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      Implementation of Targeted Temperature Management in a Patient with Cerebral Arterial Gas Embolism

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          Abstract

          Cerebral arterial gas embolism (CAGE) shows various manifestations according to the quantity of gas and the brain areas affected. The symptoms range from minor motor weakness, headache, and confusion to disorientation, convulsions, hemiparesis, unconsciousness, and coma. A 46-year-old man was transferred to our emergency department due to altered sensorium. Immediately after a controlled ascent from 33 m of seawater, he complained of shortness of breath and rigid extremities, lapsing into unconsciousness. He was intubated at another medical center, where a brain computerized axial tomography scan showed no definitive abnormal findings. Pneumothorax and obstructing lesions were apparent in the left thorax of the computed tomography scan. Following closed thoracostomy, we provided hyperbaric oxygen therapy (HBOT) using U.S. Navy Treatment Table (USN TT) 6A. A brain magnetic resonance imaging diffusion image taken after HBOT showed acute infarction in both middle and posterior cerebral arteries. We implemented targeted temperature management (TTM) to prevent worsening of cerebral function in the intensive care unit. After completing TTM, we repeated HBOT using USN TT5 and started rehabilitation therapy. He fully recovered from the neurological deficits. This is the first case of CAGE treated with TTM and consecutive HBOTs suggesting that TTM might facilitate salvage of the penumbra in severe CAGE.

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          Most cited references13

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          Mild hypothermia inhibits inflammation after experimental stroke and brain inflammation.

          We previously showed that mild hypothermia protects against experimental stroke, even when cooling was delayed by 2 hours. Protection may be due in part to inhibiting inflammation. To clarify, we examined leukocyte infiltration, microglial activation, and adhesion molecule expression in models of stroke and pure brain inflammation. Rats underwent 2-hour middle cerebral artery occlusion (MCAO; n=36) or intravenous injection with 5 mg/kg lipopolysaccharide (LPS; n=22). Temperature was lowered to 33 degrees C for 2 hours or kept at 37 degrees C. In MCAO, cooling was applied intraischemically or on reperfusion (delayed). In the LPS model, cooling began after injection. One and 3 days later, brains were assessed for neutrophils, monocytes/microglia, major histocompatibility complex class II antigen, and intercellular adhesion molecule-1 (ICAM-1). One day after MCAO, both intraischemic and delayed hypothermia decreased ICAM-1 (51% and 60%, respectively, versus normothermia; P<0.001), monocytes (63% and 57%; P<0.01), and microglia (55% and 53%; P<0.001). Similar decreases were seen at 3 days for ICAM-1 (91% and 93%; P<0.001), monocytes (62% and 54%; P<0.01), and microglia (55% and 53%; P<0.001). In the LPS model, ED-1-positive cells were not observed in the brain, but hypothermia decreased ICAM-1 (26%; P<0.05), OX6 (56%; P<0.01), and microglia (47%; P<0.01) at 1 day. Mild hypothermia decreases inflammatory responses in both brain inflammation and stroke, implicating a direct anti-inflammatory effect of cooling. This suggests that hypothermia can attenuate factors contributing to delayed ischemic injury.
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            Clinical applications of targeted temperature management.

            Targeted temperature management (TTM) has been investigated experimentally and used clinically for over 100 years. The initial rationale for the clinical application of TTM, historically referred to as therapeutic hypothermia, was to decrease the metabolic rate, allowing the injured brain time to heal. Subsequent research demonstrated the temperature dependence of diverse cellular mechanisms including endothelial dysfunction, production of reactive oxygen species, and apoptosis. Consequently, modern use of TTM centers on neuroprotection following focal or global neurologic injury. Despite a solid basic science rationale for applying TTM in a variety of disease processes, including cardiac arrest, traumatic brain injury, ischemic stroke, neonatal ischemic encephalopathy, sepsis-induced encephalopathy, and hepatic encephalopathy, human efficacy data are limited and vary greatly from disease to disease. Ten years ago, two landmark investigations yielded high-quality data supporting the application of TTM in comatose survivors of out-of-hospital cardiac arrest. Additionally, TTM has been demonstrated to improve outcomes for neonatal patients with anoxic brain injury secondary to hypoxic ischemic encephalopathy. Trials are currently under way, or have yielded conflicting results in, examining the utility of TTM for the treatment of ischemic stroke, traumatic brain injury, and acute myocardial infarction. In this review, we place TTM in historic context, discuss the pathophysiologic rationale for its use, review the general concept of a TTM protocol for the management of brain injury, address some of the common side effects encountered when lowering human body temperature, and examine the data for its use in diverse disease conditions with in-depth examination of TTM for postarrest care and pediatric applications.
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              Updates in Decompression Illness.

              Decompression sickness and arterial gas embolism, collectively known as decompression illness (DCI), are rare but serious afflictions that can result from compressed gas diving exposures. Risk is primarily determined by the pressure-time profile but is influenced by several factors. DCI can present idiosyncratically but with a wide range of neurologic symptoms. Examination is critical for assessment in the absence of diagnostic indicators. Many conditions must be considered in the differential diagnosis. High-fraction oxygen breathing provides first aid but definitive treatment of DCI is hyperbaric oxygen.
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                Author and article information

                Journal
                Ther Hypothermia Temp Manag
                Ther Hypothermia Temp Manag
                ther
                Therapeutic Hypothermia and Temperature Management
                Mary Ann Liebert, Inc. (140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA )
                2153-7658
                2153-7933
                01 September 2018
                01 September 2018
                01 September 2018
                : 8
                : 3
                : 176-180
                Affiliations
                [ 1 ]Department of Emergency Medicine, Gangneung Asan Hospital, Ulsan University College of Medicine , Gangneung, Korea.
                [ 2 ]Department of Emergency Medicine, Ajou University School of Medicine , Suwon, Korea.
                Author notes
                [*]Address correspondence to: Sangchun Choi, MD, Department of Emergency Medicine, Ajou University School of Medicine 164 Worldcup-ro Yeongtong-gu, Suwon 16499, Korea, avenue59@ 123456ajou.ac.kr
                Article
                10.1089/ther.2018.0010
                10.1089/ther.2018.0010
                6138372
                30016198
                c277250b-b506-46eb-9384-169d4921017a
                © Oh et al., 2018; Published by Mary Ann Liebert, Inc.

                This Open Access article is distributed under the terms of the Creative Commons Attribution Noncommercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are cited.

                History
                Page count
                Figures: 3, References: 19, Pages: 5
                Categories
                Case Reports

                cerebral arterial gas embolism,hyperbaric oxygen therapy,targeted temperature management

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