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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Important measures that should be implemented in patients with SAH include bed rest, headache relief.
Anticoagulants and antiplatelet drugs should be avoided in these patients.
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 , 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 .
Note that the dynamic nature of aneurysm formation increases the likelihood for development of new aneurysms and expansion of previous ones . Therefore, these patients are at increased risk for future episodes of rupture and hemorrhage.
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   especially in the context of hypertension, smoking, and excessive alcohol consumption .
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 .
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 .
The annual incidence of SAH in the U.S. is 6 to 8 individuals per population of 100,000  with a higher occurrence in Hispanics . Furthermore, there is a greater prevalence in Finland and Japan .
With regards to the patient demographics, this SAH manifests at an average age that ranges between 50 to 55 . There is a predilection for women, who exhibit a rate that is 1.6 times that of men . Additionally, the incidence in black individuals is double that of white people .
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.
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 , 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 . 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.
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.
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 , while a head injury is implicated in traumatic cases. Moreover, SAH accounts for up to 7% of stroke cases , 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 . 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.
What is Subarachnoid hemorrhage?
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:
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:
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:
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.