Friday, February 28, 2014

Pediatrics dept DiSSERTATION THESIS Bhavnagar

Thursday, February 27, 2014

DROPSY: Sanguinarine, Hydroxybutyrate Dehydrogenase and Fatigue in Epidemic Dropsy: A Retrospective Study of an Outbreak and its Control from Gujarat, India

Dept of Pediatrics and Medicine, BJMC & CH Ahmedabad- 380016 
Prof. Jayendra R Gohil,  Dr. Bankim D Mankad,  Dr. Bipin K Amin
http://www.webmedcentral.com/wmcpdf/Article_WMC002118.pdf

Diphtheria Photograph

Prof. Jayendra R GohilDr. Bhavesh A ShahDr. Alpa N Parekh
Pediatrics dept, GMC, STGH, Bhavnagar- 364002
http://www.webmedcentral.com/wmcpdf/Article_WMC002594.pdf

Bhavnagar Diphtheria Incidence from PED dep data
   Expiry shown as -x*

2005 68   
06 56   
07 62   
08 59   
09 75   
10 56   
11 34-9*
12 19-5*
13 12-2*
2014 14-4*
     2015        8-4*
    2016

Montelukast vs Budesonide as a First Line Preventive Therapy in Mild Persistent Asthma in 2 to 18 y



Pediatrics and Respiratory dept, GMC and STG Hospital, Bhavnagar, India



Thursday, February 6, 2014

BIRTH ASPHYXIA: REVIEW 2014 JAN

BIRTH ASPHYXIA Review Article
Prof Jayendra R Gohil, MD, Professor & head
Dr Heena Hasan, MBBS, Resident

Font changes are unintentional.......

ABSTRACT
Birth asphyxia is an important cause of acute neurologic injury, occurring in 2 to 3 cases per 1000 term live births in developed countries, with a higher incidence in less developed countries. Birth asphyxia related neonatal mortality and morbidity including long-term neuro-developmental sequele was seen in 25%-60% of survivors. It is estimated that around 23% perinatal deaths are due to birth asphyxia, with a large proportion of stillbirths. Asphyxia should not be confused with hypoxic ischemic encephalopathy (HIE) or cerebral palsy (CP) since not all asphyxiated neonates develop HIE or CP and there are other causes for the same.  In this article there is description of definitions, aetiologies, pathophysiology, clinical features, basic and recent investigations, older and newer treatment of birth asphyxia.
Conclusion: Although there is no specific treatment for birth asphyxia only supportive treatment (fluid and electrolytes balance, oxygenation and ventilation etc.) to prevent the complications and primary preventive measures (electronic fetal heart monitoring, training to birth attendants, home based newborn care) are helpful.
In the developed world, for the HIE, hypothermia has been the only treatment that has worked somewhat (8 -18%). The preferred cooling is whole body with a heart-lung bypass or ECMO; since that is rarely available, external whole body or external head cooling is the next best option. Prevention of reperfusion injury by early (within 6 hours) antioxidant therapy seems to hold the promise for future and should be studied.

Introduction:
          Birth asphyxia is a major cause of neonatal deaths, especially in rural India and in urban places where birth attendants trained in resuscitation are not available immediately. It also results into severe neurological long term morbidity; hardly any specific treatment is available. Perinataly asphyxiated newborns born in absence of trained manpower results in higher number of stillbirths. Prevention of the primary events and complications seem to be the best strategy at present.
Definition of birth asphyxia designed for use in hospital based settings require evaluation of umbilical cord pH, Apgar scores, neurologic clinical status, and markers of multisystem organ function1 and are not feasible for community settings2. The majority of neonatal deaths occur in the home without medical supervision; community-based definitions must rely on data gathered from verbal autopsy methods and use more general symptom- and sign-based algorithms. For example, the National Neonatology Forum of India has defined birth asphyxia as “gasping and ineffective breathing or lack of breathing at 1 minute after birth.”3 Such sign-based definitions are not, however, implemented consistently, and varying study-specific definitions may affect estimation of the proportion of neonatal deaths attributed to birth asphyxia.

               Regarding the definition according to American College of Obstetricians and Gynaecologists and the American Academy of Paediatrics, a neonate is labelled to be asphyxiated if the following conditions are fulfilled: (1) Umbilical cord arterial pH < 7; (2) Apgar score of 0 to 3 for longer than 5 minutes; (3) Neurological manifestations (e.g., seizures, coma, or hypotonia); and (4) Multisystem organ dysfunction, e.g., cardiovascular, gastrointestinal, haematological, pulmonary, or renal system.4

            Outcome of birth asphyxia depends on Apgar score at 5 minutes, heart rate at 90 seconds, time to first breath, duration of resuscitation, arterial blood gases and acid –base status at 10, and 30 minutes of age.5 It is measured as short term (early) and long-term outcome. The early outcome is either death/or presence of hypoxic ischemic encephalopathy (HIE) grade I, II or III, according to Sarnat staging.6

           Perinatal asphyxia refers to a condition during the first and second stage of labour in which impaired gas exchange leads to fetal hypoxemia and hypercarbia. It is identified by fetal acidosis as measured in umbilical arterial blood.7
           Perinatal hypoxia, ischemia, and asphyxia. These pathophyslogical terms describe respectively, lack of oxygen, blood flow, and gas exchanges to the fetus or newborn. These terms should be reserved for circumstances when there are rigorous prenatal, perinatal, and postnatal data to support their use.7
           Perinatal /neonatal depression is the preferred clinical descriptive term (over Birth Asphyxia by ACOG, but not in vogue) that pertains to the condition of the infant on physical examination in immediate postnatal period (i.e., in the first hour after birth). The clinical features of infants with these conditions include depressed mental status, muscle hypotonia and possibly disturbance in spontaneous respiration and cardiovascular function. These terms make no association with the prenatal or later postnatal condition (i.e., beyond the first hour) condition, physical exam, laboratory tests, imaging studies or electroencephalograms. After the first hour or so life, neonatal encephalopathy is the preferred descriptive terms for infants with abnormal mental status and associated findings.7
           Neonatal encephalopathy is a clinical and not an etiologic term that describes an abnormal neurobehavioral state consists of decreased level of consciousness and usually the other signs of brain stem and/or motor dysfunction. It does not imply a specific aetiology, nor does it imply irreversible neurological injury as it may be caused by such reversible conditions as maternal medications or hypoglycemia.7
            Hypoxic ischemic encephalopathy is a term that encephalopathy as described above with objective data to support a hypoxic ischemic mechanism as the underlying cause for the encephalopathy.7
            Hypoxic ischemic brain injury refers to neuropathology attributable to hypoxia and/or as ischemia as evidence by biochemical (such as creatine kinase brain bound [CK-BB] ,elecrtophyiologic (EEG), neuoroimaging (head ultrasonography), MRI, CT or pathological (post-mortem) abnormalities.7
                Neonatal Encephalopathy or Neonatal neurological syndrome8
-          term infant <7 at="" days="" o:p="" onset="">
-          depressed consciousness level
-          abdominal tone and power
-          feeding difficulty
-          seizure
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Monday, February 3, 2014

BACTERIAL INFECTION in CHILDREN with PEM GRADE III & IV at SirTG HOSPITAL, BHAVNAGAR, INDIA

Dholakia P J*, Parekh Z R**, Gohil J R **, Gosai M **, Solanki D I **
INTERNATIONAL JOURNAL OF MEDICAL AND APPLIED SCIENCES 2013; VOL2issue4:147-51.
Full text pdf
http://earthjournals.org/ijmas_228.pdf

ABSTRACT

Protein energy malnutrition (PEM) has been identified as a major health and nutrition problem in India. It is an important cause of childhood morbidity and mortality. The incidence of PEM in India in Preschool age is 3-4%. These children’s are more prone for infections. Bacterial infection & PEM is deadly combination for child.
Methods: Therefore we conducted prospective study for one year period. Patients having PEM grade III and grade IV, according to IAP classification are included in study. Blood culture, urine culture and stool culture were sent on day 1, along with routine investigations and data was analyzed.
Results: In our series of 74 patients, 9.5% are blood culture positive. Out of these, 6.8% are gram positive and 1.7% is gram negative organism. Urine cultures were positive in 5.4% of cases. Out of these 3.1% are gram negative organisms. Only 1% had stool culture positive. Anemia present in 78.9% of patients. Pneumonia was being diagnosed in 35.1% of patients, and diarrhea in 14.9% of patients. Mortality rates 5.4, of these 3.05% are in PEM grade III.
Conclusion: In the patients studied- All patients with PEM grade III & grade IV needs to be investigated for blood culture and urine culture. Stool culture is not necessary in PEM child. Preferential coverage of gram positive organisms while selecting antibiotic is necessary. Pneumonia is most common in child with PEM grade III.

Key Words : Bacterial Infection, Culture, PEM grade III &IV

Early Detection of Subclinical Diphtheritic Myocarditis by Aspartate Aminotransferase -AST- or Serum Glutamic Oxaloacetic Transaminase (SGOT) Estimation at SirTGH, Bhavnagar, India

http://www.scopemed.org/?jft=83&ft=83-1383282606
Pooja J. Dholakia, Zankhana Parekh, Jayendra R. Gohil, Dhaval I. Solanki.
From Pediatrics dept, GMC, Bhavnagar
Full text pdf 
http://www.scopemed.org/fulltextpdf.php?mno=46746

Abstracts 
Background & objectives: Diphtheria is endemic in India. Almost 50 - 60% of diphtheria deaths are due to myocarditis. Incidence of subclinical myocarditis is 68%. Aspartate Aminotransferase -AST- or Serum Glutamic Oxaloacetic Transaminase (SGOT) level can be used as marker of extent of myocardial damage during the course of diphtheria[3-7]. We therefore conducted study to detect early myocarditis due to diphtheria by measuring SGOT level.
Methods: This is a prospective study of 55 patients admitted over a 6 months period in a tertiary care hospital. Patients, from whom Corynebacterium diphtheria was isolated in throat swab culture, were enrolled in study. The clinical parameters, ECG and SGOT level were estimated on admission. All data were collected and statistical analyzed.
Results: The SGOT level was high in 65.5% (36/55) of patients. The clinical myocarditis was found in 25.8 % (6/55) patients. In 91.6% (33/36) cases of myocarditis, ECG did not reveal any abnormality, but definite elevations of the enzyme levels were noticed. The mean ± SD age of children in our study was 6.6 yr ± 3 (range 1-13) years. SGOT level was high in 36 cases; out of them 30 cases (83.3%) having duration of illness less than 7 days. Out of 6 expired cases 4 patients (66.7%) had raised SGOT level. We noticed 83.3% (5/6) cases expired due to diphtheritic myocarditis had abnormal leukocyte count (p 0.01).
Interpretation & Conclusion: We concluded elevated SGOT levels had high sensitivity and a negative predictive value to detect subclinical diphtheritic myocarditis.
Abnormal (high or low) total leukocyte count had poor prognostic value. 


Key Words: Diphtheritic Myocarditis, Leukocyte count, Serum Glutamic Oxaloacetic Transaminase, SGOT