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Hemorrhagic Stroke Symptoms
Terms in this set (45)
List four contraindications to lumbar puncture.
suspected intracranial mass lesion, platelet count <50,000-80,000 or INR >1.4 or other reason for bleeding, infection in skin over back, suspected spinal cord mass lesion or epidural abscess
Describe what is usually ordered for tubes 1-4 of collected CSF (can just say "special tests" for tube #3)
tube #1=cell count and differential, tube #2=protein and glucose concentrations, tube #3=special tests, tube #4=gram stain and cultures
Approximately what percentage of strokes are hemorrhagic as opposed to ischemic?
Into what two compartments do spontaneous intracranial hemorrhages typically occur?
List the major risk factors for an intraparenchymal hemorrhage.
hypertension, smoking, lower cholesterol, lower LDL, lower triglycerides, high alcohol consumption, anticoagulant use, cocaine or amphetamine use
List the three major sources of spontaneous intraparenchymal hemorrhage.
rupture of small/deep arteries due to long standing hypertension, rupture of small-medium size cortical arteries as a result of beta amyloid protein deposition (cerebral amyloid angiopathy), leakage of arteriovenous malformations
What is the most common cause of intraparenchymal hemorrhage in adults?
rupture of small, deep arteries due to long standing hypertension
What is the most common cause of intraparenchymal heorrhage in kids (least common in adults)?
leakage of arteriovenous malformation
Describe how an intraparenchymal hemorrhage is diagnosed.
H&P, CT or MRI
Describe the classic presentation of a patient with an intraparenchymal hemorrhage
hemiparesis and eye deviations are common, 50% headache and vomiting, patient may be comatose if large enough hemorrhage to cause uncal herniation with compression of midbrain (hemispheric bleed) or direct compression of the midbrain (pontine or cerebellar hemorrhage)
Outline the management of a patient with an intraparenchymal hemorrhage.
1) discontinue any antiplatelet or anticoagulant drugs
2) reverse anticoagulants if possible
3) manage increased intracranial pressure (elevate head of bead, lightly sedate patient if necessary and control pain, intracranial pressure monitor if GCS < 8)
4) lower blood pressure cautiously to 160/90
5) +/- ventricular drainage if hydrocephalus develops
6) +/- surgical intervention if cerebellar hemorrhage or cerebral hemisphere bleeds within 1 cm of cortex in setting of life-threatening mass effect
Can the patient typically go home the same day an intraparenchymal hemorrhage is diagnosed?
No, always admitted to the ICU after stabilization in the ER
Is surgery usually indicated for an intraparenchymal hemorrhage?
No, only if cerebellar hemorrhage or cerebral hemisphere bleeds within 1 cm of cortex in setting of life-threatening mass effect
Should an elevation of blood pressure be treated in a patient with an intraparenchymal hemorrhage?
yes but cautiously and only down to 160/90
How are deep venous thrombosis prevented in patients with an intraparenchymal hemorrhage?
with intermittent pneumatic compression stockings
At autopsy, people with hypertension-related intraparenchymal hemorrhages often have evidence of previous lacunar infarctions. Why is this not surprising?
Those infarctions are commonly caused by hypertension and the same RFs as intraparenchymal hemorrhages, which are cause by these same vessels rupturing
For hypertension-related intraparenchymal hemorrhages, what vessels are typically affected? What parts of the brain are typically affected?
small arteries deep within brain (lenticulostriate, thalamoperforators, etc.), basal ganglia most commonly, subcortical white matter (e.g. internal capsule), thalamus, cerebellum, pons
For hypertension-related intraparenchymal hemorrhages, what part of the brain is most commonly affected?
Be able to recognize a classic intraparenchymal hemorrhage on a CT scan.
looks like a white area more towards the center of the brain
What will typically cause death acutely in a patient with an intraparenchymal hemorrhage?
herniation secondary to mass effect
Who is at highest risk of acquiring cerebral amyloid angiopathy (CAA)?
people greater than or equal to 85 yo
What vessels typically rupture in CAA?
small-medium cortical vessels (superficial cortex, aka "lobar hemorrhage")
There is an increased risk of CAA in what other disease?
How does the location of a hemorrhage secondary to cerebral amyloid angiopathy differ from that of a hypertension-related intraparenchymal hemorrhage?
CAA it typically restricted to the cortex or grey-white junction and spares the areas affected by intraparenchymal hemorrhage (basal ganglia, thalamus, or pons)
What is used for secondary prevention for hemorrhages secondary to cerebral amyloid angiopathy?
treat hypertension, no anticoagulation, only use antiplatelet agents if the benefits clearly outweigh the risks, weigh the benefits and risks of statins in this population
Describe the appearance of a classic lobar hemorrhage from CAA on a CT scan.
two or more hemorrhages or microhemorrhages restricted to the cortex or "grey-white" junction and entirely sparing regions typically impacted by hypertensive hemorrhage
What is an AVM?
Arteriovenous Malformations, congenital vascular malformations where an artery leads into an abnormal segment of blood vessel instead of a capillary
Name three possible presentations that occur as a result of having an AVM.
intracranial hemorrhage, seizures, headaches, focal neurological deficits
Are most AVMs symptomatic?
No (12% develop symptoms)
What is the most common place for an AVM?
90% are in cerebral hemispheres
When an AVM ruptures, where does the blood go? (3 possible different places.)
intraparenchymally, subarachnoid space, intraventricularly (or a combination)
Do AVMs need to be treated? Why?
depends on the size and location, if it bleeds it should probably be treated
What are the treatment options for AVMs?
microsurgery (most commonly), stereotactic radiosurgery, endovascular therapy
How common are saccular (berry) aneurysms?
3.2% of the US population has them
What disorders are associated with an increased incidence of saccular aneurysms?
Ehlers-Danlos, autosomal dominant polycystic kidney disease, familial aldosteronism, bicuspid aortic valve, pseudoxanthoma elasticum
Describe the typical presentation of a ruptured saccular aneurysm.
sudden onset of the "worst headache of my life", loss of consciousness, nausea and vomting, neck or back or leg pain, photophobia, may have had similar symptoms days to weeks earlier
How is a a ruptured saccular aneurysm diagnosed?
emergent CT scan
If an imaging study is negative and you still suspect a subarachnoid hemorrhage, what other test should you do?
Describe the typical appearance of a subarachnoid hemorrhage (SAH) on a CT scan.
hyperdensity in sulci (density sign)
What are the two major risk factors for rupture of a saccular aneurysm other than associated diseases and familial factors?
hypertension, smoking, heavy alcohol consumption, stimulant medications, illicit drugs, excessive straining and Valsalva maneuvers
Why are patients with a SAH secondary to rupture of an aneurysm at risk for ischemic strokes? What medication is used to help prevent this?
due to vasospasms, phenylephrine, norepi or dopamine
Why does hydrocephalus sometimes occur after a SAH?
develops as a result of blood products blocking apertures or failure of the arachnoid granulations to deliver the CSF to the dural venous sinuses
Describe two ways in which a saccurlar aneurysm is treated.
surgical intervention via placement of a surgical clip on the aneurysm or a coil inside of it
What class of medication is nimodipine and why is it important with respect to a SAH?
calcium channel blocker, improves outcomes when used for 3 weeks
List 5 secondary causes of intracranial hemorrhage.
hemorrhagic infarction, septic embolism, brain tumor, CNS infection, abnormalities of blood vessels (vasculitis, moyamoya)
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