Treatment FAQ

which of the following treatment modalities are used to prevent cerebral vasospasms?

by Sonya McClure Published 2 years ago Updated 2 years ago
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Hypertension, hypervolemia, and hemodilution (triple-H therapy) is often utilized to prevent and treat cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH).

Nimodipine has been recommended as first-line medical treatment for preventing post-aSAH cerebral vasospasm. It is usually given orally at a dosage of 60 mg every 4 hours for 21 days after the initial subarachnoid hemorrhage.Aug 21, 2020

Full Answer

What drugs are used to treat cerebral vasospasm?

Hypertension, hypervolemia, and hemodilution (triple-H therapy) is often utilized to prevent and treat cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). Methods include intravenous fluids (IVF) +/- inotropes/pressors with targets of CVP 10-12mmHg, PAOP 15-18mmHg, CI 3-3.5L/min/m2, Hct 30-35%, SBP 160-200mmHg if aneurysm clipped and 120 …

What is cerebral vasospasm and what causes it?

Nov 07, 2017 · Other medications that may be used to prevent coronary vasospasm include calcium channel blockers (ex. Verapamil) and beta-blockers (ex. Propranolol). Both medications help protect the heart by...

How is vasospasm prevented in patients with cerebral aneurysms?

Cerebral vasospasm is a condition in which the blood vessels in the brain narrow, thereby reducing blood flow to the brain and subsequent death of brain tissue. The typical vessels involved are those in the Circle of Willis, an area at the base of the brain that connects the large arteries in the brain to each other. This condition usually occurs in patients after a

What are the treatment options for cerebral vasospasm after subarachnoid hemorrhage?

Feb 18, 2016 · At present, the most commom drugs for preventing and treating cerebral vasospasm were classified into the following drugs: calcium channel blocker, fasudil, magnesium, statins, hormones, phosphoiesterase inhabitor, endothelin-1 antagonists, nitric oxide, heparin and fibrinolysis. Calcium channel blocker (CCB) Nimodipine

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How can you prevent vasospasms?

Since vasodilator drugs cannot reverse cerebral vasospasm, treatment is directed to prevent vasospasm and to prevent or reverse ischemic deficits. The mainstay of treatment of vasospasm is the hypertensive hypervolemia dilution (triple H therapy); the mainstay of prevention is the calcium channel blocker nimodipine.

Which are mechanisms for prevention of vasospasm post cerebral bleed?

Calcium-channel antagonists have been widely investigated for prevention of vasospasm in aSAH; nimodipine is currently recommended as first-line medical treatment for preventing post-aSAH cerebral vasospasm.Aug 21, 2020

Which of the following is used for the evaluation of cerebral vasospasm?

Currently, transcranial Doppler (TCD) is the primary imaging technique used in screening for asymptomatic spasm. TCD is a noninvasive modality that extrapolates the likelihood of vasospasm on the basis of selective intracranial arterial blood flow velocity ratios, trends, and relations.Aug 21, 2020

What is Triple H therapy?

Hyperdynamic therapy, also called triple-H therapy, is the standard treatment and prophylaxis for aneurysmal-associated vasospasm. In patients who are able to tolerate cardiopulmonary stressors induced by this therapy, it is of benefit as a modality for prevention and treatment of delayed ischemic neurologic deficit.Dec 3, 2018

Can vasospasm be treated?

Treatment for vasospasm can occur through both ICU intervention and endovascular administration of intra-arterial vasodilators and balloon angioplasty. The best outcomes are often attained when these methods are used in conjunction.May 20, 2014

What is nimodipine used for?

Nimodipine is used to treat symptoms resulting from a ruptured blood vessel in the brain (subarachnoid hemorrhage). It works by increasing the blood flow to injured brain tissue. This medicine is available only with your doctor's prescription.Feb 1, 2022

What is the recommendation for treating seizures in patient with subarachnoid hemorrhage?

While antiepileptic drug use has been linked to worse prognosis, studies have evaluated treatment with almost exclusively phenytoin. When prophylaxis is used, 3-day treatment seems to provide similar seizure prevention with better outcome compared with longer-term treatment.

When should oral nimodipine therapy be started?

Nimodipine comes as a capsule and an oral solution (liquid) to take by mouth or be given through a feeding tube. It is usually taken every 4 hours for 21 days in a row. Treatment with nimodipine should be started as soon as possible, no later than 96 hours after a subarachnoid hemorrhage occurs.

Which medication is commonly used to improve neurological outcomes after subarachnoid hemorrhage?

Calcium channel blockers have been shown to reduce the incidence of ischemic neurologic deficits, and nimodipine has been shown to improve overall outcome within 3 months of aneurysmal SAH. Calcium channel blockers and other antihypertensives should be used cautiously to avoid the deleterious effects of hypotension.Dec 7, 2018

How does nimodipine prevent vasospasm?

Nimodipine. Nimodipine is a dihydropyridine agent that blocks voltage-gated calcium channels and has a dilatory effect on arterial smooth muscle. It is the only FDA-approved agent for vasospasm with a half-life of about 9 h [6].Feb 18, 2016

What is Triple-H therapy for vasospasm following subarachnoid hemorrhage?

The combination of induced hypertension, hypervolemia, and hemodilution (triple-H therapy) is often utilized to prevent and treat cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH).

What is Hyperdynamic therapy?

The cornerstone of medical therapy for cerebral vasospasm is so-called hyperdynamic therapy. Also referred to as triple-H therapy, this strategy includes the use of hypertension, hypervolemia, and hemodilution to optimize cerebral perfusion.May 14, 2010

What is cerebral vasospasm?

Cerebral vasospasm. A phenomenon occurring due to narrowing of the large and medium-sized arteries found in the brain. They are more likely to occur after an aneurysmal subarachnoid hemorrhage, which is when bleeding occurs within the compartment surrounding the brain called the subarachnoid space.

How to treat vasospasm?

Prevention is the best treatment of vasospasm and may include: 1 Decreasing bad cholesterol ( LDL) levels 2 Quitting smoking 3 Getting adequate amounts of physical activity 4 Control medical condition such as diabetes or hypertension

What is the test used to measure blood flow in the brain?

Other tests that may be used include a transcranial doppler ultrasound to measure blood flow throughout the arteries of the base of the brain, and electrocardiogram (ECG), to evaluate the electrical activity of the heart.

What imaging is used to see blood flow?

Additionally, the use of computed tomography (CT) or magnetic resonance imaging (MRI) angiography may be utilized to help observe blood flow through the affected blood vessel.

Which cells control blood vessels?

Blood vessels have varying degrees of contraction and relaxation controlled by endothelial cells, a type of cell that lines blood vessels. These cells release substances such as prostacyclin and nitric oxide that help induce blood vessel relaxation of smooth and inhibit the factors that lead to contraction.

Can atherosclerosis cause vasospasm?

Similarly, those suffering from atherosclerosis are expected to be at increased risk for developing coronary vasospasm. Vasospasm symptoms will depend on the area affected by the constricted blood vessels with the most unwanted complications causing stroke-like or coronary artery associated symptoms.

Can vasospasm cause tissue death?

Vasospasm can cut off blood circulation leading to tissue ischemia and tissue death. Knowing what is vasospasm can help you recognized symptoms they may present with and seek out help when appropriate.

What is cerebral vasospasm?

Cerebral vasospasm is a condition in which the blood vessels in the brain narrow, thereby reducing blood flow to the brain and subsequent death of brain tissue. The typical vessels involved are those in the Circle of Willis, an area at the base of the brain that connects the large arteries in the brain to each other. ...

What is the best way to diagnose cerebral vasospasm?

To diagnose cerebral vasospasm, a physician may use transcranial dopplers, CT-angiography, MR-angiography, or may obtain a cerebral angiogram.

What is the treatment for subarachnoid hemorrhage?

Most patients with subarachnoid hemorrhages are given drugs to prevent strokes from cerebral vasospasm. Once the disease is diagnosed, the treatment options elevation of blood pressure to force blood perfusion to the brain, and/or treatment through angiography.

What is a posthemorrhagic cerebral vasospasm?

Posthemorrhagic cerebral vasospasm (PHCV) is a major cause of death and permanent disability in patients with aneurysmal subarachnoid hemorrhage (aSAH), which may account for almost 50 % of the deaths among those surviving in the initial ictus [ 1 ]. Despite the improvement in the treatment of aSAH with reduced mortality by almost 50 % over the last 20 years [ 2 ], angiographic Cerebral vasospasm (CVS) is very common, affecting up to 70 % of aSAH patients, which has a predictable time course: delayed onset between day 3 and 5, maximal narrowing between day 5 and 14, and then gradual resolution over week 2–4. Nearly half of these patients, about 30 % of all aSAH survivors, will develop a delayed ischemic neurological deficit (DIND), also called symptomatic CVS [ 1 ]. The incidence of symptomatic CVS varies between 17 % and 48 % [ 3 – 5 ]. Although endovascular devices and treatment techniques are continuously developing, these minimally invasive procedures still carry treatment-specific risks. At present drug treatment is still the main therapeutic choice, and this review mainly introduces the recent development of drug treatment.

What is the FDA approved drug for vasospasm?

Nimodipine. Nimodipine is a dihydropyridine agent that blocks voltage-gated calcium channels and has a dilatory effect on arterial smooth muscle. It is the only FDA-approved agent for vasospasm with a half-life of about 9 h [ 6 ].

What is CVS in a syringe?

Cerebral vasospasm (CVS) is a common and severe complication of aneurysmal subarachnoid hemorrhage (aSAH). Despite the improvement in treatment of aSAH, CVS complicating aSAH has remained the main cause of death. CVS begins most often on the third day after the ictal event and reaches the maximum on the 5th–7th postictal days. Several therapeutic modalities have been employed to prevent or reverse CVS. The aim of this review is to summate all the available drug treatment modalities for vasospasm.

What is the role of statins in vasospasm?

Statins are HMG-CoA reductase inhibitors, which seem to have an important role in vasospasm prevention. The proposed mechanism of the action of statins involves induction of NO pathway and dilation of cerebral vessels, thereby leading to improved cerebral blood flow [ 39 ].

What is the effect of heparin on the brain?

Heparin is a pleiotropic drug, which has many effects on antagonizing molecular mechanisms of secondary brain injury after aSAH, including endothelin mediated vasoconstriction, the activity of free radicals and antifibrotic effects.

Is nicardipine a CCB?

Nicardipine is a second-generation dihydropyridine-type CCB that was developed approximately 30 years ago. Therefore, nicardipine may act in neuroprotection as a preventive factor of the CVS due to its vasodilator property and a peculiar cerebrovascular profile [ 18 ].

Is estrogen a vasodilator?

Estrogen, specifically 17β-estradiol (E2), possesses powerful vasodilatory, anti-inflammatory, and neuroprotective properties. Though its current use remains limited to in-vivo animal models of experimental SAH, E2 has potential therapeutic implications for ameliorating the DINDs which follow aneurysmal SAH [ 48 ]. Derived from cholesterol, E2 is a powerful vasodilator with the potential to prevent or reverse the vasoconstriction which occurs in CVS. Some experiments have shown that estrogen promotes vasodilatation by three mechanisms: (1) attenuating the up-regulation of endothelin-1 receptors after SAH as cited above [ 49 ]; (2) inducing the up-regulation of L-type calcium ion channels of smooth muscle cells; (3) decreasing SAH-induced inducible nitric oxide synthase (iNOS) expression, and normal endothelial nitric oxide synthase (eNOS) expression [ 50].

Does nimodipine reduce vasospasm?

[ 35] . In particular, nimodipine has been shown to improve neurologic outcomes after aSAH, but it does not decrease radiographic vasospasm and does not significantly reduce mortality. [ 36] .

Is there class A evidence for vasospasm?

Although there is a paucity of class A evidence regarding prevention and treatment of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH), a number of therapeutic strategies have been studied and found to have varying degrees of utility. [ 12]

What is the best treatment for vasospasms?

Both of these goals can be achieved through medication such as nitroglycerin, long-acting nitrates, calcium channel-blockers or beta-blockers. Treatment for vasospasms caused by bleeding inside the skull will vary depending on what caused it, where it is and how large it is.

How to diagnose vasospasm?

Diagnosis. Diagnosis of a vasospasm usually begins with a physical exam and a review of the patient’s medical history and symptoms. For vasospasms that are minor, this is often adequate to diagnose the condition. For more severe conditions other diagnostic tools will be used.

What is the cause of vasospasm?

When the vasospasm occurs in the brain, it is often due to a subarachnoid hemorrhage after a cerebral aneurysm has ruptured.

What is the risk of developing vasospasms in the toes?

Patients with Rynaud's Phenomenon are also at an increased risk of developing vasospasms in the toes or fingers.

What are the symptoms of cerebral vasospasm?

Confusion. Difficulty with speaking. Weakness on one side of the body. Patients who have experienced a cerebral vasospasm often also have stroke-like symptoms: Numbness or weakness of the face, arm or leg, especially on one side of the body. Confusion.

What diagnostic tools are used to diagnose a reduced blood flow?

For more severe conditions other diagnostic tools will be used. Imaging tests, including magnetic resonance imaging (MRI) and computed tomography (CT) angiography , are used to diagnosed the condition and observe the area affected by the reduced blood flow.

What is the best way to check blood vessels?

Other tests look exclusively at the blood vessels within the body. An angiogram may be used to view the arteries. A transcranial Doppler (TCD) ultrasound is used to measure the blood that is flowing through the arteries at the base of the brain.

What is cerebral vasospasm?

The term " cerebral vasospasm " means "narrowing" or a contracted state of the cerebral arteries in vivo. Vasospasm following subarachnoid hemorrhage is an important cause of cerebral ischemia and is the most frequent serious complication in survivors of subarachnoid hemorrhage. This article discusses the pathomechanism ...

What was the first pharmacological approach to the prevention of vasospasm?

The first pharmacological approach to the prevention of vasospasm was the use of drugs (such as res erpine) that lower the levels of active monoamines (such as norepinephrine) in the circulating blood and the brain ( 56 ).

What are the procedures for vasospasm?

Two procedures are worth consideration: (1) infusion of tissue plasminogen activator into the subarachnoid space and (2) dilatation of vasospasm by a balloon catheter or retrievable stent.

What is papaverine used for?

Papaverine is 1 of the strongest of the nonspecific vasodilatory agents and has been used for the prevention and treatment of clinical and experimental vasospasm with administration via the intravenous, intraarterial, and intrathecal routes as well as direct application to the arteries during neurosurgical procedures.

What is the function of hemoglobin in vasospasm?

Hemoglobin, released from breakdown of red blood cells in the subarachnoid space, destroys nitric oxide synthase-containing neurons in the cerebral arteries , leading to deficiency of nitric oxide, which initiates delayed vasospasm. This provides the rationale for exogenous nitric oxide delivery.

When was vasospasm first described?

Vasospasm was first described in the mid-19th century by Gull, and vasospasm theory was used to explain transient ischemic attacks ( 41 ). Identification of vasospasm in relation to ruptured intracranial aneurysm was not made until after the introduction of cerebral angiography.

What is the purpose of PDE5 inhibitors?

This is the basis for use of PDE5 inhibitors for treatment of cerebral vasospasm. Sildenafil.

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