Moderate Hypothermia as Treatment for Spinal Cord Injury

Andrew Cappuccino, MD, FACS, FAAOS

Andrew Cappuccino, MD, FACS, FAAOSAndrew Cappuccino

In this issue of Orthopedics, Dr Andrew Cappuccino, assistant team orthopedic surgeon for the NFL Buffalo Bills and the supervising and operating surgeon of Bills player Kevin Everett, discusses the use of moderate systemic hypothermia to treat spinal cord injuries.

Please explain moderate hypothermia as used for spine injuries.

Moderate hypothermia is a technique for lowering the body’s core temperature and trying to maintain temperatures between 33.5°C and 34.5°C to potentially minimize metabolic demands and edema within an injured spinal cord.

What is the success rate for this procedure? Has it been widely used in sports medicine?

Hypothermia is increasingly used in neurosurgical and cardiothoracic surgeries, and has shown promise in the treatment of stroke and sudden cardiac death patients. Use for the spine specifically has shown promise in thoracic abdominal aortic aneurysm repairs, mitigating the anoxic effects of cross-clamping the aorta. For spinal cord injuries, there is evidence of success in basic clinical research performed on animal models, but the success rates in humans currently are under investigation.

This intervention has not been widely used in sports medicine, and I am not advocating this as the standard of care for sports injuries until well-controlled double-blinded randomized studies confirm or refute its efficacy.1-16

What are the risks involved in lowering the body temperature after injury?

Significant systemic hypothermia (<33°C) can result in cardiac arrhythmia, coagulopathy, pancreatitis, and some laboratory abnormalities; therefore, patients on a cooling protocol should be monitored carefully for such complications.

Why does this procedure work?

Moderate systemic hypothermia works in animal models by minimizing damage due to many pathways, including inflammation mediated by polymorphonuclear neutrophils and ischemia from direct compression with compromise of blood supply, which results in noxious-free oxygen radical production.11-23

Will it work with every patient?

No single intervention, including systemic hypothermia, will be a panacea. However used in conjunction with other modalities, we are hoping for improved outcomes—more rapid and complete recoveries—in these catastrophic injuries.

Which cases would see the best results?

Modest hypothermia is most likely to be of benefit in cases of incomplete spinal cord injuries, when used in conjunction with other modalities, such as optimal surgical intervention in a timely fashion. We do not believe it will be of benefit in cases of complete cord injuries. However, this area requires further investigation.

Please explain Kevin Everett’s case. What is his long-term prognosis?

Kevin Everett sustained a fracture dislocation of C3-C4 while making a tackle in a professional football game. He was noted to have complete motor paralysis and lack of sensation to pinprick, light touch, and hot and cold below his neck. He reported neck pain and the inability to move any limbs, as well as difficulty breathing. On the field, he was immediately stabilized and received intravenous fluids, oxygen by mask, systemic hypothermic interventions (including iced saline infusion and ice packs to axillae and groins), and intravenous steroid boluses.

On arrival in the emergency room, he was characterized as an American Spinal Injury Association (ASIA) B classification. Within 3 hours he received a complete workup—including a computed tomography scan, magnetic resonance imaging, and radiographs—and underwent a closed reduction and surgical decompression and fusion. Modest hypothermia was maintained throughout surgery, as documented by his anesthesia record, and his temperature was not noted to be >98.4°.

Figure 1: Andrew Cappuccino with Kevin Everett
Figure 1: Andrew Cappuccino with Kevin Everett (credit: Craig Melvin).
Figure 2: Andrew Cappuccino, Bud Carpenter, and Chris Fischetti evaluate a Buffalo Bills player for cervical spine injury on sidelines
Figure 2: Andrew Cappuccino, Bud Carpenter, and Chris Fischetti evaluate a Buffalo Bills player for cervical spine injury on sidelines. (Credit: Dan Palumbo, Buffalo Bills photographer).

Immediately postoperatively no significant change was noted, although his assessment was difficult due to sedation. When sedation was lightened 8 hours postoperatively, only a flicker of movement was noted in the adductor muscles of the lower extremities, with no other motor function.

At this time a cooling catheter was placed to consistently maintain his temperature at 33°C (ASIA B). Within 24 hours of catheter placement (36 hours postoperatively), he had voluntary movement in upper and lower extremities, although weak (ASIA C). During the next 24 hours, his temperature was raised gradually and then maintained at normal temperature, while his neurological examination continued to improve. He was extubated on postoperative day 3. During the course of hospitalization, he progressed to ASIA D classification and was able to bear weight in rehabilitation with the use of a harness mechanism within 3 weeks.

He likely will have some permanent neurological deficits related to his injury, but should achieve and maintain functional independence over time.

What do you believe played a larger role in this patient’s recovery: hypothermia or rapid surgical decompression of the cord?

Considerable debate exists about early surgical decompression of the spinal cord. Many studies examining early (<72 hours) versus delayed (>72 hours) decompression show no difference in neurological outcome. Recent literature involving animal models and noted in some clinical studies supports rapid (<3 hours) decompression,24-28 which I believe to be the best course of action.

However, I would not mitigate the effects of modest hypothermia. Immediately after surgical decompression, Everett measured at ASIA B, and upon institution of the cooling catheter and persistent maintenance of his core temperature in the low-30°C range, dramatic improvement was noted—a full ASIA class within 24 hours—and improvement sustained as the cooling continued.

Furthermore, Everett received cooling interventions, including iced saline, a cooling blanket anteriorly and posteriorly, and ice packs to both groins and axillae, immediately (prior to hospitalization) resulting in early cooling. Intraoperatively his temperature was maintained in the low-30°C range as well. Prior to notable improvement, Everett’s temperature was noted never to be >98.4°.

It is impossible to attribute specific responses to either intervention more than the other, and controlled basic animal model studies are needed to clarify the comparative benefits of early decompression and moderate systemic hypothermia conclusively. It also should be noted that a full National Acute Spinal Cord Injury Study (NASCIS) II Protocol was instituted in conjunction with modest hypothermia and early surgical intervention.

Did you use a steroid protocol? If so, what role do you believe that played?

In Everett’s case, we used steroids, although this intervention is also controversial and not proven as a standard of care. It has been shown to potentially spare one spinal cord level. In this case, with a documented C3-C4 level and threatened ventilator dependence, sparing one level could have proven to be critical to overall outcome.3,25,29-35

If direct spinal cord cooling was not effective as a treatment, why does systemic moderate hypothermia work?

Many of those skeptical of the idea of hypothermia are quoting a few older studies that were completed with local and direct spinal cord cooling with epidural catheters. Cooling the cord requires significant interventions that impact the physiology of the spine, and therefore these results cannot be extrapolated to the potential benefits or risks of systemic hypothermia.

The theory for both is that the cooling will reduce metabolic demand in both models. Little scientific evidence exists to support using direct spinal cord cooling, whereas multiple basic science studies with systemic hypothermia show marked improved outcomes.9,11-23,35-46

Studies have shown that maintenance of blood flow to the spinal cord affects spinal cord injuries. Hypothermia leads to vaso-constriction. Wouldn’t this affect spinal cord blood flow?

Hypothermia can lead to vasoconstriction, but the more important effect is that of reducing the metabolic demand of the neural tissues. By reducing the metabolic demands, the damage done by hypoxia is mitigated.17

Most of the recent clinical work on hypothermia has been in thoracolumbar aneurysm surgery, where the mechanism of injury is different from trauma. Are these results applicable?

Yes, because the mechanism of injury in both cases can be related to hypoxia—in aneurysm surgery from cross-clamping the source of the blood supply, and in spinal cord injury from direct compression and edema. In spinal cord injury, there is also direct trauma and resultant cell injury and death.

There have been no large trials of this technique in trauma published to date. Are we ready to adopt this in practice?

It would be inappropriate to recommend this as an established clinical practice or standard of care at this point. I would argue for making this an option, ideally in prospective randomized trials. However, because this is not a common injury in most hospitals, it will be difficult to accrue enough participants to prove or disprove this in the near future.

I hope Everett’s case has shed light on the potential benefit of modest systemic hypothermia and will inspire spine centers to scientifically examine this in the clinical setting and the laboratory.


  1. Adams H, Adams R, Del Zoppo G, Goldstein LB; Stroke Council of the American Heart Association; American Stroke Association. Guidelines for the early management of patients with ischemic stroke: 2005 Guidelines update a scientific statement from the Stroke Council of the American Heart Association/American Stroke Association. Stroke. 2005; 36(4):916-923.
  2. Arrica M, Bissonnette B. Therapeutic hypothermia. Semin Cardiothorac Vasc Anesth. 2007; 11(1):6-15.
  3. Bethea JR, Dietrich WD. Targeting the host inflammatory response in traumatic spinal cord injury. Curr Opin Neurol. 2002; 15(3):355-360.
  4. Buki A, Koizumi H, Povlishock JT. Moderate posttraumatic hypothermia decreases early calpain-mediated proteolysis and concomitant cytoskeletal compromise in traumatic axonal injury. Exp Neurol. 1999; 159(1):319-328.
  5. Conrad MF, Crawford RS, Davison JK, Cambria RP. Thoracoabdominal aneurysm repair: a 20-year perspective. Ann Thorac Surg. 2007; 83(2): S856-S861.
  6. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002; 346(8):549-556.
  7. Kouchoukos NT, Rokkas CK. Hypothermic cardiopulmonary bypass for spinal cord protection: rationale and clinical results. Ann Thorac Surg. 1999; 67(6):1940-1942.
  8. Marion DW, Penrod LE, Kelsey SF, et al. Treatment of traumatic brain injury with moderate hypothermia. N Engl J Med. 1997 ;336(8):540-546.
  9. Rokkas CK, Cronin CS, Nitta T, et al. Profound systemic hypothermia inhibits the release of neurotransmitter amino acids in spinal cord ischemia. J Thorac Cardiovasc Surg. 1995; 110(1):27-35.
  10. Svensson LG. Paralysis after aortic surgery: in search of lost cord function. Surgeon. 2005; 3(6):396-405.
  11. van der Worp HB, Sena ES, Donnan GA, Howells DW, Macleod MR. Hypothermia in animal models of acute ischaemic stroke: a systematic review and meta-analysis. Brain. 2007; 130(12):3063-3074.
  12. Wakamatsu H, Matsumoto M, Nakakimura K, Sakabe T. The effects of moderate hypothermia and intrathecal tetracaine on glutamate concentrations of intrathecal dialysate and neurologic and histopathologic outcome in transient spinal cord ischemia in rabbits. Anesth Analg. 1999; 88(1):56-62.
  13. Westergen H, Yu WR, Farooque M, Holtz A, Olsson Y. Systemic hypothermia following spinal cord compression injury in the rat: axonal changes studied by beta-APP, ubiquitin, and PGP 9.5 immunohistochemistry. Spinal Cord. 1999; 37(10):696-704.
  14. Yoshitake A, Mori A, Shimizu H, et al. Use of an epidural cooling catheter with a closed countercurrent lumen to protect against ischemic spinal cord injury in pigs. J Thorac Cardiovasc Surg. 2007; 134(5):1220-1226.
  15. Yu CG, Jimenez O, Marcillo AE, et al. Beneficial effects of modest systemic hypothermia on locomotor function and histopathological damage following contusion-induced spinal cord injury in rats. J Neurosurg. 2000; 93(suppl 1):85-93.
  16. Yu WR, Westergren H, Farooque M, Holtz A, Olsson Y. Systemic hypothermia following spinal cord compression injury in the rat: an immunohistochemical study on MAP 2 with special reference to dendrite changes. Acta Neuropathol. 2000; 100(5):546-552.
  17. Albin MS, White RJ, Acosta-Rua G, Yashon D. Study of functional recovery produced by delayed localized cooling after spinal cord injury in primates. J Neurosurg. 1968; 29(2):113-119.
  18. Campbell JB, DeCrescito V, Tomasula JJ, et al. Bioelectric prediction of permanent post-traumatic paraplegia. Paper presented at: American Association of Neurological Surgeons Annual Meeting; 1971.
  19. Chatzipanteli K, Yanagawa Y, Marcillo AE, Kraydieh S, Yezierski RP, Dietrich WD. Posttraumatic hypothermia reduces polymorphonuclear leukocyte accumulation following spinal cord injury in rats. J Neurotrauma. 2000; 17(4):321-332.
  20. Dimar JR Jr, Glassman SD, Raque GH, Zhang YP, Shields CB. The influence of spinal canal narrowing and timing of decompression on neurologic recovery after spinal cord contusion in a rat model. Spine. 1999;24: 1623-1633.
  21. Dimar JR Jr, Shields CB, Zhang YP, Burke DA, Raque GH, Glassman SD. The role of directly applied hypothermia in spinal cord injury. Spine. 2000; 25(18):2294-2302.
  22. Ducker TB, Hamit HF. Experimental treatments of acute spinal cord injury. J Neurosurg. 1969; 30(6):693-697.
  23. Shibuya S, Miyamoto O, Janjua NA, Itano T, Mori S, Norimatsu H. Post-traumatic moderate systemic hypothermia reduces TUNEL positive cells following spinal cord injury in rat. Spinal Cord. 2004; 42(1):29-34.
  24. Buhren V, Hofmeister M, Militz M, Potulski M. Indications for surgical management of injuries of the cervical spine [in German]. Zentralbl Chir. 1998; 123(8):907-913.
  25. Fehlings MG, Perrin RG. The role and timing of early decompression for cervical spinal cord injury: update with a review of recent clinical evidence. Injury. 2005; 36(suppl 2):B13-B26.
  26. Hakato J, Wronski J. Importance of early operative decompression of spinal cord after cervical spine injuries [in Polish]. Neurol Neurochir Pol. 2004; 38(3):183-188.
  27. Karbownik J, Radek A. Results of surgical treatment of patients after spinal trauma with partial spinal cord damage [in Polish]. Neurol Neurochir Pol. 1995; 29(6):949-959.
  28. Torq JS, Guille JT, Jaffe S. Injuries to the cervical spine in American football players. J Bone Joint Surg Am. 2002; 84(1):112-122.
  29. Pharmacological therapy after acute cervical spine cord injury. Neurosurgery. 2002; 50(suppl 3):S63-S72.
  30. Bracken MB, Shepard MJ, Hellenbrand KG, et al. Methylprednisolone and neurological function 1 year after spinal cord injury. Results of the National Acute Spinal Cord Injury Study. J Neurosurg. 1985; 63(5):704-713.
  31. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. 1990; 322(20):1405-1411.
  32. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or trilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. 1997; 277(20):1597-1604.
  33. Bracken MB, Shepard MJ, Holford TR, et al. Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. J Neurosurg. 1998; 89(5):699-706.
  34. Fehlings M, Brodke D, Wang J. Steroid use in the management of spinal cord injury. Spineline. 2006; (March/April):14-17.
  35. Fehlings MG, Baptiste DC. Current status of clinical trials for acute spinal cord injury. Injury. 2005; 36(suppl 2):B113-B122.
  36. Bernard S. New indications for the use of therapeutic hypothermia. Crit Care. 2004; 8(6):E1.
  37. Bricolo A, Ore GD, Da Pian R, Faccioli F. Local cooling in spinal cord injury. Surg Neurol. 1976; 6(2):101-106.
  38. Demian YK, White RJ, Yashon D, Kretchmer HE. Anaesthesia for laminectomy and localized cord cooling in acute cervical spinal injury. Report of three cases. Br J Anaesth. 1971; 43(10):973-979.
  39. Feuer H. Management of acute spine and spinal cord injuries. Old and new concepts. Arch Surg. 1976; 111(6):638-645.
  40. Inamasu J, Nakamura Y, Ichikizaki K. Induced hypothermia in experimental traumatic spinal cord injury: an update. J Neurol Sci. 2003; 209(1-2):55-60.
  41. Koons DD, Gildenberg PL, Dohn DF, Henoch M. Local hypothermia in the treatment of spinal cord injuries. Report of seven cases. Cleve Clin Q. 1972; 39(3):109-117.
  42. Martinez-Arizala A, Green BA. Hypothermia in spinal cord injury. J Neurotrauma. 1992; 9(suppl 2):S497-S505.
  43. Meacham WF, McPherson WF. Local hypothermia in the treatment of acute injuries of the spinal cord. South Med J. 1973; 66(1):95-97.
  44. Negrin J Jr. Spinal cord hypothermia in the neurosurgical management of the acute and chronic post-traumatic paraplegic patient. Paraplegia. 1973; 10(4):336-343.
  45. Selker RG. Icewater irrigation of the spinal cord. Surg Forum. 1971; (22):411-413.
  46. Tator CH. Acute spinal cord injury: a review of recent studies of treatment and pathophysiology. Can Med Assoc J. 1972; 107(2):143-145.


Dr Cappuccino is from Buffalo Spine Surgery, Buffalo Bills, and Buffalo Catholic Health System and Kaleida Health Systems.

Dr Cappuccino has no relevant financial relationships to disclose.


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