11.1 ICP and Mechanisms of Brain Injury Flashcards
Brain Injury
- Caused by trauma, tumors, stroke, metabolic derangements, and degenerative disorders
Pathways
- Ischemia (carbon monoxide poisoning, anemia, stroke, cardiac arrest)
- Cerebral edema
- Injury from ICP
Hypoxia
- Deprivation of oxygen with maintained blood flow
Causes
- Reduced atmospheric pressure, carbon monoxide poisoning, severe anemia, failure to oxygenate blood
- Produces general depressant affect on the brain (euphoria, listlessness, drowsiness, impaired problem solving)
Ischemia
- Greatly reduced or interrupted blood flow
- Interferes with delivery of oxygen and glucose and removal of metabolic waste
Focal
- Only part of the brain is affected (stroke)
Global
- Entire brain is affected (cardiac arrest)
ICP
Cranial Cavity
- 80% brain tissue
- 10% blood
- 10% CSF
All of these contribute to ICP (normal 1-15 mmHg)
Monro-Kellie Hypothesis
- Small increases in volume of one compartment can be compensated for by decrease volume in other compartments
- Changes in one compartment causes changes in other compartments
- Brain contents cannot be compressed
Causes of ICP
- Increased volume in any of the 3 components (tissue, blood, CSF)
Examples
- Tumors, hematomas, stroke, subarachnoid bleeding, hydrocephalus, abscess, TBI
Influences
- Arterial/Venous pressure
- Intraabdominal and Intrathoracic pressure
- Posture
- ABGs
- Temperature (hypothermia)
Causes
CSF
- Hydrocephalus
- Increased production, decreased reabsorption, or both
Blood
- Increased blood volume from vasodilation of cerebral vessels (hypoxia)
- Hypoxia causes decreased blood volume and respiratory rate which leads to vasodilation. This stimulates increased cerebral blood flow and increased ICP
- Intracranial hemorrhage (ICH) or aneurysm can also cause ICP
- Obstruction of venous outflow
Brain Tissue
- Mass (tumor, brain edema, bleeding into brain tissue)
Cerebral Edema
- Cytotoxic (Caused by hypoxia accumulation of intracellular water, cells cannot pump out water of the intravascular space)
- Vasogenic (Changes in vascular permeability with disruption of the BBB, seen in tumors and may be treated with steroids or osmotic agents like mannitol)
Cerebral Edema
Brain Swelling
- Increase in tissue volume secondary to abnormal fluid accumulation
Vasogenic
- Integrity of BBB is disrupted and fluid escapes into ECF that surrounds the brain
- Tumors, prolonged ischemia, hemorrhage, brain injury, infection (meningitis)
- Focal neurologic defects, disturbances in LOC, severe intracranial HTN
Cytotoxic (metabolic) - Increased intracellular fluid
- Hypo-osmotic states (water intoxication, severe ischemia that impairs sodium-potassium pump)
BBB
- Surrounds the brain and acts as a barrier between blood stream and brain
- Only allows water and lipid soluble substances into the brain to prevent toxins and pathogens to cross into the brain
- Tight junctions of endothelial cells is what makes the protection that restrict effusion into the brain
Cerebral Perfusion Pressure
- CPP is the pressure required to perfuse the cells of the brain
- CPP = MAP - ICP
- Normal range 70-90 mmHg
- If Intracranial pressure exceeds mean arterial blood pressure tissue perfusion becomes inadequate and causes cellular hypoxia and possible neuronal death
COMPENSATION OF ICP
- CSF is first displaced
- Next cerebral blood volume and blood flow are altered
- Lastly if these fail brain tissue is displaced (herniation)
MAP
MAP = 1/3 (systolic minus diastolic) plus diastolic
Map less than 50
- Decreased cerebral blood flow
- Cerebral ischemia (syncope, blurred vision)
Map greater than 50
- Disruption of BBB
- Increased cerebral edema
Math
- Ideal CPP is between 70-100
- When CPP drops, autoregulation fails and cerebral blood flow decreases. (basically as ICP goes up blood flow decreases)
- Any CPP below 30 cannot sustain life (minimum of 50-60 is needed)
Stages of ICP
Stage 1
- Vasoconstriction and external compression of venous system
- Reabsorption of CSF to decrease pressure
Stage 2
- Increase in ICP exceeds brains compensatory mechanisms which causes oxygen deprivation and systemic vasoconstriction (to increase MAP above ICP)
- Manifestations include confusion, drowsiness, pupillary/breathing changes
Stage 3
- ICP approaches MAP which causes brain hypoxia and hypercapnia (condition starts to rapidly deteriorate)
- Causes decreased level of arousal
- Cheyne-strokes, hyperventilation, wide pulse pressure, bradycardia, sluggish pupils
Stage 4
- ICP>MABP
- Herniation, pupils dilate, death
Stages of ICP
Compensation Stages (normal appearance/activity)
Stage 1
- Everything is normal (BP, HR, LOC)
Stage 2
- Earliest signs are confusion, restlessness, lethargy (earliest indication of deterioration)
- Everything is still normal (BP, HR)
Decompensation
Stage 3
- Inability to stay awake (vigorous arousal)
- Small pupils
- Progression towards cheyne-strokes, breathing, hyperventilation
- Systolic pressure goes up and diastolic pressure goes down (wide pulse pressure)
- Heart rate slows down and bounding in nature
- REQUIRES INTERVENTION
Stage 4 (herniation)
- Comatose, unlikely to respond
- Pupils are now unequal and dilate on the same side as injury but do not respond to light.
- The end of stage 4, pupils are both dilated and fixed
- Less stable respirations such as Cheyne-strokes breathing, periods of apnea and hyperventilation.
- Pulse pressure remains wide but once herniation occurs it causes irregularities in heart rhythm.
- NOTHING CAN BE DONE MEDICALLY ONCE BRAIN HAS HERNIATED
ICP Levels
Normal - 0-15 mmHg
Compliance
- Ability for the brain tissue to buffer an increase in intracranial volume while avoiding increase in ICP
Manifestations of ICP
- Earliest indicator is change in LOC
- Cranial nerve 3 pupils become non-reactive
- Headache, vomiting, widening pulse pressure, bradycardia, irregular respirations
- LATE SIGNS IS CUSHINGS TRIAD (widened pulse pressure, bradycardia, irregular respirations)
