DEFINITIONS
Neurologic deficit as a result of potential spinal cord injury
ASSESSMENTS
Initial ICU observation for q1h neurologic checks and hemodynamic monitoring
GOALS OF CARE
Maintain rigid C-collar at all times for suspected cervical segment injury
Maintain strict log roll precautions pending diagnostic evaluation
Do not break the back of the bed.
The head may be elevated up to 20 degrees by reverse Trendelenburg provided the patient is meeting hemodynamic goals.
The patient may be log rolled from side-to-side.
Goal MAP 85-90mmHg over the first 7 days. This timeframe may be modified at the discretion of consultant on an individualized basis. The MAP goal may be achieved through a combination of low head of bed, IV fluids, colloids, and pressor support.
Preferential use of an agent with balanced alpha/beta activity is recommended to avoid paradoxical bradycardia.
Consider a baseline TTE (particularly for older patients with medical comorbidities) to guide judicious fluid management.
Goal pCO2 35-40mmHg. Goal SaO2 > 93%. Encourage incentive spirometry, bearing in mind that patients may require assistance depending on the level of injury.
Aggressive pulmonary hygiene (unless contraindicated by biomechanical instability of the spine).
Maintain a low threshold for delayed respiratory failure requiring intubation, particularly for patients with cervical segment injury.
Intubation for such patients should be performed by fiberoptic means, with the head/neck maintained in a neutral position.
If a lumbar drain is present to permit monitoring of intrathecal pressure (ITP) and spinal cord perfusion pressure (SCPP), this should supersede the MAP goal parameter during that interval. Goal ITP < 15mmHg. Goal SCPP > 65mmHg, where SCPP = MAP – ITP.
DVT prophylaxis should be provided initially by mechanical means, pending diagnostic imaging evaluation to exclude canal and/or spinal cord hematoma as well as determination of the indications for and timing of any proposed invasive intervention.
Barring contraindication, pharmacologic prophylaxis should be initiated within 72h when feasible. The use of LMWH is preferred in this setting. An initial duration of 3 months is recommended.
GI prophylaxis should be provided for patients with acute spinal cord injury.
Initial nutritional support within 72h, when clinical stability permits.
Early PT (range of motion), OT (splint), and PM&R (pre-rehab recommendations) consultations should be initiated for patients with spinal cord injury.
Diagnostic imaging evaluation will be dictated by patient-specific characteristics and initial CT-identified pathology.
Indications for and the timing of operative intervention will be dictated by a combination of presenting symptoms, objective neurologic exam findings, and imaging features, balanced against an assessment of medical comorbidities, concomitant injuries, and clinical stability to tolerate the proposed procedure
DEFINITIONS
Severe TBI – Glasgow Coma Scale (GCS) of 3 to 8 without systemic sedation and after resuscitation
Moderate TBI – GCS of 9 to 12 without systemic sedation and after resuscitation
ASSESSMENTS
GCS ≤8, minimum q 1-hour neurologic checks and hemodynamic monitoring.
GCS 9-12, minimum q 2-hour neurologic checks and hemodynamic monitoring (q 1-hour if intubated).
GCS 13-15, minimum q 4-hour neurologic checks and hemodynamic monitoring.
Recommended frequency may be altered at the discretion of consultant, based on individual patient characteristics.
GOALS OF CARE
HOB at minimum 30 degrees. This recommendation may be altered in the setting of concomitant spinal cord injury.
Maintain rigid C-collar pending the ability to clear clinically. For patients with isolated penetrating traumatic brain injury and no clinical or CT evidence of injury, the cervical collar should be discontinued. If clinical clearance is not anticipated in the setting of blunt injury, consider early (within 36-72h) MRI C-spine pre-gadolinium to exclude obvious ligamentous injury. In the setting of raised ICP and no radiographic C-spine injury, the rigid C-collar may be removed and bolsters placed to maintain neutral head position without potential for jugular compression.
Goal SBP ≥ 110mmHg (100 for age 50-69). Maximum blood pressure goal will be dictated by individual patient characteristics and intracranial pathology. Do not arbitrarily lower acutely raised blood pressure without understanding why it is elevated. Recognize a Cushing response (sudden hypertension coupled with acute bradycardia) in the appropriate clinical setting.
Goal pCO2 35-40mmHg. Goal SaO2 > 93%. Titrate continuous infusion sedation and analgesia to goal ICP and/or CPP parameters; RASS is invalid for a patient in coma. Avoid hyperventilation except for acute ICP crisis with imminent definitive intervention planned Management of ARDS in the patient with raised ICP requires direct negotiation of treatment goals between Trauma and Neurosurgery Attendings. Early tracheostomy should be considered for select patients for whom extubation within 7-10 days is not anticipated.
Consider placement of an invasive device for monitoring of intracranial pressure +/- therapeutic drainage of CSF for patients with GCS ≤8. Suspected intoxication contributing to depressed LOC, suspected DAI, the presence of coagulopathy and/or thrombocytopenia, injury pattern precluding safe placement, and/or the presence of slit ventricles may influence this decision. If an EVD is present, output, ICP, and CPP should be documented in iView q 1h. If an intraparenchymal ICP monitor is present, ICP and CPP should be documented. If a brain tissue oxygen monitor is present, the pTBO2 value should be documented q 1h.
Goal ICP < 22mmHg. The management of raised ICP occurs through an interwoven, escalating process that may include patient positioning, continuous sedation/analgesia, paralytics, barbiturates, EVD drainage, hyperosmolar therapy, and invasive surgical interventions when indicated. Consideration to initiate hyperosmolar therapy should prompt discussion with Neurosurgery. The choice of agent may depend on volume status, hemodynamic goals, and comorbid injuries. Intermittent bolus infusion is
Goal CPP > 60mmHg. Avoid aggressive attempts to raise CPP > 70mmHg, as this may contribute to the development of ARDS
Seizure prophylaxis should be provided for 7 days following severe TBI. The 4th edition BTF guideline specifies the use of phenytoin; however, levetiracetam may be used at the discretion of the neurosurgical consultant. Phenytoin levels are not monitored in the absence of a seizure event during this period. The period of AED prophylaxis may be extended for post-surgical patients (typically, 2 weeks). Indications for the use of AED prophylaxis for patients with lesser degrees of TBI should be discussed on a case-by-case basis. Neurology consultation may be appropriate to assist management of chronic AED regimens as well as for suspected new-onset convulsive or non-convulsive seizure activity.
DVT prophylaxis should be provided initially by mechanical means. The timing for the introduction of pharmacologic prophylaxis depends – at minimum – on the demonstration of radiographic stability of hemorrhagic intracranial (or spinal canal) pathology but may also be influenced by patient-specific factors (such as coagulopathy, thrombocytopenia, location or pattern of bleeding, perioperative status) on an individualized basis.
Consider correcting thrombocytopenia to a platelet count above 100,000 in the presence of documented bleed or plan for invasive intracranial procedure.
Antiplatelet therapy should not routinely be reversed in the setting of acute intracranial hemorrhage. However, planned invasive intervention, and/or radiographic progression of hemorrhage and/or clinical neurologic worsening may provide indications to consider platelet transfusion on an individualized basis.
Indications for anticoagulant therapy reversal may depend on the specific agent, measured level, timing of most recent dose (and calculated half-life), and plan for invasive intervention. This should be discussed on a case-by-case basis.
Repeat CT imaging should be performed at 6- and 24 hours for patients with an initial CT head positive for acute intracranial pathology.
Further imaging beyond this window may be recommended by the neurosurgical consultant on the basis of radiographic progression, invasive intervention, and/or change in clinical status.
Patients with isolated traumatic SAH and/or minimal initial CT findings (such as tentorial subdural blood, parafalcine blood, or minimal contusion) may not require repeat imaging at the discretion of the consultant.
Patients with evidence of a petrous temporal bone fracture on initial CT head should undergo a dedicated CT temporal bone, coupled with ENT consultation.
Patients with evidence of skull base fracture crossing a skull base foramen on initial CT head should undergo a dedicated CTA brain.
Patients with penetrating injury should undergo an initial CTA brain/neck with CTV brain, as well as delayed vascular imaging (CTA brain or DSA at the discretion of the consultant) in 3-7 days post-injury. Initial DSA may be indicated for select injuries with suspicion for acute vascular injury and/or an inability to adequately evaluate the intracranial circulation due to metallic streak artifact.
Preferential use of non-dextrose-containing, isotonic solutions for IV maintenance. In the setting of raised ICP, consider capping the total hourly IV fluids plus continuous infusion sedation/analgesia at 100-125ml/h (but do not “run the patient dry”). Avoid hyponatremia. Goal serum sodium range will depend on the patient’s ICP status.
Enteral feeding should be initiated within 72-96h – pending clinical stability – for patients not anticipated to be extubated in that time frame.
If fever is present, restore normothermia as feasible. Culture as indicated.
Early PT (range of motion), OT (splint), and PM&R (pre-rehab recommendations) consultations should be initiated for patients with severe traumatic brain injury.
Post-extubation patients should undergo evaluation by Speech Therapy prior to initiation of oral intake, as well as to identify potential cognitive/communication impairment.