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- 2. TRAUMATIC SPINAL CORD INJURY Prepared by Dr Kung Khai Shien, Cesar
- 6. Anterior Spinothalamic Tract Destruction will cause: - Loss of light touch and pressure contralateral side below the level of lesion
- 9. INTRODUCTION •Spinal cord injury (SCI) : •damage to the spinal cord that results in a loss of function. •Cord Injuries: Cervical = 60%, Thoracic = 30%, lumbar = 4%, and Sacral = 2% •Most common at C5,6,7 due to greatest mobility at these levels. •Caused by: •Cutting, compression, or stretching of the spinal cord •Unstable or sharp bony fragments pushing on the cord •Pressure from bone fragments or swelling that interrupts the blood supply to the cord causing ischemia.
- 10. MECHANISMS Distraction – Hanging), significant impact on in hyperextension (eg. the head or face. Compression of the bony spine – directly compromise the spinal canal and spinal cord. Torsion – falls, high energy vehicle collisions – can tear the spinal cord tissue. Penetration – in gun shot or stab injury
- 11. TYPES OF SPINAL CORDINJURY COMPLETE SPINAL CORD INJURIES •Total motor & sensory loss distal to the injury INCOMPLETE SPINAL CORD INJURIES •Some motor or sensory functions is spared distal to the cord injury. •Voluntary sphincter contraction, toe flexor contraction–present. •Prognosis-Good
- 12. SPINAL CORD INJURY SYNDROMES •Anterior Cord Syndrome •Central Cord Syndrome •Posterior cord syndrome •Brown-sequard syndrome •Cauda Equina Syndrome •Conus medullaris syndrome
- 13. ANTERIOR CORD SYNDROME •Due to ischemia – blood supply from anterior spinal artery is distrupted (compressed by bone fragments). •Damage to cortico-spinal and spinothalamic tracts •Posterior columns unaffected. •Flexion/rotation injury
- 14. CENTRAL CORD SYNDROME •Central gray matter is damaged. •Bladder dysfunction – present as urinary retention. •Hyperextension injury •Motor: Arm > Leg weakness •Sensory: Arms>Legs •Usually sacral sensory sparing
- 15. POSTERIOR CORDSYNDROME •Rare •Loss of proprioception and vibration •Good prognosis •Penetrating back trauma or hyperextension injury.
- 16. BROWN-SEQUARDSYNDROME •Hemisection of the cord •Usually in penetrating trauma, Knife in back or rotational or fracture/dislocation. •Ipsilateral paralysis and loss of vibration and joint position sense, with contralateral loss of pain and temperature sensation .
- 17. CAUDA EQUINASYNDROME •Presents with loss of bowel and baldder function with LMN signs on lower limbs. •Sensory signs – unpredictable. •Not a cord syndrome. Technically a LMN lesion. •Saddle anaesthesia •Loss of anal tone •Sexual dysfunction
- 18. Conus medullaris syndrome Cauda equina syndrome Vertebral level L1-L2 L2-sacrum Spinal level Sacral cord segment and roots Lumbosacral nerve roots Presentation Sudden and bilateral Gradual and unilateral Radicular pain Less severe More severe Low back pain More Less Motor strength Symmetrical, less marked hyperreflexic distal paresis of LL, fasciculation More marked asymmetric areflexic paraplegia, atrophy more common Reflexes Ankle jerks affected Both knee and ankle jerks affected Sensory Localized numbness to perianal area, symmetrical and bilateral Saddle anaesthesia,asymmetrical, unilateral Sphincter dysfunction Early urinary and fecal incontinence Tend to present late UMN or LMN Lesion? UMN & LMN LMN Impotence Frequent Less frequent 7 06/08/2014 Conus Medullaris vs. Cauda Equina Syndromes
- 19. SIGNS ANDSYMPTOMS AIRWAY: •Airway reflexes are lost and gastric stasis – can have aspiration. BREATHING: •Above C4 – diaphragm is paralysed – apnea. •T2-T12 – innervates intercostal muscles – fractures above – diaphragmatic breathing – limited expansion, decreased TV and FRC, impaired cough, inc RV. •Decreased muscle power – pneumonia is common. •ARDS and pulmonary emboli also occur
- 20. CIRCULATION: •Damage above T6 – sympathetic innervation of heart lost – loss of reflex, tachycardia, impaired LV function and risk of severe bradycardia and asystole following unopposed vagal stimulation. NEUROLOGICAL: •Spinal shock – flaccidity and areflexia – duration is variable. •Following a/c phase of spinal shock – majority of patients with lesion above T6 – autonomic dysreflexia (mass spinal reflex when area below the lesion is stimulated) •Develops severe bradycardia, hypertension, flushing and sweating above the lesion – triggered by distended bladder or bowel, pressure sores etc
- 21. TEMPERATURE: •Hypothermia due to peripheral vasodialatation. BIOCHEMICAL AND ENDOCRINE: •Increased ADH – water retention •Glucose intolerance •NG tube – hypokalemic metabolic alkalosis •Hypoventilation – respiratory acidosis •Osteoporosis and hypercalcemia
- 22. SKIN – pressure sores THROMBOELASTOGRAM – DVT and embolism. MUSCULOSKELETAL – muscle spasms and contractures. PSYCHOLOGICAL – reactive depression
- 23. DIAGNOSTIC TESTS •Complete blood count (e.g. Hb, RBC, WBC) •Arterial blood gas level PaO2:85-95 mm of Hg PaCO2:35-45 mm of Hg •X- RAYS •COMPUTERIZED TOMOGRAPHY (CT) SCANS •MAGNETIC RESONANCE IMAGING (MRI) •MYELOGRAPHY
- 25. General Pattern • Vertebral bodies • Intervertebral discs • Spinal cord/canal • Marrow Signal • Individual levels Sagittal T2 & axial T2 Rate the spinal canal and neural foramen at each level
- 26. 40 yo, fell 4 stories, lower extremity paralysis T1 hyperintense blood products compressing on the spinal cord
- 27. 40 female, MVA, Power bilateral C8 & T1 2/5
- 28. 40 female, MVA, Power bilateral C8 & T1 2/5
- 29. 40 female, MVA, Power bilateral C8 & T1 2/5
- 30. - Hemodynamic phenomenon: loss of vasomotor tone & loss of sympathetic nervous system tone - Hypotension, Bradycardia, Pokilothermia - Cause: Spinal cord injury above T6, Some drugs with effect on medulla (opioid, benzodiazepine) - Atropine, Vasopressor, beware of fluid overload Neurogenic Shock
- 31. - After spinal cord injury, temporary depressed spinal reflexes, loss of neurologic function including loss of sensation and flaccid paralysis below the level of injury - syndrome lasts days to months Spinal Shock
- 33. - Exaggerated autonomic response secondary to stimuli that would only be mildly noxious under normal circumstances - Only in lesion T6 & above - Such hypersensitivity is partially due to subnormal resting levels of catecholamines - Noxious stimuli is below T6 Autonomic Hyperreflexia
- 34. - Noxious stimuli: The 6 B’s - Bladder - Bowel - Back passage - Bones - Boils - Babies Autonomic Hyperreflexia
- 35. Autonomic Hyperreflexia 90% paroxysmal hypertension 85% have triad of • Headache • Hyperhidrosis • Cutaneous vasodilatation
- 36. - Elevate HOB - Check BP every 5 mins - Identify & eliminate the offending stimulus - Antihypertensive if HTN is extreme or doesn’t resolve quickly a) SL Nifedipine 10mg b) IV Phentolamine - Relieves spasm of skeletal and smooth muscle – IV Diazepam 5mg - Prophylaxis a) Good bowel/bladder & skin care b) Alpha blocker in resistant cases c) Prophylactic treatment(nifedipine) / anaesthetic prior to procedure Autonomic Hyperreflexia - Treatment
- 37. MANAGEMENT: The major causes of death in spinal cord injury (SCI) are aspiration and shock. Initial survey under ATLS protocol: (“ABC’s”). This is followed by a brief neurologic exam. Any of the following patients should be treated as having an SCI until proven otherwise: 1. all victims of significant trauma 2. trauma patients with loss of consciousness 3. minor trauma victims with complaints referable to the spine (neck or back pain or tenderness) or spinal cord (numbness or tingling in an extremity, weakness, paralysis) 4. associated findings suggestive of SCI include a) abdominal breathing b) priapism (autonomic dysfunction)
- 38. MANAGEMENT: Primary(Pre-hospital) management- Initial treatment of patients with cord injury focuses on two aspects -preventing further damage and resuscitation. Immobilization with a hard cervical collar Resuscitation is aimed at airway maintenance, adequate oxygen saturation, preventing bradycardia to prevent any ischemic damage to the already compromised cord
- 39. MANAGEMENT: Secondary (Hospital) Management: Medical Management Surgical Management • Surgical Decompression • Surgical Stabilization • Fixation of Vertebra • Fixation of Spine • Artificial disc implantation Spinal
- 40. MEDICAL MANAGEMENT: 1. Immobilization (Philadelphia or Aspen Collar) 2. Hypotension - Keep SBP ≥ 90mmHg - Keep MAP 85-90mmHg for 1st 7 days after SCI to improve spinal cord perfusion - Combination of factors - Pressor if necessary ( Dopamine is the choice), avoid phenylephrine 3. Oxygenation - Indication of Intubation? Level of SCI C5 & above? - During intubation, use chin lift without neck extension
- 41. MEDICAL MANAGEMENT: 4. NG Tube - Paralytic ileus is common 5.Indwelling Foley Catheter 6.DVT prophylaxis 7. Temperature regulation: vasomotor paralysis may produce poikilothermy 8. Electrolytes imbalance such as Hypokalemia
- 42. MEDICAL MANAGEMENT: 9. Detailed neuro exam
- 44. The modified Barthel Index
- 45. MEDICAL MANAGEMENT: 10. Should we give steroid? The answer: NO
- 46. SURGICAL MANAGEMENT: - When surgical decompression is indicated, it is usually combined with a stabilization procedure - Contraindication to emergency operation: a) Medically unstable patient b) Complete spinal cord injury ≥ 24 hours
- 47. SURGICAL MANAGEMENT: Modified recommendations of Schneider In patients with complete spinal cord lesions, no study has demonstrated improvement in neurologic outcome with either open decompression or closed reduction. surgery is reserved for incomplete lesions—possibly excluding central cord syndrome with extrinsic compression, After maximal possible reduction of subluxation, show: 1. progression of neurologic signs 2. complete subarachnoid block by Queckenstedt test or radiographically (on myelography or MRI) 3. compression of spinal cord 4. necessity for decompression of a vital cervical root 5. compound fracture or penetrating trauma of the spine 6. acute anterior spinal cord syndrome 7. non-reducible fracture-dislocations from locked facets causing spinal cord compression
- 48. Timing of surgical decompression
Editor's Notes
- The anterior corticospinal tract is formed at the level of the of the medullary pyramids, where the majority (90%) of descending corticospinal tract fibers decussate to form the lateral corticospinal tract. The majority of the remaining non-decussating 10% of fibers form the much smaller anterior corticospinal tract 1,2. It descends in the anterior funiculus of the spinal cord, lying close to the anterior median fissure. At each relevant level, fibers cross the anterior spinal commissure of the spinal cord to synapse with ventral horn motor neurons. The anterior corticospinal tract thus becomes smaller as it descends, ending at the level of the mid-thoracic cord. The anterior corticospinal tract is primarily responsible for gross and postural movement of the trunk and proximal musculature 3. arises from the pyramidal cells of cerebral cortex – fibres travel through • corona radiata • posterior limb of the internal capsule • cerebral peduncle ( middle 3/ 5th ) • pons • medulla oblongata ( passed through the pyramids ) – eventually fibres cross the mid line and terminate on LMN of anterior gray column of respective spinal cord segments
- Lateral spinothalamic tract pain and thermal impulses ( input from free nerve endings, thermal receptors ) transmitted to spinal cord in delta A and C fibres central process enters the spinal cord through posterior nerve root, proceed to the tip of the dorsal gray column • Second order neuron – in the dorsal horn, cross to the opposite side (decussate) – ascend in the contralateral ventral column – end in VPL nucleus of thalamus • Third order neuron – in the VPL nucleus of thalamus – project to cerebral cortex ( area 3, 1 and 2 )
- Anterior spinothalamic tract light touch and pressure impulses ( input from free nerve endings, Merkel’s tactile disks ) • First order neuron – dorsal root ganglion( all level ) • Second order neuron – in the dorsal horn, cross to the opposite side (decussate) – ascend in the contralateral ventral column – end in VPL nucleus of thalamus • Third order neuron – in the VPL nucleus of thalamus – project to cerebral cortex ( area 3, 1 and 2 )
- Men > women NON-TRAUMATIC: malignancy, infection (TB, epidural abscess), vascular (x-clamping aorta) Most common vertebrae involved are C5, C6, C7, T12, and L1 because they have the greatest ROM.
- When the bulbocavernosus reflex is positive & no sacral sensation or motor function has returned, paralysis will be permanent & complete in most patients. Spinal shock usually lasts for 24-48hrs) From our study it appears that there is a close neuroanatomic interrelation between the sacral roots innervating the external anal/urethral sphincter and the plantar Aexors of the toes. This was also suggested by Brindley,7 who emphasizes looking at the plantar flexor of the toes to control stimulation of S3. This could be important in the clinical examination of traumatic spinal cord injury patients because from our experience many subjects do not really understand what is meant when they are asked to contract the external urethral sphincter.
- – paralysis, abnormal touch, pain and temperature sensation. – vibration and joint position senses preserved
- As a result of the injury to these three main brain pathways the patient will present with three lesions: The corticospinal lesion produces spastic paralysis on the same side of the body below the level of the lesion (due to loss of moderation by the UMN). At the level of the lesion, there will be flaccid paralysis of the muscles supplied by the nerve of that level (since lower motor neurons are affected at the level of the lesion). The lesion to fasciculus gracilis or fasciculus cuneatus (dorsal column) results in ipsilateral loss of vibration and proprioception (position sense) as well as loss of all sensation of fine touch. The loss of the spinothalamic tract leads to pain and temperature sensation being lost from the contralateral side beginning one or two segments below the lesion. In addition, if the lesion occurs above T1 of the spinal cord it will produce ipsilateral Horner's syndrome with involvement of the oculosympathetic pathway.
- UMN LMN means Babinski upgoing, bulbocavernous reflex is absent
- bladder (urinary tract infection or retention, stones, or distension caused by catheter blockage), bowel (constipation, impaction), boils (skin damage), bones (fractures), babies (pregnancy, sexual intercourse, breastfeeding), and back passage (haemorrhoid or fissure) Tight clothing
- bladder (urinary tract infection or retention, stones, or distension caused by catheter blockage), bowel (constipation, impaction), boils (skin damage), bones (fractures), babies (pregnancy, sexual intercourse, breastfeeding), and back passage (haemorrhoid or fissure) Tight clothing
- Phenylephrine – non-inotropic and possible reflex increase in vagal tone and cause bradycardia
- Decompress abdomen, prevent vomit and aspiration Catheter as AUR is common and for i/o charting DVT motarlity is as high as 9% Hypovolemia and hypotension cause increased plasma aldosterone leading to hypoK
- Decompress abdomen, prevent vomit and aspiration Catheter as AUR is common and for i/o charting DVT Hypovolemia and hypotension cause increased plasma aldosterone leading to hypoK
- Decompress abdomen, prevent vomit and aspiration Catheter as AUR is common and for i/o charting DVT Hypovolemia and hypotension cause increased plasma aldosterone leading to hypoK
- Complete injury – bulbocavernous reflex is a guide to determine presence of spinal shock
- Complete injury – bulbocavernous reflex is a guide to determine presence of spinal shock