Traumatic Brain Injury TBI Presented by Bill Masten

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3 Cerebrum two hemispheres and four lobes. Cerebellum (little brain) coordinates the back and forth ballet of motion. It judges the timing of every movement precisely. Brainstem coordinates the bodies automatic and reflex activities. 3

4 Five layers to the scalp. Skull is from ¼ to 1/8 in thickness. Three layers to the dura (periosteal dura sinus meningeal) Dura matter extends into the cranial cavity in several locations (dura folds) to provide stabilization and support to the brain. Much like a seatbelt provides protection for persons in a car. Arachnoid (spider mother) delicate network of collagen and elastic fibers. Subarachnoid space filled with CSF that buffers the brain and act like a shock absorber. Pia (delicate mother) firmly attached to the brain and follows every fold and all branches of cerebral blood vessels. 4

5 Somatosensory turns touch into perception. Our sense of body position. Temporoparietal helps us figure out what s on someone's mind. Responsible for out of body experences. 5

6 Basic decisions on movement coordination. Decision to the action. 6

7 4 6 oz of CSF..Brain about 3+ pounds.floating in CSF is less then 2 oz. 7

8 Basic impulses, anger fear hunger pleasure. Heart of instinct emotion desire. Hippocampus spatial awareness memory recall. Amygdala negative emotions fearhatred. Cingulate cortex about how you think of yourself in relation to others and how you respond. Hypothalamus helps regulate the autonomic nervous system and endocrine system homeostasis. 8

9 Transmits information between left and right hemispheres. Signaling super highway is a thick band of white matter. 9

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11 Considered a clinical diagnosis. Physiologic injury to the brain without any structural alteration. Temporary LOC lasting seconds to hours. Amnesia confusion headachedizziness anxiety nausea vomiting. Can show loss of reflexes, brief periods of apnea and bradycardia during the initial LOC. Usually fully recover without long term deficits. Graded on scale 1 5, 5 the most severe. 11

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14 20 30% are to the frontal temporal lobes. Directly under the area of impact and possibly to the opposite side, coup contracoup reaction. Initially injuries the grey matter but then migrates to the white matter. Petechial hemorrages, edema swelling. Focal neurologic deficits, prolonged confusion and possible coma. Severe injury. 14

15 Axons transmit signals to the neurons. Protective white myelin sheath (therefore white matter) is sheared disrupting communication among neurons. Car accidents, falls from bicycles, slip and falls, rapid acceleration deceleration acute changes of momentum events, violent shaking (shaken baby syndrome). Difficult to predict how a person will affected from this injury. Can be temporary or permanent disruption. Can lead to I.C.P. High mortality rate based on the length of unconsciousness. 15

16 Hemorrhage into one or more of the ventricles. Blocks flow of CSF and venous cerebral blood return. Causes ICP and herniation. Permanent neurological injury is common 16

17 Intracranial components: Cerebral blood flow=10% CSF=3%, brain=87%. ICP occurs in 25 45% of stbi. Cushing s triad increase B/P sometimes widening pulse pressure to maintain CBF bradycardia in response irregular respirations. 17

18 Shearing force tearing the subarachnoid vessels. Usually a slow bleed. Diffuse headache (worst headache ever), photophobia, vomiting, LOC, neck stiffness. Might shows signs and symptoms days after the traumatic event. 18

19 More common then epidural bleeds, Occurs in about 33% of head injury patients. 50/50% between simple and complex bleeds. Usually very slow venous bleeding that cannot present for weeks even months. Headache, declining mental status and unilateral weakness. Elderly and chronic alcoholics are at a higher risk due to brain atrophy and more space for the brain to shift further during traumatic events. 19

20 Uncommon, 1% of all head trauma, most common area is the temporal/parietal regions damaging the medial meningeal artery or dura sinus. Skull fractures present in 76 85%. Usually arterial bleed. 1/3 of these patients will present with the classic LOC Lucid state neurologic decline. Confusion seizure severe headache nauseavomiting. Mortality increases with delay to neuro specialty center and intervention. 20

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22 FINR Brain app for anatomy 22

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26 ETCO2 is 1 2 mm less then PaCO2 or about 5%. 1 out of 6 patients will vomit. Vomiting does appear to correlate to an increase in ICP. 26

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29 Solid GCS documentation frequently. PTA anterograde/retrograde. Pupil size and reactivity frequently assessed individually and 10 seconds between each eye (pupils may regain reactivity once systemic hypoxia is managed). Document eye movement, requires coordination from multiple center of the brain. Abnormal respirations common in TBI. Ataxic Cheyne Stokes CNH Biot s are some. You can draw a diagram of the rhythm and depth. Also document repetitive respiratory reflexes like yawningcoughing. Hyperbaric oxygen, hypertonic saline (7.5%) and therapeutic hypothermia are under evaluation currently. 29

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