- 1. ALI AL-BUSAIDIR4 APPROACH TO TRAUMATIC BRAIN INJURY
2. OUTLINES
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.
4. ETIOLOGY
- Falls 20-30% (infants, children, elderly)
- Sports and recreational - 10-20%
5. DEFINITIONS
- Injury is clinicallyevident on physical examination.
- Not always clinically evident.
6. CLASSIFICATION
- Leading Cause - MVAapprox. 28-50%
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)
- Bleeding diathesis (low platelet count, abnormal
coagulation
11. PATHOPHYSIOLOGY
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
- tend not to be associated with underlying brain damage
17. 18. Subdural hematomas
- result from damage to bridging veins
- 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
- Mitochondrial dysfunction
- Secondary ischemia from vasospasm, focal microvascular
occlusion, vascular injury
23. 24.
- hypoxia -- decrease substrate delivery of oxygen and glucose to
injured brain
- seizures -- mayincrease metabolic demand
25. CUSHING'S REFLEX
- is seen in only one third of cases of life-threatening
increased ICP.
- 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
37. 38. 39. 40.
- Depressed level of consciousness
- Progressive , severe headache
- Severe nausea or vomiting
- Alcohol or drug intoxication
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