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

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Presentation on theme: "Management Issues in Patients with Acute and Chronic Spinal Cord Injuries Andy Jagoda, MD Professor of Emergency Medicine Residency Program Director Mount."— Presentation transcript:

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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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

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5 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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

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9 Andy Jagoda, MD, FACEP SCI: Subtypes Complete: complete transection of motor and sensory tracts Incomplete: Central Cord Syndrome Anterior Cord Syndrome Posterior Cord Syndrome Brown Sequard Syndrome

10 Andy Jagoda, MD, FACEP 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)

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12 Andy Jagoda, MD, FACEP 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)

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16 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP Anterior Cervical Cord Syndrome Typically after hyperflexion Motor loss Pain and temperature loss Dorsal column preserved Autonomic dysfunction Sacral sparing 50% Recovery

22 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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

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37 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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

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44 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 Andy Jagoda, MD, FACEP 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 H 2 O) to avoid renal damage

50 Andy Jagoda, MD, FACEP 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

51 Andy Jagoda, MD, FACEP Neurogenic Bladder Dysfunction Clean intermittent catheterizatons Needs good hand function or skilled attendants Limit fluid intake; performed q 4-6 hours Reflex bladder contractions can cause high storage pressures and incontinence Oxybutynin 5 mg po tid / Tolterodine 2 mg po bid Reflex voiding in a condom catheter Problems including urinary retention or high intravesical voiding pressure due to DSD (can be decreased with alpha blocking agents e.g. terazosin, sphincter defeating surgery, or urethral stent) Electrical stimulation

52 Andy Jagoda, MD, FACEP Neurogenic Bladder Dysfunction In the past, renal disease was a frequent cause of death in SCI patients Urinary tract complications continue to be a cause of morbidity Infection: 20% annual incidence Calculi Hydronephrosis

53 Andy Jagoda, MD, FACEP Neurogenic Bowel Dysfunction Upper motor neuron dysfunction causes constipaton with slow colonic transit and stool retention due to spasticity Reflexes allowing defecation may remain intact Cauda equina causes lower motor neuron dysfunction causing constipation with slow colonic transport and incontinence due to a flaccid sphincter

54 Andy Jagoda, MD, FACEP Neurogenic Bowel Dysfunction Diarrhea Impaction Complications of medications e.g., C. Difficile from antibiotics Constipation Manual disimpaction Stimulants

55 Andy Jagoda, MD, FACEP Hypertrophic Bone Formation Formation of new bone in soft tissue planes surrounding a joint Most commonly involves the hips Presentation: Lower extremity swelling, loss of hip ROM, fever Must be distinguished from other problems, e.g., DVT Treatment: ROM exercises, NSAIDs, irradiation, etidronate

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57 Andy Jagoda, MD, FACEP Pressure Ulceration Pressure to soft tissue above capillary pressure results in breakdown Evaluation includes assessment of ulcers depth Treatment: wet / dry dressing; topical antibiotics; debridement Myocutaneous flap

58 Andy Jagoda, MD, FACEP Spasticity Increase in upper motor neuron injury after upper motor neuron injury Spasticity causes: Resistance to passive motion, exaggerated DTRs, clonus, involuntary contraction of muscle groups Advantages of spasticity: assist mobility, imporves circulation, decrease risk of DVT and osteoporosis Disadvantages: may interfere with positioning, mobility, and spasms may be painful

59 Andy Jagoda, MD, FACEP Spasticity Prevention and treatment of noxious stimuli Muscle stretching and joint ROM Botulinum toxin: blocks presynaptic release of Ach at the NMJ Effect lasts about 3 months (collateral sprouting of axon)

60 Andy Jagoda, MD, FACEP Spasticity: Medications Baclofen: GABA-B analog. Centrally acting. 5 mg po bid / increased up to 200 mg / day Can be given intrathecally Diazepam: GABA-A agonist Tizanidine: Centrally acting muscle relaxant Clonidine: Centrally acting alpha-2 agent activates inhibitory neuron which reduces sympathetic outflow which decrease vasomotor tone and heart rate

61 Andy Jagoda, MD, FACEP Conclusions Management of acute SCI is based on preventing additional injury and providing supportive care Role of methylprednisolone in SCI is questionable Acute SCI above T7 has low sympathetic activity; chronic SCI has high sympathetic activity Pneumonia, PE, and sepsis are the most common causes of death on patients with chronic SCI Autonomic dysregulation, hypertrophic bone formation, neurogenic bladder, and spasticity underlie reasons for patients with chronic SCI to come to the ED Management of autonomic dysregulation focuses on removing noxious stimuli

62 Andy Jagoda, MD, FACEP Upper versus Lower Motor Neuron Weakness Mylopathy = Spinal cord process UMN findings (spasticity, weakness, atrophy, sensory findings, bowel and bladder complaints Radiculopathy = Nerve root process LMN findings (paresthesias, fasciculations, weakness, decreased DTR) Patient may have a radiculopathy with mylopathy below the lesions

63 Andy Jagoda, MD, FACEP Traumatic Spinal Cord Injury: Neuronal and Glial Apoptosis Immediately following SCI in rat, typical post- traumatic necrosis is seen. Apoptotic cells are seen from 6 hr-3 wk; especially in spinal white matter. After SCI in monkeys, apoptotic cells were found within remote degenerating fiber tracts. Both secondary degeneration at the site of SCI and the chronic demyelination of distant tracts appear due to apoptosis.

64 Andy Jagoda, MD, FACEP Necrotic Cellular Death Depletion of intracellular ATP Swelling of cells; early protein denaturation Disruption of organelles Rupture of plasma membrane Release of cytoplasmic contents into surrounding tissue Passive process; not ATP dependent

65 Andy Jagoda, MD, FACEP Apoptosis: Cellular Death ATP Dependent Process Condensation of nuclear chromatin into sharply delineated granular masses Margination of granular masses against nuclear membrane, with progressive condensation of nuclear contents Nucleus breaks up (karyorhexis) Dense nuclear remnants are seen

66 Andy Jagoda, MD, FACEP Apoptosis: Cellular Death (Cont) Cell shrinkage, cytoplasmic condensation Cell outline convoluted, forms extensions. Extensions separate (budding); plasma membrane seals. “Apoptotic bodies” rapidly taken up by macrophages without inflammation. Organelles such as mitochondria preserved, destroyed secondarily

67 Andy Jagoda, MD, FACEP Anatomy of the Spinal Column Anterior segment Posterior segment Ligaments Ligamenta flava: paired elastic structures joining the lamina Stretch when the spine is flexed and buckle when it is hyperextended

68 Andy Jagoda, MD, FACEP SCI: Methylprednisolone: NASCI II 162 pts. Received MP; 171 placebo 30 mg/kg; 5.4 mg/kg/hr for 23 hr Motor/Sensory scores at 6 wk/6 mo Benefit for MP when administered w/in 8 hr Motor: MP improved 16/70 compared to 11.2/70 placebo (p=0.03) Sensation to pinprick: MP improved 11.4/87 compared to 6.6/87 placebo (p=0.02) MP improved complete and incomplete

69 Andy Jagoda, MD, FACEP Neuro Exam: ASIA/NASCIS Motor: Function tested bilaterally in 14 muscle segments (0 = no contraction through 5 = normal function); scores range 0 - 70. Sensory: Response to pinprick and light touch scored bilaterally from C-2 through S-5 for 29 spinal cord segments (0 = absent through 3 = normal); scores range 0 - 87

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