Robert E. Rosenthal, MD

Yale University; BA Chemistry 1975

New York University School of Medicine; MD 1979

George Washington University School of Medicine; Residency in Internal Medicine 1979-1982

I had the great opportunity to practice and teach Emergency Medicine for over 25 years. During that period I witnessed remarkable advances in the care of patients suffering cardiovascular catastrophes, yet the continued inability to reverse brain injury following cardiac arrest remains personally frustrating. Although we are now more efficient in re-starting the arrested heart, and despite the demonstrated neuroprotection of post-resuscitative hypothermia, neurologic injury continues to complicate the recovery of most CA survivors. I find it tragic to “successfully” resuscitate a patient, only to find out days later that he/she remains severely neurologically impaired. 

            If one is to prevent neurologic injury, one must first understand the complex physiological cascade seen following ischemia/reperfusion.  In an attempt to closely model human resuscitation, and in close collaboration with my colleague, Dr. Gary Fiskum, I have developed one of the few large animal models of CA and resuscitation (ROSC). Because of close physiologic similarities to humans, this model of cardiac arrest closely mimics human CA, and allows us to provide critical care similar to that seen in human ICU’s. In recent years, our laboratory has devoted its major efforts to the study of post-resuscitative ventilation; i.e., how we provide O₂-enriched breaths to the CA survivor.  Our lab and others demonstrated significant oxidative damage to brain lipids and proteins following CA/ROSC. We hypothesized that breathing supplemental oxygen immediately post-ROSC would worsen this oxidative injury.  We showed that breathing 100% O₂ for as little as one hr after ROSC increases oxidative injury to brain lipids as well as key proteins of metabolism, worsening clinical neurological outcome. Realizing that most CA survivors will require some inspired O₂ because of underlying cardiopulmonary disease, we have since perfected a clinical protocol using pulse oximetry to rapidly lower inspired O₂ following ROSC to physiological levels, while simultaneously avoiding clinical hypoxia. Using this model, we were able to demonstrate significant neuroprotection as well as decreasing (but not eliminating) inflammation, recently shown to be a prominent component of post-ROSC neuropathology. The critical importance of these pre-clinical results has recently been supported by retrospective reports linking elevated post-resuscitative blood oxygen concentrations with increased morbidity and mortality following human cardiac arrest. 

In addition to my research interests, I am actively involved clinically as the Director of the Hyperbaric Medicine program at the R Adams Cowley Shock Trauma Center.  We run a large multiplace hyperbaric chamber which responds to emergent and non-emergent patients 24/7.  Along with a staff of four other Emergency Physicians, critical care nurses and respiratory therapists, we routinely treat patients with such emergent contiditons as necrotizing fasciitis, carbon monoxide poisoning, arterial gas embolus, and decompression sickness, as well as more chronic conditions as diabetic foot ulcers and radiation soft tissue injury.  Our chamber is the only chamber in Maryland which accepts emergency patients.  We routinely treat patients from all corners of Maryland as well as from several surrounding states.  

Additionally, I serve as chair of the Institutional Review Board for the University of Maryland Baltimore.  In that role I assist in providing ethical and regulatory review for the close to 2000 active human subjects research protocols at the UMB.  This gives me the opportunity to not only provide regulatory oversight but also to continuously learn ab out the broad spectrum of human subject research occurring daily at the University of Maryland.  

Cardiac Arrest; Stroke; Traumatic Brain Injury; Hyperoxia; Hypobaria

Most relevant publications

1. Richards, E.M., Rosenthal, R.E., Kristian, T., and Fiskum, G., Postischemic hyperoxia reduces hippocampal pyruvate dehydrogenase activity, Free Rad. Biol. Med. 40: 1960-1970 (2006)PMID: 16716897
2. Vereczki, V., Martin, E., Rosenthal, R.E., Hof, P.R., Hoffman, G.E., and Fiskum, G., Normoxic resuscitation after cardiac arrest protects against hippocampal oxidative stress, metabolic dysfunction, and neuronal death, J. Cereb. Blood Flow Metab., 26: 821-35 (2006). PMID: 16251887
3. Balan, I.S., Fiskum, G., Hazelton, J., Cotto-Cumba, C., and Rosenthal, R.E., Oximetry-guided reoxygenation improves neurological outcome after experimental cardiac arrest, Stroke 37: 3008-3013 (2006). PMID: 17068310
4. Richards, E.M., Fiskum, G., Rosenthal, R.E., Hopkins, I., and McKenna, M.C., Hyperoxic reperfusion following global ischemia decreases hippocampal energy metabolism, Stroke 38: 1578-1584 (2007) PMID: 17413048
5. Hazelton JL, Balan I, Elmer GI, Kristian T, Rosenthal R.E, Krause G, Sanderson TH, Fiskum G.  Hyperoxic reperfusion after global cerebral ischemia promotes inflammation and long-term hippocampal neuronal death. J Neurotrauma 27(4):753-62 (2010).  PMID: 20059303
6. Rosenthal RE, Chanderbhan R, Marshall G, Fiskum G. Prevention of post-ischemic brain lipid conjugated diene production and neurological injury by hydroxyethyl starch-conjugated deferoxamine. Free Radic Biol Med. 1992;12(1):29-33. PubMed PMID: 1371490