cytoplasm of pulmonary macrophages in cases of chronic eosinophilic pneumonia was first described by von Meyenburg12 and was also noted by Carrington et a1. 2 Both were uncertain as to the mechanism by which the Charcot-Leyden crystals fonned or were transferred into the macrophages. The findings with electron microscopic examination in this case suggest that there are two ways in which Charcot-Leyden crystals can fonn in macrophages; the macrophage may ingest degenerating eosinophils which already contain Charcot-Leyden crystals, or they may be fonned by phagocytosis and subsequent change of the eosinophil lysosomes. Since Charcot-Leyden crystals are known to be formed from the core portion of the lysosome,13 the outer peroxidasecontaining enzymatic matrix is presumably degraded within the phagolysosome of the macrophage. ACKNOWLEDGMENTS: We would like to thank Dr. Morris Gardener of Provo, Utah,. the patient's private physician; Dr. Ivan Turpin, a former student who initially referred the patient; Ms. Kaylee Frank, Ms. Lama Dekorver, and Ms. Marilyn Fairbanks for technical assistance; and Ms. Dale McLing for typing the manuscript.

REFERENCES 1 Liebow AA, Carrington CB: The eosinophilic pneumonias. Medicine 48:251-285, 1969 2 Carrington CB, Addington WW, Goff AM, et al: Chronic eosinophilic pneumonia. N Engl J Med 280:787-798, 1969 3 Luft J: Improvements in epoxy resin embedding methods. J Biophys Biochem CytoI9:409-414, 1961 4 Friedmann I: The nose and nasal sinuses. In Wright GP, Symmers WSC (eds): Systemic Pathology (vol 1). London, Longmans, Green and Co Ltd, 1966, p 296 5 Welsh RA: The genesis of the Charcot-Leyden crystal in the eosinophilic leukocyte of man. Am J Pathol 35:10911103, 1959 6 Kay AD, Stechschulte DJ, Austen KF: An eosinophilic leukocyte chemotactic factor of anaphylaxis. J Exp Moo 133:602-619, 1971 7 Kay AB, Austen KF: The IgE-mediated release of an eosinophilic chemotactic factor from human lung. J Immunoll07:897-902, 1971 8 Torisu M, Yoshida T, Ward PA, et al: Lymphocytederived eosinophil chemotactic factor: 2. Studies on the mechanism of activation of the precursor substance by immune complexes. J Immunoll11:1450-1458, 1973 9 Cohen S, Ward PA: In vitro and in vivo activity of a lymphocyte and immune complex-dependent chemotactic factor for eosinophils. J Exp Moo 133:133-146, 1971 10 Laster CE, Gleich GJ: Chemotaxis of eosinophils and neutrophils by aggregated immunoglobulins. J Allergy Clin Immunol48:297-304, 1971 11 Lachman PJ, Kay AB, Thompson RA: The chemotactic activity for neutrophil and eosinophil leukocytes of the trimolecular complex of the fifth, sixth, and seventh components of human complement (C567) prepared in free solution by the "reactive lysis'" procedure. Immunology 19:875-879, 1970 12 von Meyenburg H: Das eosinophile Lugenin6ltrat: Pathologische Anatomie und pathogenese. Schweiz Med Wochenschr 23:809-811, 1942 13 EI-Hashimi W: Charcot-Leyden crystals: Formation from primate and lack of formation from nonprimate eosinophils. Am J Pathol65:311-324, 1971

98 RATLIFF ET AL

Endobronchial Control of Bronchopleural Fistulae* Jack L. &tlig, M.D., F.C.C.P.; ]. Donald Hill, M.D.; Harvey Tucker, M.D.; and Robert Fallat, M.D.

This report describes a proposed solution to the problem of high-flow bronchopleoral fistulae in the adult respiratory distress syndrome. Animal studies and clinical appUcatioD demonstrate the efficacy of this treatment. he usual bronchopleural flstula leading to sponT taneous pneumothorax, subsequent to chest trauma,

associated with large raw surfaces following pulmonary resections, or seen with ventilator SUpport, l usually responds to chest tube suction and time. Bronchopleural fistulae secondary to dehiscence of a bronchial stump are different problems and are usually managed by exploration, revision and reclosure, or conversion to open chest drainage. The type of bronchopleural fistula described here seems to be perpetuated by a combination of factors, including poor lung compliance demanding very high pressures to ventilate these patients, and doubtless, the high How and pressures which hold the fistula open. Perhaps the severity of illness in these patients itself retards healing. In our hands, high-How bronchopleural fistulae constitute a lethal complication in this setting. 2 CASE REPORT

A 38-year-old man who sustained a closed head injury followed by drowning was resuscitated and subsequently developed the adult respiratory distress syndrome. Nine days after his injury, his pulmonary function had deteriorated. An open lung biopsy was performed on the patient's left lung to better clarify the nature of his disease. It revealed diffuse alveolar damage with an interstitial inHammatory response, prominent pseudomembranes, and early interstitial fibrosis. The patient's pulmonary function continued to deteriorate, and on the next day, he was given support with an extracorporeal membrane oxygenator (venoarterial bypass). Earlier in the course of his disease, the patient had developed pneumothoraces on both sides, requiring insertion of a chest tube. During the third and fourth days of membrane pulmonary bypass, the bronchopleural fistula on the right side increased in magnitude, presenting a 6OO-ml leak of air with each breath. Direct surgical intervention was untenable because of the total anticoagulation required for pulmonary bypass. The patient showed no improvement. Since the air leak was forcing the ventilator to function at its capacity, we decided to plug the bronchopleural fistula from within. To maintain anticoagulation, bypass, positive end-expirao From

Presbyterian Hospital, San Francisco. Supported in part by National Heart and Lung Institute contract NOI-HR-42917 and by general research grant 5501 RR05566-12 from the US Deparbnent of Health, Education, and WeHare. This project was approved by our Committee on Human Research. Reprint requests: Dr. Ratliff, 2009 Buchanan, San Francisco 94115

CHEST, 71: 1, JANUARY, 1977

massive bronchopleural fistala emanated from the b, i (IV order bronchus) of the posterior segment of the upper lobe (Ikeda nomenclature, 1969). Thereafter a guide wire 0.035 inch in diameter and 145 em long was advanced through the suction port of the fiberoptic bronchoscope and out through the subsubsegment identi6ed previously. A No. 3-0 split shot (fishing weight) crimped over a short strand of No. 2 mersilene suture and perforated with an 18 gauge needle was advanced over the guide wire and pushed down the tracheostomy tube with a fiberoptic bronchoscope which was likewise threaded over the guide wire. The tip of the bronchoscope was used to seat this bronchial plug in the subsegmental bronchus. On removal of the guide wire, the plug was easily identified (Fig 2), and there was minimal leakage of air through the smaIl hole in the plug. The patient developed progressive pulmonary fibrosis. Irreversible total pulmonary failure ensued, and bypass was terminated after ten days of perfusion. The bronchopleural fis~h~ w~ ~ver ~ s*~~t prC)1>~m ~~r ~ ~rnC)n

pf

the plug. The plug was inspected on two occasions thereafter and found to be well seated with minimal reaction and covered with mucus. The bronchial plug was identifled at autopsy, local tissue reaction was minimal, and the lung distal to the plug was completely atelectatic. DISCUSSION

FiGURE 1. Bronchial tree with bronchofiberscope. A, Balloontipped catheter identifying source of bronchopleural fistula. B, Guide wire left in offending airway. C, Lead shot started down wire. 0, Pushing bronchoscope down behind shot to seat shot in offending bronchus. E, Plug is seated.

tory pressure, tidal volume, and a fractional concentration of oxygen in the inspired gas of 1.0, a flexible fiberoptic bronchoscope was introduced through an air lock on the suction port of the patient's tracheostomy tube. A No.5 Fogarty embolectomy catheter was passed (Fig 1) into each lobar ori6ce of the right lung and was inflated until the lobe which fed the bronchopleural fistula had been identi6ed. Similarly, the segment, the subsegment, and the subsubsegment which fed the bronchopleural fistula were then identified. This

FiGURE

2. Lead shot in right middle pulmonary field.

CHEST, 71: 1, JANUARY, 1977

We recognized this problem over a year ago and have investigated it in the laboratory. The ideal endobronchial plug for this purpose should be easy to sterilize, radiopaque, minimally tissue reactive, precisely implantable by minimally invasive techniques, easy to monitor endobronchiaUy, and potentially removable. In an appropriate animal model in the laboratory, we found that injectable blood clots and gelatin were rapidly extruded through the fistula onto the pleural surface. We found that gelatin-capsule-shaped silicone rubber plugs were so slick that they popped back into the larger bronchi and would not remain seated. Machined brass screws were no better than lead plugs. Sponge material (Ivalon) was difficult to insert and contained interstices which harbored infecting organisms. Endobronchial silver nitrate and electric cautery produce mucosal slough and bronchial closure but over a time frame which is unacceptable for these patients. The method we have adopted proved practical, since lead shots are readily available in standard sizes, produce minimal tissue reaction, are soft enough to be worked without a machine shop in the operating theater, can be quickly sterilized by soaking in glutaraldehyde, and are radiopaque. Mersilene sutures protruding from both sides of the lead shot produce bright blue, easily visible tails by which the shot can be grasped and extracted later.

1 Zimmerman JE, Colgan 01., Mills M: Management of bronchopleural fistula complicating therapy with positive end expiratory pressure (PEEP). Chest 64:526-529, 1973 2 Ratliff JL, Hill JO, et al: Complications associated with membrane lung support by venoarterial perfusion. Ann Thorac Surg 19:537-539, 1975

ENDOBRONCHIAL CONTROL OF BRONCHOPlEURAl FISTUlAE 88