contact tip. Heat should be allowed to dissipate with adequate time spacing between repeated pulses. Maximum possible distance should be maintained between the ET tube and the surgical field. Otherwise, the tube should be meticulously wrapped with tape. A red rubber tube may be less likely to ignite as compared to a PVC tube;7 however, this purported advantage is not well documented. Alternatively, a flexible metal ET tube (Nortons tube)8 can be used in selected cases. Of course, combustible anesthetic agents should not be used during laser photoresection. If a fire should occur, the immediate intervention is removal of the combustible endobronchial materials including the ET, FOB, laser fiber, and suction catheter. This will minimize the thermal injury and help prevent smoke inhalation. The airways should be examined for the presence of remaining foreign materials and to assess the extent of the injury. A chest roentgenogram should be obtained to rule out the possibility of pneumothorax or pneumomediastinum. If significant smoke inhalation or extensive thermal injury involving peripheral airways occurs, then mechanical ventilation, including positive end-expiratory pressure, might be required. 2 Obstruction of the airways after a burn can produce Significant morbidi~ Flexible bronchoscopy can be important to aid in clearing mucous plugs. Our patient had a preexisting tracheostomy which facilitated removal of large mucous plugs. The decision to employ a tracheostomy for the management of airway complications needs to be individualized, based on the patients clinical course. Aggressive pulmonary hygiene should be instituted with humidification, hydration, aerosols with mucolytic and p2-adrenergic agonist agents, and chest physical therap~ Steroids and empiric antibiotics were also instituted in our patient for prophylactic treatment ofbronchospasm and infection, respectively. Clinical judgment needs to be exercised because empiric steroids and antibiotics are not recommended for injuries due to smoke inhalation. I Although we cannot prove that our patient benefited from the steroids and antibiotics, these drugs did not produce any apparent adverse effects. The use ofsteroids, as well as of antibiotics under similar circumstances, has been recommended by others. 2.6 Little emphasis has been given to the long-term followup of laser-induced burns of the tracheobronchial tree. We believe that long-term care is required because endobronchial granulation tissue can produce airway compromise. Regular follow-up is necessary to assess the airways for obstruction using clinical and radiographic information. Pulmonary function testing and ventilation-perfusion lung scanning could be of great value in detecting significant upper airway narrowing. Ifthere is a suspicion ofa developing airway problem, then flexible bronchoscopy can be used as a diagnostic and therapeutic tool. REFERENCES 1 Herndon DN, Thompson PB, Traber DL. Pulmonary injury in burned patients. Crit Care Clin 1985; 1:79-96 2 Schramm VL, Mattox DE, Stool SE. Acute management of laserignited intratracheal explosion. Laryngoscope 1981; 91:1417-26 3 Shapshay SM, Dumon JF, Beamis JF. Endoscopic treatment of tracheobronchial malignancy. Otolaryngol Head Neck Surg 1985; 93:205-10 4 Snow JC, Norton ML, Saluja TS, Estanislao AF. Fire hazard
918
5 6
7 8
during COl laser microsurgery on the larynx and trachea. Anesth Analg (Cleveland) 1976; 55: 146-47 Hirshman CA, Smith J. Indirect ignition of the endotracheal tube during carbon dioxide laser surgery. Arch Otolaryngol 1980; 106:639-41 Casey KR, Fairfax WR, Smith SJ, Dixon ]A. Intratracheal fire ignited by the Nd-YAC laser during treatment oftracheal stenosis. Chest 1983; 84:295-96 Andrews AH, Goldenberg RA, Moss H~ Shaker MH. Carbon dioxide laser for laryngeal laser surge~ Surg Ann 1974; 6:459-76 Healy CB. Complications of laser surge~ Otolaryngol Coo North Am 1983; 16:815-20
Failure of Corticosteroid Therapy
to Prevent Induction of Ventricular
Tachycardia in sarcoidosis· Bernard Belhassen, M.D.; Amos Pines, M.D.; and
Shlomo Laniado, M.D.
Programmed ventricular stimulation was performed in a patient with sarcoidosis who exhibited an episode of sustained ventricular tachycardia. Sustained rapid ventricular tachyarrhythmias requiring cardioversion for termination were induced by double right ventricular apical extrastimuli during control, and treatment with disopyramide, quinidine, and f1uocortolone. In contrast, only four repetitive ventricular complexes were induced during combined therapy with quinidine, mexiletine and amiodarone. While receiving the latter regimen, the patient has been asymptomatic during 28 months of follow-up. (Cheat 1989; 95:918-20)
Ventricular tachyarrhythmias and sudden death are common in patients with cardiac sarcoidosis. I.! In isolated case reports, a beneficial effect of corticosteroid therapy on ventricular ectopic activity or ventricular tachycardia was observed. 3 •4 It has been suggested that this beneficial effect could be due to the healing of cardiac sarcoid granulomas by corticosteroids. I In the present report, we describe a patient with sarcoidosis and sustained ventricular tachycardia in whom the effects of corticosteroid treatment and multiple antiarrhythmic drugs were tested by programmed ventricular stimulation. To the best of our knowledge, this is the first report evaluating the effects ofcorticosteroid therapy on ventricular tachycardia inducible by programmed ventricular stimulation in a patient with sarcoidosis. CASE REPORT A 44-year-old white man was referred from another hospital for electrophysiologic study after he experienced a syncopal episode of sustained ventricular tachycardia that required cardioversion for termination. Two years earlier, the patient was diagnosed as suffering from sarcoidosis based on the presence ofbilateral hilar adenopath~ histologic confirmation by fiberoptic bronchoscopy, and positive Kveim test. During the year prior to the present hospitalization, symptomatic ventricular arrhythmias consisting of multiple ventric*From the Departments of Cardiology and Medicine, Tel-Aviv Medical Center, Ichilov Hospital and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
Corticosteroids Fail to Prevent Ventricular Tachycardia in Sarcoidosis (Belh8Ssen, Pines, Laniado)
Table 1- Reaulta of Electropharmacologic Drug :rating.
Date 1-14-1986 1-14-1986
Drugs at TIme of Study
Serum Level
(mWL)
None Disopyramide IV
4.5
2m~W5min
1-19-1986 3-18-1986
4-22-1986
Quinidine pot 750 mg TID/4 days Fluocortolone po 40 mglday/6 weeks 20 mglday/2 weeks 1) quinidine pot 500 mg TID/l month 2) mexiletine po 200 mg TID/l month 3) amiodarone po 800 mglday/2 weeks 600 mglday/1 week 400 mglday/1 week
4.5
3.5
Induced Arrhythmia Pleomorphic vr CL 200 ms-+VF Monomorphic vr LBBB-LAD pattern CL 1BOms Pleomorphic vr CL 200 ms-+VF Pleomorphic vr CL 160 ms-+VF S4RVR
Mode of Induction
SIS1S3 (RVA) S.S.=500ms S/S/S3 (RVA) S.S.=500ms S/S/S3 (RVOT) S.S.=500 ms S/S/S3 (RVA) S.S.=600ms
Mode of Termination DC Shock
DC Shock DC Shock DC Shock
S/S/S3 (RVA,RVOT) RVP «25OImin)
*CL, cycle length; DC, direct current; ~ intravenous; LAD, left axis deviation; LBBB, left bundle branch block; RVA, right ventricular apex; PO, per os; RV
DISCUSSION
In our patient, endomyocardial biopsy was not performed, and therefore, there is no absolute proof that the ventricular arrhythmias were due to sarcoid heart disease. However, it is generally assumed that the combination of clinical diagnosis and histologic connrmation of sarcoidosis with lifethreatening ventricular tachyarrhythmias unexplained by any other heart disease strongly suggests that the ventricular arrhythmias are due to sarcoid heart disease.' In addition, endomyocardial biopsy is diagnostic only if the result is positive, while the patchy distribution of the sarcoid lesions makes a negative finding of absolutely no value.' Although ventricular tachycardia is a frequent complication of cardiac sarcoidosis, data on programmed ventricular stimulation in patients with ventricular tachycardia have been reported in only three instances.5-7 In the first patient, IS nonsustained ventricular tachycardia with a morphology different from that of the spontaneous tachycardia was induced. In the second patient, e sustained ventricular tachycardia was induced by programmed ventricular stimulation and its induction was not prevented by a combined therapy with procainamide and amiodarone. In the third patient,7 only nonsustained ventricular tachycardia could be induced by programmed ventricular stimulation, and no recurrent ventricular tachycardia occurred on empiric antiarrhythmic therap~ In our patient who had spontaneous and inducible sustained ventricular tachycardia, a combined antiarrhythmic regimen with quinidine, mexiletine, and amiodarone successfully prevented induction of ventricular tachycardia and abolished symptomatic ventricular premature complexes. In contrast, corticosteroids had no effect on ventricular premature complexes and induction of ventricular tachycardia, suggesting that corticosteroids may be less effective than antiarrhythmic therapy in the management of CHEST I 95 I 4 I APRIL, 1988
111
CONTROL
V1
V\f'\lvvVl.rwv'~f,N\]VV\f'JvIJWVWV'.~-'WVVV,.WMMNw
~~~(~~J1U~~M~((rtM~rN(t(~
AV
RV FLUOCORTO ONE III
RV
-V~~
f1!'1IvJ
':WM
FIGURE 1. Electrophysiologic drug testing data: During control, pleomorphic ventricular tachycardia degenerating into ventricular fibrillation is induced by double right ventricular apical extrastimuli. After intravenous administration of disopyramide, sustained monomorphic ventricular tachycardia is induced by double right ventricular apical extrastimuli. After oral administration of quinidine and 8uocortolone, pleomorphic ventricular tachycardia degenerating into ventricular fibrillation is induced by double extrastimuli delivered from the right ventricular apex and right ventricular outflow tract, respectivel~ After oral administration of a combined regimen of quinidine, mexiletine, and amiodarone, three and four repetitive ventricular responses are induced by double extrastimuli delivered from the right ventricular apex (left panel) and right ventricular outflow tract (right panel), respectively.
I
I
ventricular arrhythmias in patients with sarcoidosis. However, one cannot exclude the possibility that the course of corticosteroid therapy resulted in regression of sarcoid granulomas, so that antiarrhythmic drugs became more efficient. Finally, since corticosteroids may be the predisposing factor for cardiac aneurysm formation 1 and other serious adverse reactions, we suggest that their efficacy should be tested by programmed ventricular stimulation in patients with sarcoidosis and inducible ventricular tachycardia. ACKNOWLEDGMENTS: We thank Drs. S. Cabili and H. Rotmensch for referring this patient.
REFERENCES Roberts WC, McAllister Jr HA, Ferrans VJ. Sarcoidosis of the heart: A clinicopathologic study of 35 necroscopy patients (group I) and review of 78 previously described necroscopy patients (group II). Am J Med 1977; 63:86-108
920
2 Fleming HA. Sarcoid heart disease: a review and an appeal. Thorax 1980; 35:641-43 3 Gozo EG, Jr, Cosnow I, Cohen HC, Okun L. The heart in sarcoidosis. Chest 1971; 60:379-88 4 Wilkins CE, Barron T, Lowrimore MG, Massumkhavi GA, Klima T, Younis AC, et al. Cardiac sarcoidosis: two cases with ventricular tachycardia and review of cardiac involvement in sarcoidosis. Texas Heart Instit J 1985; 12:377-83 5 Bharati S, Lev M, Denes ~ Modlinger J, Wyndham C, Bauernfeind R, et al. Infiltrative cardiomyopathy with conduction disease and ventricular arrhythmia: electrophysiologic and pathologic correlations. Am J Cardioll980; 45:163-73 6 Case records of the Massachusetts General Hospital. Case 341985. N Engl J Med 1985; 313:498-509 7 Morady F, Scheinman MM, Hess OS, Chen R, Stanger E Clinical characteristics and results of electrophysiologic testing in young adults with ventricular tachycardia or ventricular fibrillation. Am Heart J 1983; 106:1306-14
Corticosteroids Fail to Prevent Ventricular Tachycardia in Sarcoidosis (Be/hassen, Pines, Laniado)