cervical fractures

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It is a simplified presentation to group the cervical spine fractures and I wish you find it helpful

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  • ORTHOPAEDIC DEPARTMENT ZAGAZIG UNIVERSITY FACULTY OF MEDICINE By Dr. Tarek A. ElHewala Lecturer of Orthopaedic Surgery Faculty of Medicine, Zagazig University
  • Spinal Injuries Less common than traumatic injuries of the extremities but: Have the lowest functional outcomes and the lowest rates of return to work after injury in all major organ systems.
  • Major Trauma High energy trauma. Polytrauma patients. Neurological involvement.
  • Spinal Injuries Incidence of spinal fracture in (NA): 64/100000 Trend: Decrease in high income countries. Strong increase in medium and low income countries.
  • Cervical Spine Injuries Account for one-third of all spinal injuries. The most commonly injured vertebrae(1) are: C2: where one-third of which are odontoid fracture. C6,C7: are the most frequently affected levels in the subaxial spine (vertebral body fracture) A neurological injury occurs in about 15% of spine trauma patients. A low GCS indicates a high risk for a concomitant cervical injury. 1- Goldberg W, Mueller C, Panacek E, Tigges S, Hoffman JR, Mower WR (2001) Distribution and patterns of blunt traumatic cervical spine injury. Ann Emerg Med 38:1721
  • Normal Anatomy Functionally, the cervical spine is divided into: The upper cervical spine [occiput (C0)C1C2] The lower (sub-axial) cervical spine (C3C7).
  • Normal Anatomy Upper Cervical Spine: The atlas-occiput junction primarily allows flexion/extension and limited rotation. Axial rotation at the craniocervical junction is restricted by osseous as well as ligamentous structures.
  • Normal Anatomy Upper Cervical Spine: The atlantoaxial joint is composed of lateral mass articulations with loosely associated joint capsules and an atlantodental articulation
  • Normal Anatomy Lower (Subaxial) Cervical Spine: The vertebrae of the lower cervical spine have a superior cortical surface which is concave in the coronal plane and convex in the sagittal plane. This configuration allows flexion, extension, and lateral tilt by gliding motion of the facets.
  • Normal Anatomy Lower (Subaxial) Cervical Spine: The C5/6 level exhibits the largest range of motion, which in part explains its susceptibility to trauma and degeneration. The facet joint capsules are stretched in flexion and therefore limit rotation in this position.
  • Biomechanics of Cervical Spine Trauma The conditions under which neck injury occurs include several key variables such as: impact magnitude. impact direction. point of application. rate of application.
  • Biomechanics of Cervical Spine Trauma For example in lower cervical spine: Vertical loading of the lower cervical spine in the forward flexed position reproduce pure ligamentous injuries. This mechanism produced bilateral dislocation of the facets without fracture. A unilateral dislocation was produced if lateral tilt or axial rotation occurred as well.
  • Biomechanics of Cervical Spine Trauma Axial loading less than 1 cm anterior to the neural position produced anterior compression fractures of the vertebral body. Burst fractures can be produced by direct axial compression of a slightly flexed cervical spine. Tear-drop fracture results from a flexion/compression injury with disruption of the posterior ligaments.
  • Spinal Cord Injury It is now well accepted that acute spinal cord injury (SCI) involves both: Primary injury mechanisms. Secondary injury mechanisms.
  • Spinal Cord Injury The primary injury of the spinal cord results in local deformation and energy transformation at the time of injury and is irreversible. It can therefore not be repaired by surgical decompression. The injury is caused by: In the vast majority of cases bony fragments that acutely compress the spinal cord. acute spinal cord distraction. acceleration-deceleration with shearing. laceration from penetrating injuries. The injury directly damages cell bodies and/or processes of neurons.
  • Spinal Cord Injury Immediately after the primary injury, secondary injury mechanisms may initiate, leading to delayed or secondary cell death that evolves over a period of days to weeks. These secondary events are potentially preventable and reversible.
  • Spinal Cord Injury A variety of complex chemical pathways are likely involved including: hypoxia and ischemia intracellular and extracellular ionic shifts lipid peroxidation free radical production excitotoxicity eicosanoid production neutral protease activation prostaglandin production programmed cell death or apoptosis
  • Spinal Cord Injury In the case of a lesion of the cord cranial to T1, a complete loss of sympathetic activity will develop that results in loss of compensatory vasoconstriction (leading to hypotension) and loss of cardiac sympathetic activation (leading to bradycardia). Secondary deteriorations of spinal cord function that result from hypotension and inadequate tissue oxygenation have to be avoided.
  • Spinal Cord Injury Injuries to the spinal cord often result in spinal shock. The phenomenon of spinal shock is usually described as: loss of sensation flaccid paralysis absence of all reflexes below the spinal cord injury. It is thought to be due to a loss of background excitatory input from supra-spinal axons
  • Spinal Cord Injury Spinal shock is considered the first phase of the response to a spinal cord injury, hyperreflexia and spasticity representing the following phases. When spinal shock resolves, reflexes will return and residual motor functions can be found.
  • History The cardinal symptoms of an acute cervical injury are: pain loss of function (inability to move the head) numbness and weakness bowel and bladder dysfunction.
  • History In patients with evidence for neurological deficits, the history should include: time of onset (immediate, secondary) course (unchanged, progressive, or improving) The history should include a detailed assessment of the injury: type of trauma (high vs. low-energy) mechanism of injury (compression, flexion/distraction, hyperextension, rotation, shear injury)
  • History In polytraumatized or unconscious patients, patients must be considered to have sustained a cervical injury until proven otherwise. The history should also comprehensively assess details of collision and injury such as: type of collision (rear-end, frontal or side impact) use of headrest/seat belt position in the car injury pattern for all passengers head contusion severity of impact to the vehicle
  • Initial Management Primary survey A full general and neurological assessment must be undertaken in accordance with the principles of advanced trauma life support (ATLS). Spinal trauma is frequently associated with multiple injuries. As always, the patients airway, breathing and circulation (ABCin that order) are the first priorities in resuscitation from trauma.
  • Initial Management Secondary survey Once the immediately life-threatening injuries have been addressed, the secondary (head to toe) survey that follows allows other serious injuries to be identified. If neurological symptoms or signs are present, a senior doctor should be present and a partial roll to about 45 may be sufficient.
  • Initial Management Secondary survey specific signs of injury including: local bruising deformity of the spine (e.g. a gibbus or an increased interspinous gap) vertebral tenderness. The whole length of the spine must be palpated, another spinal injury at a different level. Priapism and diaphragmatic breathing invariably indicate a high spinal cord lesion. The presence of warm and well-perfused peripheries in a hypotensive patient should always raise the possibility of neurogenic shock attributable to spinal cord injury in the differential diagnosis.
  • Initial Management Secondary survey At the end of the secondary survey, examination of the peripheral nervous system must not be neglected. Diagnosis of intra-abdominal trauma often difficult because of: impaired or absent abdominal sensation absent abdominal guarding or rigidity, because of flaccid paralysis paralytic ileus
  • Neurological assessment In spinal cord in