HEMORRHAGIC STROKE

Concept
A hemorrhagic stroke is bleeding (hemorrhage) that suddenly interferes with the brain's
function. This bleeding can occur either within the brain or between the brain and the skull.
Pathophysiology
 Hemorrhagic strokes usually occur spontaneously. It`s caused by vascular rupture
with bleeding into brain. The mass effect can further cause bleeding and hematoma
expansion from neighboring vessels
 Hematoma growth over several hours following presentation of symptoms is common
(30-40%)
 Hemorrhages commonly occurs at the basal ganglia, thalamus, pons, or cerebellum
Hemorrhagic strokes account for about 20% of all strokes, and are divided into categories
depending on the site and cause of the bleeding:
Intracerebral hemorrhage: It is the one that affects the fifth and sixth decade of life.
Bleeding occurs from a broken blood vessel within the brain.
Some things that increase your risk for this kind of hemorrhage are
1. High blood pressure (hypertension)
2. heavy alcohol use
3. advanced age
4. use of cocaine or amphetamines.
Other kinds of stroke can convert to an intracerebral hemorrhage. For example, a stroke that
begins without hemorrhage (a thrombotic or embolic stroke) can lead to intracerebral
hemorrhage shortly afterward. This is especially common for embolic strokes that are related
to a heart valve infection (endocarditis). In this case, a clump of bacteria and inflammatory
cells from the valve infection can become a floating mass within the bloodstream (called an
embolus). The infected clump can travel into a brain artery and become wedged there. Then,
the infection can spread through the artery.
In rare cases, intracerebral hemorrhage may happen because of a leaking arteriovenous
malformation (AVM), which is an abnormal and weak-walled blood vessel that connects an
artery and a vein. This weak blood vessel is present from birth—it is larger than a capillary
and blood that flows in can be at high pressure, causing the AVM to eventually stretch or
leak.
Subarachnoid hemorrhage: It is an Acute emergence of blood in the subarachnoid space.
Is more frequent in adolescents and young adults and it`s related to rupture of aneurysms at
the level of the Willis polygon. Bleeding from a damaged blood vessel causes blood to
accumulate at the surface of the brain. Blood fills a portion of the space between the brain
and the skull, and it mixes with the cerebrospinal fluid that cushions the brain and spinal
cord. As blood flows into the cerebral spinal fluid, it increases pressure on the brain, which
causes an immediate headache. In the days immediately following the bleeding, chemical
irritation from clotted blood around the brain can cause brain arteries that are near to this area
to go into spasm. Artery spasms can damage brain tissue. Most often, a subarachnoid
hemorrhage happens because of a leaking saccular aneurysm (a sack-like bulge in the wall
of an artery), but it also can occur because of leakage from an arteriovenous malformation.
Signs symptoms
Symptoms of a hemorrhagic stroke vary, depending on the cause:
Intracerebral hemorrhage: Symptoms almost always occur when the person is awake.
Symptoms tend to appear without warning, but they can develop gradually. Symptoms
worsen over a period of 30 to 90 minutes. Symptoms can include:
1. Sudden weakness
2. Paralysis or numbness in any part of the body
3. Inability to speak
4. Inability to control eye movements correctly
5. Vomiting
6. Difficulty walking
7. Irregular breathing
8. Stupor
9. Coma
Subarachnoid hemorrhage: When caused by a ruptured aneurysm, symptoms can include:
1. A very severe headache that starts suddenly (Some people describe it like a
"thunderclap.")
2. Loss of consciousness
3. Nausea and vomiting
4. Inability to look at bright light
5. Stiff neck
6. Dizziness
7. Confusion
8. Seizure
9. Loss of consciousness
Diagnosis
As with any pathology, it is essential in the initial evaluation the appropriate clinical history
and physical examination to be able to suspect and orient towards a certain cause.
To diagnose and classify your stroke, your doctor will need an imaging test of your brain.
Several tests can be useful, including a computed tomography (CT) scan or magnetic
resonance imaging (MRI) scan. For hemorrhagic strokes, CT scans are the fastest and most
effective test. If a subarachnoid hemorrhage is suspected, your doctor may do a lumbar
puncture, also called a spinal tap, in which a small sample of cerebrospinal fluid is removed
through a needle inserted into your back. This fluid is examined to see if it contains blood.
Another test, called an MRI angiography, can provide information about blood flow to your
brain.
If these tests show that patient are having a stroke, you will undergo tests to check for the
cause. Because a hemorrhagic stroke involves bleeding, it is important to assess the ability
of your blood to clot. If the patient takes a blood-thinning medication called warfarin
(Coumadin), which can contribute to a stroke, the blood will be tested to measure the drug
effect. If the infection endocarditis is suspected, blood samples will be drawn and checked in
a laboratory for bacteria.
Complementary studies:
 Electrocardiogram (EKG)
 chest X-ray.
 carotid Doppler
 Echocardiogram
 ECG, SaO2, blood biochemistry (glucose, urea, creatinine, sodium, potassium and
Troponin), coagulation study.
Treatment
Pharmacological treatment

 Management of cerebral edema and intracranial hypertension

Faced with signs or symptoms of intracranial hypertension, cerebral herniation,
increased degree of coma, regardless of the type of stroke.
 Osmotic diuretics; intravenous mannitol; loading dose of 1g / kg, the dose
can be repeated every 6 hours.
 Mechanical hyperventilation; with PaCO2 objective of 28-35 mmHg, only as
a transitory measure, since it only lasts a few hours.
 Barbiturates; thiopental sodium in doses of 1-5 mg / kg intravenously to
induce a barbiturate coma.
 Others: surgical evacuation, ventricular catheter placement
(ventriculostomy).
 Management of hypertension
o Blood pressure should be kept moderately high to maintain adequate perfusion of
the area.
 Pressures below 185/110 mmHg in hemorrhagic stroke are not initially
treated. If the blood pressure is maintained within this limit 1 hour after the
first measurement or if the systolic blood pressure is greater than 185
mmHg, hypotensive management is started orally with labetalol at a dose
of 100 mg every 12 hours. All this as long as there is no AMI, kidney failure,
severe heart failure, etc.
  If it is not possible to use the oral route or if the blood pressure is greater
than 230/120 mmHg in two readings separated by 5 minutes, give urgent
intravenous hypotensive treatment; Labetalol at an initial dose of 20 mg (4
ml) in 5 minutes by intravenous bolus until control of the figures is achieved
or until administration of 100 mg. Contraindicated in heart failure,
peripheral arterial ischemia and COPD.
 When the diastolic blood pressure is greater than 140 mmHg, the patient is
admitted to the intensive care unit and intravenous sodium nitroprusside is
administered.
 Seizure management
 Intravenous antiepileptic drugs should be administered if there are seizures
to prevent their recurrence, an option is phenytoin.

Surgical management:

If necessary, a surgeon will cut the skull bone to decrease the compression of the brain tissue. In
some cases, surgery is necessary to remove a large portion of the clot after a hemorrhage, but in
most patients, the body eventually reabsorbs the clotted blood on its own.

If bleeding occurred because of an abnormally formed blood vessel, surgery may be appropriate to
prevent a hemorrhage from happening again. An aneurysm can be repaired by placing a surgical
clip.

The surgical management is Indicated in patients with:

 Cerebellar hematomas with decreased stage of consciousness, signs of brainstem

compression, or obstructive hydrocephalus.
 Superficial lobar hematomas with compressive neurological deterioration.
 Hematomas open to ventricles that generate hydrocephalus.
 ISCHEMIC STROKE

Concept
It is a pathological clinical disorder of the central nervous system that occurs as a result of the
compromise of the vessels that supply it, this dysfunction is due to a circulatory alteration due to
occlusion of the brain arterial tree determining functional and vital commitment of the affected
territory.

Pathophysiology
Insufficient blood flow in a single cerebral artery can often be compensated with an efficient
collateral system, especially between the carotid and vertebral arteries through the anastomosis
in the Willis polygon and, to a lesser extent, between the major arteries that supply the cerebral
hemispheres However, normal variations of the Willis polygon and the caliber of the various
collateral vessels, atherosclerosis and other acquired arterial lesions may interfere with collateral
flow, which increases the risk that blockage in an artery causes cerebral ischemia.

Some neurons die when perfusion is <5% of normal for> 5 min; however, the extent of the
damage depends on the severity of the ischemia. If it is mild, the damage appears slowly;
therefore, even if the perfusion is 40% of normal, it may take 3 to 6 hours before the brain tissue is
completely lost. However, when severe ischemia persists for> 15 to 30 min, all affected tissue dies
(Stroke). The damage occurs more rapidly during hyperthermia and more slowly during
hypothermia. When tissues are ischemic but do not yet have irreversible damage, the rapid
restoration of blood flow can reduce or reverse the lesion. For example, the intervention can save
moderately ischemic areas (in penumbra) that often surround the areas of severe ischemia (these
areas exist due to collateral flow).

The mechanisms of ischemic injury include:

Edema.
microvascular thrombosis.
Programmed cell death (apoptosis).
Infarction with cell necrosis.

Inflammatory mediators (for example, IL-1B, tumor necrosis factor-alpha) contribute to edema
and microvascular thrombosis. Edema, if severe or extensive, may increase intracranial pressure.

Many factors can contribute to necrotic cell death; include loss of ATP deposits, loss of ionic
homeostasis (including intracellular calcium accumulation), lipid peroxidative damage of cell
membranes by free radicals (an iron-mediated process), excitatory neurotoxins (e.g.., glutamate)
and intracellular acidosis due to lactate accumulation.

Signs symptoms
The signs and symptoms of ischemic stroke depend on the part of the brain affected. Although
neurological deficit patterns often suggest the affected artery, the correlation is often inaccurate.
Embolic strokes often occur during the day; headache may precede neurologic deficits. Thrombi
tend to occur during the night and thus are first noticed on awakening.
Lacunar infarcts may produce one of the classic lacunar syndromes (eg, pure motor hemiparesis,
pure sensory hemianesthesia, ataxic hemiparesis, dysarthria–clumsy hand syndrome); signs of
cortical dysfunction (eg, aphasia) are absent. Multiple lacunar infarcts may result in multi-infarct
dementia.
A seizure may occur at stroke onset, more often with embolic than thrombotic stroke. Seizures
may also occur months to years later; late seizures result from scarring or hemosiderin deposition
at the site of ischemia.

Deterioration during the first 48 to 72 h after onset of symptoms, particularly progressively

impaired consciousness, results more often from cerebral edema than from extension of the
infarct. Unless the infarct is large or extensive, function commonly improves within the first few
days; further improvement occurs gradually for up to 1 yr.

Diagnosis

 Primarily clinical evaluation

 Neuroimaging and bedside glucose testing
 Evaluation to identify the cause

Diagnosis of ischemic stroke is suggested by sudden neurologic deficits referable to a specific

arterial territory. Ischemic stroke must be distinguished from other causes of similar focal deficits
(sometimes called stroke mimics), such as
 Hypoglycemia.
 Postictal [Todd] paralysis (a transient neurologic deficit, usually weakness, of the limb
contralateral to the seizure focus).
 Hemorrhagic stroke.
 Rarely, migraine.

Headache, coma or stupor, and vomiting are more likely with hemorrhagic stroke.

Differentiating clinically between the types of stroke is imprecise; however, some clues based on
symptom progression, time of onset, and type of deficit can help.

Although diagnosis is clinical, neuroimaging and bedside glucose testing are mandatory. CT is done
first to exclude intracerebral hemorrhage, subdural or epidural hematoma, and a rapidly growing,
bleeding, or suddenly symptomatic tumor. CT evidence of even a large anterior circulation
ischemic stroke may be subtle during the first few hours; changes may include effacement of sulci
or the insular cortical ribbon, loss of the gray-white junction between cortex and white matter,
and a dense middle cerebral artery sign. Within 6 to 12 h of ischemia, medium-sized to large
infarcts start to become visible as hypodensities; small infarcts (eg, lacunar infarcts) may be visible
only with MRI. Diffusion-weighted MRI (highly sensitive for early ischemia) can be done
immediately after initial CT neuroimaging.

Distinction between lacunar, embolic, and thrombotic stroke based on history, examination, and
neuroimaging is not always reliable, so tests to identify common or treatable causes and risk
factors for all of these types of strokes are routinely done. Patients should be evaluated for the
following categories of causes and risk factors:

 Cardiac (eg, atrial fibrillation, potential structural sources of emboli)

 Vascular (eg, critical arterial stenosis)
 Blood (eg, hypercoagulability)

For cardiac causes, testing typically includes ECG, telemetry or Holter monitoring, serum troponin,
and transthoracic or transesophageal echocardiography.
For vascular causes, testing may include magnetic resonance angiography (MRA), CT angiography
(CTA), carotid and transcranial duplex ultrasonography, and conventional angiography. The choice
and sequence of testing is individualized, based on clinical findings. MRA, CTA, and carotid
ultrasonography all show the anterior circulation; however, MRA and CTA provide better images
of the posterior circulation than carotid ultrasonography. MRA is generally preferred to CTA if
patients can remain still during MRA (to avoid motion artifact).
For blood-related causes (eg, thrombotic disorders), blood tests are done to assess their
contribution and that of other causes. Routine testing typically includes CBC, platelet count,
PT/PTT, fasting blood glucose, and lipid profile.
Depending on which causes are clinically suspected, additional tests may include measurement of
homocysteine, testing for thrombotic disorders (antiphospholipid antibodies, protein S, protein C,
antithrombin III, factor V Leiden), testing for rheumatic disorders (eg, antinuclear antibodies,
rheumatoid factor, ESR), syphilis serologic testing, Hb electrophoresis, and a urine drug screen for
cocaine and amphetamines.

A cause cannot be identified for some strokes (cryptogenic strokes).

Treatment
 General stroke treatments
 Acute antihypertensive therapy only in certain circumstances
 Antiplatelet therapy
 For acute treatment, sometimes reperfusion with recombinant tissue plasminogen activator
(IV or thrombolysis-in-situ), and/or mechanical thrombectomy
 Sometimes anticoagulation
 Long-term control of risk factors
 Sometimes carotid endarterectomy or stenting
Acute stroke treatment
Perfusion of an ischemic brain area may require a high BP because autoregulation is lost; thus, BP
should not be decreased except in the following cases:

 BP is > 220 mm Hg systolic or > 120 mm Hg diastolic on 2 successive readings > 15 min
apart.
 There are signs of other end-organ damage (eg, aortic dissection, acute MI, pulmonary
edema, hypertensive encephalopathy, retinal hemorrhages, acute renal failure).

 Use of recombinant tPA and/or mechanical thrombectomy is likely.

To lower BP, clinicians can give nicardipine 2.5 mg/h IV initially; dose is increased by 2.5 mg/h q 5
min to a maximum of 15 mg/h as needed to decrease systolic BP by 10 to 15%. Alternatively,
IV labetalol 20 mg IV can be given over 2 min; if response is inadequate, 40 to 80 mg can be given
every 10 min up to a total dose of 300 mg.
Patients with presumed thrombi or emboli may be treated with one or a combination of the
following:

 tPA, thrombolysis-in-situ, and/or mechanical thrombectomy (1)

 Antiplatelet drugs

 Anticoagulants

Most patients are not candidates for thrombolytic therapy; they should be given an antiplatelet
drug (usually aspirin 325 mg po) when they are admitted to the hospital. Contraindications to
antiplatelet drugs include aspirin-induced or NSAID-induced asthma or urticaria, other
hypersensitivity to aspirin or to tartrazine, acute GI bleeding, G6PD deficiency, and use of warfarin.

Recombinant tPA can be used for patients with acute ischemic stroke up to 3 h after symptom
onset if they have no contraindications to tPA. Some experts recommend using tPA up to 4.5 h
after symptom onset; however, between 3 h and 4.5 h after symptom onset, additional exclusion
criteria apply.
tPA must be given within 4.5 h of symptom onset—a difficult requirement. Because the precise
time of symptom onset may not be known, clinicians must start timing from the moment the
patient was last observed to be well.
Before treatment with tPA, the following are required:
 Brain hemorrhage must be excluded by CT.
 Systolic BP must be < 185 mm Hg.
 Diastolic BP must be < 110 mm Hg.
Antihypertensive drugs (IV nicardipine, IV labetalol) may be given as above.
Thrombolysis-in-situ (angiographically directed intra-arterial thrombolysis) of a thrombus or
embolus can sometimes be used for major strokes if symptoms began < 6 h ago, particularly for
strokes that are due to large occlusions in the middle cerebral artery and cannot be treated with IV
recombinant tPA. Clots in the basilar artery may be intra-arterially lysed up to 12 h after stroke
onset, sometimes even later depending on the clinical circumstances. This treatment, although
standard of care in some large stroke centers, is often unavailable in other hospitals.

Mechanical thrombectomy (angiographically directed intra-arterial removal of a thrombus or

embolus by a stent retriever device) is often used to treat patients who have had a severe stroke
and have an NIH stroke score ≥ 6 when IV and/or intra-arterial thrombolysis has been ineffective;
it must be done within 6 h of symptom onset.

Anticoagulation with heparin or low molecular weight heparin is used for stroke caused by
cerebral venous thrombosis and is sometimes used for emboli due to atrial fibrillation and for
stroke due to presumed progressive thrombosis if it continues to evolve despite use of antiplatelet
drugs and cannot be treated any other way (eg, with tPA or invasive methods).

El flujo sanguíneo cerebral puede ser interrumpido por dos formas:

La primera, por un coágulo sanguíneo (denominado «trombo») obstruye el flujo de sangre a
ciertas partes del cerebro. El trombo puede formarse en una arteria afectada por aterosclerosis. La
aterosclerosis es un proceso que se caracteriza por la acumulación de placa en el interior de la
arteria. Esta placa vuelve más gruesa la pared arterial, estrechando el vaso. La placa está
compuesta de grasa, colesterol, fibrina (una sustancia coagulante) y calcio. A medida que la placa
se acumula en las arterias, la sangre circula más lenta y dificultosamente, facilitando la
coagulación. Un vaso sanguíneo estrechado por aterosclerosis tiene mayores probabilidades de
ser obstruido por un coágulo, interrumpiéndose así el flujo sanguíneo.

La segunda, un émbolo. Esto es causado por un coágulo sanguíneo que se origina en otro lugar del
organismo, generalmente el corazón, y viaja por la sangre hasta el cerebro. Este coágulo obstruye
una arteria que conduce al cerebro o que se encuentra dentro de él.

El émbolo llega a un punto donde no puede seguir avanzando y queda atascado, obstruyendo una
pequeña arteria cerebral e interrumpiendo el flujo de sangre al cerebro.

Cerebral blood flow can be interrupted in two ways:

The first, by a blood clot (called "thrombus") obstructs the flow of blood to certain parts of the
brain. The thrombus can form in an artery affected by atherosclerosis. Atherosclerosis is a process
that is characterized by plaque buildup inside the artery. This plaque makes the arterial wall
thicker, narrowing the vessel. Plaque is made up of fat, cholesterol, fibrin (a coagulant substance)
and calcium. As plaque builds up in the arteries, blood circulates more slowly and difficultly,
facilitating coagulation. A blood vessel narrowed by atherosclerosis is more likely to be blocked by
a clot, thus interrupting blood flow.

The second, a plunger. This is caused by a blood clot that originates in another place in the body,
usually the heart, and travels through the blood to the brain. This clot clogs an artery that leads to
or is inside the brain.

The plunger reaches a point where it cannot keep moving forward and gets stuck, obstructing a
small cerebral artery and interrupting the flow of blood to the brain.