Monday, July 11, 2011
Sunday, June 19, 2011
JUNE 17TH 2011 + MARCH, APRIL + MAY 2011
The ‘GUP-SHUP ! of PEDIATRIC-MEDICINE – LATEST & USEFUL Information + a few REMINDERS (also):
So This time it is - MEGA ISSUE
Dear Reader,
We request ‘SAMAJH-DAAR’ (!) reader to excuse us – because of unavoidable – personal problem – we could not see you, in MARCH, APRIL, MAY-2011 – and Today is JUNE 17th 2011 so this the COMBINATION of 4-months – Do provide us ‘Feed back’ and tell the websites to as many as possible i.e. www..baalsanjeevani.blogspot.com
E.COLI :
We the Siblings of our ‘Ailing BHARAT MAA – This is our Family Member (!) But right now, IT HAS BECOME SUPERBUG IN THE DEVELOPED PART OF WORLD!
A particularly nasty and rare version of E.Coli called OIO4 : H4 – but figuring out how this pathogen made its way into the food supply is a trickier challenge.
Acute diarrhea is a leading cause of under –five mortality in India. Diarrhea is the passage of watery stools at least three times in a 24 hour period. However, recent change in the consistency of the stools is more important than the frequency. Mothers usually know when their children have diarrhea and provide useful working definitions in local situations.
Clinical Types of Diarrheal Diseases
Four Clinical types of diarrhea can be recognized, each reflecting the basic underlying pathology and altered physiology:
• Acute Watery
• Acute Bloody diarrhea (Dysentery)
• Persistent Diarrhea (Starts as acute watery diarrhea and lasts 14-days or longer)
• Diarrhea with severe malnutrition (marasmus or kwashiorkor) carries risk of severe systemic infection, dehydration, heart failure and vitamin and mineral deficiency.
What causes acute Diarrhea?
In India, rotavirus and enterotoxigenic E.Coli account for nearly half the total diarrheal episodes among children.
Apart from enterotoxin producing E.Coil (ETEC), which account for nearly 20% of childhood diarrhea, other forms of diarrheagenic E.Coli are enteroinvasive (EIEC), enterohemorrhagic (EHEC), attaching effacing E.coli or localized adherent (LA-EC), diffusely adherent E.Coli (DA-EC) and aggregative adherent E.coli (Agg-EC) EIEC and EHEC can cause dysentery. EHEC is a cause of hermolytic uremic syndrome also.
Yours’ Truly
Dr.(Prof.) DEEPAK SETH,
MD(PAED) MICP(USA) MNNF MNPGF FIAP
PROFESSOR & HEAD, DEPTT. OF PEDIATRICES- HIMS, NEAR LUCKNOW
MOB. 8826605719(Delhi) / 9897076071(UP/UK)
EMAIL : drdeepakseth@rediffmail.com / drdeepakseth@gmail.com
AT present I am in Delhi, D-41 Jangpura Extension, New Delhi-110014 Tel.No.24315610
Editor in Chief :
Dr. Prof. Deepak Seth,
I may be in any part of our ailing Bharat Maa (is it not shameful for us) Tomorrow!
Consultant Editor:
Dr. Prof. Neeraj Jain HIMS, Dehradun
Email neerajjain@vsnl.com / Contact No. 9412989195
Editor :
Dr. SURYA AGGARWAL,
Deptt. Of Medicine, HIMS, Dehradun (UK)
Email : agg_surya@yahoo.com / Contact No. 9811330543, 8006444404
Assistant Editor :
Mr.ABHINAV TOMAR
HIMS, Dehradun (UK)
Email : abhinav.tomar22@gmail.com / Mob. 8958484480
My PAs :
1. Ms.Deepani Seth / Email : deepani_seth@hotmail.com / Mob.9873247991
2. Ms. Kittoo Katyani Seth, Email : skatyani@gmail.com / Contact No. 001-8574176283(USA), 09456685866(India)
My 1st PA had done specialization in Designing from National Institute of Design – Ahmadabad + Bangalooroo and 2nd PA is now doing PG from Havard (US) in World Population and Public Health.
PLEASE DO TELL YOUR KNOWN TO THE IMPORTANCE AND FRUITFUL (WHICH FRUIT? )
Thursday, November 4, 2010
REMINDERS
After this article on latest developments in medical science, lets go back to some basic information that us paediatricians must always keep in mind.
· Paediatrics- is derived from the Greek words ‘Pedia’ meaning child and ‘itrike’ meaning treatment and ‘ics’ as you probably know means ‘branch of science’
· Paediatrics was born about a century back. Now, the latest strategy for the children by WHO and UNICEF is ‘Integrated Management of Neonatal Childhood Illness Scheme’ (IMNCI)
· The sorry and shameful thing is that the infant mortality rate is still very high, i.e., around 30.
Periods Of Growth
· Ovum: 0-14 days after conception i.e., The New Life has arrived on earth at conception
· Embryo: 14 days to 9 weeks
· Fetus: 9 weeks to birth
Perinatal Period is from 22 weeks of gestation to first 7 days of life (22 weeks because if the fetus is delivered, he or she can be made to live by our progressing neonatal care services)
New Born (Neonatal Period) first 4 weeks of life
Infancy- first year of life, Toddler- 1-3 years of age, Pre-School: 3-6 years. School Age: 6-10 years, Pre-Pubescent: 10-12 year in girls and 12-14 years in boys, Pubescence: 12-14 in girls and 14-16 in boys and finally Post Pubescence: 14 -18 years in girls and 16-20 yrs in boys
Important Events during Fetal Growth
Heartbeat: 4 weeks, Circulation: 8 weeks, Ovaries and Testes: 8 weeks, External Genitalia: 10 weeks, Fetal Movement: 14 weeks, Respiration: 18 weeks, Earl Sucking: 28 weeks, Suckling and Swallowing: 34 weeks
It is important that among the factors which affect growth we must remember that the four hormones are necessary and they are:
1. GH
2. Thyroxine
3 . Androgens
4. Insulin
EDITORIAL
You are welcome to send in your contributions and your critiques. Your feedback is extremely important in order to maintain the optimum level of communication and gives boost as well as direction to my efforts. So, my team and I will be meeting you every month.
On a different note: doctors or medicos in general, are usually seen by others as drab science loving geeks with no great appreciation for the more lyrical arts of the world. But anyone who has attended a casual gathering of doctors will be surprised to find the latent talents hidden behind the surgical mask and rubber gloves. One such artist I present to you, Dr.Durgesh of Najibabad, UP, an erstwhile student of the Himalayan Instt, Dehradun. The picture I have posted here was sketched by him during a tutorial in 2006.
Accept glittering best wishes on this auspicious and wonderful festival of lights. Here is wishing you all the illumination of useful knowledge and its practical utility.
MALARIA
World’s most lethal parasite is now going to be under human command, latest by 2015
There have been many trials and failures for the development of a vaccine against malaria since 1980 but now it seems that the moment of success is near at hand. There are three types of promising vaccination strategies against plasmodium.
1. Antibodies developed from mosquito enzyme called aminopeptidase injected into human beings. These antibodies when ingested by mosquito mask the enzymes in its gut. Without the enzyme, the gametocytes in the mosquito die and the cycle ends, thus rendering that mosquito harmless. Interestingly, this is A VACCINE FOR MOSQUITOES (!)
2. A VACCINE FROM MOSQUITOES: in this method, scientists grow genetically modified or irradiated parasites in the mosquitoes gut. These parasites are extracted and fragments from the weakened parasites are injected into a previously uninfected human, triggering an immune response that protects the individual from further infection.
3. A STRONGER TRADITIONAL VACCINE: Proteins from the surface of healthy sporozoites are isolated and fragments are incorporated into a scaffold. Now a chemical called an adjuvant is added to enhance the immune response by increasing the participation of B cells (antibody producing) and T cells. The resulting vaccine is injected into a previously uninfected child triggering an immune response that is partly effective at protecting individuals from future infection. A year and a half after the first injection the child receives a final booster shot to reinforce immunity.
Ref:
Extracts from article published in Scientific American Nov 2010
Author: Mary Carmichael, senior writer at Newsweek covering health and science.
Friday, June 6, 2008
Congenital Tuberculosis
Suryakant Khopkar, Asawari Setigiri,
Vilas Jadhav, Mukesh Agarwal
Edited By: Deepak Seth
Tuberculosis infection in a female of reproductive age-group is associated with profound consequences, ranging from infertility to the transmission of infection in her new born. Congenital tuberculosis is a well established clinical entity, though until pre-chemotherapeutic era the reorganization of congenital tuberculosis was mainly academic, as the condition was always fatal.
Case report
A three months old infant weighing 4.8 kg was admitted with complaints of fever, cough and breathlessness since 3 days. The baby was delivered vaginally with birth weight of 2.8 kg following an uneventful pregnancy and labor. There was no history suggestive of tuberculosis contact, including in the mother.
On examination, the baby had respiratory rate of 60/min with intercostals retractions. Air-entry was decreased and crepts were heard on both sides. Liver and spleen were palpable 2 cm each below costal margin routine haematogram revealed normal total and differential counts with ESR of 45 at the end of 1 hr and no definite evidence of septicemia. The initial X-ray of the chest showed bilateral diffuse mottling with left upper zone emphysematous bulla. Blood gas analysis showed pH 7.35, PO2- 42, PCO2-49, Sat. O2-72% and HCO3 - 15. Blood culture was sterile. Mantoux test was negative. Baby's and mother HIV were negative. Baby was started on IV Ceftriaxone and Amikacin considering staphylococcus bronchopneumonia but the baby continued to have respiratory distress and high grade fever.
Couple of day's later, gastric lavage examination revealed the acid fast bacilli with Ziehl-Neelson's staining and fluorescent microscopy. The baby was started on anti-tubercular therapy with INH (5-10 mg/kg/day), rifampicin (15-20 mg/kg/day) and Pyrazinamide (25 mg/kg/day) with prednisolone (2 mg/kg/day). After 7 days of treatment, baby developed recurrent left focal seizures with hemiparesis. CSF examination then revealed proteins 54 mg% and sugar 48 mg% and total cells 40/cumm with polymorphs 50%. CSF ADA level was raised 10 units/L (normal 10 units/ L). CSF culture was sterile and ELISA test in CSF for TB antibodies was positive. CT scan of brain showed right cortical infarct with no evidence of basal exudates or hydrocephalus.
Patient succumbed on 22nd day of admission i.e. after 2 weeks of anti-tubercular therapy. The mother's X-ray showed old calcified tuberculosis lesion at right upper zone but she was clinically asymptomatic.
Discussion
Until pre-chemotherapeutic era, recognition of the congenital tuberculosis was academic as the condition was always fatal. There have been approximately 300 reported cases in the medical literature. Surprisingly, there are few case reports from India despite of high prevalence of tuberculosis.
Recognition of congenital tuberculosis requires high index of suspicion as the manifestation are different from the older children. The disease usually manifest during first weeks of life but our patient presented little later. The common presenting manifestations are fever, respiratory distress, hepatomegaly, splenomegaly, irritability, prematurity and lymphadenopathy; sometimes indistinguishable from other causes of intrauterine or postnatal infection. Jaundice, seizure and meningitis are not very common, through may develop during the course of the disease. Infection of the fetus can occur either by transplacental route or secondary to ingestion or/and aspiration of infected amniotic fluid, usually at the time of delivery. Mother may be asymptomatic, though in some of them a radiological underlying focus is detectable.
Criteria for diagnosis of congenital tuberculosis were established in 1935 by Beitzke, which are still valid
1. The tuberculosis nature of the lesion must be proved.
· A primary complex in the liver is proof of congenital (intrauterine) origin
2. If there is no primary focus in the liver the infection is then only accepted as congenital if lesions are found in-utero, at birth or a few days later. In cases which manifest relatively later, all extrauterine sources of infection must be eliminated with certainty.
In present case, age of the child, presence of focus the mother and absence of infection in other contacts on screening, points towards a congenital origin of the disease.
Gastric aspirate for acid fast bacilli by Ziehl-Neelsen's staining, fluorescent microscopy or culture is very useful diagnostic too through over all yield is less than 20-30% with best available techniques.
Once the diagnostic of congenital tuberculosis is confirmed, with early treatment survival rate is approximately 45%. Association of tubercular meningitis with congenital tuberculosis is unusual and has poor outcome. While considering the prognosis of tuberculosis meningitis age is an important prognostic factor, and it is inversely related to mortality.
Conclusion
To conclude, early diagnosis of congenital tuberculosis depends on high index of suspicion, especially in endemic and susceptible high risk population, as the clinical manifestations are usually vague and investigations are unrewarding.
Tuesday, April 8, 2008
Prolonged Diarrhea: Chronic/Persistent/Recurrent?
Contributed by: Dr. Neeraj Jain
We all know and keep on experiencing physiological increase in number of motions (should not 'fear' (!) of Diarrhea) Acute mild to severe and chronic Diarrhea. It may keep on recurring or is persistent and keeps on troubling parents as well as treating doctors AND UNFORTUNATELY some (or majority) of patients keep on getting different, un-required and harmful 'treatment' from different doctors.
IS IT NOT OUR DUTY THAT IN OUR TROPICAL COUNTRY, WHERE WE KNOW THAT THIS PROBLEM IS SO COMMON AND HOW MAJORITY OF 'POOR CHILDREN' ARE BEING TREATED WE MUST TAKE SERIOUS STEPSTO KNOW THE SUBJECT IN TRUTH AND REALITY.
Recurrent diarrhea: Here, a child gets current episodes of acute diarrhea, clearly separated by intervening non-diarrheal periods. Arbitrarily, more than 6 episodes per year or >3 episodes/6 months or more than 2 episodes in 3 months may be defined as recurrent diarrhea.
Persistent diarrhea: A diarrheal illness starting as acute watery diarrhea, persisting for 15 days or more, is called persistent diarrhea. This is usually seen in early infancy. The term intractable diarrhea is used to define those cases of protracted diarrhea where the cause is not easily discernible, and the response to treatment is extremely unsatisfactory, The term protracted diarrhea has been applied when weight loss accompanies persistent diarrhea.
Chronic diarrhea: The onset is insidious and the course is sub-acute or chronic, with the passage of large amounts of semisolid stools. The diarrhea is usually of more than 1 month duration, Intervening normal periods may occur. This may occur at any age but is seen more often in older infants and children.
Now taking the problem in short
RECURRENT ACUTE DIARRHEA
This type of clinical syndrome is caused by recurrence of factors that cause acute diarrhea; especially recurrent infections of the gut. Each episode of recurrent acute diarrhea should be analyzed like an episode of acute diarrhea and managed accordingly. The most common predisposing factor for recurrence is an unhygienic environment, especially a contaminated water supply from tube wells, hand pumps or wells. Proper treatment of the acute episode, together with advice regarding the boiling of water and feeding bottle, is usually enough the mother should be advised about the usefulness of continued feeding of infant during the diarrheal episode (to maintain normal nutritional status), as malnutrition is also an important predisposing factor in causing recurrent diarrhea.
Nutritional advice, regarding additional food appropriate-far-age, should also be given. The child should be kept under close supervision to ensure adequate weight gain and to prevent development of malnutrition.
HOW THE CHILD IS WHOSE ACUTE DIARRHEA FAILS TO SETTLE DOWN IN 5-7 DAYS MANAGED?
Although this is not yet persistent diarrhea, but the fact remains that most parents (and the physician) would be very concerned even when the diarrhea is of 7 days' duration. A review of literature indicates that most episodes are a part of the natural history of the disease, being in nature and require no active management. However, some children do have problems and our job is to identify these cases. We should do (i) through clinical examination to detect dehydration and any systemic infection. (ii) Recording weight and comparing with any' previous record. Also recording the weight daily during the episode. (iii) Stool examination for ova and cyst, pH and reducing substances.
If the clinical examination is normal, the child is well hydrated, is maintaining or gaining weight and has normal stool examination, then no active intervention is required. Increase in non-milk calories (like cereals, pulses, curd, and banana) and some decrease in milk, while maintaining adequate calorie intake,' is all that is generally required.
Even children with LACTOSEINTOLERANCE (pH <5.5>14 days duration.
PERSISTENT/PROTRACTED DIARRHEA
This is a common and often baffling clinical problem. It is estimated to occur following 10-14 percent of episodes of acute diarrhea. It is seen more often in young infants «6 months) especially those on top-feed. Also, it is more common in malnourished children. Various causes, that may be responsible for persistent diarrhea are: (i) Resistant infection (ii) Unsuspected parenteral infection (iii) Malnutrition (iv) Disaccharidase-deficiency, including lactose-intolerance (v) Cow's milk protein intolerance (vi) Antibiotic induced diarrhea (vii) Soya protein and other food allergies (viii) Immuno-deficiency syndromes. .
In persistent or protracted diarrhea syndrome, the underlying common pathology is a persistent intestinal mucosal injury, with inadequate or no regeneration. The factors mentioned above, individually or collectively; play an important role in perpetuating mucosal injury. The maintenance of normal nutritional intake during episodes of acute diarrhea is most important for the prevention of the persistent stage. The hallmark of children with
protracted diarrhea is failure to thrive.
This is a complex problem, with a high mortality rate and requires management at the hospital level. One need not wait for 15 days before referring the child. Once weight-loss has set in, the case should be immediately referred to a specialist. In the hospital, a child with persistent diarrhea should be thoroughly examined to look for any systemic infection. A detailed stool examination, including microscopic examination, pH and reducing substances, should also be obtained. Blood counts and blood culture may be done, to exclude any systemic infection. Urine cultures and x-ray chest should be obtained to detect any occult infection. While the results of these reports are awaited, it would be prudent to withdraw all antibiotics (unless the child is very sick or has obvious signs of infections) and milk feeds, for 2-3 days. The child may be given extra low-lactose foods instead and, perhaps, a lactobacillus preparation as well. Most children would respond to this regimen unless there is an associated systemic infection, which would then need appropriate management. However, if the child's weight does not improve, enteral/parenteral alimentation and further investigations, like jejunal biopsy and sigmoidoscopy may be required. For this the child is required to be referred to a hospital with a gastroenterology unit. '
CHRONIC DIARRHEA
Most of these cases occur in older infants and children. These cases are akin to the mal-absorption syndrome. Since there is significant mal-absorption of fat always, they may not have the typical large, fatty stools seen in mal-absorption syndrome. The diarrhea may occasionally be semi-liquid type and may resemble those of persistent diarrhea except for the absence of the acute phase. These children usually do not get dehydrated unless their condition is superimposed by acute diarrhea. This factor may often be the presenting complaint.
This type of diarrhea may be due to a variety of causes, like giardiasis, gluten enteropathy and pancreatic mal-absorption. However, in our experience, it is because of heavy contamination of the gut by non specific bacteria leading to mild mucosal damage. We like to label these children as TROPICAL ENTEROPATHY. This largely occurs in low socio-economic groups of children and most episodes tend to occur during the summer or monsoon months, when gut infections tend to be high.
In all these children, weight should be carefully recorded and followed up periodically. Also 2 - 3 stool examinations may be done to rule out giardiasis or associated worm infestation. If these children maintain a good rate of weight gain, have a good appetite and have no giardia in stools; then they require good dietary (appropriate or increased calorie intake for age) and hygiene maintenance advice.
They normally tend to outgrow their problem. Presence of giardia would warrant metronidazole therapy. However if the child is not thriving (not gaining or loosing weight) and there is no giardia in the stool, then these children would require complete investigations like D-xylose absorption, fat balance study and jejunal biopsy. Now-a-days satisfactory intestinal biopsies can be obtained through GI endoscopy and hence these children should be referred to a pediatric endoscopy unit for further investigations and management.
LACTOSE-INTOLERANCE
Lactose, the sugar present in milk, is broken down in the intestine into glucose and galactose by an enzyme lactase, which is present in the superficial layers of the intestinal villi. Acute gastroenteritis may often result in the shedding of superficial layers of intestinal villi, with resultant lactose deficiency. The lactose is thus not metabolized and absorbed by the body. The lactose within the lumen of the gut is fermented by bacterial action into lactic acid, carbon dioxide and water. Stools in such a child tend to become acidic, loose and explosive. The increased water content of the stools is due to the osmotic action of unabsorbed lactose in the intestinal lumen.
Although some degree of lactose-intolerance may occur in many children with acute gastroenteritis in the first 48 hours, it usually does not cause any therapeutic problem. Clinically significant lactose intolerance should be suspected when an infant's diarrhea is perpetuated by the ingestion of cow's milk. It occurs in only 3-5 percent of cases and usually does not occur before 5-7 days of diarrhea. The chance of developing lactose intolerance is higher in malnourished children and in children following acute watery diarrhea due to Rota virus. It is rare in invasive diarrhea (dysentery).
Clinically, lactose-intolerance may be suspected if after the reintroduction of milk, diarrhea relapses, or persists beyond 1 week or so, with the passage of watery stools containing much air and a characteristic sour smell. Due to the acidic nature of the stools and frequent cleaning of perianal area develop perianal redness and this is an important sign in diagnosing this condition. These infants usually have a good appetite, as opposed to infants with infective diarrhea.
Lactose-intolerance can be confirmed by examination of the stools for reducing substances, with the help of Benedict's reagent, which gives a orange or yellow reduction. The stool pH is usually below 5.5 in such cases. The stool pH and reducing substances, should be tested in freshly passed liquid stools (within 1/2 hour) collection on plastic nappies (better as water is not absorbed by them). Contamination with urine should be avoided. These investigations are sufficient for the routine diagnosis of lactose-intolerance. Other sophisticated tests like the estimation of lactose content of the intestinal mucosa and lactose-tolerance tests, are neither easily available nor generally required.
Lactose-intolerance is usually not total and thus most children will tolerate small amount of lactose (1-2 gm/kg/day) contained in 30-50 ml/kg cow or buffalo milk. Curd is also low in lactose. Thus, a small diet of milk and curd-khichri is a very effective. Milk-withdrawal is usually not necessary for longer than 3-5 days and it should be gradually reintroduced in the diet. If diarrhea recurs or is not controlled on lactose-restricted diet then the child would require intravenous fluids and complete elimination of milk from the diet for longer time (4 to 6 weeks).
Low Lactose Foods
Milk substitutes ............ Curd, soya milk
Cereal products .............Rice or wheat porridge, khichri
Vegetables or fruits.......mashed bananas, vegetable
Non vegetarian................freshly prepared chicken soup