SPINAL TRAUMA

1. SPINAL TRAUMA

2. – Is obserwed only in 1-4 % of common traumatism. • – In most of cases is indirect. • –Divided on: • opened (with damage of skin) and closed (without damage of skin). • without violation of spinal function • with violation of spinal function • with violation of spinal function but without violation of vertebral colamn.

3. Kinds of spinal trauma are • Concussion • Contussion • Compression • Smashing with full or partial spinal rummaging, hematomielia • Traumatical radiculities. • The vertebras which are damaged very often are XII thoracic, I lumbar, V-VI cervical. • Spinal trauma without violation of spinal function does not require the neurosurgical tratment • Spinal trauma with violation of spinal function requires the neurosurgical tratment

4. REMEMBER Posttraumatical changes in the case of full or partial spinal rummaging are irreversible Clinic picture of spinal trauma with full or partial spinal rummaging • spinal shok , conducted wiw falling of motor, sensitive and reflex functions lower level of damage • pain in region of trauma • disoders of pelvic functions. SPINAL CONCASSION is characterised by functional disoders of segment apparate

5. SPINAL CONTUSSION • Pathogenesis – edema, malaxations, blood soaking of spinal tissue. • – divided on light, midle and height degree. • Clinic – disappearance of spinal functions – paralysis and anaesthesia lower than trauma level, disoders of pelvic functions, complications (bedsores, cystopielonephrities, pneumonia) during 2 weeks after trauma. • Careful neurologic assessment should be performed to determine the level of motor and sensory function, evaluate the presence of spinal shock, and assess whether the lesion is complete. Patients with a complete lesion have no sensory or motor function below the level of injury.

6. SPINAL COMPRESSION Oftenly combined with its contussion and rummaging. Conditioned by vertebras rupture with debris removal towards to vertebral chanal. Clinic the same like in the case of spinal contussion with malaxation and blood soating In addition to pulmonary disoders, high spinal cord injuries can lead to significant hypotension. Most of the arteriolar tone is mediated through the sympathetic nervous system.

7. Sympathetic nerves arise from the ventral roots of the thoracic spinal segments and are controlled by descending pathways from the brain stem. These controlling pathways may be interrupted in high thoracic and cervical cord injuries, resulting in loss of vasomotor tone. Lack of sympathetic drive to the sinoatrial node causes a predominance of vagal tone and bradycardia. This produces the classic clinical picture of spinal cord injury with hypotension and relative bradycardia. In contrast to patients with hypovolemic shock, the extremities of patients with high cord lesions are warm and well perfused because the injury ablates sympathetically mediated peripheral vasoconstriction.

8. There is a tendency for respiratory failure to develop in such patients several hours after injury secondary to fatigue. With or without intubation, they are at high risk for pulmonary complications related to atelectasis and inadequate clearance of secretions. • Hypovolemia must be presumed to be the cause of hypotension in the initial evaluation of any trauma patient, including the patient with spinal cord injury. A patient with spinal shock should be managed with volume expansion until sources of significant blood loss have been ruled out and volume deficits have been replaced

9. Once the circulating volume has been restored and hemorrhage has been controlled, persistent hypotension is best managed with a pure a-adrenergic agonist like phenylephrine. Volume status should be optimized with the use of a central venous or pulmonary artery catheter to avoid fluid overload and exacerbation of pulmonary problems. • Hemorrhage from fracture sites is a potential cause of instability in the blunt trauma patient. Although hypovolemic shock always should prompt a search for intracavitary hemorrhage, bleeding from fractures and lacerations frequently contributes to hypotension and may be its sole cause. It is important, therefore, to assess the degree of bleeding caused by fractures. The fractured pelvis can be a source of life-threatening hemorrhage and must be identified early in the evaluation of the injured patient.

10. Spinal Cord Injury with Neurologic Compromise • Patients with over 50% effacement of the spinal canal and those with deteriorating neurologic examinations are candidates for emergency surgical decompression. • Once spinal shock has resolved, a patient with an incomplete lesion demonstrates some sensory or motor function and sacral sparing of sensation. Patients with incomplete lesions and improving examination results are followed with serial neurologic testing. Stabilization is performed once the neurologic examination results have plateaued.

11. Patients with significant canal compromise and a worsening examination may benefit from early surgery to decompress the spinal cord. Those with complete injuries, especially in the cervical spine, should be observed for a time before surgery to minimize the risk of further injury to the compromised spinal cord. The loss of even a single level of function during a prematurely performed operation can have a profound effect on the patient's ultimate rehabilitation status. Patients with a stable examination and an incomplete lesion represent difficult management decisions and must have their care individualized.

12. Pharmacologic reatment Clinical trials involving several pharmacologic interventions for patients with acute spinal cord injury are ongoing. In the Second National Acute Spinal Cord Injury Study, patients with spinal cord injury who received high doses of methylprednisolone sodium succinate within 8 hours of injury had improved neurologic recovery. At 6 weeks postinjury, treated patients demonstrated modest but statistically significant improvements in motor and sensory function. This benefit continued to be observed 6 months and 1 year after injury.

13. Accepted treatment for patients with spinal cord injury consists of an initial bolus of 30 mg/kg of methylprednisolone followed by an infusion of 5.4 mg/kg/h for 23 hours. Steroid treatment begun more than 8 hours after injury has resulted in increased complications and worsened neurologic outcome, and should be avoided (296,297). • Patients with either complete or incomplete injuries should have definitive spinal stabilization at the earliest practical opportunity. Evidence from a variety of centers demonstrates prevention of early complications and significant acceleration of the rehabilitation process in patients undergoing early spinal stabilization.

14. The preoperative determination of level of consciousness and lateralizing gross motor or sensory deficits is required in all patients; a more detailed neurologic examination of the brachial plexus, deep cervical plexus, phrenic nerve, and cranial nerves should be performed in all but the most unstable patients. • A hypoglossal or spinal accessory nerve injury is particularly easy to miss unless a preoperative neurologic examination is performed. • The vagus nerve can be evaluated by examination of the vocal cords. Primary débridement and repair of all severed or lacerated “named” nerves is preferred, with the use of fine interrupted nonabsorbable suture on the perineurium.

15. Repair of a single recurrent nerve injury is controversial. An avulsed recurrent laryngeal nerve (blunt laryngotracheal disruption) should be implanted into the posterior cricoarytenoid muscle (201). If a motor nerve deficit is apparent, an expendable sensory nerve such as the great auricular can be interposed as a nerve graft to allow anastomosis without tension. If the patient's condition precludes primary repair, the nerve ends should be marked with silver clips or nonabsorbable colored suture. Secondary repair 3 weeks after injury is advised.