NEURO-ICU TREATMENT TECHNIQUES
WHAT IS A STROKE?
Stroke results from interruption of blood flow or bleeding into a specific part of the brain. The brain is supplied with blood by arteries, and this blood is drained back to the heart by veins. If one of these blood vessels becomes blocked, or if one of them ruptures, a stroke occurs. Blood carries oxygen and nutrients essential to the survival of the brain. Therefore, any interruption of blood flow can cause damage to brain cells and death of that region of the brain. In the end, the affected area of the brain can no longer function, leading to a neurological deficit.
What are the symptoms of stroke?
Stroke is characterized by the sudden onset of a global or focal neurologic deficit. The most common symptoms of stroke are:
1. Weakness or numbness on one side of the body
2. Difficulty speaking or understanding speech
3. Loss of vision in one or both eyes
4. Loss of balance and coordination
5. Severe headache
Stroke, also known as a "brain attack," is a treatable medical emergency. However, in most cases, treatment is only effective within the first few hours of onset (generally 3-6 hours). If symptoms of stroke are experienced, call 911 immediately.
Who is afflicted with strokes?
In the United States stroke is the third leading cause of death. About 150,000 people die each year from stroke, and each year stroke claims about 450,000 new victims. Stroke is most prevalent in people who are over sixty years old. It is also slightly more common in men than in women, and it is more common in African-Americans than in Caucasians. Hypertension is by far the most important risk factor for stroke. Other important risk factors include diabetes, smoking, high cholesterol, alcohol abuse, oral contraceptive use, and the presence of a previous stroke.
What are the different types of strokes?
The type of stroke that a person suffers depends on how blood flow to the brain is interrupted (i.e, whether it is blocked by a blood clot, or whether a blood vessel has ruptured). Different types of stroke include:
» Cerebral infarction and transient ischemic attacks
» Intracerebral hemorrhage
» Subarachnoid hemorrhage
» Arteriovenous malformations
» Dural Sinus Thrombosis
CEREBRAL INFARCTION AND TRANSCIENT ISCHEMIC ATTACKS
What is cerebral ischemia?
Ischemia refers to the tissue damage that results from inadequate blood flow. In the case of cerebral ischemia blood flow to a region of the brain is blocked. Since the brain requires blood to survive, regions of the brain affected by cerebral ischemia die, a process called cerebral infarction. Cerebral ischemia and infarction accounts for about 80% of all strokes.
What causes an artery in the brain to be blocked?
Arteries can form atherosclerotic plaque in their walls which causes a narrowing of the lumen of these vessels (this is called stenosis). If this narrowing occurs a blood clot or thrombus can develop in the vessel.
An artery can also be blocked by a blood clot traveling from the heart. Such a clot is known as an embolus.
What is a transient ischemic attack (TIA)?
Sometimes the cerebral ischemia lasts for a brief period of time (<24 hours) and then abates. In this case the sudden blockage of blood flow is only temporary, and the attack is known as a transient ischemic attack or TIA. Such attacks are characterized by brief periods of: loss of sensation or weakness on one side of the body or face, difficulty speaking, uncoordination, or an inability to speak or to see out of one eye. TIAs are usually brief; more than 90% last less than 30 minutes.
TIAs are an extremely important warning sign of a stroke. About one-third to one-half of people suffering from a TIA will have a major stroke within five years. People with TIAs are almost 10 times more likely to develop a stroke than people who have never experienced one.
What can be done once a TIA has occurred?
An anticoagulant drug, such as warfarin or heparin, can be administered. Anticoagulants serve to disrupt blood clots and allow blood flow in the affected artery to resume. Aspirin or ticlopidine may also be effective.
If the obstruction is due to stenosis (narrowing) of the carotid artery in the neck then an operation known as a carotid endarterectomy can be performed to remove the atherosclerotic plaque causing the occlusion.
Stenosis of intracranial segment of left internal carotid artery before (left)
and after (right) balloon angioplasty
What can be done for multiple, recurrent TIAs?
Multiple recurrent TIAs is an extremely dangerous situation. This process usually results from tight blockage (or stenosis) of a brain artery, and the chance of evolving to a completed stroke is very high. If anticoagulants are ineffective, cerebral angioplasty can be used in a neuro-ICU to open the blocked artery and allow resumption of blood flow to the threatened area of brain. This specialized technique, in which a balloon is inflated inside the blood vessel, resembles a "roto-rooter" treatment.
Can anything be done after a stroke has occurred?
Yes. A neuro-ICU is capable of rapidly and effectively managing ischemic stroke such that deficits suffered from that stroke are vastly reduced. The neuro-ICU offers a number of innovative acute treatment approaches to stroke:
- Thrombolysis with "clot-busting" drugs is aimed at increasing cerebral blood flow to brain regions affected by ischemia. Drugs mediating this treatment include tissue plasminogen activator (tPA) and urokinase. This type of drug can be administered into a vein or via a catheter directly into the occluded artery. Intravenous tPA has been shown to be effective when given within three hours of the onset of symptoms. After this so-called "therapeutic window," thrombolysis can be very dangerous and may result in excessive bleeding. A neuro-ICU allows continuous blood pressure and neurologic monitoring, which is critical after this type of treatment.
- Neuroprotection refers to treatment strategies directed toward protecting ischemic cells from progressing to infarction (cell death). Most of these agents work by blocking chemical processes that mediate secondary neuronal injury after ischemia. Hypothermia is an extremely effective means of protecting cerebral tissue from ischemic injury. Examples of experimental neuroprotective agents include excitatory amino acid blockers, calcium channel blockers, and free radical scavengers. The only neuroprotective agent approved for use in the U.S. is the calcium channel blocker nimodipine, which can prevent secondary ischemia after a ruptured brain aneurysm.
- Treatment of brain swelling (cerebral edema) can be important if the stroke is large or in close proximity to the brain stem. Intubation, hyperventilation, and mannitol can all be used to reduce swelling and secondary damage associated with a large stroke, and often can be life-saving. Placement of an intracranial pressure monitor is a key step in guiding this type of therapy.
INTRACEREBRAL HEMORRHAGE (ICH)
What is an intracerebral hemorrhage?
An intracerebral hemorrhage refers to bleeding that occurs into the substance of the brain itself. This is in contrast to a subarachnoid hemorrhage, in which blood enters the brain's fluid spaces. An ICH is usually caused by the rupture of a small artery due to high blood pressure in that vessel. Therefore, intracerebral hemorrhages usually occur in patients with hypertension. Intracerebral hemorrhage accounts for about 15% of all strokes.
What is the prognosis of ICH?
ICH has the worst prognosis of all forms of stroke. Overall, about 30% of patients with ICH will die. The damage caused by an ICH is dependent on the size of the hemorrhage, the proximity of the hemorrhage to the brain stem, and whether or not the blood enters the ventricles (CSF-filled spaces within the brain). Recurrent bleeding after ICH is unusual. For those patients that survive an ICH the outlook is often poor.
How is an ICH treated in a neuro-ICU?
The first priority in ICH treatment is the assessment of the patient's airway. Physicians in the neuro-ICU establish whether a patient is breathing normally. If the patient is unconscious, he or she is intubated. This means that a tube is passed into the patient's airway to keep it patent and ensure proper breathing.
Research has shown that brain hemorrhages can actively enlarge within the first 3 to 6 hours after ICH. Control of blood pressure at this time may limit hematoma enlargement, although this remains to be proven. This treatment must be carried out cautiously, however, to prevent excessive reduction of blood pressure which can lead to increased cerebral ischemia. Blood pressure can be continuously monitored with an arterial catheter in a neuro-ICU, thus allowing careful and precise adjustment of medications to reduce blood pressure.
Once the primary ICH is established treatment focuses on preventing any secondary brain injury. The main problem after ICH is brain swelling (or edema) that develops in regions immediately adjacent to the hemorrhage. Critical brain swelling can be detected with an intracranial pressure monitor, and can be treated with hyperventilation and mannitol.
Secondary injury can occur if the patient has seizures, which can be prevented with anticonvulsants. It can also occur if there is hydrocephalus, an excessive accumulation of fluid within the brain which can also result in increased intracranial pressure. If severe hydrocephalus is present, the bloody fluid can be drained via a ventricular drain placed in the ventricles.
In some cases surgical intervention is indicated. Generally, if the bleed or hematoma is large and readily accessible then surgery is advisable. If the hematoma is deep, however, surgery is not favored since normal brain tissue would be disrupted in order to reach the bleed.
Right middle cerebral artery aneurysm
What is a brain aneurysm?
A brain aneurysm is a ballooning of one of the arteries of the brain. Arteries at the base of the brain are most susceptible to aneurysm formation.
What is a subarachnoid hemorrhage (SAH)?
Subarachnoid hemorrhage refers to bleeding into the fluid that surrounds the brain. This fluid, known as cerebrospinal fluid (CSF), circulates in the subarachnoid space and serves to cushion the brain against injury. Following rupture of an aneurysm, blood appears in the CSF. The diagnosis can usually be established by CT scanning, but in some cases, a spinal tap (lumbar puncture) is necessary to detect the presence of bloody CSF. SAH can also result from head trauma, cocaine use, or rupture of an arteriovenous malformation.
Who is afflicted with SAH?
Aneurysmal subarachnoid hemorrhages account for 5% of all strokes and occur in 30,000 patients in North America each year. In contrast to other strokes in which the average age of the patient is in the sixties and seventies, the average patient suffering from SAH is in his or her forties. Nearly 20% of patients with SAH will die, and only half of those who survive will leave the hospital in good neurological condition. Cigarette smoking is the most important preventable risk factor for SAH.
What complications can occur as a result of an SAH?
In addition to the problems caused by the bleeding, three delayed neurological complications can occur after SAH:
Rebleeding refers to a second rupture of the brain aneurysm. Without surgery, rebleeding occurs in about 20% of patients in the first two weeks following the initial SAH, with a period of highest risk 48 hours after the initial event. After this initial time period the probability of rebleeding steadily declines. There is a 50% mortality associated with rebleeding.
Cerebral vasospasm refers to narrowing of arteries of the brain due to spasm of the vessels. If this is severe, delayed cerebral ischemia can occur, leading to a stroke or even death. Seven out of ten patients with aneurysmal SAH develop vasospasm, and of these seven people, three develop symptomatic cerebral ischemia.
Hydrocephalus refers to excessive accumulation of the fluid that surrounds the brain (CSF) due to clogging and blockage of the normal outflow pathways by blood. This can result in lethargy, confusion, and a dangerous increase in the pressure inside the skull (called intracranial pressure).
How is an SAH treated in a neuro-ICU?
Mortality from SAH has fallen dramatically in recent years, from over 50% to less than 20%, due to improvements in neurosurgical techniques and neurointensive care. In a neuro-ICU aneurysmal subarachnoid hemorrhage can be treated with state-of-the-art techniques that can prevent, reverse, or minimize the complications listed above. These include:
Prevention of rebleeding. This is usually accomplished by immediate surgery to place a clip across the neck of the aneurysm. In cases where the surgery is highly dangerous or impossible due to the location of the aneurysm, rebleeding can be prevented by placement of endovascular GDC coils within the aneurysm.
Prevention and treatment of ischemia from vasospasm. Sophisticated blood flow imaging techniques such as single photon emission computed tomography (SPECT) can be used to detect narrowing of vessels and reduction of blood flow before critical ischemia occurs. The drug nimodipine has been shown to prevent the death of brain tissue resulting from ischemia (blockage of blood flow) due to vasospasm. Induced hypertension and/or blood volume expansion has been shown to increase cerebral blood flow in regions which are ischemic as a result of vasospasm. This technique is known as hypertensive hypervolemic hemodilution, or "triple-H therapy". By increasing blood pressure and blood volume in the neuro-ICU, the amount of blood that supplies the brain is increased. This serves to reverse or minimize the effects of decreased blood flow due to vasospasm.
Treatment of hydrocephalus. Dangerous increases in intracranial pressure resulting from build-up of bloody CSF can be relieved by placement of a ventricular drain. In comatose patients, this type of treatment can be life-saving.
Can anything be done for severe SAH resulting in coma?
The neuro-ICU can aggressively treat severe SAH in the following manner. First, elevated intracranial pressure (ICP) due to hydrocephalus is treated by placement of a ventricular drain, which allows CSF drainage to lower ICP. Second, the ruptured aneurysm can be prevented from rebleeding by placing endovascular GDC coils within the aneurysm. These coils cause a blood clot (or thrombus) to form in the aneurysm, so that this part of the blood vessel is no longer functional. This important step then allows elevation of blood pressure (hypertensive hypervolemic hemodilution) to be used if necessary to treat ischemia from vasospasm.
ARTERIOVENOUS MALFORMATIONS (AVMS)
Occipital lobe arteriovenous malformation
What is an AVM?
An AVM is a tangled bundle of abnormal arteries and veins that are directly connected to each other. Under normal circumstances an artery gives rise to tiny capillaries which are interposed within the tissue of the brain. Nutrients and oxygen leave the capillaries to nourish the adjacent brain cells. The capillaries then give rise to a vein which drains blood back to the heart. In an AVM, however, blood is shunted from an artery directly into a vein without having nourished brain tissue. In fact, brain tissue is entirely displaced to the outskirts of the malformed tangle of vessels of an AVM. An AVM may be located on the surface of the brain or deep within the brain. An AVM is supplied by one or more feeding arteries, and blood exits via one or more draining vein.
Most AVMs are congenital malformations, meaning that they were present at birth. Dural AVMs are a special type of malformation which can develop in childhood or adult life. AVMs are rare; bleeding from an AVM accounts for only 1% of all strokes. Because of their rarity and complexity, AVMs should only be treated by experienced specialists.
What problems can result from having an AVM?
AVMs are usually detected when the patient develops symptoms. If no symptoms develop, it may be possible to live one's entire life with an AVM and never know it. The following represents symptoms associated with an AVM:
Bleeding. About 40-50% patients present with bleeding (or hemorrhage), which is the most feared complication of an AVM. This usually occurs in patients between ages 30 to 50. If an AVM is deep in the brain, blood is released into the brain tissue; this occurs about 2/3 of the time and is called an intracerebral hemorrhage. If an AVM is on the brain surface bleeding is released into the CSF, which is called subarachnoid hemorrhage.
Seizures (or convulsions). In 33% of patients, AVMs are diagnosed when the patient develops seizures. Patients presenting with seizures as an initial symptom are usually younger than those presenting with hemorrhage. Because of where the malformations are usually located, patients may report non convulsive seizures (episodes of odd sensations or visual hallucinations).
Headaches. In about 15% of patients the first symptom occurs as a headache. Like seizures, headaches usually first present in patients during adolescence. Typically patients have throbbing headaches which always occur in the same location.
Focal neurologic deficits. AVMs may occasionally manifest as weakness on one side of the body, sensory loss, or a speech or visual disturbance. This can result from either local brain compression, or less commonly from ischemia in adjacent brain regions if the AVM "steals" blood flow intended for that area.
What is the prognosis of an AVM?
Bleeding is the most important complication of an AVM. In most patients, the annual risk of AVM bleeding is 2-4% per year. This risk depends on various anatomic factors, including size (smaller AVMs bleed more) and the type of draining veins (deep drainage bleeds more), and on whether or not the AVM has bled previously. Prior bleeding is probably the most important risk factor for recurrent bleeding.
How is an AVM treated in a neuro-ICU?
The primary role of the neuro-ICU in AVM patients is for treating the complications of hemorrhage. This may include reduction of blood pressure (to prevent rebleeding and limit brain swelling), prevention of seizures, and treatment of brain swelling (cerebral edema) and increased intracranial pressure.
Once a ruptured AVM is stabilized, it can be treated by surgery, focal beam irradiation, or endovascular therapy aimed at blocking off the feeding arteries. Research is being done into treating AVM patients with glue which is injected into an appropriate feeding artery. The intention is to have the embolus become lodged in the feeding artery, in order to prevent blood from entering the malformation. This type of treatment generally requires monitoring in a neuro-ICU.
DURAL SINUS THROMBOSIS
What is a dural sinus thrombosis?
Once blood has perfused the brain and enriched its cells with oxygen and nutrients, it is drained by cerebral veins. These veins drain into dural venous sinuses which, in turn, drain into the jugular veins in the neck that carry blood back to the heart. A dural sinus thrombosis is the occlusion of a dural sinus by a blood clot (or thrombus). Because of this occlusion, blood flowing out of the brain is backed up, and the brain tissue becomes congested. As a result, both ischemia and hemorrhage may occur.
What are the symptoms of dural sinus thrombosis?
A dural sinus thrombosis may present as a stroke (hemorrhagic infarct), headache, or seizure. When many dural sinuses are occluded, a life-threatening increase in intracranial pressure can result.
What causes thrombosis of a dural sinus?
In 10% of cases dural sinus thrombosis is caused by an infection in the ear or nasal sinuses. More often, the cause is related to hypercoagulabilty of the blood, which may occur with pregnancy, birth control pills, or circulating antibodies.
What is the prognosis for a dural sinus thrombosis?
The outcome for patients with this disease is highly variable. Anywhere from 5 to 30% of patients with this condition will die from it. A poor prognosis is associated with coma, hemorrhagic infarction, and increased intracranial pressure. Location is also important; deeper thromboses are associated with a poorer outcome than those on the brain surface. In addition, thromboses resulting from infection are also associated with a poorer prognosis. Luckily, the chance of having a second dural sinus thrombosis after a first episode is small (<10%).
How is a dural sinus thrombosis treated in a neuro-ICU?
The mainstay of treatment for dural sinus thrombosis is anticoagulation with blood thinners (heparin and coumadin). This treatment was once controversial because the use of anticoagulants to promote blood flow was thought to exacerbate the cerebral hemorrhaging associated with the disease. However, research has shown that anticoagulation is an effective treatment for dural sinus thrombosis, because it prevents extension of the thrombus to uninvolved areas, and promotes lysis (dissolving) of existing thrombus. Seizures are a common complication and can be prevented with anticonvulsants. Increased intracranial pressure, which can be life threatening, can be managed with an intracranial pressure monitor.
What can be done if the above measures do not work?
In the most severe cases, clot-busting drugs (thrombolytics) can be delivered via a small catheter directly into the thrombus to dissolve them. Recent studies have shown that infusions of urokinase are effective at managing severe dural sinus thrombosis. This type of treatment is experimental, and probably is most effective when given immediately after a sudden major deterioration occurs. Continuous monitoring of neurologic status in a neuro-ICU can make this possible.
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August 8, 2012