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In addition, we include our experience of managing patients with acute brain injuries treated using endovascular hypothermia. Keywords.
Table of contents
- Hypothermia treatment for traumatic brain injury: a systematic review and meta-analysis.
- In cold blood
- Preventing Severe Brain Injuries By Cooling The Body
- Review ARTICLE
Various parameters are measured during hypothermia, including intracranial pressure, hemodynamics, EKG, and cardiac performance. When a patient shows any abnormality in these measurements or in any other condition, the nurse must immediately evaluate whether the situation is urgent and report it to a medical doctor if necessary. To detect excess fluctuations of body temperature, the brain, blood from the jugular vein or pulmonary artery , and bladder temperatures of patients are measured every 20 min.
In addition, we have developed special methods of nursing care that avoid temperature fluctuations.
Hypothermia treatment for traumatic brain injury: a systematic review and meta-analysis.
To prevent pulmonary complications, we employ a system of planned respiratory care. As a result of this system, the incidence of pulmonary complications during the cooling and rewarming periods has been dramatically decreased at our institution. In all of the above points, the education of the nursing staff is the most important factor. For this reason, we periodically hold lectures on nursing care during hypothermia.
In general, cell death is not directly caused by oxygen deprivation, but occurs indirectly as a result of the cascade of subsequent events. Cells need oxygen to create ATP , a molecule used by cells to store energy, and cells need ATP to regulate intracellular ion levels. ATP is used to fuel both the importation of ions necessary for cellular function and the removal of ions that are harmful to cellular function. Without oxygen, cells cannot manufacture the necessary ATP to regulate ion levels and thus cannot prevent the intracellular environment from approaching the ion concentration of the outside environment.
In cold blood
It is not oxygen deprivation itself that precipitates cell death, but rather without oxygen the cell can not make the ATP it needs to regulate ion concentrations and maintain homeostasis. Notably, even a small drop in temperature encourages cell membrane stability during periods of oxygen deprivation. For this reason, a drop in body temperature helps prevent an influx of unwanted ions during an ischemic insult. By making the cell membrane more impermeable, hypothermia helps prevent the cascade of reactions set off by oxygen deprivation.
Even moderate dips in temperature strengthen the cellular membrane, helping to minimize any disruption to the cellular environment. It is by moderating the disruption of homeostasis caused by a blockage of blood flow that many now postulate, results in hypothermia's ability to minimize the trauma resultant from ischemic injuries.
Preventing Severe Brain Injuries By Cooling The Body
Targeted temperature management may also help to reduce reperfusion injury , damage caused by oxidative stress when the blood supply is restored to a tissue after a period of ischemia. Various inflammatory immune responses occur during reperfusion. These inflammatory responses cause increased intracranial pressure, which leads to cell injury and in some situations, cell death. Hypothermia has been shown to help moderate intracranial pressure and therefore to minimize the harmful effects of a patient's inflammatory immune responses during reperfusion.
The oxidation that occurs during reperfusion also increases free radical production. Since hypothermia reduces both intracranial pressure and free radical production, this might be yet another mechanism of action for hypothermia's therapeutic effect.
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There are a number of methods through which hypothermia is induced. Core body temperature must be measured either via the esophagus, rectum, bladder in those who are producing urine, or within the pulmonary artery to guide cooling. Targeted temperature management should be started as soon as possible.
Prior to the induction of targeted temperature management, pharmacological agents to control shivering must be administered. People should be rewarmed slowly and steadily in order to avoid harmful spikes in intracranial pressure.
Cooling catheters are inserted into a femoral vein. Cooled saline solution is circulated through either a metal coated tube or a balloon in the catheter.
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The saline cools the person's whole body by lowering the temperature of a person's blood. Catheters reduce temperature at rates ranging from 1. Through the use of the control unit, catheters can bring body temperature to within 0. Furthermore, catheters can raise temperature at a steady rate, which helps to avoid harmful rises in intracranial pressure. A number of studies have demonstrated that targeted temperature management via catheter is safe and effective. Adverse events associated with this invasive technique include bleeding, infection, vascular puncture, and deep vein thrombosis DVT.
The risk of deep vein thrombosis may be the most pressing medical complication. Deep vein thrombosis can be characterized as a medical event whereby a blood clot forms in a deep vein, usually the femoral vein. This condition may become potentially fatal if the clot travels to the lungs and causes a pulmonary embolism. Another potential problem with cooling catheters is the potential to block access to the femoral vein, which is a site normally used for a variety of other medical procedures, including angiography of the venous system and the right side of the heart.
However, most cooling catheters are triple lumen catheters, and the majority of people post-arrest will require central venous access. Unlike non-invasive methods which can be administered by nurses, the insertion of cooling catheters must be performed by a physician fully trained and familiar with the procedure. The time delay between identifying a person who might benefit from the procedure and the arrival of an interventional radiologist or other physician to perform the insertion may minimize some of the benefit of invasive methods' more rapid cooling.
Transnasal evaporative cooling is a method of inducing the hypothermia process and provides a means of continuous cooling of a person throughout the early stages of targeted temperature management and during movement throughout the hospital environment. This technique uses two cannulae, inserted into a persons nasal cavity, to deliver a spray of coolant mist that evaporates directly underneath the brain and base of the skull. As blood passes through the cooling area, it reduces the temperature throughout the rest of the body. The method is compact enough to be used at the point of cardiac arrest, during ambulance transport, or within the hospital proper.
Research into the device has shown cooling rates of 2. The goal of this study was to evaluate the therapeutic window for hypothermia treatment following experimental brain injury by measuring edema formation and functional outcome. Traumatic brain injury TBI was produced in anesthetized rats by using cortical impact injury. Edema was measured in the ipsilateral and contralateral hemispheres by subtracting dry weight from wet weight, and neurological function was assessed using a battery of behavioral tests 24 hours after TBI.
In injured rats, it was found that brain water levels were elevated at 1 hour postinjury, compared with those in sham-injured control animals, and that edema peaked at 24 hours and remained elevated for 4 days. Delay of treatment by 90 or minutes postinjury did not result in this neurological protection. Immediate administration of hypothermia also significantly decreased the peak magnitude of edema at 24 hours and 48 hours postinjury, compared with that in normothermic injured control animals.
When delayed by 90 minutes, hypothermia did not affect the pattern of edema formation. When hypothermia was administered immediately or 60 minutes after TBI, injured rats showed an improvement in functional outcome and a decrease in edema. Delayed hypothermia treatment had no effect on functional outcome or on edema. Histogram showing the time course of edema mean percentage of wet weight in the two hemispheres of the brain ipsilateral [black bars] and contralateral [white bars] following cortical impact injury or sham injury in rats. Edema can be seen as early as 1 hour following injury in the ipsilateral hemisphere, with the greatest edema observed to occur between 24 hours and 4 days after TBI.
Hypothermia hypo was administered at increasing delays after injury. When applied immediately 0-minute delay or an hour later minute delay , hypothermia significantly improved balance-beam performance. When delayed by 90 minutes or minutes, the treatment had no effect. Hypothermia significantly improved posture-reflex function when applied immediately or an hour after injury, but had no effect when delayed by 90 minutes or longer.
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