management issues in patients with acute and chronic spinal cord injuries andy jagoda, md professor...

Management Issues in Patients Management Issues in Patients with Acute and Chronic Spinal with Acute and Chronic Spinal

Cord InjuriesCord Injuries

Management Issues in Patients Management Issues in Patients with Acute and Chronic Spinal with Acute and Chronic Spinal

Cord InjuriesCord Injuries

Andy Jagoda, MD

Professor of Emergency Medicine

Residency Program Director

Mount Sinai School of Medicine

Andy Jagoda, MD, FACEP

ObjectivesObjectives

• 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


Case Study: Spinal Cord InjuryCase 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

X-RayX-Ray


Case Study: QuestionsCase 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


Spinal Cord Injury: EpidemiologySpinal 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 / yearDeVivo. Causes and costs of SCI. Spinal Cord 1997; 35:809-813DeVivo. Causes and costs of SCI. Spinal Cord 1997; 35:809-813


Anatomy of the Spinal CordAnatomy 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

PicturePicture


SCI: SubtypesSCI: Subtypes

• Complete: complete transection of motor and sensory tracts

• Incomplete:

• Central Cord Syndrome

• Anterior Cord Syndrome

• Posterior Cord Syndrome

• Brown Sequard Syndrome


Anatomy: Vascular SupplyAnatomy: 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)

PicturePicture


Neurologic ExaminationNeurologic 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)

PicturePicture


Upper Versus Lower Motor Neuron WeaknessUpper 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


ASIA Impairment ScaleASIA 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


Spinal Shock Versus Neurogenic ShockSpinal 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


Complete CordComplete 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


Central Cord SyndromeCentral 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


Anterior Cervical Cord SyndromeAnterior Cervical Cord Syndrome

• Typically after hyperflexion

• Motor loss

• Pain and temperature loss

• Dorsal column preserved

• Autonomic dysfunction

• Sacral sparing

• 50% Recovery


Anterior Cord: Spinal Cord InfarctionAnterior 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


Brown - SequardBrown - 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


Cauda Equina / Conus MedularisCauda 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


SCI: PathophysiologySCI: Pathophysiology

• Early NECROTIC cellular death at focus of traumatic injury

• Extension of cellular injury continues long after trauma; ?as a result of APOPTOSIS

Morphology of Cell DeathMorphology of Cell Death


Evidence for Apoptosis in Humans: Evidence for Apoptosis in Humans: Spinal Cord InjurySpinal 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


Traumatic SCI: ManagementTraumatic 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


National Acute Spinal Cord National Acute Spinal Cord Injury Study: NASCISInjury 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


Guidelines for the Management of Acute Cervical Guidelines for the Management of Acute Cervical Spine and SCI. Spine and SCI. Neurosurg 2002;Neurosurg 2002;50 (suppl) :1-20050 (suppl) :1-200

• Evidence based practice guideline

• 22 chapters

• Chapter on pharmacologic therapy most controversial• 17 pages of editorial commentary in the

preface


IX. Pharmacological Therapy after Acute IX. Pharmacological Therapy after Acute Cervical Spinal Cord InjuryCervical 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.


Apoptosis: Therapeutic StrategiesApoptosis: Therapeutic Strategies

• Caspase inhibition

• Bcl-2 administration or up-regulation

• Mitochondrial protectants, e.g., Cyclosporin A

• Combination of anti-excitotoxic and anti-apoptotic strategies


Spinal Cord Injury: The Future?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

X-RayX-Ray

PicturePicture


MorbidityMorbidity

• 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


MortalityMortality• 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


Neurologic RecoveryNeurologic 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


One Year Prognosis after SCIOne 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-upOne Year follow-up

Admission ASIAAdmission ASIA

Neurologic decline is unusual and suggests underlying process, eg, skeletal instability, cystic degeneration, etc.


Thromboembolic DiseaseThromboembolic 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


Autonomic DysfunctionAutonomic 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

PicturePicture


Autonomic DysfunctionAutonomic 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


Autonomic HyperreflexiaAutonomic 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


Autonomic Hyperreflexia: BP ManagementAutonomic 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


Autonomic dysreflexia: One more way EMS can Autonomic dysreflexia: One more way EMS can positively affect patient survival. JEMS 2003; 28:46-51positively 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.”


Neuropathic Spinal PainNeuropathic 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, ???


Neurogenic Bladder DysfunctionNeurogenic 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


SCI and bladder recovery.SCI and bladder recovery. Arch Phys Med Rehab 996;77:1133Arch 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


Neurogenic Bladder DysfunctionNeurogenic 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


Neurogenic Bladder DysfunctionNeurogenic 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


Neurogenic Bowel DysfunctionNeurogenic 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


Neurogenic Bowel DysfunctionNeurogenic Bowel Dysfunction

• Diarrhea• Impaction• Complications of medications e.g., C.

Difficile from antibiotics

• Constipation• Manual disimpaction• Stimulants


Hypertrophic Bone FormationHypertrophic 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

PicturePicture


Pressure UlcerationPressure 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


SpasticitySpasticity• 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


SpasticitySpasticity

• 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)


Spasticity: MedicationsSpasticity: 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


ConclusionsConclusions• 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


Upper versus Lower Motor Neuron WeaknessUpper 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


Traumatic Spinal Cord Injury:Traumatic Spinal Cord Injury:Neuronal and Glial ApoptosisNeuronal 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.


Necrotic Cellular DeathNecrotic 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


Apoptosis: Cellular DeathApoptosis: 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


Apoptosis: Cellular Death (Cont)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


Anatomy of the Spinal ColumnAnatomy 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


SCI: Methylprednisolone: SCI: Methylprednisolone: NASCI IINASCI 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


Neuro Exam: ASIA/NASCISNeuro 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

management issues in patients with acute and chronic spinal cord injuries andy jagoda, md professor...

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