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Biomedical subjects

Anne-Marie Guerguerian

Publications and source records attributed to Anne-Marie Guerguerian.

5 recordsLinked to original sources
PubMed2006

Clinical trials in pediatric traumatic brain injury: unique challenges and potential responses.

In order to optimize pediatric traumatic brain injury translational and clinical research, scientific and ethical challenges need to be recognized and addressed. Having recently conducted a multisite phase II safety/feasibility trial of magnesium sulfate as a neuroprotective agent, we supplement our own experience by a mini review of similar studies, identifying challenges and possible responses from the perspective of families, investigators, funding agencies and society.

Brain Injuries↗
PubMed2004

Cerebrovascular disorders.

Arterial ischemic stroke is being recognized more commonly in the pediatric population. The etiologies differ greatly from those seen in adults. The most common etiologies are congenital heart disease and sickle cell disease. Children may present with or without hemiparesis and may have fever, headache, and depressed level of consciousness. A high index of suspicion is needed to diagnose stroke. Although clinical studies are scarce in children, besides early diagnosis, early specialized care with careful attention to detail ensuring adequate oxygenation and ventilation, prevention of hyperthermia and seizures, and maintenance of blood pressure and metabolic balance are important and likely improve outcome in these children. Selective children may also benefit from anticoagulant therapy, and, as the interval to diagnosis decreases, thrombolytic therapy may become an option although safety data are required. Children with acute stroke should be rapidly transported to and cared for in a pediatric center with a specialized stroke team or access to acute stroke protocols.

Adult↗
PubMed2003

Hypothermia for 24 hours after asphyxic cardiac arrest in piglets provides striatal neuroprotection that is sustained 10 days after rewarming.

The neuroprotective effect of hypothermia instituted after resuscitation from asphyxic cardiac arrest has not been studied in immature brain, particularly in a large animal model with recovery periods greater than 4 d. Moreover, protection from severe hypoxia seen with 3 h of hypothermia was reported to be lost when hypothermic duration was extended to 24 h in unsedated piglets, in contrast to the neuroprotection reported by 72 h of intrauterine head cooling in fetal sheep. Piglets (5-7 postnatal days) were subjected to asphyxic cardiac arrest followed by 24 h of either hypothermia (34 degrees C) or normothermia (38.5-39 degrees C). Comparisons were made with normothermic and hypothermic surgical sham animals without asphyxia. All of these groups were sedated, paralyzed, and mechanically ventilated for the first 24 h to prevent shivering and possible depletion of glucose stores. Hypothermia per se did not cause remarkable structural abnormalities. Ischemic damage was evaluated in putamen at 1 d of recovery without rewarming and at 11 d (10 d +/- SD after rewarming). Ischemic cytopathology affected 60 +/- 12% of neurons in putamen of normothermic animals compared with 9 +/- 6% in hypothermic animals at 1 d of recovery without rewarming. At 11 d of recovery from hypoxia-ischemia, the density of viable neurons (neuron profiles/mm2) in putamen was markedly reduced in normothermic animals (81 +/- 40) compared with hypothermic animals (287 +/- 22), which was the same as in sham normothermic (271 +/- 21), sham hypothermic (288 +/- 46) and naïve animals (307 +/- 51). These data demonstrate that 24 h of hypothermia at 34 degrees C with sedation and muscle relaxation after asphyxic cardiac arrest prevents necrotic striatal neuronal cell death in immature brain before rewarming, and that the effect is sustained at 11 d after injury without deleterious side effects.

Acute Disease↗
PubMed2003

Massive diltiazem overdose treated with extracorporeal membrane oxygenation.

OBJECTIVE: To describe a case of massive diltiazem overdose with a good outcome achieved after early and aggressive supportive therapy. DESIGN: Case report. SETTING: Pediatric Critical Care Unit. PATIENT: Sixteen-year-old adolescent girl. MEASUREMENTS AND MAIN RESULTS: A 16-yr-old adolescent girl presented to the emergency department 6 hrs after the intentional ingestion of 40 300-mg sustained-release diltiazem tablets (12 g of Cardura CD). She was hypotensive and required a glucagon and epinephrine infusion despite initial fluid resuscitation with saline and intravenous calcium (1 g). Multiple asystolic cardiac arrests ensued which became increasingly refractory to high-dose epinephrine. Hemodynamic support was achieved with a 48-hr period of extracorporeal membrane oxygenation for atrial standstill. Severe multiorgan dysfunction ensued (cardiac, neurologic, renal, hepatic, gastrointestinal, hematologic, and metabolic). Plasma diltiazem and its metabolites were measured and its half-life was reported between 28 and 48 hrs. A sustained decline in plasma diltiazem levels and its metabolites was not observed after two periods of charcoal hemoperfusion. Recovery of organ function occurred with sinus rhythm noted on the ninth day. The patient made a full recovery and was discharged from the critical care unit after 15 days. CONCLUSIONS: Although massive calcium channel blocker overdose can produce profound and prolonged cardiac or multiorgan dysfunction, its toxic effects may be reversible. Supportive therapy, particularly of the cardiovascular system, is the most important goal.

Adolescent↗