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Hypothermia treatment helps officer walk again/ hypothermic coma

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    Hypothermia treatment helps officer walk again/ hypothermic coma

    Hypothermia treatment helps officer walk again

    Doctors at Jackson Memorial Hospital successfully used a new procedure to help Miami Police Officer Manny Gomez walk again after he suffered a spinal cord injury.


    After falling from his police horse in January and severely bruising his spinal cord, Miami Officer Manny Gomez seemed a long shot to ever walk again.
    But movement in his left foot meant his injury was not overwhelmingly severe.
    And that gave doctors a few hours to try a procedure they have not attempted previously.
    Using new technology, doctors lowered his core body temperature several degrees for two days to reduce swelling in his spinal cord and prevent the injury from worsening.
    It worked.
    Using handrails to balance himself, Gomez this week gingerly shuffled his feet during therapy at Jackson Memorial Hospital's Rehabilitation Center.
    Helping him were therapists Alexandra Villegas and Orlando Sendon. Fellow Miami police mounted patrolmen Jose Pastor and Luis Pla watched over him, bearing all-important thimbles of Cuban coffee.
    ''It's depressing sometimes, but I feel like I've found a home,'' he says of his new surroundings at Jackson's rehabilitation center. ``All the guys have been incredible with me.''
    Gomez, 55, is a popular mounted patrolman who has worked Little Havana for almost two decades. His horses are known for their love of tasty Cuban bread.
    But on Jan. 15, as he and fellow officers were preparing for the Three Kings Day Parade, he took a freak spill off his horse (his usual horse, Sonny, was sick that day).
    Fellow officers found him sprawled on the ground, his face bloodied.
    ''Right away I felt my body getting cold,'' Gomez said.
    ``I thought that was it for me.''
    Last edited by Max; 5 Mar 2006, 3:00 PM.


    This therapy is not new & not attepted first time.
    I remember we were discussing it many times (lowering body temperature, cooling around spine etc)..At rehab I met very high walking quad who was lucky to get paralysed in winter (almoust froze)

    It is cheap way to prevent swelling in spinal cord-but yet it is not standart procedure in sci management.....

    I wonder why?


      Also, does this work only with incomplete injuries?


        Originally posted by roshni
        Also, does this work only with incomplete injuries?
        Hypothermic coma treatment of sci & brain injuries is known probably for 20 years...There is only little time window of opportubity to apply it (approx couple hours after injury) but yet its not standart procedure.. Its cheaper & it works....There is no will to apply it (in my opinion).....

        Its also works with heart attack


          HERE IS aNOTHER interesting article

          On Ice

          They call Dan O'Reilly 'The Miracle Man.'

          Diane Persson says 'They felt that if he didn't get medical intervention he really would not last long.'

          Dr. Joseph Varon says 'When I first laid eyes on Dan he was very ill. He was critically ill. He was basically near death.'

          For nearly 20 years Dr. Guy Clifton has been experimenting with hypothermia treatment on brain injury victims.

          var byString = "Catherine Stancl"; var sourceString = "Special to"; if ((sourceString != "") && (byString != "")) { document.write(byString + ", "); } else { document.write(byString); } Catherine Stancl, Special to

          Updated: Sat. Mar. 4 2006 6:50 PM ET
          They call Dan O'Reilly "The Miracle Man." Nearly 18 months ago, the 56-year-old was on the brink of death. Escaping the cold Edmonton winter for a little fun in the sun, he was on vacation with his family in Mexico and surfing with his two sons when tragedy struck.
          "This wave came that was a couple of feet above my head and I thought, wow, I can ride this one," Dan recalls.
          But the wave was bigger, and faster than Dan could handle. The wave picked him up and slammed him into the surf. His son dragged him out of the water. Dan wasn't breathing, and CPR wasn't working. But just as he was being rushed into an ambulance he suddenly gasped for breath.
          Dan was alive.
          Doctors in Mexico didn't know why Dan had almost drowned. Their best guess was that he may have suffered a heart attack or stroke in the water. The one thing they were certain of was that Dan was close to death. His wife Diane Persson had to make a decision -- keep Dan in the hospital in Mexico, or have him airlifted to Houston, Texas.
          "They felt that if he didn't get medical intervention he really would not last long," Diane says.
          In a coma, hooked up to life support, Dan was rushed to St. Luke's Episcopal Hospital in Houston. An emergency call was made to heart and critical care specialist Dr. Joseph Varon. The prognosis wasn't good.
          "When I first laid eyes on Dan he was very ill. He was critically ill. He was basically near death," Dr. Varon recalls. "His chances of making it were one per cent. He basically had no brain function whatsoever."
          When Dan was hit by the wave, his heart stopped, cutting off oxygen to the brain. The severity of the brain damage was not known.
          "They were telling me I should consider taking him off life support. They were saying that there's a very slim chance he'll ever pull out of this. And a very slim chance that he would have any quality of life if he did," Diane says.
          "A gentleman that was going to be literally a vegetable hooked up to a respirator and hooked up to a feeding tube," Dr. Varon adds.
          In a last ditch effort to save Dan from a terrible fate, Dr. Varon decided to try a radical treatment -- hypothermia. Because oxygen to the brain is cut off during a heart attack, brain damage can occur. But lowering the body temperature of the patient puts them into a hypothermic coma, slowing down body function so blood-borne oxygen is saved to help heal the brain.
          "It's pretty close to dying," Dr. Varon explains. "Your normal body temperature is somewhere around 36 to 38 degrees Celsius more or less. What we do with patients with hypothermia is we drop them to 34."
          For three days Dan's body was lowered to near death limits, his body in hibernation mode, allowing time for his body to heal itself. On Dec. 26, 2004, his birthday, Dan came back to life.
          "I'm looking at this man and say this is not possible. I mean, what do you mean that he woke up?" Dr. Varon says.
          And there was another surprise. Dan hadn't suffered a heart attack at all. An MRI showed that Dan's spine was crushed at the very spot that controls breathing. The cooling therapy not only helped to stave off severe brain damage, it also protected Dan's spinal cord, preventing him from becoming a quadriplegic. It was the best possible misdiagnosis.
          "I guess I have to go back and say it was a miracle," Dan says.
          A miracle indeed. Just over a year later, the man who should have died, or at best be confined to a wheelchair is up at the crack of dawn. Dan is working out every day; he's coaching his son's volleyball team and will soon return to teaching full time.
          The right place at the right time
          Twenty-year old Josh Ragsdale had a similar brush with death. One year ago, he fell 25 feet on his head in a work-related accident. He was rushed to Memorial Hermann Hospital in Houston, Texas. His wife Whitney was frantic.
          "I didn't think he was going to make it," Whitney recalls. "I mean just the way he looked. You know he was all bloody. I didn't think he was going to make it."
          Doctors at the hospital told Whitney to prepare for the worst— that even if Josh survived, he may not remember Whitney, or their newborn son Cason. But Josh was in the right hospital at the right time with the right person, Dr. Guy Clifton. For nearly 20 years he has been experimenting with hypothermia treatment on brain injury victims. He was conducting a preliminary study at the hospital when Josh was admitted. And it turns out that he was the perfect candidate for the study.

          "They told my mom either we're going to have to remove this bone in the side of his brain to let his brain expand," Josh explains. "Or we're going to do this hypothermia study, pretty much freeze him, keep him on ice."
          "When we got to the hospital and they mentioned this study, we had to act real fast on it because it was a matter of his life," Whitney says. "Just the fact that the study was available for him and he qualified was an act of God. So I do think it was a miracle."
          Josh's family took a leap of faith. They agreed to let Josh be part of the study. So Dr. Clifton's team put Josh into a hypothermic coma. Miraculously, just two weeks after his life-threatening fall, Josh Ragsdale woke up, walked back into his life, and back to work. The cooling worked. Josh had no brain damage.
          "I do pray a lot and you know I'm real religious but I'm real thankful for it and I think to this day I still kind of haven't grasped 100 per cent how lucky I am," Josh says.
          Cool science
          For both Dan and Josh, luck and science were on their side. They returned from the brink of death thanks to the cold grip of hypothermia. And Dr. Clifton has been working hard to perfect the treatment since he accidentally stumbled upon the benefits of cooling.
          "We were testing other drugs and found out that in the winter months our control animals who didn't get any treatment were not showing any injuries and we couldn't figure out what was going on," Dr. Clifton explains. "It turned out their temperatures were dropping a couple of degrees. The building we were in was 75 or 100 years old. It had a bad heating system. And so it was really a laboratory accident."
          When Dr. Clifton cooled injured rats down, their body functions slowed down, saving oxygen for the brain, helping it heal. His challenge at that point was to harness hypothermia and use it to save brain injury patients. Using a specially designed cooling blanket, he started a study on a handful of brain injury victims. He put them into a hypothermic coma for 48 hours. Dr. Clifton discovered that to get optimal results, he had to start freezing fast.
          "The conclusion was, that we had better find a way to literally start the hypothermia within 90 minutes or two hours of injury or it was or it's not going to work," Dr. Clifton says.
          But Dr. Clifton needed a team to test his theory. He found one in Canada, at Calgary Foothills Hospital and Dr. David Zygun. Two doctors, nearly four thousand kilometers apart, coming together to study one question; if brain injury patients are cooled fast enough, does hypothermia improve their chances for survival?
          "If we don't do studies like this, if we just accept status quo, then in 10 years we'll be treating brain injury the exact same way which means the exact same outcomes," Dr. Zygun explains. "And personally I think we all agree that the outcomes are sub-optimal at this point in time and that we can do better."
          In Houston and Calgary emergency medical teams are using air ambulance to get to victims as quickly as possible. Windows are kept open and ice packs are used to start cooling the body right away. Once the patient arrives at the hospital, more sophisticated methods are used. This time around it's a cooling vest called the Arctic Sun. It's a precise way to cool patients down, mimicking water immersion. Patients will be kept at 34 degrees centigrade for two days. Dr. Clifton's current study is the largest of its kind—240 patients will be recruited.


            Hypothermia has long been used to treat kids with brain injury. There have been many anecdotal cases of kids that have fallen into cold water and recovered remarkably from drowning. Hypothermia, likewise, has been strongly advocated by many investigators for treating brain and spinal cord injury. Hypothermia is extensively used in operative procedures, particularly in kids, that may damage the spinal cord.
            • Weigang E, Hartert M, Siegenthaler MP, Pitzer-Hartert K, Luehr M, Sircar R, von Samson P and Beyersdorf F (2006). Neurophysiological monitoring during thoracoabdominal aortic endovascular stent graft implantation. Eur J Cardiothorac Surg 29: 392-6. Objective: The aim of this study was to evaluate the benefit of neurophysiological monitoring during thoracic and thoracoabdominal endovascular stent graft implantation. Methods: The spinal cords of 21 patients undergoing endovascular stent graft implantation on the thoracic and thoracoabdominal aorta were monitored with transcranial motor-evoked potentials (tcMEP) and somatosensory-evoked potentials (SSEP). All patients underwent mild systemic hypothermia (34-35 degrees C), constant cerebrospinal fluid (CSF) pressure and vital parameter monitoring. If CSF pressure exceeded 15mmHg, CSF-drainage was carried out. Results: Three of the 21 patients (14%) exhibited short-term loss of tcMEP and SSEP after the deployment of the self-expanding endoprosthesis. We observed an intraoperative recovery of the evoked potentials in all cases. CSF-drainage was necessary in three of them. One patient, whose potentials were stable intraoperatively, developed paraparesis 3 weeks after the intervention. Conclusions: Neurophysiological monitoring has proved to be an ideal monitoring method to detect spinal cord ischemia during thoracic and thoracoabdominal endovascular stent graft implantation. Due to the advantages of endovascular therapy (no aortic cross-clamping, continuous distal perfusion, and no reperfusion injury), changes in potentials were seldom observed. Department of Cardiovascular Surgery, University Hospital Freiburg, Hugstetter Strasse 55, 79106 Freiburg, Germany.
            • Svensson LG (2005). Paralysis after aortic surgery: in search of lost cord function. Surgeon 3: 396-405. During the early 1980s, the rate of paralysis after aortic surgery was as high as 41% in patients for the most complex thoracoabdominal aortic operations. After comparing human and chacma baboon (papio ursinus) spinal cord vascular anatomy, an animal model was established to study the pathophysiology of aortic cross-clamping and the aetiology of the paralysis. Techniques, including motor evoked responses for monitoring spinal cord function, were developed that were tried in humans and later culminated in prospective and randomized studies. These established that the following were protective: combining cerebrospinal fluid with intrathecal papaverine; cooling systemically to moderate or profound hypothermia; minimizing intercostal ischaemia time; using a sequential segmental repair approach; re-attaching all patent and segmental intercostal arteries below T8 for descending thoracic aortic repair and from T6 to L2 for thoracoabdominal repairs; continuing cerebrospinal fluid drainage for at least two days and maintaining patients hypertensive after surgery. The net result has been that, in two of our recent series, the risk of permanent paralysis has been reduced to between 3.1% and 3.8%. Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Ohio 44195, USA.
            • Shiiya N, Kunihara T, Matsuzaki K and Yasuda K (2005). Evolving strategy and results of spinal cord protection in type I and II thoracoabdominal aortic aneurysm repair. Ann Thorac Cardiovasc Surg 11: 178-85. PURPOSE: We report our strategy and results of spinal cord protection in Crawford I and II thoracoabdominal aortic replacement. : METHODS: Retrospective analysis of 43 elective operations. Before 1994, we reconstructed segmental arteries during a single period of blood flow interruption in 11 of 12 patients, using distal aortic perfusion and evoked spinal cord potential (ESCP) monitoring. Deep hypothermia was used in one. Since 1994, we used multi-segmental sequential repair, in which T8-L1 arteries were sequentially reconstructed irrespective of evoked potential change, in 20 of 31 patients. In the remaining 11, deep hypothermia was used. Cerebrospinal fluid drainage (CSFD) was introduced in 1996 (n=26), and continuous infusion of naloxone in 1999 (n=17). RESULTS: In patients undergoing distal aortic perfusion without multi-segmental sequential repair, six spinal cord injuries including two deaths occurred. Change in evoked potentials was observed in nine of 10 monitored patients. With multi-segmental sequential repair, only one spinal cord injury occurred, and three of 11 monitored patients showed evoked potential change. With deep hypothermia, no spinal cord injury occurred. Multivariate analysis identified operation without multi-segmental sequential repair as a risk factor for spinal cord injury (p=0.008). CONCLUSION: Evolving strategy resulted in an improved outcome. Both multi-segmental sequential repair and deep hypothermia were more effective than our previous technique. Department of Cardiovascular Surgery, Hokkaido University Hospital, Sapporo, Japan.
            • Shiiya N, Kunihara T, Matsuzaki K and Yasuda K (2005). Evolving strategy and results of spinal cord protection in type I and II thoracoabdominal aortic aneurysm repair. Ann Thorac Cardiovasc Surg 11: 178-85. PURPOSE: We report our strategy and results of spinal cord protection in Crawford I and II thoracoabdominal aortic replacement. : METHODS: Retrospective analysis of 43 elective operations. Before 1994, we reconstructed segmental arteries during a single period of blood flow interruption in 11 of 12 patients, using distal aortic perfusion and evoked spinal cord potential (ESCP) monitoring. Deep hypothermia was used in one. Since 1994, we used multi-segmental sequential repair, in which T8-L1 arteries were sequentially reconstructed irrespective of evoked potential change, in 20 of 31 patients. In the remaining 11, deep hypothermia was used. Cerebrospinal fluid drainage (CSFD) was introduced in 1996 (n=26), and continuous infusion of naloxone in 1999 (n=17). RESULTS: In patients undergoing distal aortic perfusion without multi-segmental sequential repair, six spinal cord injuries including two deaths occurred. Change in evoked potentials was observed in nine of 10 monitored patients. With multi-segmental sequential repair, only one spinal cord injury occurred, and three of 11 monitored patients showed evoked potential change. With deep hypothermia, no spinal cord injury occurred. Multivariate analysis identified operation without multi-segmental sequential repair as a risk factor for spinal cord injury (p=0.008). CONCLUSION: Evolving strategy resulted in an improved outcome. Both multi-segmental sequential repair and deep hypothermia were more effective than our previous technique. Department of Cardiovascular Surgery, Hokkaido University Hospital, Sapporo, Japan.
            • Kotoh K, Fukahara K, Yamashita A, Seki K and Misaki T (2005). Ischemic changes in evoked spinal cord potentials during profound hypothermic circulatory arrest in thoracic aortic surgery. Surg Today 35: 271-4. PURPOSE: We examined the changes in evoked spinal cord potentials (ESCP) during profound hypothermic circulatory arrest to estimate the safe ischemic time. METHODS: We monitored ESCPs during surgery for descending thoracic or thoracoabdominal aneurysms in five patients. Evoked spinal cord potential recordings were obtained before cooling (baseline), then every few minutes during circulatory arrest, and at the end of the operation. RESULTS: After circulatory arrest, the amplitude of ESCPs decreased with time. We calculated the simple linear regression between the amplitude of ESCPs and the circulatory arrest time by the least-squares method, and found a highly linear relationship between amplitude and arrest time in all five patients. The time until disappearance of ESCPs was estimated as 50.7 +/- 20.4 min (95% level of confidence). CONCLUSION: When an ESCP disappeared, ischemic spinal cord injury had occurred. This demonstrates the potential value of estimating the time of disappearance of ESCPs to prevent ischemic spinal cord injury during descending thoracic aortic surgery. Department of Surgery, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama, 930-0194, Japan.
            • Casas CE, Herrera LP, Prusmack C, Ruenes G, Marcillo A and Guest JD (2005). Effects of epidural hypothermic saline infusion on locomotor outcome and tissue preservation after moderate thoracic spinal cord contusion in rats. J Neurosurg Spine 2: 308-18. OBJECT: Regionally delivered hypothermia has advantages over systemic hypothermia for clinical application following spinal cord injury (SCI). The effects of local hypothermia on tissue sparing, neuronal preservation, and locomotor outcome were studied in a moderate thoracic spinal cord contusion model. METHODS: Rats were randomized to four treatment groups and data were collected and analyzed in a blinded fashion. Chilled saline was perfused into the epidural space 30 minutes postcontusion to achieve the following epidural temperatures: 24 +/- 2.3 degrees C (16 rats), 30 +/- 2.4 degrees C (13 rats), and 35 +/- 0.9 degrees C (13 rats). Hypothermia was continued for 3 hours when a 45-minute period of rewarming was instituted. In a fourth group a moderate contusion only was induced in 14 animals. Rectal (core) and T9-10 (epidural) temperatures were measured continuously. Locomotor testing, using the Basso-Beattie-Bresnahan (Ba-Be-Br) scale, was performed for 6 weeks, and rats were videotaped for subsequent analysis. The lesion/preserved tissue ratio was calculated throughout the entire lesion cavity and the total lesion, spinal cord, and spared tissue volumes were determined. The rostral and caudal extent of gray matter loss was also measured. At 6 weeks locomotor recovery was similar in all groups (mean Ba-Be-Br Scale scores 14.88 +/- 3.71, 14.83 +/- 2.81, 14.50 +/- 2.24, and 14.07 +/- 2.39 [p = 0.77] for all four groups, respectively). No significant differences in spared tissue volumes were found when control and treatment groups were compared, but gray matter preservation was reduced in the infusion-treated groups. CONCLUSIONS: Regional cooling applied 30 minutes after a moderate contusive SCI was not beneficial in terms of tissue sparing, neuronal preservation, or locomotor outcome. This method of cooling may reduce blood flow in the injured spinal cord and exacerbate secondary injury. The Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami, Florida 33136, USA.
            • Tabayashi K (2005). Spinal cord protection during thoracoabdominal aneurysm repair. Surg Today 35: 1-6. Spinal cord injury after thoracoabdominal aortic surgery remains a devastating and unpredictable complication, caused by clamping of the thoracoabdominal aorta, resulting in exclusion of blood flow in critical and essential intercostal arteries. Various protective methods against spinal cord ischemia have been proposed and performed clinically. These include preoperative spinal angiography, distal aortic perfusion, hypothermia, reattachment of the intercostal artery, cerebrospinal fluid drainage, administration of neuroprotective agents, and monitoring of somatosensory and motor-evoked potentials. The information to date suggests that multimodality approaches should be used to prevent spinal cord injury after thoracic and thoracoabdominal aneurysm repair. Department of Cardiovascular Surgery, Graduate School of Medicine, Tohoku University, 1-1 Seiryo-cho, Aoba-ku, Sendai, 980-8574, Japan.
            • Bernard S (2004). New indications for the use of therapeutic hypothermia. Crit Care 8: E1. Randomised, controlled trials of therapeutic hypothermia have demonstrated improved outcomes after out-of-hospital cardiac arrest, where the initial cardiac rhythm was ventricular fibrillation. This therapy is now endorsed by the International Liaison Committee on Resuscitation. The role of therapeutic hypothermia in patients with anoxic neurological injury due to stroke, spinal cord injury or asphyxial cardiac arrest is uncertain. However, given the strong theoretical benefit and the minimal adverse side-effects, it is reasonable for clinicians to consider the use of therapeutic hypothermia in such cases. The Intensive Care Unit, Dandenong Hospital, Melbourne, Australia. <>
            • Fukuda S, Kawaguchi M, Kakinohana M and Matsumoto M (2004). [Spinal cord protection during descending thoracic and thoracoabdominal aortic surgery]. Masui 53: 1106-29. The incidence of postoperative paralysis after thoracic and thoracoabdominal aortic operations has decreased, but is still high in comparison with other operations. The analysis of the mechanism involved in the ischemic tolerance of the spinal cord could contribute to the protection of the spinal cord from ischemia. The identification of the Adamkiewicz artery and the predictive factors for postoperative paralysis in the preoperative period, the use of motor evoked potential, several adjuncts to keep the spinal cord circulation, the stabilization of the hemodynamics with good oxygenation, and hypothermia contribute to the prevention of the spinal cord ischemia. The anesthetics appropriate for the monitoring of the motor-evoked potential are propofol and fentanyl with or without ketamine. Among the anesthetic drugs, narcotics might exacerbate the motor function after the spinal cord ischemia. The analgesic drugs which do not aggravate the spinal cord dysfunction would be expected. Good cooperation of surgeons and anesthesiologists greatly contributes to the finding of the spinal cord ischemia during this operation. Department of Anesthesiology and Reanimatology, Faculty of Medical Science, University of Fukui.
            • Strauch JT, Lauten A, Spielvogel D, Rinke S, Zhang N, Weisz D, Bodian CA and Griepp RB (2004). Mild hypothermia protects the spinal cord from ischemic injury in a chronic porcine model. Eur J Cardiothorac Surg 25: 708-15. OBJECTIVES: During thoracoabdominal aortic aneurysm repair, prolonged compromise of spinal cord blood supply can result in irreversible spinal cord injury. This study investigated the impact of mild hypothermia during aortic cross-clamping on postoperative paraplegia in a chronic porcine model. METHODS: The thoracic aorta was exposed and cross-clamped in 30 juvenile pigs (20-22 kg) for different intervals at normothermia (36.5 degrees C), and during mild hypothermia (32.0 degrees C). Three pigs were evaluated at each time and temperature. Myogenic motor-evoked potentials (MEPs) were monitored, and postoperative recovery evaluated using a modified Tarlov score. RESULTS: There were no significant hemodynamic or metabolic differences between individual animals, and the groups had equivalent arterial pressures (mean 64.3+/-3.6 mmHg). Time to recovery of MEPs correlated with severity of injury; all animals with irreversible MEP loss suffered postoperative paraplegia. At normothermia, animals with 20 min of aortic cross-clamping emerged with normal motor function, but those cross-clamped for 30 min suffered paraplegia. With mild hypothermia, animals tolerated 50 min of aortic cross-clamping without evidence of neurologic injury, but were all paraplegic after 70 min of ischemia. Animals appeared to recover normal motor function after 60 min of aortic cross-clamping at hypothermia initially, but exhibited delayed-onset paraplegia 36 h postoperatively. CONCLUSIONS: Our observations indicate that mild hypothermia dramatically increases the tolerance of the spinal cord to ischemia in the pig, and therefore suggests that cooling to 32.0 degrees C should be encouraged during surgery which may compromise spinal cord blood supply. An ischemic insult of borderline severity may result in delayed paraplegia. Department of Cardiothoracic Surgery, Mount Sinai School of Medicine/New York University, One Gustave L. Levy Place, P.O. Box 1028, New York, NY 10029, USA.
            • Terada H, Kazui T, Yamashita K, Washiyama N, Suzuki K, Suzuki T, Okura K and Suzuki M (2004). [Spinal cord protection and operative results of the thoracoabdominal aortic aneurysm]. Kyobu Geka 57: 307-12. The purpose of this study was to review retrospectively recent results in 75 patients undergoing thoracoabdominal aortic operations using the technique of distal aortic perfusion with segmental aortic clamping. Between July 1997 and November 2003, 46 males (61%) and 29 females (39%) were treated. The patients ranged in age from 26 to 82 (mean 63 +/- 13) years. Indications for surgery included dissecting thoracoabdominal aortic aneurysm (n = 28), atherosclerotic thoracoabdominal aortic aneurysm (n = 46), and traumatic aneurysm (n = 1). Emergency operation was performed in 8 (11%). The extent of aneurysm was Crawford type I in 12 patients, type II in 19, type III in 34, and type IV in 10. Profound hypothermic circulatory arrest was used in 3 patients and retrograde segmental clamping technique in 5. Cerebrospinal fluid drainage and naloxone hydrochloride administration were performed as adjunctive methods since February 2000. There were 6 (8%) in-hospital deaths. The overall incidence of postoperative paraplegia or paraparesis was 8% (6/75). Although the survival rate has improved, the problem of a complete prevention of ischemic spinal cord injury on the thoracoabdominal aortic operations remains unsolved. The multimodality approach is needed to reduce the risk of this devastating complication. First Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
            • Adachi H, Kawahito K, Yamaguchi A, Murata S, Adachi K and Ino T (2004). [Repair of thoracic and thoracoabdominal aortic aneurisms by the use of hypothermic circulatory arrest]. Kyobu Geka 57: 291-4. From 1993 to 2003, repair of thoracic and thoracoabdominal aortic aneurysms using hypothermic circulatory arrest via the left thoracotomy was performed in 115 patients at our hospital. Ninety-one of them were elective cases and 24 of them were emergent cases. Hospital mortality rate was 3.3% in elective cases and 12.5% in emergent cases. Over all hospital mortality rate was 5.2%. Ischemic spinal cord injury was occurred in 2 patients (1.7%). Both of them needed total replacement of thoracoabodominal aorta by the graft. In the near future, Adamkiewicz artery may be detected by the imaging technology preoperatively and we expect the repair of thoracoabdominal aortic aneurysm may become safer operation avoiding spinal cord injury. Hypothermic circulatory arrest is a relatively safe and reliable method for the repair of thoracic and thoracoabdominal aortic aneurysms. Department of Cardiovascular Surgery, Omiya Medical Center, Jichi Medical School, Saitama, Japan.
            • Mariak Z, Lyson T and Rudzinski W (2004). [Hypothermia as a neuroprotective agent]. Neurol Neurochir Pol 38: 51-4. Hypothermia has long been employed for therapeutic purposes but its use has been limited because of the potential life-threatening side-effects. In late eighties a neuroprotective effect of bold hypothermia was demonstrated and this implied that the method could be used more safely. It has then been shown in a lot of animal experiments that post-ischaemic mild hypothermia significantly limits damage to the brain caused by cardiac arrest. Similar results have been obtained for local brain ischaemia and for experimental head trauma. Molecular basis for this neuroprotection with mild hypothermia has been found to be complex, involving attenuation of the excitotoxic effects of glutamate and diminishing the synthesis of free radicals. In the last decade some clinical series and multicenter randomised trials have shown that mild hypothermia is safe and effective in global brain ischaemia due to cardiac arrest. Clinical data suggest also its effectiveness in ischaemic stroke though no multicenter randomised study has been published to date. At present there are conflicting results of clinical trials concerning brain injuries. Although some authors have reported up to 38% improvement in the outcome, a recently published multicenter randomised trial has failed to demonstrate any practical benefit of mild hypothermia after acute brain injury. There is however virtually no data in the literature on mild hypothermia in spinal cord injury. Klinika Neurochirurgii, Akademia Medyczna, ul. M. Sklodowskiej-Curie 24a, 15-276 Bialystok.
            • Guest JD, Vanni S and Silbert L (2004). Mild hypothermia, blood loss and complications in elective spinal surgery. Spine J 4: 130-7. BACKGROUND CONTEXT: Spinal surgery carries risks of incidental spinal cord and nerve root injury. Neuroprotection, to minimize the extent of such injuries, is desirable. However, no neuroprotective strategies have been conclusively validated in nonvascular spinal surgery. Mild hypothermia resulting from general anesthesia is a readily achievable potential neuroprotective strategy. Mild hypothermia, however, has been associated with wound infection, increased operative blood loss and other complications. No previous studies have specifically evaluated whether mild hypothermia is associated with an increased risk of these complications in elective spinal surgery. PURPOSE: We investigated the association between incidental mild hypothermia, perioperative complications and operative blood loss. STUDY DESIGN/SETTING: This is a retrospective study employing cohort analysis, rank analysis and single and multivariate linear regression. The setting was the Veterans Administration Medical Center, a teaching hospital of the University of Miami. PATIENT SAMPLE: Data on a total of 70 adult veterans aged 23 to 81 years undergoing complex spinal procedures in which passive cooling was employed during surgical decompression. OUTCOME MEASURES: The variables measured were temperature, blood loss, mean arterial pressure (MAP) and duration of anesthesia. The outcome measured was the presence or absence of complications. METHODS: After 70 patients had been acquired, regression and rank analyses were performed to test for a link between mild hypothermia and blood loss. In addition, two cohorts, patients who experienced complications, and those who did not experience complications in the perioperative period, were compared for several variables including three measures of exposure to hypothermia. Surgical procedures included 60 cervical, 1 occipitocervical, 1 cervicothoracic, 7 thoracic and 1 thoracolumbar procedure. Hypothermia followed induction of anesthesia; esophageal or bladder temperature was monitored. Cooling was passive; warming utilized a forced air blanket. Temperature data from anesthetic records was used to derive mean intraoperative temperature, nadir intraoperative temperature and the rates of cooling and rewarming. The time course of hypothermia, the overall fluctuation in core temperature and the quantity of subbaseline temperature were determined. Medical and surgical complications were included. Two patients with complications considered irrelevant to hypothermia were removed from further analysis. Patients with and without complications were compared as cohorts for differences in mean values of age, comorbid risk factors, intraoperative MAP, intraoperative blood loss, anesthetic duration and temperature-related measures. Relationships between blood loss, anesthesia duration and temperature parameters were assessed in rank and regression analyses. RESULTS: Patients with complications (n=12) had longer mean anesthetic durations (p=.0001) and larger mean surgical blood losses (p=.001) than patients without complications (n=56). Neither mean nor nadir intraoperative hypothermic temperatures were statistically associated with complications. However, large hypothermic integrals (p=.04) and the total quantity of recorded temperature fluctuation (p=.01) were both associated with complications. Comorbid risk factors, MAP and age were not statistically linked to complications. Finally, no relationship between any of the temperature measures and increased blood loss was found. CONCLUSION: Operative blood loss was not linked to any index of the patient's temperature. Longer anesthesia durations were linked to complications and increased blood loss. Regarding mild hypothermia, neither mean nor nadir hypothermic temperatures were linked to complications, but the estimated total quantity of subbaseline temperature was linked, as was total fluctuation in temperature. Lengthy exposure to mild hypothermia appeared to be associated with wound infections. The use of mild hypothermia as a potential neuroprotective strategy during spinal surgery appears to be reasonably safe, but to avoid complications, the duration of hypothermic exposure should be minimized. Department of Neurological Surgery and the Miami Project to Cure Paralysis, University of Miami, Lois Pope LIFE Center, 1095 NW 14th Terrace (D4-6), and the Veterans Affairs Medical Center, Miami, FL 33136, USA.
            • Sugawara Y, Sueda T, Orihashi K, Okada K, Kochi K and Imai K (2003). Trans-vertebral regional cooling for spinal cord protection during thoracoabdominal aortic surgery: an experimental study. Hiroshima J Med Sci 52: 35-41. We developed a simple cooling method for spinal cord protection against ischemic injury during aortic surgery. The neuroprotective effects of our method were investigated using an animal study. Selective spinal hypothermia was produced by means of originally-designed cooling pads placed over the lower thoracic and lumbar vertebral column. Spinal cord ischemia was induced by cross-clamping the thoracic aorta for 60 min in beagle dogs. The neuroprotective effects were evaluated by a multi-modal study. The motor-evoked potentials of the spinal cord resulting from transcranial electric stimulation (MEPs) were recorded during both the ischemic and reperfusion periods. Hindlimb motor function was graded with the Tarlov score, and a histologic examination of the spinal cord injury was performed, at 24 hours after ischemia in animals undergoing hypothermia (hypothermia group: n = 7) or a sham (control group: n = 7). The spinal cord temperatures at the lower thoracic (T10) and lumbar (L3) levels decreased by -9.1 degrees C per hour and -8.1 degrees C per hour, respectively. The amplitude of the MEPs decreased during ischemia in both groups of animals, and significantly recovered during the early phase of aortic reperfusion in the hypothermia group. The Tarlov scores in the hypothermia and control groups were 3.3 +/- 1.0 and 1.1 +/- 1.5 (mean +/- SD, p = 0.015), respectively. Histopathologic study revealed that ischemic injury of the lumbar cord was reduced in the animals undergoing hypothermia. Trans-vertebral regional cooling reduced ischemic spinal cord injury in a canine study. The current method is potentially feasible for clinical use, especially in view of its technical simplicity and few procedure-related complications. Department of Surgery, Division of Clinical Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, Japan.
            • Reyes O, Sosa I and Kuffler DP (2003). Neuroprotection of spinal neurons against blunt trauma and ischemia. P R Health Sci J 22: 277-86. Each year in the Unites States there are over 10,000 new cases of para- and quadriplegia, and more than 100,000 cases of limited, but permanent, neurological losses. Many of these losses result from blunt trauma and ischemia to the spinal cord which leads to neuron death. Although blunt trauma directly kills neurons due to the physical trauma, over the subsequent 48 hours an even larger population of neurons dies due to secondary causes. One of leading triggers of this neuron death is ischemia due to the disruption of the blood circulation. Selective, but unavoidable, spinal cord ischemia occurs during thoracoabdominal surgery to repair aortic aneurysms. This ischemia leads to neuron death, functional neurological loss, and paraplegia in up to 33% of the cases. Thus, both blunt trauma and induced ischemia have similar triggers of neuron death. To reduce the neurological losses resulting from ischemia mechanisms must be found to make spinal neurons more tolerant to ischemic insult and other secondary causes of neuron death. In this review we discuss mechanisms being developed, predominantly using animal models, to provide neuroprotection to prevent neurological losses following blunt trauma and during induced spinal cord ischemia. In parallel, our own experiments are looking at neuroprotective techniques using adult human neurons. We believe the optimal neuroprotective approach will involve the perfusion of the ischemic region of the spinal cord with a hypothermia solution containing a combination of pharmacological agents. Divisions of Orthopedic Surgery, University of Puerto Rico.
            • Cakir O, Erdem K, Oruc A, Kilinc N and Eren N (2003). Neuroprotective effect of N-acetylcysteine and hypothermia on the spinal cord ischemia-reperfusion injury. Cardiovasc Surg 11: 375-9. The purpose of this study was to investigate the effect of N-acetylcysteine (NAC) on spinal cord ischemia-reperfusion (I-R) in rabbits. Thirty rabbits were divided into five equal groups, group I (sham-operated, no I-R), group II (control, only I-R), group III (I-R+NAC), group IV (I-R+hypothermia), group V (I-R+NAC+hypothermia). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Forty-eight hours postoperatively, the motor function of the lower limbs was evaluated in each animal according to Tarlov Score. Spinal cord samples were taken to evaluate the histopathological changes. The sham-operated rabbits (group I) showed no neurologic deficit (Score=4). Paraplegia (Score=0) developed in all rabbits in the control group (group II). Administration of 50 mg/kg of NAC (group III) resulted in significant reduction of motor dysfunction (Score=3.1+/-1.3, p=0.002). Application of hypothermia alone (group IV) showed significant recovery of motor functions (Score=3.0+/-1.1, p=0.002), and combination of hypothermia and 50 mg/kg of NAC (group V) showed complete recovery of lower limb motor function (Score=4, p=0.001). Histologic examination of the spinal cord in rabbits with paraplegia revealed several injured neurons. The cords of animals with no motor function deficits showed only minimal cellular infiltrates in the gray matter, and there was good preservation of nerve cells. NAC showed protective effects of the spinal cord. Moderate hypothermia alone also showed protective effects. Combined use of NAC and hypothermia resulted in highly significant recovery of spinal cord function. Department of Thoracic and Cardiovascular Surgery, Dicle University, School of Medicine, Diyarbakir, Turkey.
            • Inamasu J, Nakamura Y and Ichikizaki K (2003). Induced hypothermia in experimental traumatic spinal cord injury: an update. J Neurol Sci 209: 55-60. The use of induced hypothermia in the treatment of traumatic spinal cord injury (SCI) has been studied extensively between the 1960s and 1970s. Although the treatment showed some promise, it became less popular by the 1980s, mainly because of its adverse effects. However, a revival of hypothermia in the treatment of traumatic brain injury (TBI) in the last decade has encouraged neuroscientists to conduct experiments to reevaluate the potential benefits of hypothermia in traumatic SCI. All laboratory investigations studying the mechanisms of action and/or the efficacy of induced hypothermia in treating experimental traumatic SCI published in the last decade were reviewed. Although efficacy of hypothermia in improving functional outcome of mild to moderate traumatic SCI has been demonstrated, hypothermia may not be protective against severe traumatic SCI. At present, induced hypothermia has yet to be recognized or approved as a potential treatment having therapeutic value for traumatic SCI in humans. The continued search for a possible synergistic effect of induced hypothermia and pharmacological therapy may yield some promise. It has also been deduced from these laboratory studies that hyperthermia is deleterious and rigorous measures to prevent hyperthermia should be taken to minimize the propagation of secondary neuronal damage after traumatic SCI. Department of Neurosurgery, National Tokyo Medical Center, Higashigaoka 2-5-1, Meguro, Tokyo 152-8902, Japan.
            • Svensson LG, Khitin L, Nadolny EM and Kimmel WA (2003). Systemic temperature and paralysis after thoracoabdominal and descending aortic operations. Arch Surg 138: 175-9; discussion 180. HYPOTHESIS: Systemic temperature influences the development of neurologic deficits after aortic surgery. DESIGN: Retrospective case-comparison study of prospectively collected data. SETTING: Tertiary referral center. PATIENTS AND INTERVENTIONS: We examined spinal cord injury according to mild passive hypothermia (mean temperature, 36.5 degrees C; n = 25), moderate active hypothermia (temperature range, 29 degrees C-32 degrees C; n = 76), or profound hypothermia (temperature, <20 degrees C; n = 31) for complex repairs in 132 patients. Aortic dissection was present in 67 patients (51%), 41 (31%) had leaks or rupture, 39 (30%) were reoperations on the descending thoracic aorta, and 27 (20%) had concurrent arch and/or ascending thoracic aortic repairs. MAIN OUTCOME MEASURE: Occurrence of permanent and transient deficits. RESULTS: Five patients (3.8%) had permanent deficits. One (4.0%) of the 25 patients underwent mild hypothermia, 3 (3.9%) of the 76 patients who underwent moderate hypothermia, and 1 (3.2%) of the 31 patients who underwent profound hypothermia (P =.70). Reversible deficits occurred in 7 patients (total 32%) who underwent mild hypothermia, 2 patients (total 6.6%) underwent moderate hypothermia, and 1 (total 6.5%) underwent profound hypothermia (P =.004). Six were delayed neurologic deficits. Independent predictors were intercostal ischemic time (P =.02), mild hypothermia (P =.004), and no cerebrospinal fluid drainage (P =.05). The total 30-day survival was 92.4% (122 of 132 patients). The only multivariable predictor of death was acuity of surgery (namely, emergent, urgent, or elective) (P =.06). CONCLUSIONS: Moderate or profound hypothermia resulted in fewer transient neurologic deficits. Thus, we recommend active cooling and cerebrospinal fluid drainage for most patients, and profound hypothermia for patients undergoing complex repairs and reoperations. Center for Aortic Surgery, Marfan and Connective Tissue Disorder Clinic, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, Ohio 44195, USA.
            • Tetik O, Islamoglu F, Goncu T, Cekirdekci A and Buket S (2002). Reduction of spinal cord injury with pentobarbital and hypothermia in a rabbit model. Eur J Vasc Endovasc Surg 24: 540-4. OBJECTIVES: to evaluate the effects of hypothermia and pentobarbital on spinal cord ischaemia induced in a rabbit model. MATERIALS AND METHODS: thirty-two rabbits, allocated into four equal groups, had the infrarenal aorta clamped distal to the left renal artery and above the iliac bifurcation for 40 min. Groups 3 and 4 had infusion of 15 mg/kg of pentobarbital intravenously for 5 min, 15 min before the cross-clamping. Groups 2 and 4 had infusion of 20 ml of Ringer's lactate (LR) solution at 3 degrees C for 3 min during aortic cross clamp into the isolated aortic segment. Group 1 was untreated and served as control. Postoperative functions of spinal cord were assessed. RESULTS: paraplegia occurred in all rabbits in Group 1, in one in each of Groups 2 and 3, whereas no paraplegia was observed in Group 4. In addition 2 and 3 animals of Groups 2 and 3, respectively revealed varying degree of neurological disturbances, whereas all animals of Group 4 had normal function. This difference between Groups 2, 3, and 4 vs Group 1 was significant (p<0.002). So was the difference between Groups 2 and 4 (p=0.03), whereas the difference between Groups 3 and 4 was not significant. CONCLUSIONS: hypothermia and pentobarbital was more effective than hypothermia alone for prevention of spinal cord ischaemia in a rabbit model. Department of Cardiovascular Surgery, Ataturk Medical Research Hospital, Izmir, Turkey.
            • Kouchoukos NT, Masetti P, Rokkas CK and Murphy SF (2002). Hypothermic cardiopulmonary bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 74: S1885-7; discussion S1892-8. BACKGROUND: Hypothermic cardiopulmonary bypass with circulatory arrest is an important adjunct for operations on the distal aortic arch, the descending thoracic, and the thoracoabdominal aorta. The safety and efficacy of this technique when compared with other adjuncts (ie, simple aortic clamping, partial cardiopulmonary bypass, regional hypothermia) is not clearly established. METHODS: One hundred and ninety-two patients (age range, 20 to 83 years) with descending thoracic or thoracoabdominal aortic disease had resection and graft replacement of the involved aortic segments using hypothermic cardiopulmonary bypass and intervals of circulatory arrest (mean, 38 minutes). The technique was used when the location and severity of disease precluded placement of clamps on the proximal aorta (31 patients) or (in 161 patients) when extensive thoracic (47) or thoracoabdominal (114) aortic disease was present, and the risk for development of spinal cord ischemic injury was judged to be increased. Lower intercostal and lumbar arteries were attached separately to the aortic graft in 101 of the 161 patients (63%) who had extensive aortic replacement. No other adjuncts for spinal cord protection were used. RESULTS: The 30-day mortality was 6.8% (13 patients). It was 40% (8 of 20) for patients having emergent operations (acute aortic dissection or rupture) and 2.9% (5 of 172) for all others (p < 0.001). The 90-day mortality was 12.5% (24 patients). Paraplegia occurred in 4 and paraparesis in 1 (full recovery) of the 186 operative survivors whose lower limb function could be assessed postoperatively (2.7%). Among the 109 survivors with thoracoabdominal aortic disease, early paraplegia occurred in 1 of 36 with Crawford extent I, 0 of 42 with extent II, and 2 of 31 with extent III disease. One patient (extent II) developed paraplegia on the 9th postoperative day after a hypotensive episode. None of the 47 patients with aortic dissection developed paralysis. Among the 186 operative survivors, renal dialysis was required in 4 patients (2.2%), prolonged inotropic support in 18 (10%), reoperation for bleeding in 9 (5%), mechanical ventilation (> or = 48 hours) in 64 (34%), and tracheostomy in 17 (9%). Four patients (2%) sustained a stroke. CONCLUSIONS: Hypothermic cardiopulmonary bypass with circulatory arrest provides safe and substantial protection against paralysis and renal, cardiac, and visceral organ system failure that equals or exceeds that of other currently used techniques but without the need of other adjuncts. Division of Cardiovascular and Thoracic Surgery, Missouri Baptist Medical Center, St. Louis, USA.
            • Tsutsumi K, Ueda T, Shimizu H, Hashizume K, Iino Y and Kawada S (2002). Effect of post-ischemic hypothermia on spinal cord damage induced by transient ischemic insult in rabbits. Jpn J Thorac Cardiovasc Surg 50: 359-65. OBJECTIVE: The effect of post-ischemic mild hypothermia applied immediately after induced transient ischemia on the extent of neuronal damage to the spinal cord was investigated in rabbit. SUBJECTS AND METHODS: A 15-minute period of transient abdominal aortic occlusion for spinal cord ischemia at a rectal temperature of 37.3 +/- 0.3 degrees C was performed just below the left renal vein via median laparotomy. Three groups of rabbits were investigated; Group 1 (n = 8) subjected to ischemia and reperfused at the same temperature for 7 hours, Group 2 (n = 8) also subjected to ischemia and then to 6 hours of systemic hypothermia (32.5 +/- 0.5 degrees C), and Group 3 (n = 8) non-ischemic controls. All the rabbits in Group 1 and Group 2 were sacrificed at 1 week after ischemic injury. Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage. RESULTS: The mean modified Tarlov's score at 1 week after ischemic injury was 0.5 +/- 0.8 in Group 1, whereas it was 4.4 +/- 1.4 (p < .001) in Group 2. The mean total number of surviving neurons within examined sections of the spinal cord was significantly greater in Group 2 than in Group 1 (Group 1: 81 +/- 66.1 vs Group 2: 300.9 +/- 154.1, p < .001). CONCLUSION: Post-ischemic hypothermia induced immediately after reperfusion significantly reduced ischemia-induced neuronal damage in rabbit. Department of Cardiovascular Surgery, Keio University School of Medicine, Tokyo, Japan.
            • Tabayashi K, Motoyoshi N, Akimoto H, Tsuru Y, Sakurai M, Itoh T, Fukuju T and Iguchi A (2002). Epidural cooling for regional spinal cord hypothermia during most or all of descending thoracic or thoracoabdominal aneurysm repair. Acta Chir Belg 102: 224-9. PURPOSE: Hypothermia has some protective effect against ischemia of the spinal cord in thoracoabdominal aneurysm repair. Its method is divided into systemic or regional cooling. Several experimental studies of the regional cooling of the spinal cord have been performed, however, clinical reports are few. The purpose of this study is to evaluate the effect and safety of perfusion cooling of the epidural space during thoracic or thoracoabdominal aortic replacement. METHODS: Between January 1998 to June 2001 37 patients (True aneurysm: 18 patients, type B aortic dissection: 19 patients) underwent thoracic or thoracoabdominal aortic replacement with an aid of epidural perfusion cooling. The age ranged from 23 to 78 years old with a mean age of 61 years old. Separate perfusion of upper and lower body was used in all cases. Temperature was lowered to around a 31 degrees C or 32 degrees C. In cases where proximal cross-clamping was danger, deep hypothermic circulatory arrest was used. RESULTS: Ten patients underwent most or all of descending thoracic aneurysm repair with no spinal cord injury and hospital death. Number of patients of the Crawford type I, type II, and type III were 14, 8 and 5 patients, respectively. One Crawford type II patients was complicated with postoperative spinal cord injury (2.7%). There was one hospital death (2.7%) in Crawford type III. The mean epidural cooling time was 150 minutes, and mean infusion volume of cold saline was 981 cc. The mean lowest cerebrospinal fluid (CSF) temperature was 24.3 degrees C, and mean temperature differences between nasopharynx and CSF was 6.3 degrees C. CONCLUSION: Perfusion cooling of the epidural space during most or all of the descending thoracic or thoracoabdominal aneurysm repair was effective in reducing postoperative spinal cord injury and a safe method in clinical situations. Department of Cardiovascular Surgery, Graduate School of Medicine, Tohoku University, Japan.
            • Inamasu J and Ichikizaki K (2002). Mild hypothermia in neurologic emergency: an update. Ann Emerg Med 40: 220-30. Induced hypothermia to treat various neurologic emergencies, which had initially been introduced into clinical practice in the 1940s and 1950s, had become obsolete by the 1980s. In the early 1990s, however, it made a comeback in the treatment of severe traumatic brain injury. The success of mild hypothermia led to the broadening of its application to many other neurologic emergencies. We sought to summarize recent developments in mild hypothermia, as well as its therapeutic potential and limitations. Mild hypothermia has been applied with varying degrees of success in many neurologic emergencies, including traumatic brain injury, spinal cord injury, ischemic stroke, subarachnoid hemorrhage, out-of-hospital cardiopulmonary arrest, hepatic encephalopathy, perinatal asphyxia (hypoxic-anoxic encephalopathy), and infantile viral encephalopathy. At present, the efficacy and safety of mild hypothermia remain unproved. Although the preliminary clinical studies have shown that mild hypothermia can be a feasible and relatively safe treatment, multicenter randomized, controlled trials are warranted to define the indications for induced hypothermia in an evidence-based fashion. Department of Emergency Medicine, National Tokyo Medical Center, Tokyo, Japan.
            • Martelli E, Cho JS, Mozes G and Gloviczki P (2002). Epidural cooling for the prevention of ischemic injury to the spinal cord during aortic occlusion in a rabbit model: determination of the optimal temperature. J Vasc Surg 35: 547-53. PURPOSE: This experiment was designed for the determination of the optimal epidural cooling temperature for the allowance of spinal cord protection with minimal side effects during an aortic occlusion-induced spinal cord ischemia model in rabbits. METHODS: Spinal cord ischemia was induced in rabbits with infrarenal aortic occlusion for 40 minutes. Spinal cord cooling was effected with epidural infusion of normal saline solution at the following different temperatures: group 1, 17 degrees C (n = 6); group 2, 24 degrees C (n = 6); group 3, 32 degrees C (n = 6); and group 4, 39 degrees C (n = 3). Sham-operated rabbits without aortic occlusion were used as controls with epidural infusion at healthy body temperature (39 degrees C; n = 3). Motor function was assessed at 48 hours with Tarlov's criteria, and the animals were killed. The spinal cord was sectioned into multiple segments, and semiquantitative histologic scoring (0 to 5) was used to grade ischemic injury. RESULTS: Cooling solution and spinal cord temperatures showed linear correlation (r = 0.95). All the rabbits in groups 1 (except one with mild weakness), 2, and 3 were neurologically intact, and all in group 4 had paraplegia develop (P < .001). One rabbit in group 1 died from increased intracranial pressure (ICP). Mean blood pressure, ICP, and body temperature were similar among the groups. Histology correlated with the clinical findings. In groups 1 and 2, minimal histologic changes were noted. Low-grade ischemic changes were present in group 3 in the low-lumbar and mid-lumbar segments. Severe ischemic injury occurred at the same segments in group 4 (P < .05). CONCLUSION: These study results suggest that in rabbits satisfactory spinal cord protection during aortic occlusion can be achieved at moderate regional hypothermia (24 degrees C). Large volume infusion for the achievement of profound hypothermia may cause deleterious effects of increased ICP and is not warranted. Department of Surgery, Mayo Clinic, Rochester, MN 55905, USA.
            • Zvara DA (2002). Thoracoabdominal aneurysm surgery and the risk of paraplegia: contemporary practice and future directions. J Extra Corpor Technol 34: 11-7. Thoracoabdominal aneurysm surgery is associated with a high incidence of morbidity and mortality. Spinal cord ischemia and the risks of paraparesis or paraplegia remain devastating complications. The mechanisms of spinal cord injury involve both acute ischemic injury and delayed reperfusion injury. Blood flow to the spinal cord frequently arises in the segment of the aorta requiring aortic cross clamping. As such, there is an obligate period of blood flow disruption. Multiple strategies have evolved to reduce the ischemic interval and to provide adjunct interventions to reduce the impact of the ischemia. Despite a multidisciplinary approach, a spinal cord ischemia is present in approximately 4 to 16% of patients, depending on the type of aneurysm and other comorbid diseases. Cerebral spinal fluid drainage, distal perfusion techniques, intercostal artery anastomosis, hypothermia techniques, and mechanisms of ischemic preconditioning are interventions employed to reduce the risk of paraplegia after thoracal-abdominal aortic surgery. Surgeons, anesthesiologists, and perfusionist are intimately involved in the decision making as to which interventions will be employed in a given case. Although these adjuncts have been evaluated in multiple animal and human protocols, the efficacy of each intervention when looked at in isolation remains difficult to determine fully. This is attributable, in part, to the complex mechanisms of the patient injury, the inherint risks of the surgical procedure, and the confounding effects of comorbid disease states. Nonetheless, clinicians must have comprehensive understanding of these various interventions and their application. This review serves as an overview of these various interventions with special emphasis on outcome data. Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
            • Downey C (2000). Epidural cooling for spinal cord protection during thoracoabdominal aortic aneurysm repair (a case study). Can Oper Room Nurs J 18: 9-14. Aneurysms result from damage to artery walls as a result of underlying athrosclerotic and/or thromboembolic disorders. A thoracoabdominal aortic aneurysm involves vessel damage and wall weakening in the thoracic and abdominal segments of the aorta. Thoracoabdominal aortic aneurysm repair is considered to be high risk due to the nature of the intervention that requires an extensive incision with clamping of the thoracic aorta above the renal arteries. Clamping of the aorta renders all areas distal to the clamp at high risk for ischemic trauma especially to the spinal cord where the risk of neurological deficits postoperatively is 7-16% (Cambria, et al., 1997; Davison, et al., 1997). Several adjunct interventions have been tried to reduce the risk of spinal cord injury associated with the ischemia of cross clamping. Epidural cooling has been successful as an adjunct in reducing the neurological deficits. A preoperative nursing assessment indicating the appropriate nursing diagnoses and nursing care required for this patient, allowed for individualization of the plan needed to include this new procedure and plan for best patient outcomes and practices.
            • Yu J, Wang J and Xiong J (2001). [Protective effect of epidural cooling upon ischemic spinal cord injury]. Zhonghua Yi Xue Za Zhi 81: 280-2. OBJECTIVE: To evaluate the protective effect of epidural cooling on ischemic spinal cord injury. METHODS: Fourteen healthy hybrid dogs were randomly divided into two groups: control group (n = 8) and experimental group (n = 6). Spinal cord injury was induced by double aortic cross-clamping for 40 minutes. Before the clamping, the cerebrospinal fluid temperature of the animals in experimental group was decreased to 30 degrees C +/- 1 degrees C by epidural cooling until the aorta was unclamped for 5 minutes. Three days after the operation, the function of the hind limbs of the animals was evaluated by Tarlov's scale and histological examination of the spinal cord was made. RESULTS: Six dogs showed complete paraplegia (grade 0) and two showed paresis (grade 1) in the control group. The neurological outcome of the experimental group was much better than that in the control group (H = 10.68, P = 0.001). The neurological function of 4 dogs in the experimental group was in grade 4, and one in grade 3. Histological examination revealed hemorrhage of gray matter, degeneration and necrosis of neurons, and severe demyelination of myelinated nerve fibers in the spinal cord from T10 to sacral segments in dogs with paraplegia. The changes in spinal cord were slight in the dogs without severe neurological injury. CONCLUSION: Local hypothermia of spinal cord by epidural cooling provides effective protection against ischemic spinal cord injury in dog. The First Hospital Affiliated to China Medical University, Shenyang 110001, China.
            • Westergren H, Farooque M, Olsson Y and Holtz A (2001). Spinal cord blood flow changes following systemic hypothermia and spinal cord compression injury: an experimental study in the rat using Laser-Doppler flowmetry. Spinal Cord 39: 74-84. STUDY DESIGN: It is well known that changes of the body temperature as well as trauma influence the blood flow in the brain and spinal cord. However, there is still a lack of knowledge concerning the levels of blood flow changes, especially during hypothermia. OBJECTIVES: This investigation was carried out to examine the effects of systemic hypothermia and trauma on spinal cord blood flow (SCBF). METHODS: Twenty-four rats were randomized either to thoracic laminectomy only (Th VII-IX) or to 35 g spinal cord compression trauma. The animals were further randomized to either constant normothermia (38 degrees C) or to a systemic cooling procedure, ie reduction of the esophageal temperature from 38 to 30 degrees C. SCBF was recorded 5 mm caudal to the injury zone using Laser-Doppler flowmetry which allows a non-invasive continuous recording of local changes in the blood flow. The autoregulation ability was tested at the end of the experiments by inducing a 30-50 mmHg blood-pressure fall, using blood-withdrawal from the carotid artery. RESULTS: The mean SCBF decreased 2.8% and 3.5% per centigrade reduction of esophageal temperature in the animals sustained to hypothermia with and without trauma, respectively. This could be compared to a decrease of 0.2%/min when only trauma was applied. No significant differences were seen between the groups concerning auto regulatory ability. CONCLUSIONS: Our results indicate that the core temperature has a high impact on the SCBF independent of previous trauma recorded by Laser-Doppler flowmetry. This influence exceeds the response mediated by moderate compression trauma alone. Unit of Neurosurgery, Department of Neuroscience, Uppsala University, Sweden.
            • Dzsinich C, Nagy G, Selmeci L, Sepa G, Fazekas L, Kekesi V and Juhasz-Nagy S (2000). [Effect of regional hypothermia on cerebrospinal fluid parameters during thoracoabdominal aorta clamping in dogs]. Magy Seb 53: 79-84. The most feared complication of thoracoabdominal clamping is the paraplegia or paraparesis following ischemic injury of the spinal cord. Early intraoperative recognition of this complication has not been solved yet. In our earlier experiment we found significant alterations of CSF glucose, lactate, pCO2 and Neuron Specific Enolase (NSE) levels during 60 minutes thoracoabdominal aortic clamping in dogs. The analysis of these parameters proved to be proper to follow metabolism of the spinal cord during this type of surgery. In our present paper we studied protective effect of regional hypothermia using peridural cooling by registration of above parameters. Statistical analysis of our data showed prevention of production of anaerobe metabolites in animals with icy peridural irrigation. The biochemical approach is appropriate for monitoring effectiveness of regional hypothermia of the spinal cord during aortic surgery. Semmelweis Egyetem Budapest Altalanos Orvostudomanyi Kar Er- es Szivsebeszeti Klinika, Budapest.
            • Mori K, Maeda T, Shiraishi Y and Kawai Y (2001). Effects of hypothermia on blood flow and neural activity in rabbit spinal cord during postischemic reperfusion. Jpn J Physiol 51: 71-9. The effects of hypothermia on blood flow and neural activity were investigated in rabbit spinal cord during the acute phase of ischemia/reperfusion. Rabbits were exposed to ischemia for 10 or 40 min by occluding the abdominal aorta, using a balloon catheter. The body temperature was maintained either at 38 degrees C (normothermia) or 34 degrees C (hypothermia). Hyperperfusion was observed within 10 min after the cessation of ischemia in all rabbits exposed to ischemia. The magnitude of hyperperfusion in spinal cord blood flow (SCBF) was not significantly different between the 10 and 40 min ischemia rabbits, but the time for 50% recovery from the hyperperfusion was longer in the 40 min ischemia group (26.1 +/- 2.5 min) than in the 10 min group (15.1 +/- 2.1 min). The amplitude of evoked spinal cord potential decreased during ischemia and recovered to the baseline level during 8 h of reperfusion in the 10 min ischemia group. However, in the 40 min ischemia group, the amplitude was 40 +/- 8% of the baseline value after 8 h of reperfusion. Hypothermia prevented the delay of recovery from hyperperfusion and the reduction of evoked spinal cord potential. These results suggest that hypothermia plays a beneficial role in protecting tissue injury in the acute phase of ischemia/reperfusion in the spinal cord by shortening the time for recovery from postischemic hyperperfusion. Department of Physiology, Faculty of Medicine, Tottori University, Yonago, 683-8503 Japan.
            • White RJ and Albin M (2001). Spinal cord cooling. J Neurosurg 94: 183-4.
            • Kuchner EF, Hansebout RR and Pappius HM (2000). Effects of dexamethasone and of local hypothermia on early and late tissue electrolyte changes in experimental spinal cord injury. J Spinal Disord 13: 391-8. The current experiment reexamines this laboratory's frequently cited previous experimental conclusion that a mechanism underlying the beneficial effects of glucocorticoids in the treatment of spinal cord injury may be the enhanced preservation of spinal cord tissue potassium. For the first time, similar methodology also has been applied to study the effects of hypothermia. Canine spinal cords were injured at T13 by use of an epidural balloon and then were treated with local hypothermia or intramuscular dexamethasone or both. Motor recovery was assessed using a modified Tarlov scale. At either 6 days or 7 weeks, spinal cords T8 through L4 were removed and divided into 10 ordered blocks, which were analyzed for wet and dry weight, potassium concentration, and sodium concentration. Correlations between clinical motor and chemical results were evaluated. The conclusions drawn are as follows: 1) The canine severe rapid compressive injury model, unlike the previously published less severe feline impact injury model, is not associated with widespread early loss of spinal cord tissue potassium content (dry weight). 2) The dog compressive model, unlike the cat impact model, does not provide evidence that one fundamental mechanism of the confirmed beneficial action of steroids entails enhanced early preservation of tissue potassium content. 3) At 6 days, decrease in the percentage of dry weight and increase in sodium concentration, representing edema, occurred at and adjacent to the direct compression site in all lesioned dog groups except those treated with dexamethasone, demonstrating an antiedema effect of dexamethasone that was nullified by concurrent local hypothermia. 4) This antiedema effect of dexamethasone was associated with superior early motor improvement but did not lead to superior long-term function, in comparison with hypothermia. 5) At 7 weeks, decrease in the percentage of dry weight and potassium concentration, and increase in sodium concentration, all restricted to the directly compressed segment, signify necrosis. 6) This new chemical index of necrosis was highly correlated with clinical motor performance. Department of Neurosurgery, Montreal Neurological Institute, McGill University, Quebec, Canada.
            • Yu WR, Westergren H, Farooque M, Holtz A and Olsson Y (2000). Systemic hypothermia following spinal cord compression injury in the rat: an immunohistochemical study on MAP 2 with special reference to dendrite changes. Acta Neuropathol (Berl) 100: 546-52. Systemic hypothermia has been shown to exert neuroprotective effects in experimental ischemic CNS models caused by vascular occlusions. The present study addresses the question as to whether systemic hypothermia has similar neuroprotective qualities following severe spinal cord compression trauma using microtubule-associated protein 2 (MAP2) immunohistochemistry combined with the avidin-biotin-peroxidase complex method as marker to identify neuronal and dendritic lesions. Fifteen rats were randomized into three equally sized groups. One group sustained thoracic laminectomy, the others severe spinal cord compression trauma of the T8-9 segment. The control group contained laminectomized animals submitted to a hypothermic procedure in which the esophageal temperature was reduced from 38 degrees C to 30 degrees C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were sacrificed 24 h following the surgical procedure. The MAP2 immunostaining in the normothermic trauma group indicated marked reductions in MAP2 antigen in the cranial and caudal peri-injury zones (T7 and T10, respectively). This reduction was much less pronounced in the hypothermic trauma group. In fact, the MAP2 antigen was present in almost equally sized areas in both the hypothermic groups independent of previous laminectomy alone or the addition of trauma. Our study thus indicates that hypothermia has a neuroprotective effect on dendrites of rat spinal cords subjected to compression trauma. Department of Genetics and Pathology, University Hospital, Uppsala, Sweden.
            • Dimar JR, 2nd, Shields CB, Zhang YP, Burke DA, Raque GH and Glassman SD (2000). The role of directly applied hypothermia in spinal cord injury. Spine 25: 2294-302. STUDY DESIGN: The effect of intense local hypothermia was evaluated in a precision model of spinal canal narrowing and spinal cord injury in rats. The spinal cord injury was cooled with a custom cooling well used over the epidural surface. Basso, Beattie, and Bresnahan (BBB) motor scores and transcranial magnetic motor-evoked potential (tcMMEP) responses were used after injury to accurately evaluate neurologic recovery. OBJECTIVE: This study was undertaken to determine whether the prognosis for neurologic recovery in a standardized rat spinal cord injury model is altered by the direct application of precisely controlled hypothermia to the area of injury. SUMMARY OF BACKGROUND DATA: The role of hypothermia in the treatment of spinal cord injuries with neurologic deficits remains undefined. Hypothermia may decrease an area of spinal cord injury and limit secondary damage, therefore improving neurologic recovery. However, it has been difficult to consistently apply localized cooling to an area of spinal cord injury, and the use of systemic hypothermia is fraught with complications. This fact, along with the unavailability of a precise spinal cord injury model, has resulted in inconsistent results, both clinically and in the laboratory. In a rat model of spinal cord injury, 37 C and 19 C temperatures were used to study the role of hypothermia on neurologic recovery. METHODS: Male Spraque-Dawley rats (n = 52; weight, 277.7 g) were anesthetized with pentobarbital and subjected to laminectomy at T10. The rats were divided into three groups: 1) placement of a 50% spacer in the epidural space (16 rats), 2) severe (25 g/cm) spinal cord injury (16 rats), 3) 50% spacer in combination with spinal cord injury (16 rats). Eight rats in each group were tested at two temperatures: normothermic (37 C) and hypothermic (19 C). With the use of a specially designed hypothermic pool placed directly over the spinal cord for 2 hours, epidural heating to 37 C, and epidural cooling to 19 C was accomplished. Simultaneous measurements of spinal cord and body temperatures were performed. The rats underwent behavior testing using the BBB motor scores and serial tcMMEPs for 5 weeks. Statistical methods consisted of Student's t tests, one-way analysis of variance, Tukey post hoc t tests and chi2 tests. RESULTS: There was a significant improvement in motor scores in rats subjected to hypothermia compared with those that were normothermic after insertion of a 50% spacer. This improvement was observed during the 5-week duration of follow-up. In the severe spinal cord injury group and the spinal cord injury-spacer groups, no significant improvement in motor scores were obtained when the spinal cord was exposed to hypothermia. CONCLUSION: The results demonstrate that there is a statistically significant (P < 0.05) improvement in neurologic function in rats subjected to hypothermia (19 C) after insertion of a spacer that induced an ischemic spinal cord injury. This indicates that directly applied hypothermia may be beneficial in preventing injury secondary to ischemic cellular damage. The data demonstrated minimal therapeutic benefit of hypothermia (19 C) after a severe spinal cord injury. Departments of Orthopaedic Surgery and Neurological Surgery, University of Louisville, and the Kenton D. Leatherman Spine Center, Louisville, Kentucky 40202, USA.
            • Jou IM (2000). Effects of core body temperature on changes in spinal somatosensory-evoked potential in acute spinal cord compression injury: an experimental study in the rat. Spine 25: 1878-85. STUDY DESIGN: Acute spinal cord injury was induced by a clip compression model in rats to approximate spinal cord injury encountered in spinal surgery. Spinal somatosensory-evoked potential neuromonitoring was used to study the electrophysiologic change. OBJECTIVES: To compare and correlate changes in evoked potential after acute compression at different core temperatures with postoperative neurologic function and histologic change, to evaluate current intraoperative neuromonitoring warning criteria for neural damage, and to confirm the protective effect of hypothermia in acute spinal cord compression injury by electrophysiologic, histologic, and clinical observation. SUMMARY OF BACKGROUND DATA: With the increase in aggressive correction of spinal deformities, and the invasiveness of surgical instruments, the incidence of neurologic complication appears to have increased despite the availability of sensitive intraoperative neuromonitoring techniques designed to alert surgeons to impending neural damage. Many reasons have been given for the frequent failures of neuromonitoring, but the influence of temperature-a very important and frequently encountered factor-on evoked potential has not been well documented. Specifically, decrease in amplitude and elongation of latency seem not to have been sufficiently taken into account when intraoperative neuromonitoring levels were interpreted and when acceptable intraoperative warning criteria were determined. METHODS: Experimental acute spinal cord injury was induced in rats by clip compression for two different intervals and at three different core temperatures. Spinal somatosensory-evoked potential, elicited by stimulating the median nerve and recorded from the cervical interspinous C2-C3, was monitored immediately before and after compression, and at 15-minute intervals for 1 hour. RESULTS: Spinal somatosensory-evoked potential change is almost parallel to temperature-based amplitude reduction and latency elongation. Significant neurologic damage induced by acute compression of the cervical spinal cord produced a degree of effect on the amplitude of spinal somatosensory-evoked potential in normothermic conditions that differed from the effect in moderately hypothermic conditions. Using the same electromonitoring criteria,moderately hypothermic groups showed a significantly higher false-negative rate statistically (35%) than normothermic groups (10%). CONCLUSIONS: Systemic cooling may protect against the detrimental effects of aggressive spinal surgical procedures. There is still not enough published information available to establish statistically and ethically acceptable intraoperative neuromonitoring warning and intervention criteria conclusively. Therefore, an urgent need exists for further investigation. Although a reduction of more than 50% in evoked potential still seems acceptable as an indicator of impending neural function loss, maintenance of more than 50% of baseline evoked potential is no guarantee of normal postoperative neural function, especially at lower than normal temperatures. Department of Orthopedics, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China.
            • Westergren H, Farooque M, Olsson Y and Holtz A (2000). Motor function changes in the rat following severe spinal cord injury. Does treatment with moderate systemic hypothermia improve functional outcome? Acta Neurochir (Wien) 142: 567-73. Systemic hypothermia exerts neuroprotective effects following trauma and ischemia caused by vascular occlusion in the brain. In the spinal cord similar effects have been demonstrated following ischemia after aortic occlusion. We have previously presented protective effects on several morphological parameters in the early period after the injury, using an established spinal cord compression injury model and systemic hypothermia. In the present study we have evaluated the effects on motor function following severe spinal cord compression trauma and treatment with moderate systemic hypothermia. Thirty Sprague Dawley rats were randomized into three groups: In group 1 (n = 4), the animals underwent a hypothermic procedure, including a 2 h hypothermic period with a body temperature of 30 degrees C, following the initial laminectomy. In group 2 (n = 12) a 50 g compression was applied to the spinal cords for 5 min, after which the animals were kept under normothermic anesthesia for 3 h. In group 3 (n = 14), the animals underwent the same trauma procedure as in group 2 and the same hypothermic procedure as in group 1. The animals were allowed to survive for 14 days, during which the motor function was recorded. This degree of trauma results in a non-reversible paraplegia, and the addition of systemic hypothermia as described above did not alter the neurological recovery as measured by two different methods of recording the motor function up to two weeks after injury. All animals survived in group 1. However, the mortality rates in group 2 were 25% and in group 3, 50%, respectively, which mirrors the severity of the trauma. The application of systemic hypothermia and the lack of experimental therapeutic success highlight the difficulties of transferring experimental beneficial neuroprotective effects to a clinically useful treatment method. In this experimental set-up the effects of the severe primary injury may overshadow the effects of the secondary injury mechanisms, which limits the therapeutic possibilities of systemic hypothermic treatment. Department of Neuroscience and Research Group on Neuropathology, Uppsala University, Sweden.
            • Parrino PE, Kron IL, Ross SD, Shockey KS, Fisher MJ, Gaughen JR, Jr., Kallmes DF, Kern JA and Tribble CG (2000). Retrograde venous perfusion with hypothermic saline and adenosine for protection of the ischemic spinal cord. J Vasc Surg 32: 171-8. PURPOSE: Spinal cord injury and the resultant postoperative paraplegia are devastating complications of thoracic aortic surgery, for which no widely accepted protective interventions exist. We hypothesized that retrograde venous perfusion-cooling of the spinal cord with a hypothermic saline and adenosine solution would protect it from ischemic injury caused by thoracic aortic occlusion. METHODS: Adult domestic swine of either sex (weight range, 20 to 30 kg) were intubated and ventilated. A left thoracotomy was performed. The accessory hemiazygous vein was divided, and a catheter was inserted distally. The aorta was clamped at the left subclavian artery. The venous catheter was not used in the animals in the control group (n = 7); in the animals in the experimental group (n = 7), a cold (4 degrees C) saline and adenosine solution was infused into the accessory hemiazygous vein. After 30 minutes, the clamp and catheter were removed, and the chest was closed. A blinded observer evaluated the animals' hind-leg motor activity 24 hours later. The Tarlov scale was used: 0, complete paralysis; 1, minimal movement; 2, stands with assistance; 3, stands alone; 4, weak walk; 5, normal gait. The animals' rectal temperatures were measured at the end of the experiment, and blood pressure was measured throughout. Two other groups were studied to assess the effect of the intervention on spinal cord temperature. RESULTS: The animals in the control group had a mean Tarlov score of 1.7 +/- 0.6; the animals in the experimental group had a mean Tarlov score of 4.9 +/- 0.1 (P <.01). The animals in the experimental group had a significantly greater drop in spinal cord temperature than those in the control group (4. 05 +/- 0.6 degrees C vs 0.58 +/- 0.12 degrees C; P <.01). No significant difference in rectal temperatures was found, nor did any arrhythmias or hypotensive episodes occur in either group. Perfusion of the spinal cord was confirmed with angiography by using this approach. CONCLUSION: Retrograde venous perfusion-cooling of the spinal cord with a hypothermic saline and adenosine solution protects the cord from ischemic injury caused by clamping of the thoracic aorta. Departments of Surgery, Division of Thoracic and Cardiovascular Surgery, and Radiology, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA.
            • Yu CG, Jimenez O, Marcillo AE, Weider B, Bangerter K, Dietrich WD, Castro S and Yezierski RP (2000). Beneficial effects of modest systemic hypothermia on locomotor function and histopathological damage following contusion-induced spinal cord injury in rats. J Neurosurg 93: 85-93. OBJECT: Local spinal cord cooling (LSCC) is associated with beneficial effects when applied following ischemic or traumatic spinal cord injury (SCI). However, the clinical application of LSCC is associated with many technical difficulties such as the requirement of special cooling devices, emergency surgery, and complicated postoperative management. If hypothermia is to be considered for future application in the treatment of SCI, alternative approaches must be developed. The objectives of the present study were to evaluate 1) the relationship between systemic and epidural temperature after SCI; 2) the effects of modest systemic hypothermia on histopathological damage at 7 and 44 days post-SCI; and 3) the effects of modest systemic hypothermia on locomotor outcome at 44 days post-SCI. METHODS: A spinal cord contusion (12.5 mm at T-10) was produced in adult rats that had been randomly divided into two groups. Group 1 rats (seven in Experiment 1; 12 in Experiment 2) received hypothermic treatment (epidural temperature 32-33 degrees C) 30 minutes postinjury for 4 hours; Group 2 rats (nine in Experiment 1; eight in Experiment 2) received normothermic treatment (epidural temperature 37 degrees C) 30 minutes postinjury for 4 hours. Blood pressure, blood gas levels, and temperatures (epidural and rectal) were monitored throughout the 4-hour treatment period. Twice weekly assessment of locomotor function was performed over a 6-week survival period by using the Basso-Beattie-Bresnahan locomotor rating scale. Seven (Experiment 1) and 44 (Experiment 2) days after injury, animals were killed, perfused, and their spinal cords were serially sectioned. The area of tissue damage was quantitatively analyzed from 16 longitudinal sections selected from the central core of the spinal cord. CONCLUSIONS: The results showed that 1) modest changes in the epidural temperature of the spinal cord can be produced using systemic hypothermia; 2) modest systemic hypothermia (32-33 degrees C) significantly protects against locomotor deficits following traumatic SCI; and 3) modest systemic hypothermia (32-33 degrees C) reduces the area of tissue damage at both 7 and 44 days postinjury. Although additional research is needed to study the therapeutic window and long-term benefits of systemic hypothermia, these data support the possible use of modest systemic hypothermia in the treatment of acute SCI. The Miami Project, and Department of Neurological Surgery, University of Miami, Florida, USA.

            There are actually many more studies but no room to list them here.



              Thanks Wise for imput.

              I'm still wondering-why it is not standart procedure in acute sci?

              Can you give your opinion/collaborate on this?


                Originally posted by Max
                Thanks Wise for imput.

                I'm still wondering-why it is not standart procedure in acute sci?

                Can you give your opinion/collaborate on this?
                Max, can you imagine being put into hypothermia when you have acute spinal cord injury? Guy Clifton actually did a clinical trial on people with acute traumatic brain injury, and did not find any significant effect. I list some of the abstracts.

                • Clifton GL, Miller ER, Choi SC, Levin HS, McCauley S, Smith KR, Jr., Muizelaar JP, Marion DW and Luerssen TG (2002). Hypothermia on admission in patients with severe brain injury. J Neurotrauma 19: 293-301. Data from the "National Acute Brain Injury Study: Hypothermia" were examined to identify the impact of hypothermia on admission. In all patients, temperature was measured at randomization using bladder catheters with thermistors. Patients assigned to hypothermia were cooled using fluid-circulating pads. Outcome was assessed at 6 months using the dichotomized Glasgow Outcome Scale (good outcome = good recovery/moderate disability; poor outcome = severe disability/vegetative/dead). One-hundred and two patients (hypothermia, 62; normothermia, 40) were hypothermic on admission (< or =35.0 degrees C). Hypothermia-on-admission patients assigned to normothermia (n = 40) had a 78% poor outcome, and normothermia-on-admission patients assigned to normothermia had a 52% poor outcome (p < 0.004). Hypothermia-on-admission patients assigned to hypothermia had a lower percentage of poor outcomes than those assigned to normothermia (hypothermia, 61%; normothermia, 78%; p = 0.09). Patients over 45 years of age had an adverse effect of hypothermia regardless of admission temperature due to medical complications. Patients who were hypothermic on admission, age < or = 45 years (n = 81), and assigned to hypothermia had a significantly lower percentage of poor outcomes than those assigned to normothermia (hypothermia, 52%; normothermia, 76%; p = 0.02). Factors associated with hypothermia on admission were increased age, prehospital hypotension, smaller size, positive blood alcohol, larger volume of pre-hospital fluids, slightly higher injury severity, and winter enrollment The treatment effect was found in all of the four centers, which randomized the majority (80%) of the patients. It is unclear whether the improved outcome when hypothermia is maintained is a beneficial effect of very early hypothermia induction or an adverse effect of permitting the patients to rewarm passively. Vivian L. Smith Center for Neurologic Research, Department of Neurosurgery, University of Texas-Houston Medical School, 77030, USA.
                • Clifton GL (2004). Is keeping cool still hot? An update on hypothermia in brain injury. Curr Opin Crit Care 10: 116-9. PURPOSE OF REVIEW: The purpose of this review is to examine recent research results for hypothermia as a treatment for brain injury. RECENT FINDINGS: One potential application for hypothermia is as a means of control of elevated intracranial pressure in which hypothermia is induced when intracranial pressure becomes uncontrollable by conventional means. A second application is as a neuroprotectant in which hypothermia is induced very early and maintained for a specified period as a means of diminishing the biochemical cascade that produces secondary brain injury. The clinical data indicate that hypothermia reduces elevated intracranial pressure, but no conclusion can be drawn as to whether this improves outcome over existing techniques (eg, mannitol and barbiturates). There is little evidence that hypothermia acts as a neuroprotectant in trials, all of which used treatment windows of over 4 hours. SUMMARY: Hypothermia is a useful adjunct to barbiturates and mannitol to control elevated intracranial pressure. The results of trials that have tested systemic hypothermia as a neuroprotectant have been negative or equivocal, and cooling may have been induced outside the treatment window. The University of Texas Medical School at Houston, Houston, Texas 77030, USA.
                • Markgraf CG, Clifton GL and Moody MR (2001). Treatment window for hypothermia in brain injury. J Neurosurg 95: 979-83. OBJECT: 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. METHODS: 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 I hour postinjury, compared with those in sham-injured control animals, and that edema peaked at 24 hours and remained elevated for 4 days. Hypothermia (3 hours at 30 degrees C) induced either immediately after TBI or 60 minutes after TBI significantly reduced early neurological deficits. Delay of treatment by 90 or 120 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. CONCLUSIONS: 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. Vivian L. Smith Foundation for Neurologic Research and Department of Neurosurgery, The University of Texas Health Science Center at Houston, Texas, USA.
                • Clifton GL, Miller ER, Choi SC, Levin HS, McCauley S, Smith KR, Jr., Muizelaar JP, Wagner FC, Jr., Marion DW, Luerssen TG, Chesnut RM and Schwartz M (2001). Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med 344: 556-63. BACKGROUND: Induction of hypothermia in patients with brain injury was shown to improve outcomes in small clinical studies, but the results were not definitive. To study this issue, we conducted a multicenter trial comparing the effects of hypothermia with those of normothermia in patients with acute brain injury. METHODS: The study subjects were 392 patients 16 to 65 years of age with coma after sustaining closed head injuries who were randomly assigned to be treated with hypothermia (body temperature, 33 degrees C), which was initiated within 6 hours after injury and maintained for 48 hours by means of surface cooling, or normothermia. All patients otherwise received standard treatment. The primary outcome measure was functional status six months after the injury. RESULTS: The mean age of the patients and the type and severity of injury in the two treatment groups were similar. The mean (+/-SD) time from injury to randomization was 4.3+/-1.1 hours in the hypothermia group and 4.1+/-1.2 hours in the normothermia group, and the mean time from injury to the achievement of the target temperature of 33 degrees C in the hypothermia group was 8.4+/-3.0 hours. The outcome was poor (defined as severe disability, a vegetative state, or death) in 57 percent of the patients in both groups. Mortality was 28 percent in the hypothermia group and 27 percent in the normothermia group (P=0.79). The patients in the hypothermia group had more hospital days with complications than the patients in the normothermia group. Fewer patients in the hypothermia group had high intracranial pressure than in the normothermia group. CONCLUSIONS: Treatment with hypothermia, with the body temperature reaching 33 degrees C within eight hours after injury, is not effective in improving outcomes in patients with severe brain injury. Vivian L Smith Center for Neurologic Research, Department of Neurosurgery, University of Texas-Houston Medical School, 77030, USA.
                • Clifton G (2000). Hypothermia and severe brain injury. J Neurosurg 93: 718-9.
                • Clifton GL (1995). Systemic hypothermia in treatment of severe brain injury: a review and update. J Neurotrauma 12: 923-7. Laboratory studies of moderate hypothermia (30-33 degrees C) after injury show diminished neuronal loss after ischemia, diminished excessive neurotransmitter release after ischemia, prevention of blood-brain barrier disruption after ischemia and brain injury, and behavioral improvement after brain injury. Clinical literature suggests that brief periods of moderate hypothermia (> or = 30 degrees C) in humans are not associated with cardiovascular, hematologic, metabolic, or neurological toxicity. Clinical studies were, therefore, organized to investigate the potential application of moderate systemic hypothermia in patients after severe brain injury. A study of 21 elective craniotomy patients and 11 patients with severe brain injury led to the conclusion that 32 to 33 degrees C was the lowest safe temperature in patients with severe brain injury. A randomized study of moderate hypothermia in 46 patients with Glasgow Coma Score (GCS) 4-7 gave an indication of improved neurologic outcome in the hypothermia group. A multicenter, randomized protocol to test the effect of moderate systemic hypothermia in patients with severe brain injury is in progress. Funded by the National Institutes of Health, The National Acute Brain Injury Study: Hypothermia tests the hypothesis that systemic hypothermia to 32-33 degrees C if rendered within 6 h of injury improves Glasgow Outcome Scores (GOS) at 6 months after injury in patients with severe brain injury (GCS 3-8). Department of Neurosurgery, University of Texas Houston Health Science Center, USA.
                • Clifton GL (1995). Systemic hypothermia in treatment of severe brain injury. J Neurosurg Anesthesiol 7: 152-6. Department of Neurosurgery, University of Texas Houston Health Science Center, Houston 77030, USA.
                • Clifton GL, Allen S, Berry J and Koch SM (1992). Systemic hypothermia in treatment of brain injury. J Neurotrauma 9 Suppl 2: S487-95. An extensive literature suggests that there are minimal complications of systemic hypothermia in humans at and above 30 degrees C for periods of several days. Intracranial hemorrhage has been found to complicate profound hypothermia (10-15 degrees C), and ventricular arrhythmias occur at temperatures below 30 degrees C. Our initial clinical studies were with 21 patients undergoing elective craniotomy cooled to 30-32 degrees C for 1-8 h (mean 4 h). Hypothermia was induced by surface cooling with water blankets. No complications were found. Among 11 patients with severe brain injury, cooling to levels below 32 degrees C was associated with ventricular arrhythmias in 1 patient and atrioventricular block in 1 patient. Asymptomatic hypokalemia was found routinely and treated with potassium replacement. No intracranial hemorrhage or other complications were found. With surface cooling, intravascular temperature dropped at 1.6 degrees C/h. Based on the safety of surface cooling to a core temperature of 32 degrees C for 48 h, we are conducting a randomized study of this level of hypothermia in patients with severe brain injury, cooled within 6 h of injury. Department of Surgery, University of Texas Health Science Center, Medical School, Houston.
                Last edited by Wise Young; 7 Mar 2006, 11:53 PM.


                  Cooling Device Used To Help Spinal Cord Injuries

                  Cooling Device Used To Help Spinal Cord Injuries

                  POSTED: 2:36 pm EST March 24, 2006
                  UPDATED: 7:30 pm EST March 24, 2006

                  MIAMI, Fla. -- Spinal cord injuries are very difficult to treat and many times, the damage is permanent. However, a new device helps the spine heal by cooling it down.
                  When police Officer Manuel Gomez fell from his police horse, he could not feel a thing below the neck.
                  "It's incredible. I thought I was never going to walk again," he said.
                  Gomez's spinal cord was crushed, and Dr. Steve Vanni, of Jackson Memorial Hospital, said the paralysis could have been permanent.



                    How inducing hypothermia treats SCI

                    How inducing hypothermia treats SCI

                    Posted by Megan Roth
                    Thursday, May 08, 2008 12:25 AM EST

                    As has been discussed in our previous posts, spinal cord injuries are severe and affect much more than just the specific location where the injury is incurred. Such injuries can have a great many effects on the body, one of which is the reduced ability to regulate body temperature. Just ask Kevin Everett, a former professional football player who knows the effects of spinal cord injury all too well.
                    Everett was injured during a game in 2007 and immediately thereafter paramedics began attempts to cool Everett’s body between six and eight degrees. Why? What’s the reason behind this method of treatment?
                    Persons suffering a spinal cord injury are prone to hyperthermia. The functions of the autonomic nervous system undergo drastic change; thus, allowing for spikes in body temperatures. These changes in temperature may occur naturally, in response to the environment, or as a result of physical activity. In order to limit these ‘spikes’, many physicians and paramedics have turned to treatments of induced hypothermia, which can be brought about through injections of cold saline and other body-cooling methods (through a series of process before, during, and after surgery).
                    Though inducing hypothermia doesn’t guarantee lesser effects from the injury, it has been known to limit swelling and to protect the brain by slowing metabolism and lessening the bodies need for oxygen and other nutrients (which may not be transported efficiently due to the disruption of many of the body’s systems).
                    Simply knowing the effects an increase in body temperature can have on someone with a spinal cord injury can help determine the effects that injury will have. Something as simple as placing cold towels on the injured person’s forehead, arms, etc. may help decrease their body temperature and