Summer - United States Special Operations Command

first three days of injury, although one-quarter of TBIpatients reached maximal ICPs after day five. 7 Otherdelayed injuries can be due to factors released duringinjury that in time induce inflammation, production offree radicals, release of the excitatory neurotransmitterglutamate, electrolyte disturbances of the neuron, andmitochondrial dysfunction. 6 Even though affected Soldierscan be stable and functional after the TBI, thesesecondary factors can lead to severe neurological deteriorationwithin three to five days post-injury. In standardhealthcare, the concentration of care for TBIpatients goes into reducing these secondary effects. Itwould be optimal to prevent secondary injuries in orderto prevent secondary neurological damageHypothermic medicine, which is the treatmentof injuries by cooling the core body temperature belownormal physiological levels, was studied in use of braininjuries for over 50 years. Mild hypothermia has beenstudied extensively in animal models and is defined inhumans as the achievement of core body temperaturesof 33-34°C. Such treatment may be indicated to improveneurological outcomes after TBI by reducing theevolving secondary injuries through multiple means.One of these was the decrease of cerebral edema andbrain swelling. 8 In an animal-model experiment byMarkgraf in 2001, early administration of hypothermictreatment within four hours was shown to reduce maximalICPs at 24 and 48 hours after TBI. 9Mild hypothermia may also inhibit the buildupof the neurotransmitter glutamate 10,11 and reduce the8, 12metabolic rate of neurons.Hypothermic medicine may attenuate neuronaldeath by turning off several chemical pathways of cellularapoptosis. 13,14 Such treatment may also inhibit theinflammatory response by preserving the blood brainbarrier 15 or reducing pro-inflammatory cytokines. 16After trauma the reperfusion of brain tissueforms free oxygen radicals that damage the cellularmembrane of neurons leading to cell death. Hypothermictreatment increases the function of superoxide dismutase,an enzyme that limits the damage of freeoxygen radicals and protects the cellular membrane.Ultimately, hypothermic medicine may assistin the reduction of secondary insults to neurological tissue,perhaps not through all means discovered in thelaboratory, but probably through more than one factordescribed.ADVERSE EFFECTSTreatment with hypothermic medicine carriesthe adverse risks of cardiac arrhythmia and thrombocytopenia.However, arrhythmia risk is typically only increasedduring moderate hypothermia, when the body iscooled below 30°C. Since most controlled treatmentsremain above these temperatures, it is rare to find arrhythmiasin hypothermic studies. 17Even though it is a common notion that lowerbody temperatures increase hemorrhage due to impairedfunction of platelets and coagulation proteins, 18 surgicalpatients undergoing controlled hypothermia at levels between32.5 and 33.5°C for cerebral aneurysm clippingshowed no greater significant blood loss. 19EQUIPMENTVarious methods exist with which to administermild hypothermia; however, to date only surface coolingand intranasal cooling systems have been tested in humansfollowing TBI. 17The simplest method of inducing mild hypothermiafor treatment is surface cooling. In the past,techniques included applied ice packs and submergingthe patient in ice baths to drop core body temperature.The water-circulating surface cooling device consists ofblankets placed directly on the patient with regulatedcold water circulating through the blankets. The degreeof cooling treatment water is determined by feedbackfrom a rectal thermometer. Gel-coated surface coolingdevices also exist that work on the same principles asthe water-circulating blankets. Only here instead ofblankets, transfer pads coated with adhesive gel are attachedto the body along the back, abdomen, and bilateralthighs. More recently, helmets and caps have beendesigned to produce cooling in a more localized area.Invasive methods such as intravenous coolingconsist of a central venous catheter placed within the inferiorvena cava. Cooled saline is pushed through thecatheter balloons, which are in adjacent contact with thepatient’s blood. In this procedure the core body temperatureis gauged by rectal means. This measured temperatureinduces a feedback loop that regulates thetemperature of the therapeutic saline entering the body.This allows control over therapeutic measures. Anotherinvasive method includes rapid infusion of lactatedRinger’s at 4°C combined with surface cooling using icepacks. However, both these invasive methods compromisevasculature access and increase risk of infectionand hemorrhage.In a study by Hoedemaekers et al., it was shownthat surface methods of water-circulating blankets andgel pads along with cooled at a rate of 1.33°C/hr, and1.04°C/hr, respectively. Intravenous cooling with centralcatheter placement cooled at 1.46°C/hr. These threemethods were far more effective than the conventionaltreatment of running cold lactated ringers solution(0.32°C/hr) and air-circulating cooling systems(0.18°C/hr). 20A new ice water immersion system propels andcirculates a thin film of ice-cooled water directly aroundthe patient’s body in a special molded enclosed environmentto reduce core body temperatures at a rate of4.7°C to 6.6°C/hr. Patients may reach target hypothermicconditions within 20 minutes, at which time the de-A Review of the Use of Early Hypothermia in the Treatment of Traumatic Brain Injuries23