Rapid review and management of TRAUMATIC BRAIN INJURY.pptx

A rapid review for post graduate general surgery residents, for university exams

1. TRAUMATIC BRAIN INJURY Nabin Paudyal Resident, General Surgery Nobel Institute of Neurosciences

2. Introduction Major source of health loss and disability. Global burden of disease (GBD) study reports 2016 Annual incidence  27.08 million Global prevalence: 55. million Increasing in countries with middle socio-demographic indices ( 21.8 %). Fall is the main mechanism of trauma followed by road traffic accidents.

3. What is TBI? Alteration in brain function or evidence of brain pathology, caused by an external force. External force that may result in TBI include Head being struck by an object Head striking an object Acceleration-deceleration of the brain without direct external impact Penetration injury Blast/explosion Other forces yet to be defined.

4. Classification of TBI Can be classified in terms of clinical severity, mechanism of injury and pathophysiology Classification on the basis of clinical severity scores: A. Based on Glasgow Coma Scale (GCS) Mild injury (GCS of 13-15) Moderate injury (GCS 9-12) Less injury (GCS <8) B. Full Outline of Unresponsiveness Score (FOUR score)

5. Classification of TBI Can be classified in terms of clinical severity, mechanism of injury and pathophysiology Classification on the basis of clinical severity scores: C. Neuroimaging scales: 1. Marshall Scale

6. Classification of TBI Can be classified in terms of clinical severity, mechanism of injury and pathophysiology Classification on the basis of clinical severity scores: C. Neuroimaging scales: 2. Rotterdam Scale

7. Pathophysiology of TBI-related brain injury Current clinical approaches in the management of TBI revolves around surgical treatment of primary brain injury lesions (subdural and epidural hematomas) and identification, prevention and treatment of secondary brain injury. Primary brain injury: At time of trauma Due to direct impact Acceleration/deceleration injury Penetration injury Blast waves Transfer of external mechanical forces to intracranial contents  combination of focal contusions, hematomas as well as shearing of white matter tracts (DAI)

8. Epidural hemorrhage Rupture of MMA a/w skull fracture Subdural hemorrhage Extra-axial hematomas Rupture of bridging veins/ progression of superficial cortical contusions

9. Sub-arachnoid hemorrhage Following disruption of small pial vessels and occurs in sylvian fissures, interpeduncular cisterns. Intraventricular hemorrhage and superficial ICH may also extend into subarachnoid space Extra-axial hematomas

10. Intraventricular hemorrhage Following tearing of sub-ependymal veins or by extension from adjacent intraparenchymal/ SAH. Extra-axial hematomas

11. Pathophysiology of TBI-related brain injury Secondary brain injury: Occurs due to molecular injury in the neurons initiated at the time of initial trauma and continue for hours or days. Mechanisms during the secondary brain injury may be Neurotransmitter-mediated excitotoxicity causing glutamate, free radical injury to cell membranes Electrolyte imbalances Mitochondrial dysfunction Inflammatory responses Apoptosis Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury

12. Management of TBI Focused to minimize effects of Primary Brain Injury

13. Initial evaluation and treatment Pre-hospital Prevent hypotension and hypoxia [associated with poor prognosis: OR 2.67 and 2.14 respectively] Pre-hospital airway management: Includes endotracheal intubation GCS <9 SpO2 < 90 despite O2 BP monitoring Prevention of hypotension Adequate fluid resuscitation using isotonic crystalloids Neurologic assessment Stabilize and immobilize spine during transport Consider spinal fracture and take precautions

14. Initial evaluation and treatment 1. Emergency department  As per ATLS protocols ET intubation in patients with GCS <9, inability to protect airway, inability to maintain Spo2>90 despite supplemental O2, patient with signs of herniation Vitals sings monitoring. Hypoxia, hypoventilation, hyperventilation and hypotension are avoided Assess for other systemic trauma as per ATLS protocol Detailed neurologic examination should be completed as soon as possible to determine the severity of TBI. ICP monitoring should begin in ED as soon as possible CBC, blood count, electrolytes, glucose, coagulation parameters, blood alcohol level and urine toxicology should be checked.

15. 2. Anti-fibrinolytic therapy Initiate tranexamic acid therapy within three hours of injury. Indicated for GCS >8 and <13. Tranexamic acid 1 gram infusion over 10 minutes, followed by IV infusion of 1 gram over eight hours

16. 3 . Neuroimaging A non-contrast CT  Detect skull fractures, intracranial hematomas, cerebral edema Obtain head CT in all patients with GCS 14 or lower Follow up CT performed in instances of clinical deterioration. In absence of clinical deterioration, repeat imaging in 6 hours time in patients with hematoma 4. Screening for blunt cerebrovascular injury Rule out Blunt Cerebrovascular injury (BCVI) [based on Denver Criteria] High risk patients for BCVI undergo multislice CT angiography of head and neck Initiate Aspirin 81 mg in BCVI patients

17. Surgical Treatment Indications Low GCS scale Findings on head CT  hematoma volume  thickness  evidence of mass effect including midline shift

18. a. Extradural hematoma (EDH) Indications of surgery in EDH patients include Focal signs or symptoms attributable to EDH Coma [GCS<9] and pupillary abnormalities due to EDH Large hematoma volume (>30 ml) Hematoma causing elevated ICP or neurological deterioration. For patients who are awake and have no focal neurological deficits Hematoma >30 ml Clot thickness >15 mm Midline shift > 5mm Surgery technique  Craniotomy with hematoma evacuation Craniectomy may be done in cases with significant cerebral edema or midline shift Timing Within 1 -2 hours after head trauma or the onset of neurologic deterioration for comatose patients with acute EDH and signs of brain herniation

19. a. Extradural hematoma (EDH) Non-operative management Mild EDH patients (monitored in an inpatient setting) Thorough neurologic assessment (including GCS) should be performed every hourly Repeat CT scan within 7-8 hours after original CT scan Raised Intracranial pressure may require urgent intervention managed with hematoma evacuation, hyperventilation and osmotic diuresis (mannitol or hypertonic saline)

20. b. Subdural hematoma (SDH) Indications of surgery: >10mm in thickness Associated midline shift > 5mm on CT regardless of GCS GCS < or equal to 8 GCS has decreased by> or equal to 2 points from the time of injury to hospital admission If patient has asymmetric or fixed and dilated pupils ICP > 20 mmHg c. Intracerebral hemorrhage Indications of surgery: If posterior cranial fossa  Mass effect seen (obliteration of fourth ventricle, effacement of basal cisterns, brain stem compression) If cerebral hemisphere hemorrhage >50 ml, GCS 6 to 8 with frontal or temporal hematoma >20 ml with midline shift of 5mm and/or cisternal compression on CT scan

21. d. Depressed skull fracture Indications of surgery: Depression greater than the thickness of cranium Dural penetration Significant intracranial hematoma Frontal sinus involvement Cosmetic deformity Wound infection or contamination Pneumocephalus e. Refractory intracranial hypertension Decompressive hemicraniectomy

22. Management in ICU Prevention of Secondary brain injury

23. Principal focus for severe TBI is to limit secondary brain injury. Treatment efforts are aimed at intracranial pressure management and maintenance of cerebral perfusion BP management, temperature, blood glucose, seizure prevention are other important damage preventive measures.

24. a. Hemodynamic monitoring Isotonic fluids to be used  Normal saline preferred SMART-ICU trial  no benefit seen in patients with balanced crystalloids Avoidance of hypotension should be the priority. Preferred SBP > 100 mmHg Cerebral perfusion pressure  60-70 mmHg is recommended b. Ventilation Most patients are sedated and artificially ventilated ETCO2 monitoring should be used for monitoring in all ventilated patients PaO2 should be maintained above 60 mmHg. Hyperventilation should be avoided As increased PEEP is associated with increased ICP  Maintain PEEP up to 15-20 cm H2O in cases with ARDS with TBI

25. c. Antiseizure medications and EEG monitoring Antiseizure medications are generally recommended to prevent post traumatic seizures. Levetiracetam is generally recommended. Duration  Not established Used to prevent status epilepticus, systemic injury due to seizure, reduce/prevent raise in ICP. d. Venous thromboembolism prophylaxis Mechanical prophylaxis  Intermittent pneumatic compression on admission Chemoprophylaxis UFH (5000 U) three times daily OR enoxaparin 40 mg OD

26. e. Management of glucose Avoid hypo- and hyperglycemia Target range of 140-180 mg/dl. Optimal recommended level of glucose has not been studied. f. Temperature management Fever aggravates secondary brain injury, worsens ICP control Maintain normothermia Antipyretics, surface cooling devices g. Nutritional management Nutritional supplementation should begin within five to seven days. Transpyloric enteral nutrition may be considered Early nutrition rates have shown to decrease rates of pneumonia, mortality and hospital stay in some trials

27. Management of Intracranial Pressure

28. Initial management Identify patients at risk of impending herniation Signs include  pupillary asymmetry, unilateral or bilateral fixed and dilated pupil, decorticate and decerebrate posturing, respiratory depression, Cushing triad (bradycardia, irregular respiration, hypertension)

29. Prognosis Cohort studies show that patients with severe head injury have 30 percent mortality risk 30-65 percentage of patients with severe TBI will regain independence 5-15 percent patients with severe TBI are discharged from acute care in vegetative state Independent Risk factors for prognosis:

30. Prognosis risk models CRASH prediction model IMPACT model

31. Thankyou….