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Lecture 11

PAT 20A/B Lecture Notes - Lecture 11: Optic Disc, Hyponatremia, DiureticPremium

8 pages114 viewsFall 2015

Department
Pathotherapeutics
Course Code
PAT 20A/B
Professor
Kathryn Ellis
Lecture
11

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PAT 20 Pathotherapeutics
Traumatic Brain Injury
1. Discuss the relationship between ICP, BP, CPP and Cerebral Blood Flow
INTRACRANIAL PRESSURE
Normal ICP is the pressure exerted by the combined total volume of the three
components within the skull: brain tissue (78%); blood (12%); CSF (10%)
o CSF is produced in the ventricles of the
Balance between 3 components maintains intracranial pressure
If 1 component increases then the other 2 must compensate by displacement
for pressure to remain constant = Monroe-Kellie Hypothesis
o The total intracranial volume will not change
If any of the 3 components increases without a corresponding decrease in another component rapid increase
in ICP from the normal range (0-15 mmHg)
If in brain tissue or blood volume, initial response is reduction in CSF to maintain normal pressure
Compensation works only to a point
With further increase in brain tissue volume, venous blood and more CSF is forced out of the skull
Factors Influencing ICP
Blood pressure
Cardiac function
Intra-abdominal and intra-thoracic pressure
Factors Influencing Cerebral Blood Flow
Carbon dioxide (CO2=dilate=ICP)
Oxygen (O2=dilate=ICP)
Hydrogen ion concentration (acid)
CEREBRAL BLOOD FLOW (CBF)
CBF = mls of blood passing through 100mg of brain/min
Within the minute 100 g of brain tissue receives approx. 750 mls blood
Unlike other organs, the brain lacks the ability to store oxygen or glucose, and therefore the maintenance of
adequate blood flow to the brain is critical for neuronal functioning and survival
Autoregulation
The brain's intrinsic ability to regulate its own blood flow in response to its metabolic needs in spite of wide fluctuations
in systemic arterial pressure is termed autoregulation.
Autoregulation is the automatic alteration in the diameter of the cerebral blood vessels to maintain a constant
blood flow to the brain during changes in BP
The purpose of autoregulation is to ensure adequate CBF to meet the metabolic needs of brain tissue and to
maintain cerebral perfusion pressure within normal limits. (Lewis 1636)
Cerebral Blood Flow (CBF) depends on Cerebral Perfusion Pressure (CPP) and Cerebral Vascular Resistance (CVR)
Cerebral Blood Flow = amount of blood per minute to the brain in mls
Cerebral Perfusion Pressure = pressure required to provide adequate cerebral blood flow and oxygenation to
brain tissue
o CPP = MAP (diastolic + 1/3 pulse pressure) ICP
Cerebral autoregulation maintains constant CBF by compensating for changes in ICP unless:
o ICP such that CPP < 40 mm Hg
o MAP > 150 mmHg or < 50 mmHg
o Brain injury/ trauma/brain tissue
Normal ICP: 0-15 mm Hg
Increased ICP: > 20 mm Hg for > 5 minutes results in impaired cerebral perfusion
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2. Determine the etiology of Traumatic Brain Injury (T.B.I.)
TYPES OF TRAUMATIC BRAIN INJURY
Brain injuries are categorized as being mild, moderate, or severe
Mild Brain Injury
GCS 13-15: CONCUSSION
A clinical syndrome characterized by immediate and transient post-traumatic impairment of neural functions,
such as alteration of consciousness, disturbance of vision or equilibrium due to brain stem involvement
o Sudden, brief mechanical head injury with disruption of neural activity
A sudden, forceful impact (low speed) can cause the brain to make contact with the skull, possibly leading to
bleeding in or around the brain or microscopic nerve fiber damage
o No break in the skull and cannot be seen on CT or MRI
Signs of concussion = brief disruption in LOC, loss of consciousness (~5 min or less) and possible retrograde
amnesia (forgetting the event) after head trauma
Manifestations include HA, dizziness, N+V
Occurs with contra coupe injuries
Contra coupe injuy: Damage to the brain on both sides: the side
that received the initial impact (coup) or blow and the side opposite
the initial impact (countrecoup).
This occurs when the force of the initial blow is great enough to
cause brain damage at the site of initial impact between the skull
and brain and is also great enough to cause the brain to move in the
opposite direction and hit the opposite side of the skull, causing
damage at that site.
Moderate Brain Injury
GCS 9-12: Associated with POST CONCUSSION SYNDROME
Once an individual has had a concussion they are at an increased risk to concuss again
Post concussion syndrome is recognized as a mental illness (DSM IV) which may last up to 2 years or more
includes:
o Physical - headaches, dizziness, sleep disturbances, blurring vision, light and sound sensitivity, neck pain,
ringing in the ears and fatigue
o Emotional - anxiety, irritability, depression and mood swings
o Cognitive - short-term memory (S.T.M.) problems, impaired concentration and attention span, periods
of confusion and cognitive slowing (learning problems)
Chronic Traumatic Encephalopathy (CTE) research is occurring to discover if this is the cause of increase in suicide rate
and dementia in athletes who have played contact sports
Severe Brain Injury
GCS 3-8: CONTUSION
Bruising of the brain tissue itself within a focal area
o Usually occurs near the site of skull fracture
Often develops areas of hemorrhage, infarction, necrosis, and edema
Damage from coup-contrecoup injury (high speed) occurs because of mass movement of the brain inside the
skull leading to multiple contused areas
Manifestations depend on location of contusion, however, serious contusions will show signs of increased ICP
and herniation syndromes
Lacerations associated with compound fractures of the skull and actual tearing of brain tissue occurs
Many delayed consequences such as hemorrhage, hematomas, seizures and edema
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Diffuse Axonal Injury (DAI)
Can occur with mild, moderate or severe TBI
Damage occurs in subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus and brain stem
Increasing evidence supports:
o Trauma results in alterations in the function of the axon leading to
Axon swelling and disconnection
Takes 12 to 24 hours to develop following injury
Maifestatios ilude: ↓ LOC, ↑ ICP, deortiate ad deererate posturig ad gloal
cerebral edema
90% of individuals with DAI remain in a persistent vegetative state
CLINICAL COMPLICATIONS OF TRAUMATIC BRAIN INJURY
CEREBRAL EDEMA
Coo liial opliatio folloig "rai ijur
Accumulation of fluid in extra-vascular volume which has a hydrostatic pressure (pushing)
Why does this occur?
o Perfusion swelling
o d/t increase in cerebral blood volume (intravascular volume)
o Hypotonic I.V. fluid infusion
Types of Cerebral Edema
Vasogenic VESSEL (increase flow through the vessels of the brain aka filtration pressure)
o Most common
o Affects white matter
o Occurs over hours to days
o Epithelial lining of cerebral blood vessels become abnormally permeable allowing protein to leak into
the extravascular space
o Most common in traumatic brain injury
Cytotoxic edema CAN’T BREATHE (ischemia)
o Affects gray matter
o Actual swelling of cells of brain
o Occurs over minutes, may be reversible
o Main cause is ischemia, can be caused by drowning
It is better to drown in icy cold water, than a pool/ocean
Cold temperature decreases the metabolic needs of the brain
o More resistant to treatment
Interstitial Edema SWELLING
o Results from periventricular diffusion of ventricular CSF with uncontrolled hydrocephalus
o Also caused by systemic fluid volume excess with hyponatremia resulting in fluid shift into brain cells by
the administration of hypotonic solution
The sodium in the blood will shift out into the brain tissue
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