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Acute Spinal Cord Injury. Prepared by Shane Barclay MD. Pathophysiology. Spinal cord injuries are usually produced along with vertebral column injuries – ie fractures, dislocations, ligament tearing, disc herniation/disruption.
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Acute Spinal Cord Injury Prepared by Shane Barclay MD
Pathophysiology Spinal cord injuries are usually produced along with vertebral column injuries – ie fractures, dislocations, ligament tearing, disc herniation/disruption. Although spinal fractures are classified as ‘stable’ or ‘unstable’, in the rural setting assume ALL fractures are unstable.
Pathophysiology The initial cord injury can cause anything from no symptoms to a severe clinical scenario. There is a delayed cord injury syndrome that can develop over minutes to hours, so beware that neurological findings can change dramatically with time.
Spinal Shock versus Neurogenic Shock Spinal Shock Due to acute spinal cord injury Absence of all voluntary and reflex neurological activity below the lesion. • Decreased reflexes • Loss of sensation • Flaccid paralysis below injury Neurogenic shock Loss of vasomotor and SNS tone • Hypotension • Bradycardia • Poikilothermia (unable to regulate temperature. Occurs within 30 minutes of injury and only T5 and above. Lasts up to 6 weeks.
Clinical Presentation Usually spinal cord injuries associated with fractures etc will present with pain at the site of the fracture. However patients may have other systemic injuries which completely mask the spine injury. It is now recognized that even patients with a ‘normal neck CT’ can have significant cord injury. Gold standard is becoming MRI.
Diagnosis of Spinal Fracture You can clinically clear the C- spine using the ‘NEXUS’ criteria. • No evidence of intoxication. Sober and no odor of alcohol. • Normal level of alertness. Oriented x 3 and can remember objects by 5 minutes. There should also be no delay or inappropriate response to external stimuli. • No focal neurological deficits. • No painful distracting injuries. • No midline cervical tenderness. Push on the spinous processes and look for patient grimacing etc. Don’t ask if it is painful.
Diagnosis of Spinal Fracture If all 5 criteria are negative, then see if the patient can rotate their neck on their own to the left and right.
Diagnosis of Spinal Fracture If the patient fails any of these 5 criteria, they need CT and/or MRI imaging. Plain x-rays are helpful if you identify a fracture, however a ‘negative’ c-spine series does not rule out a fracture. If there is clinical suspicion a CT scan is required. Even a negative CT scan is associated with ~ 1:3000 significant spine injury.
Acute Management of Spinal Cord Injury Before discussing acute management, there is the issue ofc-spine collars. Traditionally, it was taught that c-spine immobilization and control was ‘sacrosanct’. There is now emerging ER literature suggesting that C-spine collars and precautions may be unnecessary and in some cases even detrimental to the patient. There is a separate web page link on REMSTARBC.ca The discussion is not finished!
Acute Management of Spinal Cord Injury • Do not remove athletic head gear. • Try to maintain MAP between 85 – 90 mmHg. This can be through use of IV fluids, blood products, elevation of the legs or pressors. Try to limit IV fluids as this has been associated with further cord swelling. • Maintain oxygenation, intubate if necessary. • Do NOT give methylprednisolone. • Insert urinary catheter as soon as possible.
Acute Management of Spinal Cord Injury 6. Watch for respiratory complications – usually present as mild tachypnea, shallow breaths and a weakened cough. Lesions of C5 or higher lead to diaphragmatic paresis, whereas high thoracic injury causes paralysis of the intercostal muscles. Acute respiratory failure, pulmonary edema, PE can occur in up to 85% of high cervical injury but also in up to 65% of thoracic cord injury.
Acute Management of Spinal Cord Injury 7. Pain control. 8. Temperature control. Patients with spinal cord injury may lack vasomotor control below the level of cord injury and therefore can’t sweat.
Acute Management of Neurogenic Shock Neurogenic shock is a type of ‘distributive’ shock due to loss of sympathetic tone to the blood vessels, resulting in vasodilation and bradycardia. Treatment: • Atropine prn for bradycardia. • IV fluids (N/S) for BP. • Vasopressors as needed. Recommend Phenylephrine which is a pure alpha agonist.
Scenario 58 year old male is on the roof cleaning the gutters. While reaching over, the ladder slips. He tries to grab the gutter, but it gives way and he falls ~ 12 feet down, landing initially on his feet, but then falls back hitting his neck on a rock retaining wall. EHS is called. When they arrive he is moaning in pain but responding to questions appropriately. He says his ankles are very painful. He says he has sensation in his arms and legs. Past Hx: diet controlled diabetic, mild HTN Meds: Atenolol. Motrin prn
Scenario At the scene: BP 170/85, HR 125, RR 20, He is placed in collar and clam shell, peripheral IV is started and he is transported to the hospital.
Scenario He arrives in the ER 35 minutes after the accident. He has had 200 cc N/S. When he arrives he is still oriented and responsive. GCS 15. BP 130/75, HR 55, RR 20, SpO2 99%
Scenario Exam reveals: Clear breath sounds. No chest wall tenderness. Decreased sensation from the mid torso down. Leg reflexes seem diminished to you. There is obvious deformity of both ankles but there are pedal pulses. By the time you finish your exam his BP is now 95/45, HR 40.
