Wednesday, April 1, 2009

Strokes (aka CVA, aka Brain Attack)

Studying for the neurology section of your NCLEX or USMLE can be overwhelming, but hopefully this review will make it a bit easier. Remember, not all strokes are created equal. But one thing that is, are the deficits from losing a specific section of your brain. One of the more common ways by which you can get these deficits is to lose blood supply to a certain area. Here are some common deficits, depending upon which supply of blood you lose...

· Focal Neurological Deficits: Depend upon area of brain perfused by effected artery
o Internal Carotid Artery/Opthalmic: Amaurosis fugax (transient monocular blindness-retinal ischemia: shade drawn), as well as hemispheric loss mostly from MCA territory
o ACA: Hemiplegia (leg more than arm), Confusion, Incontinence, Primitive reflexes
o MCA: Hemiplegia (arm/face more than leg), Hemianesthesia, Homonymous hemianopia, Drowsiness/Stupor (edema), Aphasia (dominant hemi), Apraxia (nondom hemi)
o PCA: Contralateral Hemisensory deficit, Aphasia, NonMacular Homon Hemianopia
o Vertebral: Ipsilateral face numb, Contralateral limb numb, Diplopia, Dysarthria, Ipsilateral Horners (ptosis, miosis, anhydrosis)
o Basilar: Pinpoint pupils, Quadriplegia, Sensory loss, Cranial nerve/Cerebellar deficit, Locked in state (all paralyzed but eyes)
o Brainstem/Cerebellar: Basilar/Vertebral; Hallmark is crossed deficit-Ipsilateral Cranial nerve deficit and Contralateral Motor deficit, Vertigo, N/V, Nystagmus, Ipsilateral limb ataxia, Rapid deterioration


Specific Stroke Treatment Protocols

Ischemic-ThromboticLarge vesselo Facts:
· Atherosclerosis main cause; Arterial dissection, Hypotension, Homocystinuria, Hyperglycemia (Delayed Calcium recovery in ischemic stroke)
· Common in Carotid bifurcation, MCA
o S/S:
· Progression of deficits over hrs to days with stuttering course
· May have been preceded by TIAs (80%)
· Often has a nocturnal onset (60%)
· Focal deficits depend upon vessel occluded (see above); Usually Carotid, MCA or Basilar
o DX:
· CT w/o contrast to r/o Hemorrhage
o TX:
· HT treated only if severe (more than 220/130) w/Labetalol or Enalapril
· Nimodipine not recommended; HOB elevated; Possible Mannitol and shunt placed



Small Vesselo Facts:
· Lacunar most common thrombotic; Usually caused by Chronic HT or DM
· Most common in small vessels of the Brainstem or Basal Ganglia
o S/S:
· Pure contra-motor hemiparesis/Clumsy hands w/Pons or Internal capsule involvement
· Pure contra-hemianesthesia w/Thalamus involvement
o DX:
· MRI best if small infarct suspected in Cortex/Brainstem
o TX:
· Antiplatelet agents


Hypoperfusion/Watershed: mainly related to low BP, with deficits often seen between the border of the ACA/MCA around the motor strip of the frontal cortex...Volume Resuscitate, Pressors, etc.



Ischemic-Embolic/Cryptogenic
o Facts:
· 50 % of all strokes
· Cardiac source (60%) from AFib/Valve Dz/MI/Cardiomyopathy; Artery source (carotid plaque, DVT w/left to right shunt); Fat/Air embolus; Often in MCA, Vertebral/Basilar
o S/S:
· Rapid onset focal deficit at maximum severity, usually with activity
· May have been preceded by TIA w/breakup of emboli within min-hrs
· May be accompanied by Seizure
· Focal deficits depend upon vessel occluded (see above); Usually MCA or Basilar
o DX:
· CT w/o contrast to r/o Hemorrhage
o TX:
· HT treated only if severe (more than 220/130) w/Labetalol or Enalapril
· TPA if all CI absent; Nimodipine not recommended
· Avoid rhythm conversion; Tx rate only


Hemorrhagic

Epidural (EDH)
o Facts:
· Not always listed as subset of Stroke although presentation often identical
· Usually from a TBI skull fracture that lacerates a meningeal artery. Hematoma puts pressure on brain causing compression, ischemia, and focal neuro deficits.
· Least common intracranial injury; Very uncommon in children/elderly
o S/S:
· Initial LOC, reawakening with clear mentation and then progressive AMS
· Sleepy, NV, Severe HA, dizziness
· Fixed, Dilated pupil on side of lesion w/contra hemiparesis is classic late finding
· Type of Herniation leads to various presentations; Transtentorial (uncal) herniation compresses oculomotor nerve causing ipsilateral fixed, dilated pupil as well as contralateral hemiparesis
o DX:
· Noncontrast CT; Shows lenticular shaped hematoma
o TX:
· Large blood collections are surgically evacuated despite neuro findings
· First step in Pt w/neuro deficit and vomiting is to protect airway by Intubation
· ICP monitor placed post evacuation and artery ligation



Subdural (SDH)o Facts:
· Not always listed as subset of Stroke although presentation often identical
· Collection of venous blood between Dura and Arachnoid
· Often seen in Pts w/Brain atrophy such as alcoholics and elderly
o S/S:
· Progressive neuro decline over days to weeks often w/no deficit initially, May mimic dementia
o DX:
· Noncontrast CT; Shows crescent shaped hematoma
o TX:
· Large blood collections are surgically evacuated despite neuro findings; Post op care in ICU



Subarachnoid (SAH)o Facts:
· 5 % of all strokes (30,000/yr) ↑ in Women (3:2); Peak 50-60 yo
· Usually from a berry aneurysm associated with HT at bifurcation of Circle of Willis
· Also from trauma, vascular anomaly or blood dyscrasias
· 2 % of population harbor aneurysms
· S/S: · Sudden severe Occipital HA with severity never experienced by Pt although a careful history may show minor S/S (NV, HA) from sentinel bleeding · N/V often follow onset of HA · Impaired consciousness and AMS w/Coma common (50%) · Seizures can occur (10%) as can retinal hemorrhage · Nuchal rigidity and other signs of meningeal irritation i/c neck/back pain · Focal neurologic deficits are frequently absent but if present often show a 3rd nerve Palsy
o DX: · CT w/o contrast immediately (faster and more sensitive for early hemorrhage than MRI); If (-)(10% missed by CT) LP for blood or xanthochromia · Cerebral arteriography to determine exact source of bleed if Pt is stable and surgery is a viable option · Bilateral carotid and vertebral arteriography to r/o other bleed source · EKG may show ST Δ, Prolonged QT, or peaked/inverted T waves
o TX: · Medical: · Sedatives to keep Pt calm · HHN Therapy to ↓ vasospasm which is most frequent cause of death for Pts who survive rupture: Hypervolemic (crystalloid or colloid fluids), Hypertensive (Dopamine), Nimodipine (60 mg q4h) · Attempt to keep BP in Pts normal range w/MAP below 100
· Other: · Obtain early neurosurgical consult; Admit to ICU · Bed rest in dark room · Prevent straining or valsalva · Pneumatic leg compression to prevent DVT · Consult physical, occupational, and speech therapists
Intracerebral (ICH)
o Facts:
· Also known as Intraparenchymal Hemorrhage; Most often in Putamen, Thalamus, Pons or Cerebellum; Often in young Pt, smoker, HT
· 25 % of all strokes; 50 % Mortality (depends on Volume/location)
· HT main cause and causes deep bleed; Also from anticoagulation/thrombolysis, Cocaine/amphetamines, AV malformation, Amyloid angiopathy
o S/S:
· Rapid (5-30m), progressive focal deficits depending on site;
· Vomiting (80 %); Headache (50%)
· Gaze deviation (towards paralyzed side = Cerebellum, Down w/unreactive pupils = Thalamus)
o DX:
· CT w/o contrast
o TX:
· Medical: Strict BP control w/MAP below 100
· Surgical: · Urgent neurosurgery consult if bleeding is in Cerebellum · Surgery for bleed elsewhere of no benefit · Other: · Induced hyperventilation to reduce edema and mass effect · Head of Bed to 30o

Other Facts of Interest
· History & Physicalo DDx includes Hypoglycemia/Hyperglycemia, Epilepsy, Tumor, Fever/Infection
o Thorough neurological exam including CN II-XII, Motor/Sensory function, Visual fields, Ability to speak/comprehend/walk, Reflexes (i/c primitive), Cerebellar function, Patient may lose appreciation of dysfunction (anosagnosia)
o Peripheral/Cervical vascular system i/c bruits/murmurs, DVT and EKG rhythm
o Cervical ROM
o Hx of previous S/S; Hx of Medications/Past surgeries/illnesses
· Diagnosticso Labs: CBC w/plts, CMP (i/c LFTs), ESR, PT/PTT, Syphilis serology, Tox screen, D-dimer, Fibrinogen, Urine Homocysteine; ABG, Cardiac enzymes Coags if hypercoag state suspected
o EKG, CXR
o CT: Door to CT interpretation goal is 45 min
· Non Contrast CT first to r/o hemorrhage (sensitivity for ischemic strokes only 50% in 6hrs)
· Next CT angio (arteriography) to evaluate vessel anatomy/patency/perfusion
o MRI: Only helpful in small infarcts in Cortex and Brainstem lesions and is not helpful in acute hemorrhages; should be avoided if Pt is unstable or will delay therapy
o Others: Carotid Doppler U/S, Transcranial Doppler, Echocardiography or U/S (RL shunt)
· Hypothermia is good for coma following cardiac arrest but no data if helpful for Stroke Pt
· Magnesium does not change morbidity/mortality rates
· Hyperglycemia delays recovery from ischemia w/data suggesting Glucose-Insulin-K helpful
· Supine position best for brain perfusion but increases ICP; Use own judgement
· If BP must be treated other acceptable medications include Clonidine, Labetalol, ACEI; Usually wait 3 wks post stroke
· Syncope occurs from stroke only w/hemorrhage, large MCA, or brainstem involvement

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