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Management Issues in Patients with Acute and Chronic Spinal Cord Injuries

Management Issues in Patients with Acute and Chronic Spinal Cord Injuries. Andy Jagoda, MD Professor of Emergency Medicine Residency Program Director Mount Sinai School of Medicine. Objectives. Review the anatomy of the spinal cord Review the pathophysiology of SCI

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Management Issues in Patients with Acute and Chronic Spinal Cord Injuries

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  1. Management Issues in Patients with Acute and Chronic Spinal Cord Injuries Andy Jagoda, MD Professor of Emergency Medicine Residency Program Director Mount Sinai School of Medicine

  2. Objectives • Review the anatomy of the spinal cord • Review the pathophysiology of SCI • Review clinical presentations of SCI • Provide an overview of diagnostic and therapeutic interventions that may be helpful in managing SCI both acutely and over time

  3. Case Study: Spinal Cord Injury • 16 yo male • Tramboline for his birthday • Brought EMS; 2 IV’s, backboard, C-collar • Nasal intubation in the field • VS: P 128; BP 90/55 • Alert • No spontaneous movement or reflexes

  4. X-Ray

  5. Case Study: Questions • How would this spinal cord injury be classified? • Does methylprednisolone play a role? • What new treatments are on the horizon? • What complications occur subacutely and over time in patients with SCI

  6. Spinal Cord Injury: Epidemiology • 12,000 new cases in the US/year • Majority from MVAs (36%) • Violence (30%), falls (20%), sports (7%) • Peak incidence: ages 15 - 35 • Rehab/medical care: • First year: $225,000 • Average lifetime: $30,000 / year DeVivo. Causes and costs of SCI. Spinal Cord 1997; 35:809-813

  7. Anatomy of the Spinal Cord • Corticospinal tracts: motor from the cerebral cortex • Cross in the lower medulla • Spinothalamic tracts: pain and temperature • Cross 1 or 2 levels above entry • Posterior column: proprioception and vibration

  8. Picture

  9. SCI: Subtypes • Complete: complete transection of motor and sensory tracts • Incomplete: • Central Cord Syndrome • Anterior Cord Syndrome • Posterior Cord Syndrome • Brown Sequard Syndrome

  10. Anatomy: Vascular Supply • Single anterior artery perfuses anterior and central cord • Paired posterior from vertebral arteries (except in the cervical cord) • Radicular arteries from aorta • Varying degrees of contribution • Great radicular artery of Adamkiewicz T-10 to L-2 (Major source of blood flow to 50% of anterior cord in 50% of patients)

  11. Picture

  12. Neurologic Examination • Document all findings • Level of consciousness • Motor strength • Sensation to light touch and pinprick • Position sense • Diaphragm, abdominal, and sphincter function • DTRs, plantar reflexes, sacral reflexes • Sacral sparing (perineal sensation, sphincter tone)

  13. Picture

  14. Picture

  15. Picture

  16. Upper Versus Lower Motor Neuron Weakness • UMN often symmetric LMN often single muscle group (with atrophy) • UMN increased (after spinal shock) LMN decreased DTR • UMN muscle tone increased LMN muscle tone decreased • UMN no fasciculations LMN fasciculations

  17. ASIA Impairment Scale • A: Complete • B: Incomplete: Sensory, but no motor function below neurological level • C: Incomplete: Motor function preserved below level; muscle grade < 3 • D: Incomplete: Motor function preserved below level: muscle grade > 3 • E: Normal

  18. Spinal Shock Versus Neurogenic Shock • Spinal shock is loss of motor and sensory after trauma • Neurogenic shock involves the sympathetic chain and is associated with autonomic instability • Best timing of exam for prognosis is undetermined: Probably 72 hours post insult though some studies use 30 days

  19. Complete Cord • No sensation • Flaccid paralysis • Initially areflexia • Hyperreflexia, spasticity, positive planter reflex (days to months) • <5% chance of functional recovery if no improvement within 24 hours

  20. Central Cord Syndrome • Hyperextension injuries, tumor, syringomylia • M U D • Paresis or plegia of arms > legs • Posterior column spared • Sensation UE > LE; sacral sparing • Perforating branches of the anterior spinal artery at greatest risk for vascular insult • Good prognosis

  21. Anterior Cervical Cord Syndrome • Typically after hyperflexion • Motor loss • Pain and temperature loss • Dorsal column preserved • Autonomic dysfunction • Sacral sparing • 50% Recovery

  22. Anterior Cord: Spinal Cord Infarction • Anterior more common than posterior • Most common in the thoracic area • Acute paralysis below the lesion • Dissociated sensory loss • Loss of pain and temperature: posterior column function remains • Loss of sphincter function • Urinary retention • Brown-Sequard may occur

  23. Brown - Sequard • Usually after penetrating trauma • Tumor • Ipsilateral motor paralysis • Ipsilateral loss of light touch and propioception (anesthesia) below the level of the lesion • Ipsilateral hyperanesthesia • Contralateral loss of pain and temperature found one or two segments below the lesion

  24. Cauda Equina / Conus Medularis • Conus Medullaris: S3-5 • Saddle anesthesia, sphincter loss • Intact LE motor and sensory • Cauda equina • Spinal cord ends at L2 • Injury to lumbosacral roots • Variable sensorimotor deficits and bowel and bladder function

  25. SCI: Pathophysiology • Early NECROTIC cellular death at focus of traumatic injury • Extension of cellular injury continues long after trauma; ?as a result of APOPTOSIS

  26. Morphology of Cell Death

  27. Evidence for Apoptosis in Humans: Spinal Cord Injury • Spinal cords from 15 patients examined: 3 hr - 2 mo following traumatic SCI. • Apoptotic cells found at the edges of the lesion epicenter and in adjacent white matter, particularly in the ascending tracts. • Apoptosis prominent in 14/15 samples when compared to 5 controls. • Apoptotic cells present around periphery of zone of injury as well as in areas of Wallerian degeneration. Emery E: Nat Med 1999;5:943

  28. Traumatic SCI: Management • ABC’s: Treat / prevent hypoxia and hypotension • Stabilize the spine to prevent additional mechanical injury • R/O other serious injuries • Careful neurological examination: level of neurological impairment • Imaging • Neuroprotective pharmacotherapy? • Early rehabilitation

  29. National Acute Spinal Cord Injury Study: NASCIS • NASCIS I: no benefit of MP (dose too low?) • NASCIS II: • 487 pts randomized: MP, naloxone or placebo • 30 mg/kg bolus then 5.4mg/kg/hr for 23 hours • Negative results in primary analysis • Positive results only in subgroup analysis; those patients treated within 8 hr; only 62 receiving MP; 67 placebo • Benefit had no clinical relevance • Steroid Rx: 2.6x inc pneumonia; length in ICU days • NASCIS III: Compared tirilazad mesylate, MP for 24 hours and 48 hours: No placebo; no functional benefit

  30. Guidelines for the Management of Acute Cervical Spine and SCI. Neurosurg 2002;50 (suppl) :1-200 • Evidence based practice guideline • 22 chapters • Chapter on pharmacologic therapy most controversial • 17 pages of editorial commentary in the preface

  31. IX. Pharmacological Therapy after Acute Cervical Spinal Cord Injury • Recommendations: Corticosteroids • Standards: None • Guidelines: None • Options: Treatment with methylprednisolone for either 24 or 48 hours is recommended as an option in the treatment of patients with acute spinal cord injury within 12 hours of injury. • B) GM-1 Ganglioside • Standards: None • Guidelines: None • Options: Treatment of acute spinal cord injury patients with GM-1 ganglioside is an option for treatment without clear evidence of clinical benefit or harm.

  32. Apoptosis: Therapeutic Strategies • Caspase inhibition • Bcl-2 administration or up-regulation • Mitochondrial protectants, e.g., Cyclosporin A • Combination of anti-excitotoxic and anti-apoptotic strategies

  33. Spinal Cord Injury: The Future? • Development of neuroprotectant agents • Nerve grafts/neural transplants • Gene therapy • Stimulating adult neurons to grow axons again; changing the environment encountered by regenerating axons

  34. X-Ray

  35. X-Ray

  36. Picture

  37. Morbidity • Acute rehabilitation phase • Pressure ulcerations in 25%; most commonly over the sacrum • Atelectasis / pneumonia in 13% • DVT in 10% • Autonomic dysreflexia in 8% • UTI Chen. Medical complications during acute rehabilitation. Arch Phys Med Rehab 1999; 80:1397

  38. Mortality • Mortality is highest in the first year after injury • Persons sustaining paraplegia at age 20 have an average subsequent life expectancy of 44 years vs 57 years for the general population • Leading cause of death are pneumonia, PE, followed by heart disease and sepsis • Renal failure is no longer a leading cause of death

  39. Neurologic Recovery • Majority of complete injuries remain complete • Initial sparing of sacral pin sensation suggests a favorable prognosis for eventual ambulation • Appearance of hemorrhage within the cord suggests unfavorable recovery Marino. Neurologic recovery after traumatic SCI. Arch Phys Med Rehab 1999; 80:1391

  40. One Year Prognosis after SCI • A: Complete • B: Incomplete: Sensory, but no motor function below neurological level • C: Incomplete: Motor function preserved below level; muscle grade <3 • D: Incomplete: Motor function preserved below level: muscle grade >3 • E: Normal One Year follow-up Admission ASIA Neurologic decline is unusual and suggests underlying process, eg, skeletal instability, cystic degeneration, etc.

  41. Thromboembolic Disease • Increased risk due to venous stasis and hypercoagulability • Highest risk in patients with cancer; flaccid paralysis • Risk of death from PE in the first year following SCI is > 200 x that of the general population • 51 / 243: 8 deaths • Prophylactic strategies • Pneumonic compression devices • Unfractionated heparin • Caval filters in patients with high cord lesions Green. SCI risk for PE (SPIRATE study). Am J Phys Med Rehab 2003;82:950

  42. Autonomic Dysfunction • High thoracic (above T6) and cervical lesions • Loss of supraspinal control of sympathetic activity with dysregulation of function • Sympathetic outflow to splanchnic beds • Acute SCI • Low sympathetic activity • Subacute and chronic SCI • High sympathetic activity

  43. Picture

  44. Autonomic Dysfunction • Resting blood pressure is low • Bradycardia with suctioning or stimulation • Usually resolves after first weeks • Orthosatic changes cause weakness, lightheadedness, fainting • Management: • Gradual mobilization • Liberal sodium intake • Compression stockings • Abdominal binding • Fludrocortisone acetate .1 mg po qd for volume expansion

  45. Autonomic Hyperreflexia • Generally in lesions above T7 • Does not occur acutely • Unmoderated sympathetic response to noxious stimuli below the level of the lesion, e.g. bladder distention or fecal impaction • Severe headache; Hypertension • Headache may be due to intracranial arterial dilatation to compensate for hypertension • Management: Place in sitting position (to decrease intracranial pressure), check for inciting stimulus, minimize all noxious stimuli

  46. Autonomic Hyperreflexia: BP Management • No scientific evidence to guide intervention • Nifedipine / nitrate historically used • Medline reports no adverse effects in these patients treated with nifedipine • Avoid nitrates if patient is using sildenafil (Viagra) • Consider alpha blocking agent (terazosin) • Admit to observation unit or hospital

  47. Autonomic dysreflexia: One more way EMS can positively affect patient survival. JEMS 2003; 28:46-51 “Bladder catherization and digital bowel emptying are not everyday EMS skills. They are, however, skills within the range of EMS abilities. Providers should contact their medical directors or training supervisors to obtain the training necessary to carry out both techniques.”

  48. Neuropathic Spinal Pain • Occurs at or below the level of injury • Reported in 6 – 50% of patients • Results from: changes in neuronal function, increased spontaneous activity and / or reduced thresholds of response • Descriptors: temperature, electric • Evaluation must look for other causes of pain, e.g. unstable spine, cystic myelopathy, other new condition e.g. renal stone • Treatment: physical therapy, anticonvulsants, antidepressants, ???

  49. Neurogenic Bladder Dysfunction • Initial bladder flaccidity; reflexes return with suprasacral injury • Acute management with indwelling catheter • Reflexes may be unable to cause efficient voiding due to tendency of reflex sphincter activity to directly oppose reflex detrusor contraction (detrusor sphincter dyssynergy) • Management must avoid high storage pressures (>40 cm H2O) to avoid renal damage

  50. SCI and bladder recovery.Arch Phys Med Rehab 996;77:1133 • Retrospective review; 19 consecutive patients • 18-68 / C4 – T12 • Correlation of perianal sensation and position sense with bladder function at one year • Presence of perianal pinprick sensation and toe position sense are positive predictors • Patients without initial position sense or the great toes will likely not regain volitional voiding • Patients without initial perianal pinprick sensation will not regain volitional voiding

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