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Review
. 2012 Dec;17(3):441-67.
doi: 10.1007/s12028-012-9747-4.

Brain resuscitation in the drowning victim

Affiliations
Review

Brain resuscitation in the drowning victim

Alexis A Topjian et al. Neurocrit Care. 2012 Dec.

Abstract

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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Figures

Fig. 1
Fig. 1
Forrest plot of studies that used therapeutic hypothermia in the treatment of asphyxia and drowning. RR of good neurologic survival is presented. A value above 1 favors therapeutic hypothermia. Jacobs et al. [90] and Shah [91] were meta-analyses. N = total number of patients studied
Fig. 2
Fig. 2
EEG patterns that may be seen in patients following anoxic brain injury. a Normal, b burst suppression, c seizures in a patient with discontinuous background, and d comatose patient with low amplitude and non-reactive background
Fig. 3
Fig. 3
Magnetic resonance imaging (MRI) of the brain in two children with divergent outcomes after drowning accidents. a–c A 4-year-old cold-water drowning victim who presented with a core temperature of 23 °C. MRI 4 days after the accident was normal as was the child’s neurological examination. d–f A 13-month-old bathtub-drowning victim who presented with a core temperature of 33 °C. MRI 4 days after the accident showed increased signal and restricted diffusion in the basal ganglia (arrows), particularly in the globus pallidus as well as the thalami. In addition, there are areas of restricted diffusion in the white matter bilaterally and to a lesser degree of the cortex most marked in the occipital and parietal regions (open arrows). This child remained in a minimally conscious state. DWI diffusion-weighted imaging, ADC apparent diffusion coefficient
Fig. 4
Fig. 4
Responses to asphyxial versus ventricular fibrillation cardiac arrest. Schematic based on the seminal work of Vaagenes et al. [249] using canine models of asphyxial versus ventricular fibrillation cardiac arrest. Despite identical (10 min) no flow durations in both models, a much more severe neuropathology was observed after asphyxial arrest. This was accompanied by poorer neurological outcome. Notably, the no flow period in asphyxial cardiac arrest was preceded in these studies by a period of ~ 7 min during which hypoxic perfusion of the brain occurred. The asphyxia scenario is highly germane to the pathobiology of drowning and thus suggests a very challenging and unique condition for the development of novel therapies

References

    1. Astrup J, Rehncrona S, Siesjo BK. The increase in extracellular potassium concentration in the ischemic brain in relation to the preischemic functional activity and cerebral metabolic rate. Brain Res. 1980;199(1):161–74. - PubMed
    1. Smith ML, Auer RN, Siesjo BK. The density and distribution of ischemic brain injury in the rat following 2–10 min of forebrain ischemia. Acta Neuropathol. 1984;64(4):319–32. - PubMed
    1. Petito CK, Feldmann E, Pulsinelli WA, Plum F. Delayed hippocampal damage in humans following cardiorespiratory arrest. Neurology. 1987;37(8):1281–6. - PubMed
    1. van Beeck EF, Branche CM, Szpilman D, Modell JH, Bierens JJ. A new definition of drowning: towards documentation and prevention of a global public health problem. Bull World Health Organ. 2005;83(11):853–6. - PMC - PubMed
    1. Papa L, Hoelle R, Idris A. Systematic review of definitions for drowning incidents. Resuscitation. 2005;65(3):255–64. - PubMed