advanced emergency trauma course

Advanced Emergency Trauma CourseGhana Emergency Medicine CollaborativePatrick Carter, MD Daniel Wachter, MD Rockefeller Oteng, MD Carl Seger, MD

C-Spine and Spinal Cord TraumaPresenter: Carl Seger, MD

Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course

EpidemiologySpinal Trauma- 10,000 new cases each year, with over 200,000 spinal injury victims living in US55% of spinal injuries occur in the C-spine15% in the thoracic, lumbar, and sacral regions10% of pts with c-spine injury have another vertebral fractureGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Spinal TraumaSpinal trauma has a huge impact physically, financially, and emotionally on societyProper treatment can minimize further damageImmobilization equipment is easy to use, inexpensive, and readily availableOur duty as EM physicians is to provide proper care and Do No HarmGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Can we make an impact?3-25% of cases of permanent neurologic impairment after spinal trauma have been attributed to injudicious manipulation by paramedical personnel, examining physicians, or radiology technicians.Francisco de Assiss Aquino Gondim, MD, e-medicine- Spinal Cord TraumaGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Prevention is key!With proper application of spinal precautions, we can positively impact patient outcomes



Evolution of SpinePrehistoric ManHunched shouldersStrong posterior neck musclesModern ManShoulders drop away, head elevatesAtrophy paraspinal musclesSacrifice protection for increased range of motionhttp://commons.wikimedia.org/wiki/File:Human_evolution.svgGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Modern ManIncreased Intellect, same aggressionHorse drawn carriages replaced by machine-powered vehiclesFists and clubs gave way to knives and gunsNew and inventive ways to inflict injury to spineGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Basic Anatomy7 Cervical12 Thoracic5 Lumbar5 Sacral4 Fused Coccygeal

Lordotic Curves Kyphyotic CurvesGrays Anatomy (Wikipedia)Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Functional Anatomy Review Vertebral Column 33 Vertebrae

Vertebrae = Body + ArchVertebral ArchPediclesLaminaeProcesses

Grays Anatomy (Wikipedia)Grays Anatomy (Wikipedia)Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


LigamentsAnterior/Posterior Longitudinal Vertebral Arch LigamentsLigamentum FlavumSupraspinatous LigamentInterspinous LigamentIntertransverse LigamentCapsular LigamentIntervertebral Disks Nucleus Propulsus Annulus FibrosusFunctional Anatomy ReviewGrays Anatomy (Wikipedia)Uwe Gille (Wikipedia)Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Spinal Stability Cervical SpineAnterior ColumnPosterior ColumnDisrupt both columns to be unstable Thoracolumbar Spine Denis ClassificationAnterior ColumnMiddle ColumnPosterior ColumnDisrupt 2 columns to be unstableGrays Anatomy (Wikipedia)https://commons.wikimedia.org/wiki/File:Cervical_vertebra_english.pngGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Normal Cervical Spinehttp://www.trauma.org/archive/spine/images/cspinealign.jpghttp://www.trauma.org/archive/spine/images/cspineLAT.jpgGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Injury PatternsAcute spinal injuries can be most easily classified according to the mechanism of traumaCategories include FLEXION, FLEXION-ROTATION, EXTENSION and VERTICAL COMPRESSION injuriesCan also include in classification whether or not a particular injury is STABLE vs. UNSTABLEGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Cervical Spine InjuriesFlexion InjuriesWedge compression fractureFlexion teardrop fractureClay Shovelers FractureBilateral Facet DislocationFlexion RotationUnilateral facet dislocationVertical CompressionJefferson Burst FractureBurst Fractures of Lower Cervical SpineHyperextension InjuriesAvulsion fracture of anterior arch of atlasExtension teardrop fracturePosterior arch of atlas fractureLaminar fractureHangmans FractureLateral FlexionUncinate Process Fracture Upper C-spine InjuriesOccipitoatlantal dissociationGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Flexion InjuriesFlexion injuries involving C1-C2 can cause atlantooccipital or atlantoaxial dislocation, with or without fracture of the odontoid Atlas = C1, Axis = C2Unstable due to the location and relative lack of muscle and ligamentous supportGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Flexion injuryOdontoid Fx with anterior dislocationSource UndeterminedSource UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Flexion InjuryIn pure flexion injury below C2, force is expended on the vertebral body anteriorly, resulting in a simple wedge fractureSimple wedge fractures are stableEven greater flexion forces a wedge shaped fragment off anterior-inferior portion of vertebral body, called a flexion teardrop injuryUsually includes ligamentous injury and is unstableGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Wedge Fracturehttp://faculty.washington.edu/alexbert/MEDEX/Winter/EM1DisordersSpine.htmhttp://emedicine.medscape.com/article/94234-mediaGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Flexion Teardrop FractureSource UndeterminedSource UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Flexion InjuryIn Australia during the 1930s, certain clay miners sustained a unique injuryWhile straining with heavy shovelful of clay, the abrupt flexion of head in opposition to the strong supraspinous ligament, resulted in avulsion fracture of spinous processClay Shovelers fracture is more often seen today due to direct blow, i.e. pool cue or baseball bat, or from sudden deceleration in MVCStable injury, no neurologic involvement

Clay Shovelers http://faculty.washington.edu/alexbert/MEDEX/Winter/EM1DisordersSpine.htm http://emedicine.medscape.com/article/94234-media



Extension InjuryMost well known is the Hangmans fracturePopular execution style in previous erasShort Drop with Sudden stop. The drop was preferred to the dangleThe skull is thrown into extreme hyperextension resulting in bilateral pedicle fractures of axisUnstable, but neurological involvement is minimal, therefore death usually due to strangulation, not cord damageGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Hangmans Fracturehttp://commons.wikimedia.org/wiki/File:Hangman%27s_fracture.JPGGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Vertical Compression InjuryExample = Jefferson FractureForce is transmitted down through skull and occipital condyles to superior articular surfaces of lateral masses of atlasSince atlas is a ring, this force pushes the masses outward resulting in fractures of anterior and posterior arches, and disruption of transverse ligamentExtremely UNSTABLEGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Jefferson FractureSource UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Jefferson FractureSource UndeterminedSource UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Injuries of Thoracic and Lumbar SpineCompression FracturesBurst FracturesFlexion Distraction Fractures



Injuries of Thoracic and Lumbar SpineCompression Fractures

http://emedicine.medscape.com/article/397896-mediaGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Injuries of Thoracic and Lumbar SpineBurst Fractures

http://emedicine.medscape.com/article/248236-mediaGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Injuries of Thoracic and Lumbar SpineFlexion Distraction Fractures Chance Fx

http://radiopaedia.org/images/143729Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Pathophysiology of Acute FracturesDirect compression of neural elements by bone fragments, disc material, and ligaments leads to damage of the central and peripheral nervous systemBlood vessel compression and disruption causes ischemiaMassive cord swelling happens within minutes at the level of injury and leads to secondary ischemiaGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Spinal Cord Lesions OverviewComplete SCI = No motor or sensory function below injury levelIncomplete SCI = Any Sensory/motor function below level of injurySpinal Cord TractsCorticospinal tract = Descending motor pathwaySpinothalamic tract (anterior)= Pain/TemperatureDorsal Column Pathway = Vibratory/Proprioception Incomplete spinal cord lesionsAnterior spinal cord syndromePosterior spinal cord syndromeCentral Cord syndromeBrown Sequard Syndrome

Source UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


PathophysiologyPrimary InjuryMechanical Injury

Secondary InjuryVascular AbnormalitiesFree Radicals/Lipid PeroxidationExcitotoxicityElectrolyte disturbancesInflammation

Edema

Source UndeterminedSource UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Cord SyndromesCentral Cord SyndromeAnterior Cord SyndromePosterior Spinal Cord SyndromeBrown Sequard Syndrome



Incomplete Spinal Cord Syndromes Anterior Spinal Cord SyndromeCorticospinal and spinothalamic tracts injuredPreservation of posterior column pathwayEtiologyAnterior spinal cord traumaFlexion of cervical spine causing cord contusionThrombosis of anterior spinal arterySource UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Incomplete Spinal Cord Syndromes Posterior Spinal Cord SyndromeRare conditionInjury to dorsal columnPreservation of corticospinal and spinothalamic pathwaysEtiologyPenetrating trauma to posterior aspect of cordHyperextension injury with vertebral arch fracture

Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma CourseSource Undetermined


Central Cord SyndromeInjury preferentially affects central portion of cordLoss of function of central fibers of corticospinal and spinothalamic tractsDecreased strength and pain/temperature of upper extremities compared with lower extremitiesEtiologyHyperextension injuriesCentral spinal stenosisDisruption of normal blood flowIncomplete Spinal Cord SyndromesSource UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Incomplete Spinal Cord SyndromesBrown Sequard SyndromeTransverse hemisection of spinal cordIpsilateral loss of motor function, proprioceptive/vibratory sensationContralateral loss of pain/temperature sensationEtiology = Penetrating injury or Lateral cord compression

Source UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Spinal vs. Neurogenic Shock Spinal ShockTemporary phenomenon characterized by loss of all spinal cord function caudal to level of injurySymptoms = Flaccid paralysis, Hypotonia, Areflexia, PriapismTypical duration = 24-72 hoursResolution = Return of Bulbocavernosus reflexOutcome = Spastic paresis, hyper-reflexia Neurogenic ShockType of distributive shock characterized by loss of adrenergic tone due to sympathetic denervationClassic Triad = Hypotension, Bradycardia, HypothermiaManagement = IVF, Vasopressor support, AtropineGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Spinal Shock vs. Neurogenic ShockSpinal Shock- the flaccidity and loss of reflexes seen after spinal cord injury. The cord may appear destroyed but actually may regain function latterNeurogenic Shock- destruction of the descending sympathetic pathways of the spinal cord. Results is hypotension and bradycardia. Pts will require vasopressors and atropine as well as fluid.Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


ManagementImmobilizationClinical C-spine ClearanceWhen to get imagesThoracic and Lumbar Spinal Immobilization and ClearanceManagement of Cervical and Thoracolumbar fractures without spinal cord injury



Aims of ImmobilizationPrevent further damage - Protect the CordHold the spine in a comfortable, anatomically correct wayPrevent movement of the spineAllow for safe concurrent management of other injuriesGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Options for ImmobilizationAnatomical RegionsHeadNeckBodyGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Head ImmobilizationManual - Hands, LegsSimple Assist Devices - Sandbags, Towels, Foam PadsAdditional Devices - StrapsHead/Neck immobilizerGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Head ImmobilizationCdang (Wikipedia)Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Head ImmobilizationStudy compared 3 methods during simulated vehicle motion, (Spine 1999;24)SandbagsHeadbandStyrofoam wedgesWedges slightly betterKey is body immobilizationGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Neck ImmobilizationCollarsPhiladelphiaStiffneckOther optionsGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Neck ImmobilizationEmrgmgmtca (Wikipedia)Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Neck ImmobilizationAnn Emerg Med 1992; 21: 1185-1188Compared C collar with Ammerman Halo orthosis, with and without spine boardPhotographic comparison during transportConclusion:A rigid cervical collar and a spine board provide significantly better immobilization than the collar alone. Further immobilization is provided by an Ammerman halo orthosisGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Body ImmobilizationBackboardsImportant for transporting patients and keeping them from possibly injuring themselves furtherGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Back BoardsCdang (Wikipedia)Ryan.mco (Wikipedia)Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Complications associated with Spinal ImmobilizationPainIncreased risk of pressure soresAspiration and limited respiratory functionIncreased risk of aspirating emesis while strapped on backboardMarked pulmonary restrictive effect of appropriately applied entire body spinal immobilization devicesGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


When to get an X-rayPatients involved in a traumatic eventwith midline tendernessWith neurologic deficitsAltered level of consciousnessPatients who are intoxicated



C-spine X-rayLateral ViewMust see to the top of T1 for film to be adequateMay need swimmers viewWill see 90% of cervical spine fracturesOdontoid viewMust include entire process and right and left c1 and c2 articulations Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Flexion and Extension FilmsObtained in injured pts without an AMS, and pts who have neck pain without fracture on AP, Lateral and odontoid viewsLooking for Instability Ligamentous spine injury



CT ScanMore SensitiveIf high suspicion for injury and have inadequate x-ray, CT is warrantedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


How do you clear a C-spine Injury?Two studies- NEXUS vs. Canadian C spineNexus Patients required to meet 5 criteriaNo mid-line tendernessNo focal neurological deficitNormal alertnessNo intoxicationNo painful, distracting injuryGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


NEXUS studyPatients who underwent C-spine X-ray for blunt trauma34,069 patients included in study818 patients had a C-spine injury8 of these patients met all 5 criteria4209 non-injured patients met all 5 criteriaGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


NEXUS StudyProblemsManagement stressorsFailure to discriminate what pain is significantWhat is a distracting injury?How drunk is intoxicated?Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Canadian C Spine RuleSource UndeterminedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Canadian C Spine RuleThe authors conclude that the CCR decision rule is more sensitive than NEXUS for identification of clinically important C-spine injuries and also is more specific, thereby decreasing the number of unnecessary C-spine radiographsProblems includeRequires active neck rotation (10% excluded)What is a Dangerous Mechanism?



MethylprednisoloneControversial treatment modality for blunt spinal cord traumaNational Acute Spinal Cord Injury Studies (NASCIS)Subsequent studies Pointillart (2000)Matsumoto (2001)Mechanism of Action Inhibition of free radical induced lipid peroxidationCurrent recommended regimenMethylprednisolone prescribed as a bolus intravenous infusion of 30 mg/kg of body weight over 15 min within 8 hours of acute closed spinal cord injuryFollowed 45 min later by an infusion of 5.4 mg/kg of body weight per hour for 23 hoursGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


SummarySpinal immobilization can reduce the likelihood of neurological deterioration in patients with unstable c-spine injuries following traumaImmobilization of the entire spinal column is necessary in patients until a spinal cord/column injury has been excluded or until the appropriate treatment has been initiatedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


SummaryA combination of rigid cervical collar with supportive blocks on a rigid backboard with straps is effective at achieving safe, effective spinal immobilization for transportSpinal immobilization devices are effective but can result in patient morbidity. They should be used for safe extrication and transport, but should be removed as soon as definitive evaluation is accomplished or treatment initiatedGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


SummaryMethylprednisolone therapy for acute spinal cord injury is controversial with only benefit when administered within 8 hours of injury Current Methyprednisolone regimen:Methylprednisolone bolus intravenous infusion of 30 mg/kg of body weight over 15 min within 8 hours of acute closed spinal cord injuryFollowed 45 min later by an infusion of 5.4 mg/kg of body weight per hour for 23 hoursAppropriate classification of SCI patients within ED to ensure prompt evaluation and treatmentCommunication between ED staff and residents is key to limiting errors and providing appropriate careGhana Emergency Medicine CollaborativeAdvanced Emergency Trauma Course


Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma CourseQuestions?Erin Silversmith (Wikipedia)


Ghana Emergency Medicine CollaborativeAdvanced Emergency Trauma CourseReferencesBaron, B., Thomas, S. Spinal Cord Injuries, in Emergency Medicine: A Comprehensive Guide. Tintinalli, Editor. 2004, McGraw-Hill. p. 1569-1583.American College of Surgeons. Spine and Spinal Cord Trauma, in Advanced Trauma Life Support for Doctors 7th edition. 2004. p. 177-204.Lin, M., Mahadevan, S. Spine Trauma and Spinal Cord Injuries, in Emergency Medicine. Adams, Editor. 2008, Saunders Elsevier. P. 765-783


Functional Anatomy Review

Vertebral Column is the central supporting structure for head/trunk and provides the bony protection for the spine. The vertebral column consists of 33 vertebra (7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral, 4 fused coccygeal)Vertebrae is comprised of the vertebral body and vertebral arch, which is comprised of 2 pedicles, 2 laminae and 7 processes (1 spinous process, 2 transverse processes and 4 articular processes).Movement of spinal columnFlexionExtensionLateral flexionRotationCircumduction (combination of all movements)LigamentsHelp maintain alignment of spinal columnAnterior/Posterior longitudinal ligaments run along vertebral bodiesVertebral arch is supported by ligamentum flavum, supraspinatous, interspinatous, intertransverse capsular ligamentsIntervertebral disksIntervertebral disks are between vertebral bodies and are comprised of a central nucleus propulsus comprised of water and cartilage, surrounded by a peripheral annulus fibrosis or fibrous cartilage.Function of disks is to act as a shock absorber and equally distribute axial load.As aging occurs, proportion of water decreases and fibrocartilage increases.When compressive forces exceed absorptive capacity of disk, annulus fibrosis ruptures and allows nucleus propulsus to protrude into the vertebral canal resulting in spinal nerve or spinal cord compression.

**Spinal Stability

** Spinal stability is an important factor in the evaluation of an injured spine and greatly affects management of spinal column injuries.

Cervical SpineMechanical Stability is provided by the two column concept.Anterior column is formed by vertebral bodies/intervetebral disks held in alignment by anterior and posterior longitudinal ligamentsPosterior Column is formed by pedicles, transverse processes, articulatin facets , laminae and spinal processes held together by nuchal ligamaentous complex (supraspinatous, interspinatous, intraspinous, capsular, ligamentum flavum)For c-spine disruption to cause instability, typically both columns must be disrupted. Some literature refers to a 4 column concept comprised of anterior, posterior columns and lateral masses (L/R) as the 4 columns. Useful in cervical spine injury severity score and prediction of injury severity and treatment/prognosisThoracolumbar SpineMechanical stability is provided by the Denis 3 column systemAnterior Column Anterior aspect of vertebral body, anterior annulus fibrosus, anterior longitudinal ligamentMiddle ColumnPosterior wall of vertebral body, posterior annulus fibrosus and posterior longitudinal ligamentPosterior ColumnBony complex of vertebral archPosterior ligamentous complex.Injury is considered unstable when it included at least two columns

*Spinal Cord Lesions:

Overview:Complete Spinal Cord Injury = Absence of sensory or motor function below the level of the injuryIncomplete Spinal Cord Injury = The presence of any sensory, motor function below the level of injury and includes even minimal presence of findings such as sacral sensation at anal mucocutaneous junction or voluntary contraction of external anal sphincter upon digital exam (i.e. anal wink)Spinal Cord Tracts:Corticospinal tract = Descending motor pathwayDescending motor pathway which originates in the cortex and travels to the medullary pyramid where the fibers cross to opposite side and descend through the spinal cord as the lateral corticospinal tract.Injury to this tract results in ipsilateral loss of motor function = muscle weakness, spasticity, Increased DTR, +BabinskisSpinal thalamic tract = Pain/TemperatureTransmits pain and temperature with receptors in the skin and muscle that forms an afferent neuron that enders spinal cord and rises one or two levels before synapsing with second neuron in gray matter.2nd neuron crosses midline in the anterior commissure and ascends as lateral spinothalamic tract.Damage to this tract results in loss of pain/temp sensation in contralateral half of body that typically occurs in 1-2 segments below the level of the lesion. Dorsal Column Pathway =Transmits vibration and proprioceptive informationAxons initially enter ipsilateral dorsal column and do not synapse until they reach the medulla where they cross the midline and ascend to the thalamus. Injury to the dorsal column leads to ipsilateral loss of vibration and position sense that begins at level of lesion. Spinal Cord Syndromes:Anterior Cord SyndromeCentral Cord SyndromeBrown-Sequard SyndromeCauda-Equina Syndrome*Pathophysiology of Spinal Cord Injuries

Primary InjuryThe primary injury is a mechanical insult to the spinal cord that results from a failure of spinal stability due to loading conditions including flexion, extension, axial load or rotation/distraction. These forces disrupt spinal stability and cause a local deformation of the spine that mechanically damages the spinal cord usually due to direct compression, contusion, or shear injury to the spinal cord. Primary injury rarely transects the spinal cord but rather leaves a rim of tissue intact. This adjacent rim of intact tissue is vulnerable to acute pathophysiological processes of secondary injury. Secondary InjuryA secondary injury pathway results from the primary injury and generates further injury to the spinal cord. The primary mediators of secondary injury cascade include Vascular abnormalitiesMechanical disruption of microvasculature that results in petechial hemorrhage and intravascular thrombosisCombination of above and vasospasm of intact vessels, edema at injury site leads to profound hypoperfusion and ischemiaFree radicals/lipid peroxidationFree radical generation (molecules that posses unpaired electrons that make them highly reactive to lipids, proteins, DNA) results in lipid peroxidation in cellular membranes propagating a cascade that leads to metabolic collapse and subsequent apoptotic cell death.Lipid peroxidation is considered to be an extremely important aspect of the secondary cascade and is a major target of pharmacologic management.Excitotoxicity/Electrolyte abnormalitiesIschemia and membrane disruption lead to release of glutamate (key neurotransmitter in CNS) that reaches toxic levels by 15 minutes post injury.Excessive glutamate leads to excitotoxicity or excess glutamate stimulation of nervous system receptors NMDA and AMPA.Receptor activation leads to disruption of cellular membrane channels, leading to large accumulation of calcium within cells, which promotes lethal enzyme activation and further generates free radicals.The result of these activities is both necrotic and apoptotic cell death.Inflammation/Inflammatory mediatorsInjury site is rapidly infiltrated by neutrophils post injury and neutrophils attract lytic enzymes and cytokines that can further damage local tissue and recruit other inflammatory cells.Inflammatory mediators are a double edged sword with both neurotoxic and neuroprotective elements.Edema at site of injury compromises blood flow and increases ischemia. Edema tends to develop within hours of injury, peaking at 3-6 days post injury and receding by 9th day post injury as edema is replaced by central hemorrhagic necrosis.*Incomplete Spinal Cord Syndromes:

Anterior Spinal Cord SyndromeDamage to the corticospinal and spinothalamic pathways with presentation of posterior column failure.Results in loss of motor function, pain and temp sensation distal to the lesionVibratory/Position and crude touch preservedEtiologyDirect anterior spinal cord traumaFlexion of cervical spine causing cord contusion or bone injury with secondary cord injuryThrombosis of anterior spinal artery causing ischemia to anterior cord.Posterior Spinal Cord SyndromeVery rare condition that does not typically occur in isolationCaused by penetrating trauma to back or hyperextension injury associated with vertebral arch fractures that results in injury to posterior spinal arteryLoss of proprioception and vibration (dorsal column) with preservation of motor function (corticospinal) and pain/temperature (spinothalamic).*Incomplete Spinal Cord Lesions:

Central Cord SyndromeInjury preferentially involves the central portion of the cord more than the peripheral regions and thus affects the centrally located fibers of corticospinal and spinothalamic tracts.The nerve tracts providing function to the upper extremities are most medial in position and thus are preferentially affected.Clinically, patients present with decreased strength, decreased pain/temperature in upper extremity than lower extremity. Bowel and bladder function are typically spared.Prognosis is good, but patients often dont regain fine motor function in upper extremities.EtiologiesHyperextension injuriesDisruption of blood flow to spinal cordCentral spinal stenosisBrown Sequard SyndromeTransverse hemisection of spinal cord or unilateral cord compression Results in ipsilateral loss of motor function, proprioceptive/vibratory sense and contralateral loss of pain and temp sensationMost traumatic syndromes result from penetrating injury but may also result from lateral cord compression 2/2 disc protrusion, hematomas, bone injury or tumors.Best prognosis for recovery.

*

Spinal Shock vs. Neurogenic Shock

Spinal Shock = Spinal shock refers to a phenomenon that occurs immediately after a spinal cord injury (within min) where the patient experiences a physiological loss of all spinal cord function caudal to the level of the injury.Characterized by flaccid paralysis, hypotonia, areflexia. Priapism in males.Spinal shock is thought to be caused by the loss of potassium within the injured cells of the cord and accumulation of the potassium in the extracellular space, resulting in reduced axonal transmission. As potassium levels wear off, spinal shock wears off. Typically lasts 24-72 hours post injuryResolution of loss of as bulbocavernosus reflex (anal sphincter contraction in response to squeezing the glanspenis or tugging on the Foley) indicates the end of spinal shock.Typically, clinical manifestations may normalize but are more often replaced by a spastic paresis and hyper-reflexia.

Neurogenic Shock = A type of distributive shock characterized by loss of adrenergic tone due to sympathetic denervation.Typically occurs in patients with partial or complete cord injury at T6 level or above.Injury at this level causes sympathetic denervation and a loss of alpha adrenergic tone, causing vasodilitation of arterial/venous vessels.Leads to loss of systemic resistance and hypotension.In addition, loss of sympathetic innervation to the heart (T1-T4) results in unopposed parasympathetic innervation via the vagus nerve that results in bradycardia.Symptoms = Classic triad (Hypotension, Bradycardia, Hypothermia), Warm/dry extremities, peripheral vasodiliation, venous pooling, decreased cardiac output.Treatment Fluid hydration followed by:BP Phenylephrine, epinephrine, Consider dopamine/dobutamineHR Atropine, Consider pacing if necessary

Transient Paralysis/Spinal ShockSpinal shock is a clinical condition characterized by a physiological loss of all spinal cord function caudal to the level or the injury with flaccid paralysis, anesthesia, absent bowel/bladder control and loss of reflex activity. Priapism may be present in males.Altered physiological state may last several hours to several weeks.Loss of function is thought to be secondary loss of potassium within the injured cells in the cord and the accumulation of potassium witin the extracellular space, resulting in decreased axonal transmission. As potassium levels normalize between the intra/extracellular spaces, the spinal shock wears off and clinical manifestations may normalize but are usually replaced by a spastic paresis reflecting morphologic injury ot the spinal cord.Transient paralysis with complete recovery is most often described in younger patients with athletic injuries.

Cauda Equina Syndrome/Conus medullaris/ConcussionThe cauda equina is comprised entirely of lumbar, sacral and coccygeal nerve roots and injury produces a peripheral nerve injury pattern rather than direct injury to spinal cord.Clinical featuresVariable motor/sensory lesions in lower extremitiesBowel/bladder dysfunctionSaddle anesthesiaPrognosis = Good 2/2 peripheral nerve ability to regenerateConus medullaris syndrome - is a sacral cord injury with or without involvement of the lumbar nerve roots. This syndrome is characterized by areflexia in the bladder, bowel, and to a lesser degree, lower limbs. Motor and sensory loss in the lower limbs is variable. Cauda equina syndrome involves injury to the lumbosacral nerve roots and is characterized by an areflexic bowel and/or bladder, with variable motor and sensory loss in the lower limbs. Because this syndrome is a nerve root injury rather than a true SCI, the affected limbs are areflexic. This injury is usually caused by a central lumbar disk herniation. A spinal cord concussion is characterized by a transient neurologic deficit localized to the spinal cord that fully recovers without any apparent structural damage.

****

Methylprednisolone in management of acute spinal cord injury:

High dose methylprednisolone (Solumedrol) is recommended on the basis of the National acute spinal cord injury studies and is the only effective neuroprotective agent to be tested in controlled multicenter clinical trialsMethylprednisolone is hypothesized to work through inhibition of free radical induced lipid peroxidation and reducing intracellular calcium overload and tissue lactate levels, improving microcirculation and inhibiting post-traumatic cord ischemia.National Acute Spinal Cord Injury StudiesNASCIS I First study conducted in 1979, NASCIS results published in 1984Comparison:100 mg bolus followed by 25 mg q 6 hrs for 10 days1000 mg bolus followed by 250 mg q 6 hrs for 10 days.Prospective, RCT, double-blinded, multicenter trial in 330 patients. Primary outcome measures = Sensory and Motor assessment at 6 weeks, 6 months and 1 year after the SCINo statistical difference between the two groups with respect to either modality at all time points.Adverse events: 4-fold increase in wound infections in high dose group. Trends towards increased sepsis, pulmonary embolis and death in high dose group.NASCIS IISubsequent animal studies suggested that only higher doses of MP have a neuroprotective effect after SCI, prompting the NASCIS II study conducted in 1985 with results published in 1990.Prospective RCT, double blinded, multicenter trialPatients randomized to one of 3 treatment arms:MPSS 30 mg/kg bolus followed by 5.4 mg/kg/hr infusion for 23 hoursNaloxone 5.4 mg/kg bolus followed by infusion for 23 hours (Note naloxone had shown promise in previous animal exp)Placebo infusionN = 487 patients who arrived to hospital within 12 hours Exclusion criteria = Patients with isolated peripheral nerve injury, pregnant women and patients with other serious injuriesPrimary outcome measures = Neurologic outcome (6 weeks, 6 months and 1 yr), MortalityNeurologic outcome was an assessment of motor and sensory function.Motor = 14 muscle groups (power 0-5) for total score of 0-70 pointsSensory = pinprick and tactile sensation in 29 dermatomes (graded between 1-3)Total score ranged between 29-87 points.No difference between the three groups in initial analysisComplicationsIncreases in wound infection, GI bleeding, Pulmonary embolism in steroid groupPost-hoc analysisExamination of patients (subgroup = 62) treated with MPSS within 8 hours of injury found a benefit with improvement in motor scores at 6 months and 1 year.Motor scores demonstrated improvement of 17.2 points compared with 12.0 points in the control groupSensory scores also demonstrated improvement in steroid group at 6 months but effect disappeared by 1 yearMost improvement in motor scores was observed in patients with incomplete spinal cord injury. NASCIS IIIThird study conducted in 1991, published in 1997Prospective RCT, Double blinded multi-center trial of MP in 499 patientsOnly patients presenting within 8 hours were included.Exclusion criteria = pregnancy and patients with serious illnessTreatment arms: All patients administered bolus of 30 mg/kg and then were randomized to one of three armsMP 5.4 mg/kg/hr infusion for 23 hoursMP 5.4 mg/kg/hr infusion for 47 hoursTrilizad mesylate 2.5 mg/kg bolus q 6 hrs for 48 hrsTrilazad has same lipid peroxidation effect as MP but lacks glucocorticoid effectResultsRandomization did not generate equal treatment groupsPatients receiving trilizad mesylate demonstrated significantly worse motor function than pts receiving MPAmong MP groups, no significant difference in outcomes Post analysis of patients receiving treatment before 3 hours compared with before 8 hours demonstrated a statistically significant difference in motor score in patients receiving 48 hours of infusion compared with 24 hours. Difference was noted at 6 weeks and 6 months but was less apparent at 1 yr. No sensory improvement was noted.Complications: 2-fold increase in severe pneumonia, 4-fold increase in severe sepsis and 6-fold increase in mortality 2/2 respiratory complications in 48 hr group compared with 24 hour group infusion.Other Clinical Studies to evaluate MP in treatment of Acute SCI***

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