Hypertensing Spinal Cord Injury - gold standard or wacky?
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This document discusses the concept of maintaining higher blood pressure levels, known as hypertension, after a spinal cord injury to improve spinal cord perfusion pressure and reduce secondary injury. It notes that while animal studies and some human trials have shown improved neurological outcomes, the evidence is still limited. It calls for larger randomized controlled trials in humans that also incorporate multi-modal monitoring and standardized outcome measures to further evaluate if inducing hypertension after spinal cord injury should be considered the gold standard of care.
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Hypertensing Spinal Cord Injury - gold standard or wacky?
- 1. HYPERTENSING SCI GOLD STANDARD OR WACKY?
- 2. THE WHY? 15 cases per million $2 billion annually Just one level more
- 3. PRIMARY INJURY COMPRESSION LACERATION TRACTION ISCHAEMIC TRANSECTION Case courtesy of Dr Ahmed Abdrabou, Radiopaedia.org, rID: 22719
- 4. TIME IS SPINE SECONDARY INJURY
- 6. BORROWED FROM THE BRAIN Spinal Cord Perfusion Pressure= MAP – Intraspinal Pressure SCPP= MAP – ISP
- 7. Normal text is in Gotham Book font Case courtesy of Dr Abdulmajid Bawazeer, Radiopaedia.org, rID: 77009 SPINAL CORD PERFUSION PRESSURE (SCPP) SCPP= MAP – ISP
- 8. https://www.wingsforlife.com/us/research/multi-modal-monitoring-of-patients-with- severe-acute-traumatic-spinal-cord-injury-2470/ Normal text is in Gotham Book font SCPP
- 9. GUIDELINES MAP >85mmHg for 7 Days
- 10. SWELLING AFTER SCI HUMANS ? 3-14 DAYS IN ANIMALS
- 11. THE PROS IMPROVED PERFUSION PRESSURE REDUCE SECONDARY INJURY IMPROVED NEUROLOGICAL OUTCOME
- 13. THE EVIDENCE 2 Systematic Reviews 2 Prospective Trials 790 patients (127 in prospective trials)
- 14. THE EVIDENCE Measurement of neurological outcome Follow up variable Results variable
- 15. THE FUTURE RCT
- 16. THE FUTURE RCT Multi modal monitoring
- 17. THE FUTURE RCT Multi modal monitoring Outcome Measures
- 19. REFERENCES Sabit B, Zeiler FA, Berrington N. The Impact of Mean Arterial Pressure on Functional Outcome Post-Acute Spinal Cord Injury: A Scoping Systematic Review of Animal Models. Journal of Neurotrauma: Mary Ann Liebert Inc.; 2017. p. 2583-2594. DOI 10.1089/neu.2016.4735 Saadeh YS, Smith BW, Joseph JR, et al. The impact of blood pressure management after spinal cord injury: A systematic review of the literature. Neurosurgical Focus: American Association of Neurological Surgeons; 2017.DOI 10.3171/2017.8.FOCUS17428 Walters BC, Hadley MN, Hurlbert RJ, et al. Guidelines for the management of acute cervical spine and spinal cord injuries: 2013 update. 2013:82-91.DOI 10.1227/01.neu.0000430319.32247.7f
Editor's Notes
- Every year in Australia there are about 15 new cases of SCI per million population. Though relatively small numbers, there are estimated to be between 10 and 20 thousand Australians living with spinal cord injury, the economic burden is over 2 billion dollars annually. With improvement in emergency and intensive care medicine, survival after spinal cord injury has improved, however functional outcome may vary from minimal disability to severe functional impairment and ventilator dependence. No treatment yet exists that can reverse the primary damage to the spinal cord, so management focuses on preventing secondary neurological injury. I like to think of our management as “just one level more”, aiming to help the patient to improve 1 motor level more. Just one level more can have a significant impact on quality of life. For a patient with a high cervical cord injury just one level could mean independence from a ventilator (C3/4), or being able to feed yourself (C5) or drive your wheelchair (C6).
- The primary injury. In traumatic spinal cord injury the mechanism may result in focal compression, laceration or traction injury to the cord. Ischaemic injury may result from interference to the arterial supply.
- After the initial injury further damage continues with an inflammatory cascade that results in -Swelling -disruption of the microvascular supply -Neuronal excitotoxicity and oxidative damage -worsening ischaemia and cell death An ischaemic penumbra can extend caudally from the injury site leading to secondary neurological injury above the level of the primary injury. We are not only trying to gain just one level but also trying not to lose a level either. This all starts within minutes after SCI and contributes to the secondary neurological injury. Current acute and intensive care management focuses on minimising this damage.
- Many treatments have been investigated but to date none have been proven in a large prospective trial. Most guidelines and accepted practice advocate for early surgical decompression, some as early as within 8 hours of the injury to reduce external compression on the spinal cord. Other treatments such as methylprednisolone have been used in the past to reduce spinal cord oedema. There are ongoing studies investigating other pharmacological agents that may reduce inflammation such as rizulole (used in ALS) or promote neuroregeneration (such as anti nogo). And there is hypertensive therapy.
- It is well established practice to defend cerebral perfusion pressure in TBI, guided by intracranial pressure monitoring where possible. The basis of hypertensive therapy in spinal cord injury is to defend the spinal cord perfusion pressure like we do the CPP.
- Whilst the spinal cord is not encased in the skull it is encased in the dura and swelling tends to extend radially, narrowing the epidural space and compromising blood and CSF flow. This can result in worsening oedema leading to further spinal cord compression. Intraspinal pressure rises and spinal cord perfusion pressure falls.
- Here are some fluorescence images of blood flow in an injured spinal cord at difference perfusion pressures measured intraoperatively in a tr You can see there is an obvious difference in flow with a perfusion pressure above 60, demonstrating the importance of spinal cord perfusion pressure in the injured cord.
- International guidelines advocate for targeting a MAP of >85mmHg for 7 days post injury, though this is not based on high level evidence. Due to a paucity of evidence practice does vary. For example a survey in the UK revealed 23 % of NICU specialists aiming for MAP >60 mmHg, 54 % >80 mmHg, and 15 % aimed for what they considered to be a normal map for age. A study in emergency management in Australia found that while more than half of the patients with acute TSCI in the study had an MAP <85 mmHg on arrival to the ED, only 63% of these received treatment for this in accordance with guidelines. We know from post mortem examinations that there is greater spinal cord white matter degeneration in individuals who suffered severe hypotension post-injury compared with those who did not, so defence of spinal cord perfusion pressure is important from very early on.
- The recommended 7 days stems from the majority of protocols of the existing studies which has come originally from one of the 2 published prospective studies (by Vale in 1990) which itself was based on a prior study in monkeys that showed that spinal cord swelling peaked at 7 days post injury. Even this timeline of swelling has not been consistent across all animal studies.
- So why do it? Well, it’s relatively easy to do. Increased MAP leads to improved spinal cord perfusion and hopefully reduce secondary neurological injury. There is evidence to suggest targeting a higher MAP can lead to improved neurological particularly motor outcome scores.
- Well it’s not always that easy to achieve the target MAP, and MAP is a very rough surrogate for spinal cord perfusion pressure. We are often dealing with competing injuries for example in multi trauma that preclude hypertensive therapy. Overperfusion can lead to cord haemorrhage and oedema There are complications associated with the treatment such as central line infections, pneumothorax Complications associated with high vasopressor use, especially in those with cardiac risk factors It may prolong ICU length of stay and delay rehab
- Well 2 systematic reviews have looked high MAP target in traumatic spinal cord injury , which included 9 and 11 trials respectively, 2 of which were prospective trials. The prospective trials were both performed in the 1990s, included a total of 127 patients and had no control groups. It seems that these are the trials that the MAP target of 85 stemmed from. One study which only looked at C spine injuries, targeting a MAP of >90 for 7 days, followed patients up to 6 weeks and found that 82% of patients had stable or improved neurological function measured by Frankel grade. The other prospective trial treated patients with a MAP >85mmhg for 7 days and found that at 12 months patients had a stable or improved ASIA score.
- The remainder of the retrospective studies had mixed results. Many had variable follow up time, variable outcomes measures, poor documentation of adverse events associated with treatment, and often used dopamine or phenylephrine. Overall there is a suggestion that targeting a higher MAP may lead to improved neurological outcome, with little evidence of harm. There is also a suggestion that patients with incomplete injuries are the most likely to show neurological improvement with hypertensive therapy. One more recent study had minute to minute measurements and found that patients who had fewer measurements below the target (as opposed to overall average MAP over 7 days) had better neurological outcomes.
- No future statement would be complete without proclaiming that we need more randomised controlled trials. There have been two recent randomised controlled trials that were designed to examine blood pressure control in spinal cord injury. One trial was terminated in 2019 and the other is ongoing. Aside from RCTs though we also need to review where we are getting our targets from. The current guidelines are based on poor evidence and are somewhat historical. Ideal MAP will relate to spinal cord perfusion pressure and intraspinal pressure which will be different for every patient. The duration of therapy has been extrapolated from animal studies and we are yet to track the timing of the inflammatory process in humans, though there are promising studies investigating blood and CSF biomarkers that may provide more information. In short, I think we need more than an RCT, we need more information to guide our target pressures and duration.
- While we do not routinely monitor intraspinal pressures, like we do with intracranial pressures, studies have used intraspinal pressure monitors inserted under the dura to calculate accurate spinal cord perfusion pressures and have demonstrated the feasibility and safety of this. These observational studies have demonstrated a link between spinal cord perfusion pressure but not MAP, and motor functional outcome. While this might still fall under the “wacky”, multi modal monitoring to guide blood pressure management is an option and maybe one day the better option in spinal cord injury.
- Like in the brain injury literature we also need to work on meaningful outcome measures. Patients with spinal cord injury will be the first to tell you that the ASIA score is not a meaningful measure of their functional outcome. We also rarely perform a proper ASIA assessment at the recommended 72hours post injury. It is very difficult to assess the effect of hypertensive treatment, or in fact any of our intensive care therapies, if we don’t know the baseline neurology.
- At our centre we routinely aim for a MAP of >85mmHg for 5 days in all spinal cord injured patients. Note that they usually arrive to us after surgical decompression. If the patient was on high doses of vasopressor or the MAP target was difficult to achieve I would drop the MAP target. If there is evidence of ongoing improvement I tend to extend this to 7 days. There is evidence that this is one of the few things we can do for these patients in ICU that may help to improve neurological outcome, with little evidence of harm, so yes for now this is my gold standard.
- At our centre we routinely aim for a MAP of >85mmHg for 5 days in all spinal cord injured patients. Note that they usually arrive to us after surgical decompression. If the patient was on high doses of vasopressor or the MAP target was difficult to achieve I would drop the MAP target. If there is evidence of ongoing improvement I tend to extend this to 7 days. There is evidence that this is one of the few things we can do for these patients in ICU that may help to improve neurological outcome, with little evidence of harm, so yes for now this is my gold standard.