Approach to traumatic brain injury
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Transcript of Approach to traumatic brain injury
- 1. ALI AL-BUSAIDIR4 APPROACH TO TRAUMATIC BRAIN INJURY
2. OUTLINES
- Introduction
- Definition
- Pathophysiology
- Severe head injury
- Minor head injury
- Second impact syndrome
- Cerebral herniation
3. INTRODUCTION
- Traumatic brain injury (TBI) encompasses a broad range of pathologic injuries to the brain of varying clinical severity that result from head trauma.
- MVC ---- young
- Fall ---- elderly
4. ETIOLOGY
- MVAapprox. 28-50%
- Falls 20-30% (infants, children, elderly)
- Assaults 9-10%
- Sports and recreational - 10-20%
5. DEFINITIONS
- Head injury:
- Injury is clinicallyevident on physical examination.
- Traumatic brain injury:
- Not always clinically evident.
6. CLASSIFICATION
- Clinical severity scores
- Neuroimaging scales
- Leading Cause - MVAapprox. 28-50%
- 0-20%
7. 8. 9.
- PROGNOSISCohort studies have suggested that patients with severe head injury (GCS 8) have about a 30 percent risk of death and only about 25 percent achieve long-term functional independence .
10.
- Specific outcome predictors include :
- GCS at presentation (especially the GCS motor score)
- CT findings (subarachnoid hemorrhage, cisternal effacement, midline shift)
- Pupillary function
- Age
- Associated injuries
- Hypotension
- Hypoxemia
- Pyrexia
- Elevated ICP
- Reduced CPP
- Bleeding diathesis (low platelet count, abnormal coagulation
11. PATHOPHYSIOLOGY
- primary brain injury
- secondary brain injury.
12. PRIMARY BRAIN INJURY
- occurs at the time of trauma.
- Common mechanisms include direct impact, rapid acceleration/deceleration, penetrating injury, and blast waves.
- The damage that results includes a combination of focal contusions and hematomas, as well as shearing of white matter tracts (diffuse axonal injury) along with cerebral edema and swelling.
13. 14. Diffuse axonal injury
- 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.
- present with profound coma without elevated intracranial pressure (ICP), and often have poor outcome.
- Involves the gray-white junction in the hemispheres
15. 16. Epidural hematomas
- Typically associated with torn dural vessels such as the middle meningeal artery
- are almost always associated with a skull fracture
- are lenticular-shaped
- tend not to be associated with underlying brain damage
17. 18. Subdural hematomas
- result from damage to bridging veins
- Are crescent-shaped
- are often associated with underlying cerebral injury
19. 20. Subarachnoid hemorrhage
- can occur with disruption of small pial vessels
- commonly occurs in the sylvian fissures and interpeduncular cisterns.
- may also extend into the subarachnoid space .
21. Intraventricular hemorrhage
- Is believed to result from tearing of s ubependymal veins, or by extension from adjacent intraparenchymal or subarachnoid hemorrhage.
22. SECONDARY BRAIN INJURY
- a cascade of molecular injury mechanisms :
- 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
23. 24.
- Examples:
- hypotension
- hypoxia -- decrease substrate delivery of oxygen and glucose to injured brain
- fever
- seizures -- mayincrease metabolic demand
- hyperglycemia
25. CUSHING'S REFLEX
- is seen in only one third of cases of life-threatening increased ICP.
- Triad of:
- hypertension
- bradycardia
- diminished respiratory effort
26. INITIAL EVALUATION AND TREATMENT 27. Prehospital
- The primary goal of prehospital management for severe head injury is to prevent hypotension and hypoxia
- Early endotracheal intubation is generally recommended for patients with a GCS of 8 or less if performed by well-trained personnel.
- If this expertise is not available, bag-mask ventilation is recommended.
28. Prehospital
- In a meta-analysis of clinical trials and population-based studies , hypoxia (PaO2 90 mm Hg)
- Vital signs including heart rate, blood pressure, respiratory status (pulse oximetry, capnography), and temperature require ongoing monitoring.
32. Emergency department
- A neurologic examination should be completed as soon as possible
- Neurologic status should be continuously assessed. Deterioration is common in the initial hours after the injury.
33. 34. Emergency department
- The patient should be assessed for other systemic trauma.
- evaluate and manage increased intracranial pressure
- A complete blood count, electrolytes, glucose, coagulation parameters, blood alcohol level, and urine toxicology should be checked if indicated
35. Neuroimaging
- Computed tomography (CT) is the preferred imaging modality in the acute phase of head trauma
- should be performed as quickly as possible
- CT scan will detect skull fractures, intracranial hematomas, and cerebral edema
36. Neuroimaging
- Risk stratification
37. 38. 39. 40.
- LOC
- PTA
- Depressed level of consciousness
- Progressive , severe headache
- Severe nausea or vomiting
- Alcohol or drug intoxication
- Age 3 feet
- or five stairs)
42. NEW ORLEAN CRITERIA 43. COMPARISON OF THE CANADIAN CT HEAD RULE AND THE NEW ORLEANS CRITERIA IN PATIENTS WITH MINOR HEAD INJURY
- Design, Setting, and PatientsIna prospective cohort study (June 2000-December 2002)that included 9 emergency departments in large Canadian community and university hospitals, the CCHR was evaluated in a convenience sample of2707 adultswho presented to the emergency department with blunt head trauma resulting inwitnessed loss of consciousness ,disorientation, or definite amnesia and a GCS score of 13 to 15 . The CCHR and NOC were compared in a subgroup of 1822 adults with minor head injury and GCS score of 15.
- JAMA. 2005;294:1511-1518.
44. COMPARISON OF THE CANADIAN CT HEAD RULE AND THE NEW ORLEANS CRITERIA IN PATIENTS WITH MINOR HEAD INJURY
- ResultsAmong 1822 patients with GCS score of 15, 8 (0.4%) required neurosurgical intervention and 97 (5.3%) had clinically important brain injury.The NOC and the CCHR both had 100% sensitivity but the CCHR was more specific (76.3% vs 12.1%,P 70 mm Hg and