Anesthesia Considerations for Traumatic Brain Injury - Dr.Qazi.pptx

Essential strategies for managing anesthesia in patients with TBI. It emphasizes the prevention of secondary brain damage by maintaining cerebral perfusion pressure and avoiding factors like hypotension and hypoxemia.

1. Anesthesia Considerations for Traumatic Brain Injury Presented by Dr. Qazi Said Rahim

2. Traumatic brain injury Traumatic brain injury (TBI) refers to damage to the brain caused by an external force, leading to temporary or permanent impairment of cognitive, physical, and psychosocial functions. Any trauma patient with an altered level of consciousness must be considered to have a traumatic brain injury (TBI) until proven otherwise TBIs can be categorized as either primary or secondary injuries.

3. Primary Brain Injuries Initial direct injury (physical or mechanical) on the brain parenchyma and skull *an inflammatory cascade including cerebral edema, axonal injury, and decreased CPP. Primary brain injuries can lead to elevated intracranial pressure (ICP), which compromises cerebral blood flow and can result in death shortly after head trauma. It Includes: Subdural hematoma Epidural hematoma Intraparenchymal hemorrhage Nonfocal , diffuse neuronal injury

4. Secondary Brain Injury Indirect brain injury resulting from consequence of the primary injury, like Electrolyte abnormalities, hypoxemia, glycemic imbalance, hypotension, loss of autoregulation, increased ICP, and hyper or hypocarbia . They are potentially preventable injuries. Contributors to Morbidity and Mortality : Systemic Hypotension : Systolic blood pressures <90 mm Hg. Hypoxia : PaO2 <60 mm Hg. Hypercapnia : PaCO2 >50 mm Hg. Hyperthermia : Temperature >38.0°C.

5. Major Contributors to Poor Neurological Recovery : Hypotension and hypoxemia. Hypoxemia is the single most important parameter correlating with poor neurological outcome Management Dilemma in Severe Head Trauma with Other Severe Injuries: Emergency neurosurgery and damage control laparotomy are nearly impossible to perform simultaneously. Control of life-threatening hemorrhage takes precedence over neurosurgical intervention. Attempts to increase cerebral perfusion pressure in the presence of life-threatening hemorrhage will exacerbate bleeding. Once non-neurosurgical hemorrhage is controlled, attention can be directed toward the neurosurgical emergency, specifically toward restoring cerebral perfusion pressure. Prolonged periods of cerebral hypoperfusion in this situation are associated with negative neurological outcomes

6. Evaluation of TBI Patients HISTORY TAKING SHOULD INCLUDE Neurological state (consciousness, pupillary response) and vital parameters at the scene and during transport Estimated blood loss. Nature of treatment at scene and in transit. Use of airbags, seat-belts, crash-helmets Time, place, mechanism, vehicle speed (in relation to the accident) Past medical history Suspected influence of drugs or alcohol Possible medical reason for the accident (e.g. fit, heart attack, spontaneous intracranial haemorrhage , stroke) Use of anticoagulants or antiplatelet therapy

7. Preoperative Evaluation Evaluation of type and severity of TBI Identification of associated injuries.(orthopedic, abdominal, or thoracic injuries) Review of relevant imaging and laboratory findings. Identification of any secondary insults. (hypotension, hypoxemia, hyper- and hypocarbia , hypo- and hyperglycemia, seizures, and coagulopathy.) Goal: To Prevent Secondary brain injury. Clinical Assessment with GCS determining severity of TBI

8. Glasgow Coma Scale The Glasgow Coma Scale (GCS) is the most reliable clinical assessment tool for determining the severity of TBI in a nonsedated , nonparalyzed patient. Scoring Mild : 13-15 Moderate : 9-12 Severe : < 8 A GCS score of 8 or less on admission is associated with approximately 35% mortality

9. Examination of pupils for size, symmetry, and reaction to light.

10. Laboratory Evaluation (Pre-op) Preoperative laboratory tests should be reviewed, including hemoglobin, platelet count, clotting parameters, electrolytes, glucose, and blood gases. A sample should be sent for type and screen (or type and crossmatch if significant blood loss is expected).

11. Neuroimaging (Pre-op) CT preferred for acute TBI: detects fractures, hemorrhage, cerebral edema. MRI may be used. Acute intracranial hemorrhage may require emergency evacuation due to intracranial hypertension. Traumatic subarachnoid hemorrhage may lead to cerebral vasospasm. Increased ICP without hematoma suggests cerebral edema. Skull fractures require careful handling to prevent further injury, risk of pneumocephalus , CNS infection. Chronic intracranial hemorrhage may need burr-hole evacuation or craniotomy.

12. Anesthetic Management Goals: Early cerebral decompression for expanding intracranial hematoma. Maintain cerebral perfusion pressure (CPP) and treat increased intracranial pressure (ICP). Avoid secondary insults: hypotension, hypoxemia, hyper- and hypocarbia , hypo- and hyperglycemia, seizures, coagulopathy. Provide adequate analgesia and amnesia. Facilitate early postoperative neurologic evaluation when feasible. Avoid hypercarbia related to the administration of hypnotic agents or sedatives such as benzodiazepines, narcotics, etc., prior to induction of anesthesia

13. Intraoperative Monitoring Standard ASA monitors: ECG, noninvasive BP, pulse oximetry , capnography , temperature. Additional monitoring for TBI patients: Arterial catheterization for continuous BP monitoring and blood sampling. ICP monitoring to assess intracranial pressure. EEG monitoring for suspected seizure activity. Advanced neuromonitoring : Jugular venous oximetry and brain tissue O2 tension monitoring.

14. Venous Access: Placement of two large bore IV lines (>/=18 gauge) One very important consideration: placement of these lines should not delay the start of the surgical intervention. If difficult IV then place a central line, (the femoral vein is most appropriate) ,if fails, then tibial or humeral intra-osseous lines should be placed Vasopressor administration with Central Venous Cathers (CVC) Avoid delaying intracranial hematoma evacuation for CVC placement. Subclavian venous access may be preferred over internal jugular to minimize ICP increase. Temperature monitoring

15. ICP Monitoring Cerebral Perfusion Pressure (CPP): Normal: 80-100 mm Hg (MAP - ICP = CPP) ICP monitoring is not required for conscious, alert patients Monitored via intraparenchymal probe or intraventricular catheter Avoid in intentionally anticoagulated or bleeding diathesis patients Intervene when ICP exceeds 20-25 mm Hg Current Brain Trauma Foundation guidelines recommend maintaining CPP between 50 and 70 mm Hg and ICP at less than 20 mm Hg for patients with severe head injury.

16. Indications for ICP monitoring. Severe Head Injury (GCS Score ≤ 8 after cardiopulmonary resuscitation) Plus one of the following: Abnormal admitting head CT scan OR Normal CT scan plus ≥ 2 of: Age > 40 years Systolic blood pressure > 90 mm Hg Decerebrate or decorticate position Additional Risk Factors: Sedated patients Multisystem injury with altered consciousness Treatment increasing ICP risk (e.g., high-volume IV fluids) Abnormal transcranial Doppler waveform (excl. arterial hypotension and hypocapnia )

17. Choice of Anesthetic Agents: Agents should maintain hemodynamic stability, preserve cerebral perfusion, and avoid increases in ICP and secondary brain injury. No specific anesthetic agent has shown superior neurologic outcomes in TBI patients. Ketamine is gaining interest for perioperative use in TBI patients: Ketofol (ketamine/ propofol admixture) resulted in better hemodynamic stability and lower vasopressor requirement compared to propofol alone. Ketamine can be safely used for analgesia and sedation in TBI patients. Propofol may be preferred for maintenance anesthesia in severe TBI patients undergoing decompressive hemicraniectomy : Lower intraoperative mean arterial pressure compared to sevoflurane with similar brain relaxation scores.

18. Anesthesia Strategy Premedication: No premedication preferred for patients with possible intracranial hypertension. Rapid Sequence Induction and Intubation (RSII): Fentanyl 2-4 mcg/kg IV Lidocaine 1-1.5 mg/kg IV Propofol 1.5-2 mg/kg IV Etomidate 0.2-0.6 mg/kg IV for hypotensive patients before induction Succinylcholine 1-1.5 mg/kg; consider defasciculating dose of nondepolarizing NMBA followed by succinylcholine if contraindicated. ( rocuronium 1 mg/kg IV)

19. Anesthesia Strategy Maintenance: Isoflurane or sevoflurane <1 MAC or propofol 70-140 mcg/kg/minute, titrated to processed EEG monitoring when possible. Low-dose ketamine (up to 10 mg/ hr ) or dexmedetomidine (0.2 to 0.6 mcg/kg/ hr ) may be used as adjuncts. Fentanyl 1-2 mcg/kg every 1-2 hours depending on hemodynamic status. Rocuronium / vecuronium titrated to one to two twitches in train-of-four. Antiemetic: Ondansetron 4 mg IV one hour prior to emergence.

20. Pain Control Alternatives: Fentanyl, morphine, or hydromorphone titrated to effect postoperatively. OR morphine (3-5mg IV) or hydromorphone (0.5mg IV) administered 30 minutes prior to emergence, further titrated to effect postoperative neurologic examination. Acetaminophen 1000 mg IV may be administered to supplement analgesia without compromising neurologic assessment.

21. Airway Management ● Cervical spine injury Assume cervical spine injury unless formally cleared. Reported incidence of cervical spine injury in severe head injury patients: 4-8%; many are mechanically unstable, associated with spinal cord injury. Minimize cervical spine movement during airway management to avoid spinal cord injury. ● Aspiration Risk: Assume full stomach and aspiration risk. Decision for RSII based on predicted difficulty with airway management and other patient factors.

22. Hemodynamic Management: Maintain adequate cerebral blood flow (CBF) to prevent secondary injury. Autoregulation of CBF may be impaired or abolished following TBI. "Pressure-passive" patients are at risk of secondary hemorrhage, edema, and elevated ICP. Goal Intracranial Pressure and Cerebral Perfusion Pressure (CPP): Maintain ICP <22 mmHg and CPP target of 60 to 70 mmHg. Avoid aggressive attempts to achieve CPP above 70 mmHg. Goal Blood Pressure: SBP ≥100 mmHg for patients 50 to 69 years old. SBP ≥110 mmHg for patients 15 to 49 or >70 years old. Consider MAP and CPP alongside SBP. Higher SBP may be required to achieve adequate CPP, particularly in patients with severely increased ICP.

23. Fluid Management: Administer warm, non-glucose-containing isotonic crystalloid solution to maintain euvolemia . Avoid colloids like albumin due to concerns about increasing ICP in patients with altered blood-brain barriers. The Saline versus Albumin Fluid Evaluation (SAFE) study reported higher mortality among TBI patients receiving albumin compared to saline. Resuscitation with albumin was associated with increased ICP and interventions for elevated ICP. Avoid starch-based colloids due to concerns about altered coagulation and potential adverse outcomes. Electrolyte Imbalances: Common in TBI patients and should be regularly assessed intraoperatively alongside other laboratory values.t

24. Intraoperative Ventilation and Oxygenation: Goals : PaO2 >60 mmHg. Peripheral O2 saturation >90 percent. Hypoxemia associated with increased mortality and poor neurologic outcome. Conflicting studies on hyperoxia outcomes; maintain PaO2 of 60 to 200 mmHg. Ventilation guided by blood gases rather than ETCO2. Hypercarbia should be avoided, as it increases CBF and may increase ICP. Hyperventilation used selectively to reduce ICP or improve surgical exposure. Limit duration to prevent brain ischemia. Monitor cerebral oxygenation or CBF if prolonged hyperventilation required.

25. Management of ICP CSF drainage is the fastest way to reduce ICP > 20 mmHg.(If CSF drain present) Elevate the patient's head and keep the neck neutral to improve venous return. Administer mannitol slowly (0.25-1 gm/kg over 15 minutes) in stable patients for ICP reduction, transient increase in oxygen transport, and CBF increase. Monitor and replace urinary losses to prevent hypovolemia and hypotension with mannitol administration to avoid kidney damage. Rebound increase in ICP may occur due to worsening vasogenic edema.(damaged BBB) Hyperventilation can temporarily treat ICP but should be cautious with as excessive hyperventilation can lead to cerebral vasoconstriction and oxygen deprivation. (maintain pac02 near 35mmhg. And not less than 20-25mmhg)

26. Management of ICP (Cont’d) Hypertonic saline reduces cerebral water content, decreasing ICP and improving brain blood flow without causing hypotension. Prevent hypernatremia Avoid hypotonic solutions to prevent cerebral edema and worsened ICP; use isotonic solutions for fluid resuscitation (e.g., 0.9% saline). Avoid glucose-containing solutions and albumin unless hypoglycemia is present. Hypothermia may help control ICP by decreasing metabolic rate (approx. 5-7% per degree Celsius of cooling). Corticosteroids are not recommended due to adverse effects on mortality and morbidity in TBI.

27. Other Managements Temperature Management: Intraoperative normothermia is the goal for most TBI patients. Therapeutic hypothermia continuation for those pre-treated. Fever worsens outcome; aggressively treated. Therapeutic hypothermia not shown to improve TBI outcome. Glucose Management: Aim for blood glucose between 80 and 140 mg/ dL . Antiseizure Drugs: Phenytoin or fosphenytoin recommended for prevention of early post-traumatic seizures. Administer slowly to prevent hypotension and bradycardia. Intraoperative Glucocorticoids: Not recommended for TBI patients due to harm.

28. Emergence and Transfer of Care: Patients with epidural hematoma or isolated depressed skull fracture can often be awoken from anesthesia and extubated at the end of craniotomy. Follow usual extubation procedures, especially for patients with difficult intubation or airway concerns. Patients with severe TBI, SDH, or other intracranial lesions, or polytrauma may remain intubated and transported to the ICU. Immediate postoperative CT scan may be required for intracranial decompression confirmation or ruling out progression of intracranial hemorrhage. Continue all intraoperative monitoring during transport. Use a standardized handoff checklist for safe transfer of care to the ICU staff.

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