Fellowship:Harvard Medical School (2001) MA
Board Certification: Pediatric Anesthesia, American Board of Anesthesiology (2013)
Fellowship:University of Florida College of Medicine (1998) FL
Residency:University of Florida College of Medicine (1996) FL
Residency:Bowman Gray School of Medicine of Wake Forest University (1993) NC
Internship:Duke University School of Medicine (1991) NC
Medical Education:Ohio State University (1990) OH
Board Certification: Anesthesia, American Board of Anesthesiology (1998)
- Independent Studies (5)
Management of high-risk reentry sternotomy in an infant for repair of a giant pseudoaneurysm of the right ventricular outflow tract.
Annals of cardiac anaesthesia
2014; 17 (1): 59-61
Improved survival from congenital heart disease has led to an increasing need for complex reoperation by reentrant sternotomy. Peripheral cannulation and initiation of cardiopulmonary bypass prior to sternotomy to avoid the risk of cardiac injury and massive hemorrhage is an option in adults and larger children, but femoral vessel size precludes this strategy in infants. We describe the management of a high-risk reentry sternotomy in an infant for repair of a giant pseudoaneurysm after prior homograft repair of tetralogy of Fallot, using surgical dissection for suprasternal cannulation of the innominate artery and subxyphoid cannulation of the inferior vena cava.
View details for DOI 10.4103/0971-9784.124145
View details for PubMedID 24401306
Anesthesia and the developing brain: relevance to the pediatric cardiac surgery.
2014; 4 (2): 295-310
Anesthetic neurotoxicity has been a hot topic in anesthesia for the past decade. It is of special interest to pediatric anesthesiologists. A subgroup of children potentially at greater risk for anesthetic neurotoxicity, based on a prolonged anesthetic exposure early in development, are those children receiving anesthesia for surgical repair of congenital heart disease. These children have a known risk of neurologic deficit after cardiopulmonary bypass for surgical repair of congenital heart disease. Yet, the type of anesthesia used has not been considered as a potential etiology for their neurologic deficits. These children not only receive prolonged anesthetic exposure during surgical repair, but also receive repeated anesthetic exposures during a critical period of brain development. Their propensity to abnormal brain development, as a result of congenital heart disease, may modify their risk of anesthetic neurotoxicity. This review article provides an overview of anesthetic neurotoxicity from the perspective of a pediatric cardiac anesthesiologist and provides insight into basic science and clinical investigations as it relates to this unique group of children who have been studied over several decades for their risk of neurologic injury.
View details for DOI 10.3390/brainsci4020295
View details for PubMedID 24961762
Acute and sustained isoflurane neuroprotection: The effect of culture age and duration of oxygen and glucose deprivation
2013; 27 (4): 444-453
Organotypic hippocampal slice (OHS) cultures provide the opportunity to dissect factors influencing volatile anaesthetic neuroprotective efficacy. It was hypothesized that three conditions-OHS culture age, oxygen glucose deprivation (OGD) duration and day of evaluation for cell death after OGD-influence isoflurane's ability to provide acute and sustained protection against OGD-induced cell death.OHS were prepared from PND 9-11 rat pups and maintained in vitro for 0.5, 1, 2 or 3 weeks. The slices were exposed to OGD for 0, 10, 30, 60 or 90 minutes with or without 1.5% isoflurane. Sytox staining was used to determine the amount of cell death on post-OGD days 1, 3 and 7 and was compared to the amount of cell death in culture-age matched controls (no OGD).The duration of OGD necessary to produce cell death was inversely related to culture age. All culture ages showed evidence of both acute and sustained neuroprotection, but the magnitude of protection depended on OHS culture age, duration of OGD and post-OGD day of evaluation. In 1 and 2-week old slices early isoflurane neuroprotection was best observed with 90 minutes OGD and late isoflurane protection was best observed with 10 minutes OGD.In OHS, acute and sustained isoflurane neuroprotection in OGD-induced cell death is dependent on the conditions being studied.
View details for DOI 10.3109/02699052.2012.750755
View details for Web of Science ID 000316954300009
View details for PubMedID 23473549
- Anesthesia during surgical repair for congenital heart disease and the developing brain: neurotoxic or neuroprotective? PEDIATRIC ANESTHESIA 2011; 21 (5): 554-559