Targeted temperature management in intensive care of severe traumatic brain injury
Background. Hyperthermia causes cerebral injury and worsens neurological outcomes in severe traumatic brain injury (TBI). The aim of the work was to study neurological outcomes in patients with severe TBI and refractory hyperthermia, while providing the target temperature management (TTM) with using an esophageal cooling device in the intensive care as compared to the control group. Materials and methods. Twenty patients aged 23 to 54 years with a diagnosis of severe TBI were examined. They were divided into 2 groups: I (n = 10) — these patients underwent a standard intensive care based on the international guidelines for the management of severe head injury (2007, 2016); II group (n = 10) — the TTM was carried out with the help of the Blanketrol II (CSZ, USA) and invasive technology using the Esophageal Cooling Device (ACT, USA) to achieve normothermia in the range of 36.5–37 C. The indication for the use of TTM was the development of febrile and hectic fevers of non-infectious origin in patients with TBI. The trigger for the start of TTM was hyperthermia ≥ 38.3 C, which can not be ameliorated by pharmacological correction with antipyretics. The TTM was performed to achieve the target value of the body’s normothermia. Exclusion criterion from the study was a neurological deficit ≤ 4 on the Glasgow Coma Scale (GCS). All patients were assessed neurological status on the GCS at the stages: initially, on days 5, 10 and at the time of discharge from the hospital. The outcomes of the TTM were determined on the scale of Cerebral Performance Categories (CPC) at the stages: the maximum score when in the ICU and at the time of discharge. Results. There were no deaths in any group of patients examined. An analysis of the dynamics of neurologic recovery at the time of discharge from the hospital showed a significant improvement in the group of patients using TTM on the GCS in comparison with control group. During the analysis of poor outcomes, in the group using TTM, a decrease in the severity of neurologic damage was revealed compared to the control group of patients. Thus, the most unfavorable outcome of severe TBI as a delay of neurologic recovery at the level of the apallic syndrome or akinetic mutism of the corresponding CPC-4 in the first group developed in 30 % of patients, while in the second group — in no patient. We did not find any clinically significant side effects when using the Esophageal Cooling Device. It should be emphasized that factors limiting the application of the Esophageal Cooling Device for the purpose of arresting hyperthermia of the central origin have been identified, such as the inability to conduct enteral nutrition and the lesser accuracy of monitoring the body temperature when using a rectal sensor. Limitations of this study are a small sample of patients and heterogeneity of traumatic brain injury, which requires additional studies. Conclusions. An analysis of the dynamics of neurologic recovery after severe TBI at the time of discharge from the hospital showed a significant improvement in the group of patients using the TTM of 13.50 ± 1.36 points on the GCS in comparison with 11.50 ± 1.80 points in the control group (p < 0.05). According to the best scores on the scale of outcomes of the CPC when in the ICU, a good neurologic recovery was achieved in 20 and 50 % of the corresponding CPC 1–2, and a poor neurologic recovery at the level of the CPC 3–4 was found in 70 and 50 % of patients in the control group and the main group with the application of TTM, respectively. At the discharge from the hospital, neurologic recovery at the level of CPC 1–2 was detected in 30 compared to 80 %, and at the level of CPC 3–4 — in 70 and 20 % of patients in the control and TTM group, respectively. Intergroup differences in mean values on the scale of the CPC at the time of discharge from the hospital were reliable: 2.90 ± 0.94 and 2.00 ± 0.77 (P = 0.02) in the control and TTM groups, respectively. The use of target temperature management to maintain normothermia creates more favorable conditions for a more complete restoration of impaired neurological functions after severe TBI.
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Fernandez A., Schmidt J.M., Claassen J. et al. Fever after subarachnoid hemorrhage: risk factors and impact on outcome // Neurology. 2007; 68(13): 1013–1019. doi:10.1212/01.wnl.0000258543.45879.f5
Stocchetti N., Rossi S., Zanier E.R. et al. Pyrexia in head-injured patients admitted to intensive care // Intensive Care Med. 2002; 28(11):1555–1562.doi: 10.1007/s00134-002-1513-1
Walter E.J., Carraretto М.The neurological and cognitive consequences of hyperthermia // Critical Care. 2016. 20: 199. doi: 10.1186/s13054-016-1376-4.
White M.G., Luca L.E., Nonner D. et al. Cellular mechanisms of neuronal damage from hyperthermia // Prog. Brain Res. 2007; 162: 347–371.doi: 10.1016/S0079-6123(07)63001-5
Kiyatkin E.A. Physiological and pathological brain hyperthermia // Prog. Brain Res. 2007; 162: 219–243.doi:10.1016/S0079-6123(06)62012-8
Kochanek P.M., Jackson T.C. The brain and hypothermia – from Aristotle to Target Temperature Management // Crit. Care Med. 2017; 45: 305-310.doi: 10.1097/CCM.0000000000002182
Nielsen N. Wetterslev J.,Cronberg T. et al. Target temperature management at 330C versus 360C after cardiac arrest // NEJM. 2013; 369: 2197-2206.doi:10.1056/NEJMoa1310519
CarneyN., TottenA.M.,O’ReillyC. et al.Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Brain Trauma Foundation // Neurosurgery. 2017; 80(1): 6-15. doi: 10.1227/NEU.0000000000001432.
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