Bronchoscopically Induced Bronchospasm

serum bilirubin level was 0.4 mg/l00 ml. A test for hepatitisB antigen was negative. There was no evidence of influenzalike illness preceding this episode. The therapy with rifampin was"discontinued, and within seven days the proteinuria and light-ehain K and A immunoglobulins disappeared from the urine. The patient's renal function returned to normal (serum creatinine level, 1.3 mg/l00 ml) within two weeks of stopping the therapy with rifampin (Fig 2). The patient is doing well and continues to receive isoniazid (Isonex) and ethambutol (Myambutol). DISCUSSION

Rifampin has been shown to be an immunosuppressive agent;':" and antibodies to rifampin have also been demonstrated by various workers. 3,13-16 Proteinuria with light-chain immunoglobulins has also been reported.v" Graber et al 2 listed various possible mechanisms to explain the light-chain proteinuria induced by rifampin therapy. Further acute renal failure has also been reported 7-12 by various workers but always with intermittent rifampin therapy and preceded by inHuenzalike illness in the majority of cases, thereby making one think of some immunologic type of renal involvement. Renal biopsy performed in all cases until now has shown only acute tubular necrosis 7-12 and cortical'< necrosis without any deposition of immunoglobulins.tP Renal biopsy was not done in our patients, and none of the patients' sera were investigated for specific antibodies to rifampin because there was no method of testing available here at that time. Until now, practically all of the cases of acute renal failure reported in the literature were reversible, 7-12 except for one case with permanent renal damage." Both of our patients had only mild renal damage, reversing to normal renal function after the discontinuation of the rifampin therapy. There was no influenza-like illness preceding the renal damage in these two patients. Thus, further study is needed to establish the exact pathogenesis of the immunoincompetence, the passage of light-chain immunoglobulins in the urine, and the renal functional damage in rifampin-treated patients. Although renal side effects have so far only been described with intermittent therapy,7-12 we emphasize by reporting these two cases that there should be an awareness of the possibility of these complications occurring with a continuous daily regimen of rifampin. Further, with a word of caution, we believe that all patients receiving rifampin therapy, even for the first time, should be very closely monitored from the renal point of view. It is especially important because of the fact that rifampin has been released to be used in North American countries only for the last three years. Santosh Kumar, M.B., B.S., M.D. Jagdishchandra A. Mehta, M.B., F.C.C.P.and Hargovind L. Trivedi, M.B., F.C.C.P. Department of Medicine, McMaster University St. Joseph's and Chedoke Hospitals Hamilton, Ontario, Canada Reprint requests: Dr. Trivedi, St. Joseph's Hospital, Hamilton, Ontario L8N lY4, Canada

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1 Graber CD, Patrick CC, Galphin RL: Light chain proteinuria and cellular mediated immunity in rifampin treated patients with tuberculosis. Chest 67 :408-410, 1975 2 Graber CD, Jebaily J, Galphin RL: Light chain proteinuria and humoral immunoincompetence. Am Rev Respir Dis 107:713-717, 1973 3- DukorP, Schuman G, Dietrich FM: Immunological studies with rifampicin. Scand J Respir Dis (suppl) 84:73-82, -'.1973 4 Dujani B~ Kasik JB, Thompson JS: Rifampin and the immune system (abstract). Read before the Interscience Conference on Antimicrobial Agents and Chemotherapy, Atlantic City, NJ, September 1972 5 Ruben FL, Winkelstein A, Potiadis IG: Suppression of cell mediated .immunity- by rifampin ( abstract). Read before the meeting of the American Thoracic Society, Cincinnati, May Igf4 6 Nilson BS: Rifampin: An immunosuppressant? Lancet 2:374, 1971 7 Kleinknecht D, Homberg JC, Decroix G: Acute renal failure after rifampicin. Lancet 1: 1238-1239, 1972 8 Cordonnier D, Muller JM: Acute renal failure after . rifampicin. Lancet 2:1364-1365, 1972 9 Poole G, Stradling P, Worlledge S: Potentially serious side effects of high-dose twice weekly rifampicin. Br Med J 3:343-347, 1971 10 Ramgopal V, Leonard C, Bhathena D: Acute renal failure associated with rifampicin. Lancet 1: 1195, 1975 11 Mattson K, Riska H, Forsstrom J, et al: Acute renal failure following ri£ampin administration. Scand J Respir Dis 55:291-297, 1974 12 Cochran M, Moorhead PJ, Platts M: Pennanent renal damage with ri£ampin. Lancet 1: 1428, 1975 13 Algeorge G, Rudescu D, Alexandrescu D: Rifampicin dependent antibodies in twice-weekly treated patients. Scand J Respir Dis (suppl) 84:98, 1973 14 Herman H, Eule H: Immunological and hematological investigations on patients with adverse reactions during treatment with rifampicin plus INH, once weekly. Seand J Respir Dis (suppl) 84:87-93, 1973 15 Worlledge S: The detection of rifampicin-dependent antibodies. Scand J Respir Dis (suppl) 84: 60-63, 1973 16 Virgilio R: Rifampicin-dependent antibodies during intermittent treatment. Scand J Respir Dis (suppl) 84: 83-86, 1973

Bronchoscopically Induced Bronchospasm To the Editor: Sahn and Scoggin! pointed out a problem which we have been aware of for many years, and that is bronchoscopically induced bronchospasm. We have learned the lesson the hard way also. I would like to point out two features of the problem that these investigators didn't discuss. First, Sahn and Scoggin! used only a I-percent solution of lidocaine for "adequate local anesthesia." They did not mention the number of milliliters, but we wonder

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if a I-percent solution is adequate. We use 5 ml of a 4percent solution of lidocaine (for a total of 200 mg) to anesthetize the larynx and tracheobronchial tree. We have now performed over 4,500 examinations with the fiberoptic bronchoscope using the oral route of intubation and have encountered no episodes of serious laryngospasm." More importantly, we premedicate any asthmatic patient, whether symptomatic or asymptomatic, with a drip infusion of aminophylline, giving 100 to 300 mg before and during the procedure and more during the postbronchoscopic period if any suggestion of bronchospasm appears. We can also leave the oral airway in place if it appears as though the patient may be in some distress. Having the intravenous needle in place for the drip infusion of aminophylline also gives us a quick route for administering a steroid bolus, should it be needed. Edward C. Rosenow, III , M.D ., F.C.C.P. and Howard A. Andersen, M.D., F.C.C.P. Division of Thoracic Disease Mayo Clinic, Rochester, Minn REFERENCES

1 Sahn SA, Scoggin C: Fiberoptic bronchoscopy in bronchial asthma: A word of caution. Chest 69:39-42, 1976 2 Hodgkin JE, Rosenow EC III, Stubbs SE: Oral introduction of the flexible bronchoscope. Chest 68:88-90, 1975

Iatrogenic Superior Vena Cava Syndrome A Complication of Internal Jugular Venous Catheters To the Editor: English and associates- have described the percutaneous catheterization of the internal jugular vein. The rate of major complications ranges from 0.2 percent- to 0.3 percent." The reported complications include extravasation of fluids," pneumothorax.- laceration of the ascending cervical artery," air embolism;' mediastinal inflltration.s extensive neurologic damage," and thrombophlebitis with septicemia.' Minor complications, such as hematomas, carotid arterial puncture, and catheterization of the internal mammary vein are not included in these complication rates. This case report details the placement of an internal jugular venous catheter which resulted in superior vena cava syndrome in a patient with a superior sulcus tumor. CASE REPORT

A 7l-year-old Mexican American man had a history of periumbilical pain for two months, a 9-kg (20-lb) weight loss, and a long history of smoking, but denied any history of tuberculosis. On physical examination, bronchial breath sounds were

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FIGURE 1. j arrowed superior vena cava. present in the right apex, with scattered rales throughout the chest. There was no compromise of the brachial plexus, Homer's syndrome was absent, and there were no stigmata of obstruction of the superior vena cava. The chest x-ray film on admission demonstrated a mass in the apex of the right lung, with associated deviation of the trachea to the right and volume loss on that side. Following precipitous upper gastrointestinal bleeding, a catheter was placed into the right internal jugular vein during resuscitation. Subsequently, superior vena cava syndrome developed in two hours, despite a central venous pressure of 3.0 cm H20. A catheter was introduced into the left antecubital vein, and subsequent injection of contrast material demonstrated the narrowed superior vena cava seen in Figure 1. Following the removal of the catheter from the right internal jugular vein, the superior vena cava syndrome completely resolved. DISCUSSION

In this case, passage of the jugular catheter through a compromised superior vena cava precipitated the symptoms of obstruction of the superior vena cava. The initial central venous pressure of 3 cm H 20 suggested that there was no obstruction; however, the tip of the catheter had passed through the obstruction to measure the true right atrial pressure. Wesley M. Nottage, M.D . Department of Radiology University of California, Irvine Reprint requests: Dr. Nottage, Department of Radiology, 101 The City Drive South, Orange, Calif 92668

CHEST, 70: 4, OCTOBER, 1976