Response of Brain Tissue to Trauma
- occurs at cellular level
1. Injury:
-causes massive vasodilation
- causes changes in permeability of capillary walls
- fluid leaks into interstitial carebral tissues which leads to:
2. Cerebral Edema:
- fluid from brain vessels migrates into cerebral tissues; therefore increase in size and
volume or brain; whichleads to increased pressure
**** Increase in ICP: increase in pressure in Cranial Cavity!
Cranial Cavity:
1. Cerebral tissue: 80%
2. Blood: 10%
3. CSF: 10%
CHANGES IN ANY OF THESE LEADS TO INCREASE IN ICP!!
Normal ICP:
4-15 mmHg
- fluctuates
- measured with SENSORS
ICP; BP; & CPP:
- need O2 and Glucose
1. BP: eg. 120/80; therefore Mean is 100
Mean Arteriole Pressure (MAP) needs to be higher than ICP
2. CPP: to overcome ICP; therefore there is delivery of O2 and nutrients
SWELLING CAUSES INCREASED ICP.
MAP = Driving Force
ICP = Resistence
CPP = MAP - ICP
= 100 mmHg - 15 mmHg; This is a NORMAL reading
- therefore the CPP that is NORMAL is: 85 mmHg
Regulatory Mechanisms
Protect brain from increases in ICP by maintaining CPP
1. Pressure Autoregulation:
Maintains CPP:
eg. EXERCISE increases BP which leads to
Vasoconstriction
eg. ORTOSTATIC HYPERTENSION decreases BP which
leads to Vasodilation
Problems:
1. Systolic BP increases >150 mmHg which leads to zero AUTOREGULATION which
leads to H/A (Tension)
2. Increased ICP > 30-33 mmHg leads to zero AUTOREGULATION; therefore
decreased blood flow to brain; therefore increased ICP from cerebral edema; which
leads to poor perfusion and ultimately brain damage/death
2. Metabolic Regulation
Cerebral blood vessels sensitive to:
i) PCO2
ii) PO2
iii) Temperature
Vasodilation occurs when:
i) oxygenation poor (decreased PO2)
ii) Resps fail (increased PCO2)
iii) Fever
iv) Acidosis
WHY??? Dilation!
NSG:
Keep: PCO2 low; PO2 high; Temp normal or low
WHAT HAPPENS WHEN ICP IS SUSTAINED?
1. Body compensates initially (if ICP is at 20 mmHg > 10 minutes)
2. CSF production decreases; then CSF absorption increases
3. Decreased BS to brain leads to decreased volume
4. Babies: Skull expands
5. Compression of brain tissue
6. CUSHING'S TRIAD (opposite of shock)
- decreased HR and RR; increased BP
THEREFORE INCREASED ICP WHICH LEADS TO
DECOMPENSATION!!!!
Steps of Decompensation:
1. Increased ICP
2. Decreased cerebral blood flow
3. Brain ischemia
4. Cerebral vasodilation: increased CO@, decreased O2
5. Cerebral edema
6. Increased ICP+++
7. Brain tissue compressed
8. Blood vessels compressed which leads to more increased ICP
9. Brain death
Nursing Care Increased ICP
1. Assessment: SUBTLE changes
2. LOC: increased agitation, restlessness, personality changes
decreased alertness: WHY? Cerebral hypoxia!
3. Pupil reaction: unequal (because increased ICP)
4. Motor strength and function:
First: Spontaneous
Second: if not alert --- test response to stimuli (eg. tickle;
increase pressure; NO PAINFUL
STIMULI!!!
5. Vital signs: Problems with increased ICP before changes in VS: Increased ICP =
decreased HR, increased BP, wide pulse pressure
6. Vomiting/H/A:
- vomiting: pressure on vomiting centre
- H/A: increased pressure on pain sensitive arterioles
7. Suctioning: BE CAREFUL
8. Increase HOB
9. Positioning
10. Pain control
11. Turn slowly
12. Reassure
13. Careful discussion
14. Therapeutic touch