Acute and Critical Care

Review Article

Neurosurgery
Target temperature management in traumatic brain injury with a focus on adverse events, recognition, and prevention: Kwang Wook Jo; Acute Crit Care. 2022;37(4):483-490. Published online November 10, 2022; DOI: https://doi.org/10.4266/acc.2022.01291

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Traumatic brain injury (TBI) is a critical cause of disability and death worldwide. Many studies have been conducted aimed at achieving favorable neurologic outcomes by reducing secondary brain injury in TBI patients. However, ground-breaking outcomes are still insufficient so far. Because mild-to-moderate hypothermia (32°C–35°C) has been confirmed to help neurological recovery for recovered patients after circulatory arrest, it has been recognized as a major neuroprotective treatment plan for TBI patients. Thereafter, many clinical studies about the effect of therapeutic hypothermia (TH) on severe TBI have been conducted. However, efficacy and safety have not been demonstrated in many large-scale randomized controlled studies. Rather, some studies have demonstrated an increase in mortality rate due to complications such as pneumonia, so it is not highly recommended for severe TBI patients. Recently, some studies have shown results suggesting TH may help reperfusion/ischemic injury prevention after surgery in the case of mass lesions, such as acute subdural hematoma, and it has also been shown to be effective in intracranial pressure control. In conclusion, TH is still at the center of neuroprotective therapeutic studies regarding TBI. If proper measures can be taken to mitigate the many adverse events that may occur during the course of treatment, more positive efficacy can be confirmed. In this review, we look into adverse events that may occur during the process of the induction, maintenance, and rewarming of targeted temperature management and consider ways to prevent and address them.

Citations

Citations to this article as recorded by

Trends and hotspots in research of traumatic brain injury from 2000 to 2022: A bibliometric study
Yan-rui Long, Kai Zhao, Fu-chi Zhang, Yu Li, Jun-wen Wang, Hong-quan Niu, Jin Lei
Neurochemistry International.2024; 172: 105646. CrossRef
Severe traumatic brain injury in adults: a review of critical care management
Siobhan McLernon
British Journal of Neuroscience Nursing.2023; 19(6): 206. CrossRef

Case Reports

Thoracic Surgery
Early laparoscopic exploration for acute mesenteric ischemia after cardiac surgery: Sue Hyun Kim, Ho Young Hwang, Min Jung Kim, Kyu Joo Park, Ki-Bong Kim; Acute Crit Care. 2020;35(3):213-217. Published online April 19, 2019; DOI: https://doi.org/10.4266/acc.2018.00423

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Abstract PDF

Acute mesenteric ischemia (AMI) after cardiac surgery is a rare but fatal complication. Early diagnosis and intervention can be lifesaving. We report two cases of patients who underwent early diagnostic laparoscopy for suspicious AMI after cardiac surgery and demonstrated favorable outcomes. An 83-year-old male with severe left ventricular dysfunction underwent off-pump coronary artery bypass grafting. Severe ileus with gaseous distension of the small bowel was developed on the 3rd postoperative day and computed tomographic angiography (CTA) showed pneumatosis intestinalis of small bowel suggestive of AMI. An immediate bedside laparoscopy was performed and it showed preserved perfusion of small bowel. He recovered without complication under supportive medical management. Another 69-year-old male who underwent aortic valve replacement complained of whole abdominal tenderness with severe distension on the 3rd postoperative day. The CTA found segmental non-enhancing bowel wall with air bubbles suggestive of AMI with possible microperforation. A diagnostic laparoscopy demonstrated small-bowel infarction with pus-like fluid collection in the peritoneal cavity. The operation was converted to laparotomy and complete resection of ischemic segments of small bowel was done. He recovered well without any other complications and discharged home on the 35th postoperative day.

Citations

Citations to this article as recorded by

The Challenge of Pneumatosis Intestinalis: A Contemporary Systematic Review
Gennaro Perrone, Mario Giuffrida, Valentina Donato, Gabriele Luciano Petracca, Giorgio Rossi, Giacomo Franzini, Sara Cecconi, Alfredo Annicchiarico, Elena Bonati, Fausto Catena
Journal of Personalized Medicine.2024; 14(2): 167. CrossRef
Gastrointestinal complications after cardiac surgery
Klara Schwarzova, Sameer Damle, Frank William Sellke, Michael Phillip Robich
Trauma Surgery & Acute Care Open.2024; 9(1): e001324. CrossRef
The role of bed-side laparoscopy in the management of acute mesenteric ischemia of recent onset in post-cardiac surgery patients admitted to ICU
Carlo Bergamini, Giovanni Alemanno, Alessio Giordano, Desiré Pantalone, Giovanni Fontani, Anna Maria Di Bella, Veronica Iacopini, Paolo Prosperi, Jacopo Martellucci
European Journal of Trauma and Emergency Surgery.2022; 48(1): 87. CrossRef
Minimally invasive acute care surgery
Caroline E. Reinke, Robert B. Lim
Current Problems in Surgery.2022; 59(2): 101031. CrossRef
In Brief
Caroline E. Reinke, Robert B. Lim
Current Problems in Surgery.2022; 59(2): 101033. CrossRef
Mesenteric ischemia postcardiac surgery—Elusive and less stratified complexity
Mohammed Idhrees, Ian Williams, Mohamad Bashir, Bashi V. Velayudhan
Journal of Cardiac Surgery.2022; 37(7): 2040. CrossRef

Inhospital Spontaneous Acute Subdural Hematoma (SADH) Patient with Antiplatelet Therapy due to Acute Cerebral Ischemia: A Case Report: Hyo Chang Kim, Chun Sik Choi, Jae Young Yang, Hyun Chul Shin, Yu Sam Won, Young Jun Kwon; Korean J Crit Care Med. 2011;26(2):94-97.; DOI: https://doi.org/10.4266/kjccm.2011.26.2.94

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Abstract PDF: A case of "spontaneous" acute subdural hematoma caused by aspirin and plavix therapy has not been described previously. As an isolated cerebrovascular event related to aspirin and plavix therapy, this is the first report described in the literature. It also represents a new differential diagnosis for nontraumatic acute subdural hematomas.

Foot Necrosis Following Percutaneous Cannulation of the Dorsalis Pedis Artery: A Case Report: Hyun Young Lee, Bo Yeon Yu, Sang Hun Kim, Tae Hun An, Chuog Dal Chung, Byung Sik Yu, Keum Young So, Kyung Joon Lim, Nam Soo Cho; Korean J Crit Care Med. 2009;24(3):156-159.; DOI: https://doi.org/10.4266/kjccm.2009.24.3.156

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Abstract PDF: Arterial canuulation is generally used to monitor blood pressure and sample blood for gas analysis. Radial and dorsalis pedis arteries are commonly used for arterial cannulation. It is a simple, safe, and uncomplicated procedure, but some complications have been reported, including bleeding, hematoma, infection, pseudoaneurysm, and thromboembolism. Although thromboembolism is not common, it could be serious because it can lead to digital ischemia and necrosis. We present a case of foot necrosis following dorsalis pedis artery cannulation in a 65-year-old patient who underwent small bowel resection.

Original Articles

The Effects of Mild Hypothermia on the Expression of the Apoptosis-related Proteins following Transient Global Ischemia in Gerbil Hippocampus: Young Min Kim, Kyu Nam Park, Seung Pil Choi, Tai Yong Hong, Se Kyung Kim; Korean J Crit Care Med. 2007;22(1):30-41.

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Abstract PDF: BACKGROUND
The neuroprotective mechanisms of hypothermia remain unclear. Recently, attenuation of apoptosis by hypothermia has been suggested as one of the responsible mechanisms. The aim of this study is to investigate the effects of post-ischemic hypothermia on apoptotic neuronal death as well as expression of some apoptosis-related proteins in a gerbil transient global ischemia model.
METHODS
Following 5 minutes of ischemia, normothermia (NT, 37+/-0.5degrees C) or mild hypothermia (HT, 33+/-0.5degrees C) was immediately induced and maintained for 3 hours. The hippocampal CA1 neurons were examined on day 2, 3, 4, and 7 after ischemia for the survived neuronal densities, DNA nick end labeling and immunohistochemical expressions of Bcl-2, Bax, and caspase 3 in each group. Additionally, DNA gel electrophoresis and western blot analysis for each protein in hippocampus were performed. RESULTS: The neuronal death in CA1 area on day 3, 4, and 7 was significantly reduced in HT group compared to NT group. The number of TUNEL positive cells in HT group was also significantly reduced than NT group on day 3, 4, and 7. DNA laddering of hippocampus on day 4 and 7 also reduced in HT group. Expressions of Bax on days 2, 3 and activated caspase 3 on days 3, 4 were reduced in HT group. Western blots also disclosed a decrease in the intensity of the Bax on day 2 and 3 in HT group compared to NT group. CONCLUSIONS: These results suggest that mild post-ischemic hypothermia attenuates the apoptotic neuronal death through the inhibition of the intrinsic pathway of caspase activation following transient global ischemia and these effects may be related to a reduction of pro-apoptotic events.

The Changes of Regional Cerebral Blood Flow according to Inhalational Anesthetic Agents after Transient Bilateral Carotid Artery Occlusion in the Rabbit: Hyeong Geun Joo, Hae Kyu Kim; Korean J Crit Care Med. 2005;20(2):121-130.

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Abstract PDF: BACKGROUND
Cerebral hyperperfusion syndrome is a recognized complication of carotid endarterectomy, with a reported incidence of 0.3 to 1.2%. Monitoring of regional cerebral blood flow (rCBF) may limit neurological damage. This study was planned to investigate the changes of rCBF according to inhalational anesthetic agents. METHODS: 2.40+/-0.04 kg weighed New Zealand White Rabbits were undergone transient brain ischemia by bilateral carotid artery ligation for 20 minutes. The rCBF was measured by Bowman Perfusion Monitor.
RESULTS
The value of rCBF in pre-ligation state was not significantly different among the three groups. rCBF in sevoflurane group was decreased to 46% of baseline value during ischemia and increased to 143% just after reperfusion. rCBFs in isoflurane and enflurane groups were abruptly increased instead of decrease like sevoflurane group. The values of rCBF was more increasing after reperfusion in isoflurane and enflurane groups. rCBFs in all groups were return to baseline value 10 minutes after reperfusion. CONCLUSIONS: This results was suggested that sevoflurane might be contributed to create a neurologic damage during ischemia and the hyperperfusion was seen in all three anesthetic agents. The clinical investigation may be needed to establish the value of this experiment.

The Effects of Intrathecal Ketamine and NBQX on Neurologic Injury and Spinal Cord Glutamate Receptor mRNA Expression in Transient Spinal Ischemia in the Rat: Seung Hoon Baek, Jung Min Hong, Kyoo Sub Chung; Korean J Crit Care Med. 2005;20(1):24-31.

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Abstract PDF: BACKGROUND
Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. Excitatory amino acids have been known to cause neurologic injury after neuronal ischemia. The purpose of this study was to elucidate the effects of intrathecal ketamine or NBQX on neurologic outcome and NMDA receptor gene expression in transient spinal ischemia. METHODS: Sprague-Dawley rats were anesthetized with enflurane, divided by 4 groups: Control (C group), Intrathecal ketamine 0.1 mg (K-1 group), Intrathecal ketamine 0.2 mg (K-2 group), and intrathecal NBQX 1 nM (N group). Spinal ischemia was produced by both induced hypotension and thoracic aortic cross clamping. After spinal ischemia, neurologic scores were assessed after 1, 2, 3 hours. After 3 hours rats were euthenized and spinal cords were removed for the assay of NMDAR and mGlu1 mRNA. RESULTS: The neurol ogic scores of K-2 and N groups were significantly lower than C group and K-1 group. There were no significant difference between K-1 group and C group. The NMDAR and mGlu1 gene expression was increase in C and K-1 group compared to sham operation. In K-2 and N groups, the gene expressions were significantly lesser than C group.
CONCLUSIONS
The NMDAR and mGlu1 gene expressions were increased in transient spinal ischemia. Intrathecal ketamine and NBQX were effective in preventing neurologic injury after transient spinal ischemia. The NMDA antagonistic action of ketamine might involve to prevent neurologic injury.

Effects of Amrinone and Dobutamine on Regional Myocardial Function and Oxygen Balance in Normal and Stunned Myocardium in Dogs: Jun Suh Park, Jong Eun Park, Sung Tae Jeong, Seongwook Jeong, Sung Su Chung, Kyung Yeon Yoo; Korean J Crit Care Med. 2005;20(1):14-23.

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Abstract PDF: BACKGROUND
We examined the effects of amrinone and dobutamine on regional mechanical function, coronary blood flow (CBF), and myocardial oxygen consumption (MVO2) in normal and stunned myocardium in an open-chest canine model.
METHODS
Dogs were instrumented to measure aortic and left ventricular pressures, pulmonary and left anterior descending (LAD) coronary blood flows, and subendocardial segment length in the region supplied by LAD. Incremental doses of either amrinone (2~10microgram/ml of LAD flow, n=13) or dobutamine (0.05~0.375microgram/ml of LAD flow, n=14) were directly infused into a coronary artery before (normal) and after a 15 min of LAD occlusion and subsequent 30 min-reperfusion (stunned). Percent segment shortening (%SS) and percent post-systolic shortening (%PSS) were evaluated. Myocardial extraction of oxygen (EO2) and lactate (Elac) was calculated. RESULTS: Amrinone or dobutamine in the normal myocardium caused dose-dependent increases in %SS that were comparable (range, 20~40%) but had no effect on %PSS. MVO2 increased in parallel with %SS for both amrinone and dobutamine. With amrinone, CBF increased more than MVO2, resulting in a modest decrease in EO2, whereas with dobutamine, CBF increased in proportion to MVO2, resulting in no change in EO2. After the ischemia and reperfusion, %SS and Elac were reduced, but similar %SS and CBF responses to both agents were observed, except that both agents caused progressive reductions of %PSS. CONCLUSIONS: These results indicate that both amrinone and dobutamine exert positive inotropic effects in normal and stunned canine myocardium. It is also indicated that amrinone causes direct coronary vasodilation, which is not affected by ischemia and reperfusion, while dobutamine has no direct effect on coronary vascular tone in either normal or stunned myocardium.

Case Report

Aortic Dissection Presenting as Lower Leg Ischemia: A Case Report: Young Shin Bae, Yeon Woo Kim, Young Gi Min, Young Ju Lee; Korean J Crit Care Med. 2004;19(2):134-138.

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Abstract PDF: We report a 47-year-old man who presented with acute right leg pain without any other symptoms on visit to ER. But he had the severe back pain when the leg pain developed. Contrast CT revealed no enhancement on right common iliac artery and aortic dissection from the lower level of right renal artery to the iliac artery bifurcation. Angiographic stent insertion was performed immediately, but the patient showed reperfusion syndrome and died after 3 days. Aortic dissection with the isolated peripheral vascular complications is rare. Aortic dissection should be included in the differential diagnosis of patients with acute lower leg ischemia like peripheral arterial occlusive disease.

Original Articles

The Effect of Low-dose Dopamine on Splanchnic and Renal Blood Flow in Patients with Septic Shock under the Treatment of Norepinephrine: Jong Joon Ahn, Tae Hyung Kim, Ki Man Lee, Tae Sun Shim, Chae Man Lim, Sang Do Lee, Woo Sung Kim, Dong Soon Kim, Won Dong Kim, Younsuck Koh; Korean J Crit Care Med. 2001;16(1):36-41.

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Abstract PDF: BACKGROUND
Norepinephrine, which is frequently administered as a vasopressor to the patients with septic shock, can decrease splanchnic and renal blood flows and aggravate splanchnic and renal ischemia. The low-dose dopamine (LDD) has been frequently combined with norepinephrine to ameliorate renal and splanchnic hypoperfusion in patients with septic shock. However, the effect of the LDD on the splanchnic and renal blood flow has not been fully elucidated. This investigation was carried out to determine the effect of the LDD on the splanchnic and renal blood flow in the patients with septic shock under the treatment of norepinephrine.
METHODS
Eleven patients with septic shock were included in this study. All of them were under the norepinephrine treatment as the mean arterial pressure (MAP) was less than 70 mm Hg in spite of the adequate fluid resuscitation. With stabilization of MAP, the LDD (2 g/kg/min) was administered for two hours in each patients. Hemodynamics, gastric intramucosal pH (pHi), gastric regional PCO2 (rPCO2), rPCO2 - PaCO2, urine volume, urine sodium excretion and creatinine clearance were compared between with and without the LDD infusion. Diuretics was not used during the study period.
RESULTS
Age of patients (n=11) was 64 12 and the APACHE III score was 84 17. The mortality rate of the subjects was 64%. Dosage of norepinephrine was 0.55 0.63 g/kg/min during the study period. There were no significant differences in hemodynamics (central venous pressure, cardiac output, pulmonary artery occlusion pressure, mixed venous gas), pHi, rPCO2, rPCO2 - PaCO2 depending on the concomitant infusion of the LDD. The volume of urine tended to increase (P=0.074) after concomitant LDD, but the changes in urine sodium excretion and creatinine clearance were not significantly different.
CONCLUSIONS
The combined infusion of the LDD with norepinephrine did not improve splanchnic and renal blood flow in the patients with septic shock.

Molecular Biologic Study on the Changes of Glutamate Receptor (mGluR5) in Rat Hippocampus after Brain Ischemia: Hae Kyu Kim, Pyong Ju Kim, Seong Wan Baik, Inn Se Kim, Kyoo Sub Chung; Korean J Crit Care Med. 2000;15(2):75-81.

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Abstract PDF: BACKGROUND
Metabotropic glutamate receptors (mGluRs) participate in the induction of synaptic plasticity phenomena, such as long-term potentiation and long-term depression that are thought to be at the origin of learning and memory. They are also likely to play a role in modulating glutamate-induced neurotoxicity. It will become apparent that mGluRs are excellent targets for the development of drugs that modulate excitatory synaptic transmission. But there were several controversies about the exact role of group 1 mGluRs subtype 5 (mGluR5). This study was designed for evaluation of the neuroprotective role of mGluR5.
METHODS
Fifty male Sprague-Dawley rats were divided into three groups, control, MK-801 and lamotrigine. The hippocampus and basal ganglia were removed at 6 hours and 3 days after the one hour transient middle cerebral artery occlusion. The gene expression of mRNA of the brain samples were evaluated by using reverse transcriptase polymerase chain reaction technique.
RESULTS
The gene expression of mGluR5 mRNA in hippocampus was increased by 101.96 +/- 18.45% at 6 hours after ischemia and decreased by 50.70 +/- 15.73% at 3 days after ischemia (p<0.01). MK-801 and lamotrigine attenuated the ischemia-induced increases of gene expression of mGluR5 mRNA. In MK-801 group, the expression in basal ganglia was increased by only 0.23 +/- 5.41% at 6 hours after ischemia and decreased by 9.82 +/- 4.35% at 3 days after ischemia. In MK-801 group, the expression in hippocampus was decreased by 3.45 +/- 8.24% and 9.35 5.69% at 6 hours and 3 days after ischemia. In lamotrigine group, the expressions in hippocampus and basal ganglia were decreased by 26.66 +/- 9.85% and 9.45 +/- 5.22% at 6 hours after ischemia.
CONCLUSIONS
From these results, the role of mGluR5 was defined as a mediator for neuronal damage after transient focal cerebral ischemia in hippocampus and basal ganglia.

Effects of Mg2+ Intravenous Pretreatment on Brain Energy Metabolism in Acute Ischemic-Reperfusion Model in Cats: 31P and 1H Magnetic Resonance Spectroscopic Study: Eun Ha Suk, Ji Young Kang, Sung Kwan Chun, Pyung Hwan Park, Kun Ho Lim, Jung Hee Lee, Tae Hwan Lim; Korean J Crit Care Med. 1999;14(2):132-136.

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Abstract PDF: BACKGOUND: This study was purposed to evaluate the effects of Mg2+ pretreatment on cerebral ischemic injury in cats.
METHODS
Global cerebral ischemia was induced by ligation of both innominate arteries following ligation of inferior vena cava under lowered mean blood pressure for 20 minutes followed by 3 hrs of reperfusion. Ten cats were divided into 2 groups: Group 1 (n=5) is the control group, for group 2 (n=5) (Mg2+ group), the animals were pretreated with 90 mg/kg of Mg2+ intravenously before subjected to ischemia.
RESULTS
Phosphocreatine/inorganic phosphate (Pcr/Pi) and pH decreased after ischemia and did not recovered during reperfusion. And there were no significant differences between the two groups. The ratios of lactate/N-acetyl aspartate (Lac/NAA) and lactate/creatine (Lac/Cr) increased after ischemia and not recovered during reperfusion. But the ratios were higher for the group 2 than the group 1 during reperfusion (p<0.05). For the Mg2+ group, blood pressure during reperfusion was lower than the control group.
CONCLUSIONS
Mg2+ intravenous pretreatment had no protective effect on this global cerebral ischemia animal model. Even it deteriorated brain energy metabolism by lowering blood pressure.

The Effects of Nitric Oxide on Oxygen Balance in Cerebral Ischemia: Doo Ik Lee, Young Kyu Choi, Oak Za Chi; Korean J Crit Care Med. 1998;13(2):179-185.

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Abstract PDF: Bockground: Nitric oxide (NO) is an important regulator of blood flow and also works as a neuronal messenger via cyclic GMP. Recent studies regarding the therapeutic utility of nitric oxide synthase (NOS) inhibitors in reducing ischemia-induced neuronal damage are very controversial. The possible neuroprotective effect of NO or NOS inhibitors in ischemic neuronal damage could occur at the vascular and or neuronal level. This study investigated whether the NOS inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME) would alter oxygen balance in ischemic cerebrocortex of isoflurane-anesthetized rats.
METHODS
Fifteen minutes after middle cerebral artery occlusion, L-NAME (1.5 mgxmin-1kg-1) was infused intravenously to the L-NAME group (n=14), and normal saline was given to the control group (n=14) for 45 minutes. Regional cerebral blood flow was determined with [14C]iodoantipyrine, and arterial and venous oxygen saturations were determined by microspectrophotometry.
RESULTS
Regional cerebral blood flow of the ischemic cortex was significantly lower than that of the contralateral cortex in both groups. In the control group, ischemic cortex; 55+/-13, contralateral cortex; 110+/-29 mlxmin-1100 g-1, and in the L-NAME group, ischemic cortex; 35+/-13, contralateral cortex; 90+/-24 mlxmin-1100 g-1. Compared with the blood flow in the ischemic cortex of the control group, L-NAME significantly reduced ischemic blood flow by 36%. Venous oxygen saturation was significantly increased in the ischemic cortex (41+/-1% in control, 44+/-3% in L-NAME) but decreased in the contralateral cortex (65+/-3% in control, 61+/-3% in L-NAME) by L-NAME. Ischemic cortical oxygen consumption in the L-NAME group was 39% lower than that in the corresponding control group, whereas the difference was only 11% in the contralateral sides between groups. The ratio of oxygen supply to consumption was lower in the ischemic than in the nonischemic regions in both groups. In the ischemic cortex, this ratio was significantly lower in the control group (1.7+/-0.1) than in the L-NAME group (1.9+/-0.1). In contrast, the ratio tended to be decreased by L-NAME in nonischemic regions.
CONCLUSIONS
These observations suggest that despite a decrease in cerebral blood flow, inhibition of nitric oxide synthesis mildly improves the oxygen supply and consumption balance in the ischemic cortex.

The Effect of Brain Hypothermia on Brain Edema Formation after Transient Ischemia: Seung Sig Kang, Kyu Taek Choi, Chung Gill Leem, In Hea Cho, Sung Lyang Chung, Pyung Hwan Park; Korean J Crit Care Med. 1998;13(1):43-48.

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Abstract PDF: BACKGOUND: When ischemia reduces blood supply, hypothermia remains the sine qua non for reducing demand. An alternative to whole body deep hypothermia is an isolated cerebral hypothermia via perfusion of cooled blood through one internal carotid artery. The goal of this study was to evaluate the effect of isolated cold hemisphere perfusion during the cerebral ischemia on the formation of brain edema.
METHODS
The studies were designed to perfuse a saline solution into both carotid arteries with a different temperature (left 15degreesC, right 38degreesC) in the same animal. Cerebral ischemia was produced by a combination of the both carotid artery saline perfusion and systemic hypotension to a mean arterial blood pressure of 40 mmHg for 10 minutes. Ninety minutes after reperfusion, brain water contents were measured using the kerosene/bromobenzene density gradient and compared with warm saline perfusion and normal control group.
RESULTS
Brain water content of cold saline perfusion hemisphere measured at 90 minutes after ischemia showed decreased water content compared to warm saline perfusion hemisphere (p<0.05).
CONCLUSIONS
Cerebral cold saline perfusion during the ischemia decreased the formation of brain edema. These results showed hypothemia is one of the most effective ways to protect brain from the ischemia.

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