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UP, IAP Journal July 2010 is out , check - Welcome to The Indian ...

  1. 1. From the pen of the Editors ears back the State Chapter had a journal of its own by the name of "The Child Today". It used to be published sometimes regularly and sometimes erratically. Then, it got stopped being published. This year we have tried to fill this void by coming out with UP Pedinfo. The first copy was a limited edition copy due to financial constraints and sent only to a few people by post. But, it was sent to a large number of members from UP by e-mail. It was also posted on the State Chapter website www.upiap.com. It had little academic content. The second issue of this journal cum newsletter is in your hands now as a hard copy. It will also be sent bye-mail and would also be posted on the website. This issue has more academic content. It also contains information about the activities that have taken place and/or are being planned for the future. We hope that you would go through it and be enlightened. Editors UP Pedinfo Editorial Board Editor in Chief Editors Dr. Ajay Kalra Dr. Ashok Rai Dr. Vineet Saxena Assistant Editors Dr. Premasish Mazumdar Dr. Shrish Bhatnagar Dr. K.L. Srivastava Dr. Savitri Thakur Dr. Ashraf Malik Advisors Dr. B.D. Bhatia Dr. G.K. Malik Dr. S.K. Yachha Members Dr. Meena Singh Dr. Dr. R.S. Sethi Dr. Dr. Mala Kumar Dr. Dr. Rashmi Kumar Dr. Dr. Manazar Ali Dr. Dr. Tabassum Shahab Dr. Dr. R. Dayal Dr. Dr. Vipin M. Vashishtha Dr. Dr. Priti Dabadghao Dr. Dr. Ashish Prakash Dr. Dr. Ujjal Poddar Dr. Dr. V.L. Bhatia Dr. Dr. B. Das Dr. Dr. Alka Agarwal Dr. Dr. Piyali Bhattacharya Dr. Dr. Amit Upadhayaya Dr. P.C. Misra A.K. Kaushik Archana Kumar V.N. Tripathi K.M. Shukla Farzana Beg K.P. Kushwaha Atul Agarwal N.C. Prajapati R.P. Singh Anshu Srivastava Shubha Phadke Lalit Kumar Rakesh Bhatia Benani Poddar Sanjay Niranjan
  2. 2. 2 UP PEDINFO CONTENTS 1. Presidential Address 1 2. President'sletter 4 3. The Rolling out of Neonatal Resuscitation Programme in Uttar Pradesh Vineet Saxena 5 Lead Article 4. Personal Practice Primer : Use of Antibioticsin suspected bacterial infectionsin neonates Vipin M. Vashishtha 6 Review Articles 5. Hydronephrosisin the fetusand neonate Premasish Mazumdar 10 6. Role of Zinc, Probioticsand Vitamin A in acute diarrhea PC. Mishra, Anubha Nigam, Alok Rai, Gaurav Garg 16 7. Patent DuctusArteriosus Neeraj Kumar Yadav 18 8. Malaria - brief review of recommendations Rajesh Kumar, Senthil Kumar 21 Original Articles 9. Dengue Hemorrhagic Fever with Osteopetrosis Om ShankarChaurasiya, Anil Kaushik 23 10. Feeding Practicesand growth in low birth rate babies KP Kushwaha, Mahima Mittal, Bhoopender Sharma, Anita Mehta, Satish Srivastava, Di/shad Ansari, Arvind Kumar, Vinay Bajpai, 26 11. Letters 28 12. Journal Watch Shrish 8hatnagar, Niranjan Kumar Singh 29 13. Spot the diagnosis 9, 30 14. News Report of UP Pedicon 2009 31 15. Registration Form UP Pedicon 2010 33 16. Registration Form State branch membership 35 17. Advertisements 15, 22 18. UP Pedicon 2010 - Call for Scientific/Award Papers
  3. 3. 3 Presidential Address : Dr. Ajay Kalra, Professor Pediatrics S.N. Medical College, Agra 30th Annual Conference of Up State Branch of Indian Academy of Pediatrics Allahabad - Hotel Kanha Shyam - 14th November'2009 Honorable Chairman, Hon'ble President of Indian Academy of Pediatrics Dr. Panna Choudhary, Vice President Dr. Atul Agarwal, Past Presidents of UP IAP, distinguished guests, members of the organizing committee, members of Indian Academy of Pediatrics and friends. I am deeply touched by the immense honor which you have bestowed upon me by electing me unanimously to the highest office of our academy in the state. I am also aware of the responsibility of this task. Before I proceed further, I would like to pay my homage to our past president Dr. Gyan P. Lal whom we have unfortunately lost last year soon after he demitted office. The academy in UP is 30 years young now. Over the years, it has gained in stature, influence and prestige due to great efforts of our learned predecessors. I am full of admiration and appreciation of their contribution and accept their heritage with utmost humility as a sacred trust. I will try my best to carry forward their illustrious work. The conference is being held in the holy city of Allahabad which is not only known for its sacredness due to the Sangam but is also the great centre of culture and education. It is in this city that many important deliberations have been held which have given new direction to this country. One of the important historical places in this regard is the "Anand Bhawan". Today also happens to be "The Children's Day" which is celebrated all over the country in memory of the greatest son of this city born in this Anand Bhawan and the architect of modern India, Pandit Jawaharlal Nehru. It was therefore most appropriate for this conference of advocates of child health to be held today on this day and in this city of the person whom children fondly called "Chacha Nehru". Friends, now let us have a quick view of the status of child health in our state. We have the highest infant mortality rate in the country (73/1000 live births as compared to national average of 57/1000), one of the lowest immunization rates in the country (51% fully immunized as against the all India data of 63%); 42% of our children are under nourished (which is the same as of the national level) and the prevalence of anemia in pre-school children is more than 70%. No wonder, the Vice President of our country was constrained to express his anguish over the situation by slamming health indices in the state. The situation thus leads to frustration and helplessness on the status of child health in the state and we often end up into blaming the system. But the answer to these problems also arises from this situation of helplessness. For, it is said that, "Worst things in your life have within them the seeds of the best-Jeo Kogel'. The answer is, that in the face of helplessness think of empowerment. When I say empowerment, it does not mean getting power by fighting elections and then sticking on to it. What it means is to strengthen ourselves to the extent that we are able to be the harbinger of change or to be the change itself. It seems there are some ways by which we can do so. We can empower ourselves by increasing our membership. This increase is not to be an increase for the purpose of filling registers. It is not an increase for the purpose of trade unionism or for our vested interest. But it is to form a great team whose members know each other, who are able to communicate with each other, who are able to learn from each other and who work jointly for the welfare of the child. Today our membership stands at 748 as compared to 1580 members from our state in the
  4. 4. 4 Central IAP while there are more than 3000 Pediatricians in the state. We have branches in only 28 out of 75 districts. It is indeed a challenge to increase the membership and the branches and to convert them from passive into active units. This empowerment is by acquiring knowledge and keeping ourselves updated. This is getting better now in this era of information technology. Further, the Central IAP every year makes a plan of action which we can use to enhance the knowledge of our members. This year, under the leadership of Dr. Panna Choudhary, one of the most successful programmes of the central IAP was the neonatal resuscitation programme. Impressed by this programme, the Central Government has adopted it and has brought out the "Navjat Shishu Suraksha Karyakaram" based on this. The Rajasthan, Madhya Pradesh and Gujarat governments have also recently adopted this Central programme. The process of gaining knowledge is continuous. We must be prepared to learn, unlearn and re-learn. In the last few decades, the medical profession was busy dealing with sickness and diseases. The focus has now shifted from being disease centric to health centric. We realize that there it is more important to use less medicines to preserve and promote good health rather than treat with too many medicines. "The superior doctor prevents illness. The mediocre attends to impending illness. The inferior doctor treats actual illness" ...........Chinese Proverb By empowerment I also mean capacity building in the government medical colleges and hospitals. After years of lukewarm attitude, the medical colleges and hospitals are now being equipped again. New faculty and staff are being inducted. The young faculty and staff are enthusiastic, knowledgeable and ready to deliver the goods. We should be able to tap their energy and inspire them to bring about a new work culture where a pediatric physician, a pediatric surgeon, a pediatric neurologist, a pediatric cardiologist and many others would learn to form a team and work together. I feel optimistic that with the new life infused in these institutions, they can become centres of service and excellence. This empowerment also means not only strengthening ourselves but also educating and training the paramedical staff employed in the private hospitals and clinics. In fact, 90% of the health services are provided
  5. 5. 5 by the private sector. This private sector employs a large number of paramedical staff who do not have any opportunity of inservice training and is not available for national health schemes. If we can provide inservice training to this untapped manpower, the results would be tremendous. We can begin by running workshops for paramedics on five subjects viz. essential care of new born, breast feeding, safe injection practices, ORS and routine immunization. We have already started working on a module for this and hopefully we would be able to provide it to those interested after January. Such an attempt was initiated at Surat in Gujarat by my friend Dr. Digant Shastri. It was so successful that the Gujarat Government adopted it and has made this training mandatory for licensing private clinics and hospitals. Another way of empowerment is by Research. collection and sharing of data. In this field, we are woefully way behind. Our friend Dr. Vipin Vashistha from our own state has given a lead by his research which has brought international recognition to the Indian Academy of Pediatrics. He was able to solve the mystery behind the mysterious deaths in Western UP, Haryana and other states by finding out that the cause was actually seeds from a locally growing weed and not Encephalitis as believed till that time. Thus, research can take place even in the smallest and remotest of set ups. It can start with documentation of observations. As I said earlier, if we wish to see a change, we have to begin ourselves. The onus to do so lies with us. For, "Changes are not brought about by those with credentials but by those with concerns" -Anonymous So, friends, what does the team 2010 of UP IAP propose to do this year ? We do not wish to make any promises because we do not want such a picture to emerge by the end of our tenure where we may have to say we could do nothing due to lack of funds. But, the team 2010 does hope to be able to do the following :- 1. Increase of our membership strength. 2. Bring out a directory of the state chapter for which ground work has already been done by my predecessor Dr. D.K. Tiwari. 3. Launch a website so that all informations of central and state IAP activities can be accessed. 4. Bring out at least two copies of the newsletters to keep the members and branches informed and to encourage them to participate to their maximum. 5. Bring out at least two copies of the journal so that
  6. 6. 6 injection practices and immunization. With Dr. Vineet Saxena continuing as secretary, I am sure we will be able to achieve our objectives. Finally let us remember that : "The destiny of our beloved land lies not with us but with our children"....... Mahatma Gandhi. Before I end, on behalf of all the members and on my own behalf, I would like to thank the chairman and members of the organizing committee for having invited us for this 30`h National Conference of UP Pedicon and having worked so hard to make it successful. They have gone much beyond our expectations. Jai Hind the research and academic interest of our members are taken care of. 6. Establish liaison with government and NGOs to achieve the most in child health programmes. 7. To encourage members for parent education programmes. 8. To encourage members to participate in all child health programmes of the government and in routine immunization in particular. 9. To provide module and inputs for inservice training of para-medical staff of private sectors on essential new-born care, breast feeding, safe
  7. 7. 7 4 President's Letter Friends, The state chapter seems to be driving at a reasonably good speed. During its present tenure, it has been able to steer in the following directions :- Website : This has been launched as www.upiap.com. It provides a host of information viz. the constitution, conference guidelines, past office bearers, past conferences, rules for award papers, norms for orations, minutes of Executive Board meetings, information related to the immediate past and forthcoming State Pedicon, the Journal/newsletter UP Pedinfo, office bearers of city/district branches and phone numbers and addresses of members. Journal : The state chapter has brought out two issues of the journal cum newsletter "UP Pedinfo". These can also be visited on the website. Publication of journal as a hard copy not only costs money but also environment. We wish all members would become electronic savvy at the earliest, so that in future all journals can be sent as CDs or posted on the website only. We feel that keeping members informed on the website and through the newsletter brings in transparency in our affairs. Activities : A state level workshop on Diarrhea Management has been held at Lucknow. Districts level workshops are being held on 7th August at Rae Bareilly, 17`h August at Gorakhpur, 26" August at Jhansi and 29th August at Mathura. CMEs and other academic activities are also being organized by different city branches especially on Respiratory Infections and Asthma. They are also preparing to participate in annual events which are outlined below. I am sure that all members would enthusiastically join these efforts. Herewith, I would like to make a special mention of the state chapter' s participation in one of the most important National and Central IAP programmes in child health i.e. the Neonatal Resuscitation Programme. This programme is being run as "Navjat Shishu Suraksha Karyakaram" at the government level with the IAP acting as nodal body. It is also being run as "First Golden Minute" at the private sector level by the IAP with the help of generous academic grant from Johnson & Johnson. The state chapter has played a very crucial role in planning and finalizing this programme at the national level. At the state level, it has been able to do extremely well by planning everything before hand. The Secretary, Dr. Vineet Saxena is one of the national coordinators and has worked day and night to run this programme. This programme has also given the state chapter an opportunity to work in liaison with the state government. More information on this is available in the article on this subject in this issue of the journal. The in service re-orientation and training programme on child health and diseases for paramedics in private sector has been successfully initiated at two places in Agra. MoU : I am also extremely happy to inform all members that in the first week of June, 2010, the State Chapter signed a memorandum of understanding (MoU) with the State Unicef to collaborate in activities related to child welfare. The credit for this goes to the efforts made by the President Elect - Dr. Ashok Rai and the Secretary Dr. Vineet Saxena. We are looking forward to a lasting and fruitful collaboration between these two organizations. Directory : The directory of members of IAP is on the website. I wonder whether at all we now need to get it published as a hard copy. Conference : UP Pedicon 2010 is being held at Hotel Ramada, Varanasi on 27`h and 28`h November, 2010. The organizers are working very hard for the success of this conference. Further information on this is available on the website and in this journal. Membership : The drive to increase the membership has not picked up well. But, I hope that with so much good work being done at the level of State Chapter, more Pediatricians would be induced to join our fold. The IAP is not only an organization; it is a mission which needs hands of all. Wishing you all good health and happiness. (AJAY KALRA) drajaykalra@yahoo.com
  8. 8. 8 Annual activitiesof Central IAP which would need to be run by all District Branches ORS Week : Around and including 29`" July (ORS Day)- Report by 31 August. World Breast feeding week : August 1 - 7 - Report by 31st August. Teenage day:1'` August- Report by31" August. IAP Child and Adolescent healthcare week-around and including14th November- Report by 30th November. Best IAP branch awards-Activities Report on prescribed form by 30th November.
  9. 9. 9 The Rolling outof NeonatalResuscitation Programmein Uttar Pradesh Vineet Saxena
  10. 10. Uttar Pradesh has the highest infant mortality in the country. It stands third in rank as far as the neonatal mortality rate in the country is concerned (37/1000 population as compared to the national figure of 47.6/1000). The high infant mortality rate is because of this high neonatal mortality rate. Considering the first minute as the most crucial timeto save these newborn babies, The Indian Academy of Pediatrics has proceeded to consider it as a golden opportunity to intervene effectively and it therefore launched this programme in 2009 with the name " First Golden Minute" (FGM). The Government of India has also launched this programme under the name "Navjat Shishu Suraksha Karyakaram" (NSSK) with collaboration of IAP, All India Institute of Medical Sciences and the National Neonatology Forum. Also, the Indian Academy of Pediatrics has received a handsome academic grant from Johnson & Johnson to run this FGM course in the private sector. The course is for all those who participate in neonatal resuscitation in the delivery room and care for newborn. It intends to train two lac persons in the next three years. All those trained would be given a certificate which would be valid for two years. Trained persons from this pool would be available to the government as trainers and providers under NSSK. The course has two arms - (1) Trainer Course to train district instructors (DIs) and (2)Provider Course for providers to be trained by District Instructors for providing care in the maternity homes. It has two components (a) Basic newborn care and (b) Advanced newborn care. The basic course is being rolled out in UP for 70districts. Out of these, 50 have already been identified. Instructor Courses have already been held in three districts viz. Agra, Allahabad and Lucknow. In the Instructor courses four district instructors are trained for each district. Thus, the total numbers of instructors that we would be having in the
  11. 11. state would be 4x numbers of districts inthe state identified for training. Each district instructor course would have a maximum of 40 DIs to be trained. The DIs would be preferably Pediatricians but may also include enthusiastic Obstetricians and Anesthetists. The DIs will then train the providers in the private sectors. These providers would be Pediatricians, Obstetricians, nursing home doctors and at least one paramedical staff from each private maternity centre. The district courses are to run as two days courses on concurrent day. The provider courses are also two days courses preferably to be run onconcurrent day, but can also be run on twoconsecutive Sundays, if the need be. Each DI course will have 40participants while each provider course will have 32 participants. The ratio of instructor to participant is not to exceed 1 is to 8. It is calculated that as the programme is rolled out, we would be having 7000providers every three months and by the end of three years, we can have two lac providers. It is a matter of great satisfaction that FGM/NSSK Workshops could be successfully conducted at the following places in the state :- Date Place No of persons trained 5`h -6`h March 2010 Jhansi 35 16`" - 1 7 `" March 2010 Agra 31 18`h -19`h March 2010 Allahabad 39 26`" -27`h March 2010 Kanpur 38 29`" -30`h March 2010 Kanpur 32 29`" -30`h March 2010 Agra 44 30`" -31`" March 2010 Jhansi 42 6 & 7 May 2010 Allahabad 42 With members showing a lot of enthusiasm, we are sure that we will be able to go beyond our targets even well ahead of the dealines. 10 Review Articles
  12. 12. Hydronephrosis in the fetus and neonate Premasish Mazumdar The introduction of fetal ultrasonography (US) has allowed for the detection of many intrauterine anomalies. Indeed, most anomalies are detected during routine fetal US done at 18- 20 weeks gestation. Urinary tract anomalies are particularly readily identified. Of these, hydronephrosis is the most common, comprising 50% of congenital malformations. Fetal hydronephrosis is found in 0.59% to 1.4% of fetuses (1). The many underlying causes as well as the wide spectrum of outcomes have resulted in a significant debate about the proper evaluation and management of prenatally identified hydronephrosis. Evaluation may include discomfort and radiation exposure, and definitive treatment involves surgical correction with variable efficacy and attendant risks, making it desirable to limit unnecessary intervention whenever possible. At the same time, severe cases may result in irreversible prenatal renal damage, and less severe conditions that persist and evolve after birth also can lead to permanent renal scarring and permanent damage during childhood (2). For some fetal conditions, the associated oligohydramnios can result in lung hypoplasia, if it is present in midgestation. Evaluation and management of each case must balance these opposing factors by avoiding overevaluation of benign conditions while ensuring appropriate care of the more significant ones. Aetiology Hydronephrosis may be caused by obstruction due to either urologic or nonurologic factors. The most common of these are outlined in Table 1. Of the cases identified prenatally, 48% have no specific cause and resolve before birth, and another 15% are due to physiologic changes in which no specific anatomic anomaly can be discerned. Anatomic anomalies can occur at any level of the urinary tract and may affect one or both sides, but they commonly occur where embryonic structures divide, including ureteropelvic or vesicoureteral obstructions (accounting for about 11% of cases), vesicoureteral reflux (9% of cases), or obstruction at the urethrovesicular junction (posterior urethral valves [PUV], about 1% of cases identified prenatally). Grading of Severity A uniform grading system of hydronephrosis severity is required to compare results between patients and different series, guide ongoing follow-up and management, and predict outcome.. Among the 50% of prenatally identified cases that do not resolve before birth, persistent uropathy may occur in 12% of mild, 45% of moderate, and 88% of severe hydronephrosis cases (3). The most widely used grading system is that adopted by Table 1. Causes of hydronephrosis No Identified Cause UrologicAnomalies  Ureteropelvic junction (UPJ) anomalies Anatomic anomalies Dysfunction of the UPJ  Ureterovesicularjunction anomalies Vesicoureteral reflux Megaureter U reterocele/ectopic ureter  Vesicourethral anomalies Posterior urethral valves Urethral atresia Urogenital sinus and cloacal anomalies  Miscellaneous disorders Collagen anomalies Prune-belly syndrome Tumors Neurologic impairment Consultant Neonatologist, Agra. E mail: premasishl@yahoo.com
  13. 13. Premasish Mazumdar 11 the Society for Fetal Urology (SFU) (Table 2, Fig 1) (4). Other grading systems often are employed in parallel with the SFU designations and rely primarily on measurement of the anteroposterior diameter of the pelvis in the transverse view. Dilation in excess of 10 mm in late gestation is considered significant hydronephrosis (5), and additional measurement cutoffs have been identified at different gestational ages.The highest positive predictive value comes from third trimester measurements (6), with no patients who have measurements of less than 10 mm requiring later surgery (7). Ultrasonographic examinations in late gestation also may help determine the morphology of the kidneys and predict outcomes better (9). Prenatal Evaluation and Management Hydronephrosis identified in the fetus require repeat ultrasonography at appropriate intervals either to identify resolution or ensure that there is no disease progression. Serial evaluation of amniotic fluid volume Table 2. Severity of Hydronephrosis by Ultrasonography: Society for Fetal Urology Grade 0 : Normal Grade 1 : Split renal pelvis Grade 2 : Further dilation of the pelvis with a few visible calyces Grade 3 : Renal pelvis dilation with many obvious distended calyces Grade4 : Findings of Grade 3 plus a thinned renal parenchyma Fig. 1. Showing VS pictures of different grades of severity of fetal hydronephrosis Grade 4
  14. 14. 12 Hydronephrosis in the fetus and neonate Grade 0
  15. 15. 13 Hydronephrosis in the fetus and neonate also is undertaken as part of severity assessment. Several factors aid in formulating management decisions, including the presence of oligohydramnios or evidence of abnormal renal function (3). As the normal kidney can manufacture enough urine to ensure adequate amniotic fluid volume, unilateral disease almost never requires prenatal intervention. Indeed, even bilateral disease can be managed conservatively unless oligohydramnios develops (10). Most of these cases occur in males, with obstruction due to PUV or urethral atresia, and the development of oligohydramnios before about 20 weeks' gestation is highly associated with failure in lung growth, resulting in potentially fatal hypoplasia. There is, therefore, much interest in identifying cases of PUV, including identification of the socalled "keyhole sign" on ultrasonography besides bladder wall thickness and overall dilation(Fig 2) (11). When the ultrasonographic evaluation reveals severe hydronephrosis, corrective or palliative intervention during fetal life may be considered. Evidence of abnormal renal function in the fetus may be helpful in determining the need for intervention, and normal values of the parameters of fetal urine are shown in Table 3.The utility of these measurements when abnormal in predicting outcome can be greatly increased by obtaining serial measurements 48 to 72 hours apart (12). Evidence of poor or deteriorating renal function in the presence of oligohydramnios may prompt consideration of fetal intervention. Before making the decision, it is important to rule out other major anomalies Fig2. Bladder ultrasound showing sonographic finding of bladder outlet obstruction such as bladder wall thickening and key-hole Q sign suggesting a dilated posterior urethra.
  16. 16. 14 Hydronephrosis in the fetus and neonate Table 3. Normal Fetal Urine Values Comments Sodium: 75-100mg/dL normal values decreases during gestation Chloride: <90 mmol/L Calcium: <8 mg/dL sensitive indicator of dysplasia Beta-2microglobulin:<4mg/dL greater than 13 mg/dL associatedwith fetal death Osmolarity:<200 mmol/kg Total protein:<0.2 g/L Urinary fetal markers obtained from a freshly aspirated fetal bladder tap can be used to prognosticate fetal renal function for possible prenatal intervention, although favorable markers do not always translate to favorable postnatal renal function or chromosomal disorders and to ensure that the kidneys are otherwise normal, without evidence of dysplasia. The decision to intervene is difficult because fetal intervention does not necessarily improve long-term outcome, and more than one third of patients have chronic renal failure, with another 22% having persistent renal insufficiency. The placement of draining vesicoamniotic shunts is risky. Shunt failure or displacement is common, and the procedures are associated with mortality or fetal loss rates as high as 43%, due to provoked preterm birth and infections (13). On the other hand, such shunts can correct the early severe oligohydramnios, allowing for normal lung development and survival after birth, when conventional interventions may be performed. Postnatal Evaluation All babies who have a prenatal diagnosis of hydronephrosis should undergo at least a follow-up ultrasonographic examination after birth. This includes those who had transient pelvic dilation in the second trim est er that resolved on ultrasonographic examinations before birth because as many as 29% of these patients have identifiable abnormalities on postnatal examinations and 12% have significant nephropathies (6)(14). Similarly, patients who have mild hydronephrosis on fetal examinations may show worsening on postnatal evaluation, although the degree of dilation is stable or resolves after birth in most of these patients (15). Consultation with a pediatric urologist should be requested, if it has not been done in the
  17. 17. 15 Hydronephrosis in the fetus and neonate antenatal period. Most practitioners wait a minimum of 7 to 10 days after birth to perform the first ultrasonographic examination. Such delay is advocated to ensure that the normal postbirth water losses will have occurred and that the infant's hydration status will have normalized, reducing the likelihood of false-negative study results. Some investigators have found that early studies, performed at 48 hours after birth, while the baby is still hospitalized, may be adequate for initial evaluation. Although later studies ultimately may show some worsening of the hydronephrosis, cases of more severe disease always are evident on 48-hour ultrasonographic evaluations (16). In addition, in none of the mild-to- moderate cases was the change between 48 hours and 7 to 10 days significant, nor did it change management. To ensure safety, almost all patients are given prophylactic antibiotics while awaiting ultrasonography, although little data support the value of this practice. The most common regimens are amoxicillin or a first-generation cephalosporin at a dose of 10 to 25 mg/kg per day. The need for additional evaluation should be based on the findings of the postnatal ultrasonographic examination, which delineate obstructive processes that may require intervention. Beyond this, some practitioners advocate VCUG for all patients who have the antenatal diagnosis of hydronephrosis (17) to identify reflux that ultimately might result in renal injury. This practice captures all possible cases of reflux, but many practitioners note that reflux primarily occurs in patients who have more severe dilation or other abnormal ultrasonographic findings and that those who have minimal unilateral dilation on postnatal ultrasonography (diameter </=15 mm) can be discharged without further evaluation. Others have found that the diagnosis of significant reflux is rare in patients who have mild degrees of unilateral dilation on prenatal examination and two normal ultrasonographic readings after birth (the initial one and afollow-up at 8 to 12 weeks), and they conclude that VCUG may not be indicated in these cases (18). It is widely agreed that bilateral disease warrants VCUG and that significant disease also should be evaluated for renal function. Diuretic renography is the method of choice to evaluate renal function and drainage in the significantly dilated upper urinary tract system when there is no reflux. It is relatively non-invasive and gives quantitative data on function and drainage. The radionuclide of choice is 99mtechnetium mercaptoacetyl-triglycine (MAG 3) due to its high initial renal uptake (19) but 99m-technetium diethyltriamine pentaacetic acid (DTPA) is also usable. If
  18. 18. 16 Hydronephrosis in the fetus and neonate there is no washout in the first 30 min of the study, a diuretic (usually furosemide) is given to challenge the system. Hydronephrotic systems that are not obstructed will usually drain after the diuretic, but those that are obstructed will not. Many will fall in between and this is where an experienced clinician is essential. The half-time (T1/2) of drainage of tracer has been described by Kass et al. to help objectively evaluate obstruction (20). A T1/2 of less than 10 min is unobstructed, T1/2 greater than 20 min is obstructed and T1/2 between 10 and 20 min is equivocal. Many investigators are experimenting with MR urography as an alternative. This is particularly useful in neonates who have severe hydronephrosis and poor renal function. With current MR urography, T2-weighted sequences can evaluate neonatal hydronephrosis and localize the site of obstruction. Determination of functional impairment and evaluation of renal parenchyma can be assessed using gadolinium enhanced T1-weighted sequences. Unfortunately, at this time, sedation or anesthesia is required to perform the study; hence, it has not gained popularity. These recommendations have been combined into a management algorithm (21): 1. All patients who have a prenatal diagnosis should undergo ultrasonographic examination in postnatal week 1. a. Those who have minimal dilation (</=15 mm) are discharged. b. Those who have bilateral disease should undergo VCUG and renography. Severe cases should be considered for surgical intervention according to the criteria in Table 4; milder disease is followed with observation. c. Those who have unilateral disease are considered for surgery if the dilation is severe; the others are fol l owed wit h repeat ultrasonography after 8 to 12 weeks of observation. 2. If fol l ow- up ul t ras onography documents improvement, the patient can be discharged. If there is persistent hydronephrosis of Grade 2 or higher, renography is performed and surgery or continued observation is considered according the criteria in Table 4. Management The fundamental management paradigm is to
  19. 19. 17 Hydronephrosis in the fetus and neonate prevent renal injury and chronic failure from obstruction and reflux, avoiding unnecessary invasive monitoring or surgery while still ensuring sufficient monitoring to identify those patients in whom surgery is required. High-grade obstruction still requires surgical intervention, but the biggest change in recent management has been the shift from immediate surgery for repair of all obstruction to a practice of serial imaging for less severe cases and intervention according to the criteria outlined in Table 4 (20). As a result, only about 25% of patients who have unilateral disease eventually require surgery, and the use of a 15-mm cutoff identifies patients who have an ultimate need for surgery in most cases (23). The more severe the disease, the greater the risk of long-term problems and the stronger the indication for surgical intervention, but in some recent series, many patients who had Grade 3 or 4 disease and nearly all of those who had Grade 1 or 2 disease improved without surgical intervention (24). For patients who have bilateral disease, postnatal evaluation soon after birth is necessary to identify PUV, so a catheter can be placed for temporary drainage and comfort while preparing for valve ablation or vesicostomy. Hydronephrosis from other causes usually is followed with observation and periodic monitoring, with surgical intervention indicated for worsening hydronephrosis or deterioration of renal function. Research directions Table 4. Criteria for Surgery or Observation (22) Consider Surgery:  Anteroposterior diameter >30 mm  Anteroposterior diameter >20 mm with calyceal dilation  Renal function <30%  Worsening renal function  Worsening hydronephrosis  Febrile breakthrough infections or symptoms Continued Observation:  Prophylactic antibiotics  Renal ultrasonography every 2 to 12 months, as indicated  Repeat renography if ultrasonography documents worsening or symptoms develop  Discharge if improved, surgery if indicated
  20. 20. 18 Hydronephrosis in the fetus and neonate Research is being currently directed towards finding new biomarkers of early renal injury due to obstruction. The predictive value of radiographic findings (e.g., renal pelvic diameter and renal functional measurements) using multivariate analysis to risk stratify patients are also being evaluated. bewsides treatment options for prenatal urethral valves. The aim is to better selectvfetal and neonatal patients who would benefit the most. Conclusions Hydronephrosis is a common condition in the fetus and newborn that has a wide range of causes and severity. Most cases resolve without therapy and can be managed conservatively, especially if the initial severity grades are mild. For more severe cases, close monitoring for progression, associated alterations in renal function or reflux, and the occurrence of symptoms can be used effectively to identify those patients in need of surgical intervention. Although many affected patients have some degree of permanent renal impairment, this approach appears to minimize risks while avoiding unnecessary procedures and interventions. References 1. Woodward M, Frank D. Postnatal management of antenatal hydronephrosis. BJU Int. 2002; 89: 149-156. Sidhu G, Beyene J, Rosenblum N. Outcome of isolated antenatal hydronephrosis: a systematic review and meta-analysis. Pediatr Nephrol. 2006; 21:218-224. Lee RS, Cendron M, Kinnamon D, Nguyen HT. Antenatal hydronephrosis as a predictor of postnatal outcome: a metaanalysis. Pediatrics. 2006;118: 586-593. Fernbach SK, Maizels M, ConwayJJ. Ultrasound grading of hydronephrosis: introduction to the system used by the Society for Fetal Urology. Pediatr Radio!. 1993;23:478-480 Arger PH, Coleman BG, Mintz MC, et al. Routine fetal genitourinary tract screening. Radiology. 1985; 156: 485-89 Ismaili K, Hall M, Donner C, et al. Avnie FE. Brussells Free University Perinatal Nephrology Study Group: results of systematic screening for minor degrees of fetal renal pelvis dilatation in an unselected population. Am J Obstet Gynecol. 2003;188:242-246 7. Wollenberg A, Neuhaus T, Willi U, Wisser J. Outcome of fetal renal pelvic dilatation diagnosed during the third t ri m es t er. Ul t ras o und Obs t et Gy nec ol. 2005;25:483-488 8. De Kort EHM, Bambay Oetono S, Zegers SHJ. The long-
  21. 21. Premasish Mazumdar 19 term outcome of antenatal hydronephrosis up to 15 millimetres justifiesa noninvasive postnatal follow-up. Acta Pediatr. 2008;97:708-711 Dhillon H. Prenatally diagnosed hydronephrosis: the Great Ormond Street experience. Br J Urol. 1998;81:39-44 Herndon C, Ferrer F, Freedman A. Consensus on the prenatal management of antenatally detected urological abnormalities. J Urol. 2000; 164: 1052-1056. Bernades LS, Aksnes G, Saada J, et al. Keyhole sign: how specific is it for the diagnosis of posterior urethral valves? Ultrasound ObstetGynecol. 2009;34:419-423 Johnson MP, Corsi P, Bradfield, W, et al. Sequential urinalysis improves evaluation of fetal renal function in obstructive uropathy. Am J Obstet Gynecol. 1995;173:59-65 Holmes N, Harrison MR, Baskin, LS. Fetal surgery for posterior urethral valves: long-term postnatal outcomes. Pediatrics. 2001;108: E7 Cordero L, Nankervis CA, Oshaughnessy RW, et al. Postnatal follow-up of antenatal hydronephrosis: a healthcare challenge. J Perinatol. 2009;29:382-387 Morin L, Cendron M, Crombleholme TM, et al. Minimal hydronephrosis in the fetus: clinical significance and implications for management. J Urol. 2000; 155: 2047-2049 16. Wiener J, O'Hara S. Optimal timing of initial postnatal ultrasonography in newborns with prenatal hydronephrosis. J Urol. 2002;168:1826-1829 Belarmino J, Kogan B. Management of neonatal hydronephrosis. Early Hum Dev. 2006;82:9-14 Ismaili K, Avni FE, Hall M. Brussels Free University Perinatal Nephrology (BFUPN) Study Group: results of systematic voiding cystourethrography in infants with antenatally diagnosed renal pelvis dilation. J Pediatr. 2003;141:21-24 Riccabona M. Assessment and management of newborn hydronephrosis. World J Urol 2004; 22:73-8. Kass EJ, Majd M, Belman AB. Comparison of the diuretic renogram and the pressure perfusion study in children. J Urol 1985;134:92-6. Yiee J, Wilcox D. Management of fetal hydronephrosis. Pediatr Nephrol. 2008 23:347-353 Ransley PG, Dhillon HK, Gordon I, et al. The postnatal management of hydronephrosis diagnosed by prenatal ultrasound. J Urol. 1990;144:584-587 Coplen D, Austin P, Yan Y, Blanco V, Dicke J. The magnitude of fetal renal pelvic dilatation can identify obstructive postnatal hydronephrosis and direct postnatal evaluation and management. J Urol. 2006; 176:724-727 24. Chertin B, Pollack A, Koulikov D. Long-term follow up of antenatally diagnosed megaureters. J Pediatr Urol. 2008; 4:188-191
  22. 22. W G U t L C a m n e a t ~114Nt Blue Cross Laboratories Ltd., Mumbai C Bludrox (Cefadroxil), Bluedrox-500, Bludrox-250 DT, Bludrox-P DT, Bludrox-P Dry Syrup
  23. 23. 17 Review Articles Role of zinc, probiotics and vitamin A in acute diarrhea PC Mishra*, Anubha Nigam*, Alok Rai*, Gaurav Garg** Role of zinc There were several studies (1,2,3,4) conducted to evaluate the effect on morbidity and mortality of providing daily zinc for 14 days to children with diarrhea which proves that lower rates of child morbidity and mortality with zinc treatment represent substantial benefits from a simple and inexpensive intervention that can be incorporated in existing efforts to control diarrheal disease. Zinc supplements given during diarrhea reduce the duration and severity of treated episodes. If given for 14 days during and after diarrhea, zinc reduces the incidence of diarrhea and pneumonia in the subsequent two to three months. Provision of zinc during diarrhea may thus be a feasible strategy for both treatment of diarrhea and prevention of subsequent morbidity and mortality. On a global scale, the addition of zinc treatment to the management of childhood diarrhea could save the lives of almost400,000 children each year (5). More recently studies of the impact of experimental Zn deficiency on intestinal structure and function have been performed (Roy & Tomkins, 1989). During experimental Zn deficiency, a characteristic cyclical change in body weight occurs and the animals develop watery diarrhoea and become somewhat anorexic. For this reason there has been much discussion on the design of an appropriate control group. Food intake-matched groups are most commonly used and in the present review most of the results refer to comparisons between experimental Zn deficiency and animals receiving a Znreplete diet but in the same quantity that their deficient counterparts were receiving. Microscopic appearances of the small intestine are quite characteristic; there is atrophy of the jejunal mucosa and a range of changes of ultra-structure visible on light microscopy. Atrophy of the jejunal mucosa may be quantified by measurements of mucosal weight (expressed as mg/mm intestine) or mucosal mass as assessed by DNA per mg/mm intestine. All these can be explained by the necessity for Zn during DNA synthesis; a reduction in the number of jejunal mucosal cells might be expected during Zn deficiency (6). Role of probiotics Similar studies to evaluate efficacy of probiotics in prevention and treatment of diarrhea associated w ith the use of antibiotics revealed that probiotics can be used to prevent antibiotic associated diarrhea (10) and S boulardii and lactobacilli have the potential to be used in this situation. Probiotics or Biological agents ("biotherapeutic agents") have been used to treat a variety of infections, most notably infections of mucosal surfaces such as the gut and vagina.  Probiotics are live organisms that improve the microbial balance of the host.  Probiotics have special properties that make them useful in fighting infections of mucosal surfaces such as the gut and vagina.  Different species of lactobacilli have the potential for use in clinical practice as also the yeast Saccharomyces boulardii.  Probiotics are becoming increasingly available as capsules and dairy based food supplements sold in health food stores and some supermarkets but its not an OTC (over the counter) product in the market. The relative lack of side effects makes probiotics a possible way of preventing antibiotic associated diarrhea. Probiotics have been used to prevent or treat diarrhea of other causes-namelytraveller's diarrhea and infantile infectious diarrhea studies showed positive results, and some reviews have been encouraging (9). *Department of Pediatrics, MLN Medical College, Allahabad
  24. 24. 18 Review Articles **Department of Pediatrics , SN Medical College, Agra
  25. 25. 19 Review Articles PC Mishra et al 17 The way in which probiotics affect the gut has drawn much interest. To combat the problems of gastrointestinal infection, a probiotic must be non-pathogenic and must act against pathogens by different mechanisms from antibiotics for example, by competition. More importantly, they should have a fairly rapid onset of action and survive the challenges of gastric acid, bile, or concurrentantibiotics. It is also desirable that they modify immune processes to destroy the invading organism. Saccharomyces boulardii and lactobacilli display these common properties. Probiotics are a possible solution in the prevention of antibiotic associated diarrhea. Increasing availability, lower costs, and relative lack of side effects of probiotics make them very useful. Role of Vitamin A The effect of experimental vitamin A deficiency on gut mucosa has been described in several studies recently. In contrast to the situation with Zn deficiency, changes in mucosal morphology in vitamin A deficiency are relatively mild (8), although there are significant differences in the mucosal morphology of a vitamin A-deficient animal when infected with experimental rotavirus infection. Recent measurements of electrogenic activity in the small and large intestine of the rat during vitamin A deficiency have shown some complex results. In the small intestine there are changes in short-circuit current activity in response to bethanecol in vitamin A deficiency ( 7). Similar appearances occur in the proximal large intestine but in the distal large intestine there is a completely opposite result, i.e. a decrease in short-circuit current after stimulation with bethanecol ( Nzegwu & Levin, 1992) (6). The relationship of vitamin A deficiency and child survival has been documented in a number of studies. Total dietary vitamin A intake was strongly and inversely associated with the risk of diarrhea. Under IMNCI program, vitamin A is regularly given to children above 6 month of age at every 6 month interval till the age of 5 years .Thus it helps to reduce the morbidity and mortality caused by diarrhea and dehydration in under 5 age children. Relationship of vitamin A, measles and diarrhea still needs research exploration today as significant number of deaths occurs due to diarrhea and dehydration. Vitamin A supplementation does not reduce the overall incidence and prevalence of common childhood illnesses; however, it reduces the incidence of more severe episodes of diarrhea. References 1. Bhutta ZA, Bird SM, Black RE, et al. Therapeutic effects of oral zinc in acute and persistent diarrhea in children in developing countries: Pooled analysis of randomized controlled trials. American Journal of Clinical Nutrition. 2000. 72(6):1516-1522. 2. Photo: PATH/Carib Nelson. Prasad, A. S. (2009). Impact of the Discovery of Human Zinc Deficiency on Health. J. Am. Coll. Nutr. 28: 257-265 3. Sandstead HH, PrasadAS, Penland 1G, Beck FW, Kaplan J, Egger NG, Alcock NW, Carroll RM, Ramanujam V, Dayal, HH, Rocco CD, Plotkin RA, Zavaleta AN (2008). Zinc deficiency in Mexican American children: influence of zinc and other micronutrients on T cells, cytokines, and anti inflammatory plasma proteins. Am. J. Clin. Nutr. 88: 1067-1073 4. Bhandari N, Mazumder S, Taneja 5, Dube B, Agarwal R, Mahalanabis D, Fontaine 0, Black RE, Bhan MK (2008). Effectiveness of Zinc Supplementation Plus Oral Rehydration Salts Compared With Oral Rehydration Salts Alone as a Treatment for Acute Diarrhea in a Primary Care Setting: A Cluster Randomized Trial. Pediatrics 121: e1279-e1285 5 Jones G, Sketetee RW, Black RE, Bhutta ZA, Morris SS, and Bellagio Child Survival Study Group. How many child deaths can we prevent this year? Lancet 2003; 362:65-71. 6 Andrew tomkins, Ron Behrens and Swapan Roy. The role of zinc and vitamin A deficiency in diarrhoeal syndromes in developing countries. Proceedings of the Nutrition Society 1993; 52: 131-142 Nzegwu H & Levin RJ. Vitamin A deficiency and small intestinal secretory function in rat. Gut 1991; 32: 1324-1328. Ahmed F, Jones DB & Jackson AA. The interaction of vitamin A deficiency and rotavirus infection in the mouse. British Journal of Nutrition 1990; 63: 363-373. Alfredo Guarino; Andrea Lo Vecchio; Roberto Berni Canani. Probiotics as Prevention and Treatment for Diarrhea. Curr Opin Gastroenterol. 2009; 25(1): 18-23 Guandalini S. Probiotics for children with diarrhea: an update. J Clin Gastroenterol. 2008 Jul; 42 Suppl 2: S53-7.
  26. 26. 20 Review Articles Patent ductus arteriosus Neeraj Kumar Yadav Introduction Ductus arteriosus is persistent terminal portion of sixth brachial arch. It is a blood vessel that connects a baby's aorta and pulmonary artery while the baby is in the womb. This connection allows blood to be pumped from the right side of the heart straight to the aorta without stopping at the lungs for oxygen. In the womb, only a small amount of a baby's blood needs to go to the lungs because the baby gets oxygen from the mother's blood stream. The baby's pulmonary artery, which carries blood to the lungs is not needed at this time. What is PDA Ductus Arteriosus is a passageway which normally is present in every baby before birth. Patent ductus arteriosus (PDA) is a heart problem that occurs after birth in some babies. Before birth, the two major arteries -the aorta and the pulmonary artery-are normally connected by a blood vessel called the ductus arteriosus, which is an essential part of the fetal circulation. The high level of oxygen to which a body is exposed to after birth causes the ductus artery to close in most cases within 24 hours. When it does not close or remains open (patent), it is termed as patent ductus arteriosus. Since the pressure in the aorta is much higher than in the pulmonary artery, lots of blood will go to the pulmonary artery and it will enlarge. The lungs will get much more blood than they really need, which can put a strain on the heart and increase the blood pressure in the lung arteries. In fetal life prostaglandin-E2 (PGE2) is produced by ductus arteriosus to maintain its patency. Ductus closure occurs in two phases (i)functional closure by smooth muscle constriction (ii) anatomic occlusion of lumen over next several days due to extensive neointimal thickening and loss of muscle cells from the inner muscle media. After birth, construction of ductus arteriosus and obliteration of lumen results into separation of pulmonary and systemic circulation The initial functional closing of ductus depends on alteration in the balance between dilating and contracting forces. The ductus arteriosus has high level intrinsic tone during fetal life(1). After delivery, an increase in arterial Pao2 plays an additional important role in dutcus arteriosus constriction(2). A cytochrome P-450 hemoprotein that is located in the plasma membrane of the vascular smooth muscle cells appears to act as a receptor in the oxygen mediated contractile pathway(3,4). Oxygen inhibits, K-ion channels(5,6), which in turn causes membrane depolarization, an increase smooth muscle intracellular calcium(7) and formation of potent vasoconstrictor endothelin-1(8). Prenatal administration of steroid causes significant reduction in incidence of PDA (9). Incidence- In term babies 50% ductus closure occurs within 24hrs, in 90% by 48hrs and in all by 72hrs. The rate of ductus closure is delayed in preterm infant. About 3,000 infants are diagnosed with PDA each year in the United States. It is more common in premature infants (babies born too early) but also occurs in full-term infants. Premature babies with PDA are more vulnerable to its effects. PDA is twice as common in girls as in boys. PDA represents 5-10% of all congenital heart diseases, excluding those in premature infants(10). It occurs in approximately 8 of 1000 live premature births. In term infants, the incidence is about 1 in 2000 births. The female-to-male ratio is 2:1. PATENT DUCTUS ARTERIOSUS (PDA) Department of Pediatrics, Sarojini Medical College, Agra E-mail : neerajyadu@rediffmail.com
  27. 27. N K Yadav 19 Causes  Prematurity  Low birth weight  Prostaglandins  Maternal rubella in the first trimester of pregnancy is thought to be a cause of the seasonal incidence of PDA.  High altitude and low atmospheric oxygen tension have been associated with persistence of the PDA.  Hypoxia Clinical Feature  Poor feeding habits  Fast breathing  Shortness of breath  Sweating while feeding  Tiring very easily  Poor growth The condition also varies depending on how wide the ductus arteriosus opening is. A small opening may not produce any symptoms. A larger opening may produce a heart murmur.  A ductus arteriosus with a moderate-to-large left-to- right shunt may be associated with a hoarse cry, cough, lower respiratory tract infections, atelectasis, or recurrent pneumonia.  When the defect is large, congestive heart failure (CHF) with dyspnea and poor weight gain or failure to thrive are the main presentations. Clinical examination  Bounding peripheral pulses and wide pulse pressure.  Hyperdynamic precordium  Systolic thrill  Accentuation of the pulmonic component of the second heart sound is heard.  Continuous or machinery murmur is best heard at the upper left sternal border or left infraclavicular area.  Occasionally, auscultation of the PDA reveals numerous clicks or noises resembling shaking dice or a bag of rocks.  The murmur may be only a systolic ejection murmur. Investigation  Investigation of choice-The two dimensional echocardiographic visualization of ductus with pulsed wave, continuous wave measurement or color Doppler measurement appears to be not only very sensitive but also specific for identifying ductus patency. Other measurement of LA:Ao ratio is also sensitive.  X-ray chest: cardiomegaly, prominence of pulmonary artery segment and plethoric pulmonaryvasculature.  Electrocardiography- tall T wave characteristic of the volume overloading of left ventricle.  Hemoglobin, complete blood count, platelet count, serum creatinine, blood urea and bleeding profile. Management- Supportive, medical and surgical management  Oxygen to correct hypoxemia  Sodium and fluid restriction  Correction of anemia  Medical management consists of amelioration of CH F symptoms  Prophylaxis against infective endocarditis.  Indomethacin is currently the drug of choice for closure of the ductus in premature infant  Dose <7days:0.2mg/kg IV, then 0.1 mg/ kg IV at 12 and 36 h after initial dose >7 days: 0.2 mg/kg IV, then 0.2 mg/kg IV at 12 and 36 h after initial dose. Indomethacin is much more likely to achieve ductus closure if given on first day of life; its effectiveness wanes with increasing postnatal age (11).  During treatment monitor vital of baby and urine output.  Contraindication- poor renal function, bleeding disorder or thrombocytopenia, necrotizing enterocolitis and sepsis.  Ibuprofen- The dose is 10 mg/kg bolus followed by 5 mg/kg/d for 2 additional days. Cardiac surgery:  Indications for surgical treatment include the following: 1. Failure of indomethacin treatment 2. Contraindications to medical therapy (eg, thrombocytopenia, renal insufficiency) 3. Signs and symptoms of CHF 4. PDA found in an older infant. 5. Infants found to have an asymptomatic PDA after the neonatal period should undergo surgical ligation preferably before the age of 1
  28. 28. year to
  29. 29. 20 Patent Ductus Arteriosus prevent future complications of a PDA. Contraindications to surgery include pulmonary vascular obstructive disease. Surgical methods of closing PDA  Ligation (with or without division of the PDA) without cardiopulmonary bypass can be performed through a left posterolateral thoracotomy.  Video-assisted thoracoscopic surgery (VATS) ligation of PDA is less invasive than the posterolateral thoracotomy. It has been shown to be safe and effective. Timing of surgery is at 1-2 years or whenever the diagnosis is made in an older infant. In infants with CHF, failure to thrive, pulmonary hypertension, or recurrent pneumonia, the operation is more urgent ( within 3-6 months).  A Cochrane Database of Systematic Reviews article showed no statistically significant difference in closure between ibuprofen and indomethacin. A decision to use one drug versus another should be based upon the infant's presentation and comorbidities. A similar Cochrane Database of Systematic Reviews article looking at initial treatment of symptomatic PDA in preterm infants showed no difference in risks or benefits of surgery versus the use of cyclooxygenase inhibitors.  Prostaglandin E-1(PGE1) should be used to maintain patency of the ductus arteriosus once it is established that a ductal dependent lesion exists. However, PGE is a pulmonary vasodilator and could cause exacerbation of CHF by means of increasing pulmonary blood flow. Complications  Left heart failure  Pulmonary hypertension  Right heart hypertrophy and failure  Eisenmenger physiology  Bacterial endocarditis  Myocardial ischemia  Necrotizingenterocolitis Prognosis If a small PDA remains open, heart symptoms may or may not eventually develop. Persons with a moderate or large PDA will usually develop heart problems sooner or later unless the PDA is closed.
  30. 30. Closure with medications can work very well in some situations, with few side effects. Early treatment with medications is more likely to be successful. Surgery carries its own significant risks. It may eliminate some of the problems of a PDA, but it can also introduce a new set of problems. The potential benefits and risks should be weighed carefully before choosing surgery. Prevention Preventing preterm deliveries, where possible, is the most effective way to prevent PDA Reference 1. Kajino H, Chan YQ, Seinder SR et al: Factors that increase the contractile tone of ductus arteriosus also regulate anatomical remodeling. American Journal Physiology 281:R291-R301, 2001. Kennedy JA, Clarc SL: Observation on physiological reaction of the ductus arteriosus. American Journal Physiology 136:140-147, 1942. Coceani F, Wreight J, Breen C: Ductus arteriosus: Involvement of sarcolemmal cytochrome P-450 in 02 const rict ion. Canadian Journal Physiology Pharmacology 167:1448-1450, 1989b. Cocaeni F, Kelsey L, Ackerley C, et al: Cytochrome P450 during ontogenic development: Occurrence in the ductus artreiosus and other tissues. Canadian Journal Physiol Pharmacol 72:217-226, 1994. Michelakis E, Rebeykal, Bateson J, et al: Voltage gated potasium channels in human ductus arteriosus. La ncet356:134-137,2000. Reeve HL, Tolarova S, Nelson DP et al: Redox control of oxygen sensing in the rabbit ductus artriosus. Journal Physiol 533:253-261, 2001. NakanishiT, Gu H, Hagiwara N, Momma K: mechanism of oxygen induced contraction of ductus arteriosus isolated from fetal rabbit. Cric Res 72: 1218-1228, 1993. Coceeani F, Armstrong C, Kelsey L: Endothelin is a potent constrictor of the lamb ductus arteriosus . Canadian Journal Physiol Pharmacol 67:902-904, 1989. Waffarn F, Siassi B, Cable L, Schimdt PL:Effect of antenatal glucocorticoid on clinical closure for patent ductus arteriosus: American Journal Dis Child: 137, 336-338,1983. Dude11 GG, Gersony WM: Patent ductus arteriosus in neonates with severe respiratory disease. Journal pediater 104:741-748, 2001. Schimdt B, Davis P, Moddemman D et al. Long term effect of indomethacin prophylaxis in extremely low birth weight infants. N England Journal Med 344: 1966-1972,2001.
  31. 31. Malaria brief review of recommendations Rajesh Kumar, Senthil Kumar Introduction Malaria is a mosquito-borne infectious disease caused by a eukaryotic protozoa of the genus Plasmodium. It is widespread in tropical and subtropical regions, including parts of the Americas (22 countries), Asia, and Africa. Each year, there are approximately 350-500 million cases of malaria, killing between one and three million people, the majority of whom are young children. Five species of the plasmodium parasite can infect humans; the most serious forms of the disease are caused by Plasmodium falciparum. Malaria caused by Plasmodium vivax, Plasmodium ovale and Plasmodium malariae causes milder disease in humans that is not generally fatal. A fifth species, Plasmodium knowlesi, is a zoonosis that causes malaria in macaques but can also infect humans [1]. Diagnosis Charles Laveran first visualized the malaria parasite in blood in 1880, the mainstay of malaria diagnosis has been the microscopic examination of blood. Microscopic examination of blood films Two sorts of blood films are traditionally used. Thin films are similar to usual blood films and allow species identification because the parasite's appearance is best preserved in this preparation. Thick films allow the microscopist to screen a larger volume of blood and are about eleven times more sensitive than the thin film, so picking up low levels of infection is easier on the thick film. From the thick film, an experienced microscopist can detect parasite levels down to as low as 0.0000001% of red blood cells [2]. Antigen tests For areas where microscopy is not available, or where laboratory staff are not experienced at malaria diagnosis, there are commercial antigen detection tests that require only a drop of blood. The first rapid diagnostic tests were using P. falciparum glutamate dehydrogenase as antigen. PGIuDH was soon replaced by P.falciparum lactate dehydrogenase. PLDH does not persist in the blood but clears about the same time as the parasites following successful treatment. The lack of antigen persistence after treatment makes the pLDH test useful in predicting treatment failure. Depending on which monoclonal antibodies are used, this type of assay can distinguish between all five different species of human malaria parasites, because of antigenic differences between their pLDH isoenzymes [3]. TREATMENT[4] Recommendations on treatment for uncomplicated falciparum malaria 1. Artesunate+sulfadoxine-pyrimethamine The total recommended treatment is 4 mg/kg of artesunate given once a day for 3 days and a single administration of sulfadoxinepyrimethamine(25/1.25 mg base/kg ) on day 1. 2. Artesunate + mefloquine The total recommended treatment is 4 mg/kg of artesunate given once a day for 3 days and 25 mg base/kg bw of mefloquine usually split over 2 or 3 days. 3. Artemether-lumefantrine This is currently available as co-formulated tablets containing 20 mg of artemether and 120 mg of lumefantrine. The total recommended treatment is a 6-dose regimen of artemether-lumefantrine twice a day for 3 days Recommendations on second-line antimalarial treatment for uncomplicated falciparum malaria 1. Artesunate (2 mg/kg once a day) + tetracycline (4 mg/kg four times a day) or doxycycline (3.5 mg/kg once a day) or clindamycin (10 mg/kg twice a day). Any of these combinations to be given for7 days Review Articles
  32. 32. 22 Rajesh Kumar et al 2. Quinine (10 mg salt/kg three times a day) + tetracycline or doxycycline or clindamycin. Any of these combinations to be given for 7 days. Recommendations on the treatment of severe malaria Artesunate 2.4 mg/kg i.v. or i.m. given on admission,then at 12 h and 24 h, then once a day is the recommended choice in low transmission areas or outside malaria endemic areas For children in high transmission areas, the following antimalarial medicines are recommended as there is insufficient evidence to recommend any of these antimalarial medicines over another for severe malaria: 1. artesunate 2.4 mg/kg i.v or i.m given on admission, then at 12 h and 24 h, then once a day 2. artemether 3.2 mg/kg i.m. given on admission then 1.6 mg/kg per day 3. quinine 20 mg salt/kg i.v on admission, then 10 mg/kg every 8 h; infusion rate should not exceed 5 mg salt/kg per hour. Concomitant use of antibiotics The threshold for administering antibiotic treatment should be low in severe malaria. Septicaemia and severe malaria are associated and there is diagnostic overlap, particularly in children. Unexplained deterioration may result from a supervening bacterial infection. Although enteric bacteria (notably Salmonella) have predominated in most trial series, a variety of bacteria have been cultured from the blood of patients diagnosed as having severe malaria, and so broad spectrum antibiotic treatment should be given initially. Treatment of other types of malaria Chloroquine 25 mg base/kg divided over 3 days, combined with primaquine 0.25 mg base/kg, taken with food once daily for 14 days is the treatment of choice for chloroquine-sensitive infections. In moderate G6PD deficiency, primaquine 0.75 mg base/kgshould be given once a week for 8 weeks. In severe G6PD deficiency,primaquine should not be given. References 1. Collins WE, Barnwell JW. "Plasmodium knowlesi: Finally being recognized". J Infect Dis 2009;199 (8): 1107-1108. 2. Warhurst DC, Williams JE. "Laboratory diagnosis of malaria". J Clin Pathol 1996; 49(7): 533-38. 3. McCutchan, Thomas F, Robert C Piper, and Michael T Makler. "Use of Malaria Rapid Diagnostic Test to Identify Plasmodium knowlesi Infection". Emerging Infectious Diseases (Centers for Disease Control) 2008; 14 (11): 1750-1752. WHO Guidelines in the treatment of malaria 2006.
  33. 33. 'ee 6i e4t G G ~ i 4 e 2 Aristo Pharmaceuticals Ltd., Mumbai C Makers of Pedpro - the ideal protein for children
  34. 34. Original Articles Dengue hemorrhagic fever with osteopetrosis Om Shankar Chaurasiya and Anil Kaushik Introduction Osteopetrosis, also known as marble bone disease belongs to a group of disorders in children associated with increase in skeletal density. Osteopetrosis is caused by defect in bone resorption by osteoclasts leading to hyperostosis. At least 9 types of Osteopetrosis have been described, with variations in clinical and radiological features [1]. The autosomal dominant form is usually asymptomatic and diagnosed incidentally in late childhood/adulthood. We report a case of dengue hemorrhagic fever who was incidently found to have osteopetrosis manifesting in early childhood. Case Report A six year old female child of a government employee resident of Jhansi, presented with history of fever (8 days), generalized bodyache (8days), epistaxis (2 days), appearance of bluish spots on body (2days). The patient was born full term by normal vaginal delivery at home. Birth weight was not recorded. Antenatal and immediate postnatal period were uneventful. At 2 years of age, she was noted to have lack of visual activity from her left eye along with deviation of eye. Developmental history was normal. The patient was immunized for age and a product of non-consanguineous marriage and elder sibling aged 4 years was healthy. There was no family history of neurological illness.Patient had one episode of fracture of right lower limb following a fall while walking on high heel sandal. Fracture healed in 6-8 weeks following successful plaster application. At admission the infant weighed 13.5 kg (67% of expected). Height 98 cm(84 % of expected). pallor was present. Two 2, 2.5 cm pupuric spots seen over cheek. On abdominal examination, liver is enlarged 3.0 cm below costal margin, soft to firm, non tender, well defined margin,with liver span 10 cm and spleen is enlarged 2 cm below costal margin non tender and firm in consistency. Neurological examination revealed higher mental status, motor, sensory system normal with left second cranial nerve palsy and left optic disc pallor. No dysmorphic features or neurocutaneous markers were present. Respiratory and Cardio-vascular examination was normal. Investigations revealed : Hb 6.4 gm%, TLC 5400/cu mm, platelet count 18000/cu mm. Peripheral blood smear showed 4 premature myeloid cells per 100 cells examined.Blood sugar, liver function tests, urea, creatinine, sodium and potassium were within normal limits. Serum calcium was 7.4 mg%.Serum phosphorus 3.1mg%, alkaline phosphatase was 146u/l, acid phosphatase 1.74. Serum was positive for IgM and IgG of dengue and rapid malarial antigen test was negative for P.vivax and P.falciparum. Blood culture was sterile. HIV spot test was negative. Radiographs of limbs showed generalized increase in bone density and 'bone within bone' appearance. Radiographs of skull showed sclerosis and thickening of orbital rims and anterior cranial fossa. Sella was small. Ultrasonography abdomen showed hepatosplenomegaly with no other abnormality. During PICU stay patient received one unit whole blood ,9 units PRP, 2 units FFP,I/V Fluids and inj ceftrioxone. Parents refused bone marrow biopsy. Based on the clinical presentation, classical radiological findings and haematological picture the diagnosis of osteopetrosis was made. Discussion Malignant recessive osteopetrosis or osteopetrosis with precocious manifestations is a rare disorder occurring with an incidence of 1:200000 population [2]. It is an autosomal recessive condition presenting in neonatal period or early infancy. Its various manifestations are a result of hyperostosis. The initial presentation of these patients may be with pallor, failure to thrive, nasal obstruction or visual impairment. Lorea Cortes et al found nasal obstruction as an early symptom in their series of 26 patients over a period of 10 years [3], whereas Gerritsen EJ et al reported ocular manifestations as an early symptom in their series of 33 patients over 16
  35. 35. 24 Om Shankar Chaurasiya et al Fig. 1: Showing generatized increase of bone density in limbs years [4]. Our patient was brought with symptoms of nasal obstruction aggravated by recurrent upper respiratory infection. He was also noted to have impaired vision. Haematological findings are due to obliteration of bone marrow cavity by bone, causing myelophthisic anaemia, which manifests as a leukoerythroblastic picture on peripheral blood smear (neutrophilia, i m m at ur e gra nul oc y t es , nuc l eat ed RBCs). Hepatosplenomegaly is due to extra medullary haematopoiesis. Thrombocytopenia, leukopenia and
  36. 36. 30 Review Articles haemolytic anaemia may occur due to hypersplenism [5]. In our case, haemoglobin level was relatively preserved as a result of compensatory haematopoiesis. However, many patients of malignant recessive osteopetrosis become transfusion dependant [6]. The radiological findings were increase in bone density with defective metaphyseal remodelling. A 'bone within bone' appearance is characteristic and diagnostic and was seen in the above case. This finding differentiates osteopetrosis from other sclerosing dysplasias. This is due to the cyclical nature of the disease, so that the dense shadow of bone at the time of formation of abnormal bone is seen within the outline of the current normal or abnormal shadow. Irregular condensation of bone at metaphysis may produce parallel plates of dense bone at the end of long bones, a finding that is normally seen in older children. Base of skull is dense, with or without involvement of vault and sella is small. Orbital margins are markedly increased in density. Sphenoid, mastoid and frontal sinuses are underornon-pneumatised [7]. Visual impairment is seen due to bony encroachment on optic foramina. It is a common initial symptom as reported by Gerritsen et al [4]. Optic atrophy is present in a significant number of cases. In the series reported by Phadke et al [8], optic atrophy was present in 3 out of 6 cases. Visual impairment is responsible for lack of acquisition of certain early development milestones like social smile, as seen in our case. Early visual impairment in combination with haematological impairment is associated with a poor outcome [4]. Hearing impairment may be due to bony encroachment on auditory nerve, sclerosis of middle ear ossicles and/or middle ear effusion [6]. Various other cranial nerve palsies can similarly be present due to bony encroachment on foramina [6]. Our patient had clinical evidence of hearing impairment.
  37. 37. Degue Hemorrhagic fever with Osteopetrosis 25 Spastic quadriparesis and pseudobulbar palsy were present in our case. This may be due to associated neurodegenerative disorder, which has been reported to occur in osteopetrosis [6]. Other neurological manifestations described in osteopetrosis are macrocephaly, seizures, hydrocephalus, psychomotor retardation and strabismus [3]. Hypocalcemia, low serum phosphorous levels and elevated serum alkaline phosphatase levels are known to occur in osteopetrosis [1] Serum calcium was marginally lower in our case. In the series of cases reported by Phadke et al, serum calcium levels were normal [8]. Hypocalcemia is related to decrease in osteoclastic activity and can be the cause of seizures occasionally. Infants with malignant osteopetrosis also suffer from recurrent infections as a result of defect in macrophage function [1]. Chronic anaemia, recurrent infections, feeding problems due to bulbar nerve involvement and nasal congestion lead to failure to thrive in these children. Fractures are common and one of the classical features of osteopetrosis. They are usually transverse and heal with normal callus. They occur after moderate trauma and are thus rare in infancy. Skeletal maturation is normal. The course of illness in autosomal recessive osteopetrosis is progressive and these children do not survive long. Survival at 6 years is about 30% [4]. The cause of death is usually severe anaemia, bleeding or overwhelming infection. Mortality is higher in first two years of life. Children who are not transfusion dependent and alive at 2 years have a relativelyfavourable prognosis. The defi niti ve treatment is bone marrow transplantation. Recipients of HLA identical bone marrow transplant have 79% 5-year survival [9]. Supportive t reat m ent i nc ludes t r eat m ent of anaemia, thrombocytopenia and infections. Prednisolone may arrest progress of anaemia and thrombocytopenia. Oral cellulose phosphate, low calcium diet, recombinant human interferon gamma may also be beneficial [1]. Neurosurgical unroofing of optic foramina has been tried. Genetic ally, recessive osteopetrosis is a heterogenous disease and a number of genetic loci are likely. Recently mutations in the gene coding for an osteoclast specific vacuolar pump have been found in a subset of affected children. The near future will see other genes being mapped, cloned and mutational analysis hopefully made available [6]. Appropriate genetic counselling could then be offered, References 1. Hall BD. Genetic skeletal dysplasia (Osteopetrosis, Pyknodysostosis, dysosteoscelerosis and cortical hyperostosis). In : Richard E Behrman, Robert M Kleigman, AnnM Arvin, editors, Nelson Textbook of Paediatrics. 15`h ed. Prism Books. WB Saunders, Philadelphia 1996;1980-1. 2. Johnson CC, Lavy N, Lord T, Vellios G, Merritt AD, Deiss WP. Osteopetrosis : A clinical, genetic, metabolic, morphological study of the dominantly inherited benign form. Medicine 1968;47:149-67. 3. Loria Cortes R, Quesada-Calvo E, Cordero-Chavveri C. Osteopetrosis in children : A report of 26 cases. J Paediatrics 1977;91:37-43. 4. Gerritsen EJA, Vossen JM, Van Loo IHG, Hermans J, Helfrich MH, Griscelli C. Autosomal recessive osteopetrosis. Variability of findings at diagnosis and during the natural course. Paediatrics 1994;93:247-53. 5. Alter BP, Young NS. Bone marrow failure syndromes. In:Nathan DG, Oski FA, editors. Haematology of infancy and childhood. 4th ed. Pennsylvania, WB Saunders Co 1993;216-316. 6. Wilson CJ, Vellodi A. Autosomal recessive osteopetrosis : diagnosis, management and outcome. Arch Dis Child 2000;83:449-52. 7. Jacobs P, Renton P. Congenital skeletal anomalies : Skeletal dysplasias : chromosomal disorders. In : David Sutton, editor. A textbook of radiology and imaging. 4th ed, Churchill Livingstone 1987;22-3. 8. Phadke SR, Gupta A, Pahi J, PandeyA, Gautam P, Agarwal SS. Malignant recessive osteopetrosis. Indian Paediatr 1999;36:69-74. 9. Gerritsen EJA, Vossen JM, Fasth A, Freiedrich W, Morgan G, Padmos A. Bone marrow transplantation for osteopetrosis. A report from the Working Party on Inborn Errors of the European Bone Marrow Transplantation Group.J Pediatr 1994;125:896-902.
  38. 38. 26 Original Articles Feeding Practices and Growth in LBW Babies KP Kushwaha, Mahima Mittal, Bhoopender Sharma, Anita Mehta, Satish Srivastava, Dilshad Ansari, Arvind Kumar, Vinay Bajpai World over efforts have been made to develop a feeding practice guideline, for all LBW babies which would ensure their proper growth along with minimal morbidity and mortality (1), but the dilemma still remains the feeding options for LBW infants, particularly when breastfeeding is not possible ,include human donor milk and artificial infant formula multi component fortifiers (HMF, MCT oil, etc) (1). Although used regularly in neonatal units of developed countries (2), in developing countries their use is limited due to risk of contamination (3). Animal milk is also used as a breast milk substitute in some nurseries although no policy statement for its proper preparation is available as such (1). In order to develop a feeding protocol which would best suit LBW babies of our neonatal unit, we monitored the growth and morbidity patterns of LBW babies on different feeding protocols .We developed protocols according to aforementioned feeding options keeping in mind all the feeding practices prevalent in this region. LBW babies without any medical, surgical or congenital problem were divided into four groups according to weight Group A (< 1200 gms, n =32), Group B (1201-1500gms, n=30), group C (1501-1800gms, n=60), group D (1801-2500gms, n=88). All mothers were informed regarding the various feeding options given below along with their advantages and disadvantages. They were also told about the benefits of breast milk and breast feeding. After providing this information the parents were allowed to make a choice regarding the feeding mode they would like to follow. Babies were then divided into four feeding groups according to the feeding practice they chose to follow - Final groups (after 6 month of follow up) Group 1-LBW babies who were exclusive breast fed Group 2 - LBW babies given Animal milk and breast milk with Supplements, (Rice water, human milk fortifier, coconut oil and MCT oil etc.) Group 3 - LBW babies being given milk, both animal milk and breast milk (Without supplements) Group 4 - LBW babies being given exclusively top fed (animal milkorformula milk) As soon as the babies were able to tolerate feeds they were given feeds according to the choice through gavage tube, later switching over to katori or breast feeding. when the feeding was established and when babies weighed 2500 gms, they were discharged with adequate vitamin and calcium supplementation. The mothers were also motivated to bring their babies every month up to 6 month for follow-up .At subsequent OPD visits all the anthropometric measurements, to assess the growth, were recorded. Feeding practice were recorded and counseling was imparted regarding the difficulties encountered. Follow-up was good up to 3 months after which the attendance became poor and by end of the study only 62 babies were left. Those babies whose feeding group changed in between were also excluded. Results It was noted that although babies belonging to group 2, 3, 4 (supplemented babies) fared better than their exclusively breast fed counterparts in all parameters of growth (i.e. weight, height, head circumference, chest circumference) and also that group 3 excelled in all the four groups, but babies in group one also maintained their growth within normal limits (according to CDC Growth Charts) throughout. When the rate of weight gain was analyzed by calculating the time taken for doubling of weight, the
  39. 39. KP Kushwaha et al 27 results in all groups were comparable .Group 1 babies (exclusively breast fed) in Group A (<1200 gms) & B(1201-1500 gms) doubled their weight by approximately 10 week, which was similar to time taken by babies in same weight category in group 2, 3, & 4. Morbidity patterns were also tabulated and it was found that common ailments on the whole were diarrhea, respiratory tract infections, neonatal hyperbilirubinemia, conjunctivitis etc. Diarrhea) disease in breastfed infants i.e..Group 1, was strikingly low in all weight categories, especially in group A (<1200 gms ) where the incidence was only 33% in group 1, as compared to 100% &72% in group 2 & 3 babies. Discussion Although the study shows that babies had achieved better biological parameters with supplementation it also reemphasizes that babies grow equally well on breast milk alone. RCT's who have reported significantly lower growth rate human donor milk as compared to infant formula4,are very old and are of limited value due to use of donor drip milk (predominantly foremilk) ,instead of expressed breast milk. Studies consistent with our findings are ones who have followed these babies up to 7-8 years and have not reported any adverse effect on growth parameters'. Higher incidence of diarrhea, along with economic burden due to high cost of some supplements e.g. humanized powder milk, human milk fortifiers etc. and population not literate enough to prepare these preparations hygienically and avoiding to prescribed norms etc.are few of the many constraints which limit supplementation of any kind even in LBW babies. Additional benefits of breast milk, apart from growth are achievements of better neuro developmental state and beneficial effect on chronic diseasesf i. Use of animal milk although, could be a cost effective alternative for supplementation as it is easily available and we have not encountered any major complication on its use in our study although larger scale studies are required to establish proper recommendations. We thus, recommend all LBW babies to be started with expressed breast milk in all neonatal units with an aim to establish and continue exclusive breast feeding for long term benefits. Acquisition of slightly better growth parameters on other feeds cannot outweigh the long-term benefits of breast milk. Fortification is not recommended due to risk of contamination. Animal milk however can be considered as alternative in these circumstances, due to the easy availability of pure milk in our setup and less chances of contamination. References 1. Edmond K, Bahl R, Optimal feeding of LBW infants technical Review WHO: 2006;1-4, 56. 2. European Society of Pediatric Gastroenterology and Nutrition. Committee on Nutrition of the Preterm Infant, Nutrition and feeding of preterm infants, Acta Pediatricia Scandinavica supplement, 1987, 336:1-14. 3. Lucas A et al Randomized outcome trial of human milk fortification and developmental outcome in preterm infant's American Journal of Clinical Nutrition, 1996, 64: 142-151. 4. Gross SJ Growth and biochemical response of preterm infants fed human milk or modified infant formula New England Journal of Medicine 1983, 308: 237-241. 5. Morley R, Lucas A. Randomized diet in the neonatal period and growth performance until 7.5 -8 y of age in preterm children. American Journal of Clinical Nutrition, 2000,71; 822-828. 6. Singhal A et al. Breast milk feeding and lipoprotein profile in adolescents born preterm- follow up of a prospective randomized study. Lancet, 2004, 363;
  40. 40. 1571-8.
  41. 41. 28 Letters Use of Electronic Media - On Wed, 6/9/10, Dr.Sanjiv Kumar <drsanjv.kumar@gmail.com> wrote: From: Dr.Sanjiv Kumar <drsanjiv. kumarPgmail.com> Subject: Good use of electronic media To: "Dr Ka Ira Ajay Agra" <drajaykalra@y yahoo.com> Date: Wednesday, June 9, 2010, 10:15 AM Last year our Aligarh branch had a very good and fruitful experience with electronic media specially 92.7 Big FM. On ORS Day as well as Breast feeding week, we made messages related to ORS & Breast feeding & distributed them among our members. Few of our members recorded these messages in the studio. These messages were aired hourly on ORS day & on whole of the breast feeding week. Since these were public interest messages, so we made use of our relations and the Big FM people were kind enough to air our messages free of cost. This came out to be very effective. I think all our branches should explore the possibilities in their areas to make use of these media in spreading the public interest messages. Another suggestion is that we can make hoardings carrying public interest messages on different fields like ORS, breast feeding, vaccinations, good nutrition practices, importance of cleanliness etc. These hoardings can be put at important sites in the city. We can write all the messages on the same board or can make different boards topic-wise and rotate them on monthly or two-monthly interval. After having talks with CMO & MNA, these boards can be put free of charge. DrSanjiv Kumar, Aligarh Executive Board Member, State IAP Dear All, Forwarding herewith a letter from Dr. Sanjiv Kumar of Aligarh. His work is worth trying at other places. I had also mentioned about this in my first letter addressed to you all. Ajay Kara
  42. 42. Respected Sir This is a very nice suggestion and in fact since the beginning of the year IAP Lucknow branch has regularly been using the local FM media for giving messages of public importance on special days marked on IAP Calendar. Dr Archana Kumar, President and Dr Sanjay Niranjan, Secretary have been regular invitees for such talks on Air FM channel and we plan to continue with our efforts in future too, in order to reach out to maximum number of people DrShrish Bhatnagar Pediatric Gastroenterologist Joint Sec. IAP-Lucknow district unit Sahara Hospital, Lucknow. Ph:09918208555, drshrishbhatnagarr?a gmail.com; pedgastrolko@hotmail.com Polio - Won the battle? As far as the cases of Polio are concerned, Aligarh seems to have almost won the battle.Since last November,not a single case has been found positive in Aligarh district.Even in whole UP state,only two cases have been found in last 6 months.This is very encouraging as compared to the last year's statistics. This year a new addition to the polio eradication programme was the use of bivalent polio vaccine.lt was used in February & April and is to be used again in June.We are keeping our fingers crossed on next three months of high infectivity.lf these months are also polio-free,then we can say that we are going to win over polioverysoon.Let us hopeforthe best. DrSanjivKumar, Aligarh Distt. Coordinator, Polio Eradication comm. of IAP State Executive Board Member
  43. 43. Journal Watch Shrish Bhatnagar*, Niranjan Kumar Singh** 1. Usage pattern and exposure assessment of food colours in different age groups of consumers in the State of Uttar Pradesh, India. (Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2010;27(2):181-9.) Dixit S, Purshottam SK, Gupta SK, Khanna SK, Das M. E link: http://www.biomedsearch.com/nih/Usagepatte rn-exposu re-assessment- food/19890754.html The present study investigated the nature and levels of colours in food items and to undertake risk assessment vis-a-vis intake among different age groups of consumers in the State of Uttar Pradesh, India. A total of 478 edible foodstuffs were analyzed, and of six permitted colours, Sunset Yellow FCF (SSYFCF) and Tartrazine were most popular, and two non-permitted colours, namely Metanil Yellow and Rhodamine B, were encountered. The study showed a marked improvement in the trend of use of non-permitted colours over previous surveys, with 90% foods now resorting to approved food colours. However, 59% of foods employing permitted colours exceeded the maximum allowable limit, with average quantities crossing the threshold of 100 mg kg(-1) in most food commodities. The intake of SSYFCF exceeded the acceptable daily intake (ADI) for children and adolescents by 88% and 39%, respectively, These results indicate that children and adolescents are more vulnerable to higher intakes of food colours compared with the adult population. Comments : There has been a steady increase in awareness in state of UP about use of permitted colours but still the level are much high than the maximum allowable limit. A definite cause of concern.
  44. 44. 2. Redefining urinary tract infections by bacterial colony counts. (Pediatrics. 2010;125(2):335-41) Coulthard MG, Kalra M, Lambert Hi, Nelson A, Smith T, Perry JD. E Link: http://pediatrics.aappublications.org/ cgi/content/abstract/125/2/335 This study was to determine the best urinary bacterial concentration to diagnose urine infections. Authors studied a quantitative culture of paired urine samples from children that were promptly tested together after serial dilution. The initial diagnosis of urinary tract infection made from the result of the first urine culture and subsequently modified according to the second sample result, and then the ratio of their colony counts was considered. A total of 203 children (aged 2.0 weeks to 17.7 years) were screened for urine infection in a hospital setting. The 36 children who had a urinary tract infection, defined as having the same uropathogen in both urine samples at concentration within 25-fold of each other, had a mean colony count of 1.7 x 10(7) colony-forming units/mL. Among the 167 children who did not have a urinary tract infection, 12 (7.2%) would have had a false-positive diagnosis made on the first sample, which was revealed because the second sample result was different (n = 7) or had a > or =25-fold different colony count (n = 5). Raising the threshold from 10(5) to 10(6) colony-forming units/mL reduces the false-positive rate 4.8%. If 2 samples are cultured, the false-positive rates fall to 3.6% and 0.6%, respectively. The minimum urinary bacterial concentration that is used to diagnose a urine infection should be increased from > or =10(5) to > or =10(6) colony-forming units/mL, because that would reduce the false-positive rate from 7.2% to 4.8% if 1 sample was cultured and from 3.6% to 0.6% if 2 samples were cultured. *Consultant Pediatric Gastroenterologist,SaharaHospital,Lucknow **Consultant Pediatrician,VivekanandaPolyclinic &Institute of Medical Sciences,Lucknow
  45. 45. 30 Shrish Bhatnagar Comments: This study suggests that increasing the cutoff to =106 CFU/ml halves the false positive rate; and culturing 2 urine samples reduces the false positive rate to a minimum. Further prospective studies are required to validate these findings. Presently culture of a midstream urine sample showing =105 CFU/ml remains the gold standard for diagnosis of UTI in young infants and children. 3. Pro- and Prebiotic Supplementation Induces a Transient Reduction in Hemoglobin Concentration in Infants (JPGN2009;49:626-630) Mikael Kuitunen, Kaarina Kukkonen, and Erkki Savilahti E link http://journals.lww.com/jpgn/Abstract/2009/ 11000/Pro_and_Prebiotic_Supplementation_Induc es_a.14.aspx This study is the first to explore the effect of pro- and prebiotics on hematologic values in Infants. The authors investigated the effect of prenatal probiotic and 6 months of pro- and prebiotic supplementation of infants on their hematologic values at 6 months and 2 years and factors affecting these values. In a prospective randomized controlled probiotic intervention trial in infants at high risk for allergy, blood samples were obtained consecutively from 98 infants at 6 months and from 658 children at 2 years to measure hematologic values. Fecal samples at 3 and 6 months were collected to measure immunologic development by calprotectin, a-1-antitrypsin, tumor necrosis factor-a, and immunoglobulin A. At 6 months, infants in the probiotic group had significantly lower hemoglobin (Hb) values than did the placebo group, mean (SD): 119.8 g/L (6.3) versus 123.3 g/L (8.4), P=0.025. Adjustment for factors that might affect Hb values (breast-feeding duration, solid-food introduction, and sex), revealed no need for adjustment. A significant negative correlation emerged between Hb values at 6 months and fecal calprotectin (good marker of intestinal inflammation, with higher levels in inflammatory bowel disease and bacterial gastroenteritis than in healthy controls) at age 3 months r=-0.301, P=0.009, which was affected neither by breast-feeding, sex, nor study group. At 2 years, hematologic values in both groups became similar. Probiotics cause a gut mucosal inflammation with decreased Hb values during i nt e r ve nt i o n, c orrec t ed aft er hal t i ng t he supplementation. Comments : A definite cause of concern as pro- and prebiotics are part of majority of medical prescriptions these days.
  46. 46. News Report of UP Pedicon 2009 The 30`h Annual conference of the UP State branch of Indian Academy of Pediatrics was held at Allahabad on 14`h & 15`h November'09. The conference was inaugurated by the President of IAP Dr. Panna Choudhury who was the chief guest. The guest of honor was the Vice President Dr. Atul Agarwal. In his inaugural address, Dr. Panna Choudhury gave a detailed account of the activities of Central IAP and requested members to actively participate in them. Dr. Ajay Kalra Professor Pediatrics at S.N. Medical College took over as President of the state branch from Dr. D.K. Tiwari of Saharanpur. In his presidential address Dr. Kalra outlined the grim picture of child health in the state. However, he felt that instead of feeling sorry or frustrated we should take up the challenge. The conference was attended by over 300 delegates. Several important topics were covered in the two days of the conference. Key note addresses were delivered by Dr. Prof. K.N. Agarwal on Iron and brain development and by Dr. Raina President of the Pediatrics Surgeon Association of India on Management of Empyema thoracis. Dr. Vineet Saxena provided the details and concept of Neonatal Resuscitation Programme of IAP and the Navjat Shishu Suraksha Karyakram of Government of India. The faculty in the two days conference included Dr. Rohit Agarwal, Dr. Yash
  47. 47. Paul, Dr. Praveen Khilnani, Dr. Rajiv Uttam, Dr. V. Bhatnagar (from outside the state) and Dr. Rajiv Saran, Dr. K.L. Srivastava, Dr. D.K. Agarwal, Dr. B.D. Bhatia, Dr. Vipin Vashistha, Dr. V.N. Tripathi, Dr. K.P Kushwaha, Dr. O.P. Mishra, Dr. Manazar Ali, Dr. Farzana Beg, Dr. S.N. Singh, Dr. Arvind, Garg, Dr. N.C. Prajapati, Dr. S. Phadke, Dr. Ashok Rai, Dr. Rajpal Singh, Dr. Lalit Kumar, Dr. Amit Upadhayay, Dr. Rajesh Kumar and Dr. Premasish Mazumdar (from the state). A two days workshop on basic Pediatric Intensive Care preceded the conference at Jagriti Hospital. The cultural evening where more than 700 people were present was a delightful experience. Another highlight was the presence of several past presidents of IAP viz. Dr. V.K. Agarwal, Dr. Kanwal Kalra, Dr. M.M. Maithani, Dr. D.K. Sharma, Dr. Rajiv Saran, Dr. K.L. Srivastava and Dr. B.D. Bhatia. Dr. V.K. Agarwal was awarded the life time achievement award. The success of the conference was due to the untiring efforts made by the organizers headed by Professor P.C. Mishra as Organizing Chairperson, Dr. Avanindra Agarwal as Organizing Secretary, Dr. Ghanshyam Mishra as Joint Organizing Secretary, Dr. D.K. Singh as Scientific Secretary and the work of a wonderful team including Dr. Ajai Gopal and Dr. R.C. Chourasia.
  48. 48. 42 Session on Asthma management organized by Lucknow Branch of IAP Inaugural ceremony of UP Pedicon 2009, Allahabad Regional workshop on management of Diarrhoea organized by Lucknow branch of IAP Members of Aligarh IAP receiving one of the five awards presented to their branch at Pedicon 2009 LUCKNO DISTRICT U LUX1;AMEW OF POM
  49. 49. 31" UP PEDICON 2010 Hotel Ramada, Varanasi 27th - 28th November, 2010 REGISTRAITON FORM Please use Capital Letters Date ............................... First Name .................................................................................................................................................... Middle Name ................................................................................................................................................. Last Name .................................................................................................................................................... Address ........................................................................................................................................................ City ................................................................................................. Postal Code .......................................... Phone (with STD Code) .................................................................................................................................. Fax ................................................ Mobile ......................................... E-mail.............................................. Accompanying person/Spouse ............................................./Children (age) ............................................... Paid in favour of (UP PEDICON-2010) Payable at Varanasi Cash Rs .............................................................................................. Date................................................. DD No..................................... Date .......................................Amount .......................................................... Drawn on ...................................................................................................................................................... (cheques will not be accepted) REGISTRATION FEES (In Rupees) Till31st May,2010 Upto 31.07.10 Upto 31.09.10 Upto 31.10.10 Spot IAP Members 2000.00 2500.00 2800.00 3000.00 3500.00 PG Students 1200.00 1500.00 2000.00 2500.00 3000.00 Accompanying delegates 1500.00 2000.00 2200.00 2500.00 3000.00 Signature SECRETARIAT Dr. Alok C. Bharadwaj Smile Vaccination Clinic 8-Sigra Kamlanagar, Near Sigra Police Station, Varanasi Mob : 09335625522,09839056960 E : alokcbhardwaj@rediffmail.com Place