Week 10: HEMORRHAGIC STROKE & ICP Flashcards
Study guide and notes
Mortality for subarchnoid hemorrhade
18%
Mortality forr intracerbrals
52% in first 30 days
what is a intracerebral hemorrhage
bleeding occurs w/i tissues of brain
what is a Subarachnoid hemorrhage. how does it result, what happens in the brain
bleeding occurs in subarachnoid space directly into CSF
- Both:
- result when an artery or arteriole in the brain ruptures and bleeds (from atherosclerosis
- Take up space in the brain & press on surrounding brain tissue
Intracerebral hemorrhage (ICH) common? where? form?
- Forms from a localized hematoma w/i the brain
- Most common type of hemorrhagic stroke (making up 10% of all strokes) :
Intracerebral hemorrhage result from (4)
- HTN (main cause)
- Trauma
- Bleeding disorders
- Illicit drug use (esp cocaine or amphetamines)
Risk factors for intracerbral hemorrhage (ICH) (3)
- HTN (doubles risk)
- Older age
- Antithrombotic therapy (anticoagulants or antiplatelets)
intracerbral hemorrhage (ICH) inital symptoms (6- how long til it comes on,
- May occur w exertion or emotions (might elevate high BP)
- Symptoms come on gradually (over minutes or hours)
- Typically when pt is awake
- HA, vomiting, LOC
- May have seizures
Subarachnoid hemorrhages (SAH) most common cause
by the rupture of a saccular (berry) aneurysm
Subarachnoid hemorrhages (SAH) result from (3)
- Trauma
- Bleeding disorders
- Illicit drug use
risk factors for SAH (3)
- htn
- smoking
- family hx
initial symptoms for SAH (5)
- “Thunderclap” HA (worst headache they ever had)
- May have warning HA (days or weeks prior)
- Neck pain/stiffness
- Vomiting
- brief LOC
treatment for SAH (4)
- Stabilizing pt
- Ensuring secure airway
- Maintaining cardiovascular function
- Preventing seizures
Surgical interventions (2 locations)
- Depends on location of bleed
- Cerebellum: surgical evacuation of hematoma = indicated
- Supratentorial (higher): surgery is controversial
for who is ICH usaly reserved for?
usually reserved for pts w a life-threatening hemorrhage that hasn’t responded well to meds
Open craniotomy
= most commonly used technique
- Surgeon removes flap of bone -> removes hematoma - bone flap is replaced -> skin is sutured or stapled shut
SAh needs to be treated to prevent rebleeding. 2 main ways.
- Clipping
- Endovascular coiling
Clipping
Open craniotomy -> place tiny spring-loaded clips at base of aneurysm to ut off blood flow & prevent it from rebleeding
Endovascular coiling
- Minimally invasive; performed through a blood vessel
- Catheter is passed up from the groin to the artery in the brain that contains the aneurysm -> tiny platinum coils are released into the aneurysm that block any more blood from entering & prevent aneurysm from leaking
Following a SAH, pts often experience ____________ in the brain -> (increase or decrease) blood flow & makes brain ________worse
Following a SAH, pts often experience vasospasm in the brain -> reduces blood flow & makes brain ischemia worse
Oral nimodipine (CCB) used to prevent
= used to prevent vasospasms
CCB (oral nimodipine) MOA, route
- Acts to relax smooth muscles in arteries (specifically in brain)
- Doesn’t work well on other parts of body so not used for HTN
- Give PO
-If pt has dysphagic/unable to swallow, administer via feeding tubes
- Serious cardiovascular events (inc death) when given IV
Medical tx for SAH
Manage BP
What is the blood pressure goal for SAH?
- If SBP >220 -> lower to 140-160
- If SBP 150 - 220 -> lower to 140
- Avoid going lower than 140 bc pt needs that min BP to perfuse their brain - aka cerebral perfusion pressure (CPP)
- The brain can become hypoxic (if too low)
Autoregulation: CBF
Controls cerebral blood flow (CBF); makes little adjustments to ensure that the brain always receives just the right amount of blood
- By constricting or dilating arteries
autoregulation: what should MAP be
between 50-150 mmHg
autoregulation: - When systemic BP is low,
arteries in the brain dilate to increase blood flow (so that brain gets enough O2)
autoregulation:
- When systemic BP is high,
arteries in the brain constrict to decrease blood flow (so that pressure in brain doesn’t get too high)
autoregulation:
- Too low:
cerebral blood vessels dilate but as pt goes into shock & they don’t have enough BP to perfuse the brain, the amount of blood flow to the brain isn’t enough no matter how much arteries dilate -> brain becomes hypoxic -> arteries collapse due to inadequate blood flow
autoregulation:
- Too high:
cerebral blood vessels can’t compensate anymore & give up -> start to dilate, allowing more & more blood into brain -> increasing pressure -> does more damage -> makes it even more difficult for blood vessels to control blood flow
which factor has the strongest influence on causing arteries in the brain to dilate, increasing blood flow to the brain?
elevated CO2 levels
Factors that affect CBF
(3)
a. Oxygen
b. CO2
c. Blood pH
Arteries in brain dilate when (3)
- CO2 is elevated (hypercapnia)
- O2 is low (hypoxia)
- pH is low (acidosis)
arteries in the brain contrict when (3)
- CO2 is low (ex: hyperventilation)
- pH is high (alkalosis)
what do the artieres in the brain do compared to the blood vessels in the lung? (which causes what in certain patients)
they do the opposite: - One of the mechanisms that causes ppl w COPD to develop pulmonary HTN and cor pulmonale
meds that will need to be stopped, why, antidotes, etc 2 drugs)
Stop (& if possible, reverse) anticoagulant & antiplatelet therapies
- Warfarin: Antidote = vit K BUT may require multiple doses & may take days to fully reverse effects
- => use 4-factor prothrombin complex concentrate: blood product that contains the coagulation factors that are affected by warfarin (2, 7, 9, 10)
- Really quick effect - causes INR to decline in 10 min
- Heparin= Reversal agent = protamine sulfate
other aspects of care? (6)
- prevention of venous thromboemolism
- maintance of normal fluid volume f
- prevention of fever
- prevention and/ or management of seizures
- prevent hypoglycemia and hyperglycemia (in diabetes)
- asses and manage ICP
-Prevention of venous thromboembolism (4)
Avoid anticoagulant drugs => use intermittent pneumatic compression devices
- Remove compression sleeves each shift
- Assess skin underneath
- Keep them in place until pt is able to mobilize
Maintenance of normal fluid volume f (3)
Q: Always Avoid hypotonic solutions (ex: D5W): will dilute the blood & cause water to shift from vascular space into cells of body, causing them to swell -> makes cerebral edema worse
- NS = used to replace fluids as it won’t cause major fluid shifts
- If pressure is increasing in the brain, administer hypertonic fluids (hypertonic saline, osmotic diuretics - ex: mannitol)
prevention of fever (3, )
- Associated w worse outcomes (greater disability, higher mortality rates)
- Fever associated double the risk of death
around clock if fever develops - Administer antipyretics
fever common cause: 2
- Aspiration pneumonia => follow safety precautions when feeding
- UTI => remove catheters asap
prevention and/ or management of sexiures (2.1)
- May have higher risk for strokes
- Monitor for seizure activity & be prepared to administer anti-seizure meds
- may be administered prophylactically (but not routine)
Prevent hypoglycemia & hyperglycemia (in diabetics) (3)
- Hypoglycemia damages neurons
- Hyperglycemia exacerbates brain injury & is associated w worse outcomes
- BG btw 6-10 mmol/L = safe target for those critically ill in ICU
hemorrhagic stroke and SIADH
if hemorrhagic stroke damages the pituitary gland & causes SIADH (syndrome of inappropriate antidiuretic hormone), what clinical manifestations should the nurse watch for? (3- why)
oliguria, confusion, low serum osmolality
why? Bc in SIADH the pituitary gland put out too much ADH -> kidneys decrease urine output & hold onto water
- as more & more water accumulates in body, it begins to dilute the blood, causing serum osmolality to go down
- As concentration of blood decreases, it makes the blood hypotonic compare to cells -> water is drawn into cells & they swell
- Brain = sensitive to changes in water balance => SIADH may cause neurological changes (ex: confusion)
ICP signs and symptoms
Changes in LOC
Eyes:
- papilledema
- Pupillary changes
- Impaired eye movement
Posturing
- Decerebrate
- Decorticate
- Flaccid
Decreased motor function
- Changes in motor ability
- Posturing
Headache
Seizures
- Impaired sensory and motor function
Changes in VS
- Cushing triad:
- Increase systolic BP
- Decrease pulse
- Altered resp pattern
Vomiting
Changes in speech
Infants:
- Buldging fontanels
- Cranial suture separation
- Increased head circumfrance
- High pitched cry
3 components of skull volume
Increase in any of the following results in ICP bc the skull can’t expand to allow the brain to swell
- Pressure gets directed inward & causes brain tissue to get squeezed
1. Brain tissue (80%)
2. Blood (10%)
3. CSF (10%)
- Additional mass can by occupied by: edema, tumours, abscesses, infection
Conditions that cause ICP (5)
- Hemorrhagic stroke
- Subdural or epidural hematoma
- Brain tumours
- Brain abscess
- Typically surrounded by edema
subdural or epidural hematoma
Typically occur as a result of a head injury
- Subdural: outside of the membrane (dura mater) surrounds the brain (dura & arachnoid)
- May be acute or chronic (developing slowly over time, sometimes expanding if re-bleeding occurs)
- Epidural: bleeding occurs/accumulates outside of the touch outer membrane (dura mater) but inside skull
brain tumors
- Both benign & cancerous
- Can also cause inflammation & edema which takes up additional space
brain abscess
- Localized collection of pus, usually caused by bacterial infection
- Typically surrounded by edema
traumatic brain injury
- May result in skull fractures, bleeding, cerebral contusion, & cerebral edema
early signs of ICP (5.2)
- Drowsiness (change in LOC = usually first sign)
- Also anxiety, agitation,
changes in cognition - HA (esp constant ache that worsens upon awakening)
- Nausea
- Sudden vomiting that may not be preceded by nausea
- Double vision or blurred vision
and pulmonary changes? what do
- => assess pupils regularly
- Helpful bc pt doesn’t need to be awake & able to respond
- Assess even in pts who are comatose or sedated
as pressure increase what three things happen to the pupils
- Pupil on the affected side dilates
- Both pupils dilate
- Pupils stop responding to light -> become fixed & dilated (really ominous finding)
later/ominous signs (4- what does it mean)
- Decorticate or decerebrate posturing
- Cushing’s triad
- coma
- respiratory arrest
*these signs all indicate that there’s so much pressure in the brain that brain stem herniation & coning is imminent
3 parts to cushings triad
- Increasing systolic BP (widening pulse pressure)
- Bradycardia
- Irregular resps
- Shallow breathing w periods of apnea
what is cushings triad, well ICP builds up so what happens? more blood is forced in so what happens?
- As ICP builds up, blood flow (& O2) to the brain decreases which stimulates the SNS -> increases SBP in an attempt to force more blood to brain & improve oxygenation
- As more blood is forced into the brain, it causes pressure to increase -> PSNS is activated
Cushings triad: what receptor is used what does it do, what does the pressure in brain do?
- Baroreceptors in the aortic arch are activated by the high BP & cause parasympathetic response
- Pressure in brain squeezes the intracranial vagal nerve -> parasympathetic response
- Bc of pressure in brain, it squeezes the resp centre in the brain -> isn’t able to regulate resps
Brainstem herniation (3, when does it occur)
- Fatal
- Occurs when there’s so much ICP that it tries to push some of the brain out of skull
- Only opening = foramen magnum (hole at the base of the skull where the spinal cord enters)
what is conning with brainstem herniation?
Pressure forces the brainstem & possibly part of cerebellum down the foramen magnum -> causes blood vessels to tear
Activities that elevate ICP (5)
- Valsalva maneuver:
- Flexing at waist
- Coughing, sneezing
- Lying flat/Trendelenburg
- Pain, stress, and anxiety
- Valsalva maneuver: what is it, fix it
weight lift closes throat, which keeps air from escaping lungs -> forcefully contract muscles in abdomen & rib cage, creating rigid compartments of liquid in lower torso & air in upper torso
- Used when ppl are on the toilet trying to have a BM
- To avoid: administer stool softener
flexing at the waist, what is it, how to avoid
- To tie shoes, sitting cross legged..
- Ppl will sometimes initially hold breath which mimics portions of the valsalva maneuvre
- To avoid: teach pt to avoid
coughing and sneexing, how to avoid
- To avoid: administer antitussive (cough) & antihistamine (sneezing)
- Some opioids (ex: codeine) = common antitussives
- Teach pt not to cough when performing deep breathing exercises (which prevent the development of atelectasis & hypostatic pneumonia)
lying flat/ trendelenburg, why is it bad how to/ what to avoid
- More fluid goes to head if it’s tilted down
- To avoid: elevate HOB to 30 (low Fowlers)
- Doesn’t make heart work too hard to pump blood uphill
- Pain, stress, anxiety: what to does to body and how to reduce or avoid it
- Boosts BP & increases ICP
- To avoid: reduce stimulation
- Provide regular, effective analgesics
- Reduce environmental noise & lights
- Keep calm
- Organize nursing care to reduce stimulation (cluster a few small tasks together to allow quiet time inbtw)
- Tell family members to avoid arguments or raised voices
Short-term strategies (8)
- remove causes of ICP
- Hypervenitilation therapy
- reduce BP w antihypertensive meds
- rescue fluid volume in brain w meds
- reduce fever and. or chills
- adminster glucocorticoids
- sedatives and barbiturates
- decompressive craniectomy
Remove cause of ICP: in subdural hematoma
remove collection of blood by drilling small burr holes into skull to permit drainage
remove cause of ICP: in lesions
surgery to remove tumor, reduce its size, or drain an abscess
remove cause of ICP Hydrocephalus (what is it, what does it do, how it is in the brain, draining?)
-> insert external ventricular (ventriculostomy) drain to allow excess fluid to drain
- When catheter is in place in brain, can also be connected to a transducer that directly measures the ICP + can measure the amount of CSF output + take a sample for testing if needed
Importance of ventriculostomy drain at zero mark for drainage?
- Bc when pt’s lying down, the tragus is at the same level as the ventricles in the brain where CSF accumulates
- Older models come w a level w an air bubble inside; newer models have a laser level
hyperventilation therapy
if on a mechanical ventilator, increasing resp rate will cause CO2 levels in the blood to drop, making the blood more alkaline & causing vasoconstriction of the cerebral arteries (which reduces ICP)
reduce BP w antihypertensive meds (why, when it it used)
- May also decrease ICP bc it reduces the volume of blood in the brain
- Only used for severe HTN
- A higher BP may be needed to maintain adequate CPP
- Increased pressure from swelling may prevent a sufficient amount of blood from entering the brain -> high BP is needed
rescue fluid volume in brain with meds. 3 main medications
- IV mannitol
- IV hypertonic Saline
- IV furosemide
what does IV mannitol do? type of drug?
Osmotic diuretic: pulls free water out of tissues of the brain & into the blood where fluid can be filtered/eliminated by kidneys
where does IV hypertonic work, is it common?
- More widely used a sa first-line treatment
- Works in similar manner to mannitol; pull fluid out of tissues & into blood -> kidneys excrete
Iv furosemide: type of drug, where does it work, can you use other drugs with it, caution for?
- Strong loop diuretic
- Works on kidneys to increase excretion of sodium & chloride
- May be used w mannitol to increase fluid loss
- Use w caution as it may increase risk of dehydration & electrolyte imbalances (ex: hypokalemia)
How to decrease fever and. or chills? (2 ways)
Administer antipyretics (ex: acetaminophen) as needed
- Avoid NSAIDs bc they may increase risk of bleeding
Cooling devices
- intravascular cooling (cool IV fluids)
- cooling blankets
Administer glucocorticoids: why? med used, what it does
- Specific situations
- Have strong anti-inflammatory effects so might help reduce edema relating to inflammation (ex: from brain tumour)
- Ex: dexamethasone
Administer glucocorticoid: what does it do for ICP, what might happen?
Aren’t helpful for ICP due to bleeding
- Might make situation worse bc glucocorticoids may cause kidneys to retain more sodium & water
sedatives and barbiturates: 3 functions
- Reduce brain metabolism
- Reduce sympathetic stimulation
- Reduce CBF
sedative and barbiturates: in ICU, a drug for each
- In ICU, pts may be sedated & ventilated as we wait for ICP to decrease
Propofol = commonly used anesthetic agent
Pentobarbital = barbiturate
Decompressive Craniectomy: ICP? how does it work, surgery amt?
- If pt has life-threatening ICP
- Bone flap is removed & dura mater is opened to allow the brain to swell -> Will need special care (ex: helmet)
- Second surgery is needed later on to close the opening of the skull
Glasgow coma scale
- Eye opening
- 4 - spontaneous
- 3 - to speech
- 2 - to pressure
- 1 - no response - Verbal response
- 5 - oriented
- 4 - confused
- 3 - words
- 2 - sounds
- 1 - no response - Motor response
- Apply peripheral stimulus (ex: press on nail bed w pen)
- 6 - obeys commands
- 5 - localizes to pain
- 4 - normal flexion
- 3 - abnormal flexion
- 2 - extension
- 1 - no response
glasgow coma scale: mild, moderate, and severe ratings.
- Mild: 13-15
- Moderate: 9-12
- Severe: 8 or less
Q: How should the nurse score a clients GCS motor response, if after applying a peripheral stimulus, one arm slowly flexes and the other extends?
score of 3
glascow coma scale: what to record?
- Record best response as it’s more likely to reflect pt’s overall neurological condition
- If one side is worse, it may reflect focal brain damage or local injury
other head injuries: COupe and Contracoupe injuries: how does it happen what is it?
When the initial impact on the head causes an injury to one side of the brain (coup) & then the brain sloshes over & smacks the other side of the skull, causing injury to the other side (contrecoup)
- Often caused by head injuries
head injuires: Basilar skull fracture (what is it, is it bad)
- fracture at the base of skull
- Extremely dangerous
signs and symptoms of basilar skull fractures (^)
- Bleeding from the fracture at base of skull
- Raccoon eyes (bruising)
- Battle sign (bruising behind ear)
- Hemotympanum (blood accumulated in middle ear) - Seen when looking into ear w otoscope
- Leakage of CSF from the ear (otorrhea) or nose (rhinorrhea)
- Halo sign
what is a Halo sign?
- When fluid is dripped onto a piece of paper, look for halo sign
- Blood forms a spot in the centre & a more lightly stained ring forms around it
- Fluid can be sent to lab to confirm whether it contains CSF
can you insert a GI tube with a basilar skull fracture why/ why not?
Do not attempt to insert NG
Bc the fracture may create an opening in the skull at the back of the cavity & there’s a risk that the NG tube may enter the pt’s brain & cause tissue damage
characterisic on conussions, condition type?
- Characteristic S/S experienced by an individual after a mild-mod traumatic brain injury
- Aren’t a clearly defined condition
conussion: fencing posture
= typical of injury to brainstem
Related to decorticate & decerebrate posturing in which the pt extends their arm when struck in the head
signs and symptoms of concussions ( 7.2)
- Possible LOC at time of injury
- Confusion
- Lack of awareness of surroundings
- Amnesia-> Time of injury and -> Might involve loss of recall of events preceding injury or events immediately after injury
- HA
- Dizziness
- N/V
Post-concussion syndrome: why expreince it, when are symptoms in, improvement? recovery time? how long are symptoms for?
Also experienced by 30-80% of ppl w mild-mod brain injury
Symptoms are usually the greatest in the 7-10 days after the injury
- Slowly improve w time
- Most pts recovers w/i 3 months
- Minority (10-15%) have symptoms that persist for 1+ years
post concussion syndrome signs and symptoms (6)
- HA
- Dizziness
- Fatigue
- Insomnia
- Loss of concentration & memory
- Noise sensitivity
STUDY GUIDE
STUDY GUIDE
post concussion syndrome: Tx (3)
usually aimed at managing symptoms
- Analgesics or migraine meds for HA
- Counselling
- Tx for seizures (slight increase in epilepsy for the first 5 years after injury)
post concussion syndrome: living with it, what can happen, problems?
Living w post-concussion syndrome is stressful
- Can make depression & anxiety worse if ppl have a predisposition for this
- Another layer of stress (work or school performance)
- Test’s person’s ability to cope
part 1: HEMORRHAGIC STROKE
part 1
What percentage of strokes are hemorrhagic strokes?
15 percent of all strokes
ICH: Where does the bleeding occur (in what area of the skull/brain)?
occurs into the brain tissue itself (intracerebral or intraparenchymal hemorrhage) or into the subarachnoid space or the ventricles (subarachnoid hemorrhage or intraventricular hemorrhage)
ICH: What are people typically doing when the hemorrhage occurs
common during activites
ICH: main cause (from what)
caused by a ruptured vessel, hypertension is the most important risk factor but other causes
ICH: how quickly or slowly do symptoms occur
usally a sudden onset, with progression over minutes to ours due to ongoing bleeding
ICH: common signs and symptoms (6)
neurological deficts, headache, N/V, decreased LOC, HTN
In what order do the symptoms typically progress (in the most common type of ICH)?
Sudden onset focal neurological deficit
Decrease in conscious level (measured using the Glasgow coma scale)
Headache
Nausea
Vomiting
Lethargy or confusion.
SAH: : where does the bleeding go into via in the skull/ nrain
into the cerebro-spinal fluid filled space: between arachnoid and the pia mater membranes (surface of brain)
SAH: main causes (4)
rupture of cerbral aneurysm, AVM’s, trauma, illicit drug use (cocaine)
SAH: prognosis (neuro problems, death rate for ruptured aneursyms)
25%: from a ruptured aneurysm die.
50%: peristant neurological deficits
-?> silent killer significant morbidity and cognitive difficulites
SAH: typical signs and symptoms
considered the slient killer. not many warning signs of an aneurysm ruptures.
possible: N/V, seizures, stiff neck, focal neuro deficits, change in LOC
COLLABORATIVE ACUTE CARE FOR HEMORRHAGIC STROKE
COLLABORATIVE ACUTE CARE FOR HEMORRHAGIC STROKE
main drug therapy for pt with hemorrhagic stroke
Managment of HTN: Once BP is stabilized low dose anticoagulation can be initiated for DVT prophylaxis.
Patients who are on blood thinners and experience a hemorrhagic stroke should be given reversal agents as soon as possible to reduce risk for further bleeding.
What drugs are contraindicated in clients with acute hemorrhagic stroke?
anticoauglants and platelet inhibotrs: increase bleeding
target BP with antihypertensive (look at sldies)
but at least under 160mm Hg
what are some surgical treatments for hemorrhagic stroke?
immediate evacuation of aneurysm-induced hematomas or cerebellar hematomas larger than 3cm.
If a hemorrhagic stroke results in bleeding into the ventricles of the brain (causing hydrocephalus), what is the treatment for this?
srugical insertion of an external ventricular drain (EVD) to drain excess CSH that is not draining due to lack os absorption or obstruction
If a client has a subarachnoid hemorrhage, what drug is given every 2-4 hours, starting from the time that the aneurysm ruptures? Why?
Calcium channel blocker, Nimodipine. for 21 days to decrease effects of vasospasm and minimize cerbral damage
what is endovascular coiling?
A metal coil is inserted into the lumen of the aneurysm via interventional neuroradiology. The coils immediately help reduce the blood pulsations within the aneurysm to protect against rupture. Coils are less invasive than the traditional clipping of an aneurysm.
what is clipping an aneurysm?
A metal clip is placed at the base of the aneurysm.
INTRACRANIAL PRESSURE
INTRACRANIAL PRESSURE
what are the three compents that make of the volume within the skull
brain tissue, blood, and cerbrospinal fluid (CSF)
What 6 factors influence intracranial pressure (ICP)?
BP, cardiac function, intra-abdominal and intrathoracic pressure, body postiton, temperature, and blood gasses (mainly CO2 levels)
What is the difference between “primary injury” and “secondary injury”?
primary: occur at the inital time of an injury that results in displacement, bruising or damage of the three components.
Secoundary: is the resulting hypoxia, ischemia, hypotension, edemia, or increased ICP that follows primary injury
what is normal ICP
from 5 to 15mm Hg
what is an abnormally elevated ICP?
pressure greated then 20mm Hg
How does the body compensate for increased ICP?
Change CSF volume: via the displacement of CSH into the spinal subarachnoid space or the basal subarchnoid cisterns, and to a lesser degree by altering CSF production and absorption rates.
Changes in cerebral veins vasodilation or vasoconstriction also help.
How much (%) of the body’s oxygen and glucose does the brain use?
20% of the bodies
What happens when the ability of the body to compensate for increased ICP is exceeded?
- increase ICP, neuronal compression, and ischemia
What is autoregulation?
The brains ability to regulate its own blood flow in response to its metabolic needs in spite of wide fluctuations in systemic arterial pressure.
When autoregulation is working properly… What happens to cerebral blood vessels (constrict or dilate) when systemic blood pressure is high (hypertension)?
cerbral vessels are maximally contstricted
How do the following factors affect cerebral blood flow: Carbon dioxide levels in arterial blood?
An increase in PaCO2 relaxes smooth muscle, dilates cerebral vessels, decreases cerebro-vascular resistance and increases CBF. Alternately, a decrease in PaCO2 will reverse this process and decrease CBF.
How do the following factors affect cerebral blood flow: oxygen levels in arterial blood
PaO2 below 50mm Hg results in cerebral vascular dilation, this decreases cerebral vascular resistance and increases CBF. If PaO2 is not raised anaerobic metabolism begins, which results in an accumulation of lactic acid. As lactic acid increases, hydrogen ions accumulate and the cerebral environment becomes more acidic.
How do the following factors affect cerebral blood flow: pH of arteral blood
Within this acidic environment vasodilation occurs to attempt to increase blood flow. The combination of a severely low PaO2 and elevated hydrogen ion concentration may produce a state where autoregulation is lost and compensatory mechanisms fail to meet tissue metabolic demands.
What is cerebral perfusion pressure (CPP)?
CPP is the pressure needed to ensure adequate brain tissue perfusion. CPP is equal to the MAP minus the ICP.
What is brain compliance?
Brain compliance is the expandability of the brain. It is represented as the volume increase for each unit increase in pressure. With low compliance, small increases in volume result in greater increases in pressure.
What is brain herniation, and why is it bad
Herniation occurs as the brain tissue is forcibly shifted from the compartment of greater pressure to a compartment of lesser pressure. In this situation, intense pressure is placed on the brain stem and if herniation continues brain stem death is imminent.
Why is increased ICP dangerous?
Increased ICP is a life-threatening situation resulting from an increase in any or all of the 3 components pf the skull. Increased ICP is clinically significant because it diminishes CPP and increases risk for brain ischemia and infarction, and is associated with a poor prognosis.
What are the mechanisms that can increase ICP:
o By increasing the brain tissue component?
Displacement and herniation of brain tissue can cause irreversible pathophysiological processes that lead to further ischemia and edema.
What are the mechanisms that can increase ICP:By increasing the blood volume component?
Slow increases in ICP can preserve blood flow better than a rapid increase, sustained increases in ICP result in brain stem compression and herniation.
What are the mechanisms that can increase ICP: by increasing the CSF volume
Increase in CSF can lead to cerebral acidosis, impaired autoregulation, and systemic hypertension which promotes the spread of cerebral edema and this distorts brain tissue
What is a sensitive and early indicator of altered neurological status (including increased ICP)?
A change in LOC is the earliest indicator in a change in neurological status, caused by impaired CBF
What causes changes in the level of consciousness during increased ICP?
Impaired CBF deprives the cells of the cerebral cortex and the RAS of oxygen.
What are the 3 signs of Cushing’s Triad?
Increasing systolic blood pressure, bradycardia with a full and bounding pulse, and irregular resp pattern
Is Cushing’s Triad an early or late sign of increased ICP?
Late sign, doesn’t occur until ICP has been increased for some time or suddenly markedly increases.
What ocular signs can be seen with increased ICP?
Compression of the oculomotor nerve results in dilation of the pupil ipsilateral (same side as) to the mass or lesion, sluggish or no response to light, inability to move the eye upward, and ptosis of the eyelid.
How does increased ICP affect motor function?
Contralateral hemiparesis or hemiplegia may be seen. Patient may exhibit localization to a painful stimuli or a withdrawal from the stimuli. Decorticate or decerebrate posturing may be noxious stimuli.
What are the following and what are their significance: Decorticate posturing?
Internal rotation and adduction of the arms, with flexion of the elbows, wrists, and fingers as a result of interruption of voluntary motor tracts. May also have extension of the legs.
What are the following and what are their significance: Decerebrate posturing?
Results from disruption of motor fibres in the midbrain and brain stem and may indicate more severe damage. Arms are stiffly extended, adducted, and hyperpronated. There is also hyperextension of the legs with plantar flexion of the feet.
What are the characteristics of headache caused by increased ICP; and what makes them worse?
Typically a continuous headache, straining, agitation, or movement may make them worse.
What are the characteristics of vomiting caused by increased ICP?
Described as projectile due to the force of vomitus ejection
What diagnostic tests may be performed when a client is thought to have increased ICP?
MRI, CT, MRA, CTA, EEG, ICP measurement, licox catheter to measure brain tissue oxygenation, transcranial doppler studies.
What diagnostic test SHOULD NOT be performed when a client is thought to have increased ICP (due to the risk for brain herniation)?
A lumbar puncture.
why is ventriculostomy used
It is the gold standard for measuring ICP as it directly measures the pressure within the ventricles and facilitates removal or sampling of the CSF.
Regarding ventriculostomy to measure ICP:
o What is a ventriculostomy?
A catheter is inserted into the lateral ventricle and coupled to an external transducer
How should the ventriculostomy transducer be positioned?
It should be kept level with the foramen of Monro(intraventricular foramen) the reference point on the patient for this is the tragus of the ear.
What complication is the client with a ventriculostomy at increased risk for?
Infection is a serious consideration with ICP monitoring, prophylactic systemic antibiotics may be administered to reduce the chances of infection.
Why are the following treatments used in clients with increased intracranial pressure (ICP): Osmotic diuretics, such as Mannitol?
Used to treat ICP in acute situations, decreases ICP in two ways: plasma expansion and osmotic effect. Helps move fluid from the tissue into the blood and ICP is decreased by the decrease in total brain fluid content.
What are the goals of collaborative care for a client with increased ICP?
The goals are to determine and treat the underlying cause of increased ICP and support brain function.
Why are arterial blood gasses (ABGs) helpful in guiding the treatment of increased ICP?
Ensuring adequate oxygenation is the first step in the care of a person with increased ICP, ABG’s guide the oxygen therapy.
Why are the following treatments used in clients with increased intracranial pressure (ICP): hypertonic saline
It reduces swelling and improves CBF drawing water out of the brain tissue.
Why are the following treatments used in clients with increased intracranial pressure (ICP): corticosteroid drugs, such as dexamethasone
Used to treat vasogenic edema surrounding tumours and abcesses, they have limited value in the treatment of those with head injuries and are not recommended for use with them. They stabilize the cell membrane and inhibit synthesis of prostaglandins preventing formation of proinflammatory mediators.
Why are the following treatments used in clients with increased intracranial pressure (ICP): sedatives, such as propofol
Treatment with sedation and analgesia with propofol can reduce cerebral metabolism.
Why are the following treatments used in clients with increased intracranial pressure (ICP): Barbiturates, such as pentobarbital?
Used in patients whos ICP is refractory to all other treatments. Barbiturates also decrease cerebral metabolism which decreases ICP.
Why are the following treatments used in clients with increased intracranial pressure (ICP): nutritional therapy
Patients with increased ICP are in a hypermetabolic and hypercatabolic state that increases the need for glucose toprovide adequate fuel for metabolism.
Why should fever, agitation, shivering, pain, and seizures be avoided in a person with increased ICP?
These can also increase ICP and should be reduced in patients at risk.
How should a fever be treated in a client with increased ICP?
Yes, it should be well controlled to maintain a temperature between 36-37 degrees using antipyretic agents, cool baths, cooling blankets, ice packs, or intravascular cooling devices.
What are the 3 categories that are assessed in the GCS?
responsiveness, eye opening, verbal and motor response to stimuli
THE GLASGOW COMA SCALE AT 40
THE GLASGOW COMA SCALE AT 40 (reminder you need to memorize it!
What is the purpose of the preliminary check?
Used to identify any factors that may interfere with your assessment
What are the 4 steps to assessment?
Check, observe, stimulate, and rate
What are you supposed to observe for?
Observe the patient noting any spontaneous behaviours in any of the three components of the scale
Describe how a nurse should assess verbal response.
Ask the patient to tell you their name, where they are, and what month it is
If a client doesn’t open his eyes to sound, what stimulus should the nurse should apply?
Physical peripheral stimulus, start at a low level by pressing on the nail bed for up to 10 seconds
Describe how a nurse should assess motor response.
Ask them to grasp and release your fingers with their hand, or ask them to open their mouth and stick out their tongue
If a client can’t follow a command for a motor response, what type of stimulus should a nurse apply?
A central stimulus is needed, trapezius pinch, supraorbital notch
What is the difference between “normal” and “abnormal” flexion?
Normal the elbow bends and rapidly moves away from the body and from the stimulus, in abnormal flexion the elbow bends slowly and the arm comes across the body
What should the nurse do if, when testing motor response, the client flexes one arm and extends the other arm?
record the better side response?
What should the nurse record if it’s not possible to assess an area (e.g.testing verbal response on a client with an endotracheal tube, or testing motor response on a paralyzed client)?
not testable
NEUROLOGICAL ASSESSMENT
NEUROLOGICAL ASSESSMENT
What changes occur in the pupils as ICP increases (and how do the changes progress)?
If the oculomotor nerve is compressed, the pupil on the affected side will become larger until it fully dilates. If ICP continues to increase both pupils will dilate. When testing pupils with a penlight, the normal reaction is brisk constriction, a sluggish reaction can indicate early pressure on the CN III nerve. A fixed pupil shows no response to light which usually indicates an increase in ICP.
cribe the following types of abnormal breathing that may occur with altered ICP:
o Cheyne-Stokes respirations
chcle of hyperventilation and apnea
cetral neurogenic hyperventilation
sustained, regular rapid and deep breathing
apneustic breathing
prolonged inspiratory phase, or paused alternating with expriatry pauses
cluster breathing or Biots respirations
cluster of breaths follow each other with irregular pauses between
What is the nursing care for a client with increased ICP, specifically in regards to:
o Airway management?
Patient should be kept laying on one side with frequent position changes to prevent the tongue from blocking the airway. Accumulated secretions should also be removed by suctioning. An oral airway can be used for a comatose patient. Patients who are unable to maintain a patent airway or effective ventilation requires intubation and mechanical ventilation.
Management of client anxiety, fear, pain?
Use of sedatives, analgesics, and paralytics is common but poses challenges for the ICU team to appropriately assess the neurological state. IV propofol is useful in the treatment of pain and anxiety because of its rapid onset, short half life, and oxygen saving properties. Dexmedetomidine is an alpha adrenergic agonist.
ataxic breathing
Completely irregular with some breaths deep and some shallow. Random, irregular pauses, slow rate.
how shoed the HOB be postioned
at a 30 degree angle to enhance respiratory exchange and aid in decreasing cerbral edema
Fluid and electrolyte balance?
IV fluids should be closely monitored with the use of a limited volume device or a volume control apparatus. Intake and output and daily weights should be monitored.
What additional factors can increase ICP?
Valsalva manoeuvre, coughing, sneezing, hypoxemia, pain, fever, and environmental stimuli can increase ICP.
What body position is recommended for a person with increased ICP?
head up position
What body positions should be avoided in a person with increased ICP?
Preventing extreme neck flexion, the bed should be positioned so that it decreases ICP
Why is it important to be slow and gentle, when turning and repositioning clients?
Rapid changes in position may increase ICP
HEAD TRAUMA
HEAD TRAUMA
What are the clinical manifestations of a “basilar skull fracture”?
Otorrhea, bulging of tympanic membrane caused by blood or CSF, battle sign, tinnitus or hearing difficulty, rhinorrhea, facial paralysis, conjugate deviation of gaze, vertigo, bilateral raccoon eyes.
If a client with head injury has clear fluid leaking from the nose or ears, how can this be tested to verify if it is cerebrospinal fluid (CSF)?
There are 2 methods for testing the fluid, use a dextrostix or Tes-Tape strip to determine if glucose is present, CSF will give a positive reading for glucose.
What type of brain injury is a concussion?
A concussion is classified as a diffuse brain injury, it is considered a mild brain injury, patient may or may not lose total consciousness with this injury. Concussion is a sudden, transient, mechanical head injury with disruption or neural activity and a change in LOC.
Describe postconcussion syndrome?
It is seen anywhere from 2 weeks to 2 months after the concussion. Symptoms include persistent headache, lethargy, personality and behaviour changes, shortened attention span, decreased short term memory, and changes in intellectual ability.
What are the clinical manifestations of a concussion?
Clinical manifestations of a concussion may include a brief disruption in LOC, amnesia regarding the event, and a headache.
Describe the following in regards to an epidural hematoma:
o What is it?
A collection of blood that results from bleeding between the dura and the inner surface of the skull. It produces compression of the dura mater and thus of the brain.
what causes an epidural hematoma
A torn artery, linear fracture to the thin squamous portion of the temporal bone and laceration of the middle meningeal artery or one of its branches (arterial related)
Venous epidural hematomas are less common and are associated with a tear of the dural venous sinus and develops slowly (venous related)
how was does a epidural hematoma develop
Arterial is a neurological emergency, venous develops more slowly
what is a subdural hematoma
A collection of blood that results from bleeding between the dura mater and the arachnoid layer of the meningeal covering of brain.
symptoms of a epidural hematoma
Typically symptoms include unconsciousness at the scene, with a bried lucid interval followed by a decreased LOC. Other symptoms may be a headache, nausea and vomiting, or local findings. Rapid surgical intervention is required to prevent cerebral herniation.
What is the difference between an ‘acute’, ‘subacute’ or a ‘chronic’ subdural hematoma?
- An acute subdural hematoma manifests signs within 48 hours of the injury
- A subacute subdural hematoma usually occurs within 2-14 days of the injury
- A chronic subdural hematoma develops over weeks or months after a seemingly minor head injury.
BRAIN TUMOURS
BRAIN TUMOURS
What is the difference between a primary and a secondary tumour?
A PRIMARY tumour is arising from the tissues within the brain, a SECONDARY tumour results from a metastasis from a malignant neoplasm elsewhere in the body (most common type).
What is the difference between a malignant and a benign brain tumour? (this is explained on page 319, in the chapter on cancer)
Benign neoplasms are well differentiated and malignant neoplasms are undifferentiated. Malignant tumour cells have the ability to invade and metastasize, unlike benign neoplasms.
Why is it that all brain tumours will eventually cause death if they are not treated?
All tumours grow which causes increasing tumour volume which leads to increased ICP.
What are some common signs and symptoms of a brain tumour?
The clinical manifestations range and depend mainly on the location, rate of growth and the size of the tumour. Headaches are very common, they are usually dull and constant. Seizures are common in gliomas and brain metastases. Nausea and vomiting can occur due to increased ICP
Why are corticosteroids (e.g. dexamethasone) usually prescribed for clients with a brain tumour?
They are useful in reducing cerebral edema associated with neoplasms, they are typically prescribed at the time of diagnosis and continued following surgery until radiation and chemotherapy are finished.
