Acute and Critical Care

Original Article

Basic science and research
Therapeutic hypothermia reduces inflammation and oxidative stress in the liver after asphyxial cardiac arrest in rats: Yoonsoo Park, Ji Hyeon Ahn, Tae-Kyeong Lee, Bora Kim, Hyun-Jin Tae, Joon Ha Park, Myoung Cheol Shin, Jun Hwi Cho, Moo-Ho Won; Acute Crit Care. 2020;35(4):286-295. Published online November 30, 2020; DOI: https://doi.org/10.4266/acc.2020.00304

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Background
Few studies have evaluated the effects of hypothermia on cardiac arrest (CA)-induced liver damage. This study aimed to investigate the effects of hypothermic therapy on the liver in a rat model of asphyxial cardiac arrest (ACA).
Methods
Rats were subjected to 5-minute ACA followed by return of spontaneous circulation (RoSC). Body temperature was controlled at 33°C±0.5°C or 37°C±0.5°C for 4 hours after RoSC in the hypothermia group and normothermia group, respectively. Liver tissues in each group were collected at 6 hours, 12 hours, 1 day, and 2 days after RoSC. To examine hepatic inflammation, mast cells were stained with toluidine blue. Superoxide anion radical production was evaluated using dihydroethidium fluorescence straining and expression of endogenous antioxidants (superoxide dismutase 1 [SOD1] and SOD2) was examined using immunohistochemistry.
Results
There were significantly more mast cells in the livers of the normothermia group with ACA than in the hypothermia group with ACA. Gradual increase in superoxide anion radical production was found with time in the normothermia group with ACA, but production was significantly suppressed in the hypothermia group with ACA relative to the normothermia group with ACA. SOD1 and SOD2 levels were higher in the hypothermia group with ACA than in the normothermia group with ACA.
Conclusions
Experimental hypothermic treatment after ACA significantly inhibited inflammation and superoxide anion radical production in the rat liver, indicating that this treatment enhanced or maintained expression of antioxidants. Our findings suggest that hypothermic therapy after CA can reduce mast cell-mediated inflammation through regulation of oxidative stress and the expression of antioxidants in the liver.

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Hypothermic treatment reduces matrix metalloproteinase-9 expression and damage in the liver following asphyxial cardiac arrest in rats
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Review Article

CPR/Resuscitation
Management of post-cardiac arrest syndrome: Youngjoon Kang; Acute Crit Care. 2019;34(3):173-178. Published online August 31, 2019; DOI: https://doi.org/10.4266/acc.2019.00654

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Abstract PDF

Post-cardiac arrest syndrome is a complex and critical issue in resuscitated patients undergone cardiac arrest. Ischemic-reperfusion injury occurs in multiple organs due to the return of spontaneous circulation. Bundle of management practicies are required for post-cardiac arrest care. Early invasive coronary angiography should be considered to identify and treat coronary artery obstructive disease. Vasopressors such as norepinephrine and dobutamine are the first-line treatment for shock. Maintainance of oxyhemoglobin saturation greater than 94% but less than 100% is recommended to avoid fatality. Target temperature therapeutic hypothermia helps to resuscitated patients. Strict temperature control is required and is maintained with the help of cooling devices and monitoring the core temperature. Montorings include electrocardiogram, oxymetry, capnography, and electroencephalography (EEG) along with blood pressue, temprature, and vital signs. Seizure should be treated if EEG shows evidence of seizure or epileptiform activity. Clinical neurologic examination and magnetic resonance imaging are considered to predict neurological outcome. Glycemic control and metabolic management are favorable for a good neurological outcome. Recovery from acute kidney injury is essential for survival and a good neurological outcome.

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Original Article

CPR/Resuscitation
Comparison between Gel Pad Cooling Device and Water Blanket during Target Temperature Management in Cardiac Arrest Patients: Yoon Sun Jung, Kyung Su Kim, Gil Joon Suh, Jun-Hwi Cho; Acute Crit Care. 2018;33(4):246-251. Published online November 30, 2018; DOI: https://doi.org/10.4266/acc.2018.00192

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Abstract PDF Supplementary Material

Background
Target temperature management (TTM) improves neurological outcomes for comatose survivors of out-of-hospital cardiac arrest. We compared the efficacy and safety of a gel pad cooling device (GP) and a water blanket (WB) during TTM.
Methods
We performed a retrospective analysis in a single hospital, wherein we measured the time to target temperature (<34°C) after initiation of cooling to evaluate the effectiveness of the cooling method. The temperature farthest from 33°C was selected every hour during maintenance. Generalized estimation equation analysis was used to compare the absolute temperature differences from 33°C during the maintenance period. If the selected temperature was not between 32°C and 34°C, the hour was considered a deviation from the target. We compared the deviation rates during hypothermia maintenance to evaluate the safety of the different methods.
Results
A GP was used for 23 patients among of 53 patients, and a WB was used for the remaining. There was no difference in baseline temperature at the start of cooling between the two patient groups (GP, 35.7°C vs. WB, 35.6°C; P=0.741). The time to target temperature (134.2 minutes vs. 233.4 minutes, P=0.056) was shorter in the GP patient group. Deviation from maintenance temperature (2.0% vs. 23.7%, P<0.001) occurred significantly more frequently in the WB group. The mean absolute temperature difference from 33°C during the maintenance period was 0.19°C (95% confidence interval [CI], 0.17°C to 0.21°C) in the GP group and 0.76°C (95% CI, 0.71°C to 0.80°C) in the WB group. GP significantly decreased this difference by 0.59°C (95% CI, 0.44°C to 0.75°C; P<0.001).
Conclusions
The GP was superior to the WB for strict temperature control during TTM.

Citations

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Efficacy and safety of the Arctic Sun device for hypoxic-ischemic encephalopathy in adult patients following cardiopulmonary resuscitation: A systematic review and meta-analysis
SaurabhC Sharda, MandipSingh Bhatia, RohitR Jakhotia, Ashish Behera, Atul Saroch, AshokKumar Pannu, HMohan Kumar
Brain Circulation.2023; 9(3): 185. CrossRef
Factors influencing deviation from target temperature during targeted temperature management in postcardiac arrest patients
Kanae Ochiai, Yasuhiro Otomo
Open Heart.2023; 10(2): e002459. CrossRef
Water Temperature Variability Is Associated with Neurologic Outcomes in Out-of-Hospital Cardiac Arrest Survivors Who Underwent Targeted Temperature Management at 33°C
Seok Jin Ryu, Dong Hun Lee, Byung Kook Lee, Kyung Woon Jeung, Yong Hun Jung, Jung Soo Park, Jin Hong Min, Dong Ki Kim
Therapeutic Hypothermia and Temperature Management.2022; 12(2): 74. CrossRef
Comparison of hydrogel pad and water-circulating blanket cooling methods for targeted temperature management: A propensity score-matched analysis from a prospective multicentre registry
Kyoung Tak Keum, Yong Hwan Kim, Jun Ho Lee, Seong Jun Ahn, Seong Youn Hwang, Joo Suk Oh, Su Jin Kim, Soo Hyun Kim, Kyung Woon Jeung
Resuscitation.2021; 169: 78. CrossRef
Use of a Servo-Controlled Cooling Gel Pad System to Regulate Body Temperature in Critically Ill Children
Gema Pérez, Gema Manrique, Julia García, Sara de la Mata, Débora Sanz, Jesús López-Herce
Pediatric Critical Care Medicine.2020; 21(12): e1094. CrossRef
Management of post-cardiac arrest syndrome
Youngjoon Kang
Acute and Critical Care.2019; 34(3): 173. CrossRef

Case Reports

Repeated Hypothermia for Rebound Cerebral Edema after Therapeutic Hypothermia in Malignant Cerebral Infarction: Jeong Ho Hong, Jin Heon Jeong, Jun Young Chang, Min Ju Yeo, Han Yeong Jeong, Hee Joon Bae, Moon Ku Han; Korean J Crit Care Med. 2013;28(3):221-224.; DOI: https://doi.org/10.4266/kjccm.2013.28.3.221

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Abstract PDF

Malignant cerebral infarction has a high risk of fatal brain edema and increased intracranial pressure with cerebral herniation causing death. One of the major causes of death is a rebound cerebral edema during rewarming phase. A 66-year-old male patient presented with the right hemiplegia and global aphasia due to malignant cerebral infarction in the whole territory of middle cerebral artery with the occlusion of the proximal internal carotid artery. Being refused decompressive hemicraniectomy, he received the therapeutic hypothermia for 6 days. After rewarming for 6 hours, mentality was suddenly decreased and dilated left pupil. Follow-up CT revealed that midline shifting was more aggravated. We decided on repeated hypothermia for rebound cerebral edema and successfully controlled. We report our experience with repeated hypothermia for rebound cerebral edema following therapeutic hypothermia in malignant cerebral infarction.

Citations

Citations to this article as recorded by

Dexmedetomidine Use in Patients with 33℃ Targeted Temperature Management: Focus on Bradycardia as an Adverse Effect
Hyo-yeon Seo, Byoung-joon Oh, Eun-jung Park, Young-gi Min, Sang-cheon Choi
The Korean Journal of Critical Care Medicine.2015; 30(4): 272. CrossRef
Therapeutic Hypothermia after Decompressive Craniectomy in Malignant Cerebral Infarction
Jun Young Chang, Jeong-Ho Hong, Jin-Heon Jeong, Sung-Jin Nam, Ji-Hwan Jang, Jae Seung Bang, Moon-Ku Han
Korean Journal of Critical Care Medicine.2014; 29(2): 93. CrossRef

Treatment of Carbon Monoxide Poisoning with Therapeutic Hypothermia: Young Hwan Lee, You Dong Sohn, Seung Min Park, Won Wong Lee, Ji Yun Ahn, Hee Cheol Ahn; Korean J Crit Care Med. 2013;28(3):218-220.; DOI: https://doi.org/10.4266/kjccm.2013.28.3.218

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Abstract PDF

Carbon monoxide (CO) is a well-known chemical asphyxiant, which causes tissue hypoxia with prominent neurological injury. Therapeutic hypothermia (TH) has been shown to be an effective neuroprotective method in post-cardiac arrest patients. A 26-year-old man presented to the emergency department with severe CO poisoning. On arrival, the patient was comatose. His vital signs were blood pressure, 130/80 mm Hg; heart rate, 126/min; respiratory rate, 26/min; body temperature, 36degrees C; and O2 saturation, 94%. Initial carboxyhemoglobin was 45.2%. Because there was no available hyperbaric chamber in our local area, he was intubated and treated with TH. The target temperature was 33 +/- 1degrees C for 24 hours using an external cooling device. The patient was then allowed to reach normothermia by 0.15-0.25degrees C/hr. The patient was discharged after normal neurological exams on day 11 at the hospital. TH initiated after exposure to CO may be an effective prophylactic method for preventing neurological sequelae.

Citations

Citations to this article as recorded by

Dexmedetomidine Use in Patients with 33℃ Targeted Temperature Management: Focus on Bradycardia as an Adverse Effect
Hyo-yeon Seo, Byoung-joon Oh, Eun-jung Park, Young-gi Min, Sang-cheon Choi
The Korean Journal of Critical Care Medicine.2015; 30(4): 272. CrossRef

Original Articles

Implementation of Therapeutic Hypothermia after Pediatric Out-of Hospital Cardiac Arrest in One Tertiary Emergency Center: Woo Jin Kim, Jin Joo Kim, Jae Ho Jang, Sung Youl Hyun, Hyuk Jun Yang, Gun Lee; Korean J Crit Care Med. 2013;28(1):25-32.; DOI: https://doi.org/10.4266/kjccm.2013.28.1.25

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Abstract PDF

BACKGROUND
Cardiac arrest in infants and children is rare than adults yet, it is critical. The efficacy and feasibility of therapeutic hypothermia after cardiac arrest in adults is proved through many studies however, there are few data on pediatric out-of hospital cardiac arrest. We analyzed several variables in pediatric therapeutic hypothermia after out-of hospital cardiac arrest.
METHODS
Infants and children (1 to 17 years old), who were admitted to our emergency intensive care units following the return of spontaneous circulation after out-of hospital cardiac arrest from Jan 2008 to Apr 2012, were included in this study. Basal patients' characteristics and variables about therapeutic hypothermia were analyzed.
RESULTS
A total of seventy-six patients visited our emergency center after a pediatric cardiac arrest during the study period. Among this, sixty-three patients received pediatric advanced life support, twenty one patients were admitted to intensive care units and nine patients received therapeutic hypothermia. Overall, the survival discharge was 7.9% (5 of 63). Among the admitted patients, 3 patients (14.3%) had a good Cerebral Performance Category (CPC). Two patients received endovascular cooling and seven patients received surface cooling. The mean time from the induction of therapeutic hypothermia to reaching the temperature with in the therapeutic range was 193.9 minutes. There were no critical adverse events during induction, maintenance and the rewarming period of therapeutic hypothermia.
CONCLUSIONS
Therapeutic hypothermia after pediatric out-of hospital cardiac arrest was performed safely and effectively in one emergency center. The standardized pediatric therapeutic hypothermia protocol should be established in order to be used widely in pediatric intensive care units. Further, larger studies are needed on the subject of pediatric therapeutic hypothermia.

Citations

Citations to this article as recorded by

Epidemiological and Survival Trends of Pediatric Cardiac Arrests in Emergency Departments in Korea: A Cross-sectional, Nationwide Report
Jae Yun Ahn, Mi Jin Lee, Hyun Kim, Han Deok Yoon, Hye Young Jang
Journal of Korean Medical Science.2015; 30(9): 1354. CrossRef

The Changing Pattern of Blood Glucose Levels and Its Association with In-hospital Mortality in the Out-of-hospital Cardiac Arrest Survivors Treated with Therapeutic Hypothermia: Ki Tae Kim, Byung Kook Lee, Hyoung Youn Lee, Geo Sung Lee, Yong Hun Jung, Kyung Woon Jeung, Hyun Ho Ryu, Byoeng Jo Chun, Jeong Mi Moon; Korean J Crit Care Med. 2012;27(4):255-262.; DOI: https://doi.org/10.4266/kjccm.2012.27.4.255

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Abstract PDF: BACKGROUND
The aim of this study was to analyze the dynamics of blood glucose during therapeutic hypothermia (TH) and the association between in-hospital mortality and blood glucose in out-of-hospital cardiac arrest survivors (OHCA) treated with TH.
METHODS
The OHCA treated with TH between 2008 and 2011 were identified and analyzed. Blood glucose values were measured every hour during TH and collected. Mean blood glucose and standard deviation (SD) were calculated using blood glucose values during the entire TH period and during each phase of TH. The primary outcome was in-hospital mortality.
RESULTS
One hundred twenty patients were analyzed. The non-shockable rhythm (OR = 8.263, 95% CI 1.622-42.094, p = 0.011) and mean glucose value during induction (OR = 1.010, 95% CI 1.003-1.016, p = 0.003) were independent predictors of in-hospital mortality. The blood glucose values decreased with time, and median glucose values were 161.0 (116.0-228.0) mg/dl, 128.0 (102.0-165.0) mg/dl, and 105.0 (87.5-129.3) mg/dl during the induction, maintenance, and rewarming phase, respectively. The 241 (180-309) mg/dl of the median blood glucose value before TH was significantly lower than 183 (133-242) mg/dl of the maximal median blood glucose value during the cooling phase (p < 0.001).
CONCLUSIONS
High blood glucose was associated with in-hospital mortality in OHCA treated with TH. Therefore, hyperglycaemia during TH should be monitored and managed. The blood glucose decreased by time during TH. However, it is unclear whether TH itself, insulin treatment or fluid resuscitation with glucose-free solutions affects hypoglycaemia.

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