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Severe Arrhythmias in Coxsackievirus B3 Myopericarditis

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Severe Arrhythmias in Coxsackievirus B3 Myopericarditis Arch Dis Child: first published as 10.1136/adc.53.2.174 on 1 February 1978. Downloaded from 174 Short reports Oh, W., and Karecki, H. (1972). Phototherapy and insensible Table Results of clinical chemistry water loss in the newborn infant. American Journal of Diseases of Children, 124, 230-232. Oh, W., Yao, A. C., Hanson, J. S., and Lind, J. (1973). Date: September Peripheral circulatory response to phototherapy in Investigation newborn infants. Acta Paediatrica Scandinavica, 62, 49-54. (normal max) 6 7 9 10 14 23 Smales, 0. R. C. (1978). Simple method for measuring Blood urea 13-2 18-6 23-0 11-2 9*5 3-9 oxygen consumption in babies. Archives of Disease in (2*7-7 5 mmol/l) Childhood, 53, 53-57. Alananine Wilcoxon, F. (1945). The signed ranks test. Biometrics aminotransferase 2562 4987 7185 Bulletin, 1, 80. (100-500 nkat/1) Wu, P. Y. K., and Berdahl, M. (1974). Irradiance in incubators Aspartate aminotransferase 8000 7935 6000 under phototherapy lamps. Journal of Pediatrics, 84, (75-400 nkat/1) 754-755. Glutamin oxalotransferase 226 68 10 (9-19 IU/1) 0. R. C. SMALES Glutamic Department of Child Health, University Hospital and phosphorotransferase 687 207 16 (5-17 IU/1) Medical School, Nottingham NG7 2UH. Creatine kinase 133 11 12 (0-1 17 IU/1) Lactic dehydrogenase 1368 691 217 (115-457 IU/1) Severe arrhythmias in Alkaline phosphatase 75 100 117 (25-103 IU/1) Coxsackievirus B3 myopericarditis Bilirubin 7 13 18 (0-22 ,umol/l) Proven viral myopericarditis onlyrarely presents with Conversion: SI to traditional units-Blood urea: 1 mmol/l 6 02 life-threatening arrhythmias. This report describes mg/100 ml. Bilirubin: 1 ,umol/l 0-06 mg/100 ml. the first such case with serological evidence of recent Coxsackievirus B3 infection. 0a 125 mg/day, phenytoin 50 mg three times a day, Case report prednisolone 20 mg per day, and frusemide 40 mg IV copyright. immediately. A urinary catheter was inserted. A previously healthy 12-year-old girl was admitted to hospital on 6 September 1976 with a 4-day history of Progress. Ventricular fibrillation did not recur and sore throat, shivering, malaise, occasional vomiting, urinary output was satisfactory. By 14 September and with 'fainting attacks' on the 2 preceding days. lung fields were radiologically normal and cardiac On examination she was apyrexial, blood pressure size was decreasing. On the 17th, paroxysmal atrial 100/90 mmHg, pulse 80 beats/min. There were no fibrillation occurred with a ventricular rate of 130/ cardiac murmurs, no pericardial rub, and no signs of min. Phenytoin was stopped and Kinidin durules 1 http://adc.bmj.com/ cardiac failure. She had slight neck stiffness. A few bd started. Pulse rate was easily controlled and she hours after admission she had a cardiac arrest. was gradually mobilised. The pacemaker electrode After resuscitation, chest x-ray showed marked was removed on the 23rd. She was discharged on 4 cardiomegaly. Subsequently, multifocal ventricular October taking digoxin 0 125 mg/day and Kinidin ectopic beats occurred which were resistant to durules 1 bd. Digoxin was stopped one month later. lignocaine and to mexiletine. She was seen in the outpatient clinic on 3 December; During the next 36 hours ventricular fibrillation there were no abnormal physical signs but she on September 27, 2021 by guest. Protected occurred on 14 occasions. Each time it was terminated complained of breathlessness, for example, when by DC defibrillation (100-200 J) but was followed by climbing stairs. Chest x-ray was normal; ECG is severe bradycardia (<30 beats/min) which only shown in the Fig. partially responded to atropine 0-6 mg IV. On 9 September she became breathless and was oliguric, Investigations. Results ofclinical chemistry are shown blood urea had risen to 23 mmol/l (138-6 mg/100 ml; in the Table and ECGs in the Fig. Hb 12 g/dl; white see Table), and chest x-ray showed pulmonary cell count 15@6 x 109/1. ESR 4 mm in the first hour oedema. At this stage she was transferred to this (Westergren). On 20 October echocardiography hospital. On examination blood pressure was 100/60 showed a small pericardial effusion. mmHg, pulse 60 beats/min (see ECG, Fig.), jugular venous pressure raised 4 cm, liver enlarged 3 cm. A Viral studies. On 9 September Coxsackievirus B3 bipolar endocardial pacing catheter was introduced neutralisation titre 32, and on the 21st, 512. Attempts via the left antecubital fossa and 'on demand' pacing to isolate the virus from stools and throat washings was started at 90 beats/min. She was given digoxin were unsuccessful. Arch Dis Child: first published as 10.1136/adc.53.2.174 on 1 February 1978. Downloaded from aVR WfL3 WF H: J.- t--1,1 copyright. aVF http://adc.bmj.com/ * -i--0- -+ -4- ; -14~~~~~~~ ffb4,+3t t on September 27, 2021 by guest. Protected VI Fig. Electrocardiograms. (A) Immediately before endocardial pacing. Junctional (nodal) bradycardia-P waves can be seen deforming S-T segments in S2. Right bundle branch block and left posterior hemiblock (QRS axis approximately + 1400). (B) Next day. Changes in VI- V3 very suggestive ofseptal myocardial infarction. (C) 2 months after discharge from hospital. Rhythm: junctional or 1st degree A- V block. P waves visible at end of T wave in V1. P-R interval 340 ms. Right bundle branch block and left posterior hemiblock still present. Arch Dis Child: first published as 10.1136/adc.53.2.174 on 1 February 1978. Downloaded from 176 Short reports Chest x-rays. On 9 September showed cardiomegaly, man, 1962). An additional factor in this case was globular heart, changes in lung fields suggesting repeated DC defibrillation. However, the presence of cardiac failure. On 16 September cardiomegaly, lung a marked rise in enzyme levels in the first blood fields clear. On 5 November heart size at upper limit sample (before defibrillation) and the absence of any of normal. additional evidence of liver dysfunction suggests that in this case extensive myocardial damage was the Discussion major source of the enzymes. This patient had features of acute myopericarditis References coexistent with evidence of Coxsackievirus B3 Coltman, C. A., Jr. (1962). Influenza myocarditis. Journal of the American Medical Association, 180, 204-208. infection. This association has previously been Forfang, K., and Lippestad, C. T. (1974). Transient left described but several features of this case are unusual. posterior hemi-block in acute myocarditis. Journal of Patients with viral myopericarditis usually present Electrocardiology, 7, 83-85. with chest pain or dyspnoea and have clinical features Gould, L., Diaz, R., and Gomprecht, R. (1972). Complete or heart block in myocarditis-recovery with a pacemaker. caused by pericarditis, pericardial effusion, cardiac Chest, 62, 230-233. failure secondary to myocarditis. In contrast, this Lim, C-H., Toh, C. C. S., Chia, B-L., and Low, L-P. (1975). patient presented with syncope-in retrospect Stokes- Stokes-Adams attacks due to acute non-specific myo- Adams attacks-and the clinical course was domi- carditis. American Heart Journal, 90, 172-178. nated by Sainani, G. S., Krompotic, E., and Slodki, S. J. (1968). Adult life-threatening arrhythmias. This resembles heart disease due to the Coxsackie virus B infection. in some respects the description by Lim et al. (1975) Medicine, 47, 133-147. of 10 patients with myocarditis, although with the Smith, W. (1970). Coxsackie B myopericarditis in adults. exception of one case associated with adenovirus American Heart Journal, 80, 34-46. infection they were to a Thompson, W. M., Jr., and Nolan, T. B. (1966). Atrioventri- unable prove viral aetiology. cular dissociation associated with Adams-Stokes syndrome All their patients were young, and most were female. presumably due to mumps myocarditis. Journal of Pedia- They presented with syncope and heart block trics, 68, 601-607. requiring temporary endocardial pacing in 9 cases. Verel, D., Warrack, A. J. W., Potter, C. W., Ward, C., and Rickards, D. F. (1976). Observations on the A2 England However, ventricular fibrillation was not a major copyright. problem in these patients; it occurred in only one influenza epidemic. American Heart Journal, 92, 290-296. case and another had ventricular tachycardia. With CHRISTOPHER WARD the exception of one patient with persistent heart Cardio-Thoracic Unit, Northern General Hospital, block all recovered fully. Sheffield S5 7A U. Bradycardia, usually sinus, is common in viral myocarditis especially when caused by influenza (Verel et al., 1976). Atrioventricular block has also Improved tube for nasojejunal been described. Isolated case reports have docu- feeding in low birthweight infants http://adc.bmj.com/ mented the use of temporary endocardial pacing in myocarditis caused by 3 viruses: mumps (Thompson In the last few years nasojejunal infusion of milk and Nolan, 1966), Coxsackievirus B2 (Gould et al., formulas has been widely used for the feeding of 1972), and adenovirus (Lim et al., 1975)-and other low birthweight infants. The techniques of trans- clinically similar cases have been described which pyloric intubation previously described are those of lacked evidence of a viral aetiology. Junctional Rhea and Kilby (1970) and Cheek and Staub (1973). (nodal) bradycardia, which caused the patient's slow Besides the enthusiastic experiences of many, heart rate, seems to be uncommon in viral myoperi- difficulties and complications relating to both on September 27, 2021 by guest. Protected carditis. The intraventricular conduction defect was methods of intubation have been encountered also unusual; right bundle branch block with left (Boros and Reynolds, 1974; Chen and Wong, 1974; posterior hemiblock has only twice been described in Van Callie and Powell, 1975). Modifications of the suspected viral myopericarditis (Forfang and Lippe- original methods have been made by Rhea et al.
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