Traumatic brain injury lecture g
- 1. TRAUMATIC BRAIN INJURY What really matters!!! Riyadh Abdullah Almogahed ICU resident AQSH.
- 2. THE INCREDIBLE STORY OF HOLT
- 3. Traumatic brain injury (TBI) 1-a non-degenerative, non-congenital insult to brain from an External mechanical force, 2-permanent or temporary impairment of physical, and psychosocial functions, diminished altered state of consciousness. 3-(GCS)(1) within 48 hours as being severe GCS= 8, moderate GCS = 9-12, mild GCS= 13-15. (2)
- 4. Modes of injuries to the brain include: Road Traffic Accidents "RTA“ 50%. Falls 20-30% of total cases of TBIs. Persons aged 75 years and older . Pediatric age group also frequently withstands TBI due to falls. Firearms cause 12% of TBI Occupation related TBIs cause 45-50% of all TBIs. Drug abuse and Alcohol are main causes of TBIs and are often associated with the leading causes of TBI namely RTAs, and fall from heights
- 5. PATHOLOGY OF TBI: (1) Primary injury, which takes place immediately after trauma (2) Secondary injury, a process which starts at the time after trauma and produces effects that may continue for a long time
- 6. TYPES OF TBI: SKULL FRACTURES CONTUSIONS “COUP AND COUNTERCOUP” INTRACRANIAL HEMORRHAGES: EDH/SDH/ICH/SAH/IVH CONCUSSION DIFFUSE AXONAL INJURY
- 7. GENERAL PATHOPHYSIOLOGY: initial phases second stage SPECIFIC PATHOPHYSIOLOGY: CEREBRAL BLOOD FLOW HYPOPERFUSION AND HYPERPERFUSION CEREBROVASCULAR AUTOREGULATION AND CARBON DIOXIDE (CO2) REACTIVITY CEREBRAL VASOCONSTRICTION. CEREBRAL METABOLIC DYSREGULATION: OXIDATIVE STRESS AND EXCITOTOXICITY:
- 8. CEREBRAL TISSUE EDEMA: INFLAMMATION NECROSIS VS APOTOSIS:
- 10. DIAGNOSTICS IN TBI SKULL RADIOGRAPH CT BRAIN : BONE WINDOW,BRAIN WINDOW, SUBDURAL WINDOW MRI, MRA, MRV ANGIOGRAPHY FLUID BIOMARKERS !
- 11. Midline shift Cisterns High or mixed density lesion Notes I None Present None No visible pathology on CT scan II 0-5 mm Present None III 0-5mm Compressed or absent None Swelling IV >5 mm None V Any Any Any Any lesion surgically evacuated VI >25 cm cubic Not surgically evacuated Marshall CT classification in Traumatic brain injury
- 12. ADRENERGIC HYPERACTIVITY: TBI in particular leads to immediate and profound SNS activation with massive release of both central and peripheral catecholamine. Detrimental effect on cardiovascular, respiratory, inflammation. Paroxysmal sympathetic hyperactivity: 1-Hyperthermia; 2-Tachycardia; 3-Tachypnea; 4-Agitation, 5-Diaphoresis. 6-Dystonia
- 13. GUIDELINES FOR THE MANAGEMENT OF SEVERE TRAUMATIC BRAIN INJURY 4TH EDITION SEPTEMBER 2016
- 14. MANAGEMENT OF TRAUMATIC BRAIN INJURY 1.Decompressive Craniectomy: A LARGE frontotemporoparietal DC is recommended over a small frontotemporoparietal DC for reduced mortality and improved neurologic outcomes in patients with severe TBI
- 15. 2.Prophylactic Hypothermia Early (within 2.5 hours), short-term (48 hours post-injury) prophylactic hypothermia is not recommended to improve outcomes in patients with diffuse injury
- 16. 3. Hyperosmolar Therapy While mannitol was previously thought to reduce intracranial pressure through simple brain dehydration, both mannitol and hypertonic saline work to reduce intracranial pressure, at least in part, through reducing blood viscosity, leading to improved microcirculatory flow of blood constituents and consequent constriction of the pial arterioles, resulting in decreased cerebral blood volume and intracranial pressure
- 17. 3. Hyperosmolar Therapy Although hyperosmolar therapy may lower intracranial pressure, there was insufficient evidence about effects on clinical outcomes to support a specific recommendation, or to support use of any specific hyperosmolar agent, for patients with severe traumatic brain injury.
- 18. 4. Cerebrospinal Fluid Drainage An EVD” external ventricular drainage” 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 Glasgow Coma Scale (GCS) <6 during the first 12 hours after injury may be considered
- 19. 5. Ventilation Therapies Normal ventilation is currently the goal for severe TBI patients in the absence of cerebral herniation and normal partial pressure of carbon dioxide in arterial blood (PaCO2) ranges from 35-45 mm Hg.
- 20. 5. Ventilation Therapies Low PaCO2, therefore, results in low CBF and may result in cerebral ischemia while high PaCO2 levels can result in cerebral hyperemia and high intracranial pressure (ICP). Therefore, providing optimal CBF is important under normal and abnormal conditions. Prolonged prophylactic hyperventilation with partial pressure of carbon dioxide in arterial blood (PaCO2) of 25 mm Hg or less is not recommended.
- 21. 6. Anesthetics, Analgesics, and Sedatives • Administration of barbiturates to induce burst suppression measured by EEG as prophylaxis against the development of intracranial hypertension is not recommended. • High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment. Hemodynamic stability is essential before and during barbiturate therapy. • Although propofol is recommended for the control of ICP, it is not recommended for improvement in mortality or 6- month outcomes. Caution is required as high-dose propofol can produce significant morbidity.
- 22. 7. Steroids The use of steroids is not recommended for improving outcome or reducing ICP. In patients with severe TBI, high-dose methylprednisolone was associated with increased mortality and is contraindicated.
- 23. 8. Nutrition Feeding patients to attain basal caloric replacement at least by the fifth day and, at most, by the seventh day post-injury is recommended to decrease mortality. Transgastric jejunal feeding is recommended to reduce the incidence of ventilator-associated pneumonia. A moderate approach to insulin therapy should be adopted as the practice of “tight glucose control” could have deleterious effects in patients with severe TBI
- 24. 9. Infection Prophylaxis Early tracheostomy is recommended to reduce mechanical ventilation days. However, there is no evidence that early tracheostomy reduces mortality or the rate of nosocomial pneumonia. The use of povidone-iodine oral care is not recommended to reduce VAP and may cause an increased risk of acute respiratory distress syndrome. Antimicrobial-impregnated catheters may be considered to prevent catheter-related infections during EVD..
- 25. 10. Deep Vein Thrombosis Prophylaxis Low molecular weight heparin (LMWH) or low-dose unfractioned heparin may be used in combination with mechanical prophylaxis. However, there is an increased risk for expansion of intracranial hemorrhage. In addition to compression stockings, pharmacologic prophylaxis may be considered if the brain injury is stable and the benefit is considered to outweigh the risk of increased intracranial hemorrhage. There is insufficient evidence to support recommendations regarding the preferred agent, dose, or timing of pharmacologic prophylaxis for deep vein thrombosis
- 26. 11. 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 days of injury). At the present time there is insufficient evidence to recommend levetiracetam over phenytoin regarding efficacy in preventing early post-traumatic seizures and toxicity
- 27. 15. Blood Pressure Thresholds Maintaining systolic blood pressure SBP at ≥100 mm Hg for patients 50 to 69 years old or at ≥110 mm Hg or above for patients 15 to 49 or over 70 years old may be considered to decrease mortality and improve outcomes. (211)
- 28. 16. Intracranial Pressure Thresholds Treating ICP above 22 mm Hg is recommended because values above this level are associated with increased mortality. (211)
- 29. 17. Cerebral Perfusion Pressure Thresholds: The recommended target cerebral perfusion pressure (CPP) value for survival and favorable outcomes is between 60 and 70 mm Hg. Avoiding aggressive attempts to maintain CPP above 70 mm Hg with fluids and vasopressors may be considered because of the risk of adult respiratory failure.
- 30. THE LUND THERAPY: 1) Stress reduction with adequate sedation and catecholamine blockade; 2) Maintenance of euvolemia through the use of erythrocyte transfusion and maintenance of a normal albumin level; 3) Preservation of cerebral perfusion pressure (60–70 mm Hg for adults and 40–55 mm Hg for children and adolescents); 4) Avoidance of cerebrospinal drainage; 5) Use of early nutrition; and 6) Use of mechanical ventilation to promote normal oxygenation and ventilation.
- 31. THE LUND THERAPY: In part the protocol advocated by the group from Lund emphasizes the use of metoprolol, a selective beta1- antagonist, and clonidine, an alpha 2-agonist, which are used to limit the posttraumatic hyperadrenergic stress response. Combined, these drugs can be used to lower MABP, hypothetically reducing capillary hydrostatic pressure to the point where fluid filtration halts and reabsorption can occur. Although this induced reduction in MABP may lower cerebral perfusion pressure, the Lund group has used hemodynamic (247) and microdialysis data to suggest that this effect is well tolerated by patients with brain injuries.