Rapid review regarding management of TRAUMTIC SPINAL CORD INJURY.pptx

paudyalnabin 96 views 38 slides May 11, 2024
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About This Presentation

A rapid review for post graduate general surgery residents about Traumatic spinal cord injury


Slide Content

TRAUMTIC SPINAL CORD INJURY Dr. Nabin Paudyal Resident, Neurosurgery Nobel Institute of Neurosciences

Introduction Spinal cord trauma remains one of the most devastating event often resulting in severe and permanent disabilities AANS data  ~450,000 persons in USA have Traumatic Spinal Cord Injury (TSCI). ~11000 new cases are admitted to US hospitals every year.

Pathophysiology and Mechanism of injury TSCI pathophysiology can be categorized into 2 phases Primary injury  Results from compression of spinal cord by pressure (caused by bone fragments, blood products, soft tissues and/or foreign bodies) Secondary events Vasogenic shock causing spinal ischemia (release of cytokines and vasoactive proteins cause inflammation and cord edema worsen ischemia promoting cell death) Dying neurons release free radicals and cause oxidative damage and excitotoxicity.

Classification of traumatic spinal cord injury Universal stratification of the spinal injury and its severity is done using American Spinal Injury Association (ASIA) scoring. Can present with either complete or incomplete injury to spinal cord. Each injury has distinct clinical features.

Complete Injury (ASIA-A) No motor and sensory function below the neurological level of injury NO SACRAL SPARING In acute settings  Reflexes are absent, males have continuous priapism Urinary retention causing bladder distension may occur. In cervical and thoracic injury  sympathetic dysfunction including hypotension and bradycardia

Incomplete injury (ASIA B through D) Preservation of voluntary anal contraction and bulbocavernosus reflex Various degrees of motor function and sensation caudal to the level of injury Sensation is preserved to a greater extent than motor function.

Types of incomplete spinal injury Central cord syndrome Incomplete pattern of injury Mechanism  hyperextension injury which is exacerbated by pre-existing cervical spondylosis and/or cervical canal stenosis Features  greater motor impairment in upper limbs compared to lower bladder dysfunction variable degree of caudal sensory loss

Types of incomplete spinal injury Anterior cord syndrome Incomplete pattern of injury Mechanism  injury affecting the anterior two thirds of the spinal cord often secondary to anterior spinal artery injury caused by vascular occlusion or ligation Corticospinal tracts, spinothalamic tracts and descending autonomic tracts are involved Features Complete motor paralysis Loss of pain and temperature

Types of incomplete spinal injury Lateral hemi section/ Hemi cord syndrome/ Brown-Sequard syndrome Unilateral damage to the dorsal column/ corticospinal tract and spinothalamic tract Mechanism Ballistic and penetrating injuries. Features ipsilateral weakness, loss of vibration and proprioception  contralateral loss of pain and temperature sensation two spinal levels below the injured level

Spinal shock Condition immediately following spinal cord injury. Caused by physiologic insult rather than anatomic insult characterized by reflex depression of spinal cord function. Transient and temporal course  Gradual return of ano-cutaneous reflex, plantar reflex. Transient loss of complete spinal cord function below the level of injury with unremarkable imaging. Pathophysiology : Loss of potassium within injured cells transient weakness May be concurrent with neurogenic shock  features of hypotension, hypothermia and bradycardia

Management of spinal trauma [ A polytraumatized patient should be assumed to have spinal trauma until otherwise.]

Evaluation- In the field History of unconsciousness/ spinal cord trauma  cervical precautions using cervical collar Airway, Breathing, Circulation. Rapid transfer to trauma center.

In the trauma bay Reassess patient’s airway, breathing and circulation Vitals monitoring  Keep targeted MAP between 85-90 Trauma series CT  CT C-spine (with/without contrast), Contrast CT chest and abdomen. Plain radiographs may be used Head and neck injury suspects  CT head with CT angiography of brain (Rule out atlanto-occipital / atlanto-axial injury, C-spine fracture)

Role of MRI in spinal trauma In cases where no spinal fracture is present  MRI enables to demonstrate spinal cord/ edema/ occult ligamentous injury MRI enables localizing hematoma, identifying ligamentous integrity, traumatic disc herniation, degree of spinal stenosis Limitations less widely available, time for investigation, inability to use in patient with metals.

MRI should be used in all patients with spinal cord injury to help guide management MRI should be used in all patients with spinal cord injury to help guide prognostication. All MRI done should be sagittal T2 sequence.

Medical Management Cardiovascular complication CVS complications require prompt medical attention to prevent neurologic compromise and morbidity Spinal injuries at T6 or above  autonomic dysreflexia (hypotension, cardiac arrhythmia) Manage and prevent hypotension. Fluid resuscitation and vasopressors may be used. Target MAP > 85 to 90 mmHg for 7 days. ( Walter et al ) If vasopressor required  Dopamine followed by Norepinephrine can be used. Management of Spinal Cord Injury

Respiratory complications Cervical trauma owing to C3- C5 level and thoracic accessory muscle innervation may lead to respiratory complications Patients with high spinal injury often require ventilatory support and continued mechanical ventilation Influenza vaccination, pneumococcal vaccination is recommended in patients with SCI Aggressive chest physiotherapy, deep suctioning, respiratory recruitment maneuvers (like spirometry) are beneficial in promoting airway compliance and clearance.

Role of steroids In patients with acute non-penetrating TSCI  Methylprednisolone is recommended. NASCIS I study compared high dose vs low dose methylprednisolone Result was no difference in high dose vs low dose with wound infection and mortality rates being higher in high dose group (p= 0.01)

NASCIS II Study Methylprednisolone was administered in initial dosage of 30mg/kg followed by 5.4mg/kg/h for 23 hours. Post-hoc analysis  Reported improvement of motor and sensory scores at 6 months. Findings were not statistically significant NASCIS III study In patients who arrive within 3 hours of hospital  24 hours regimen is appropriate In patients who arrive within 3-8 hours after injury 48 hours regimen should be initiated. Statistically not significant

Other studies regarding the MPSS in acute SCI 2012 Cochrane review  overall increase in ASIA motor scores when MPSS was used, if given within 8 hours of injury. 2013 AANS/CNS spine guidelines  MPSS not recommended AOSpine 2017 expert’s panel systematic review No significant increase in motor scores in patients receiving MPSS therapy.

Surgical management of spinal cord injury. Prompt decompression and/or fixation enhances restoration neurological function. Surgery is considered in patients who are likely to benefit from decompression Mechanical stabilization Fracture reduction Deformity correction Mechanism, type of injury, severity of other bodily injuries and clinical examination findings are crucial in determining the timing of intervention needed

STASCIS trial showed that early surgery (< 24 hours) showed > 2 grade improvement in ASIA IMPAIREMENT SCORE (AIR) Drovak et al found improved motor recovery in patients who underwent decompression and stabilization within 24 hours. Early intervention within 72 hours of injury is associated with fewer overall complications during admission such as pneumonia, pressure sores and UTI. Badhiwala et al showed that decompressive surgery within 24 hours experienced greater recovery, higher total motor and sensory scores and had better ASIA grades at 1 year after surgery.

Rehabilitation A. Dietary rehabilitation Nutritionist must be involved in designing diet plans when available Paraplegia  28kcal/kg ; quadriplegia 23 kcal/kg Early feeding within 72 hours recommended if safe NG feeding and other feeding routes may be used if required B. Bowel management High cervical injury  Impairment in esophageal sphincter control may increase the risk of GERD and lead to delayed gastric emptying with high post-feed residuals Lesions above T10  Gall bladder disease increases, colonic stasis, ileus occurs Lesions below T10 External anal sphincter dysfunction, loss of voluntary control  Increases bowel distention

Such patients should increase daily fluid intake, increase water content of stool and increase fiber intake Stool softeners  Docusate, PEG given on scheduled basis Bulk formers, Bowel stimulants (Cisapride) can be given dosage titrated as per condition Target stool passage once every alternate day. PR should be performed on a daily basis C. VTE/ DVT prophylaxis Standard of care for patients in acute stage Mechanical and thromboprophylaxis should be used at least for initial 2 weeks following injury LMWH is the recommended drug. To be started within 72 hours of injury. The Spinal Cord Consortium recommends 8 weeks of pharmacologic DVT following acute SCI Use of IVC filters are not recommended

D. Urogenital complications Involuntary reflux detrusor contractions  mimics overflow incontinence (detrusor-sphincter dyssynergia) Patients have reduced awareness of bladder filling Increased risk of UTI, Hydronephrosis, renal stones and post-renal kidney failure. Bladder scans  followed by urinary catheterization  removed for void trials If patients cant void themselves Self intermittent catheterization, alpha-inhibitors, acetylcholine antagonists If these don’t relieve symptoms Suprapubic catheterization E. Increased prevalence of psychiatric disorders is seen among these patients Low threshold to offer appropriate mental health resources when needed. F. Mobility and disposition Early engagement using a physiotherapist assistance with at least 20 min of activity is recommended. Physical therapy rehabilitation disposition during discharge in patients requiring specialized care

Investigational Therapeutic Options in Spinal Trauma Spinal cord cooling  Limited evidence and conflicting evidence Role of Gangliosides (GM1) Animal studies show GM1 agents induce regeneration and sprouting of neurons. No such human studies Not recommended. Electric stimulation Shows promising results in improving neurologic function in chronic spinal injury. Most studies has revolved around lumbar region to help lower extremity function. Electric current stimulates neuronal outgrowths and increases excitability of neuronal networks below the lesion. Novel human oscillating field stimulator has been proven safe in Phase I trial

Role of Riluzole in Spinal cord injury Secondary spinal cord damage is often attributed to uncontrolled activation of voltage-gated sodium channels. Riluzole (sodium channel blocker)  has been postulated as a potential tool to reduce neuronal apoptosis in acute phase following TSCI. Currently on Phase III trial.

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References National Center for Biotechnology Information (2022). PubChem Compound Summary for CID 5070, Riluzole. Retrieved June 4, 2022 from  https://pubchem.ncbi.nlm.nih.gov/compound/Riluzole . Wang, T. Y., Park, C., Zhang, H., Rahimpour , S., Murphy, K. R., Goodwin, C. R., ... & Abd-El-Barr, M. M. (2021). Management of Acute Traumatic Spinal Cord Injury: A Review of the Literature. Frontiers in surgery, 8. Young W. NASCIS. National Acute Spinal Cord Injury Study. J Neurotrauma. (1990) 7:113–4. doi : 10.1089/neu.1990.7.113 Young W, Bracken MB. The second national acute spinal cord injury study. J Neurotrauma. (1992) 9:S397–405. doi : 10.1089/neu.1992.9.151 Bracken MB, Shepard MJ, Holford TR, Leo-Summers L, Aldrich EF, Fazl M, Fehlings MG, Herr DL, Hitchon PW, Marshall LF, Nockels RP. 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. Journal of neurosurgery. 1998 Nov 1;89(5):699-706.

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