correspondence
TRANSCRIPT
The Clinical Establishment (Registration and Regulation)Act was enacted by the Union government to ensure thatuniform and acceptable standard of health care is meted tothe citizens in the private sector [1]. Till date, only 5 Statesand 4 Union territories have implemented it. As a part ofproviding standard treatment by private hospitals,treatment guidelines have been formulated for most broadspecialties and super specialties. The standard treatmentpolicy is intended to provide a ring of protection for bothpatients and doctors [2]. For the patients, it assures thedelivery of a rational, safe, standard and uniformtreatment. For the doctors who follow standard guidelines,it offers protection against medico-legal issues arising outof non-standard treatment. For Pediatrics and Pediatricsurgery, the standard treatment guidelines (published atwww.clinicalestablishments.nic.in) cover only a limitednumber of conditions [3]. There is no mention ofmanagement of common ailments like respiratoryinfection, diarrhea, malaria, typhoid, hepatitis, HIV,tuberculosis, envenomations and chronic diseases likeasthma, diabetes and epilepsy. Similarly, developmentaldisorders like cerebral palsy, attention deficit hyper-activity disorder and autism have not found a place.Delivery room management of perinatal asphyxia,
Standard Treatment Guidelines forPediatrics under ClinicalEstablishment Act 2010
neonatal sepsis and screening for metabolic diseases havealso been ignored.
We assume that the standard guidelines availablethrough the website are only a sample and not anexhaustive list of common pediatric and pediatric surgicalconditions. There is a haste in implementing the aboveprogram in various states. Standard guidelines need to beelaborate, focusing on common clinical conditions, andconditions associated with serious morbidity and mortalityif not identified or treated appropriately. We urge theAcademy to share the common pediatric protocols, that arealready in place, with the appropriate authorities, so thatthe same can also be incorporated in the website.
Acknowledgement: BS Sanjay Kumar Bommidi.*VENKATESH SOMA AND CHANDRASEKARAN
VENKATESHDepartments of Pediatrics; JIPMER and
*Mahatma Gandhi Medical College and Research Institute,Puducherry, India.
1. Kumar R. Healthcare and medical education reforms inIndia: What lies ahead? J Family Med Prim Care.2013;2:123-7.
2. Phadke A. The Indian Medical Association and the ClinicalEstablishment Act, 2010: irrational opposition toregulation. Indian J Med Ethics. 2010;7:229-32.
3. Ministry of Health and Family Welfare, Government ofIndia. Protocol for Dengue Fever in Children. Availablefrom: http://clinicalestablishments.nic.in/WriteReadData/853.pdf. Accessed April 21, 2014.
Benign infantile seizures with mild gastroenteritis, firstdescribed from Japan in 1982 [1], have been commonlyreported from Asia [1-3]. More recently, many cases arealso being reported from non-Asian countries, albeitinfrequently [4,5]. Typically, previously healthy infantsaged 6 months to 3 years, present with generalized,afebrile, isolated or cluster seizures. The laboratoryexamination, including blood glucose, serum electro-
Benign Infantile Seizures with MildGastroenteritis
lytes, and CSF, as well as the interictal EEG andneuroimaging are normal [4,5]. Subsequent recoveryfrom the episode is complete [4].
An 11-month-old girl presented with a 15-minutegeneralized tonic seizure, associated with mild gastro-enteritis of 2 days duration. There was no dehydration,and seizures subsided without any anti-convulsanttreatment. Her serum glucose, electrolytes and ioniccalcium, and hemogram were within normal range. Thestool microscopy did not show pus cells, and bacterialculture did not reveal any organisms. Studies forRotavirus were not done. Interictal EEG and MRI werenon-contributory. Development quotient done after three
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months (using DASII) was 84. There was no recurrenceof seizures, or developmental delay on follow-up overnext 13 months. The final diagnosis made was Benigninfantile seizures with mild gastroenteritis.
This syndrome – recognized only in the last decade –is still not accepted by the International League AgainstEpilepsy [6]. Rotavirus has been reported as the mostcommon etiological agent in this condition in differentstudies [4,5]. However, other organisms have also beenreported [3], and it has not been possible to attribute theconvulsions to any organism, as yet [2]. The clinicalsymptoms are reported to precede the convulsions by anaverage of 2 days [4], similar to that in our case.
The importance of recognition of this condition is thatit helps in avoiding unnecessary long term anti-epileptictherapy, and favorably counsel the parents about the lowrisk of recurrence of seizures.
DEVENDRA MISHRA AND NIRAJ KUMAR NIKUNJDepartment of Pediatrics,
MAMC, New Delhi, [email protected]
REFERENCES
1. Uemura N, Okumara A, Negoro T, Watanabe K. Clinicalfeatures of benign convulsions with mild gastroenteritis.Brain Dev. 2002;24:745-9.
2. Narchi H. Benign afebrile cluster convulsions withgastroenteritis: an observational study. BMC Pediatr.2004;4:2.
3. Abe T, Kobayashi M, Arki K, Kodama H, FujitaY, Shinozaki T, et al. Infantile convulsions with mildgastroenteritis. Brain Dev. 2000;22:1367-70.
4. Youssef WF, Ramírez RP, Plana JC, Marfa MP. Benignafebrile convulsions in the course of mild acutegastroenteritis: a study of 28 patients and a literaturereview. Pediatr Emerg Care. 2011;27:1062-4.
5. Caraballo RH, Gañez L, Santos Cde L, Espeche A,Cersósimo R, Fejerman N. Benign infantile seizures withmild gastroenteritis: study of 22 patients. Seizure.2009;18:686-9.
6. Engel J, Jr. Report of the ILAE Classification Core Group.Epilepsia. 2006;47:1558-68.
I read the recent review article [1] on management ofpatent ductus arteriosis (PDA) in very low birth weight(VLBW) infants with interest. I wish to seekclarifications regarding authors’ conclusion about birthweight <800 g (without any reference to gestational age)being a deciding factor for treatment when babies withPDA are symptomatic or require positive pressureventilator support. The reference quoted [2] reportssignificant effect on mortality and morbidity in thepresence of persistent PDA only with gestational age<25 weeks. Moreover, there is evidence that the rate ofspontaneous closure in babies weighing >1000g at birthis significantly high [3], and hence interventions forductal closure may be relevant only in those having birthweight ≤1000g. Furthermore, neither individualrandomized controlled trials nor meta-analyses of thosetrials have been able to demonstrate any long termbenefits of interventions for ductal closure in babies withPDA, irrespective of the gestational age and birth weight[4,5]. In this context, should management of these infantsbe guided only by clinical judgement on an individualbasis, irrespective of gestational age or birth weight?
Management of Patent DuctusArteriosus
ALTHAF ANSARYDepartment of Paediatrics and Neonatology,
Royal Alexandra Hospital, Paisley, UK. PA2 [email protected].
REFERENCES
1. Ibrahim TK, Haium AAA, Chandran S, Rajadurai VS.Current controversies in the management of patent ductusarteriosus in preterm infants. Indian Pediatr. 2014;51:289-94.
2. Tauzin L, Joubert C, Noel AC, Bouissou A, Moulies ME.Effect of persistent patent ductus arteriosus on mortalityand morbidity in very low-birth weight infants. ActaPediatr. 2012;101:419-23.
3. Nemerofsky SL, Parravicini E, Bateman D, Kleinman C,Polin RA, Lorenz JM. The ductus arteriosus rarely requirestreatment in infants >1000 grams. Am J Perinatol.2008;25:661-6.
4. Benitz WE. Patent ductus arteriosus: to treat or not to treat?Arch Dis Child Fetal Neonatal Ed. 2012;97:F80-2.
5. Smith CL, Kissack CM. Patent ductus arteriosus: time tograsp the nettle? Arch Dis Child Fetal Neonatal Ed.2013;98:F269-71
AUTHOR’S REPLY
We thank the reader for his comments and providing usthe opportunity to further discuss the controversies in themanagement of PDA in VLBW infants. We agree with thereader that spontaneous closure of PDA is significantlyhigh in VLBW infants with birth weight >1000g [1-2],
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and the presence of PDA is associated with significantmorbidity and mortality in infants of gestational age <25weeks [3]. However, it is not clear from the literaturewhere to draw the demarcation line as far as the birthweight is concerned. An unpublished audit done in ourdepartment revealed that birth weight was a betterpredictor than gestational age with regard to PDA-relatedmorbidities. We found that morbidities such as massivepulmonary hemorrhage and severe intra-ventricularhemorrhage were significantly higher in babies with birthweight less than 800g with untreated PDA, regardless ofgestational age. Hypothermia, peri-natal asphyxia, lackof antenatal steroids and intrauterine growth retardationwere additional risk factors.
If treatment for the PDA is based on clinical judgmentalone, we might end up in over treating it, and exposingthe neonates to treatment - related morbidities. Hence werecommend that the treatment strategies should be based
on birth weight as well, in addition to hemodynamicsignificance of PDA and need for assisted ventilation.
VICTOR SAMUEL RAJADURAIHead of Department of Neonatology,
KK Women’s and Children’s Hospital, Singapore [email protected]
REFERENCES
1. Nemerofsky SL, Parravicini E, Bateman D, Kleinman C,Polin RA, Lorenz JM. The ductus arteriosus rarely requirestreatment in infants >1000 grams. Am J Perinatol.2008;25:661-6.
2. Clyman R, Narayanan M. Patent ductus arteriosus: aphysiologic basis for current treatment practices. In:Current Topics in Neonatology. Philadelphia:WBSaunders. 2007. p. 71-97.
3. Tauzin L, Joubert C, Noel AC, Bouissou A, Moulies ME.Effect of persistent patent ductus arteriosus on mortalityand morbidity in very low-birthweight infants. ActaPediatr. 2012;101:419-23.
We read the two recent publications [1,2] related toSevere acute malnutrition (SAM), and wish to highlightcertain issues. The prevalence of bilateral pitting edemawas found to be 8.1% [1] and 27% [2]. These proportionsare very high. Recent National Nutrition MonitoringSurvey Report [3] has reported the time trends inprevalence of Kwashiorkor as 1.2% (1975-79), 0.2%(1988-1990), 0.8% (1996-1997) and 0% (2011-2012)[3]. The reasons for high prevalence of bilateral pittingedema found in Uttar Pradesh and Madhya Pradesh needto be elaborated.
The study that was conducted in twelve NutritionRehabilitation Centers (NRCs) in Uttar Pradesh [1]documented high defaulter rates (49% and 46%) amongstSAM children with complications admitted to NRCs anduncomplicated SAM children, respectively. With such ahigh defaulter rate, the results documenting mortality of1.2% amongst SAM children admitted to NRCs are notvalid. What were the reasons for high defaulter rateamongst complicated and uncomplicated SAM children?This information could help immensely in improving thefunctioning of NRCs in other states for efficientmanagement of children with SAM.
Management of Children withSevere Acute Malnutrition
The discharge and recovery rates were 17.8%(complicated SAM) and 28.7% (uncomplicated SAM),which reflect that inadequate services were provided toSAM children who were admitted to NRCs in UttarPradesh.
UMESH KAPIL AND N SAREENDepartment of Human Nutrition, AIIMS, New Delhi, India.
1. Singh K, Badgaiyan N, Ranjan A, Dixit HO, Kaushik A,Kushwaha KP, et al. Management of children with severeacute malnutrition: Experience of nutrition rehabilitationcentres in Uttar Pradesh, India. Indian Pediatr. 2014;51:21-5.
2. Kumar R, Singh J Joshi K, Singh HP, Bijesh S. Co-morbidities in hospitalized children with severe acutemalnutrition. Indian Pediatr. 2014;51:125-7.
3. National Nutrition Monitoring Bureau. NIN HyderabadPress, NNMB Technical Report No. 26; 2012.
AUTHOR’S REPLY
The 8.1% prevalence of bilateral pitting edema amongchildren with SAM admitted in the 12 NRCs in UttarPradesh should not be confused with the prevalence ofKwashiorkor as found in the nutrition surveys in thecommunity. The proportion of patients admitted in a healthfacility with a certain health condition may not correlatewith its prevalence in the community. It would also beimportant to note that the frontline workers during theirtraining on identification and referral of children with
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SAM are specifically trained on the need to identify andrefer children with bilateral pitting edema to the NRCs asthese children are at a much high risk of death. Thesefrontline workers make special effort in convincing thefamily of children with bilateral pitting edema foradmission and treatment in NRCs.
The paper mentions that of the total program exits,1.2% children died. The focus of this paper was on theoutcomes of children with SAM while in the program. Theoutcome of children who defaulted is beyond the scope ofthe paper. The paper also acknowledges and highlights thehigh default rates and has recommended furtherinvestigation for corrective action.
NRCs are meant for the stabilization, transition and theinitial part of the rehabilitation phase of management ofchildren with SAM with medical complications; the majorpart of the rehabilitation (4-6 weeks) needs to beundertaken in the community using therapeutic foods. Achild with SAM needs to be treated with therapeutic foodfor 6-8 weeks for full recovery; low recovery rates seen atNRC cannot be taken as a failure or inadequacy of NRCs.
KARANVEER SINGHUNICEF, 73, Lodi Estate, New Delhi 11003, India.
The National Vector-Borne Disease Control Programme(NVBDCP), the National Antimalarial Programme(NAMP) and the WHO Guidelines 2010 recommend theuse of artemesinin combination therapy (ACT) for thetreatment of uncomplicated and complicated malaria dueto P. falciparum, and in chloroquine-resistant malaria dueto P. vivax [1,2]. Having stated this, the pertinent questionarises as to why the WHO Guidelines recommend the useof ACT even in malaria non-endemic zones likePondicherry where drug resistance has not beendocumented, and especially when there is good responseto other antimalarials like chloroquine, quinine,sulfadoxine-pyrimethamine and primaquine. Recentstudies indicate the evidence of resistance even toartemesinin combination therapy [3]. Is there not a needto take necessary steps before the ACT drug resistancebecomes a common phenomenon? Is it not logical toreassess the use of ACT, and use it only in cases ofchloroquine resistance malaria, in severe complicatedmalaria, in cases of heavy parasitemia, malaria inendemic areas, and in cases where there is poor responseto non- ACT antimalarials, rather than in all cases?Should ACT not be the preserved drug used in selectivecases, especially with increasing incidence of drugresistant malaria? Should not the policy of treatment ofmalaria be different in the areas of stable and unstablemalaria transmission zones, rather than having a blanket
rule and uniform guidelines of usage of ACT throughoutthe country? It is also important to address the issue ofincreasing incidence of P. falciparum in unstabletransmission zones and also the situation in the stateswhere P. falciparum has not been rampant. There needs tobe a reassessment as far as the use of ACT is concerned.As pediatricians, we have a much larger and responsiblerole to play for malaria to be controlled in our community.The WHO guidelines and the IAP Consensus Statementneeds to review the issue of ACT in falciparum malaria inchildren according to the areas of stable and unstablemalaria transmission zones. At the same time, there is alsoa need to introduce the ACT in Integrated Management ofNeonatal and Childhood Ilness (IMNCI) guidelines forthe effective implementation of ACT at the primary healthcentres in malaria-endemic zones [4].
SRIRAM POTHAPREGADADepartment of Pediatrics,
Indira Gandhi Medical College and Research Institute,Pondicherry, India.
1. Directorate General of Health Services. National Vectorborne Disease control programme. Diagnosis andTreatment of Malaria 2013. New Delhi: Ministry of Healthand Family welfare; Government of India, 2013.
2. World Health Organization. Treatment of P. falciparummalaria. Guidelines for Treatment of Malaria. Geneva:World Health Organization; 2010. p.13-47.
3. Breman JG. Resistance to artemesinin-based combinationtherapy. Lancet Infect Dis. 2012;12:820-2.
4. Kundu R, Ganguly N, Gosh TK, Chaudhary P, Shah RC.Diagnosis and management of malaria in children:Recommendations. Indian Pediatr. 2008;45:731-5.
Artemesinin-based CombinationTherapy in Malaria Non-endemicAreas