Nontraumatic subarachnoid hemorrhage (SAH) represents about 3% of all strokes in the USA. Worldwide the incidence of SAH is 2–16/100,000 people, and it has not undergone changes in the last three decades. Females are more commonly affected than males (F:M = 1.24:1), as are some ethnic groups (African Americans and Hispanics) compared to white Americans [1, 2]. SAH incidence increases with age (onset ≥ 50 years), while the prevalence rate is 3.2% [3]. In about 80% of cases, the cause of SAH is the rupture of a cerebral aneurysm (annual rupture rate 0.95%) [4]; in 15% of SAH, there is no evidence of source of bleeding with neuroimaging studies; and finally the remaining 5% of cases is explained by other causes (arteriovenous malformations, vasculitis). SAH is responsible for significant morbidity and mortality. Mortality rates vary widely between different studies (8–67%), but most of these studies do not take into account prehospital mortality (about 10–15%) [5].

A significant reduction of SAH mortality rates has been observed worldwide (30-day mortality 32–42%) [6], attributable to the improvements in patient care (neurosurgical intensive care, endovascular therapy, microsurgical techniques) which have increased the survival in hospitalized patients. Despite the reduction in fatality rates, about 50% of survivors have significant permanent reduction in health-related quality of life (loss of working capacity, social independence, and personal/family relationships at a 5-year follow-up). This quality of life reduction has multifactorial causes such as impairment of physical functions, cognitive deficits (executive function and memory), mood disorders (anxiety, depression, and posttraumatic stress disorder), and personality disorders [7, 8].

Several risk factors have been identified, both nonmodifiable (age, female sex, previous aneurysmal SAH, familiarity) and modifiable (hypertension, cigarette smoking, alcohol abuse, sympathomimetic drugs use). Other risk factors are some genetic diseases (autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome type IV, Marfan syndrome, neurofibromatosis type I, fibromuscular dysplasia), cerebral aneurysms of the anterior circulation in patients <55 years, cerebral aneurysms of the posterior circulation in male patients, cerebral aneurysms >7 mm in diameter, and finally patients with significant legal or financial problems over the last 30 days. It is unknown whether there are factors playing a predominant role but, if present simultaneously, many of them can interact among themselves with a synergistic effect [9–14]. Antihypertensive treatment is recommended and may reduce the risk of SAH, as well as avoiding tobacco and alcohol use and eating a diet rich in vegetables [2].

Most of cerebral aneurysms are not diagnosed during life, or their detection is incidental. Inflammation appears to play an important role in the pathogenesis and growth of intracranial aneurysms [2]. Clinically the aneurysm may present with headache, bitemporal hemianopsia and bilateral hyposthenia of the lower limbs (anterior communicating artery), unilateral third cranial nerve palsy (posterior communicating artery), facial or orbital pain, epistaxis, progressive visual loss and/or ophthalmoplegia (intracavernous internal carotid artery), and with symptoms of brain stem dysfunction (posterior circulation).

SAH is the most common clinical presentation of an aneurysm [6]. A severe, sudden headache (thunderclap headache, often described as the worst headache a patient has ever had) is the typical onset of SAH, and it occurs in about 80% of patients, accompanied by nausea, vomiting, photophobia, neck pain and stiffness, and loss of consciousness [15]. Physical examination should include evaluation of level of consciousness, fundus oculi, meningeal signs, and presence of focal neurological deficits. Focal neurological deficits (including cranial nerve palsies) are present in 10% of SAH patients and are associated with worse prognosis when caused by the presence of thick subarachnoid clots or intraparenchymal hemorrhage.

A transient increase in intracranial pressure (ICP) is responsible for nausea, vomiting, and syncope; coma and even brain death can occur in case of more severe and prolonged increase in ICP values. Terson syndrome (vitreous hemorrhage associated with SAH) occurs in up to 40% of SAH patients [16, 17]. A sudden increase in ICP may cause preretinal hemorrhages associated with more severe SAH and increased mortality.

Occasionally some patients may have atypical SAH presentation with seizures, acute encephalopathy, concomitant subdural hematoma, and traumatic brain injury, making diagnosis more difficult. Some patients (10–43% of cases) experience days or weeks before aneurysmal SAH the so-called “sentinel” headache caused by a small blood loss from the aneurysm [18, 19]. Unfortunately this event often represents only retrospective information since sentinel headache is temporary, and head CT is negative in 50% of cases.

Initial assessment and management of SAH patients with impaired consciousness must focus on stabilizing airway, breathing, and circulation [2, 15, 22–24]. Once stabilized, patients should undergo head CT and, if the patient is unable to protect airway, must be immediately intubated. The most common indications for endotracheal intubation include coma, hydrocephalus, seizures, and the need for sedation. We must also avoid extreme values of blood pressure that could trigger rebleeding; therefore, controlling hypertension is critical [34]. On the basis of randomized controlled clinical trials, it is recommended to maintain mean arterial pressure (MAP) <110 mmHg or systolic blood pressure < 160 mmHg until ruptured aneurysm treatment, avoiding hypotension not to compromise cerebral perfusion [35, 36]. Usually blood pressure control is achieved by treating patient’s pain, otherwise administering labetalol IV (5–20 mg), hydralazine (5–20 mg), or continuous nicardipine infusion (5–15 mg/h). To treat patient’s pain, short-acting opioids are used.

In the management of cerebral aneurysms, there are two effective treatments: surgical clipping and endovascular coiling. The goal is to completely obliterate the aneurysm and exclude it from circulation whenever possible. Clipping consists in excluding the aneurysm sac from circulation by positioning a vascular clip at the aneurysm neck with microsurgical technique. Coiling is an endovascular treatment and consists in bringing an endovascular microcatheter to the aneurysm sac and releasing through these very thin metallic coils until complete aneurysm occlusion. The choice between this two treatment options depends on several factors including patient age, aneurysm localization and morphology, and the relationship with adjacent vessels. Since deciding on the most appropriate treatment for each patient is complex, it is important that the assessment is performed by a multidisciplinary team consisting of cerebrovascular neurosurgeons, endovascular-trained physicians, and neurointensivists to reach a consensus on therapy [2, 15, 22, 23, 30, 43]. A prospective randomized controlled clinical trial—ISAT (International Subarachnoid Aneurysm Trial)—was performed to evaluate patients with treatable aneurysms and candidates for both endovascular coiling and surgical clipping [45, 46]. Patients assigned to the coiling group showed a significantly better outcome (in terms of disability-free survival at a 1-year follow-up, evaluated with modified Rankin scale) and a lower risk of epilepsy compared to the clipping group. On the other hand, the risk of rebleeding and only partial aneurysm occlusion was lower in the clipping group. Overall, endovascular coiling should be preferred compared to surgical clipping whenever possible. Many aneurysms are not equally eligible for clipping or coiling. Characteristics such as advanced age, poor clinical grading, underlying multiple systemic comorbidities, aneurysms of basilar artery tip and vertebrobasilar circulation, aneurysms of intracavernous internal carotid artery, and high surgical risk make endovascular coiling preferable. Other features such as giant, fusiform aneurysms, with an elevated neck/body ratio (>0.5), localized at arterial bifurcations and middle cerebral artery aneurysms or associated with large parenchymal hematomas make surgical clipping more suitable. In young patients, surgical clipping is preferable as it provides better protection against SAH recurrence. After every aneurysm repair surgery, it is recommended to perform an immediate cerebrovascular imaging examination to identify promptly any residues or recurrences of aneurysmal pathology requiring further treatment [2]. Regardless of the chosen treatment, aneurysms should be treated as early as possible to prevent rebleeding and to safely and effectively treat vasospasm [6].

The general goals of anesthesiologic management include hemodynamic control to minimize the risk of aneurysm re-rupture and strategies to protect the brain from ischemic injury. Depending on SAH severity, patients will exhibit a different degree of cerebrovascular reactivity impairment and of cerebral autoregulation impairment, making brain perfusion strictly dependent on MAP value. Therefore the patient should not be exposed to hypotension, with associated risk of DCI, or hypertension, with risk of rebleeding [47, 48]. The goal is to maintain the transmural pressure gradient through the aneurysm wall and to maintain the cerebral perfusion pressure (CPP), given by the subtraction MAP-ICP. A sudden increase in blood pressure along with a rapid reduction in ICP can alter the gradient and increase the risk of aneurysm rupture. It is therefore important to avoid hypotension or hypertension during induction of anesthesia, intubation, surgical incision, and opening of dura. Prior to induction of anesthesia, a central venous access and also an arterial access with intra-arterial blood pressure monitoring must be obtained to be able to continuously calculate CPP and the transmural pressure gradient through the aneurysm wall [49]. Many pharmacological agents have been used for neuroprotective purpose during aneurysm surgery, but no one has shown a significant improvement in outcome.

In the early stage, SAH is often associated with severe systemic and intracranial consequences rather than further brain damage [60–63]. More than 75% of SAH patients experience a systemic inflammatory response syndrome (SIRS), probably due to high levels of inflammatory cytokines, associated with permanent neurocognitive dysfunction. SAH patients have an increased risk of developing several neurological complications, including hydrocephalus, cerebral edema, delayed cerebral ischemia, rebleeding, seizures, and neuroendocrine disorders leading to alteration of sodium, water, and glucose homeostasis. SAH also triggers alterations mediated by the hypothalamus increasing the orthosympathetic and parasympathetic tone, responsible for cardiac and pulmonary complications. Increased levels of circulating catecholamines are thought to be the basis of several cardiac manifestations including ECG alterations, arrhythmias, contractility disorder (Takotsubo cardiomyopathy), troponinemia, and myocardial necrosis. A similar pathophysiologic mechanism is probably the basis of pulmonary complications such as neurogenic pulmonary edema. It is important to recognize and treat all these systemic complications since they are associated with an increased risk of delayed cerebral ischemia and poor neurological outcome after SAH.