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TRAUMATIC BRAIN INJURY
- 1. TRAUMATIC BRAIN INJURY STRATEGIES AND RATIONALE TO DECREASE SECONDARY BRAIN INJURY PRESENTER - DR YOGESH RATHOD MODERATOR – DR SHALINI NAIR
- 2. TRAUMATIC BRAIN INJURY Consists of two types of injuries:- Primary Brain injury is the damage sustained as a direct result of the impact on the skull and intracranial contents. Secondary brain injury refers to the changes that evolve over a period of time (from hours to days) after the primary brain injury. It includes an entire cascade of cellular, chemical, tissue, or blood vessel changes in the brain that contribute to further destruction of brain tissue.
- 3. PATHOPHYSIOLOGY Primary brain Injury — heterogenous. Common mechanisms direct impact rapid acceleration/deceleration penetrating injury blast waves. External mechanical force damage results in focal contusions and hematomas shearing of white matter tracts (diffuse axonal injury) cerebral edema and swelling.
- 4. Secondary brain Injury These mechanisms include: Neurotransmitter-mediated excitotoxicity (e.g. glutamate), free-radical injury to cell membranes Electrolyte imbalances Mitochondrial dysfunction Inflammatory responses Apoptosis Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury Current clinical approaches to the management of TBI center around primary and secondary brain injury concepts.
- 5. INTRACRANIAL SECONDARY BRAIN DAMAGE Hemorrhage Extradural Subdural Intracerebral Intraventricular Subarachnoid Swelling Venous congestion/hyperemia Edema Vasogenic Cytotoxic Interstitial Infection Meningitis Brain abscess
- 6. EXTRACRANIAL SECONDARY BRAIN DAMAGE Hypoxia Hypotension Hyponatremia Hyperthermia Hypoglycemia
- 7. LIBERATION OF CHEMICALS (EAAs, PAF & Free Radicals of O2) DISRUPTION OF BBB EDEMA NEURAL DEATH CONTINUATION OF VICIOUS CYCLE Neurotoxic cascades ISCHAEMIA AND REPERFUSION INJURY
- 8. Calcium channel disturbance Local tissue damage EAAs NMDA glutamate receptors of calcium channels in the surroundings cells massive influx of Ca++ ions metabolic failure of the cells and cellular edema. Oxygen free radical production Cellular metabolic failure free radicals of oxygen + PAF free radical generation and the destruction of super oxide dismutase damaged cells and blood vessels Ischemia and vascular damage arachidonic acid cascade prostaglandin, prostacyclin leukotrienes release with free radical generation further vascular damage increase in vascular permeability and vasogenic oedema further brain swelling & raised ICP, a decrease in CPP and more global ischaemia.
- 9. Hematoma formation Exrtadural hematomalocal ischemia, a shift of midline structures and possible fatal brainstem damage Subdural and subarachnoid hemotoma local compression and swelling of the brain substance and an increase in ICP Blood in the subarachnoid space can cause vasospasm and further aggravate cerebral ischemia.
- 10. Respiratory failure LOC accompanied by a period of central apnea and can lead to severe hypoxia. Aspiration of vomit can cause further injury to lungs impairing ventilation. Any hypoxia will aggravate cerebral ischemia and increases cerebral blood flow and cerebral blood volume, thus increasing ICP. Thus any degree of respiratory failure is particularly hazardous for the patient with head injury. Blood Loss CPP = MAP – ICP Raised ICP + fall in MAP cerebral ischaemia. Hypotension from blood loss is not uncommon in multiple injuries and should be strenuously avoided and corrected. Blood loss can lead to anemia and make cerebral ischemia more likely
- 11. Infection and Seizure A major source of concern . Any patient with a CSF leak or air in the intracranial cavity and open fracture of the skull should be given an appropriate prophylactic antibiotic regimen Epileptic seizures Early epilepsy is most likely to be associated with intracranial haematoma and depressed skull fracture. If the seizures are not controlled, they can cause cerebral hypoxia
- 12. STRATEGIES AND RECOMMENDATIONS FOR TRAUMATIC BRAIN INJURY
- 13. TREATMENT RECOMMENDATIONS Decompressive craniectomy Bifrontal DC is not recommended to improve outcomes. But reduces ICP and minimizes days in the ICU. A large fronto-temporo-parietal DC (not less than 12 x 15 cm or 15 cm diameter) is recommended over a small FTP DC for reduced mortality and improved neurologic outcomes. Ventilation therapies Prolonged prophylactic hyperventilation with PaCO2 of 25 mm Hg is not recommended. Hyperventilation is recommended as a temporizing measure for the reduction of elevated ICP. Hyperventilation avoided during the first 24 h when CBF often is reduced critically. If hyperventilation is used, SjO2 or BtpO2 measurements are recommended to monitor oxygen delivery.
- 14. Prophylactic hypothermia Early (within 2.5 h), short-term (48 h post-injury), prophylactic hypothermia is not recommended to improve outcomes in patients with diffuse injury. Hyperosmolar therapy Mannitol is effective for control of raised ICP at doses of 0.25 to 1 g/kg body weight. Arterial hypotension (systolic blood pressure ,90 mm Hg) should be avoided. Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial causes. Cerebrospinal fluid drainage An EVD system zeroed at the midbrain with continuous drainage of CSF may be considered to lower ICP burden more effectively than intermittent use. Use of CSF drainage to lower ICP in patients with an initial GCS of 6 or lower during the first 12 h after injury may be considered.
- 15. Anesthetics, analgesics, and sedatives Barbiturates for burst suppression in EEG as prophylaxis against development of intracranial HTN not recommended. High-dose barbiturate recommended to control elevated refractory ICP. Hemodynamic stability essential. Propofol is recommended for the control of ICP, but not recommended for improvement in mortality or 6- month outcomes. Caution is required as high-dose propofol can produce significant morbidity. Steroids Not recommended for improving outcome or reducing ICP. Rather high dose methylpred was a/w increased mortality and is contraindicated. Nutrition Feeding patients to attain basal caloric replacement at least by the 5th day and at most by the 7th day recommended to decrease mortality.
- 16. Infection prophylaxis Early trach recommended to reduce mechanical ventilation days if overall benefit outweighs the complications. No evidence that early trach reduces mortality or the rate of nosocomial pneumonia. PI oral care is not recommended to reduce VAP and may cause an increased risk of ARDS. Antimicrobial-impregnated catheters may be considered during EVD to prevent infections. DVT Prophylaxis LMWH or low-dose unfractionated heparin may be used in combination with mechanical prophylaxis. But an increased risk for expansion of ICH. Compression stockings + pharmacologic prophylaxis may be beneficial. Insufficient evidence to support recommendations regarding the preferred agent, dose, or timing of pharmacologic prophylaxis for DVT. Seizure prophylaxis Prophylactic use of phenytoin or valproate is not recommended for preventing late PTS. Phenytoin is recommended to decrease the incidence of early PTS (within 7 d of injury), when the overall benefit outweighs the complications. However, early PTS have not been associated with worse outcomes. Insufficient evidence to recommend levetiracetam over phenytoin regarding efficacy in preventing early PTS and toxicity.
- 17. MISCELLANEOUS Antagonists or blockers of the NMDA glutamate receptor (dizocilpine) have been successful in preventing brain injury in animals. Nimodipine have also been shown to have some brain protective effects. Ketamine is an NMDA receptor antagonist that has been shown to improve neurological outcome in a rat brain injury model, but no practical value in a clinical settings. Nitric oxide production of free radicals (by blocking nitric oxide synthase, outcome is improved) Antagonists to PAF and leucocytes antibody treatment may also limit secondary brain injury.
- 18. Intracranial pressure monitoring Management of severe TBI patients using information from ICP monitoring is recommended to reduce in hospital and 2-week post-injury mortality. Monitored in all salvageable patients with a TBI (GCS 3-8 after resuscitation) and an abnormal CT scans. Indicated in patients with severe TBI with a normal CT scan if >2 OR 2 of the following features are noted at admission: age >40 years, unilateral or bilateral motor posturing, or SBP <90 mm Hg. Advanced cerebral monitoring Jugular bulb monitoring of AVDO2 may be considered important parameter to reduce mortality and improve outcomes at 3 and 6 mo post-injury. Cerebral perfusion pressure monitoring Management of severe TBI patients using guidelines-based recommendations for CPP monitoring is recommended to decrease 2-wk mortality. MONITORING RECOMMENDATIONS
- 19. Blood pressure thresholds - Maintaining SBP at >100 mm Hg OR equal for patients 50 to 69 years old or at >110 mm Hg or equal or above for patients 15 to 49 or >70 years old may be considered to decrease mortality and improve outcomes. Intracranial pressure thresholds - Treating ICP >22 mm Hg is recommended because values above this level are associated with increased mortality. A combination of ICP values and clinical and brain CT findings may be used to make management decisions. Cerebral perfusion pressure thresholds - The recommended target CPP value for survival and favorable outcomes is between 60 and 70 mm Hg. Whether 60 or 70 mm Hg is the minimum optimal CPP threshold is unclear and may depend upon the autoregulatory status of the patient. Avoiding aggressive attempts to maintain CPP >70 mm Hg with fluids and pressors may be considered because of the risk of adult respiratory failure. Advanced cerebral monitoring thresholds - Jugular venous saturation of <50% may be a threshold to avoid in order to reduce mortality and improve outcomes. THRESHOLD RECOMMENDATIONS
- 20. Diffuse axonal injury CT scan of the brain showing diffuse axonal injury (DAI). Note the deep shearing-type injury in or near the white matter of the left internal capsule (arrow).
- 21. Frontal cerebral contusion CT scan of the brain depicting cerebral contusions. The basal frontal areas (as shown) are particularly susceptible.
- 22. Traumatic epidural hematoma CT scan demonstrating a right epidural hematoma (EDH, arrow). Note the lenticular shape.
- 23. Traumatic subdural hematoma CT scan showing a left acute subdural hematoma (SDH, arrow). Subdural hematomas are typically crescent-shape. In this case the SDH is causing significant mass effect and shift of midline structures to the right.
- 24. Perimesencephalic nonaneurysmal subarachnoid hemorrhage Head CT of three different patients demonstrating subarachnoid hemorrhage in the characteristic pattern of perimesencephalic hemorrhage with blood in the interpeduncular and ambient cisterns.
- 25. Intracerebral Hemorrhage CT obtained less than six hours from symptom onset in a patient with spontaneous acute intracerebral hemorrhage. The CT scan shows a hyperdense hemorrhage predominantly in the left frontal lobe.
- 26. SUMMARY TBI encompasses a broad range of pathologic injuries of varying clinical severity. TBI is universally categorized as mild, moderate, and severe based on GCS. The pathophysiology of TBI includes primary and secondary brain injury. The pathoanatomical sequelae of primary TBI include intra- and extra parenchymal hemorrhages and DAI. Secondary TBI results from a cascade of molecular injury mechanisms and can be exacerbated by modifiable systemic events such as hypotension, hypoxia, fever, and seizures Surgical treatment of primary brain injury lesions is central to the initial management. Likewise, the identification, prevention, and treatment of secondary brain injury is the principle focus of neurointensive care management.
- 27. NO QUESTIONS! JUST SELF HELP! INDIAN JOURNAL OF NEUROTRAUMA BRAIN TRAUMA FOUNDATION GUIDELINES 2016 UPTODATE NEUROTRAUMA TEXTBOOKS
Editor's Notes
- — A cascade of molecular injury mechanisms that are initiated at the time of initial trauma and continue for hours or days. These lead in turn to neuronal cell death and to cerebral edema with increased ICP that can further exacerbate the brain injury. Mimics like ischemic cascade in acute stroke. These various pathways of cellular injury have been the focus of extensive preclinical work into the development of neuroprotective treatments to prevent secondary brain injury in TBI. No clinical trials of these strategies have demonstrated clear benefit in patients. However, a critical aspect of ameliorating secondary brain injury after TBI is the avoidance of secondary brain insults, which would otherwise be well-tolerated but can exacerbate neuronal injury in cells made vulnerable by the initial TBI. Examples include hypotension and hypoxia (which decrease substrate delivery of oxygen and glucose to injured brain), fever and seizures (which may further increase metabolic demand), and hyperglycemia (which may exacerbate ongoing injury mechanisms). &lt;number&gt;
- &lt;number&gt;
- as measured by the GOS-E score at 6month post-injury in severe TBI patients with diffuse injury (without mass lesions), and with ICP elevation to values 20mmHg for &gt;15 min within 1 hr period that are refractory to first-tier therapies. &lt;number&gt;
- Shearing mechanisms lead to diffuse axonal injury (DAI), which is visualized pathologically and on neuroimaging studies as multiple small lesions seen within white matter tracts . Severe DAI presents with profound coma without elevated ICP, and often have poor outcome. This typically involves the gray-white junction in the hemispheres, with more severe injuries affecting the corpus callosum and/or midbrain. MRI (in particular diffusion tensor imaging) is more sensitive than CT for detecting DAI, and the sensitivity of the test declines if delayed from the time of injury. &lt;number&gt;
- Focal cerebral contusions are the most frequently encountered lesions. Contusions are commonly seen in the basal frontal and temporal areas, which are susceptible due to direct impact on basal skull surfaces in the setting of acceleration/deceleration injuries. Coalescence of cerebral contusions or a more severe head injury disrupting intraparenchymal blood vessels may result in an intraparenchymal hematoma. &lt;number&gt;
- Extra-axial (defined as outside the substance of the brain) hematomas are generally encountered when forces are distributed to the cranial vault and the most superficial cerebral layers. These include epidural, subdural, and subarachnoid hemorrhage. In adults, epidural hematomas (EDH) are typically associated with torn dural vessels such as the middle meningeal artery, and are almost always associated with a skull fracture. EDHs are lenticular-shaped and tend not to be associated with underlying brain damage. For this reason, patients who are found to have EDHs only on CT scan may have a better prognosis than individuals with other traumatic hemorrhage types. &lt;number&gt;
- •Subdural hematomas (SDH) result from damage to bridging veins, which drain the cerebral cortical surfaces to dural venous sinuses, or from the blossoming of superficial cortical contusions. They tend to be crescent-shaped and are often associated with underlying cerebral injury. &lt;number&gt;
- •Subarachnoid hemorrhage (SAH) can occur with disruption of small pial vessels and commonly occurs in the sylvian fissures and interpeduncular cisterns. Intraventricular hemorrhage or superficial intracerebral hemorrhage may also extend into the subarachnoid space. &lt;number&gt;
- •Intraventricular hemorrhage is believed to result from tearing of subependymal veins, or by extension from adjacent intraparenchymal or subarachnoid hemorrhage. &lt;number&gt;