Taufan Arif, [Link]., Ns., M.

Kep
 Definition
• Stroke is a descriptive term for the sudden
onset of acute neurologic deficit persisting for
more than 24 hours and caused by the
interruption of blood flow to the brain.
• Each year, approximately 795,000 people have
a stroke; 610,000 of these are first attacks, and
185,000 are recurrent attacks
 Classification
• Strokes are classified as ischemic and
hemorrhagic
• Hemorrhagic strokes can be further
categorized as subarachnoid hemorrhages
(SAHs) and intracerebral hemorrhages (ICHs).
• Approximately 87% of all strokes are ischemic,
10% are ICHs, and 3% are SAHs.
Subarachnoid hemorrhages
intracerebral hemorrhages
 Ischemic Vs Hemorrhage Stroke
Ischemic Hemorrhage
• Due to occlusion of an • Due to rupture of
artery supplying brain cerebral artery
tissue • ICH in brain tissue
• Most common stroke at • SAH around brain
88% surface
• Reversible with • Reversible with surgery
fibrinolysis or and medical
mechanical clot management
disruption
 Etiology
• The brain cannot store oxygen or glucose, so
requires a constant flow of blood to supply
these nutrients.
• The blood supply to the brain can be altered
through several different processes.
• These etology include embolism, thrombosis,
and compression or spasm of the vessels.
 Etiology
• Ischemic stroke due to embolism or thrombus
formation accounts for approximately 85% of
all strokes.
• Edema occurs in the area of ischemic or
infarcted tissue and contributes to further
neuronal cell death.
 Etiology
• If ischemia is not reversed, neuronal cell death
and infarction of brain tissue occurs.
• The penumbra is an area of tissue that
surrounds the core ischemic area.
• The penumbra receives some blood flow from
adjacent vessels but perfusion is marginal. If
CBF is improved, the penumbra may recover.
 Risk Factor
1. hypertension 9. Dyslipidemia
2. Cardiac disease (coronary [Link]
artery disease, heart failure,
atrial fibrillation, endocarditis, (cancer, pregnancy,
patent foramen ovale, high RBCs, sickle
myocardial infarction, carotid cell)
artery disease),
3. Diabetes [Link]
4. Increased age [Link]
5. Race (African American)
6. Male gender [Link] inactivity
7. Stroke History [Link] or illicit
8. Family history drugs.
 Pathophysiology
• The pathophysiology of stroke varies based on
the precipitating event.
• Thrombosis and embolism formation,
described below, result in acute ischemic
stroke.
 Thrombosis
• Thrombosis is the most common cause of
ischemic stroke usually due to atherosclerosis
and the formation of plaque within an artery.
• Thrombosis can form in large vessels or small
vessels
• A thrombus then forms at the site of the plaque
and causes brain tissue ischemia along the course
of the affected vessel, which results in infarct
• Thrombosis due to atherosclerosis of large
cerebral vessels results in large areas of infarct.
 Thrombosis
• Considerable edema often develops, further
increasing ischemia by compressing areas
surrounding the infarct.
• Significant functional deficits are common. If
thrombus forms in a smaller branching artery,
a lacunar infarct develops.
• Lacunar infarcts result in smaller areas of
neuronal cell death.
 Embolism
• Embolism refers to the occlusion of a cerebral
vessel, most often by a blood clot but also by
infectious particles, fat, air, or tumor
fragments.
• Embolism is often associated with heart
disease that results in bacterial vegetations or
blood clots that are easily detached from the
wall or valves of the heart and then travel to
the brain, lodging in a cerebral vessel.
 Embolism
• Chronic atrial fibrillation, valvular disease, prosthetic
valves, cardiomyopathy, and atherosclerotic lesions of
the proximal aorta are common causes of embolism.
• Less common causes include atrial myxomas, patent
foramen ovale, and bacterial endocarditis.
• The fragmented substance easily lodges at the
bifurcation of the middle cerebral artery, sometimes
breaking apart and traveling further into the cerebral
vascular system.
• The onset of an embolic occlusion is rapid, with
symptoms that develop without warning.
 Clinical Presentation
• Common signs and symptoms include weakness
in an extremity or on one side of the body,
sensory changes, difficulty speaking or
understanding speech, facial droop, headache,
and visual changes.
• Clinical presentation of stroke varies based on the
area of ischemia or infarction.
• The National Institute of Health Stroke Scale
(NIHSS) is often used to evaluate and monitor
patients after stroke.
How to rapid assessment?
Stroke in a cerebral hemisphere
• Signs and symptoms occur on the side of the
body contralateral to the stroke.
• Weakness or paralysis occurs in one or both
extremities, and sensory loss may also be
noted.
• Visual field deficits are also contralateral to
the lesion.
• Dominant hemisphere strokes often produce
receptive, expressive, or global aphasia.
cerebral hemisphere
 Cerebellar or Brain Stem Stroke
• Motor and sensory function may be impaired on one
or both sides of the body.
• Loss of equilibrium, decreased fine motor abilities, and
nausea or vomiting are typical.
• Cranial nerve deficits are common and include
dysarthria, nystagmus, dysphagia, and decreased
cough reflex.
• Careful evaluation of airway protection and
swallowing ability is essential to determine aspiration
risk.
• Patients with severe deficits often require a feeding
tube and potentially a tracheostomy.
• In patients with cerebellar stroke, obstructive
hydrocephalus may occur due to occlusion of
the ventricular drainage system by edema.
• Surgical decompression of the posterior fossa
may be necessary and an external ventricular
drain may be placed.
• Brain stem stroke because of basilar artery
occlusion results in quadriplegia and loss of
facial movements (locked-in syndrome).
 Diagnostic Test
• The goal of initial diagnostic testing in acute
stroke is to rule out intracranial hemorrhage
(ICH), because treatments for hemorrhagic and
ischemic stroke differ significantly.
• CT scanning is available at most hospitals, can be
performed quickly, and is an excellent tool for
detecting intracranial bleeding.
• Specialized MRI scans can detect areas of
ischemia.
 Diagnostic Test
• Other tests that may be done acutely include
cerebral angiography and carotid ultrasound.
• Transthoracic or transesophageal
echocardiography is used to assess cardiac
causes of stroke.
• Hypercoagulable states are detected through
laboratory work.
• All patients who present with stroke receive
an ECG
 Principles of Management of Acute
Ischemic Stroke
• The goals of treatment are to restore
circulation to the brain when possible, stop
the ongoing ischemic process, and prevent
secondary complications.
 Evaluation of Conditions That Mimic
Acute Ischemic Stroke
1. Other conditions may mimic acute ischemic stroke
and must be ruled out.
2. Hypoglycemia may cause stroke-like symptoms and is
easily detected by using a bedside monitor to check
blood glucose.
3. Radiologic tests are performed on all patients with
signs and symptoms of stroke to rule out intracranial
bleeding.
4. Other conditions that may mimic acute ischemic
stroke include toxic or metabolic disorders, migraines,
seizures, mass lesions such as brain tumors or
abscesses, and psychological disorders.
 Fibrinolytic Therapy
• Function restore perfusion to the affected area.
• IV administration of recombinant tissue
plasminogen activator (rtPA) is considered in all
patients who meet the inclusion/exclusion
criteria (Table 12-6) and can be treated within 3
hours of the onset of symptoms.
• Patients who can be treated between 3 and 4.5
hours after symptom onset can also receive rtPA,
although there are several additional exclusion
criteria
 Fibrinolytic Therapy
• The recommended dose for rtPA is 0.9 mg/kg, with 10% of
the total dose given as a bolus over 1 to 2 minutes followed
by the remainder of the dose as an infusion over 1 hour.
• The maximum dose recommended is 90 mg.
• Vital signs and neurologic checks are done every 15
minutes for the first 2 hours, then every 30 minutes for 6
hours, and then hourly until 24 hours following initial
treatment.
• Following rtPA administration, antiplatelet or anticoagulant
medicines are avoided for 24 hours.
• Placement of nasogastric tubes, bladder catheters, and
invasive lines is delayed to decrease the risk of
hemorrhage.
 Blood Pressure Management
• a marked or sudden decrease in blood pressure
can significantly decrease cerebral perfusion.
• For patients who are not eligible for fibrinolytic
therapy, blood pressure is not treated emergently
unless the systolic blood pressure exceeds 220
mm Hg or the diastolic blood pressure exceeds
120 mm Hg.
• Because of the risk of hemorrhage, blood
pressure management is more stringent in
patients who are eligible for or who have
received fibrinolytic therapy (Table 12-7).
 BLOOD PRESSURE MANAGEMENT FOR STROKE ACCORDING TO THE
AMERICAN STROKE ASSOCIATION GUIDELINES

BLOOD PRESSURE TREATMENT

Nonthrombolytic Candidates
DBP >140 mm Hg Sodium nitroprusside (0.5 mcg/kg/min); aim for
10%-20% reduction in DBP
SBP >220 mm Hg, DBP 121-140 10-20 mg of labetalol‡ given by IVP over 1-2 min;
mm Hg, or MAP† >130 mm Hg may repeat or double labetalol every 20 min to a
maximum dose of 300 mg
SBP <220 mm Hg, DBP = 120 Emergency antihypertensive therapy is deferred in
mm Hg, or MAP† <130 mm Hg the absence of aortic dissection, acute
myocardial infarction, severe congestive heart
failure, or hypertensive encephalopathy
 BLOOD PRESSURE TREATMENT
Thrombolytic Candidates Pretreatment
SBP >185 mm Hg or 1-2 inches of nitroglycerine paste (Nitropaste) or 1-2 doses of 10-20 mg
DBP >110 mm Hg of labetalol‡ given by IVP;
if BP is not reduced and maintained to <185/110 mm Hg, the patient
should not be treated with tPA

During and After Treatment

Monitor BP BP is monitored every 15 min for 2 hr, then every 30 min for 6 hr, and
then hourly for 16 hr
DBP >140 mm Hg Sodium nitroprusside (0.5 mcg/kg/min)
SBP >230 mm Hg or 10 mg of labetalol‡ given by IVP over 1-2 min; may repeat or double
DBP 121-140 mm Hg labetalol every 10 min to a maximum dose of 300 mg or give initial
labetalol bolus and then start a labetalol drip at 2-8 mg/min
If BP not controlled by labetalol, consider sodium nitroprusside

SBP 180-230 mm Hg 10 mg of labetalol‡ given by IVP; may repeat or double labetalol every
or DBP 105-120 mm 10-20 min to a maximum dose of 300 mg or give initial labetalol bolus
Hg and then start a labetalol drip at
2-8 mg/min
 Management of Increased ICP
• Cerebral edema occurs in the area of infarct
and may lead to increased ICP.
• Hemicraniectomy may be used to alleviate
increased ICP in patients with large infarcts,
particularly in the distribution of the middle
cerebral artery.
• Aggressive treatment of fever is warranted to
avoid increases in cerebral metabolic demand.
 Management of Increased ICP
Monitoring neurologic status:
• Level of consciousness
• coma score,
• pupillary size and reaction to light,
• eye movement,
• motor and sensory function.
 Management of Increased ICP
Adequate Oxygenation and ventilation:
• Pao2 and Paco2 are maintained at normal levels
 evaluated
• intubation and mechanical ventilation For
patients with impaired consciousness.
• Both hypercarbia and severe hypoxemia can
result in cerebral vasodilation and increased ICP.
 hyperventilation
• Suctioning and other pulmonary care measures
may increase ICP but are performed as clinically
indicated
 Management of Increased ICP
Blood Pressure and Fluid Management
• Management of blood pressure is determined
by the level of ICP and CPP
• the goal is to maintain a CPP of at least 50 to
60 mm Hg.
• If the patient is hypotensive, non–glucose-
containing fluids are infused to ensure
euvolemia.
 Management of Increased ICP
Positioning
• elevating the head of the bed 30° optimizes
ICP and CPP
• Hip flexion is minimized.
• The head and neck are maintained in a neutral
position, avoiding flexion, hyperextension, or
rotation  Cervical collars
 Management of Increased ICP
CSF Drainage  Drainage of small amounts of CSF may be used
to decrease ICP in patients with an intraventricular catheter.
 Management of Increased ICP
Minimizing Environmental Stimuli
• The environment is kept calm and quiet.
• Patient care activities (suctioning, bathing,
turning) are spaced out to avoid
overstimulation and allow recovery time.
 Management of Increased ICP
Preventing Increased Cerebral Metabolic Demand
• Seizure activity increases cerebral metabolic
demand and ICP  The prophylactic use of
anticonvulsants
• For each elevation of 1°C, cerebral metabolic
demand increases by approximately 6%.
• Methods to normalize temperature include
antipyretics, air- or water-filled cooling blankets.
 Management of Increased ICP
Analgesia and Sedation
• Analgesia and sedation are used to prevent
elevation of ICP due to pain or agitation.
• Commonly used agents include fentanyl for
analgesia and midazolam for sedation.
 Management of Increased ICP
Medications to Decrease Cerebral Edema
• Osmotic diuretics reduce cerebral edema by
pulling extracellular fluid from brain tissue
into the blood vessels.
• Mannitol is commonly used and is given as a
bolus dose of 0.25 to 1 g/kg body weight.
• Hypertonic saline is also used by many
practitioners to increase serum osmolality and
pull water into the vascular space
 Management of Increased ICP
Surgical Treatment
• surgical evacuation of the hematoma is likely
to reduce ICP.
• In cases of diffuse cerebral edema, a portion
of the skull may be removed to increase
compliance and allow the brain to swell
outside the contained area of the skull. This
procedure is referred to as a craniectomy
 Glucose Management
• Hyperglycemia is associated with worse
outcomes after stroke and is treated;
• lowering blood glucose to 140 to 180 mg/dL is
a common goal.
• Hypoglycemia is deleterious and must be
avoided.
 Definition
• Subarachnoid hemorrhage (SAH) is bleeding into
the subarachnoid space, usually as the result of a
ruptured aneurysm or arteriovenous
malformation (AVM).
• Computed tomographic angiography (CTA) and
magnetic resonance angiography (MRA) can
detect up to 95% of all aneurysms.
• Known risk factors for SAH include hypertension,
smoking, and alcohol or stimulant use
Type aneurisma
 Etiology
• Cerebral aneurysm rupture accounts for
approximately 85% of all cases of spontaneous
SAH.
• AVM rupture is responsible for roughly 6% of
all SAHs
 Etiology, Risk Factors, and
Pathophysiology
• Hypertension is the most common cause of
ICH.
• Other causes include vascular malformations
(arteriovenous malformations or cavernous
malformations), coagulopathy, amyloid
angiopathy, tumor, vasculitis, venous
infarction, and illicit drug abuse.
 Clinical Presentation
• Intracranial hemorrhage presents with a
sudden onset of neurologic deficits often
associated with a severe headache,
nausea/vomiting, decreased consciousness,
and sometimes seizures.
 Diagnostic Tests
• Intracranial hemorrhage is most often
diagnosed using CT scanning, although MRI is
sometimes used, cerebral angiography.
WHAT is it??
 Principles of Management of
Intracerebral Hemorrhage
• Initial priorities of care for the patient with
ICH include blood pressure control and
correction of coagulopathy.
• Fresh frozen plasma, platelets, vitamin K, or
prothrombin complex concentrate may be
ordered; the goal is rapid correction of
coagulopathy.
 Principles of Management of
Intracerebral Hemorrhage
• Operative management may or may not be indicated
based on size and location of hemorrhage.
• Cerebellar hemorrhage may require a suboccipital
craniectomy to evacuate the clot and decrease
pressure on vital structures.
• Intraventricular hemorrhage may cause hydrocephalus,
which is treated by placement of an external
ventricular drain.
• Antiepileptic drugs (AEDs) are recommended for
patients who experience a seizure or who show
electrographic evidence of seizure on EEG.
 Nursing Assesment
• Neurologic assessment in the critical care unit
can be broken down into the following
components: level of consciousness, mental
status, motor examination, sensory
examination, and cranial nerve examination.
 level of consciousness
• Normal
• Confused
• Letahargic
• Obtunded
• Stupor
• Comatose