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Summary Contemporary management of aneurysmal subarachnoid haemorrhage. An update for the intensivist
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Contemporary management of aneurysmal subarachnoid haemorrhage. An update for the intensivist
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Intensive Care Med (2024) 50:646–664https://doi.org/10.1007/s00134-024-07387-7
REVIEW
Contemporary management of aneurysmal
subarachnoid haemorrhage. An update for the
intensivist
Chiara Robba1,2* , Katharina M. Busl3, Jan Claassen4, Michael N. Diringer5, Raimund Helbok6,7, Soojin Park4,8,
Alejandro Rabinstein9, Miriam Treggiari10, Mervyn D. I. Vergouwen11 and Giuseppe Citerio12,13
© 2024 The Author(s)
Abstract
Aneurysmal subarachnoid haemorrhage (aSAH) is a rare yet profoundly debilitating condition associated with high
global case fatality and morbidity rates. The key determinants of functional outcome include early brain injury,
rebleeding of the ruptured aneurysm and delayed cerebral ischaemia. The only effective way to reduce the risk of
rebleeding is to secure the ruptured aneurysm quickly. Prompt diagnosis, transfer to specialized centers, and meticu-
lous management in the intensive care unit (ICU) significantly improved the prognosis of aSAH. Recently, multimo-
dality monitoring with specific interventions to correct pathophysiological imbalances has been proposed. Vigi-
lance extends beyond intracranial concerns to encompass systemic respiratory and haemodynamic monitoring, as
derangements in these systems can precipitate secondary brain damage. Challenges persist in treating aSAH patients,
exacerbated by a paucity of robust clinical evidence, with many interventions showing no benefit when tested in
rigorous clinical trials. Given the growing body of literature in this field and the issuance of contemporary guidelines,
our objective is to furnish an updated review of essential principles of ICU management for this patient population.
Our review will discuss the epidemiology, initial stabilization, treatment strategies, long-term prognostic factors, the
identification and management of post-aSAH complications. We aim to offer practical clinical guidance to intensivists,
grounded in current evidence and expert clinical experience, while adhering to a concise format.
Keywords: Subarachnoid haemorrhage, Vasospasm, Delayed cerebral ischaemia, Outcome, Intensive care, Aneurysm
Epidemiology and need for intensive care hypertension and smoking [1]. The incidence of aSAH
management increases with age and is 1.3 times higher in women
Aneurysmal subarachnoid haemorrhage (aSAH) is char- than in men [1, 2]. Although the prognosis of aSAH
acterized by bleeding in the subarachnoid space from the has improved over the last decades, 12% of patients die
rupture of an intracranial aneurysm (Fig. 1) [1]. aSAH before reaching the hospital, and the 90-day case-fatality
accounts for only 2–5% of all strokes, and global inci- of patients hospitalized for aSAH is approximately 30%
dence declined from 10.2 per 100,000 person-years in [3]. Survivors often suffer from functional and cognitive
1980 to 6.1 in 2010, with significant variabilities across sequelae that decrease quality of life and hamper the abil-
regions, age, and sex [1]. The global decrease in aSAH ity to return to work. Since half of patients with aSAH are
incidence paralleled a global reduction in prevalence of younger than 55 years, many are in their most produc-
tive working years. Hence, the economic burden is high
due to the loss of productive years of life[4]. In the United
*Correspondence: kiarobba@gmail.com
2
IRCCS Policlinico San Martino, Genoa, Italy Kingdom, total costs from aSAH are estimated to be £510
Full author information is available at the end of the article million ($645, €591) per year. On a community level, the
, 647
loss of productive years of life after aSAH is similar in
magnitude to that of ischaemic stroke. Take‑home message
Major determinants of poor functional outcome and
The review highlights significant progress in managing aneurysmal
case fatality are early brain injury, rebleeding of the subarachnoid hemorrhage (aSAH), underscoring the crucial role of
ruptured aneurysm, and delayed cerebral ischaemia timely diagnosis, transfer to specialized centers, and intensive care in
(DCI) [5, 6]. Rapid diagnosis, transfer to dedicated cen- improving prognosis.
It presents monitoring and intervention strategies in intensive care
tres, management strategies to prevent rebleeding, and aimed at addressing both intracranial and systemic complications,
haemodynamic management to preserve organ perfusion despite persistent challenges due to the lack of robust evidence for
in the early phase after aSAH can improve the chances of many treatments. Future research focusing on closing knowledge
gaps, particularly in early and late complications management,
favourable outcomes [7]. Admission to high-volume cen- is deemed essential to enhance long-term outcomes for aSAH
tres, defined by the management of at least 35 patients patients.
per year, is also associated with better functional out-
comes after aSAH [8].
Criteria for admission to the intensive care unit (ICU) World Federation of Neurosurgical Societies (WFNS)
are not well defined but determined by the need for spe- scale [10], (electronic supplementary material, ESM,
cialized care to manage early and delayed intracranial and Figure S1). The WFNS scale (full range 0–5) transforms
extracranial complications. Management in dedicated the Glasgow Coma Scale (GCS) score into different
neuroICUs has been shown to improve patient outcomes levels (3–6, 7–12, 13–14 with/without motor deficit,
[7]. The optimal duration of ICU management is not well and 15). Similarly, the Hunt and Hess Scale is a clini-
defined. In studies comparing neurointensivist-managed cal grading system ranging from a score of 1 to 5, based
ICUs, the median ICU stay was around 11–12 days, on neurological symptoms and signs ranging from mild
which parallels the time window to address aSAH-related headache to a comatose state [11].
complications [9]. However, these studies do not take Imaging-based scales such as the Fisher scale [12]
into account disease severity. aSAH patients may neces- or modified Fisher scale [13, 14] quantify the extent of
sitate critical care management for many weeks. In con- subarachnoid, intraventricular, and intraparenchymal
trast, good-grade patients may require fewer days of haemorrhage and are associated with outcomes. The
monitoring in the ICU, although often even good-grade Subarachnoid haemorrhage Early Brain Oedema Score
aSAH patients benefit from close neurologic observation (SEBES) has been proposed to quantify global cerebral
by specially trained staff during the risk period for vasos- oedema [15], and seems to be associated with increased
pasm and DCI. intracranial pressure and outcomes after aSAH [16].
Clinical presentation and severity scales Early complications before aneurysm securing
Although the clinical presentation of patients with aSAH Early brain injury, defined as a cascade of events that
may vary, the characteristic presenting symptom is develop in the first hours after subarachnoid haem-
a thunderclap headache, a sudden severe headache gen- orrhage, is related to a variety of pathophysiologi-
erally described as the “worst headache of life”. Other cal mechanisms, which include cerebral oedema from
symptoms include nausea, vomiting, confusion, distur- bleeding, microcirculatory alterations, oxidative and
bance in vision and language, focal neurological deficits inflammatory cascade, and blood–brain-barrier break-
and loss of consciousness [1]. down, thus leading to neuronal damage [17].
Severity scales are based on neurological examina- Early management of patients includes intubation
tions and early computed tomography (CT) findings and mechanical ventilation in comatose patients to
[10]. The most widely utilized clinical assessment scale protect the airway and optimize ventilation, neuroim-
to capture clinical severity in patients with aSAH is the aging (non-contrast head CT, and if negative lumbar
(See figure on next page.)
Fig. 1 After the rupture of an intracranial aneurysm, a cascade of events ensues. Arterial blood under pressure enters the subarachnoid space,
inducing swift mechanical effects, such as abrupt increases in intracranial pressure and related cerebral impact. This sets off intracranial repercus-
sions in the form of early brain injury, accompanied by immediate systemic consequences, impacting cardiovascular and respiratory functions.
The presence of blood in the subarachnoid space may contribute to cerebral vasospasm, delayed cerebral ischemia, hydrocephalus, and seizures.
Systemically, there can be hyperglycaemia, an inflammatory response, electrolyte imbalances (primarily hypo/hypernatremia), and hormonal dis-
turbances. ICP intracranial pressure, CBF cerebral blood flow, NPO neurogenic pulmonary oedema, ECG electrocardiography, BBB brain blood barrier,
DCI delayed cerebral ischemia, LV left ventricle
, 648
Fig. 1 (See legend on previous page.)
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