498
Editorial correspondence
The Journal of Pediatrics September 1979
studies.'-' Thus "inoperative" or "impaired" autoregulation is directly involved in the pathogenesis of hypoxic-ischemic brain damage.
7o
9
O)
o
o
Hans C. Lout Ph.D., M.D. Department of Neonatology Rigshospitalet Tagensvej 18 2200 Copenhagen N Denmark
60
-g 5oB--~
EL ~0"
"
~-A
m
REFERENCES
30-
1.
2010
2.
d-~C
3.
lb 2'o io ;o s'o io Syst. BP (mmHg) 9 : Newborns with birth weight.~ 2000g 0 : Newborns with birth weight.,:2OOOg A :Regression line:y=O.g6x-18.6 r=075
Fig. 1. ,Proportional relationships between BP and CBF in patient group as a whole. B and C, spontaneous variations of BP and CBF indicating lacking autoregulation of CBF.
Lou HC, Lassen NA, and Friis-Hansen B: Low cerebral blood flow in hypotensive perinatal distress, Acta Neurol Scand 56:343, 1977. Lou HC, Skov H, and Pedersen H: Low cerebral blood flow as a risk factor in the neonate, J PEDIAIR (in press). Lou HC, Lassen NA, Tweed WA, Johnson G, Jones M, and Palahnink RJ: Pressure-passive cerebral blood flow and break down of the blood-brain barrier in experimental fetal asphyxia, Acta Paediatr Scand 68:57, )979.
Mitral valve prolapse and ventricular arrhythmias To the Editor:
significant relationship between BP and CBF in the most asphyxic group depends on one measurement it is difficult to conceive that this proportionality is not a fact, since it is identical with the proportionality in the less asphyxic group and with the patient group as a whole (Figure). In experimental studies, a similar proportional relationship has been obtained in severe asphyxia? We want to compliment Vannucci et al for their effort in interpreting our data, and we too are aware of the fact that our data also reflect the increase of BP and CBF during intrauterine development. This r.elationship is, however, less significant. Multiple regression analysis of birth weight, BP, and CBF of the patient group as a whole shows that BP and CBF is still interdependent with high significance (P < 0.001). Hence the proportionality between BP and CBF is not dependent on the "development effect" but is rather due to inoperative autoregulation. This interpretation is in accordance with the demonstrated covariation of BP and CBF in two patients. Finally, we agree that perivascular acidosis, due for instance to hypercarbia or to previous or present tissue hypoxia, is the vasodilatator stimulus which may make the autoregulation mechanism inoperative. This in itself is not "pathologic" but may be regarded as a compensatory mechanism which, with unchanged perfusion pressure, will increase oxygen delivery to the brain. If, however, hypotension occurs, hypoperfusion will result and atrophic lesions may develop as demonstrated in our follow-up
I read with interest the article of Pickoff et al 1 on the presentation of mitral valve prolapse in children as premature ventricular contractions (PVC). Although PVCs are an important clue to the presence of underlying cardiac disease, the pediatrician should be aware of the diverse aspects o f mitral valve prolapse (MVP) in children which can be detected on thorough history and physical examination. I reported-' 23 children with MVP diagnosed by echocardiography. In contrast to the six children studied by Pickoff et al, none of our patients presented with an irregular pulse. PVCs were noted on routine electrocardiogram in two patients; however, these were abolished with exercise. The most common complaints of the children that we studied were chest pain and exercise intolerance, with a fewer number of patients complaining of excessive sweating, psychologic difficulties, dizziness, or syncope. Our patients also differed in auscultatory findings from Pickoff et al's in that nine had the classical click-murmur combination. In addition, one had the well-described3 audible honk after exercise. Other abnormalities that stood out in the evaluation of our patients weye a 31% incidence of the straight back syndrome, aortic root enlargement in 13%, and prolongation of the Q-Tc interval in 31%. Dr. Pickofs point of a need for collaboration of data on symptoms, physical findings and disability of children with MVP as would be provided by the registry proposed by Criley 4 is important. Only when the pediatrician becomes aware of the not
Volume 95 Number 3
Editoriai correspondence
infrequent incidence of the disease in children, and its diverse presentations and sequelae, will we be able to predict what the real outcome of children with mitral valve prolapse will be. Linda M. Brown, M.D. Resident in Pediatrics Box 15 12901 N. 30th St. Tamfla, FL 33612 REFERENCES
1. PickoffAS, Gelband H, Ferrer P, Garcia O, and Tamer D: Premature ventricular contractions as the presenting.feature of mitral valve prolapse in childhood, J PEDIATR 94:614, 1979. 2. Brown LM: Mitral valve prolapse in children, in Barness LA, editor: Advances in pediatrics, vol 25, Chicago, 1978, Year Book Medical Publishers, Inc., pp 327-348. 3. Pickering P: Clicks, whoops, and honks, Arch Dis Child 47:731, 1972. 4. Criley JM: Needed: A mitral prolapse registry, Medical World News 19:53, 1978.
Reply To the Editor: We believe that our patients represent a subgroup of children with mitral valve prolapse not previously described. Differences in the mode of presentation and auscultatory findings in our series occur as a function of the specific population of children we examined, in whom an active search for mitral valve prolapse was undertaken and the presenting complaint was arrhythmia. The purpose of our report was to alert the pediatrician that children with premature ventricular contractions may have mitral valve prolapse demonstrable on echocardiography, even in the presence of a normal physical examination. To be sure, the six patients reported are not representative of the usual presentation of mitral valve prolapse in children at our institution. As emphasized by Dr. Brown's series, 1 as well as what amounts to 164 children with mitral valve prolapse reported in other recent series2, ~ most children present with typical ausculatory findings and are either asymptomatic or experience symptoms repeatedly associated with the mitral valve prolapse syndrome. Nevertheless, in view of the uncertainty that exists concerning the long-term prognosis of children with mitral valve prolapse, as well as what we feel is the important and immediate need to institute endocarditis prophylaxis, we suggest approaching pediatric patients with idiopathic ventricular arrhythmias with the diagnosis of mitral valve prolapse in mind. Arthur S. Pickoff, M.D. Pediatric Cardiology Department of Pediatrics School of Medicine P.O. Box 016820 University of Miami MiamL FL 33101
499
9 REFERENCES
1. Brown LM: Mitral valve prolapse in children, in Barness LA, editor, Advances in pediatrics, Vol 25, Chicago, 1978, Year Book Medical Publishers, Inc, pp 327-348. 2. Schmaltz AA, Ibrahim ZI, and Apitz J: Clinical and angloand echocardiographic findings in 45 children with mitral valve prolapse syndrome, Eur J Cardiol 7:49, 1978. 3. Schwartz DC, Bisset GIII, Meyer RA, and Kaplan S: Mitral valve prolapse in children: clinical spectrum and long-term follow-up in 119 cases, Pediatr Res 13(part 2):351, 1979.
Benign "'subdural'" collections To the Editor: Robertson and colleagues I present a discussion of benign subdural collections in the March, 1979, issue of THE JOVRNAL. They describe patients with fluid on subdural taps compatible with Rabe's criteria for subdural collections of fluid? Accompanying computerized tomographic (CT) evaluations of the brain showed ventricular enlargement, wide sulci, large cisterns, prominent interhemispheric fissure, and decreased density over the cerebral convexities. The CT findings were felt to resemble cerebral atrophy. We have seen a similar CT appearance occurring in acute bacterial meningitis in children. Our CT findings have also been those generally attributable to cerebral atrophy. Our findings in bacterial meningitis and the findings of Robertson and his colleagues raise a question regarding the usual clinical criteria for the diagnosis of subdural collections. It seems entirely possible that the fluid from some "subdural" taps may be subarachnoid fluid, perhpas loculated and containing elevated protein, rather than subdural fluid. The usually accepted clinical criteria for subdural collections may be inappropriate and in need of revision. The person placing a needle through the fontanelle cannot distinguish between the subdural and subarachnoid spaces. If conditions such as bacterial meningitis in childhood lead to an enlargement of the subarachnoid space, it may be possible for a needle to enter that space and to retrieve fluid. The diagnostic subdural tap does not necessarily tap the subdural space. The anatomy of the spaces and potential spaces which can be entered upon inserting a needle through the fontanelle needs to be reconsidered in light of the information provided by CT scan. Russell D. Snyder, M.D. Professor o f Neurology and Pediatrics University of New Mexico Medical Center Albuquerque, N M 87131 REFERENCES
Robertson WC, Chun RWM, Orrison WW, and Sackett JF: Benign subdural collections of infancy, J PEDIATR 94:382, 1979.
Editorial correspondence
The Journal of Pediatrics September 1979
studies.'-' Thus "inoperative" or "impaired" autoregulation is directly involved in the pathogenesis of hypoxic-ischemic brain damage.
7o
9
O)
o
o
Hans C. Lout Ph.D., M.D. Department of Neonatology Rigshospitalet Tagensvej 18 2200 Copenhagen N Denmark
60
-g 5oB--~
EL ~0"
"
~-A
m
REFERENCES
30-
1.
2010
2.
d-~C
3.
lb 2'o io ;o s'o io Syst. BP (mmHg) 9 : Newborns with birth weight.~ 2000g 0 : Newborns with birth weight.,:2OOOg A :Regression line:y=O.g6x-18.6 r=075
Fig. 1. ,Proportional relationships between BP and CBF in patient group as a whole. B and C, spontaneous variations of BP and CBF indicating lacking autoregulation of CBF.
Lou HC, Lassen NA, and Friis-Hansen B: Low cerebral blood flow in hypotensive perinatal distress, Acta Neurol Scand 56:343, 1977. Lou HC, Skov H, and Pedersen H: Low cerebral blood flow as a risk factor in the neonate, J PEDIAIR (in press). Lou HC, Lassen NA, Tweed WA, Johnson G, Jones M, and Palahnink RJ: Pressure-passive cerebral blood flow and break down of the blood-brain barrier in experimental fetal asphyxia, Acta Paediatr Scand 68:57, )979.
Mitral valve prolapse and ventricular arrhythmias To the Editor:
significant relationship between BP and CBF in the most asphyxic group depends on one measurement it is difficult to conceive that this proportionality is not a fact, since it is identical with the proportionality in the less asphyxic group and with the patient group as a whole (Figure). In experimental studies, a similar proportional relationship has been obtained in severe asphyxia? We want to compliment Vannucci et al for their effort in interpreting our data, and we too are aware of the fact that our data also reflect the increase of BP and CBF during intrauterine development. This r.elationship is, however, less significant. Multiple regression analysis of birth weight, BP, and CBF of the patient group as a whole shows that BP and CBF is still interdependent with high significance (P < 0.001). Hence the proportionality between BP and CBF is not dependent on the "development effect" but is rather due to inoperative autoregulation. This interpretation is in accordance with the demonstrated covariation of BP and CBF in two patients. Finally, we agree that perivascular acidosis, due for instance to hypercarbia or to previous or present tissue hypoxia, is the vasodilatator stimulus which may make the autoregulation mechanism inoperative. This in itself is not "pathologic" but may be regarded as a compensatory mechanism which, with unchanged perfusion pressure, will increase oxygen delivery to the brain. If, however, hypotension occurs, hypoperfusion will result and atrophic lesions may develop as demonstrated in our follow-up
I read with interest the article of Pickoff et al 1 on the presentation of mitral valve prolapse in children as premature ventricular contractions (PVC). Although PVCs are an important clue to the presence of underlying cardiac disease, the pediatrician should be aware of the diverse aspects o f mitral valve prolapse (MVP) in children which can be detected on thorough history and physical examination. I reported-' 23 children with MVP diagnosed by echocardiography. In contrast to the six children studied by Pickoff et al, none of our patients presented with an irregular pulse. PVCs were noted on routine electrocardiogram in two patients; however, these were abolished with exercise. The most common complaints of the children that we studied were chest pain and exercise intolerance, with a fewer number of patients complaining of excessive sweating, psychologic difficulties, dizziness, or syncope. Our patients also differed in auscultatory findings from Pickoff et al's in that nine had the classical click-murmur combination. In addition, one had the well-described3 audible honk after exercise. Other abnormalities that stood out in the evaluation of our patients weye a 31% incidence of the straight back syndrome, aortic root enlargement in 13%, and prolongation of the Q-Tc interval in 31%. Dr. Pickofs point of a need for collaboration of data on symptoms, physical findings and disability of children with MVP as would be provided by the registry proposed by Criley 4 is important. Only when the pediatrician becomes aware of the not
Volume 95 Number 3
Editoriai correspondence
infrequent incidence of the disease in children, and its diverse presentations and sequelae, will we be able to predict what the real outcome of children with mitral valve prolapse will be. Linda M. Brown, M.D. Resident in Pediatrics Box 15 12901 N. 30th St. Tamfla, FL 33612 REFERENCES
1. PickoffAS, Gelband H, Ferrer P, Garcia O, and Tamer D: Premature ventricular contractions as the presenting.feature of mitral valve prolapse in childhood, J PEDIATR 94:614, 1979. 2. Brown LM: Mitral valve prolapse in children, in Barness LA, editor: Advances in pediatrics, vol 25, Chicago, 1978, Year Book Medical Publishers, Inc., pp 327-348. 3. Pickering P: Clicks, whoops, and honks, Arch Dis Child 47:731, 1972. 4. Criley JM: Needed: A mitral prolapse registry, Medical World News 19:53, 1978.
Reply To the Editor: We believe that our patients represent a subgroup of children with mitral valve prolapse not previously described. Differences in the mode of presentation and auscultatory findings in our series occur as a function of the specific population of children we examined, in whom an active search for mitral valve prolapse was undertaken and the presenting complaint was arrhythmia. The purpose of our report was to alert the pediatrician that children with premature ventricular contractions may have mitral valve prolapse demonstrable on echocardiography, even in the presence of a normal physical examination. To be sure, the six patients reported are not representative of the usual presentation of mitral valve prolapse in children at our institution. As emphasized by Dr. Brown's series, 1 as well as what amounts to 164 children with mitral valve prolapse reported in other recent series2, ~ most children present with typical ausculatory findings and are either asymptomatic or experience symptoms repeatedly associated with the mitral valve prolapse syndrome. Nevertheless, in view of the uncertainty that exists concerning the long-term prognosis of children with mitral valve prolapse, as well as what we feel is the important and immediate need to institute endocarditis prophylaxis, we suggest approaching pediatric patients with idiopathic ventricular arrhythmias with the diagnosis of mitral valve prolapse in mind. Arthur S. Pickoff, M.D. Pediatric Cardiology Department of Pediatrics School of Medicine P.O. Box 016820 University of Miami MiamL FL 33101
499
9 REFERENCES
1. Brown LM: Mitral valve prolapse in children, in Barness LA, editor, Advances in pediatrics, Vol 25, Chicago, 1978, Year Book Medical Publishers, Inc, pp 327-348. 2. Schmaltz AA, Ibrahim ZI, and Apitz J: Clinical and angloand echocardiographic findings in 45 children with mitral valve prolapse syndrome, Eur J Cardiol 7:49, 1978. 3. Schwartz DC, Bisset GIII, Meyer RA, and Kaplan S: Mitral valve prolapse in children: clinical spectrum and long-term follow-up in 119 cases, Pediatr Res 13(part 2):351, 1979.
Benign "'subdural'" collections To the Editor: Robertson and colleagues I present a discussion of benign subdural collections in the March, 1979, issue of THE JOVRNAL. They describe patients with fluid on subdural taps compatible with Rabe's criteria for subdural collections of fluid? Accompanying computerized tomographic (CT) evaluations of the brain showed ventricular enlargement, wide sulci, large cisterns, prominent interhemispheric fissure, and decreased density over the cerebral convexities. The CT findings were felt to resemble cerebral atrophy. We have seen a similar CT appearance occurring in acute bacterial meningitis in children. Our CT findings have also been those generally attributable to cerebral atrophy. Our findings in bacterial meningitis and the findings of Robertson and his colleagues raise a question regarding the usual clinical criteria for the diagnosis of subdural collections. It seems entirely possible that the fluid from some "subdural" taps may be subarachnoid fluid, perhpas loculated and containing elevated protein, rather than subdural fluid. The usually accepted clinical criteria for subdural collections may be inappropriate and in need of revision. The person placing a needle through the fontanelle cannot distinguish between the subdural and subarachnoid spaces. If conditions such as bacterial meningitis in childhood lead to an enlargement of the subarachnoid space, it may be possible for a needle to enter that space and to retrieve fluid. The diagnostic subdural tap does not necessarily tap the subdural space. The anatomy of the spaces and potential spaces which can be entered upon inserting a needle through the fontanelle needs to be reconsidered in light of the information provided by CT scan. Russell D. Snyder, M.D. Professor o f Neurology and Pediatrics University of New Mexico Medical Center Albuquerque, N M 87131 REFERENCES
Robertson WC, Chun RWM, Orrison WW, and Sackett JF: Benign subdural collections of infancy, J PEDIATR 94:382, 1979.
