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Biomedical subjects

V Nadkarni

Publications and source records attributed to V Nadkarni.

At least 19 recordsLinked to original sources
PubMed2005

International Resuscitation Network Registry: design, rationale and preliminary results.

There is a lack of high-quality information about the effectiveness of resuscitation interventions and international differences in structure, process and outcome after out-of-hospital cardiac arrest and cardiopulmonary resuscitation because data are not collected uniformly. An internet-based international registry could make such evaluations possible, and enable the conduct of large randomized controlled trials of resuscitation therapies. A prospective international cohort study was performed that included 571 infants, children and adults (a) who experienced cardiac arrest requiring chest compressions or external defibrillation, (b) outside the hospital in the study communities and (c) upon whom resuscitation was attempted by EMS personnel. Cardiac arrest was defined as lack of responsiveness, breathing or movement in individuals for whom the EMS system is activated for whom an arrest record is completed. All data were collated via a secure and confidential web-based method by using automated forms processing software with appropriate variable range checks, logic checks and skip rules. Median number of missing responses for each variable was 0 (interquartile range 0, 0). Twenty-seven percent of the patients had a first recorded rhythm of ventricular fibrillation or ventricular tachycardia, 60% had a witnessed arrest, and 34% received bystander CPR. Mean time from call to arrival on scene was 7.1+/-5.1 min. Six percent of the patients survived to hospital discharge. The resuscitation process was highly variable across centers, and survival and neurological outcome were also significantly and independently different across centers. This study shows that it is possible to collect data prospectively describing the structure, process and outcome associated with cardiac arrest in multiple international sites via the internet. Therefore, it is feasible to conduct adequately powered randomized trials of resuscitation therapies in international settings.

Adolescent↗
PubMed2001

Tools for predicting risk of mortality in the ICU setting: do we need a crystal ball or rose colored glasses?

Hematopoietic stem cell transplantation (HSCT) applied to children is associated with high risk for organ failure, ICU admission, morbidity and mortality. "Respiratory failure" after HSCT carries a historically grave prognosis. Factors associated with high risk for critical care complications in HSCT patients have been identified, but are dependent on timing and intensity of interventions. Several ICU severity of illness scoring systems predict prognosis on the basis of physiologic stability, organ system involvement, and intensity of supportive measures; but these tend to underestimate post-transplantation mortality risk. Adjustment of scoring systems and logistic regression factor analysis are promising adjuncts, but have not been adequately validated. Specific endpoints such as death, length of ICU or hospital stay, and neurologic function are relatively easy to quantify; but, quality of life is difficult to assess and report. What constitutes "heroic therapy" in one institution may qualify as "routine" care in another. Therefore, tools to predict mortality in the pediatric HSCT recipient requiring intensive care are difficult to apply to the individual patient, and remain more an art than science. This manuscript attempts to briefly define and review the pertinent types of PICU severity of illness and mortality prognosis scoring systems, and their application to pediatric HSCT patients. Pitfalls in application of physiology, organ system failure, therapeutic intensity, disease specific, and history-based scoring systems are discussed. Prospective validation studies for severity of illness systems and the evolution to concurrent registry-style data collection and analysis are necessary for the HSCT patient requiring ICU care.

Child↗
PubMed2001

An advisory statement from the Pediatric Working Group of the International Liaison Committee on Resuscitation.

The International Liaison Committee on Resuscitation (ILCOR), with representation from North America, Europe, Australia, New Zealand, Africa, and South America, was formed in 1992 to provide a forum for liaison between resuscitation organizations in the developed world. This consensus document on resuscitation extends previously published ILCOR advisory statements on resuscitation to address the unique and changing physiology of the newly born infant within the first few hours after birth and the techniques for providing advanced life support. After careful review of the international resuscitation literature and after discussion of key and controversial issues, consensus was reached on almost all aspects of neonatal resuscitation, and areas of controversy and high priority for additional research were delineated. Consensus on resuscitation for the newly born infant included the following principles: Personnel trained in the basic skills of resuscitation should be in attendance at every delivery. A minority (fewer than 10%) of newly born infants require active resuscitative interventions to establish a vigorous cry and regular respirations, maintain a heart rate > 100 beats per minute (bpm), and maintain good color and tone. When meconium is present in the amniotic fluid, it should be suctioned from the hypopharynx on delivery of the head. If the meconium-stained newly born infant has absent or depressed respirations, heart rate, or muscle tone, residual meconium should be suctioned from the trachea. Attention to ventilation should be of primary concern. Assisted ventilation with attention to oxygen delivery, inspiratory time, and effectiveness judged by chest rise should be provided if stimulation does not achieve prompt onset of spontaneous respirations and/or the heart rate is < 100 bpm. Chest compressions should be provided if the heart rate is absent or remains < 60 bpm despite adequate assisted ventilation for 30 seconds. Chest compressions should be coordinated with ventilations at a ratio of 3:1 and a rate of 120 "events" per minute to achieve approximately 90 compressions and 30 rescue breaths per minute. Epinephrine should be administered intravenously or intratracheally if the heart rate remains < 60 bpm despite 30 seconds of effective assisted ventilation and chest compression circulation. Common or controversial medications (epineprine, volume expansion, naloxone, bicarbonate), special resuscitation circumstances affecting care of the newly born, continuing care of the newly born after resuscitation, and ethical considerations for initiation and discontinuation of resuscitation are discussed. There was agreement that insufficient data exist to recommend changes to current guidelines regarding the use of 21% versus 100% oxygen, neuroprotective interventions such as cerebral hypothermia, use of a laryngeal mask versus endotracheal tube, and use of high-dose epinephrine. Areas of controversy are identified, as is the need for additional research to improve the scientific justification of each component of current and future resuscitation guidelines.

Environment↗
PubMed2000

Vasopressin pressor effects in critically ill children during evaluation for brain death and organ recovery.

BACKGROUND: Vasopressin (VP) shows promise as a pressor agent in animals and adult human cardiac arrest and resuscitation, but has not been studied for pressor effect in critically ill or arrested children. VP infusion is routine treatment for diabetes insipidus during brain death evaluation and organ recovery. We hypothesized that low dose VP infusion during organ recovery in critically ill children exerts a pressor effect, without major organ toxicity. METHODS: 34 VP-treated and 29 age-matched critically ill controls (C) < or =18 years were retrospectively reviewed during brain death evaluation and organ recovery. VP infusion protocol titrated VP dose clinically to urine output, with high variability. Pressor and inotrope management was titrated clinically to BP, cerebral perfusion and central venous pressures (when available) and peripheral perfusion with similar protocol targets for pre-load in VP and C groups. Outcome measures include dose, type and number of pressors and inotropes. Organ function was assessed at recovery and 48 h post-transplant by independent surgeon and transplant program organ function criteria. Analysis by Odds Ratio (OR), and chi-square. RESULTS: VP dose averaged 0.041+/-0.069 U/kg/h. Average baseline mean arterial pressure (MAP) before VP infusion was 79+/-17 mmHg VP and 76+/-14 mm Hg C (P=0.6). Subsequent average MAP were: 82+/-21 mmHgVP after VP infusion versus 71+/-16 mmHg C (P=0.01) and 80+/-14 mmHg VP versus 68+/-22 mmHg C (P=0.01). Ability to wean/stop pressors and inotropes was: dopamine (14/23) 42% VP versus (10/26) 38% C (P=0.75), dobutamine (4/7) 57% VP versus (0/6) 0% C (P=0.026), epinephrine (4/5) 80% VP versus (0/6) 0% C (P=0.006), norepinephrine/phenylephrine (4/4) 100% VP versus (2/5) 40% C (P=0. 057). Alpha agonist pressor dependence was successfully weaned from 7/9 (78%) VP versus 0/9 (0%) C: odds ratio=7.3, (P<0.01). There was no VP induced dysrhythmia, hypertension, anuria or toxicity reported. Good organ recovery function was not significantly different at recovery or 48 h post-transplant for kidney (79% VP versus 69% C, P=0.068), liver (87% VP versus 95% C, P=0.533), or heart (90% VP versus 71% C, P=0.11). CONCLUSIONS: Low dose vasopressin infusion exerts a pressor effect in critically ill children treated for diabetes insipidus during brain death and organ recovery. VP treated patients were 7.3 times more likely to wean from alpha agonists than comparably managed age matched controls, without adverse affect on transplant organ function. We speculate that further prospective assessment of VP safety and efficacy as a pressor adjunct for resuscitation of critically ill children is warranted.

Adolescent↗
PubMed2000

International Guidelines for Neonatal Resuscitation: An excerpt from the Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: International Consensus on Science. Contributors and Reviewers for the Neonatal Resuscitation Guidelines.

The International Guidelines 2000 Conference on Cardiopulmonary Resuscitation (CPR) and Emergency Cardiac Care (ECC) formulated new evidenced-based recommendations for neonatal resuscitation. These guidelines comprehensively update the last recommendations, published in 1992 after the Fifth National Conference on CPR and ECC. As a result of the evidence evaluation process, significant changes occurred in the recommended management routines for: * Meconium-stained amniotic fluid: If the newly born infant has absent or depressed respirations, heart rate <100 beats per minute (bpm), or poor muscle tone, direct tracheal suctioning should be performed to remove meconium from the airway. * Preventing heat loss: Hyperthermia should be avoided. * Oxygenation and ventilation: 100% oxygen is recommended for assisted ventilation; however, if supplemental oxygen is unavailable, positive-pressure ventilation should be initiated with room air. The laryngeal mask airway may serve as an effective alternative for establishing an airway if bag-mask ventilation is ineffective or attempts at intubation have failed. Exhaled CO(2) detection can be useful in the secondary confirmation of endotracheal intubation. * Chest compressions: Compressions should be administered if the heart rate is absent or remains <60 bpm despite adequate assisted ventilation for 30 seconds. The 2-thumb, encircling-hands method of chest compression is preferred, with a depth of compression one third the anterior-posterior diameter of the chest and sufficient to generate a palpable pulse. * Medications, volume expansion, and vascular access: Epinephrine in a dose of 0.01-0.03 mg/kg (0.1-0.3 mL/kg of 1:10,000 solution) should be administered if the heart rate remains <60 bpm after a minimum of 30 seconds of adequate ventilation and chest compressions. Emergency volume expansion may be accomplished with an isotonic crystalloid solution or O-negative red blood cells; albumin-containing solutions are no longer the fluid of choice for initial volume expansion. Intraosseous access can serve as an alternative route for medications/volume expansion if umbilical or other direct venous access is not readily available. * Noninitiation and discontinuation of resuscitation: There are circumstances (relating to gestational age, birth weight, known underlying condition, lack of response to interventions) in which noninitiation or discontinuation of resuscitation in the delivery room may be appropriate.

Blood Volume↗
PubMed1999

Osmotic response element enhancer activity. Regulation through p38 kinase and mitogen-activated extracellular signal-regulated kinase kinase.

Hypertonicity induces a group of genes that are responsible for the intracellular accumulation of protective organic osmolytes such as sorbitol and betaine. Two representative genes are the aldose reductase enzyme (AR, EC 1.1.1.21), which is responsible for the conversion of glucose to sorbitol, and the betaine transporter (BGT1), which mediates Na+-coupled betaine uptake in response to osmotic stress. We recently reported that the induction of BGT1 mRNA in the renal epithelial Madin-Darby canine kidney cell line is inhibited by SB203580, a specific p38 kinase inhibitor. In these studies we report that the hypertonic induction of aldose reductase mRNA in HepG2 cells as well as the osmotic response element (ORE)-driven reporter gene expression in transfected HepG2 cells are both inhibited by SB203580, suggesting that p38 kinase mediates the activation and/or binding of the transcription factor(s) to the ORE. Electrophoretic gel mobility shift assays with cell extracts prepared from SB203580-treated, hypertonically stressed HepG2 cells further show that the binding of trans-acting factors to the ORE is prevented and is thus also dependent on the activity of p38 kinase. Similarly, treatment of hypertonically stressed cells with PD098059, a mitogen-activated extracellular regulated kinase kinase (MEK1) inhibitor, results in inhibition of the hypertonic induction of aldose reductase mRNA, ORE-driven reporter gene expression, and the binding of trans-acting factors to the ORE. ORE-driven reporter gene expression was not affected by p38 kinase inhibition or MEK1 inhibition in cells incubated in iso-osmotic media. These data indicate that p38 kinase and MEK1 are involved in the regulation of the hyperosmotic stress response.

Aldehyde Reductase↗
PubMed1999

Resuscitation of the newly born infant: an advisory statement from the Pediatric Working Group of the International Liaison Committee on Resuscitation.

The International Liaison Committee on Resuscitation (ILCOR), with representation from North America, Europe, Australia, New Zealand, Africa, and South America, was formed in 1992 to provide a forum for liaison between resuscitation organizations in the developed world. This consensus document on resuscitation extends previously published ILCOR advisory statements on resuscitation to address the unique and changing physiology of the newly born infant within the first few hours following birth and the techniques for providing advanced life support.

Delivery Rooms↗
PubMed1999

Assessment of infant cardiopulmonary resuscitation rescue breathing technique: relationship of infant and caregiver facial measurements.

OBJECTIVE: Although a few infants ever require resuscitation, pediatric cardiopulmonary resuscitation (CPR) is performed most commonly under 1 year of age. American Heart Association guidelines for pediatric basic life support recommend that the caregiver place his/her mouth over the infant's mouth and nose to create a seal. The way CPR is currently taught encourages parents to attempt to seal the nose and open the mouth of the infant for rescue breathing. Recent studies suggest some parents may have trouble sealing an infant's nose and open mouth, but their study participant numbers were small. The aim of this report is to estimate, among a large cohort, the ability of caregivers to create a seal to their infants for the provision of rescue breathing according to current guidelines. METHODS: Infants up to 1 year of age (n = 281) and their caregivers were enrolled from Philadelphia pediatric offices. Facial measurements of the infants were obtained to estimate the length needed to seal the nose and open mouth, and the nose and closed mouth. Mouth widths of the caregivers were compared with their infant's nose and mouth lengths. One-way analysis of variance with Tukey's postmortem analysis and ordinary least squares means regression were used for univariate analysis with analysis of covariance used to control for the effects of multiple variables when necessary. Infant measurements were stratified into 3-month age quadrants to compare against matched adult caregiver measurements. RESULTS: Most caregivers (n = 270) were female. Females had smaller mouth widths than males (4.9 +/- 0.5 cm vs 5.2 +/- 0.5 cm). Infant nose and mouth length increased during the first year of life, with the largest increase between 0 to 3 months and 3 to 6 months (4.2 +/- 0.4 cm to 4.7 +/- 0.4 cm). As infant age and face length increased, a progressively higher rate of adult females were estimated not to be able to cover their infant's nose and open mouth, with the greatest increase again between 0 to 3 months (9%) and 3 to 6 months (40%). All female caregivers except 1 were predicted to be able to seal their infant's nose and closed mouth by our measurements. CONCLUSIONS: Infant face length grows rapidly during the first year of life with the most rapid growth occurring during the first 6 months. As early as 3 to 6 months of infant age, many adult caregivers' facial measurements, especially female, predict that they may not be able to form a seal for mouth-to-nose and open-mouth infant rescue breathing. By related measurements, nearly 100% of caregivers should be able to seal their infant's nose and closed mouth. If facial measurement predictions correlate with functional inability to seal an infant's nose and open mouth, infant CPR rescue breathing instruction will need to emphasize head position and creation of a seal over the mouth and nose without teaching that the mouth be open. pediatric basic life support, infant CPR, rescue breathing, sudden infant death syndrome, acute life-threatening episode.

Adult↗
PubMed1999

An advisory statement from the Pediatric Working Group of the International Liaison Committee on Resuscitation.

The International Liaison Committee on Resuscitation (ILCOR), with representation from North America, Europe, Australia, New Zealand, Africa, and South America, was formed in 1992 to provide a forum for liaison between resuscitation organizations in the developed world. This consensus document on resuscitation extends previously published ILCOR advisory statements on resuscitation to address the unique and changing physiology of the newly born infant within the first few hours after birth and the techniques for providing advanced life support. After careful review of the international resuscitation literature and after discussion of key and controversial issues, consensus was reached on almost all aspects of neonatal resuscitation, and areas of controversy and high priority for additional research were delineated. Consensus on resuscitation for the newly born infant included the following principles: Common or controversial medications (epinephrine, volume expansion, naloxone, bicarbonate), special resuscitation circumstances affecting care of the newly born, continuing care of the newly born after resuscitation, and ethical considerations for initiation and discontinuation of resuscitation are discussed. There was agreement that insufficient data exist to recommend changes to current guidelines regarding the use of 21% versus 100% oxygen, neuroprotective interventions such as cerebral hypothermia, use of a laryngeal mask versus endotracheal tube, and use of high-dose epinephrine. Areas of controversy are identified, as is the need for additional research to improve the scientific justification of each component of current and future resuscitation guidelines.

Documentation↗
PubMed1998

Abnormal renal and hepatic glucose metabolism in type 2 diabetes mellitus.

Release of glucose by liver and kidney are both increased in diabetic animals. Although the overall release of glucose into the circulation is increased in humans with diabetes, excessive release of glucose by either their liver or kidney has not as yet been demonstrated. The present experiments were therefore undertaken to assess the relative contributions of hepatic and renal glucose release to the excessive glucose release found in type 2 diabetes. Using a combination of isotopic and balance techniques to determine total systemic glucose release and renal glucose release in postabsorptive type 2 diabetic subjects and age-weight-matched nondiabetic volunteers, their hepatic glucose release was then calculated as the difference between total systemic glucose release and renal glucose release. Renal glucose release was increased nearly 300% in diabetic subjects (321+/-36 vs. 125+/-15 micromol/min, P < 0.001). Hepatic glucose release was increased approximately 30% (P = 0.03), but increments in hepatic and renal glucose release were comparable (2.60+/-0.70 vs. 2.21+/-0.32, micromol.kg-1.min-1, respectively, P = 0.26). Renal glucose uptake was markedly increased in diabetic subjects (353+/-48 vs. 103+/-10 micromol/min, P < 0.001), resulting in net renal glucose uptake in the diabetic subjects (92+/-50 micromol/ min) versus a net output in the nondiabetic subjects (21+/-14 micromol/min, P = 0.043). Renal glucose uptake was inversely correlated with renal FFA uptake (r = -0.51, P < 0.01), which was reduced by approximately 60% in diabetic subjects (10. 9+/-2.7 vs. 27.0+/-3.3 micromol/min, P < 0.002). We conclude that in type 2 diabetes, both liver and kidney contribute to glucose overproduction and that renal glucose uptake is markedly increased. The latter may suppress renal FFA uptake via a glucose-fatty acid cycle and explain the accumulation of glycogen commonly found in the diabetic kidney.

3-Hydroxybutyric Acid↗
PubMed1998

Effects of physiological hyperinsulinemia on systemic, renal, and hepatic substrate metabolism.

To determine the effect of physiological hyperinsulinemia on renal and hepatic substrate metabolism, we assessed systemic and renal glucose release and uptake, systemic and renal gluconeogenesis from glutamine, and certain aspects of systemic and renal glutamine and free fatty acid (FFA) metabolism. These were assessed under basal postabsorptive conditions and during 4-h hyperinsulinemic euglycemic clamp experiments in nine normal volunteers using a combination of isotopic techniques and renal balance measurements. Hepatic glucose release (HGR) and glutamine gluconeogenesis were calculated as the difference between systemic and renal measurements. Infusion of insulin suppressed systemic glucose release and glutamine gluconeogenesis by approximately 50% during the last hour of the insulin infusion (P < 0.001). Renal glucose release and glutamine gluconeogenesis decreased from 2.3 +/- 0.4 to 0.9 +/- 0.2 (P < 0.002) and from 0.52 +/- 0.07 to 0.14 +/- 0.03 micromol. kg-1. min-1 (P < 0.001), respectively. HGR and glutamine gluconeogenesis decreased from 8.7 +/- 0.4 to 4.5 +/- 0.5 (P < 0.001) and from 0.35 +/- 0.02 to 0.27 +/- 0.03 micromol. kg-1. min-1 (P < 0.002), respectively. Renal glucose uptake (RGU) increased from 1.61 +/- 0.19 to 2.18 +/- 0.25 micromol. kg-1. min-1 (P = 0.029) but accounted for only approximately 5% of systemic glucose disposal (40.6 +/- 4.3 micromol. kg-1. min-1). Both systemic and renal FFA clearance increased approximately fourfold (P < 0.001 for both). Nevertheless, renal FFA uptake decreased (P = 0.024) and was inversely correlated with RGU (r = -0.582, P = 0.011). Finally, insulin increased systemic glutamine release (P = 0.007), uptake (P < 0.005), and clearance (P < 0.001) but left renal glutamine uptake and release unaffected (P > 0.4 for both).

Adult↗
PubMed1997

Renal glucose production and utilization: new aspects in humans.

According to current textbook wisdom the liver is the exclusive site of glucose production in humans in the postabsorptive state. Although many animal and in vitro data have documented that the kidney is capable of gluconeogenesis, production of glucose by the human kidney in the postabsorptive state has generally been regarded as negligible. This traditional view is based on net balance measurements which, other than after a prolonged fast or during metabolic acidosis, showed no significant net renal glucose release. However, recent studies have refuted this view by combining isotopic and balance techniques, which have demonstrated that renal glucose production accounts for 25% of systemic glucose production. Moreover, these studies indicate that glucose production by the human kidney is stimulated by epinephrine, inhibited by insulin and is excessive in diabetes mellitus. Since renal glucose release is largely, if not exclusively, due to gluconeogenesis, it is likely that the kidney is as important a gluconeogenic organ as the liver. The most important renal gluconeogenic precursors appear to be lactate, glutamine and glycerol. The implications of these recent findings on the understanding of the physiology and pathophysiology of human glucose metabolism are discussed.

Animals↗