Ascorbic acid combined with ibuprofen in hypoxic ischemic encephalopathy: a randomized controlled trial

Aly, Hany; Abd-Rabboh, L; El‐Dib, Mohamed; Nawwar, F; Hassan, H. M.; Aaref, Mansour M.; Abdelrahman, S Elmusharaf; El‐Sayed, Amr

doi:10.1038/jp.2009.1

Cited by 25 publications

(26 citation statements)

References 22 publications

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“…Antioxidants have not been studied in drowning. One randomized trial found no benefit from ascorbic acid and ibuprofen in asphyxiated neonates [203]. There were no articles associated with CA.…”

Section: Post-hypoxic Pharmacologymentioning

confidence: 99%

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Brain Resuscitation in the Drowning Victim

et al. 2012

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Drowning is a leading cause of accidental death. Survivors may sustain severe neurologic morbidity. There is negligible research specific to brain injury in drowning making current clinical management non-specific to this disorder. This review represents an evidence-based consensus effort to provide recommendations for management and investigation of the drowning victim. Epidemiology, brain-oriented prehospital and intensive care, therapeutic hypothermia, neuroimaging/monitoring, biomarkers, and neuroresuscitative pharmacology are addressed. When cardiac arrest is present, chest compressions with rescue breathing are recommended due to the asphyxial insult. In the comatose patient with restoration of spontaneous circulation, hypoxemia and hyperoxemia should be avoided, hyperthermia treated, and induced hypothermia (32–34 °C) considered. Arterial hypotension/hypertension should be recognized and treated. Prevent hypoglycemia and treat hyperglycemia. Treat clinical seizures and consider treating non-convulsive status epilepticus. Serial neurologic examinations should be provided. Brain imaging and serial biomarker measurement may aid prognostication. Continuous electroencephalography and N20 somatosensory evoked potential monitoring may be considered. Serial biomarker measurement (e.g., neuron specific enolase) may aid prognostication. There is insufficient evidence to recommend use of any specific brain-oriented neuroresuscitative pharmacologic therapy other than that required to restore and maintain normal physiology. Following initial stabilization, victims should be transferred to centers with expertise in age-specific post-resuscitation neurocritical care. Care should be documented, reviewed, and quality improvement assessment performed. Preclinical research should focus on models of asphyxial cardiac arrest. Clinical research should focus on improved cardiopulmonary resuscitation, re-oxygenation/reperfusion strategies, therapeutic hypothermia, neuroprotection, neurorehabilitation, and consideration of drowning in advances made in treatment of other central nervous system disorders.

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Section: Post-hypoxic Pharmacologymentioning

confidence: 99%

“…2 LOE 5 studies showing benefit [205, 207], and 3 showing a neutral effect in CA or HIE [203, 206, 208]. …”

Section: Post-hypoxic Pharmacologymentioning

confidence: 99%

Brain Resuscitation in the Drowning Victim

et al. 2012

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“…In human preterm neonates (<28 weeks gestation) indomethacin reduces white matter loss [137] although ibuprofen combined with ascorbic acid treatment in neonates reportedly has little effect on brain injury after severe HI [138]. Consistent with previous studies [86, 139–142], we have shown that COX-2 is elevated in the brain after P3 HI and that ibuprofen significantly prevents this effect as well as P3 HI-induced increases in numbers of activated microglia, IL-1 β , and TNF- α levels [143].…”

Section: Role Of Neuroinflammation In Producing Neuronal Injurymentioning

confidence: 99%

Disruption of the Serotonergic System after Neonatal Hypoxia-Ischemia in a Rodent Model

Buller

Wixey

Reinebrant

2012

Neurology Research International

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Identifying which specific neuronal phenotypes are vulnerable to neonatal hypoxia-ischemia, where in the brain they are damaged, and the mechanisms that produce neuronal losses are critical to determine the anatomical substrates responsible for neurological impairments in hypoxic-ischemic brain-injured neonates. Here we describe our current work investigating how the serotonergic network in the brain is disrupted in a rodent model of preterm hypoxia-ischemia. One week after postnatal day 3 hypoxia-ischemia, losses of serotonergic raphé neurons, reductions in serotonin levels in the brain, and reduced serotonin transporter expression are evident. These changes can be prevented using two anti-inflammatory interventions; the postinsult administration of minocycline or ibuprofen. However, each drug has its own limitations and benefits for use in neonates to stem damage to the serotonergic network after hypoxia-ischemia. By understanding the fundamental mechanisms underpinning hypoxia-ischemia-induced serotonergic damage we will hopefully move closer to developing a successful clinical intervention to treat neonatal brain injury.

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“…111 Only one randomized-controlled clinical study in term infants who were asphyxiated has been performed, which found that the combination of AA with ibuprofen had no effect on outcome at 6 months of age. 112 …”

Section: Resultsmentioning

confidence: 99%