Those measures can predict the need for intubation 9. Predictors of the need for tracheostomy are ASIA A lesions, extent of the lesion, smoking, and previous lung disease. Some studies advocate that early tracheostomy within 10 days in these patients leads to a shorter ICU stay and reduction in the length of time of mechanical ventilation Hypotension after SCI is frequent. It may be due to hypovolemia in a context of polytrauma, or due to the direct cervical or thoracic spinal trauma itself, leading to neurogenic shock.
Neurogenic shock results from the interruption of sympathetic tone due to disruption in supraspinal control, and an intact parasympathetic influence via the vagus nerve, leading to an imbalance in the autonomic control. There is, therefore, loss of peripheral vascular tone and bradycardia Although the deleterious consequences of hypotension in SCI have not been assessed in a controlled prospective way, there is convincing evidence that hypotension contributes to secondary injury after acute SCI, reducing spinal cord flow and perfusion. Based on this, the current recommendation is to strictly avoid hypotension, and maintain mean arterial pressure MAP at mmHg for seven days after injury level III evidence 3.
In order to achieve that goal, the mainstay of treatment is intravenous fluid therapy mainly with crystalloids to maintain a euvolemic or slightly hypervolemic status, in association with vasopressors 2. It is important to have invasive blood pressure monitoring with an arterial line. The main predictors of poor cardiovascular function requiring resuscitation and support are high cervical and complete lesions Cardiovascular instability may be transient and episodic, but can also be recurrent in the first 7—10 days after injury.
The best vasoactive amine is still a matter of debate. The last guideline does not address this controversy. A systematic review tried to answer several questions regarding the use of vasopressors in acute SCI. However, it was inconclusive in determining which vasopressor is better, what the optimal therapy duration is and what the MAP level is below which one should initiate vasopressor support In cervical or high thoracic lesions with both hypotension and bradycardia, a drug with chronotropic and inotropic effects as well as vasoconstrictor properties might be required. Norepinephrine or alternatively, dopamine could be good options.
For low thoracic lesions, where hypotension is usually the result of peripheral vasodilation, a pure vasopressor drug such as phenylephrine could be appropriate Recently, some studies have addressed the frequency of side effects and rates of complications related to the use of vasoactive drugs in this population. A higher rate of side effects with the use of dopamine compared to norepinephrine and phenylephrine was described, especially in the population older than 55—60 years 15 , 16 , Recently, Altaf and collaborators compared the effects of norepinephrine versus dopamine on MAP, the intrathecal pressure monitored with a lumbar intrathecal catheter and spinal cord pressure perfusion the difference between MAP and intrathecal pressure.
The conclusion was that norepinephrine was able to maintain MAP with a lower intrathecal pressure and correspondingly higher spinal cord pressure perfusion Progressive edema and hemorrhage contribute to the ongoing mechanical pressure on the microvascular circulation. Surgical decompression aims to relieve this pressure, thereby reducing secondary hypoxia and ischemia 2. Indications for surgery include significant cord compression with progressive neurological impairment and a fracture not amenable to, or not responding to, close reduction, such as unstable vertebral fractures.
The Surgical Timing in Acute Spinal Cord Injury Study was a prospective, observational study that compared patients who had undergone surgery before and after 24 hours from injury. The first group was more than twice as likely to have a two grade ASIA Impairment Scale improvement and a similar complication rate compared to the group with late surgery Those findings were confirmed in a prospective Canadian cohort study even after adjusting for preoperative status and neurological level The final report is planned to be published in the end of Methyprednisolone MP is a synthetic corticosteroid that upregulates anti-inflammatory factors and decreases oxidative stress, enhancing endogenous cell survival in animal models of SCI.
It reduces edema, prevents intracellular potassium depletion and inhibits lipid peroxidation 1. Since the s, clinical trials have been trying to demonstrate its benefits in humans. The National Spinal Cord Injury Study I, published in , examined mg bolus MP followed by the same dose daily for 10 days, compared to mg bolus and then daily. No difference in motor or sensitive neurological recovery was observed between groups, and wound infections were more prevalent in the high-dose group At one year, there was no significant difference in neurological function among the groups.
A subanalysis found that the subset of patients who received the corticosteroid within eight hours had a modest improvement in motor recovery. Wound infections were more frequent among MP patients The National Spinal Cord Injury Study III, published in , compared three treatment groups: MP for 48 hours, the same drug administered for 24 hours and tirilazad mesylate a potent lipid peroxidation inhibitor.
Patients were treated within eight hours of SCI.
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In a post hoc analysis, in patients treated between three to eight hours from trauma, the hour regimen was associated with a greater motor, but not functional, recovery. In addition, the group with the longer duration had more severe sepsis and pneumonia Recently, a meta-analysis and systematic review concluded that evidence from multiple randomized controlled trials and also from observational studies do not support methylprednisolone use in acute SCI since it has no long-term benefits.
Besides, it increases gastrointestinal hemorrhage and has a trend to increase overall adverse events Neuroprotective agents aiming to reduce secondary insults are potential key therapies in SCI. Multiple approaches have been studied, and many others are currently under investigation.
Gangliosides are glycolipid molecules present in neuronal membranes. Laboratory studies have shown that they can enhance axonal regeneration, besides having a variety of neuroprotective effects, such as prevention of apoptosis and anti-excitotoxic activity. GM-1 Sygen was suggested as a therapeutic option until the guideline although without demonstrated clinical benefit However, a randomized controlled trial of the ganglioside compound reported no difference in neurological recovery after six months, therefore, it is no longer recommended 3 , The study was negative, with no differences in motor scores between groups Nimodipine is an L-type calcium channel blocker thought to prevent calcium- dependent apoptotic enzymes and block presynaptic release of glutamate.
In comparison with placebo, however, no difference in neurological status at one year was noted Tirilazad mesylate, a drug that attenuates peroxidation of neuronal membranes, was analyzed together with MP in the National Spinal Cord Injury Study III trial, with no difference between groups. There are no placebo-controlled studies In animal studies, hypothermia decreased basal metabolic rate in the central nervous system, reduced inflammation, apoptosis, excitotoxicity, edema, gliosis, and increased angiogenesis.
As well, traumatic SCI models showed improvement with the decreased temperature In the remaining patients, This study which is not yet recruiting plans to evaluate different durations of hypothermia, starting within six hours post-trauma.enter
Riluzole, a sodium-channel blocker, reduces secondary injury by blocking pathological activation of sodium channels and reducing the release of glutamate in preclinical models of SCI. It will be completed in Minocycline is an antibiotic with anti-inflammatory properties including inhibition of tumor necrosis factor alpha, interleukin 1 beta, cyclooxygenase-2 and nitric oxide synthase. In pre-clinical models, it decreased lesions sizes and neuron loss. Fibroblast growth factor has been shown to protect against excitotoxicity and to reduce free radical production in animal models of SCI.
Cytokine granulocyte colony stimulating factor is neuroprotective in SCI by promoting cell survival and inhibiting tumor necrosis factor alpha and interleukin 1 beta.
There were two small, non-randomized studies that demonstrated improvements in ASIA motor scores with the drug use 38 , A wide number of strategies are being developed worldwide to help recovery in SCI patients. There are numerous targets and therapeutic opportunities using endogenous and exogenous repair mechanisms. The aim is to surpass barriers to recovery such as the loss of structural framework, cystic cavitation, scarring and inhibitory molecular signaling 2. Cell-based therapies are promising modalities of regeneration.
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A wide number of cell types have been studied or are being evaluated in ongoing studies — embryonic stem cells, induced pluripotent stem cells, olfactory ensheathing cells, Schwann cells, mesenchymal cells, and activated autologous macrophages. In preclinical studies, cellular transplantation alone, or in combination with other therapies, was associated with neurological recovery, without any subtype showing superiority over the other.
Small human studies also disclosed some degree of improvement, with no major adverse events. However, it is important to notice that, independent of treatment, most patients will undergo some spontaneous recovery in the first six months after injury. Therefore, confounding factors cannot be excluded from these results 1. Embryonic and induced pluripotent stem cells are capable of remyelinate axons, modulate the inflammatory response, regenerate lost neural circuits and modify the microenvironment.
Schwann cells are able to remyelinate central nervous system axons and, in animal models, have reduced cystic cavitation, enhanced tissue sparing and enhanced recovery. Olfactory ensheathing cells are phagocytes capable of clearing microbes and debris and also of secreting neurotropic factors. In animals, they enhanced axonal regeneration and remyelination and also improved outcomes.
Mesenchymal cells can differentiate along their connective tissue lineages and modulate inflammatory response at systemic and local environment levels. They have been shown to decrease inflammatory cell infiltration, increase pro-survival trophic factor levels and promote tissue sparing 1 , 2.
It should be noted that cellular transplantation remains an investigational and experimental therapy, with no formal recommendations. Spinal cord injury management has substantially changed over the last years. Key early interventions are increasingly being recognized, as well as the need to better study these patients. Neuroprotective and neuroregenerative strategies are probably more effective when done together, and they are an extensive field of current and future research.
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