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Archive for the ‘Subarachnoid Hemorrhage (SAH)’ Category


Subarachnoid hemorrhage care at Mayo Clinic in Rochester, Minn., ranks No. 1 for neurology and neurosurgery in the U.S. News & World Report Best Hospitals rankings

Reporter: Aviva Lev-Ari, PhD, RN

 

A Mayo Clinic study found that 63.3 percent of people treated for aneurysmal subarachnoid hemorrhages at Mayo Clinic in Rochester, Minnesota, from 2001 to 2013 had no or few lasting symptoms.

Mayo Clinic in Phoenix/Scottsdale, Ariz., and Mayo Clinic in Jacksonville, Fla., are ranked among the Best Hospitals for neurology and neurosurgery by U.S. News & World Report.

SOURCE

https://www.mayoclinic.org/diseases-conditions/subarachnoid-hemorrhage/care-at-mayo-clinic/mac-20361025

 

Overview

The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes (see the image below). It occurs in various clinical contexts, the most common being head trauma. However, the familiar use of the term SAH refers to nontraumatic (or spontaneous) hemorrhage, which usually occurs in the setting of a ruptured cerebral aneurysm or arteriovenous malformation (AVM).

The classic presentation can include the following:

  • Sudden onset of severe headache (the classic feature)
  • Accompanying nausea or vomiting
  • Symptoms of meningeal irritation
  • Photophobia and visual changes
  • Focal neurologic deficits
  • Sudden loss of consciousness at the ictus
  • Seizures during the acute phase

Physical examination findings may be normal or may include the following:

  • Mild to moderate BP elevation
  • Temperature elevation
  • Tachycardia
  • Papilledema
  • Retinal hemorrhage
  • Global or focal neurologic abnormalities

Complications of SAH include the following:

  • Hydrocephalus
  • Rebleeding
  • Vasospasm
  • Seizures
  • Cardiac dysfunction

Diagnosis

Diagnosis of SAH usually depends on a high index of clinical suspicion combined with radiologic confirmation via urgent noncontrast CT, followed by lumbar puncture or CT angiography of the brain. After the diagnosis is established, further imaging should be performed to characterize the source of the hemorrhage.

Laboratory studies should include the following:

  • Serum chemistry panel
  • Complete blood count
  • Prothrombin time (PT)/activated partial thromboplastin time (aPTT)
  • Blood typing/screening
  • Cardiac enzymes
  • Arterial blood gas (ABG) determination

Imaging studies that may be helpful include the following:

  • CT (noncontrast, contrast, or infusion)
  • Digital subtraction cerebral angiography
  • Multidetector CT angiography
  • MRI (if no lesion is found on angiography)
  • Magnetic resonance angiography (MRA; investigational for SAH)

Other diagnostic studies that may be warranted are as follows:

  • Baseline chest radiograph
  • ECG on admission
  • Lumbar puncture and CSF analysis

See Workup for more detail.

Management

Current treatment recommendations include the following:

  • Antihypertensive agents (eg, IV beta blockers) when mean arterial pressure exceeds 130 mm Hg
  • Avoidance of nitrates (which elevate ICP) when feasible
  • Hydralazine and calcium channel blockers
  • Angiotensin-converting enzyme (ACE) inhibitors (not first-line agents in acute SAH)
  • In patients with signs of increased ICP or herniation, intubation and hyperventilation

Other interventions for increased ICP are as follows:

  • Osmotic agents (eg, mannitol)
  • Loop diuretics (eg, furosemide)
  • IV steroids (controversial but recommended by some)

Surgical treatment to prevent rebleeding includes the following options:

  • Clipping the ruptured aneurysm
  • Endovascular treatment [1(ie, coiling)

The choice between coiling and clipping usually depends on the location of the lesion, the neck of the aneurysm, and the availability and experience of hospital staff.

SOURCE

https://emedicine.medscape.com/article/1164341-overview

 

Pharmaco-Therapy for SAH

  • Nimodipine is a drug used for SAH

Nimodipine is a second generation calcium channel blocker used in the treatment of cerebral vasospasm after subarachnoid hemorrhage.  Nimodipine is not widely used and has not been implicated in causing clinically apparent acute liver injury.

Introduction

Nimodipine is a second generation calcium channel blocker used in the treatment of cerebral vasospasm after subarachnoid hemorrhage.  Nimodipine is not widely used and has not been implicated in causing clinically apparent acute liver injury.

 

Background

Nimodipine (nye moe’ di preen) belongs to the dihydropyridine class of calcium channel blockers (similar to amlopidine and felodipine) and is used to treat cerebral vasospasm after subarachnoid hemorrhage.  Like other calcium channel blockers, nimodipine acts by inhibition of the influx of calcium ions into smooth muscle cells during depolarization which results in vasodilation.  Nimodipine has high lipid solubility and was developed specifically to treat cerebral vasospasm.  Clinical trials have suggested that nimodipine reduces infarct size and complications after subarachnoid hemorrhage.  Nimodipine was approved for use in the United States in 1988 but is not widely used, largely because of its restricted indications.  Nimodipine is available in generic forms and under the commercial name Nimotop as capsules of 30 mg.  The recommend dose in adults is 60 mg every 4 hours for 21 days starting as soon as possible or within 96 hours of the diagnosis of subarachnoid hemorrhage.  Like most calcium channel blockers, nimodipine is generally well tolerated and side effects are largely due to its vasodilating activities and can include headache, dizziness, flushing, fatigue, nausea, diarrhea, peripheral edema, palpitations and rash.

 

Hepatotoxicity, Outcome and Management

Nimodipine has been associated with only rare reports of serum enzyme elevations during therapy.  These elevations are usually mild, transient and not associated with symptoms or need for dose modification.  Nimodipine is not widely used and has not been linked to instances of clinically apparent liver injury.  Thus, hepatotoxicity from nimodipine must be rare, if it occurs at all.

 

Likelihood score: E  (Unlikely cause of clinically apparent liver injury).

 

The reason why some calcium channel blockers cause liver injury (verapamil, diltiazem, amlodipine) while others (such as nimodipine) do not is not known. Because liver injury from calcium channel blockers is rare, those that are uncommonly used may just not have had enough exposures to manifest idiosyncratic cases of liver injury. Nimodipine is metabolized in the liver largely via CYP 3A4 and is susceptible to drug-drug interactions with agents that induce or inhibit CYP 3A4.

 

Drug Class:  Cardiovascular AgentsCalcium Channel Blockers

 

Other Drugs in the Subclass, Calcium Channel Blockers:  AmlodipineDiltiazemFelodipineIsradipineNicardipineNifedipineNisoldipineVerapamil

 

SOURCE

https://livertox.nih.gov/Nimodipine.htm

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