to a loss of thermoregulation. hyperthermia in the preperfusion period can also be caused by an increase in the production of oxygen radicals, which influences brain metabolism. these oxygen radicals attack cell membranes, leading to a disruption of intracellular organelles and subsequent cellular death. virtually all patients who undergo dhca develop impaired glucose metabolism and require insulin to control blood sugars. thrombocytopenia and clotting factor deficiencies prove to be a significant cause of early death after dhca. careful monitoring intra-procedure and post-procedure is needed. although dhca is necessary for some procedures, the use of anesthesia can provide optimum operation time and organ protection but can also have serious impacts on cellular demand, brain cells, and serious systemic inflammatory results. possible disadvantages of dhca includes alteration in organ functions of the liver, kidney, brain, pancreas, intestines and smooth muscles due to cellular damage. permanent neurological injury has been seen in 3-12% of patients when using dhca. cases of partial or complete limb motor loss, impaired language, visual defects, and cognitive decline have all been reported as consequences of dhca. other neurological complications are increase risk for seizures postoperative due to delayed return of cellular blood flow to the brain. when compared to moderate hypothermia (temperature dropped to 26-31 °c), there was less bleeding volume experienced during surgery thus leading to less use of packed red blood cells or plasma post surgery. longer recovery time postoperatively have been noted with dhca as compared to moderate hypothermia, but the length of hospital stay and death has no correlated difference. most patients can tolerate 30 minutes of dhca without significant neurological dysfunction or adverse effects, but after an extended period of 40 minutes or more, prevalence of increase brain injury have been noted. research one of the anticipated medical uses of long circulatory arrest times, or so-called clinical suspended animation, is treatment of traumatic injury. in 1984 cpr pioneer peter safar and u.s. army surgeon ronald bellamy proposed suspended animation by hypothermic circulatory arrest as a way of saving people who had exsanguinated from traumatic injuries to the trunk of the body. exsanguination is blood loss severe enough to cause death. until the 1980s, it had been thought impossible to resuscitate people whose heart stopped because of blood loss, resulting in these people being declared dead when cardiac resuscitation failed. traditional treatments such as cpr and fluid replacement or blood transfusion are not effective when cardiac arrest has already occurred and bleeding remains uncontrolled. safar and bellamy proposed flushing cold solution through blood vessels of patients with deadly bleeding, and leaving them in a state of cold circulatory arrest with the heart stopped until the cause of bleeding could be surgically repaired to allow later resuscitation. in preclinical studies at the university of pittsburgh during the 1990s, the process was called deep hypothermia for preservation and resuscitation, and then suspended animation for delayed resuscitation. the process of cooling people with fatal bleeding for surgical repair and later resuscitation was finally called emergency preservation and resuscitation for cardiac arrest from trauma (epr-cat), or epr. it is presently undergoing human clinical trials. in the trials, patients who experience clinical death for less than five minutes duration from blood loss are being cooled from normal body temperature of 37 °c to less than 10 °c by pumping a large quantity of ice-cold saline into the largest blood vessel of the body (aorta). by remaining in circulatory arrest at temperatures below 10 °c (50 °f), it is believed that surgeons have one to two hours to fix injuries before circulation must be restarted. surgeons involved with this research have said that epr changes the definition of death for victims of this type of trauma.