LETTERS
TO T H E E D I T O R
Clinical notes
"Clinical Notes" represent clinical and/or laboratory experiences which can be presented in 200 to 400 words; 3 or 4 references, and, if contributory, one illustration or short table. "Clinical Notes" are subject to the same critical peer review and editing as papers published in other sections of the JouRY At.
Complete heart block in viral myocarditis To the Editor." Arrhythmias are common in patients with myocardifiS but complete heart block is rare? Complete heart block, however, which required the implantation of a permanent cardiac pacemaker occurred in an adolescent who had viral myocarditis. Because acquired complete heart block is unusual in pediatrics, this patient is presented and the indications for implantation of permanent epicardial pacemakers in children are discussed.
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CASEREPORT
A previously healthy 15-year-old girl whose family physician had documented normal heart rates on multiple examinations suddenly developed fatigue, blurred vision, and syncope. On admission to a local hospital she had ankle and facial edema, bradyeardia (48 beats per minute), orthopnea, and fever. Digitalis and diuretic therapy were begun, and she was transferred to University of Iowa Hospitals. Ghildhood immunizations were complete and she had experienced no rheumatic manifestations. No heart block, cardiac arrhythmias, myocarditis, or deafness were known among family members. On physical examination she was normotensive, but the pulse rate was 43 beats per minute. There was a left ventricular impulse and "cannon" sounds were heard synchronously with the cannon "a" waves in the jugular venous pulse. The second heart sound was normal. Prominent third and fourth heart sounds were heard over the apex and along the left sternal border. There was a Grade 2/6 basal systolic ejection murmur which radiated faintly to the posterior chest. No diastolic murmur was heard. There was no hepatosplenomegaly. Increased heart size and left pleural effusion were noted in a chest roentgenogram. The electrocardiogram (Fig. 1) revealed complete heart block with multifocal ventricular beats; the atrial rate was 100 per minute while the ventricular rate was 40-50 per minute. The hemoglobin was 11.6 gm/dl and white blood cell count was 16,800 mm 3 with 'a normal differential. The erythrocyte sedimentation rate was 78 m m per hour. The C-reactive protein was 2 + . The results of monospot test was negative. Serologies for anti-nuclear antibodies, syphilis, histoplasmosis, blastomyocosis, and coccidiomyocosis were nonreac-
Fig. 1. Preoperative electrocardiogram showing complete heart block. Multifocal ventricular beats are seen. No conducted sinus beats are recorded. five. Antistreptococcal titers (antistreptolysis O and antiDNAse) were 240 Todd units in the third and sixth weeks of illness, respectively. Attempts at viral isolation from throat, stool, urine, and pleural fluid in the third and fourth week of illness were unsuccessful in both tissue cultures and suckling mice. However, a 16-fold increase in neutralizing serum antibody t O Coxsackie B 1 was demonstrated. At rest the patient complained of dizziness, blurred vision, and orthopnea. Because of persistent symptomatic complete heart block a transvenous pacemaker was inserted percutaneously via the femoral vein into the right ventricle with dramatic symptomatic improvement. The intrinsic heart rate remained at 40 beats per minute for two weeks and a permanent epicardial cardiac demand pacemaker was inserted. The patient was seen six months after the insertion o f the pacemaker. She was well. The cardiac pacemaker was functioning at a rate of 68 per minute. No multifocal ventricular b e a t s were recorded (Fig. 2). No conducted sinus beats were recorded, suggesting her conduction system had not recovered. COMMENT The etiologic agent was not isolated in this case but a 16-fold rise in neutralizing antibody titer to CoxsackieB1, an established cause of myocardifis, was found. Other excluded causes o f myocarditis are diphtheria, rheumatic fever, streptococcal infecThe Journal o f P E D I A T R I C S Vol. 87, No. 5, pp. 831-842
831
832
Letters to the Editor
The Journal of Pediatrics November t975
variety of systemic infections. 1 It has been reported only once in association with infectious mononucleosis. This is a report of a 4year,old gift with serologically proved infectious mononucleosis whose presenting symptom was severe ataxia; she made a complete recovery after resolution of her viral illness. CASE REPORT
.......
...... !
Fig. 2. Postoperative electrocardiogram, continuous recording from lead V1, showing paced ventricular beats at a rate of 68 beats per minute. No conducted sinus beats are recorded. tions, pyogenic bacteremia, tuberculosis, parasitic diseases, other viral infections, and rickettsial disease. 2 This patient demonstrates a rare complication of viral myocarditis: complete heart block. Arrhythmias, including first and second degree heart block, are common occurrences in patients with recognized myocarditis though these conduction abnoi'maiities are usually transient. 3 These conduction abnormalities are thought to be due to focal lesions involving the conduction system, including the bundle of His, which are seen in patients dying of myocarditis. ~ Richard M. Sehieken, M.D. Martin G. Myers, M.D. Department of Pediatri'es Division of Pediatric Cardiology and Infectious Diseases University of Iowa Iowa City, Iowa 52242 REFERENCES
1. Stocker FP, Czoniczer G, Massell BF, and Nadas AS: Transient complete A-V block in two siblings during acute rheumatic fever, Pediatrics 45:850, 1970. 2. Gore I, and Saphir O: Myocarditis. A classification of 1402 cases, Am Heart J 34:827, 1947. 3. Smith WG: Coxsackie B myopericarditis in adults, Am Heart J 80:34, 1970. 4. Butch GE, Sun SE, Cololough HL, Sohal RS, and DePasquale NP: Coxsackie B viral myocarditis a n d valvulitis identified in routine autopsy specimens by immunofluroescent techniques, Am Heart J 74:12, 1967.
Acute cerebellar ataxia of childhood associated with infectious rnononucteosis To the Editor: Acute eerebellar ataxia of childhood is usually a benign, selflimited disease which has been seen accompanying br following a From Rush Medical College and the lllinois State Psychiatric Institute.
A 4-year-old girl was brought to the hospital two days after developing an unsteady gait. She had complained of generalized headache, but seemed otherwise well. On admission~ the patient was alert and afebrile. The pharynx was inflamed, and many small, firm, tender lymph nodes were palpable in the anterior and posterior cervical regions. The spleen was easily palpable, and the hepatic border could be felt 2 cm below the costal margin. Neurologic examination revealed severe gait and truncal ataxia. There was a mild end-point tremor on finger-nose testing. The rest of the neurologic examination was normal. On admission, the peripheral white blood cell count was 10,800, with 17% polymorphonuclear cells, 58% lymphocytes, and 18% band forms; some atypical lymphocytes were seen. A heterophile antibody (Paul-Bunnell) test Was positive. The cerebrospinal fluid contained 14 mononuclear cells per high-power field; concentrations of protein and glucose were normal, and Gram stain and bacterial culture were negative. Titers of serum antibodies to herpes virus, cytomegalovirus, mumps and poliovirus, Coxsackie B, and arboviruses were less than 1:8. The serum liter of toxoplasma antibody was less than 1:16. The serum titer to Epstein-Ban" virus was 1:128. Hospital eourse. The day after admission, multiple vesicles appeared on the soft palate. Two days later she developed a spiking fever (up to 103.3 ~ orally), appeared ill and irrRable, and had a nonproductive cough and rhinorrhea. Submandibular and axillary lymph nodes were now palpable. Twelve days after admission the ataxia, as well as the malaise, had improved. Follow-up neurologic examination three weeks after discharge revealed no abnormalities. DISCUSSION Acute cerebellar ataxia of childhood is a well-defined syndrome, but its etiology is still a matter for conjecture. A history of a febrile illness preceding or accompanying the onset of cerebellar symptoms is common. Infectious mononucleosis may be seen in the same age group (early childhood) which is the target for acute cerebellar ataxia," but the association of acute cerebellar ataxia with infectious mononucleosis is rarely observed. A review of the neurologic literature revealed only six such cases2-G; only one of these was a child. Donna Bergen, M.D. Herbert Grossman, M.D. Rush-Presbyterian-St. Luke's Medical Center 1753 IV.. Congress Parkway Chicago, 11l. 60612 REFERENCES
1. Cottom DG: Acute cerebellar ataxia, Arch Dis C h i l d 32:163, 1957.
TO T H E E D I T O R
Clinical notes
"Clinical Notes" represent clinical and/or laboratory experiences which can be presented in 200 to 400 words; 3 or 4 references, and, if contributory, one illustration or short table. "Clinical Notes" are subject to the same critical peer review and editing as papers published in other sections of the JouRY At.
Complete heart block in viral myocarditis To the Editor." Arrhythmias are common in patients with myocardifiS but complete heart block is rare? Complete heart block, however, which required the implantation of a permanent cardiac pacemaker occurred in an adolescent who had viral myocarditis. Because acquired complete heart block is unusual in pediatrics, this patient is presented and the indications for implantation of permanent epicardial pacemakers in children are discussed.
'
];];z;:]~!:I
CASEREPORT
A previously healthy 15-year-old girl whose family physician had documented normal heart rates on multiple examinations suddenly developed fatigue, blurred vision, and syncope. On admission to a local hospital she had ankle and facial edema, bradyeardia (48 beats per minute), orthopnea, and fever. Digitalis and diuretic therapy were begun, and she was transferred to University of Iowa Hospitals. Ghildhood immunizations were complete and she had experienced no rheumatic manifestations. No heart block, cardiac arrhythmias, myocarditis, or deafness were known among family members. On physical examination she was normotensive, but the pulse rate was 43 beats per minute. There was a left ventricular impulse and "cannon" sounds were heard synchronously with the cannon "a" waves in the jugular venous pulse. The second heart sound was normal. Prominent third and fourth heart sounds were heard over the apex and along the left sternal border. There was a Grade 2/6 basal systolic ejection murmur which radiated faintly to the posterior chest. No diastolic murmur was heard. There was no hepatosplenomegaly. Increased heart size and left pleural effusion were noted in a chest roentgenogram. The electrocardiogram (Fig. 1) revealed complete heart block with multifocal ventricular beats; the atrial rate was 100 per minute while the ventricular rate was 40-50 per minute. The hemoglobin was 11.6 gm/dl and white blood cell count was 16,800 mm 3 with 'a normal differential. The erythrocyte sedimentation rate was 78 m m per hour. The C-reactive protein was 2 + . The results of monospot test was negative. Serologies for anti-nuclear antibodies, syphilis, histoplasmosis, blastomyocosis, and coccidiomyocosis were nonreac-
Fig. 1. Preoperative electrocardiogram showing complete heart block. Multifocal ventricular beats are seen. No conducted sinus beats are recorded. five. Antistreptococcal titers (antistreptolysis O and antiDNAse) were 240 Todd units in the third and sixth weeks of illness, respectively. Attempts at viral isolation from throat, stool, urine, and pleural fluid in the third and fourth week of illness were unsuccessful in both tissue cultures and suckling mice. However, a 16-fold increase in neutralizing serum antibody t O Coxsackie B 1 was demonstrated. At rest the patient complained of dizziness, blurred vision, and orthopnea. Because of persistent symptomatic complete heart block a transvenous pacemaker was inserted percutaneously via the femoral vein into the right ventricle with dramatic symptomatic improvement. The intrinsic heart rate remained at 40 beats per minute for two weeks and a permanent epicardial cardiac demand pacemaker was inserted. The patient was seen six months after the insertion o f the pacemaker. She was well. The cardiac pacemaker was functioning at a rate of 68 per minute. No multifocal ventricular b e a t s were recorded (Fig. 2). No conducted sinus beats were recorded, suggesting her conduction system had not recovered. COMMENT The etiologic agent was not isolated in this case but a 16-fold rise in neutralizing antibody titer to CoxsackieB1, an established cause of myocardifis, was found. Other excluded causes o f myocarditis are diphtheria, rheumatic fever, streptococcal infecThe Journal o f P E D I A T R I C S Vol. 87, No. 5, pp. 831-842
831
832
Letters to the Editor
The Journal of Pediatrics November t975
variety of systemic infections. 1 It has been reported only once in association with infectious mononucleosis. This is a report of a 4year,old gift with serologically proved infectious mononucleosis whose presenting symptom was severe ataxia; she made a complete recovery after resolution of her viral illness. CASE REPORT
.......
...... !
Fig. 2. Postoperative electrocardiogram, continuous recording from lead V1, showing paced ventricular beats at a rate of 68 beats per minute. No conducted sinus beats are recorded. tions, pyogenic bacteremia, tuberculosis, parasitic diseases, other viral infections, and rickettsial disease. 2 This patient demonstrates a rare complication of viral myocarditis: complete heart block. Arrhythmias, including first and second degree heart block, are common occurrences in patients with recognized myocarditis though these conduction abnoi'maiities are usually transient. 3 These conduction abnormalities are thought to be due to focal lesions involving the conduction system, including the bundle of His, which are seen in patients dying of myocarditis. ~ Richard M. Sehieken, M.D. Martin G. Myers, M.D. Department of Pediatri'es Division of Pediatric Cardiology and Infectious Diseases University of Iowa Iowa City, Iowa 52242 REFERENCES
1. Stocker FP, Czoniczer G, Massell BF, and Nadas AS: Transient complete A-V block in two siblings during acute rheumatic fever, Pediatrics 45:850, 1970. 2. Gore I, and Saphir O: Myocarditis. A classification of 1402 cases, Am Heart J 34:827, 1947. 3. Smith WG: Coxsackie B myopericarditis in adults, Am Heart J 80:34, 1970. 4. Butch GE, Sun SE, Cololough HL, Sohal RS, and DePasquale NP: Coxsackie B viral myocarditis a n d valvulitis identified in routine autopsy specimens by immunofluroescent techniques, Am Heart J 74:12, 1967.
Acute cerebellar ataxia of childhood associated with infectious rnononucteosis To the Editor: Acute eerebellar ataxia of childhood is usually a benign, selflimited disease which has been seen accompanying br following a From Rush Medical College and the lllinois State Psychiatric Institute.
A 4-year-old girl was brought to the hospital two days after developing an unsteady gait. She had complained of generalized headache, but seemed otherwise well. On admission~ the patient was alert and afebrile. The pharynx was inflamed, and many small, firm, tender lymph nodes were palpable in the anterior and posterior cervical regions. The spleen was easily palpable, and the hepatic border could be felt 2 cm below the costal margin. Neurologic examination revealed severe gait and truncal ataxia. There was a mild end-point tremor on finger-nose testing. The rest of the neurologic examination was normal. On admission, the peripheral white blood cell count was 10,800, with 17% polymorphonuclear cells, 58% lymphocytes, and 18% band forms; some atypical lymphocytes were seen. A heterophile antibody (Paul-Bunnell) test Was positive. The cerebrospinal fluid contained 14 mononuclear cells per high-power field; concentrations of protein and glucose were normal, and Gram stain and bacterial culture were negative. Titers of serum antibodies to herpes virus, cytomegalovirus, mumps and poliovirus, Coxsackie B, and arboviruses were less than 1:8. The serum liter of toxoplasma antibody was less than 1:16. The serum titer to Epstein-Ban" virus was 1:128. Hospital eourse. The day after admission, multiple vesicles appeared on the soft palate. Two days later she developed a spiking fever (up to 103.3 ~ orally), appeared ill and irrRable, and had a nonproductive cough and rhinorrhea. Submandibular and axillary lymph nodes were now palpable. Twelve days after admission the ataxia, as well as the malaise, had improved. Follow-up neurologic examination three weeks after discharge revealed no abnormalities. DISCUSSION Acute cerebellar ataxia of childhood is a well-defined syndrome, but its etiology is still a matter for conjecture. A history of a febrile illness preceding or accompanying the onset of cerebellar symptoms is common. Infectious mononucleosis may be seen in the same age group (early childhood) which is the target for acute cerebellar ataxia," but the association of acute cerebellar ataxia with infectious mononucleosis is rarely observed. A review of the neurologic literature revealed only six such cases2-G; only one of these was a child. Donna Bergen, M.D. Herbert Grossman, M.D. Rush-Presbyterian-St. Luke's Medical Center 1753 IV.. Congress Parkway Chicago, 11l. 60612 REFERENCES
1. Cottom DG: Acute cerebellar ataxia, Arch Dis C h i l d 32:163, 1957.
