Neurosurgical management of traumatic brain injury (TBI) Dr. Mohammed Muneam M.B CH.B A.B.H.S Neurosurgery Introduction: 6–60% of patients with GCS score ≤ 8 have 1 or more other organ system injured.1 25% have “surgical” lesions. There is a 4–5% incidence of associated spine fractures with significant head injury (mostly C1 to C3). When a detailed history is unavailable, remember: the loss of consciousness may have preceded (and possibly have caused) the trauma. Therefore, maintain an index of suspicion for e.g.: aneurysmal SAH, hypoglycemia, etc. in the differential diagnosis of the causes of trauma and associated coma. Brain injury from trauma results from two distinct processes: 1. primary brain injury: occurs at time of trauma (cortical contusions, lacerations, bone fragmentation, diffuse axonal injury, and brainstem contusion). 2. secondary injury: develops subsequent to the initial injury. Includes injuries from intracranial hematomas, edema, hypoxemia, ischemia (primarily due to elevated intracranial pressure (ICP) and/or shock), vasospasm (OUR focus should be on reducing secondary injuries). Classification Of Head Trauma A simple system based only on GCS score is as follows: 1-Minimal: GCS 15 2-Mild: GCS 14 3-Moderate: GCS 9-13 4-Sever: 5-8 5-Critical: 3-4 Intracranial hypertension (IC-HTN) The critical parameter for brain function and survival is not actually ICP, rather it is adequate cerebral blood flow (CBF) to meet CMRO2 demands. CBF depends on cerebral perfusion pressure (CPP), which is related to ICP. cerebral perfusion pressure = mean arterial pressure intracranial pressure CPP= MAP- ICP Cerebral autoregulation is a mechanism whereby over a wide range, large changes in systemic BP produce only small changes in CBF. Due to autoregulation, CPP would have to drop below 40 in a normal brain before CBF would be impaired. Normal Intracranial Constituents brain parenchyma & ECF :1400 ml cerebral blood volume (CBV): 150 ml cerebrospinal fluid (CSF): 150 ml Traumatic Intracranial hypertension cerebral edema hyperemia traumatically induced masses hydrocephalus hypoventilation (causing hypercarbia → vasodilatation) systemic hypertension (HTN) venous sinus thrombosis increased muscle tone sustained posttraumatic seizures (status epilepticus) cerebral vasospasm hyponatremia Management of TBI A-Rapid primary survey The primary survey is performed simultaneously with resuscitation and includes the “A, B, C, D, Es” of trauma care.in accordance with Advanced Trauma Life Support (ATLS) principles (American College of Surgeons, The Committee on Trauma). A: Airway maintenance (while taking care to protect the cervical spine) B: Breathing and ventilation C: Circulation and control of hemorrhage D: Disability assessment including a brief evaluation of neurologic status (ask the patient to move his/her extremities, ask if he/she can feel?) and Glasgow Coma Scale (GCS) E: Exposure and environmental control, which includes fully exposing the patient and measures to prevent hypothermia. B-Resuscitation & stabilization (with primary survey) Major goals avoid hypoxia (pO2 < 60 mm Hg) avoid hypotension (SBP ≤ 90 mm Hg): 67% positivepredictive value (PPV) for poor outcome (79% PPV when combined with hypoxia) SPINAL PRECAUTIONS 1-positioning: elevate HOB 30–45° & keep head midline 2- Hypotension (shock) monitor BP and avoid hypotension (SBP < 90 mm Hg), hypotension in TBI can occurs in ● in terminal stages ● in infancy, where enough blood can be lost intracranially or into the subgaleal space to cause shock ● scalp wounds Important notes IVF of choice is isotonic (NS + 20 mEq KCl/L) avoid hypotonic solutions (lactated ringers) if mannitol is required, patient should be maintained at euvolemia also exercise caution with fluids in CSW & SIADH pressors (dopamine) are preferable to IV fluid boluses in head injury arterial line for BP monitoring and frequent ABGs CVP line if high doses of mannitol are needed (goal: keep patient euvolemic 3-oxygenation avoid hypoxia (PaO2 < 60 mm Hg or O2 saturation < 90%). Intubate if: 1. depressed level of consciousness 2. need for hyperventilation 3. severe maxillofacial trauma: 4. need for pharmacologic paralysis for evaluation or management (What is the risk of intubation in TBI?)= pneumonia , basal skull fracture , GCS 4-paralytics and sedatives 1- intracranial hypertension 2-for intubation. 3-or where use is necessary for transport or to permit evaluation of the patient (to get a combative patient to hold still for a CT scan). 5-Early prophylactic hyperventilation (risks?) avoid hyperventilation: keep PaCO2 at the low end of eucapnia (35 mm Hg) (USE IT LATER ON IN DOCUMENTED IC-HTN) 6-Mannitol in E/R: indicated in evidence of intracranial hypertension evidence of mass effect (focal deficit, e.g., hemiparesis) sudden deterioration prior to CT (including pupillary dilatation) after CT, if a lesion that is associated with increased ICP is identified after CT, if going to O.R. to assess “salvageability Contraindications: hypotension hypovolemia. mannitol may slightly impede normal coagulation CHF. 7-Prophylactic antiepileptic drugs AED 8-Anti-ulcer medication 9- indwelling (Foley) catheter: to prevent distension from urinary retention 10-Biochemical investigation: 11- temperature regulation: aggressive control of fever (fever is a potent stimulus to increase CBF, and may also increase plateau waves) 12-Analgesics. 13-Aggressive management of hyperglycemia prevent hyperglycemia: (aggravates cerebral edema) usually present in head injury (steroids) C-Secondary Survey 1-History: allergies, medications, illnesses, pregnancy, last meal. mechanism of injury, time of injury presence and location of pain in conscious patient loss of consciousness, vomiting, seizures occurrences of transient or persistent neurologic symptoms hx of congenital malformation, IC pathology, previous operations 2-General physical examination: 1. visual inspection of cranium Evidence of basal skull fracture check for facial fractures periorbital edema, proptosis 2-cranio-cervical auscultation 3-physical signs of trauma to spine 4-evidence of seizure: single, multiple, or continuing (status epilepticus) 3-Neurologic exam: GCS, Cranial nerves, Motor, sensory, reflexes Important note: look for signs of intracranial hypertension: 1. pupillary dilatation (unilateral or bilateral) 2. asymmetric pupillary reaction to light 3. decerebrate or decorticate posturing (usually contralateral to blown pupil) 4. progressive deterioration of the neurologic exam not attributable to extracranial factors 4-Radiological investigations: CT: An unenhanced (i.e., non-contrast) CT scan of the head usually suffices for patients seen in the emergency department presenting after trauma or with a new neurologic deficit. Enhanced CT or MRI may be appropriate after the unenhanced CT in some circumstances, but are not usually required emergently. Skull X-rays: significant ICI can occur with a normal skull X-ray, SXRs affect management of only 0.4–2% of patients in most reports. MRI scans in trauma: Usually not appropriate for acute head injuries. Arteriogram in trauma: useful with non-missile penetrating trauma. D-Initiation of definitive management 1- ICP monitoring: For salvageable patients with severe traumatic brain injury GCS ≤ 8 after cardiopulmonary resuscitation), treatment for IC-HTN should be initiated for ICP > 22 mm Hg. keep ICP ≤ 22 mm Hg & keep CPP ≥ 50 mm Hg. (TYPES OF ICP MONITORS) 2- Initiate treatment if ICP > 22 mm Hg. See below table 3- second tire therapy: 1. high dose barbiturate therapy 2. hyperventilate to PaCO2 = 25–30 3. hypothermia 4. decompressive surgery: 5. lumbar drainage 6. hypertensive therapy 4- surgical Indication in TBI: 1- traumatic intracranial masses 2- decompressive craniectomy may be considered for IC-HTN that cannot be controlled medically