Thoraco lumbar injuries can be categorized based on which spinal columns are affected. Injuries involving the middle column and at least one other column are considered unstable. Burst fractures involve failure of the anterior and middle columns and may require early stabilization, especially if they involve over 50% canal compromise, over 20 degrees of kyphosis, or over 45-50% canal compromise. Flexion distraction injuries can be categorized into types A through D depending on whether they involve bone or ligaments at one or two spinal levels.
Introduction by Dr. Zameer Ali. Overview of spinal vertebrae anatomy: cervical, thoracic, lumbar, sacral, and coccyx.
Key facts on spinal cord anatomy, injuries, and recovery statistics. 43% with multiple injuries; 50 per million with injuries; mortality causes detailed.
Mechanism of injury significance and prevalence data. Common causes include RTAs (51%) and sports. Demographics: 10-15 per million affected, predominantly young males.
Diagnosis challenges due to head trauma or intoxication. Common injury types highlighted, including osteoporosis-related fractures being more prevalent.
Details on thoracolumbar fractures (30-50% of spinal injuries) and definitions of spinal stability essential in surgical care. Importance of addressing neural function preservation.
Concept of functional spinal units, criteria for stability/instability, and implications for surgical intervention.
Introduction to scoring systems for thoracic/lumbar stability, with specific scoring points for elements like anterior/posterior integrity and radiographic criteria.
Estimation of multiple spinal fractures occurrence, Denis classification of spinal injuries based on CT analysis.
Detailed analysis of spinal stability theories and fracture classifications (compression, burst, flexion-distraction) relating to stability and neurological outcomes.
Mechanisms of spinal cord injury discussed, treatment groupings, physiological responses, and neurological damage progression.
Various grading systems (Frankel, ASIA) to classify spinal cord injuries and their implications for prognosis and recovery.
Discussion on surgical techniques and the role of decompression in managing spinal injuries along with emerging techniques for stabilization.
Central, Brown-Séquard, Anterior, and Posterior cord syndromes explained. Symptoms, causes, and recovery outcomes discussed.
Summary of spinal trauma management, including physiological responses to injury and impact on recovery.
Some important factsSpinal cord ends below lower border of L1 Cauda equina is below L1 Mid dorsal spinal cord & neural canal space are of same diameter hence prone for complete lesion Mechanical injury - early ischaemia, cord edema - cord necrosis Neurological recovery unpredictable in cauda equina ie. peripheral nerves
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Thoraco lumbar injuriesFractures and dislocations of the spine are serious injuries that most commonly occur in young people. Nearly 43% of patients with spinal cord injuries sustain multiple injuries.
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Kraus et al.estimated that each year 50 people in 1 million sustain a spinal cord injury
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Of those whodie within 1 year of their accidents, 90% die en route to the hospital. Overall, 85% of patients with a spinal cord injury who survive the first 24 hours are still alive 10 years later compared with 98% of patients of similar age and sex without spinal cord injury.
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cause common ofdeath According to the National Spinal Cord Injury Association, the most cause common of death is respiratory failure whereas in the past it was renal failure.
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An increasing numberof people with spinal cord injury are dying of unrelated causes, such as cancer or cardiovascular disease, similar to that of the general population. Mortality rates are significantly higher during the first year after injury than during subsequent years.
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history A detailedhistory of the mechanism of injury is important but frequently is unobtainable at the initial examination.
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Statistics prevalence10 - 15 per million age group 18 - 35 years male/female - 3:1 RTA 51% - cars Domestic 16% Industrial 11% Sports 16% - diving incidents Self harm 5%
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most common causesThe most common causes of severe spinal trauma are motor vehicle accidents, falls, diving accidents, gunshot wounds
Delay in diagnosisThe most common causes of misdiagnosis were head trauma, acute alcoholic intoxication, and multiple injuries. Patients with decreased levels of consciousness or comatose patients often do not complain of back pain.
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Delay in diagnosisProfuse bleeding from severe facial or scalp lacerations may divert attention from the cervical spinal injury
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Most isolated thoracicand lumbar spine fractures are related to osteoporosis and involve minimal or no trauma. In fact, osteoporosis-related fractures far outnumber trauma-related thoracic and lumbar fractures. Osteoporosis leads to approximately 750,000 vertebral fractures each year in the United States
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The annual rateof trauma-related thoracic and lumbar fractures is approximately 15,000 (14). Thoracic and lumbar fractures account for 30% to 50% of all spinal injuries in trauma patients
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In trauma patients,thoracic and lumbar fractures are concentrated at the thoracolumbar junction, with 60% of thoracic and lumbar fractures occurring between the T11 and L2 vertebral levels (15
Spinal instability Aspine injury is considered unstable if normal physiological loads cause further neurological damage ,chronic pain and unacceptable deformity
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Stability and Instabilityof the Vertebral Column The concept of spinal stability is central to the field of spine surgery.
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Spinal fusion andfixation surgery, in fact, is performed primarily to restore stability of the spinal column after instability from injury, degeneration, or decompression to address neural tissue
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Spinal instability isvariably defined, widely interpreted, and inconsistently measured
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Treatment and outcomeof spine injuries are integrally related to the neurological status, definition of spinal stability in trauma should be centred on preservation of neural function.
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Historically, discussions ofspinal stability have focused on the vertebral column and not on neural structures or neural function
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Functional spinal unitcomposed of two adjacent vertebrae and their intervening ligaments and inter vertebral disc,
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the anterior structuresare the vertebral body and the intervertebral disc, and the posterior structures are the facet joints, laminae, spinous processes, and posterior intervertebral ligaments.
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functional spinal unitis stable if all anterior structures plus one posterior structure are intact, or alternatively, if all posterior structures and one anterior structure are intact
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White and panjabi For assessing spinal instability Thoraco lumbar stability usually follows the middle column if it is intact then injury is usually stable
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Thoracic and lumbarspine stability score element /point score Ant. element unable to function….2 Post elem. Unable to function ….2 Disruption of costovertebral articulation …1 Radiographic criteria 4 Saggital displacement >2.5mm (2 points)
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Relative sagittal planeangulation >5 degrees…..2 points Spinal cord or cauda equina damage…2 pts Dangerous loading anticipated …1 pt Instability if score greater than 5
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Lumbar spine stabilityscale Ant. element unable to function….2 Post elem. Unable to function ….2 Radiographic criteria 4 pts Flex. /ext. x rays Saggital plane translation >4.5 mm or 15% 2 pts
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Sagittal plane rotation2 pts >15 degrees at L1 –L4 >20 degrees at L4 – L5 >25 degrees at L5-S1 0r Resting x rays
Roughly three typesof spinal instability are recognized First degree mechanical instability potential for late kyphosis E.g. severe compression fractures Seat belt type injuries
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Second degree (neurologicinstability) Potential for late neurologic injury E.g. burst fractures without neurological deficits
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Third degree (mech.andneur. Instability ) E.g. fracture dislocations/severe burst fractures with neurologic deficit
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McAfee Factors indicativeof instability in burst fractures >50% canal compromise >15 to 25 degrees of kyphosis >40 % loss of anterior vert.body height
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MULTIPLE SPINAL FRACTURESIf a spinal fracture is identified at any level, the entire spine should be examined with anteroposterior and lateral views to document the presence or absence of spinal fractures at other levels.
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Multiple-level spinal fractures,which may be contiguous or separated, are estimated to occur in 3% to 5% of patients with spinal fractures
Denis developed athree-column concept of spinal injury using a series of more than 400 CT scans of thoracolumbar injuries
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Assesment of spinalstability 3 structural elements to be considered Posterior coloumn Middle coloumn Anterior coloumn All fractures involving middle coloumn and at lest one other coloumn should be regarded as unstable.
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The anterior columncontains the anterior longitudinal ligament, the anterior half of the vertebral body, and the anterior portion of the annulus fibrosus.
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The middle columnconsists of the posterior longitudinal ligament, the posterior half of the vertebral body, and the posterior aspect of the annulus fibrosus.
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The posterior columnincludes the neural arch, the ligamentum flavum, the facet capsules, and the interspinous ligaments
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Denis classification Minorspinal injuries 1 Articular processe fracture (1%) 2 transverse process fracture (14%) 3 Spinous process fracture (2%) 4 Pars interarticularis fracture(1%)
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Major spinal fracturesCompression fractures 48% Burst fracture 14 % Fracture dislocation 16 % Seat belt type factures 5 %
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Compression fracture 4subtypes on basis of end plate involvement A fracture of both end plates 16% B Fracture of superior end plate 62% C fracture of inferior end plate 6 % 4 both end plates intact 15%
Burst Fracture Failureof anterior and middle column Axial compression +/- failure of posterior column Compression or tensile force Most common at T/L junction
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Burst fracture subtypes4 subtypes on basis of end plate involvement A fracture of both end plates 24% B Fracture of superior end plate 49% C fracture of inferior end plate 7 % 4 both end plates intact 15% Burst lateral flexion 5 %
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Early stabilization isrequired in both saggital and coronal plane in patients with 1 neurological deficit 2 Loss of vertebral body height >50 % 3 angulations of >20 degree 4 Canal compromise of >50 % scoliosis of >10 degree
Flexion Distraction InjuryType A one level bony injury Type B one level ligamnetous injury Type C two level injury through bony middle column Type D two level injury through ligamentous middle column
Pathophysiology of spinalinjuries Stable and unstable injuries- Stable-vertebral components will not be displaced by normal movements. Unstable-Significant risk of displacements and consequent damage to neural tissues
McAfee et al. determined the mechanisms of failure of the middle osteoligamentous complex and developed a new system based on these mechanisms
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Wedge compression fractures cause isolated failure of the anterior column and result from forward flexion. They rarely are associated with neurological deficit except when multiple adjacent vertebral levels are affected
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stable burst fractures the anterior and middle columns fail because of a compressive load, with no loss of integrity of the posterior elements
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unstable burst fractures the anterior and middle columns fail in compression, and the posterior column is disrupted. The posterior column can fail in compression, lateral flexion, or rotation.
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Chance fractures are horizontal avulsion injuries of the vertebral bodies caused by flexion about an axis anterior to the anterior longitudinal ligament. The entire vertebra is pulled apart by a strong tensile force.
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flexion distraction injuries the flexion axis is posterior to the anterior longitudinal ligament. The anterior column fails in compression while the middle and posterior columns fail in tension. This injury is unstable because the ligamentum flavum, interspinous ligaments, and supraspinous ligaments usually are disrupted
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Translational injuries are characterized by malalignment of the neural canal, which has been totally disrupted. Usually all three columns have failed in shear
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Kelly and Whitesides described the thoracolumbar spine as consisting of two weight-bearing columns: the hollow column of the spinal canal and the solid column of the vertebral bodies.
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Classification of SpinalCord injury Many Grading Systems Impairment Based Frankel ASIA Yale Motor Index
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Type of bonyinjury Flexion Extension Flexion with rotation Compression
The presence ofan incomplete or complete spinal cord injury must be determined and documented by neurological examination
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Important dermatome landmarksare the nipple line (T4), xiphoid process (T7), umbilicus (T10), and inguinal region (T12, L1), as well as the perineum and perianal region (S2, S3, and S4).
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Complete /Incomplete spinalcord injury . Evidence of sacral sensory sparing can establish the diagnosis of an incomplete spinal cord injury If voluntary contraction of the sacrally innervated muscles is present, then the prognosis for recovery of motor function is good
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Some lumbar spineinjuries may present as isolated root injuries with weakness of the foot or leg, depending on the specific root involved
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spinal shock rarelylasts longer than 24 hours, it may last for days or weeks. A positive bulbocavernosus reflex or return of the anal wink reflex indicates the end of spinal shock. .
If no motoror sensory function below the level of injury can be documented when spinal shock ends, a complete spinal cord injury is present and the prognosis is poor for recovery of distal motor or sensory function
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Signs in anUnconscious patients Diaphragmatic breathing Neurological shock (Low BP & HR) Spinal shock - Flaccid areflexia Flexed upper limbs (loss of extensor innervations below C 5 ) Responds to pain above the clavicle only Priapism – may be incomplete.
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Signs of spinalinjury Forehead wounds – think of hyperextension injury Localized bruise Deformities of spine - Gibbus, feel a step & Priapism Beevors sign – tensing the abdomen umbilicus moves upwards in D 10 lesions
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Evaluation Radiographic EvaluationPlain Xray CT MRI Mylography Spinal Stability Classification of Fractures Treatment of Specific Injuries
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Imaging evaluation X- rays CT scan MRI myelography CT scan significantly outperforms plain radiography however it should not replace plain radiography as a screening test for evaluation of spinal injury
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Radiographic Evaluation MRIIndicated in all cases of neuro deficit? Both intrinsic and extrinsic cord injuries Mylogram Replaced by MRI
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SCIWORA Spinal cordinjuries without roentgenographic abnormalities (SCIWORA) have been reported by Dickmen et al. to occur predominantly in children.
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Spinal cord injuriesin children frequently occur without fracture-dislocation. Because of the inherent elasticity of the juvenile spine, the spinal cord is vulnerable to injury even though the vertebral column is not disrupted.
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SCIWORA ismost common in children younger than 8 years of age. The recovery of neurological function depends on the patient's neurological status at presentation.
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Patients with incompleteinjuries tend to recover, and those with complete injuries have a poor prognosis for recovery of neurological function
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Pathophysiology Primary Neurologicaldamage Direct trauma, haematoma & SCIWORA < 8yrs old In 4hrs - Infarction of white matter occurs In 8hrs - Infarction of grey matter and irreversible paralysis Secondary damage Hypoxia Hypoperfusion Neurogenic shock Spinal shock
GENERALISATIONS (1) thegreater the sparing of motor and sensory functions distal to the injury, the greater the expected recovery; (2) the more rapid the recovery, the greater the amount of recovery; and (3) when new recovery ceases and a plateau is reached, no further recovery can be expected
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By definition, anincomplete spinal cord injury is one in which some motor or sensory function is spared distal to the cord injury.
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Complete -flaccid paralysis + total loss of sensory & motor functions Incomplete - mixed loss - Anterior sc syndrome - Posterior sc syndrome - Central cord syndrome - Brown sequard’s syndrome - Cauda equina syndrome
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An incomplete spinalcord syndrome may be a Brown-Séquard syndrome, central cord syndrome, anterior cord syndrome, posterior cord syndrome, or rarely monoparesis of the upper extremity. Ninety percent of incomplete lesions produce either a central cord syndrome, a Brown-Séquard syndrome, or an anterior cervical cord syndrome.
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. A completespinal cord injury is manifested by total motor and sensory loss distal to the injury. When the bulbocavernosus reflex is positive and no sacral sensation or motor function has returned, the paralysis will be permanent and complete in most patients
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Goals of SpineTrauma Care Protect against further injury during evaluation and management Expeditiously identify spine injury or document absence of spine injury
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Optimize conditions formaximal neurological recovery Maintain or restore spinal alignment Minimize loss of spinal mobility Obtain a healed and stable spinal column Facilitate rehabilitation
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TIMING OF SURGERY The timing of surgery for spinal cord injuries is controversial. Most authors agree that in the presence of a progressive neurological deficit, emergency decompression is indicated
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indications for surgicaltreatment of thoracolumbar spine injuries include burst fractures with 50% or more canal compromise, 30 degrees or more of kyphosis, late neurological deficits, and clearly unstable fractures and fracture-dislocations.
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. In patientswith complete spinal cord injuries or static incomplete spinal cord injuries, some authors advocate delaying surgery for several days to allow resolution of cord edema, whereas others favor early surgical stabilization
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decompression 1 anteriordecompression and fusion with instrumentation 2 posterior decompression and fusion with instrumentation 3 combined anterior decompression and posterior decompression
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DECOMPRESSION Therole of decompression also is controversial Compression of the neural elements by retropulsed bone fragments can be relieved indirectly by the insertion of posterior instrumentation or directly by exploration of the spinal canal through a posterolateral or anterior approach.
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The posterolateral techniquefor decompression of the spinal canal is effective at the thoracolumbar junction and in the lumbar spine. This procedure involves hemilaminectomy and removal of a pedicle with a high-speed burr to allow posterolateral decompression of the dura along its anterior aspect
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risk and complicationsof surgery, including inadequate decompression, increased neurological deficit, failure of internal fixation, and the need for implant removal
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Degree of canalstenosis no reliable correlation between the degree of compromise of the spinal canal and the severity of the neurological deficit.
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Vertebral Compression FracturesThey rarely are associated with neurological deficit, except when multiple adjacent vertebral levels are affected..
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Medical management is the mainstay of treatment for these acute, painful compression fractures and includes bed rest, analgesics, braces, and physical therapy
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Silverman showed thatwith each successive fracture, pulmonary force vital capacity was reduced by an average of 9%
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minimally invasive spinalsurgery techniques have evolved, acutely painful vertebral compression fractures can be treated with a percutaneous procedure termed vertebroplasty.
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This procedure entailsplacing large spinal needles into the fractured vertebral body through a channel made in the pedicle and injecting bone cement into the fractured bone
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Balloon Kyphoplasty has evolved as the next step in the treatment of vertebral compression fractures. This is a minimally invasive procedure that involves reduction and fixation.
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Posterior instrumentation posteriorinstrumentation is a safe and effective treatment for thoracolumbar instability These implants have been developed because of the deficiencies of Harrington rods, such as breakage, cutting out of hooks, and loss of fixation
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. Biomechanical studiessuggest that these newer devices offer improved fixation, but because they may be technically more difficult to insert, neurological risks are increased
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Anterior instrumentation hasevolved significantly, now allowing correction of a deformity, stabilization of spinal segments during decompression, and bone grafting to be performed simultaneously. These implants are useful in the treatment of thoracolumbar burst fractures
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Anterior internal fixationdevices allow treatment of mechanical instability and neurological compression in a single-stage surgical procedure
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ANTERIORVERTEBRAL BODY EXCISION FOR BURST FRACTURES may be selected primarily or may be necessary in certain burst fractures left untreated for more than 2 weeks and not believed to be candidates for posterior instrumentation and indirect decompression of the spinal canal
Central cord syndrome Central cord syndrome is the most common. It consists of destruction of the central area of the spinal cord, including both Gray and white matter . The centrally located arm tracts in the cortical spinal area are the most severely affected, and the leg tracts are affected to a lesser extent
Sensory sparing isvariable, but usually sacral pinprick sensation is preserved This syndrome usually results from a hyperextension injury in an older person with pre-existing osteoarthritis of the spine. The spinal cord is pinched between the vertebral body anteriorly and the buckling ligamentum flavum posteriorly
Brown sequard syndrome brownSéquard syndrome is an injury to either half of the spinal cord and usually is the result of a unilateral laminar or pedicle fracture, penetrating injury, or a rotational injury resulting in a subluxation. It is characterized by motor weakness on the side of the lesion and the contralateral loss of pain and temperature sensation. Prognosis for recovery is good, with significant neurological improvement often occurring.
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Anterior cord syndrome Anterior cord syndrome is caused by a hyperflexion injury in which bone or disc fragments compress the anterior spinal artery and cord.
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It is characterizedby complete motor loss and loss of pain and temperature discrimination below the level of injury.
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The posterior columnsare spared to varying degrees resulting in preservation of deep touch, position sense, and vibratory sensation. Prognosis for significant recovery in this injury is poor.
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Posterior cord syndromePosterior cord syndrome involves the dorsal columns of the spinal cord and produces loss of proprioception vibrating sense while preserving other sensory and motor functions. This syndrome is rare and usually is caused by an extension injury
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A mixedsyndrome A mixed syndrome usually is an unclassifiable combination of several syndromes. It describes the small percentage of incomplete spinal cord injuries that do not fit one of the previously described syndromes
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Conus medullaris syndrome,Conus medullaris syndrome, or injury of the sacral cord (conus) and lumbar nerve roots within the spinal canal, usually results in areflexic bladder, bowel, and lower extremities. Most of these injuries occur between T11 and L2 and result in flaccid paralysis in the perineum and loss of all bladder and perianal muscle control.
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The irreversiblenature of this injury to the sacral segments is evidenced by the absence of the bulbocavernosus reflex and the perianal wink. Motor function in the lower extremities between L1 and L4 may be present if nerve root sparing occurs.
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Cauda equina syndromeCauda equina syndrome, or injury between the conus and the lumbosacral nerve roots within the spinal canal, also results in areflexic bladder, bowel, and lower limbs. With a complete cauda equina injury, all peripheral nerves to the bowel, bladder, perianal area, and lower extremities are lost.
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the bulbocavernosus reflex,anal wink, and all reflex activity in the lower extremities are absent, indicating absence of any function in the cauda equina
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Cauda equina syndromewidespread neurological disorder Difficulty with micturition Loss of anal sphincter tone or faecal incontinence Saddle anesthesia about the anus, perineum or genitals Widespread (>one nerve root) or progressive motor weakness in the legs or gait disturbance Sensory level
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Hypoxia Lesions aboveC 5 – damage to diaphragm leads to 20% reduction in vital capacity Lesions at D 4-6 – reduces vital capacity if < 500ml patient is ventilated Intercostal nerve paralysis Atelectasis – poor cough V/Q mismatch Reduced compliance of lung – muscle fatigue.
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Neurogenic shock Lesionsabove D6 Minutes – hours (fall of catecholamines may take 24 hrs) Disruption of sympathetic outflow from D1 - L2 Unapposed vagal tone Peripheral vasodilatation Hypotension, Bradycardia & Hypothermia BUT consider haemmorhagic shock if – injury below D6, other major injuries, hypotension with spinal fracture alone without neurological injury.
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Spinal shock Transientphysiological reflex depression of cord function – ‘ concussion of spinal cord’ Loss anal tone, reflexes, autonomic control within 24-72hr Flaccid paralysis bladder & bowel and sustained Priapism Lasts even days till reflex neural arcs below the level recovers.