The Treatment of Pediatric Gastroenteritis: A Comparative Analysis of Pediatric Emergency Physicians’ Practice Patterns

Freedman, Stephen B.; Sivabalasundaram, Vithika; Bohn, V; Powell, Elizabeth C.; Johnson, David W.; Boutis, Kathy

doi:10.1111/j.1553-2712.2010.00960.x

Cited by 66 publications

(53 citation statements)

References 34 publications

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“…In this study we have addressed the hypothesis that rotavirus infection triggers the release antagonists, but no etiology is done 90 .…”

Section: Results and Discussion Of The Papersmentioning

confidence: 99%

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Rotavirus Disease Mechanisms Diarrhea, Vomiting and Inflammation : How and Why

Hagbom¹

2015

Linköping University Medical Dissertations

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Rotavirus infections cause diarrhea and vomiting that can lead to severe dehydration. Despite extensive tissue damage and cell death, the inflammatory response is very limited. The focus of this thesis was to study pathophysiological mechanisms behind diarrhea and vomiting during rotavirus infection and also to investigate the mechanism behind the limited inflammatory response. An important discovery in this thesis was that rotavirus infection and the rotavirus toxin NSP4 stimulate release of the neurotransmitter serotonin from intestinal sensory enterochromaffin cells, in vitro and ex vivo. Interestingly, serotonin is known to be a mediator of both diarrhea and vomiting. Moreover, mice pups infected with rotavirus responded with central nervous system (CNS) activation in brain structures associated with vomiting, thus indicating a cross-talk between the gut and brain in rotavirus disease. Our finding that rotavirus infection activates the CNS led us to address the hypothesis that rotavirus infection not only activates the vagus nerve to stimulate vomiting, but also suppresses the inflammatory response via the cholinergic anti-inflammatory pathway, both of which are mediated by activated vagal afferent nerve signals into the brain stem. We found that mice lacking an intact vagus nerve, and mice lacking the α7 nicotine acetylcholine receptor (nAChR), being involved in cytokine suppression from macrophages, responded with a higher inflammatory response. Moreover, stimulated cytokine release from macrophages, by the rotavirus toxin NSP4, could be attenuated by nicotine, an agonist of the α7 nAChR. Thus, it seems most reasonable that the cholinergic anti-inflammatory pathway contributes to the limited inflammatory response during rotavirus infection. Moreover, rotavirus-infected mice displayed increased intestinal motility at the onset of diarrhea, which was not associated with increased intestinal permeability. The increased motility and diarrhea in infant mice could be attenuated by drugs acting on the enteric nervous system, indicating the importance and contribution of nerves in the rotavirus mediated disease. In conclusion, this thesis provides further insight into the pathophysiology of diarrhea and describe for the first time how rotavirus and host cross-talk to induce the vomiting reflex and limit inflammation. Results from these studies strongly support our hypothesis that serotonin and activation of the enteric nervous system and CNS contributes to diarrhea, vomiting and suppression of the inflammatory response in rotavirus disease

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“…In this study we have addressed the hypothesis that rotavirus infection triggers the release antagonists, but no etiology is done 90 .…”

Section: Results and Discussion Of The Papersmentioning

confidence: 99%

“…A future alternative treatment strategy can be to prevent dehydration by reducing vomiting through use of 5--HT 3 receptor antagonists. In the US and Canada 5--HT 3 receptor antagonist are already used to treat vomiting in children with acute gastroenteritis, although no etiology is done 90 .…”

Section: Treatment and Preventionmentioning

confidence: 99%

Rotavirus Disease Mechanisms Diarrhea, Vomiting and Inflammation : How and Why

Hagbom¹

2015

Linköping University Medical Dissertations

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“…A recent analysis of practice patterns revealed that 67% of U.S. pediatric emergency physicians routinely administer antiemetics to toddlers and young children, with ondansetron as the agent of choice of those responding. 46 Ondansetron was 1 of the 10 most frequently prescribed drugs in children 2 to 17 years of age: fifth most common in 2 to 4 year olds (19 occurrences per 100 hospitalizations), second most common in 5 to 11 year olds (30 occurrences per 100 hospitalizations), and most common in 12 to 17 year olds (30 occurrences per 100 hospitalizations). 47 Use in this condition is despite the fact that published guidelines do not recommend routine administration.…”

Section: Discussionmentioning

confidence: 99%

Fatal Cardiac Arrest in 2 Children

Brenner¹,

Boucher²

2016

Pediatr Emer Care

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“…There is significant evidence that ondansetron is associated with a much lower rate of side-effects than other antiemetics and that it decreases the risk of persistent vomiting, the use of intravenous fluids, and hospital admission in children [44 ,45]. One study that evaluated current gastroenteritis therapies by pediatric emergency care providers in the United States and Canada found that ondansetron is routinely administered for mild-to-moderate dehydration with persistent vomiting in patients who failed oral rehydration attempts [46 ]. DeCamp et al [47] published a recent meta-analysis that reviewed six ondansetron-based studies over the past decade.…”

Section: Use Of Antiemetics With Rapid Fluid Resuscitationmentioning

confidence: 98%

Pediatric rapid fluid resuscitation

Simpson

Teach

2011

Current Opinion in Pediatrics

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Rapid fluid resuscitation is most commonly used for children with moderate-to-severe dehydration, or for patients in shock to restore circulation. Concerns regarding potential for fluid overload and electrolyte disturbances and regarding the method of rehydration (i.e., enteral versus parenteral) raise some debate about the safety and efficacy of rapid fluid resuscitation in the pediatric patient. Recent studies show that early, aggressive fluid resuscitation of up to 60 ml/kg within 1-2 h may be necessary to replenish circulating intravascular fluid volume. Complications of severe electrolyte disturbances, cerebral edema, or uncontrolled hemorrhage are uncommon and can often be avoided with early clinical assessment and reassessments throughout the resuscitation. In the mildly to moderately dehydrated child, enteral fluid resuscitation with the aid of an antiemetic such as ondansetron can be as effective and efficient as intravenous fluid resuscitation.

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The Treatment of Pediatric Gastroenteritis: A Comparative Analysis of Pediatric Emergency Physicians’ Practice Patterns

Cited by 66 publications

References 34 publications

Rotavirus Disease Mechanisms Diarrhea, Vomiting and Inflammation : How and Why

Rotavirus Disease Mechanisms Diarrhea, Vomiting and Inflammation : How and Why

Fatal Cardiac Arrest in 2 Children

Pediatric rapid fluid resuscitation

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