Spinal compression, decompression surgery and the beneficial effects of hypothermia

Release date: 24-Nov-2011

Organisation: National Stroke Research Institute and University of Melbourne, Department of Medicine, Austin Health, Heidelberg, Victoria, Australia

Prof Alan Mackay-Sim describes two papers on cooling the spinal cord. He explains how this approach may prolong the time during which surgical intervention can be effective.

Trauma to the spine can lead to vertebral bone, disc or other tissue pressing on the spinal cord, resulting in impaired function. Surgery can remove these fragments, realign vertebrae and reduce the pressure (decompression surgery). However, its value in improving outcomes is yet to be confirmed and thus is not standard practice. Previous research includes a small prospective study which showed significant improvements in function associated with early spinal stabilisation and decompression surgery, concluding that larger trials are needed to confirm the usefulness of the surgery. The clinical case for decompression surgery was recently reviewed (Cadotte et al, 2010) and the results of a large trial (the STACSIS trial) led by Dr Michael Fehlings in Canada, are expected soon. However, there are practical problems in getting spinal injured persons quickly into operating theatres. The limited evidence is that sooner after injury is better and that after 24 hours there may be no benefit. Is there a way around this?

The Papers
Melbourne neurologist, Dr Peter Batchelor with a team of scientists in Dr David Howells’ laboratory at Austin Health and the Department of Medicine, University of Melbourne, have been investigating the consequences of spinal cord compression and decompression surgery in rats and whether hypothermia might be beneficial in delaying the effects of sustained compression spinal cord injury. In a paper published last year they showed that hypothermia could reduce the effects of spinal cord compression (Batchelor et al, 2010). They cooled the animals from normal body temperature (37.3°C) to 33°C for eight hours from the time of spinal cord contusion (bruising) injury, with compression exerted by a small wedge that squeezed the spinal canal by 45%. They assessed the animals’ gait and spinal cord structure at 12 weeks. They found that animals compressed for eight hours, but not cooled, were severely affected. However, animals compressed and cooled for eight hours had much smaller deficits, similar to animals compressed for just two hours without cooling. They propose that hypothermia immediately after injury can “buy time”, potentially pushing open the “time window” during which decompression surgery will be effective.

The second, more recent study published in May 2011 addresses a potential mechanism for the effect of compression and decompression (Batchelor et al, 2011). At the time of spinal cord injury there is rapid deterioration of neurological signs and symptoms. They hypothesised that this may happen because compression causes an increase in pressure within the spinal canal, blocking the flow of cerebral spinal fluid along the canal, and causing local tissue swelling. To test this they measured intracanal pressure after spinal cord contusion injury, with and without spinal cord compression, and asked if intracanal pressure was related to neurological outcome. They then applied hypothermia to test whether it altered intracranial pressure and the neurological outcome. First they showed that intracanal pressure in the healthy spinal cord was maintained despite a spinal cord compression up to 40%, after which it rose moderately. In contrast, after spinal cord bruising, even 20% compression increased intracanal pressure significantly, with a marked increase after further compression. They then showed that 45% compression for eight hours following injury led to severe gait and structural deficits. Finally, they showed that hypothermia reduced intracranial pressure after spinal cord contusion injury and 45% spinal cord compression.

These studies provide clear evidence that the benefits of decompressing the spinal cord after traumatic spinal cord injury depend on the size of the compression and the period elapsed, after injury, before decompression surgery occurs. Importantly the studies show that early hypothermia can reduce the effects of spinal cord compression, functionally and structurally. Finally they show a mechanism for the hypothermic effect may be via its reduction in pressure within the spinal canal, thereby reducing tissue swelling.

This animal study supports a small study in humans that demonstrated that clinical improvement varied inversely with the time until decompression after spinal cord injury (Papadopoulos et al, 2002). These papers by Dr Batchelor and collaborators demonstrate very clearly in an animal model that:

  • compression of the spinal cord after injury leads to poorer recovery
  • decompression soon after injury is better than later;
  • immediate cooling of the body can slow down the damaging effects of spinal cord compression.

This approach may be useful in people because it is not usually possible to get patients into the operating room soon enough for decompression to be optimally effective. Hypothermia could extend the period for optimal surgical intervention.

Professor Alan Mackay-Sim
National Centre for Adult Stem Cell Research
Griffith University
Member of the Spinal Cord Injury Network’s Research Development Committee

November 2011

Cadotte DW et al. (2010) The timing of surgical decompression for spinal cord injury. F1000 Med Rep. 2; 67.

Batchelor PE et al. (2011) Intracanal pressure in compressive spinal cord injury: reduction with hypothermia. J Neurotrauma. 28(5); 809-20.
Link to abstract - www.ncbi.nlm.nih.gov/pubmed/21250916

Batchelor PE et al. (2010) Hypothermia prior to decompression: buying time for treatment of acute spinal cord injury. J Neurotrauma. 27(8); 1357-68.
Link to abstract - www.ncbi.nlm.nih.gov/pubmed/20504158

Papadopoulos SM et al. (2002) Immediate spinal cord decompression for cervical spinal cord injury: feasibility and outcome. J Trauma. 52(2); 323-32.

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