- Email: [email protected]
Deterioration of Ventricular Tachycardia to Ventricular Fibrillation after Rapid Intravenous Administration of Magnesium Sulfate
of nitrous oxide in laminated, wire-reinforced endotracheal tubes.' A wide variety of foreign bodies also have been reported to cause endotracheal tube obstruction, including nasal turbinates avulsed during nasotracheal .intubation, 4 surgical tape," dried lubricant," a broken endotracheal tube stylet sheath" and retained plastic debris from the manufacturing of the Murphy eye." Another common complication of endotracheal tube use is right mainstem bronchus intubation which has been reported, in one series, to occur in 9.6 percent of all cases of intubation. 7 Alveolar hyperinflation, atelectasis and rightsided tension pneumothorax can result from right mainstem bronchus intubation. We are unaware, however, of any previously reported cases of tension pneumothorax resulting from ball-valve endotracheal tube obstruction. As demonstrated by the removed specimen (Fig 1 and 2) obstruction of an endotracheal tube by such a ball-valve mechanism requires both endotracheal tube ports to be involved in the occlusion. In this case, a mass of dried secretions and clotted blood was adherent inside the tube, completely occluding the Murphy eye. The remainder of the dried secretions and clot extended beyond the tip of the endotracheal tube. The large diameter and mobility of this mass allowed it to open and close over the distal endotracheal tube port. Inspiratory pressure would move the mass away from the distal port allowing inspiratory flow to occur; expiratory pressure distal to the endotracheal tube would push the mass into the distal port, occluding expiratory flow. The repeated ball-valve action of this mass resulted in pulmonary hyperinflation and consequent barotrauma, as manifested by a tension pneumothorax and subcutaneous emphysema. Whenever airway obstruction is suspected in an intubated patient, prompt, thoughtful intervention is necessary to locate and relieve the obstruction. By utilizing physical examination findings, manual ventilation, a suction catheter, and by deflating the endotracheal cuff the problem should be localizable to either the patient, the endotracheal tube, the cuff or the ventilator circuit. In this patient, difficult passage of the suction catheter suggested a problem related to the endotracheal tube. Urgent extubation and rein tubation revealed the nature of the endotracheal tube obstruction, while the physical findings allowed prompt recognition and treatment of the tension pneumothorax. REFERENCES
1 Petersen G~ Baier H. Incidence of pulmonary barotrauma in a medical I.C. U. Crit Care Med 1983; 11:67-69 2 Hosking M~ Lennon RL, \Varner MA, Gray JR, Masley ~ De Luca LA, et al. Endotracheal tube obstruction: recognition and management. Milit Med 1989; 154:489-91 3 Munson ES, Stevens OS, Redfern RE. Endotracheal tube obstruction by nitrous oxide. Anesthesiology 1980; 52:275-76 4 Ripley JF, McAnear JT, Tilson HB. Endotracheal tube obstruction due to impaction of the inferior turbinate. J Oral Maxillofac Surg 1984; 42:687-88 5 Zmyslowski W~ Kam 0, Simpson GT. An unusual cause of endotracheal tube obstruction [letter). Anesthesiology 1989; 70:833 6 Harrington JF. An unusual cause of endotracheal tube obstruction [letter]. Anesthesiology 1984; 61:116-17 7 Petty TL. Complications occurring during mechanical ventilation. Heart Lung 1976; 5:112-13
Deterioration of Ventricular Tachycardia to Ventricular Fibrillation after Rapid Intravenous Administration of Magnesium Sulfate* Sand Viskin, M.D.; Bernard Belhassen; M.D.; and Shlomo Laniado, M.D.
We report the case of a patient who had development of ventricular fibrillation following rapid intravenous administration of magnesium sulfate (2 g over 5 s) for treatment of sustained monomorphic ventricular tachycardia. Initial slowingof the tachycardia was followed by gradual widening of QRS complexes and electrical alternaDS, leading to ventricular fibrillation within 3 min of magnesium admin(Che.t 1992; 101:1445-41) istration.
vr =ventricular
=
tachycardia; VF ventricular 8brillation; LVEF = left ventricular ejection fraction; RBBB = right bundle
branch block
magnesium sulfate is a well-established treatI ntravenous ment of polymorphic ventricular tachycardia (VT) asso-
ciated with QT prolongation. I Recently, the use of magnesium was proposed as an alternative therapy for sustained monomorphic Vf. 2 Reservations concerning rapid administration of magnesium sulfate have been expressed, mainly relating to possible cardiac arrest:" however, electrocardiographic documentation of the sequence of events leading to cardiac arrest is not available. ~.5 We report the case of a patient who had development of ventricular fibrillation (VF) following rapid administration of magnesium sulfate for treatment of sustained monomorphicVf. CASE REPORT
A 65-year-old man was hospitalized with an extensive anterior myocardial infarction complicated by severe left ventricular dysfunction (left ventricular ejection fraction [LVEF] = 21 percent, right hundle branch block [RBBB], and left anterior hemiblock). Two weeks later, he developed multiple episodes of sustained VI: The tachycardia was of monomorphic configuration, with rates ranging from 160 to 180 heats/min. VI' resulted in hemodynamic deterioration and invariably required electrical cardioversion for termination. Spontaneous deterioration of VT to VF, however, was never ohserved. Successive treatment with intravenous lidocaine, procainamide, hretylium tosylate, amiodarone, and magnesium sulfate (6 g over 24 h) failed to terminate or to prevent the episodes of sustained VI'. Nonoliguric renal failure occurred (with gradual increase of serum creatinine levels up to 4.5 mg/dl) and led to discontinuation of magnesium sulfate infusion. The last serum magnesium level, obtained shortly before discontinuation of treatment, was 3.7 mg/dl, Three days later, during a new episode of sustained monomorphic VI', which occurred while the patient was receiving a continuous infusion of procainamide and amiodarone (2 mglmin and 0.5 mgl min, respectively), a bolus of 2 ~ of magnesium sulfate (as a 10 percent solution) was administered over a period of 5 s (Fig 1). Progressive slowing of the VI', from 160 to 130 heats/min, was *From the Department of Cardiology, Ichilov Hospital, Tel Aviv Medical Center and Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. CHEST I 101 151 MA'(. 1992
1445
I II
11rvvvv'J I II III I II III
I~ II III I II III FICURE 1. Simultaneous recording of leads I, II, and III during sustained monomorphic ventricular tachycardia and following administration of 2 g of magnesium sulfate over 5 s (panel A). Fifty seconds after magnesium administration, slowing of tachycardia from 160 to 130 beats/min is observed (panel B). Gradual widening of QRS complexes with electric alternans occurs 80 s after magnesium administration (panel C) leading to frankly disorganized ventricular activity 80 s later (panels D and E). observed within the first minute following magnesium administration; however, gradual widening of QRS complexes and electrical alternans appeared afterwards and led to frankly disorganized ventricular activity culminating in VF within 3 min. The patient was successfully resuscitated with a single 300-J direct current shock, and remained in sinus rhythm for several hours without further changes in QRS-T morphology or QT interval. Additional episodes of vr were terminated by rapid ventricular pacing; nevertheless, the patient died of cardiogenic shock two days later. DISCUSSION
Slow infusion of magnesium sulfate has been repeatedly found to be safe when administered to patients in sinus rhythm," as well as during supraventricular? or ventricular tachyarrhythmias.P Rapid intravenous bolus of magnesium sulfate (2 g/5 s), administered to patients with reentrant supraventricular tachyarrhythmias' has recently raised controversy regarding the safety of such dosing." Our patient experienced deterioration of sustained vr to VF after receiving magnesium sulfate at this rapid infusion rate. Although spontaneous arrhythmia degeneration cannot be excluded, a direct causal effect of magnesium in the induction of VF is suggested by the following: (1) absence of such deterioration during many similar episodes of vr documented both before and after the administration of the rapid bolus of magnesium sulfate; (2) the sequence of events, culminating in VF within 3 min of the magnesium bolus; and (3) slowing rather than acceleration of vr preceding the degeneration to VF. Of note, the patient had received higher doses of magnesium sulfate at slower infusion rates several days before. This was accompanied by a slight elevation of serum magnesium levels (3.4 rng/dl) but had no detrimental 1448
consequences. It was only three days after discontinuation of magnesium infusion that the 2-g bolus in question was administered. Thus, although serum magnesium levels were not obtained following resuscitation from VF, and notwithstanding the deterioration of renal function, we believe that the rate of magnesium administration, rather than the total amount administered, played an important role in deterioration of vr to VF. Also, the fact that magnesium was administered while the patient was under the influence of other antiarrhythmic agents argues against a "pure" magnesium-related side effect. However, such a setting is likely the one that will be encountered in clinical practice since magnesium sulfate is not considered a first-line drug for sustained monomorphic vr. The mechanism of deterioration of Vl' to VF in our patient is unclear. Marked widening of the QRS complex and slowing of the ventricular rate before VF induction reflect a strong negative dromotropic effect, similar to that of class 1 antiarrhythmic drugs. Such effect could be due to the rate of drug administration. Magnesium sulfate has not been shown to affect intraventricular conduction and refractoriness significantly when infused slowly (infusion rates of 1 g/min)." On the other hand, blockade of conduction over accessory bypass tracts may occur with faster infusion rates (2 g of magnesium sulfate over 15 s or less).?" Also, decreased intraventricular conduction following magnesium administration has been observed during rapid ventricular pacing. 6 Regardless of the mechanism involved, and as interest in the clinical use of magnesium sulfate increases, a word of caution against its rapid intravenous administration, even during resuscitation for ventricular arrhythmias, is in order. Deteriorationof ventricular Tachycardia (Viskin, Belhassen, Laniado)
REFERE:-.ICES
I Tzivoni D, Banal S, Schuger C , Benhorin J. Keren A, Cottlieb S, et al . Treatment of torsade de pointes with magnesium sulfate . Circulation 1981l: 77:392-97 2 Allen BJ, Brodsky MA, Cappart'lli EV, Luckett CR , Iseri U : Magn esium sulfah' therapy for sustained monomorphic ventricula r tachycardia. Am J Cardiol191l9; 64:1202-04 3 Atwood J. Walsh M. Hellman J. Rapid bolus magnesium sulfate for supraventricular tachycardia. Am J Cardiol 1990: 65:826 4 Richards A, Stather-Dunn L, Moodley J. Cardiopulmonary arrest after the adm inistration of magnesium sulfate. S Afr Med J 198.'5: 67:145 5 McCuhhin JII , Siha i BM , Abdellu Tl'I: , Anderson (;D . Card iopulmonary arrest due to acute maternal hypermagnesemia. Lancet 1981: l :m'5R 6 DiCarlo LA, Morady F, de Buitleir M , Krol RB, Schurig L, Annesley TM . Efft'cls of magnesium sulfate on cardiac conduction and refractoriness in humans. J Am Coli Cardiol 19I16; 7:13.'56-62 7 Wesley HC, Haine -s DE, Lerman BB, DiMarl" Jp, Crampton RS. Efft'Ct of intravenous magnesium sulfate (Ill supraventricular tachyeardin. Am J Cardiol 1989: 6.1:1129-31 8 Viskin S, Belh assen B, Sheps D , Laniado S. Termlnat ion of paroxysmal reentrant junctional tachycardia hy magnesium sulfate : comparison with adenosine triphosphute [abstract] . Circulation 1990; 82: 111-43.'5
Primary Pulmonary Disease Due to Mycobacterium AviumIntracellulare* [cnnnc M . Reich . .\ I.D . -From the Division of Pulmonarv Medicine, Bess Kaiser Medical Center, and Center for lIealtli Research . Kaiser Permanente, Northwest Region , Portland, Oregon. Rt'll1int requests : Dr. Reich . .J.ll-l Sorth Kaiser Center Drice, Portland, Oregoll 97227
Primary pulmonary disease due to Mycobacterium amum· intracellulare (MAl) presented in an immunologically intact (Ches: 1992; 101:1447·48) child exposed to pet birds.
=
MAl Mycobacterium acium-lntracellulare complex; MB = mycobacteria; NTM = nontuberculous mycobacteria; PRIMAe: primary pulmonary disease due to MAl
T
Il{' rarity with which MAl leads to primary pulmonary aspects disease in humans is one of tilt' more puzzlin~ of its peculiar epidemiology; only three cases, all involving children, have been reported .' In a comprehensive review of the subject of NTM.' this pattern was not cited, and in a review of the roentgenographic features of NTM;' absence of the primary pattern was listed (along with ahsence of pleural effusion) as one of the two roentgenographic attributes of MAl which dlfferenttated it from tuberculosis. CASE REPOIIT
A three-year-old girl, pr eviously in go(KI health, presented in 19RO with complaints of a nonproductive l'lugh and fever of one month's duration . A CR showed atelectasis of the right lower and middle lobe and It,ft hilar adenopathy; the right hilum was obscured hy the atelectatic shadows (Fig I). Complete blood count results were normal ; the ab solute lymphocyte cou nt was 4.OOOIcll mm . Primary tuberculosis was suspected on dinical and roentgenographic grounds. A Mantoux test showed no ind uration to .'5 TV at 4R h . TIlt' hilar adenopathy d iminished over time. Brnnchoscopy revealed extrinsic compression of the bronchus Intermedins from the med ial aspect and overlying friahle erythematous mucosa , Bronchial washings were negat ive on smear and culture for MB. At thoracotomy, the two atelectatic lobes were removed along with specimens of enlarged right hilar lymph nodes, The lung and lymph nodes exhibited numerous confluent caseating granulomata. Stains to demonstrate MB and fungi were negative.
L M 6 - 80 FIGI·I\I·: 1. Att,let'lasis of middle and lower lohe and contralateral hilar adenopathy are evid ent. CHEST I 101 I 5 I MAy' 1992
1447
1 Petersen G~ Baier H. Incidence of pulmonary barotrauma in a medical I.C. U. Crit Care Med 1983; 11:67-69 2 Hosking M~ Lennon RL, \Varner MA, Gray JR, Masley ~ De Luca LA, et al. Endotracheal tube obstruction: recognition and management. Milit Med 1989; 154:489-91 3 Munson ES, Stevens OS, Redfern RE. Endotracheal tube obstruction by nitrous oxide. Anesthesiology 1980; 52:275-76 4 Ripley JF, McAnear JT, Tilson HB. Endotracheal tube obstruction due to impaction of the inferior turbinate. J Oral Maxillofac Surg 1984; 42:687-88 5 Zmyslowski W~ Kam 0, Simpson GT. An unusual cause of endotracheal tube obstruction [letter). Anesthesiology 1989; 70:833 6 Harrington JF. An unusual cause of endotracheal tube obstruction [letter]. Anesthesiology 1984; 61:116-17 7 Petty TL. Complications occurring during mechanical ventilation. Heart Lung 1976; 5:112-13
Deterioration of Ventricular Tachycardia to Ventricular Fibrillation after Rapid Intravenous Administration of Magnesium Sulfate* Sand Viskin, M.D.; Bernard Belhassen; M.D.; and Shlomo Laniado, M.D.
We report the case of a patient who had development of ventricular fibrillation following rapid intravenous administration of magnesium sulfate (2 g over 5 s) for treatment of sustained monomorphic ventricular tachycardia. Initial slowingof the tachycardia was followed by gradual widening of QRS complexes and electrical alternaDS, leading to ventricular fibrillation within 3 min of magnesium admin(Che.t 1992; 101:1445-41) istration.
vr =ventricular
=
tachycardia; VF ventricular 8brillation; LVEF = left ventricular ejection fraction; RBBB = right bundle
branch block
magnesium sulfate is a well-established treatI ntravenous ment of polymorphic ventricular tachycardia (VT) asso-
ciated with QT prolongation. I Recently, the use of magnesium was proposed as an alternative therapy for sustained monomorphic Vf. 2 Reservations concerning rapid administration of magnesium sulfate have been expressed, mainly relating to possible cardiac arrest:" however, electrocardiographic documentation of the sequence of events leading to cardiac arrest is not available. ~.5 We report the case of a patient who had development of ventricular fibrillation (VF) following rapid administration of magnesium sulfate for treatment of sustained monomorphicVf. CASE REPORT
A 65-year-old man was hospitalized with an extensive anterior myocardial infarction complicated by severe left ventricular dysfunction (left ventricular ejection fraction [LVEF] = 21 percent, right hundle branch block [RBBB], and left anterior hemiblock). Two weeks later, he developed multiple episodes of sustained VI: The tachycardia was of monomorphic configuration, with rates ranging from 160 to 180 heats/min. VI' resulted in hemodynamic deterioration and invariably required electrical cardioversion for termination. Spontaneous deterioration of VT to VF, however, was never ohserved. Successive treatment with intravenous lidocaine, procainamide, hretylium tosylate, amiodarone, and magnesium sulfate (6 g over 24 h) failed to terminate or to prevent the episodes of sustained VI'. Nonoliguric renal failure occurred (with gradual increase of serum creatinine levels up to 4.5 mg/dl) and led to discontinuation of magnesium sulfate infusion. The last serum magnesium level, obtained shortly before discontinuation of treatment, was 3.7 mg/dl, Three days later, during a new episode of sustained monomorphic VI', which occurred while the patient was receiving a continuous infusion of procainamide and amiodarone (2 mglmin and 0.5 mgl min, respectively), a bolus of 2 ~ of magnesium sulfate (as a 10 percent solution) was administered over a period of 5 s (Fig 1). Progressive slowing of the VI', from 160 to 130 heats/min, was *From the Department of Cardiology, Ichilov Hospital, Tel Aviv Medical Center and Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. CHEST I 101 151 MA'(. 1992
1445
I II
11rvvvv'J I II III I II III
I~ II III I II III FICURE 1. Simultaneous recording of leads I, II, and III during sustained monomorphic ventricular tachycardia and following administration of 2 g of magnesium sulfate over 5 s (panel A). Fifty seconds after magnesium administration, slowing of tachycardia from 160 to 130 beats/min is observed (panel B). Gradual widening of QRS complexes with electric alternans occurs 80 s after magnesium administration (panel C) leading to frankly disorganized ventricular activity 80 s later (panels D and E). observed within the first minute following magnesium administration; however, gradual widening of QRS complexes and electrical alternans appeared afterwards and led to frankly disorganized ventricular activity culminating in VF within 3 min. The patient was successfully resuscitated with a single 300-J direct current shock, and remained in sinus rhythm for several hours without further changes in QRS-T morphology or QT interval. Additional episodes of vr were terminated by rapid ventricular pacing; nevertheless, the patient died of cardiogenic shock two days later. DISCUSSION
Slow infusion of magnesium sulfate has been repeatedly found to be safe when administered to patients in sinus rhythm," as well as during supraventricular? or ventricular tachyarrhythmias.P Rapid intravenous bolus of magnesium sulfate (2 g/5 s), administered to patients with reentrant supraventricular tachyarrhythmias' has recently raised controversy regarding the safety of such dosing." Our patient experienced deterioration of sustained vr to VF after receiving magnesium sulfate at this rapid infusion rate. Although spontaneous arrhythmia degeneration cannot be excluded, a direct causal effect of magnesium in the induction of VF is suggested by the following: (1) absence of such deterioration during many similar episodes of vr documented both before and after the administration of the rapid bolus of magnesium sulfate; (2) the sequence of events, culminating in VF within 3 min of the magnesium bolus; and (3) slowing rather than acceleration of vr preceding the degeneration to VF. Of note, the patient had received higher doses of magnesium sulfate at slower infusion rates several days before. This was accompanied by a slight elevation of serum magnesium levels (3.4 rng/dl) but had no detrimental 1448
consequences. It was only three days after discontinuation of magnesium infusion that the 2-g bolus in question was administered. Thus, although serum magnesium levels were not obtained following resuscitation from VF, and notwithstanding the deterioration of renal function, we believe that the rate of magnesium administration, rather than the total amount administered, played an important role in deterioration of vr to VF. Also, the fact that magnesium was administered while the patient was under the influence of other antiarrhythmic agents argues against a "pure" magnesium-related side effect. However, such a setting is likely the one that will be encountered in clinical practice since magnesium sulfate is not considered a first-line drug for sustained monomorphic vr. The mechanism of deterioration of Vl' to VF in our patient is unclear. Marked widening of the QRS complex and slowing of the ventricular rate before VF induction reflect a strong negative dromotropic effect, similar to that of class 1 antiarrhythmic drugs. Such effect could be due to the rate of drug administration. Magnesium sulfate has not been shown to affect intraventricular conduction and refractoriness significantly when infused slowly (infusion rates of 1 g/min)." On the other hand, blockade of conduction over accessory bypass tracts may occur with faster infusion rates (2 g of magnesium sulfate over 15 s or less).?" Also, decreased intraventricular conduction following magnesium administration has been observed during rapid ventricular pacing. 6 Regardless of the mechanism involved, and as interest in the clinical use of magnesium sulfate increases, a word of caution against its rapid intravenous administration, even during resuscitation for ventricular arrhythmias, is in order. Deteriorationof ventricular Tachycardia (Viskin, Belhassen, Laniado)
REFERE:-.ICES
I Tzivoni D, Banal S, Schuger C , Benhorin J. Keren A, Cottlieb S, et al . Treatment of torsade de pointes with magnesium sulfate . Circulation 1981l: 77:392-97 2 Allen BJ, Brodsky MA, Cappart'lli EV, Luckett CR , Iseri U : Magn esium sulfah' therapy for sustained monomorphic ventricula r tachycardia. Am J Cardiol191l9; 64:1202-04 3 Atwood J. Walsh M. Hellman J. Rapid bolus magnesium sulfate for supraventricular tachycardia. Am J Cardiol 1990: 65:826 4 Richards A, Stather-Dunn L, Moodley J. Cardiopulmonary arrest after the adm inistration of magnesium sulfate. S Afr Med J 198.'5: 67:145 5 McCuhhin JII , Siha i BM , Abdellu Tl'I: , Anderson (;D . Card iopulmonary arrest due to acute maternal hypermagnesemia. Lancet 1981: l :m'5R 6 DiCarlo LA, Morady F, de Buitleir M , Krol RB, Schurig L, Annesley TM . Efft'cls of magnesium sulfate on cardiac conduction and refractoriness in humans. J Am Coli Cardiol 19I16; 7:13.'56-62 7 Wesley HC, Haine -s DE, Lerman BB, DiMarl" Jp, Crampton RS. Efft'Ct of intravenous magnesium sulfate (Ill supraventricular tachyeardin. Am J Cardiol 1989: 6.1:1129-31 8 Viskin S, Belh assen B, Sheps D , Laniado S. Termlnat ion of paroxysmal reentrant junctional tachycardia hy magnesium sulfate : comparison with adenosine triphosphute [abstract] . Circulation 1990; 82: 111-43.'5
Primary Pulmonary Disease Due to Mycobacterium AviumIntracellulare* [cnnnc M . Reich . .\ I.D . -From the Division of Pulmonarv Medicine, Bess Kaiser Medical Center, and Center for lIealtli Research . Kaiser Permanente, Northwest Region , Portland, Oregon. Rt'll1int requests : Dr. Reich . .J.ll-l Sorth Kaiser Center Drice, Portland, Oregoll 97227
Primary pulmonary disease due to Mycobacterium amum· intracellulare (MAl) presented in an immunologically intact (Ches: 1992; 101:1447·48) child exposed to pet birds.
=
MAl Mycobacterium acium-lntracellulare complex; MB = mycobacteria; NTM = nontuberculous mycobacteria; PRIMAe: primary pulmonary disease due to MAl
T
Il{' rarity with which MAl leads to primary pulmonary aspects disease in humans is one of tilt' more puzzlin~ of its peculiar epidemiology; only three cases, all involving children, have been reported .' In a comprehensive review of the subject of NTM.' this pattern was not cited, and in a review of the roentgenographic features of NTM;' absence of the primary pattern was listed (along with ahsence of pleural effusion) as one of the two roentgenographic attributes of MAl which dlfferenttated it from tuberculosis. CASE REPOIIT
A three-year-old girl, pr eviously in go(KI health, presented in 19RO with complaints of a nonproductive l'lugh and fever of one month's duration . A CR showed atelectasis of the right lower and middle lobe and It,ft hilar adenopathy; the right hilum was obscured hy the atelectatic shadows (Fig I). Complete blood count results were normal ; the ab solute lymphocyte cou nt was 4.OOOIcll mm . Primary tuberculosis was suspected on dinical and roentgenographic grounds. A Mantoux test showed no ind uration to .'5 TV at 4R h . TIlt' hilar adenopathy d iminished over time. Brnnchoscopy revealed extrinsic compression of the bronchus Intermedins from the med ial aspect and overlying friahle erythematous mucosa , Bronchial washings were negat ive on smear and culture for MB. At thoracotomy, the two atelectatic lobes were removed along with specimens of enlarged right hilar lymph nodes, The lung and lymph nodes exhibited numerous confluent caseating granulomata. Stains to demonstrate MB and fungi were negative.
L M 6 - 80 FIGI·I\I·: 1. Att,let'lasis of middle and lower lohe and contralateral hilar adenopathy are evid ent. CHEST I 101 I 5 I MAy' 1992
1447