed-days and 50,000 medical consultations annually, plus considerable prescribing ofdrugs. In 1986 prices, the total smoking-

Table 2-Smoldng aa a CafJlJe ofMortality and Morbidity Attributable risks (%)

Direct causal relation Lung cancer Laryngeal cancer Cancer of the oral cavity Esophageal cancer Chronic obstructive pulmonary disease Probable causal relation Pancreatic cancer Cancer of the urinary bladder Ischemic heart disease Aortic aneurysm Diseases of the peripheral vessels

Men

Women

83 47 40 34 67

22 20 19 15 16

44 30 20

6

45

53

18

Reprint requests: Dr. Bense, ftJatangsv 232, 145 52 Norsberg, Sweden

REFERENCES 1 West JB, Dollery CT. Distribution of blood Howand ventilationperfusion ratio in the lung, measured with radioactive CO •. J Appl Physioll960; 15:405-10 2 West JB. Distribution of mechanical stress in the lung, a possible factor in localization of pulmonary disease. Lancet 1971; 24:83944 3 Bense L, Hedenstierna G, Lewander R, Wiman LG, Thornshum S. Regional lung function of non-smokers with healed spontaneous pneumothorax. Chest 1986; 90:352-57 4 Bense L, Eklund G, Wiman LG. Bronchial anomaly and the deteriorated regional ventilation in patients with healed spontaneous pneumothorax. Chest 1989; 96(suppl):I43S 5 Bense L, Wiman LG, Nilsson B. On the etiology ofspontaneous pneumothorax. Proceedings of the IVth SEP Congress, MilanoStresa, 1985. SEP; A17 6 Bense L, Eklund G, Wiman LG. Smoking and the increased risk of contracting spontaneous pneumothorax. Chest 1987; 92:1009-12 7 Bense L, Wiman LG, Hedenstiern G. Onset of symptoms in spontaneous pneumothorax; correlations to physical activity. Eur J Respir Dis 1987; 71:181-86 8 Bense L. Spontaneous pneumothorax related to falls in atmospheric pressure. Eur J Respir Dis 1984; 65:544-46 9 Kizer KW Spontaneous pneumothorax and diving. Pressure 1982; 11:12-13 10 Bense L. Number ofx-ray examinations and duration of drainage during pneumothorax can be considerably reduced. Llikartidningen 1989; 86:3673-74 11 Hjalte K, lsacsson SO, Lindgren B, Wilhelmssen L. How much do medical injuries from tobacco consumption cost? Uikartidningen 1985; 82:2978-81 12 Williams A. Economics of coronary artery bypass grafting. Br Med J 1985; 291:325-29 13 Williams A. Screening for risk of CHD: is it a wise use of resources? In: Oliver H, Ashley-Miller M, Wood D, eds. Strategy for screening for risk of coronary heart disease. London: John Wiley & Sons Ltd, 1987; 97-105

Early Description of ARDS 7b the

Editor:

Although Ashbaugh and colleagues coined the acronym ARDS in 1967,' the syndrome had already been described under various names such as shock lung. Recently, while reading a military medical handbook used by my grandfather-a physician who served in the Canadian Forces in World War I-I discovered an accurate description of ARDS caused by poison gas attack.· The book CHEST 1991 1 I JANUARY, 1991

281

describes: .. . . . edema of the lungs, with general asphyxia. Livid cyanosis with great dyspnea is the outstanding clinical feature . . . A yellow serous 8uid fills the air passages in such quantities that it may drip from the mouth of the living patient when the stretcher is tilted head downwards. Death in this stage may occur at any time from the first to the fourth or fifth day. . .. Secondary infection of the bronchiolar passages and lungs may develop, causing purulent bronchitis, bronchopneumonia, pleurisy, or even empyema and It8Dgrene of the lung. These may be fatal in the second or third week." The seven-page description includes accurate physical and gross pathologic findings and appropriate treatment considering the medical technology of 1915. The role of secondary infection was recognized long before modern case series reported this complication." This report may represent one of the earliest detailed descriptions of ARDS. Unfortunately, poison gas causing epidemic ARDS may not be a historic curiosity, as recent Third-World regional con8icts have seen the reemergence of poison gas as a weapon. Even in the nuclear age, we should not forget the lessons of the First World War on the dangers inherent from the proliferation of chemical weapons. A Bruce Montgomery, M.D., Associate Director, Clinical Research, Genentech, Inc., San Francisco

REFERENCES 1 Ashbaugh DC, Bigelow DB, Petty TL, Levine BE. Acute respiratory distress in adults. Lancet 1967; 2:319-23 2 Sloggett AT, ed. Memorandum of the treatment of injuries in war. London: Harrison and Sons, 1915; 115-22 3 Montgomery AB, Stager MA, Carrico CJ, Hudson LD. Causes of mortality in patients with the adult respiratory distress syndrome. Am Rev Respir Dis 1985; 132:485-489

Antiarrhythmic Effect of H-2 Antihistamines 1b the FAuor:

Histamine, since its isolation from ergot,' has been recognized to possess arrhythmogenic activity. This property is considered to be mostly due to HI receptor-mediated slowing of atrioventricular conduction and H2-mediated increase in sinus rate and ventricular automaticity.1.3 Cellular events, which parallel the above effects, include activation of adenylate cyclase of cyclic adenosine monophosphate' and the generation of an inward (Ca' , ) current due to opening of slow channels.' Clinical conditions where histamine's arrhythmogenesis has been recognized include secondary disorders of the heart such as anaphylaxis" and drug reactions."" The authors tried to determine whether ventricular arrhythmias associated with primary myocardial diseases could have been mediated by cardiac histamine release. Myocardial mast cells were examined by light (toluidine blue stain) and electron microscopy in biopsy fragments from ten patients with complex ventricular arrhythmias (Lown 3-4B) who underwent ventricular endomyocardial biopsy (three to five biopsies per patient) for histologic evaluation. Cardiac contractility was normal (LVEF >0.50) in four patients, moderately depressed (LVEF between 0.40 and 0.50) in four patients, and severely compromised (LVEF 0.20 and 0.25, respectively) in two. In every case, the valvular pattern, coronary network, plasma electrolytes (Na' , K' , Ca' • , Mg"), and thyroid function

test results were within normal limits. In this patient population, cardiac histamine (H) release, was also evaluated in simultaneous blood samples from the aorta (Ha) and coronary sinus (Hcs) taken at the beginning of cardiac catheterization (in order to avoid possible interference due to biopsy and angiography). Histamine level was then determined by 8uoronefelometric method using a TechniconAutoanalyzer2 after blood samples were treated with perehloric acid. Our study included evaluation of antiarrhythmic effect of H2antihistamines, monitoring (24-h Holter) cardiac rhythm before and after 5 days of therapy with 1 glday cimetidine. Histologic results provided evidence of myocarditis in six patients (healing in four; healed in two) and of cardiomyopathic changes in four cases. Myocardial mast cells were significantly increased (6 ± 31section) and partially degranulated at ultrastructural examination in patients with myocarditis, compared with cardiomyopathic patients (1 ± 1/ section) and normal control subjects (four patients undergoing surgery for atrial septal defect) (1 ± 1/section). As far as cardiac histamine is concerned, Hcs was found to be 10-30 percent higher (8± 1.4 Jl.glml) than Ha (6± 1.2 Jl.glml, confidence <0.1 Jl.glml) in patients with myocarditis, while unchanged Hcs vs H values were observed in the cardiomyopathy group. Analysis of cardiac rhythm revealed, following cimetidine treatment, reduction >80 percent of ventricular extrasystolic beats in four of six and >50 percent in two of six patients with myocarditis, and no response of ventricular extrasystoles associated with cardiomyopathy. In conclusion, in patients with ventricular arrhythmias and histologic evidence of myocarditis our data document: 1) increased number and degranulation of myocardial mast cells; 2) rise of myocardial histamine release; and 3) susceptibility of ventricular arrhythmias to H2-antihistamines. These results suggest that histamine might have a role in the pathogenesis of electrical instability associated with in8ammatory disorders of the heart. Andrea Frustaci, M.D., F.C.C.P.; Marina Caldarulo, M.D.; \Gleriodi Hienzo, M. D.; Matteo A. Russo, M.D., and Nicola Gentiloni, M.D., Catholic University School of Medicine, Rome, Italy

Reprint requests: Dr: Frustaci, Cardiology, Catholic University, Largo GemeUi 8, 00168 Rome, Italy

REFERENCES 1 Barger G, Dale HH. The presence in ergot and physiological activity of beta-iminazolylethylamine. J Physiol 1910; 40:

XXXVIII·XXXIX

2 Wit AL, Rosen MR. Pathophysiologic mechanism of cardiac arrhythmias. Am Heart J 1983; 106:798-811 3 Wolff AA, Levi R. Histamine and cardiac arrhythmias. Cire Res 1986; 58:1-16 4 Verma JC, McNeill JH. Cardiac histamine receptors: difference between left and right atria and right ventricle. J Pharmacol Exp Ther 1977; 200:352-62 5 Sperelakis N, Vogel S. Development of electrical activity in cardiac pacemaker cells. In: Carpenter DO, ed. Cellular pacemakers, vol 1. Mechanism of pacemaker generation. New York: John Wiley, 1982; 9-66 6 Levi R, Allan G. Histamine-mediated cardiac effects. In: Briston M, ed. Drug-induced heart disease. Amsterdam: Elsevier/ North-Holland, 1980; 377-95 7 Herman EH, Young RSK. Acute cardiovascular alterations induced by low doses of adriamycin, rubidazone and daunorubicin in the anesthetized beagle dog. Cancer Treat Rep 1979; 63:1771-79

262 Communications to the Edilor