CASE REPORTS

ing globulin and other thyroid hormones in the dialysate.

compensate and maintain a euthyroid state. Our studies did not show a transient increase in serum thvrotropin level, which would have reflected this compensatory process. Detailed analyses of the serum thyroid hormones were not done during the initial phase of the peritoneal dialysis (<I month). More detailed studies during the initiation of this treatment on a greater number of patients should detect the compensatory process. A recent report" supports our finding that most patients receiving continuous ambulatory peritoneal dialysis remain euthyroid. The long-term follow-up (> 12 months) was confined to only a few cases, however, so conclusions regarding the possible development of hypothyroidism cannot be reached. Because the incidence of subclinical or latent hypothyroidism in the general population is high (3.0 percent)2' and may be even greater in the uremic population,' patients receiving continuous ambulatory peritoneal dialysis may be especially susceptible to thyroid failure. Patient B may have had latent hypothyroidism (thyrotropin level 14 1,U per ml) before dialysis and may not have been able to compensate for the extra loss of thyroxine via the dialysate even after his serum total iodine level had returned to normal. As a consequence he remained hypothyroid while receiving continuous ambulatory peritoneal dialysis. Once this type of dialysis gains wider acceptance in the long-term management of chronic renal failure, an increased prevalence of clinical hypothyroidism might be anticipated in this population even when excessive exposure to iodine is avoided.
REFERENCES
1. Ramirez G, Jubiz W, Gutch CF, et al: Thyroid abnormalities in renal failure-A study of 53 patients on chronic hemodialvsis. Ann Intern Med 1973 Oct; 79:500-504 2. Lim V, Fang V, Katz Al, et al: Thyroid dysftunction in chronic renal failure. J Clin Invest 1977 Sep; 60:522-534 3. Hershman JM, Krugman LG, Kopple JD, et at: Thyroid function in patients undergoing maintenance hemodialysis: Unexplained low seruim thyroxine concentration. Metabolism 1978 Jutl; 27:755-759 4. Felicetta J, Green WL, Haas L, et al: Thyroid function and lipids in patients with chronic renal disease treated by hemodialysis: With comments on the free thyroxine index. Metabolism 1979 Jutl; 28:756-763 5. Spector DA, Davies PJ, Helderman H, et al: Thyroid function and metabolic state in chronic renal failLure. Ann Intern Med 1976 Dec; 85: 724-730 6. Silverberg DS, Ulan RA. Fawcett DM, et al: Effects of chronic hemodialysis on thyroid function in chronic renal failure. Can Med Assoc J 1973 Aug; 109:282-286 7. Ramirez G, O'Neill W, Jubiz W, et al: Thyroid dysfunctien in uremia: Evidence for thyroid and hvpophyseal abnormalities. Ann Intern Med 1976 Jun; 84:672-676 8. Czernichow P, Dauzet MC, Broyer M, et al: Abnormal TSH. PRI and GH response to TRH releasing factor in chronic renal failure. J Clin Endocrinol Metab 1976 Sep; 43:630-637 9. Emmanouel DS, Lindheimer MD. Katz Al: Pathogenesis of endocrine abnormalities in uremia. Endocr Rev 198(0 Winter; 1:28-44 10. Kosowicz J, Malczewska B, Czekalski S: SeruLm reverse triiodothvronine (3,3'5'-L-triiodothyronine) in chronic renal failuLre. Nephron 1980: 26(2) :85-89 11. Yee E, Foss K, Schmidt RW: Use of povidone iodine in continuous

The rate of dialysate thyroxine loss (29 ocg a day) by these patients was equivalent to about 30 percent of the normal human thyroxine production rate. Despite this thyroxine loss, most of our patients on continuous ambulatory peritoneal dialysis were able to

version of thyroxine to 3,3',5'-triiodothyronine (reverse-Ta) and to 3,5, 3'-triiodothyronine (T3) in hunmans. J Clin Endocrinol Metab 1977 Apr; 44:733-742 14. Feldman HA, Singer I: Endocrinology and metabolism in uiremia and dialysis. Medicine (Baltimore) 1975 May; 54:345-376 15. Cuttelod S, Lemarchand-Wraud T, Magnenat P, et al: Effect of age and role of kidneys and liver on thyrotropin turnover in man. Metabolism 1974 Feb. 23:101-113 16. Vagenakis AG, Downs P, Braverman LE, et al: Control of thyroid hornoone secretion in normal subjects receiving iodides. J C'lin Invest 1973 Feb; 52:528-532 17. Alexander NM, Nishimoto M: Protein-linked iodotyrosines in seruLm after topical application of povidone-iodine ( Betadine ). J Clin Endocrinol Metab 1981 JulI; 53:1115-108 18. Braverman LE. Ingbar SH, Vagenakis AG. et at: Enhanced susceptibility to iodide myxedema in patients w ith Hashimoto's disease. J C'lin Endocrinol Metab 1971 Jan; 32:515-521 19. Grav RS, Irvine \VJ, Toft J. et al: Unrecognized thyroid failure in diabetes mellitus. J Clin lab Inimrunol 1979 Auig; 2:221-224 20. Nolph KD. Sorkin M. Rubin J, et al: ContinuLous armbuLlatory peritonieal dialysis: Three-year experience at one center. Ann Intern Med 1980 May; 92:609-613
21. Gavin LA, MMcNahbon FA, Castle JN, et al: Alterations in serum thyroid horniones and thyroxine-binding globuLlin in patients wit'h nephrosis. J Clin Endocrinol Nfctab 1978 Jan: 46: 125-131) 22. Nicoloff JT, Low JC, Dussault JH, et al: SiMLultanecous measurement of thyroxine and triiodothyronine peripheral turnover kinietics in

Invest 1972 Mar: 15:473-483 23. TLunbridge WM: The epidemliology of hypothyroidisnm. C'lin Endocrinol Mletab 1979 Mar; 8:21-27
man. J Clin

Corticosteroid Therapy and Death in Cases of Adult Bronchial Asthma

FELIX W. LEUNG, MD SILVERIO M. SANTIAGO, MD WILLIAM B. KLAUSTERMEYER, MD Los Angeles

THE EFFICACY of corticosteroids in the treatnment of acute bronchial asthma is well documented and has led to recom-mendations that corticosteroids be used early in treating status asthmaticus.'-' An opposing view is that corticosteroids be given only after other therapies have failed; this is based on concern for the potential complications of steroid use.i'-'i Whereas the efficacy and side efTects of corticosteroids in the treatment of bronchial asthma are well recognized, their role in fatal cases is less well defined. We report deaths in five cases of bronchial asthma and analyze the role of corticosteroids in these fatal cases. The treatment of severe asthma is often by nonspecialty physicians. An increased awareness of the complexities of corticosteroid use in bronchial asthma may prevent fatalities. From 1973 to 1980 there were 530 patients with a history of bronchial asthma admitted to Wadsworth Veterans Administration (VA) Hospital (Los Anaeles). Of these patients 192 were admitted primarily for an exacerbation of bronchial asthma, 41 having multiple admissions, for a total of 280 admissions during this period. Five fatal cases were identified among these patients treated for asthma. In one patient corticosteroid
Refer to: LeuLng FWV. Santiago SMI. KlaustermeEer WB: Corticosteroid therapy and death in cases of adtult bronchial asthmlna. W\est J Med 1983 Apr; 138:565-569. From the Allergy and ImmUnology and PuLlmonary Diseasc Sections, Medical and Research Services. Wadsworth VA Mledical Centcr. and Department of Medicine, UCLA School of Mledicine. Los Angeles. Submitted, revised, April 26, 1982. Reprint requLests to William B. Klaustermeyer. NID. Allerey and ImmuLnology Section 691 '111R. Wadsworth VA Medical Center, Lo;s Angeles. CA 90073.

ambulatory peritoneal dialysis (CAPD)-A techniquie to reduLce the incidence of infectious peritonitis. Trans Am Soc Artif Intern Organs 1980 Jul; 26:223-224 12. Abreau C, Vagenakis A, Azizi F, et al: A single method for measturing total thyroxine and free thyroxine index in seruim. J NelCl Med 1973 Oct; 14:740-746 13. Gavin LA, Castle IN. McMahon FA, et al: Extrathyroidal con-

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CASE REPORTS
ABBREVIATIONS USED IN TEXT Paco2 = partial arterial carbon dioxide pressure Pao2=partial arterial oxygen pressure VA = Veterans Administration

therapy was withheld because of a diagnosis of acute pancreatitis thought to be due to a single 60-mg dose of intravenously given methylprednisolone. Failure to institute corticosteroid therapy was probably a factor in the deaths of two others. The development of unusual infections complicating corticosteroid therapy contributed to the death of the remaining two patients. The objective of this review is to emphasize the value of early use of corticosteroids in status asthmaticus and the need for surveillance for complications of treatment.

Reports of Cases
CASE 1. A 55-year-old man was admitted for shortof breath that had lasted for two days. The patient had a six-year history of bronchial asthma and had been treated with oral and inhaled bronchodilators. During the two months before admission, the patient was seen in a community hospital emergency department five times for shortness of breath. He had symptomatic improvement with intermittent positive-pressure breathing treatments with isoetharine and on each occasion was discharged on a regimen of theophylline with ethylenediamine (aminophylline) alone. The day before admission the patient was seen at another hospital where he was noted to have respirations of 34 a minute, a heart rate of 1 12 beats a minute and diffuse expiratory wheezing. Arterial blood gas determinations made while the patient was breathing room air showed a pH of 7.45, a partial arterial carbon dioxide pressure (Paco2) of 36 mm of mercury (normal 35 to 40) and a partial arterial oxygen pressure (Pao2) of 57 (normal 76 to 84, corrected for age). Hematocrit was 43 percent. He was given aminophylline intravenously and intermittent positive-pressure breathing treatment with isoetharine and was sent home following subjective improypment. The next day the patient returned to the same emergency department with a reexacerbation. Intravenous administration of aminophylline was restarted and after intermittent positive-pressure breathing treatment with isoetharine was given, the patient was transferred to Wadsworth VA Hospital. Initial -assessment showed a thin man appearing to be in moderate respiratory distress. His temperature was 37.0C (98.6'F), pulse rate 112 a minute, respirations 27 per minute and blood pressure 110/63 mm of mercury. Chest examination showed diffuse expiratory wheezing. Peak expiratory flow rate was 120 liters per minute. An arterial blood gas study was not done. The patient was treated with intravenous aminophylline, aerosolized isoetharine delivered by hand-held nebulizer and supplemental oxygen given at 2 liters a minute. Peak expiratory flow rates
ness

did not improve during three hours of treatment in the emergency department. He received 0.25 mg of terbutaline sulfate subcutaneously and was transported to the ward with oxygen being given nasally. While the patient was in transit from the emergency department to the ward a coughing spell developed, followed by severe shortness of breath. He had respiratory arrest and resuscitative measures were instituted. Arterial blood gas determinations while the patient was receiving nasal oxygen showed a pH of 7.0, a Paco., of 102 mm of mercury and a Pao, of 28. An electrocardiogram showed sinus tachycardia. There was no pneumothorax noted on a chest roentgenogram. Hematocrit was 47 percent. IDifficulty in maintaining adequate ventilation was encountered and the patient died. Postmortem findings showed diffuse mucous plugging of the bronchioles. Comment. With a history of five visits to an emergency department for asthmatic exacerbations in the two months before admissiodn, the patient should have been promptly admitted. The lack of improvement in peak expiratory flow after treatment with aminophylline and sympathomimetics in the emergency department should have prompted the use of more aggressive therapy, including administration of corticosteroids and admission to an intensive care unit rather than a ward. The hemoconcentration reflected by the rise in hematocrit in a 24-hour period suggested that fluid therapy was not optimal for replacing fluid deficit. CASE 2. A 59-year-old man was admitted for treatment of paralysis agitans (Parkinson's disease). He had a 20-year history of asthma treated with inhaled sympathomimetics. On the fifth hospital day he was noted to be short of breath. Room air arterial blood gas determinations showed a pH of 7.40, a Paco2 of 34 mm of mercury and a Pao2 of 70 mm of mercury. He was started on a regimen of aminophylline, 200 mg by mouth every six hours. In the evening of the same day acute respiratory distress developed. His mental state was depressed and examination of the chest showed diffuse inspiratory and expiratory wheezing. Arterial blood gas determinations made while the patient was breathing room air showed a pH of 7.21, a Paco. of 74 mm of mercury and a Pao2 of 40 mm of mercury. Intravenous administration of aminophylline was started. He was also given 0.3 mg of terbutaline subcutaneously, intermittent positive-pressure breathing treatment with isoetharine and nasal oxygen at 2 liters a minute. Two hours later arterial blood gas studies done with the patient receiving 2 liters a minute of supplemental oxygen showed a pH of 7.37, a Paco2 of 29 mm of mercury, and a Pao2 of 80 mm of mercury. The patient's condition improved and he was kept on the ward overnight. Corticosteroid therapy was not instituted. He was transferred to the medical intensive care unit the next morning because of recurrence of depressed mental state and respiratory distress. Endotracheal intubation and mechanical ventilation were required.
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Bilateral tension pneumothoraces developed and the patient had cardiorespiratory arrest. Bilateral chest tubes were inserted during resuscitation. The patient became comatose and died several days later. No postmortem examination was done. Comment. The severity of this patient's asthmatic exacerbation should have prompted the use of more aggressive therapy, including the administration of corticosteroids and earlier transfer to an intensive care unit. This could have averted his subsequent deterioration and obviated the need for continued use of intermittent positive-pressure breathing treatment or mechanical ventilation. It is possible that bilateral pneumothoraces associated with intermittent positive-pressure breathing treatment accounted for his deterioration7 and mechanical ventilation then aggravated the condition. CASE 3. A 51-year-old man was admitted for treatment of shortness of breath. He had a seven-year history of severe asthma requiring admission to hospital and corticosteroid treatment on two previous occasions. The day before admission he was seen in the emergency department for shortness of breath. Arterial blood gas determinations made while he was breathing room air showed a pH of 7.40, a Paco2 of 42 mm of mercury and a Pao, of 63 mm of mercury. He was given aminophylline intravenously and 60 mg of methylprednisolone. He improved subjectively and was sent home. The following day the patient returned to the emergency department because he had epigastric pain. He was admitted with a diagnosis of pancreatitis. Serial serum amylase levels during the next two days were 176, 635 and 400 mg per dl (normal <190). A twohour urinary diastase level was 3,069 mg per dl (normal < 600). He was thought to have acute pancreatitis, possibly due to the corticosteroid that he received intravenously the day before admission. He continued to receive aminophylline and inhaled sympathomimetics. Corticosteroid therapy was withheld. His abdominal pain subsided six days after admission. The patient's oral bronchodilator therapy was interrupted in preparation for an upper gastrointestinal radiographic study, the findings of which were unremarkable. He was subsequently discharged, though he noted increasing shortness of breath. On the morning after discharge the patient was examined in the allergy clinic and was observed to have pronounced wheezing and shortness of breath. He was admitted to the chest service and given fluids and aminophylline intravenously and inhaled isoproterenol. The patient seemed to respond clinically. Corticosteroid therapy was withheld for fear of precipitating pancreatitis again. At 3 the following morning the patient was found slumped over a chair, cyanotic and without a palpable blood pressure. Cardiorespiratory resuscitation was unsuccessful. Postmortem examination showed diffuse mucous plugging of the airways. Careful microscopic examination of the pancreas showed no evidence of pancreatitis.
APRIL 1983 * 138 * 4

Comment. The presence of extensive mucous plugging in the airways suggests that this patient died in status asthmaticus. The diagnosis of acute pancreatitis due to the intravenous administration of a single 60-mg dose of methylprednisolone resulted in the withholding of corticosteroids from this patient who had clearly shown a need for this medication on two previous occasions. In two recent critical reviews on drug-induced pancreatitis,89 a probable association was noted between corticosteroid administration and acute pancreatitis. The duration of corticosteroid treatment before the onset of symptoms of pancreatitis ranged from one week to seven years and averaged 37 weeks; dosages of corticosteroid ranged from 8 mg to 200 mg of prednisone a day.8 Fatal cases in adults have been reported.10-12 There is, however, no report of a single dose of corticosteroid precipitating acute pancreatitis. The worsening condition that developed after oral bronchodilator therapy was interrupted in preparation for an upper gastrointestinal study confirms the need for continuous monitoring and treatment of asthmatic patients. In the event oral bronchodilator therapy is interrupted, aerosolized and intravenous medication should be continued. CASE 4. A 50-year-old man was admitted because of shortness of breath for two days. He had a 20-year history of bronchial asthma and two previous hospital admissions for status asthmaticus. At the time of admission his temperature was 36.8C (98.2F), respirations 44 per minute and blood pressure 130/80 mm of mercury. Chest examination showed diffuse expiratory wheezing. Findings on the chest film were normal. Arterial blood gas studies done while the patient was breathing room air showed a pH of 7.49, a Paco., of 30 mm of mercury and a Pao, of 57 mm of mercury. He responded to treatment that included intermittent positive-pressure breathing with isoetharine and intravenous administration of aminophylline. On the fifth hospital day an acute episode of shortness of breath developed. His forced vital capacity was 2.55 liters and forced expiratory volume in one second was 1.00 liter. Intravenous administration of methylprednisolone (125 mg every six hours) was started and continued for seven days. The forced vital capacity and forced expiratory volume in one second improved to 4.34 liters and 1.44 liters, respectively, and he was then treated with corticosteroids given by mouth. On the 12th hospital day a temperature of 38.9C (102F) developed. A chest roentgenogram showed left lower lobe consolidation. Penicillin and amikacin sulfate were given, with no apparent response. On the 19th hospital day a generalized seizure occurred and he had a cardiorespiratory arrest. Resuscitation efforts were unsuccessful. Postmortem examination showed findings of an old, as well as a recent but nonacute, myocardial infarction and left lower lobe bronchopneumonia due to Legionella pneumophila. Comment. Legionnaires' disease was not suspected in this patient. The acquisition of the disease was probably related to the immunosuppressive effects of corti567

CASE REPORTS
TABLE 1.-Relevant Factors in Asthma Deaths and Their Presence (+) or Absence (-) in Our 5 Cases
1 2
Cases 3 4 5

Long history of asthma ........ + Previous admission with severe attack ...............Recent hospital admission or emergency care ............. + Insufficient treatment or assessment or intensive care + Underuse of steroids ....... .... +

+
+

+
+
-

+ +
-

+
-

+
+

+
-

+................ Pneumothorax.
Unusual infections ........
....

costeroids. In cases of legionnaires' disease identified at Wadsworth VA Hospital, 9 of 24 patients received pharmacologic doses of corticosteroids within ten days of the onset of illness."3 The disease was fatal in immunosuppressed hosts unless specific therapy was giVen. CASE 5. A 43-year-old man was admitted for evaluation of a two-week history of fever, chills, worsening dyspnea and cough unresponsive to administration of tetracycline. He had a history of childhood asthma. He was admitted to hospital for exacerbations of asthma in 1970 and 1974, and on each occasion was treated with intravenous administration of methylprednisolone, in addition to aminophylline and inhalation of sympathomimetics. Outpatient treatment consisted of the administration of prednisone, 20 mg every other day, aminophylline and hydroxyzine hydrochloride, and inhalation of isoproterenol. There was no history of intravenous drug use or previous heart disease. Examination on admission showed his temperature to be 38.2C (100.8F), pulse rate 120 beats per minute, blood pressure 100/60 mm of mercury and respiratory rate 24 a minute. Examination of the chest showed an increase in the anteroposterior diameter, hyperresonance and diffuse wheezing. No cardiac murmurs or gallops were heard. Hepatomegaly was noted. Following admission, laboratory studies obtained values that included a hematocrit of 36 percent and a leukocyte count of 29,200 per cu mm, with 77 percent neutrophils, 20 percent band forms and 3 percent lymphocytes. Arterial blood gas determinations made while the patient was breathing room air showed a pH of 7.49, a Paco, of 36 mm of mercury and a Pao, of 65 mm of mercury. The patient was treated with intravenous administration of aminophylline, ampicillin and methylprednisolone (125 mg every six hours). Blood cultures grew Pseudomonas aeruginosa. Gentamicin sulfate and carbenicillin therapy was started and the prednisone dosage tapered to 10 mg given every other day. The patient continued to be febrile and subsequent blood cultures continued to grow P aeruginosa. Extensive diagnostic workup, including laparotomy and right heart catheterization, did not reveal the site of infection. After eight
568

weeks of receiving antibiotic therapy, grand mal seizures developed and he had a cardiorespiratory arrest. He became comatose and died. Postmortem examination showed polypoid vegetations on the mitral valve with perforation of the anterior and posterior leaflets. There was no evidence of rheumatic scarring. Amyloid involvement of the blood vessels of the heart, liver, kidneys, pancreas, adrenal glands and lymph nodes was found on microscopic examination. Conmment. A detailed analysis of this case was previously reported.14 For our present discussion it is enough to point out that this patient clearly required corticosteroids for control of acute and chronic asthma. Corticosteroids affect host defense mechanisms and could have contributed to the development of P aeruginosa endocarditis and the lack of response to appropriate and adequate antibiotic therapy.

Discussion

Although many factors are associated with death from asthma, underuse of corticosteroids has been incriminated as a specific cause of death.'5-'8 Other factors include the following: a long history of asthma,'9 previous admissions for severe attacks 15,16,19 recent hospital admission,1",; insufficient assessment and treat7,2 ment, 161,17.19 cardiac arrhythmia,20 pneumothorax,7"' excessive diurnal variation in peak expiratory flow rates22 and delay in getting treatment at the hospital.23 Table 1 summarizes the presence of these factors in our five cases. All of our patients had a long history of asthma and three had previous admissions for severe attacks. One had been recently admitted to hospital and another had several recent emergency department visits. Insufficient assessment and treatment were evident in three cases. Underuse of corticosteroids was present in three cases. Pneumothorax developed in one patient who received intermittent positive-pressure breathing therapy and two had fatal infectious complications. The fatal outcome in cases 1, 2 and 3 could possibly have been averted with the use of corticosteroids. The last two patients succumbed to unusual infections that developed in the presence of corticosteroid use and its immunosuppressive effects. Our series of five patients thus shows that the use of corticosteroids in the management of status asthmaticus can be a demanding situation for a physician. It requires recognition of the need for corticosteroid therapy, as well as surveillance for complications of treatment. The recognition of severe asthma during an acute attack, however, may be the most important factor in preventing death. Respirations of more than 35 per minute, a heart rate of more than 120 per minute, the presence of pulsus paradoxus, a silent chest in a symptomatic patient, the use of accessory muscles of breathing, altered consciousness and an exhausted patient are all ominous clinical signs. An elevated Paco, level, respiratory acidosis, hypoxemia and a significantly decreased forced expiratory volume at one second (less
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CASE REPORTS

than 800 ml) or a decreased peak flow rate (less than 60 liters per minute) are laboratory findings that indicate a severe attack. All of these factors should be assessed while a patient is receiving maximal bronchodilator therapy. If a patient fails to respond, intravenous corticosteroid therapy should be instituted promptly, with the recognition that the onset of effect on the asthmatic airway following intravenous administration of a corticosteroid has been determined to be two hours.24 A delay in the use of the drug deprives a patient of its potential benefits. Corticosteroids should also be administered to patients with severe asthmatic exacerbations who have received systemic corticosteroids in the previous 12 months. The development of infections in patients immunosuppressed by corticosteroids is well documented. Although infrequent, fatal infections can occur in asthmatic patients receiving corticosteroids. Patients must be carefully monitored for infections and other complications. Prompt treatment of complications helps avert fatal outcomes.
REFERENCES
1. Rebtick AS, Read J: Assessment and management of severe asthma. Am J Med 1971 Dec; 51:788-798 2. Pierson WE, Bierman CW, Kelley VC: A double-blind trial of corticosteroid therapy in status asthmaticus. Pediatrics 1974 Sep; 54:282288 3. Senior RM, Lefrak SS, Korenblat PE: Status asthmaticus. JAMA 1975 Mar 24; 231:1277-1279 4. Drugs for asthma. Med Lett Drugs Ther 1978 Aug 11; 20:69-72 5. Report to the Medical Research Council by the subcommittee on clinical trials in asthma: Controlled trial of effects of cortisone acetate in status asthmaticuLs. Lancet 1956 Oct 20; 2:803-806 6. Fontana VJ: Changing pattern of childhood asthma-Steroid-induced. New York J Med 1970 Jun 15; 70:1651-1654 7. Karetzky MS: Asthma mortality: An analysis of one year's experience, review of the literature and assessment of current modes of therapy. Medicine (Baltimore) 1975 Nov; 54:471-484 8. Mallory A, Kern F: Drug induced pancreatitis: A critical review. Gastroenterology 1980 Apr; 78:813-820 9. Nakashima Y, Howard JM: Drug-induced acute pancreatitis. Surg Gynecol Obstet 1977 Jul; 145:105-109 10. Nelp WB: Acute pancreatitis associated with steroid therapy. Arch Intern Med 1961 Nov; 108: 102-110 11. Cortese AF, Glenn F: Hypocalcemia and tetany with steroid-induced acute pancreatitis. Arch Surg 1968 Jan; 96:119-122 12. Jain R, Ramanan SV: latrogenic pancreatitis-A fatal complication in the induLction therapy for acute lymphocytic leukemia. Arch Intern Med 1978 Nov; 138:1726 13. Kirby BD, Snyder KM, Meyer RD, et al: Legionnaires' disease: Clinical features of 24 cases. Ann Intern Med 1978 Sep; 89:297-309 14. Winston DJ, Enriquez L, Meyer RD: Pseudomonas aeruginosa endocarditis and amyloidosis in an asthmatic patient. Ann Allergy 1978

Chest Wall Stimulation for Pacemaker Inhibition

NORA GOLDSCHLAGER, MD BRIAN ANDREWS, MD San Francisco
PROPER SENSING FUNCTION of a ventricular-inhibited

(demand) pacemaker generator requires a stable intracardiac signal having sufficient amplitude, duration and slew (rate of change in voltage).'-3 Intracardiac signals that do not meet the sensing requirements of the pacemaker generator may be sensed intermittently or not at all, resulting in the delivery of inappropriately early pacing stimuli. If these stimuli fall during a critical time period during ventricular repolarization, repetitive ventricular beating may result. Chest wall stimulation, during which electrical stimuli are delivered to the body surface via an external pacemaker generator, can produce signals capable of being sensed by the implanted demand pacemaker generator, which will then inhibit.4 We report the case of a patient with acute myocardial infarction in whom chest wall stimulation was used successfully for 12 hours in order to inhibit an implanted pulse generator that caused repeated episodes of ventricular tachycardia and fibrillation because of failing to sense intracardiac signals.

Report of a Case A 77-year-old man was admitted to the coronary care unit complaining of chest pain unrelieved by sublingual nitroglycerin. Three years earlier he had had a nontransmural anterior myocardial infarction complicated by bradycardia-tachycardia syndrome and bundle branch block, and a permanent unipolar ventricular demand pacing system (Ela Stilith 60) was implanted
and its rate set at 51 per minute. Because of stable postinfarction angina, shortness of breath and periodic supraventricular tachycardias, the patient was placed on a daily regimen of 0.25 mg of digoxin, 1.4 grams of quinidine gluconate, 80 mg of propranolol and sublingual nitroglycerin tablets. On physical examination at admission the patient appeared to be in respiratory distress, coughing bloodtinged sputum. Blood pressure was 150/1 10 mm of mercury and apical pulse 100 per minute and irregular. Pertinent findings included normal central venous pressure, bilateral rales, a sustained nondisplaced left ventricular apical impulse and an S3 gallop. Results of the following laboratory studies were within normal limits: complete blood count, analysis of urine, blood urea nitrogen level and electrolyte determinations, including serum potassium. Arterial blood gas analysis showed
Refer to: Goldschlager N, Andrews B: Chest wall stimulation for pacemaker inhibition. West J Med 1983 Apr; 138:569-573. From the Cardiology Division and Department of Medicine, San Francisco General Hospital Medical Center, and the Department of Medicine, University of California, San Francisco, School of Medicine. Submitted, revised, March 17, 1982.

Nov; 41:30)3-306

15. Poukkula A, Huhti E, Kaipainen WJ: Fatal asthma: Circumstances Feb; 11:13-17 16. Ormerod LP, Stableforth DE: Asthma mortality in Birmingham 1975-7: 53 deaths. Br Med J 1980 Mar 8; 1:687-690 17. Cochrane GM, Clark TJH: A survey of asthma mortality in patients between ages 35 and 64 in the Greater London hospitals in 1971. Thorax 1975 Jun; 30:300-305 18. Management of severe acute asthma (Editorial). Br Med J 1975 Oct 11; 2:65-66 19. MacDonald JB, MacDonald ET, Seaton A, et al: Asthma deaths in Cardiff 1963-74: 53 deaths in hospital. Br Med J 1976 Sep 25; 2:721-723 20. Scoggin CH. Sahn SA, Petty TL: Status asthmaticus: A nine-year experience. JAMA 1977 Sep 12; 238:1158-1162 21. Burke GJ: Pneumothorax complicating acute asthma. S Afr Med J 1979 Mar 24; 55:508-510 22. Hetzel MR, Clark TJH, Branthwaite MA: Asthma: Analysis of sudden deaths and ventilatcry arrests in hospital. Br Med J 1977 Mar 26;
at death. Ann Clin Res 1979

1:808-811 23. Bateman JRM, Clarke SW: Sudden death in asthma. Thorax 1979 Feb; 34:40-44 24. Ellul-Micallef R, Fenech FF: Intravenous prednisolone in chronic

brcnchial asthma. Thcrax 1975 Jun; 30:312-315 25. Klaustermeyer WB, Hale FC: The physiologic effect of an intravenous glucocorticoid in bronchial asthma. Ann Allergy 1976 Aug; 37:
80-86

Reprint requests to Nora Goldschlager, MD, Cardiology Division, San Francisco General Hospital Medical Center, San Francisco, CA 94110.

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