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Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a life-threatening condition that refers to bleeding into the subarachnoid space. Most cases are attributed to a ruptured aneurysm. Additionally, there are risk factors such as hypertension, atherosclerosis, smoking, and other conditions as well.


Presentation

Up to 50% of patients with SAH experience symptoms prior to rupture. The most common feature is a headache, which is frequently accompanied by nausea, emesis, photophobia, and possibly nuchal pain and rigidity. Moreover, the hallmark complaint is "this is the worst headache of my life." Other manifestations include dizziness, visual impairment, diplopia, and orbital pain. Patients may also develop seizures, ptosis, bruits, dysphagia, motor dysfunction, and sensory losses.

The history of the patient often provides a clue regarding the diagnosis. Approximately 60% to 70% of patients report that SAH may be preceded by physical or emotional stress such as head trauma, defecation, or sexual intercourse.

The proposed characteristics which should raise suspicion for SAH are 1) age of patient 40 years or above, 2) pain or stiffness of the neck, 3) loss of consciousness, 4) manifestations induced by physical or emotional exertion, 5) emesis, 6) transportation to the hospital by an ambulance, and 7) diastolic blood pressure of at least 100mm Hg or systolic blood pressure of at least 160mm Hg.

Physical exam

Specific neural deficits will reflect the site of an expanding aneurysm. For example, an affected anterior communicating artery produces paresis of the bilateral lower extremities along with a positive bilateral Babinski sign. An aneurysm in the intracranial vertebral artery results in vertigo among other deficits. Furthermore, a lesion in the MCA leads to paresis of the contralateral face, hand, and vision in addition to left sided aphasia. Finally, an affected ICA or posterior communicating artery causes oculomotor nerve palsy and retro-orbital headaches.

Weakness
  • On postoperative day 10, the patient developed new bilateral lower extremity weakness; MRI of the lumbar spine demonstrated worsening acute spinal SDH above the laminectomy defect, from L4-T12.[ncbi.nlm.nih.gov]
  • A 69-year old female patient developed suddenly left-sided face and body weakness and numbness and visual neglect on the left. She was newly detected with paroxysmal atrial fibrillation on the ground of thyrotoxicosis.[ncbi.nlm.nih.gov]
  • CONCLUSIONS: The present meta-regression provides weak evidence for dose-dependent reductions in vasospasm, DIND and mortality associated with acute statin use after aneurysmal subarachnoid hemorrhage.[ncbi.nlm.nih.gov]
  • Bursts and Breaks: Causes of Hemorrhagic Stroke When blood vessels of the brain are weak, abnormal, or under unusual pressure, a hemorrhagic stroke can occur.[msdmanuals.com]
Fever
  • The impact of fever on DCI and clinical outcomes was assessed.[ncbi.nlm.nih.gov]
  • “For it happens in this, as the physicians say it happens in hectic fever, that in the beginning of the malady it is easy to cure but difficult to detect, but in the course of time, not having been either detected or treated in the beginning, it becomes[content.nejm.org]
  • […] with poor functional outcome at 14 days (OR, 1.5 per quartile; 95% CI, 1.3 to 1.8; P 0.001), although not at 3 months (P 0.09); the effect remained (OR, 1.6 per quartile; 95% CI, 1.2 to 2.1; P 0.001) after correction for admission Glasgow Coma Scale, fever[ncbi.nlm.nih.gov]
  • CASE DESCRIPTION: A 56-year-old man developed prolonged fever and headache. Magnetic resonance imaging showed a mass lesion around the brainstem. No laboratory data were suspicious for inflammatory diseases or autoimmune diseases.[ncbi.nlm.nih.gov]
  • Fever burden and cognitive outcome after subarachnoid hemorrhage. Neurology. 2003 ; 60 : A230.(Abstract.)[dx.doi.org]
Coarctation of the Aorta
  • […] of the aorta fibromuscular dysplasia INVESTIGATIONS Bedside ECG: tall peaked T waves, ST depression, prolonged QT, arrhythmia Echo: neurogenic cardiomyopathy Laboratory hyponatraemia hypovolaemia from SIADH or cerebral salt wasting - worsens vasospasm[lifeinthefastlane.com]
  • MR Angiography MRA can be used to screen for intracranial aneurysms in asymptomatic patients who have a family history of aneurysms or who have polycystic kidneys, coarctation of the aorta, or collagen vascular disease, putting them at a higher risk for[spinwarp.ucsd.edu]
Vomiting
  • Clinical features include headache; nausea; vomiting, nuchal rigidity, variable neurological deficits and reduced mental status.[icd9data.com]
  • OUTCOMES: Through 2 years of follow-up, intermittent migraine was found in the patient, but the symptoms of occipital pain, nausea, and vomiting did not occur again.[ncbi.nlm.nih.gov]
  • CASE REPORT: A 55-year-old woman presented at the Emergency Department of our hospital complaining of vomiting and headache of sudden onset.[ncbi.nlm.nih.gov]
  • CASE DESCRIPTION: A 61-year-old woman presented with the worst headache of her life and an acute onset of nausea and vomiting and was shown to have a grade 2 subarachnoid hemorrhage (SAH) on computed tomography scan.[ncbi.nlm.nih.gov]
  • PATIENT CONCERNS AND DIAGNOSES: A 45-year-old right-handed man was admitted to the hospital with a sudden onset of severe headache associated with nausea, vomiting, and mild photophobia for 6 hours. The patient was fully conscious and totally alert.[ncbi.nlm.nih.gov]
Nausea
  • Clinical features include headache; nausea; vomiting, nuchal rigidity, variable neurological deficits and reduced mental status.[icd9data.com]
  • BACKGROUND: Patients with subarachnoid hemorrhage (SAH) by hemorrhagic arteriovenous fistulas (AVFs) usually presents with meningeal signs, including headache and nausea, and focal neurologic deficit is found in rare cases.[ncbi.nlm.nih.gov]
  • OUTCOMES: Through 2 years of follow-up, intermittent migraine was found in the patient, but the symptoms of occipital pain, nausea, and vomiting did not occur again.[ncbi.nlm.nih.gov]
  • Six days after the surgery, the patient continued to complain of nausea and headache. By 13 days, the patient reported relief from her symptoms. There was no evidence of cerebral aneurysm, or vascular malformation in both cases.[ncbi.nlm.nih.gov]
  • CASE DESCRIPTION: A 61-year-old woman presented with the worst headache of her life and an acute onset of nausea and vomiting and was shown to have a grade 2 subarachnoid hemorrhage (SAH) on computed tomography scan.[ncbi.nlm.nih.gov]
Hypertension
  • Lumbar puncture revealed an opening pressure of 360 mmH2O, suggestive of intracranial venous hypertension. Grave disease was diagnosed by endocrinological investigation.[ncbi.nlm.nih.gov]
  • Use of prophylactic or therapeutic hypervolemia or prophylactic-induced hypertension were associated with a lower risk of unfavorable outcome. Time from admission to surgery was significant in some models.[ncbi.nlm.nih.gov]
  • We conclude that smoking, hypertension, and alcohol abuse are important risk factors for SAH. Reduction of exposure to these risk factors might result in a decreased incidence of SAH.[ncbi.nlm.nih.gov]
  • KEYWORDS: Pseudotumor cerebri; basal vein of Rosenthal; idiopathic intracranial hypertension; stent; subarachnoid hemorrhage; transverse sinus stenosis[ncbi.nlm.nih.gov]
  • Given an SAH incidence of 6/100 000 person-years, 9 a prevalence of hypertension approximating 10%, and an RR of hypertension of 3, the incidence of SAH in patients without hypertension is 5/100 000 person-years and that of patients with hypertension[doi.org]
Neck Pain
  • A patient with subarachnoid hemorrhage may have a sudden, intense headache, neck pain, and nausea or vomiting. Sometimes this is described as the worst headache of one’s life.[strokecenter.org]
  • A history of neck pain (LR 4.1; 95% confidence interval [CI] 2.2 to 7.6) and neck stiffness on physical examination (LR 6.6; 95% CI 4.0 to 11.0) were the individual findings most strongly associated with SAH.[ncbi.nlm.nih.gov]
  • After comparing the performance of the three candidate decision rules, the investigators refined the decision tool to combine the six factors that were most predictive of SAH: age 40 or older, neck pain or stiffness, witnessed loss of consciousness, onset[neurologyreviews.com]
  • Other symptoms: Decreased consciousness and alertness Eye discomfort in bright light ( photophobia ) Mood and personality changes, including confusion and irritability Muscle aches (especially neck pain and shoulder pain) Nausea and vomiting Numbness[nlm.nih.gov]
Photophobia
  • PATIENT CONCERNS AND DIAGNOSES: A 45-year-old right-handed man was admitted to the hospital with a sudden onset of severe headache associated with nausea, vomiting, and mild photophobia for 6 hours. The patient was fully conscious and totally alert.[ncbi.nlm.nih.gov]
  • Snapshot A 45-year-old woman presents to the emergency room with a stiff neck, photophobia, and an extremely severe headache that began while she was enjoying a glass of sweet Alabama southern tea.[step2.medbullets.com]
  • Pathophysiology Clinical features Characteristic features Thunderclap headache : sudden , severely painful headache : - spreads over the entire head (holocephalic) and radiates to the neck and back (may present with opisthotonus ) Meningism : : neck stiffness, photophobia[amboss.com]
  • It is often associated with photophobia and meningism .[radiopaedia.org]
  • It is often associated with photophobia and meningism. Focal neurological deficits often present either at the same time as a headache or soon thereafter 2.[radiopaedia.org]
Diplopia
  • […] stiffness or pain, onset of headache on exertion, vomiting, witnessed loss of consciousness, and elevated BP 160/100 Also consider the following signs: stroke‐like symptoms, seizure or 3rd cranial nerve palsy from mass effect, 6th cranial nerve palsy with diplopia[emergencymedicinecases.com]
  • Other manifestations include dizziness, visual impairment, diplopia, and orbital pain. Patients may also develop seizures, ptosis, bruits, dysphagia, motor dysfunction, and sensory losses.[symptoma.com]
  • […] poor if happens at onset) Meningism [neck stiffness and photophobia due to meningeal irritation] (prognostically poor) Seizures (only in 7% but highly suggestive) Early seizures predict late seizures and poor outcome New neurology (prognostically poor) Diplopia[oxfordmedicaleducation.com]
  • The most common symptoms are headache (48%), dizziness (10%), orbital pain (7%), diplopia (4%) and visual loss (4%).[patient.co.uk]
Facial Pain
  • These symptoms, which can occur minutes to weeks before a rupture, include: Severe headache Facial pain Double vision, droopy eyelid or other vision problems If these symptoms are present, they should always be brought to a doctor’s attention quickly[ufhealth.org]
Stroke
  • Childhood ischemic stroke is attributed to vasculopathy with moyamoya syndrome. Hemorrhagic stroke is commonly attributed to aneurysms accompanying HbSS cerebral vasculopathy in SCD.[ncbi.nlm.nih.gov]
  • CASE PRESENTATION: The Norwegian Acute Stroke Pre-hospital Project (NASPP) has developed a Mobile Stroke Unit (MSU) model, which is staffed with anesthesiologists also trained in pre-hospital clinical assessment of acute stroke patients and interpretation[ncbi.nlm.nih.gov]
  • CONCLUSIONS: cSAH may be a rare complication of cardioembolic stroke. Copyright 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved. KEYWORDS: Embolic stroke; atrial fibrillation; cSAH; cortical sulci[ncbi.nlm.nih.gov]
  • KEYWORDS: CT Angiography; Coil; Dissection; Hemorrhage; Stroke[ncbi.nlm.nih.gov]
  • Stroke. 2005;36:2773-2780 Published online before print November 10, 2005, doi: 10.1161/01.STR.0000190838.02954.e8 ( Stroke. 2005;36:2773.) 2005 American Heart Association, Inc.[web.archive.org]
Headache
  • Abstract Headache is the presenting complaint in roughly 2% of ED visits. 1 Of all those with headache, about 1% will have Subarachnoid Hemorrhage (SAH), 2-4 meaning 99% of ED headache patients do not have SAH.[web.archive.org]
  • BACKGROUND: The headache preceding an intracranial aneurysm rupture is called a sentinel headache (SH), and it is characterized by a sudden, intense, and persistent headache.[ncbi.nlm.nih.gov]
  • Conclusions Less than one in 10 headache patients concerning for SAH are ultimately diagnosed with SAH in recent studies.[doi.org]
  • Although the presentation of a thunderclap headache or the worst headache of a patient's life easily triggers the evaluation for SAH, subtle presentations are still missed.[ncbi.nlm.nih.gov]
Seizure
  • None of the patients with epilepsy after discharge had electrographic seizures while hospitalized.[ncbi.nlm.nih.gov]
  • Preventing a seizure may prevent rebleeding, 3 although in multivariate models seizures and rebleeding are not associated. 8 Benefit from prophylaxis, however, assumes that seizures are harmful and PHT is harmless.[dx.doi.org]
  • Seizures During Hospitalization Twenty-seven (5%) patients had seizures in the hospital. Clinical variables associated with in-hospital seizures are listed in Table 2.[web.archive.org]
Meningism
  • CONCLUSIONS: Tuberculosis in the central nervous system may present as tuberculoma and tuberculous meningitis. Vasculitis secondary to tuberculous meningitis can cause infarcts, and, rarely, aneurysm formation.[ncbi.nlm.nih.gov]
  • KEYWORDS: Spinal cord; lumbar puncture; meningitis; schwannoma; subarachnoid hemorrhage[ncbi.nlm.nih.gov]
  • Conclusion: SAH in meningitis could be explained by vasculitis or undetected ruptured mycotic aneurysm induced by acute inflammation from meningitis.[n.neurology.org]
  • Applies To Middle meningeal hemorrhage following injury ICD-9-CM Volume 2 Index entries containing back-references to 852.0 : ICD-9-CM codes are used in medical billing and coding to describe diseases, injuries, symptoms and conditions.[icd9data.com]
  • Subsequent chemotherapy is essential to prevent carcinomatous meningitis and disease progression. Copyright 2018 Elsevier Inc. All rights reserved.[ncbi.nlm.nih.gov]
Confusion
  • On postoperative day 2, he became confused; and head CT demonstrated intracranial SAH with blood products along the superior cerebellum and bilateral posterior Sylvian fissures.[ncbi.nlm.nih.gov]
  • Some people remain in a coma, but most often patients wake up feeling confused and sleepy. Within a few minutes or few hours, the patient may again begin to feel confused and sleepy.[ufhealth.org]
  • Symptoms include rapid onset of a severe headache (often called a “thunderclap headache”), nausea, confusion, altered consciousness, seizure, visual disturbances, cardiac arrhythmias, and focal neurological deficits such as hemiparesis, sensory loss,[link.springer.com]
  • Common symptoms of a subarachnoid hemorrhage include: Loss of consciousness Double vision Nausea or vomiting Severe headache — the worst headache pain you've ever had that feels different from other headaches Trouble speaking Drooping eyelid Confusion[hopkinsmedicine.org]

Workup

Patients with characteristic symptoms should raise suspicion for SAH as they warrant immediate medical evaluation and management. The workup includes a thorough history, a complete exam with a neural assessment, and the appropriate workup.

Imaging

CT scan without contrast demonstrates a sensitivity greater than 90% with excellent detection if performed within 6 hours of onset of the clinical picture. MRI is also sensitive but its availability may be limited. Cerebral angiography and CT angiography are alternative tests if other modalities are inconclusive.

Lumbar puncture

If the CT fails to detect SAH, then a lumbar puncture is the next step unless the patient has elevated ICP, in which case the procedure can exacerbate the bleeding. Evaluation of the cerebrospinal fluid (CSF) yields findings such as the presence of red blood cells (RBCs), although this may result from trauma. Other typical features include xanthochromia and elevated pressure.

Laboratory tests

In addition to the critical imaging studies, comprehensive laboratory tests should be obtained in order to understand the overall clinical picture. These include a complete blood count (CBC) to rule out infection, a coagulation panel for the exclusion of bleeding disorders, cardiac enzymes to evaluate myocardial infarction, and a metabolic panel. Additionally, blood typing and screening are very important in the event that a transfusion is required.

Other

These patients should also have an electrocardiogram (ECG) done, which may reveal ST changes, abnormalities such as QRS or QT prolongation, or T wave peaking or inversion.

Xanthochromia
  • Traditional teaching is that a positive tap is Xanthochromia or blood in the CSF What exactly is Xanthochromia? The word xanthochromia is simply Greek for “yellow color.” It refers to the yellow color that CSF can take in certain situations.[tamingthesru.com]
  • Key Words: subarachnoid hemorrhage, aneurysm, thunderclap headache, sentinel headache, lumbar puncture, xanthochromia, emergency department, head CT, CTA, angiography, MRI, nimodipine, risk factors, prehospital care, diagnosis, management, analgesia,[web.archive.org]
  • We assess the sensitivity and specificity of xanthochromia as adjudicated by visual inspection and spectrophotometry at predicting the presence of cerebral aneurysm in patients with suspected subarachnoid hemorrhage who have a normal computed tomography[ncbi.nlm.nih.gov]
  • Complications were in 4 percent and xanthochromia was found in 13 percent. Total length of stay was 7.8 hours (0.95 CI; 7.5 - 8.2).[ncbi.nlm.nih.gov]
  • Diagnostic studies differed in assessment of history and physical examination findings, CT technology, analytical techniques used to identify xanthochromia, and criterion standards for SAH.[doi.org]
Hyponatremia
  • RESULTS: The rate of complications in the NPM-SAH group was higher than in the PM-SAH group, including early hydrocephalus, delayed cerebral ischemia, clinical vasospasm, pneumonia, and hyponatremia.[ncbi.nlm.nih.gov]
  • Pooled data [ 26, 27 ] demonstrated lower incidences of hyponatremia (Na serum 2 c).[doi.org]
  • In addition, triple-H therapy may carry significant medical morbidity, including pulmonary edema, myocardial ischemia, hyponatremia, renal medullary washout, indwelling catheter-related complications, cerebral hemorrhage, and cerebral edema.[ncbi.nlm.nih.gov]
  • ., left ventricular function) References: [1] [5] Treatment Initial treatment Strict bedrest Analgesia ( acetaminophen ) IV fluids for hydration and to avoid hyponatremia Reverse anticoagulation Control BP ; : maintain BP below 160 mm Hg to prevent rebleeding[amboss.com]
  • It is the most common cause of hyponatremia in these patients and may respond to fludorcortisone [Stroke 20: 1156, 1989; Clin Neurol Neurosurg 90: 209, 1988].[openanesthesia.org]
T Wave Inversion
  • ECG Electrocardiographic manifestations are non-specific, but commonly include: deep, symmetric T wave inversions 12 often referred to as "cerebral T waves" prolongation of the QT interval sinus bradycardia Three distinct patterns of subarachnoid hemorrhage[radiopaedia.org]
  • ECG changes in 50‐100% of patients due to neurogenic myocardial stunning and coronary vasospasm: deep, wide precordial Twave inversion, bradycardia, and prolonged QT – beware of anticoagulating these patients on the assumption of acute coronary syndrome[emergencymedicinecases.com]
  • ECG may show Tall T waves, ST depression, Giant T wave inversions secondary to raised ICP, QT prolongation and arrhythmias.[emdidactic.blogspot.com]
  • ‡Q wave, QTc prolongation ( 0.4 ms), T-wave inversion, or ST-T–segment abnormality. §Available in 230 patients; in 50 patients, the day 14 or discharge mRS score was used.[circ.ahajournals.org]

Treatment

Since this is a life-threatening condition, patients should be promptly stabilized and admitted to the ICU or stroke center. In order to prevent complications, the medical team should immediately manage the cardiovascular, respiratory, and neurologic manifestations.

Pharmacologic treatment

According to current recommendations, intravenous nicardipine is administered if the mean arterial pressure (MAP) is above 130mm Hg. The blood pressure should be maintained in a particular range so as to not exacerbate or produce complications. Another essential component in the management of these patients is vasospasm prophylaxis with nimodipine for 21 days.

Surgical intervention

To decrease the likelihood of rebleeding, the aneurysm should be occluded through clipping or coiling within the first 24 hours of rupture. The goal is to create a bypass of the blood flow. Clipping is an option for accessible masses or in cases wth hematomas that can be evacuated.

If the rupture occurred more than 24 hours ago, the neurosurgeons may choose to operate after 10 days to reduce the probability of angry brain complications although the risk for rebleeding and fatality is increased.

Furthermore, acute hydrocephalus may warrant drainage and shunt placement. Other sequelae may also require surgery.

Other

Important measures that should be implemented in patients with SAH include bed rest, headache relief.

Contraindications

Anticoagulants and antiplatelet drugs should be avoided in these patients.

Prognosis

The prognosis of SAH due to a ruptured aneurysm tends to be poor even with prompt intervention. Specifically, SAH is deadly in as much as 50% of patients [3], with the majority dying after the initial rupture and others meeting a fatal outcome from a further rupture a few weeks later. SAH is also associated with severe neurological and cognitive disabilities [1].

Note that the dynamic nature of aneurysm formation increases the likelihood for development of new aneurysms and expansion of previous ones [14]. Therefore, these patients are at increased risk for future episodes of rupture and hemorrhage.

Etiology

SAH is caused by a ruptured aneurysm in nearly 80% of cases. Structural defects in the walls of the cerebral vessels contribute to aneurysm formation [4] [5] especially in the context of hypertension, smoking, and excessive alcohol consumption [6].

About 20% of SAH cases are the result of nonaneurysmal conditions such as peri mesencephalic hemorrhage, cerebral arteriovenous malformations, arterial dissection, rare diseases, as well as anticoagulant treatment [6].

There are risk factors for the formation of an aneurysm, which include hypertension, cerebral atherosclerosis, abnormalities in the circle of Willis, chronic use of analgesic drugs, hypertensive diseases in pregnancy, positive family history for stroke, and persistent headaches. Certain genetic disorders may predispose affected individuals to the development of this defect as well. Marfan syndrome, Ehlers-Danlos syndrome, and adult polycystic kidney disease are among the examples.

Predictors of rupture include an aneurysm that measures 3mm or less in diameter as well as a positive family history of the cerebrovascular disease [7].

Epidemiology

The annual incidence of SAH in the U.S. is 6 to 8 individuals per population of 100,000 [8] with a higher occurrence in Hispanics [9]. Furthermore, there is a greater prevalence in Finland and Japan [8].

With regards to the patient demographics, this SAH manifests at an average age that ranges between 50 to 55 [1]. There is a predilection for women, who exhibit a rate that is 1.6 times that of men [8]. Additionally, the incidence in black individuals is double that of white people [10].

Sex distribution
Age distribution

Pathophysiology

SAH refers to bleeding into the subarachnoid space, which most commonly stems from a ruptured aneurysm. Specifically, saccular aneurysms (also known as berry aneurysms) are found in the terminal segment of the internal carotid artery (ICA) and the anterior arteries of the circle of Willis. Intracranial arteries are susceptible to developing aneurysms since these vessels have a thin adventitia layer, absent external elastic lamina, and no support in the subarachnoid space.

The growth of these lesions is influenced by the hemodynamics and structure of the large cerebral arteries, which are under significant hydrostatic pressure due to the turbulent and rapid changes in blood flow. Moreover, the arterial wall stress is highest at bifurcation points. The likelihood of rupture is determined by the La Place's law, which explains that the radius and transmural pressure of an aneurysm determine the amount of tension in the wall.

Unruptured aneurysms can also cause brain injury since the compressive force of the lesion damages tissue and limits perfusion.

Complications

There are numerous complications that can arise from SAH such as rebleeding, which is a very serious risk that likely occurs due to the instability of the thrombus. About 20% of patients experience rebleeding episodes within 2 weeks. Risk factors for this sequel are anxiety [11], as well as hypertension and seizures.

A predominant cause of morbidity and mortality in patients with SAH is delayed cerebral ischemia, which results from vasospasm [12]. The most common vessels involved are the ICA and the proximal segments of the anterior cerebral artery (ACA) and middle cerebral artery (MCA).

Aneurysms of the ACA, ICA, and other vessels can rupture and induce intracranial hemorrhage. Additionally, intraventricular hemorrhage (IVH) can emerge from ruptured aneurysms in the brain vasculature.

Hydrocephalus can develop, especially in older individuals and/or those with vasospasms, subdural hematoma, intraventricular bleeding, and systolic heart failure. Consequently, acute hydrocephalus can increase the ICP, which leads to loss of consciousness and possibly even coma.

Other complications of SAH include subdural hematoma, left ventricular systolic dysfunction, myocardial infarction [13], and seizures.

Prevention

Universal recommendations advocate for a healthy lifestyle that helps prevent cerebrovascular disease. For example, all individuals are advised modify risk factors through strict blood pressure control, smoking cessation, alcohol restriction, weight management, and proper diet.

Prevention of rupture

There are challenges that present with regards to management of patients with incidental findings. Since the probability of rupture does increase with age, the medical team and the patient should discuss the risks of rupture and complications of surgery in order to make the best decision. Note that the screening of first-degree family members of affected individuals does not give promising results.

Summary

Subarachnoid hemorrhage (SAH) is the extravasation of blood into the space between the arachnoid membrane and pia mater. The majority of nontraumatic cases of SAH are attributed to a ruptured cerebral aneurysm [1], while a head injury is implicated in traumatic cases. Moreover, SAH accounts for up to 7% of stroke cases [2], and thus shares risk factors such as hypertension, atherosclerosis, and alcohol abuse.

The characteristic features of SAH are a severe "a thunderclap headache," nausea, emesis, altered mental status, and other neurologic manifestations [3]. Due to elevated intracranial pressure (ICP) and damage to the brain tissue and vasculature, SAH can also result in serious complications such as episodes of rebleeding, vasospasm, hydrocephalus, intraventricular hemorrhage, intracerebral hemorrhage, and seizures.

Patients suspected to have SAH should be evaluated and treated urgently. The clinical assessment includes patient and family history, identification of all risk factors, a detailed physical exam with neurologic focus, and the appropriate studies. The latter consists of computed tomography (CT) scan, and a lumbar puncture if the former is negative for SAH. Furthermore, various blood tests should be obtained to rule out other causes of the clinical picture.

Emergency treatment is crucial since SAH is associated with high rates of morbidity and mortality. Initial management is composed of stabilization, maintenance of blood pressure within a therapeutic range, and emergent surgical intervention to prevent rebleeding and other complications. Procedures such as clipping or coiling of an aneurysm are usually performed immediately.

Patient Information

What is Subarachnoid hemorrhage?

Subarachnoid hemorrhage (SAH) refers to bleeding in an area known as the subarachnoid space. This space is the protective cushion between the brain and the tissue that surrounds it.

What causes it?

There are numerous causes but the most common one is a ruptured aneurysm. An aneurysm is a bulge that forms in the large arteries of the brain in some people. When it bursts, the blood spills into the arachnoid space. Other causes include abnormalities in the structure of arteries, rare genetic diseases, the use of anticoagulant medications, and head injuries.

The factors that increase the risk for the formation of aneurysms are:

  • Hypertension
  • Atherosclerosis
  • Smoking
  • Alcohol abuse
  • Certain genetic diseases such as Marfan syndrome
  • Certain abnormalities in the vessels of the brain

What are the signs and symptoms?

SAH more commonly occurs between the ages of 50 and 55 although it can develop at any age. The following are the signs and symptoms:

How is it diagnosed?

Any patient with the above signs and symptoms should be evaluated immediately. The clinician will ask important questions about the history, perform a full physical exam including a detailed neurologic exam, and order the following tests:

  • CT scan without contrast
  • MRI if needed
  • Cerebral angiography and CT angiography if CT scan is negative
  • If CT is negative, the patient should have a lumbar puncture
  • Laboratory tests: complete blood count, coagulation panel, cardiac tests metabolic tests, and blood typing and screening
  • EKG

How is it treated?

This life-threatening condition must me treated immediately. Patients should be admitted to the ICU or stroke center. The treatment includes the following:

  • Very high blood pressure is treated carefully
  • Spasm of cerebral vessels should be prevented with specific medications such as calcium channel blockers
  • Surgery: neurosurgeons block blood flow of the affected artery since the risk of recurrent bleeding is usually high. They can clip or place coils in the vessel.
  • The patient should be placed on bed rest to prevent more bleeding
  • Treatment with medications that prevent constipation (so that the patient does not strain and exert pressure)
  • Headache relief

What is the prognosis?

This is a life-threatening condition and should be treated urgently. Survivors may experience further episodes of aneurysm formation and rupture in the future. Also, patients who survive SAH may develop neurologic disabilities.

References

Article

  1. Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. New England Journal of Medicine. 2006;354(4):387-396.
  2. Feigin VL, Rinkel GJ, Lawes CM et al. Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies. Stroke. 2005; 36 (12): 2773–80.
  3. van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007; 369 (9558): 306–18.
  4. Brisman JL, Song JK, Newell DW. Cerebral aneurysms. New England Journal of Medicine. 2006; 355(9):928-939.
  5. Wiebers DO, Piepgras DG, Meyer FB, et al. Pathogenesis, natural history, and treatment of unruptured intracranial aneurysms. Mayo Clinic Proceedings. 2004;79(12):1572-1583.
  6. van Gijn J, Rinkel GJ. Subarachnoid haemorrhage: diagnosis, causes and management. Brain. 2001;124 (Pt 2):249-278.
  7. You SH, Kong DS, Kim JS, et al; Characteristic features of unruptured intracranial aneurysms: predictive risk. Journal of Neurology, Neurosurgery, and Psychiatry. 2010 May;81(5):479-84.
  8. Linn FH, Rinkel GJ, Algra A, et al. Incidence of subarachnoid hemorrhage: role of region, year, and rate of computed tomography: a meta-analysis. Stroke. 1996;27(4):625-629.
  9. Bruno A, Qualls C. Risk factors for intracerebral and subarachnoid hemorrhage among Hispanics and non-Hispanic whites in a New Mexico community. Neuroepidemiology. 2000;19(4):227-232.
  10. Broderick JP, Brott T, Tomsick T, et al. The risk of subarachnoid and intracerebral hemorrhages in blacks as compared with whites. New England Journal of Medicine. 1992;326(11):733-736.
  11. Morris PG, Wilson JT, Dunn L. Anxiety and depression after spontaneous subarachnoid hemorrhage. Neurosurgery. 2004; 54(1):47-52; discussion 52-4.
  12. Jaeger M, Soehle M, Schuhmann MU, Meixensberger J. Clinical Significance of Impaired Cerebrovascular Autoregulation After Severe Aneurysmal Subarachnoid Hemorrhage. Stroke. 2012;43(8):2097-101.
  13. van der Velden LB, Otterspoor LC, Schultze Kool LJ, Biessels GJ, Verheugt FW. Acute myocardial infarction complicating subarachnoid haemorrhage. Netherlands Heart Journal. 2009; 17(7-8):284-7.
  14. Wermer MJ, van der Schaaf IC, Velthuis BK, et al. Follow-up screening after subarachnoid haemorrhage: frequency and determinants of new aneurysms and enlargement of existing aneurysms. Brain. 2005;128 (Pt 10):2421-2429.

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Last updated: 2018-06-21 23:31