Anaesthesia for clipping of intracranial aneurysms

Key points.

• •Treatment for intracranial aneurysms is tailored to the characteristics of the aneurysm and the patient.
• •Surgical clipping has a low recurrence rate but higher morbidity; the long-term outcome is comparable to coiling.
• •Goals of anaesthesia include minimising transmural pressure changes while maintaining perfusion.
• •Induced hypertension and reduced CMRO₂ decreased the risk of focal ischaemia during temporary clipping.
• •Adenosine can be used to cause circulatory arrest, which aids visualisation and clipping during intraoperative aneurysm rupture.

Learning objectives.

By reading this article, you should be able to:

• •Describe the anatomy, classification and natural history of intracranial aneurysms.
• •Detail the perioperative strategy for managing patients undergoing surgical clipping.
• •Have a clear strategy to manage an intraoperative aneurysm rupture.

An aneurysm is a localised dilation of an artery resulting from weakening of the arterial wall. Intracranial vessels are particularly prone to developing aneurysms because of their thinner tunica media and adventitia layers.¹ Ruptured intracranial aneurysms account for ∼85% of non-traumatic subarachnoid haemorrhages (SAH) and are associated with high mortality and morbidity.² The general prevalence of intracranial aneurysms is estimated to be 3–5%, varying by geographical region.³ The average age of diagnosis, based on imaging findings, is around 50 yrs, with a female preponderance of 1.24:1 compared with males.⁴

Anatomy and pathophysiology

Intracranial aneurysms most commonly occur at the circle of Willis, typically at bifurcation points where the mechanical stress from turbulent blood flow is greatest (Fig 1, Fig 2). The pathophysiology of intracranial aneurysm formation is complex and multifactorial. While genetic factors play a role, it is also driven by the interplay of haemodynamic stress, extracellular matrix degradation and inflammatory responses. Chronic exposure to high wall shear stress leads to endothelial dysfunction and media thinning. In addition, an imbalance between matrix metalloproteinases (MMPs) and their tissue inhibitors promotes the breakdown of elastin and collagen, reducing vessel integrity.⁶ These changes, combined with inflammatory cell-mediated remodelling, contribute to aneurysm formation and rupture risk.⁶

Fig 1.

Circle of Willis anatomy and incidence of location of intracranial aneurysms.⁵

Fig 2.

Clipping of an unruptured right MCA bifurcation aneurysm.

Intracranial aneurysms can be classified based on size (typically of the maximal dome diameter) or by shape (Table 1). Apart from dome diameter, variables such as aneurysm neck diameter and dome-to-neck ratio are also evaluated to guide treatment planning. Aneurysms with neck diameter >4 mm, dome-to-neck ratio <2, or both are considered wide-necked aneurysms, while giant aneurysms are those measuring 25 mm or more in diameter.⁹

Table 1.

Risk of rupture of intracranial aneurysms.

Classification	Size (mm)	5-yr risk of rupture for anterior circulation7 (%)	5-yr risk of rupture for posterior circulation7 (%)
Small	<7	0	2.5
Moderate	7–12	2.6	14.5
Large	13–24	14.5	18.4
Giant	>25	40	50
Factors that increase risk of rupture (PHASES risk prediction score components)8: •Size •Location on the posterior circulation or anterior cerebral arteries •Japanese or Finnish ethnic background •Hypertension •Age >70 yrs •Previous subarachnoid haemorrhage from another aneurysm

Intracranial aneurysms can also be classified by shape. Saccular aneurysms, which account for the vast majority, are acquired lesions that lack the two strongest layers of blood vessel walls—the internal elastic lamina and tunica media.¹⁰ Fusiform aneurysms, characterised by circumferential dilation, are most commonly found in the vertebro-basilar circulation. Dissecting aneurysms result from a tear in the intima, leading to blood accumulation within the subadventitial layers and the formation of a false lumen, causing lumen narrowing and potential ischaemic sequelae. Intracranial aneurysms can also develop in association with arteriovenous malformations (AVMs) because of altered flow dynamics. Aneurysms associated with AVMs have a higher risk of rupture. Defining the anatomic relationship between the aneurysm and the AVM nidus, typically through angiographic imaging, is crucial for planning the treatment strategy.

Ruptured and unruptured intracranial aneurysms

Intracranial aneurysms may rupture and can lead to SAH with or without intraventricular extension or intraparenchymal haemorrhage. The risk of rupture is dependent on many factors including size, shape and location of aneurysm, with the size of aneurysm being the best predictor of rupture (Table 1).

Patients with aneurysmal SAH often present with a sudden, severe ‘thunderclap’ headache. This is likely caused by intracranial pressure (ICP) equating that of arterial pressure as blood occupies the subarachnoid space.¹¹ This is often accompanied by other neurological signs and symptoms including loss of consciousness, seizure, nausea, vomiting and focal neurological deficits. Signs of meningism can also occur from blood tracking into the ventricles and further into the spinal canal.¹¹ These signs and symptoms, along with the Glasgow Coma Scale (GCS) score, form the basis of the clinical grading systems (e.g. Hunt and Hess scale, World Federation of Neurosurgical Societies [WFNS] grade) predicting outcome and mortality (Table 2). Radiological grading of SAH is usually according to the Fisher or modified Fisher scale. Aneurysmal SAH carries a 30-day mortality rate of 45%, with rebleeding occurring in 30–40% of patients within the first month.^2,11

Table 2.

Grading of SAH.¹².

Grade	World federation of neurosurgical societies (WFNS) scale		Hunt and Hess scale
	Glasgow coma scale (GCS)	Motor deficit	Clinical description/neurological deficit
1	15	Absent	Asymptomatic, mild headache, slight nuchal rigidity
2	13–14	Absent	Moderate to severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy
3	13–14	Present	Drowsiness, confusion or mild focal deficit
4	7–12	Present or absent	Stupor, moderate to severe hemiparesis
5	3–6	Present or absent	Deep coma, decerebrate posturing, moribund appearance

Apart from cases diagnosed after rupture, the majority of patients with intracranial aneurysms (85%) are asymptomatic, with aneurysms often discovered incidentally during the investigation of other conditions.¹³ Large unruptured aneurysms can compress brain tissue or cranial nerves, resulting in symptoms such as headache, visual disturbances, dilated pupils and loss of balance. Factors such as aneurysm size, location and patient comorbidities all influence the balance of risks between intervention and conservative management.

Treatment modalities for intracranial aneurysms

Treatment strategies for intracranial aneurysms are contingent on both aneurysm characteristics (e.g. size, location, morphology, presence of perforating arteries arising from the aneurysm, presence of intra-aneurysmal calcification or thrombosis) and the patient's overall risk profile. The two main treatment options are endovascular therapy and surgical clipping, with alternative options such as aneurysm ‘wrapping’ or parent artery sacrifice reserved for select cases. The goal of all therapies is to obliterate the aneurysm from the circulation and reduce the risk of rupture or rebleeding.

Endovascular coiling involves implanting coils into the aneurysm via an intra-arterial catheter. In high-income countries, the majority of intracranial aneurysms are now treated with coiling as it is less invasive and the recovery time is quicker. Coiling is also preferred for posterior circulation aneurysms, where surgical access is more challenging, and has lower postoperative morbidity compared with surgical clipping. However, it has a higher recurrence rate and is less suitable for wide-necked or complex aneurysms because of the risk of coil migration and incomplete occlusion. In such cases, adjunct techniques such as flow diversion or stent/balloon-assisted coiling may be required.

Aneurysms that are unsuitable for endovascular treatment are typically managed with surgical clipping. These include aneurysms with complex morphology, a wide neck, middle cerebral artery (MCA) location where surgical access is often favourable and in younger patients where long-term durability is a priority. Surgical clipping involves placing a metal clip across the aneurysm neck via a craniotomy. While clipping has a lower recurrence rate, it is associated with higher postoperative morbidity.¹⁴ Surgical alternatives for aneurysms that are not amenable to clipping include aneurysm wall reinforcement (commonly known as ‘wrapping’) and parent artery sacrifice, which may be performed with or without bypass revascularisation. These techniques are particularly useful for complex aneurysms, such as giant, fusiform or dissecting aneurysms.

The International Subarachnoid Aneurysm Trial demonstrated that endovascular coiling improved survival and reduced dependency at 1 yr compared with clipping (23.7% compared with 30.6%), although long-term outcomes at 5 yrs were similar.^15,16 The latest American Heart Association/American Stroke Association guidelines describe the choice of treatment modality as ‘highly nuanced’ and recommend coiling over clipping for ruptured aneurysms of the posterior circulation.¹⁷

Anaesthetic management for clipping procedures

General principles

Transmural pressure (TMP), the difference between mean arterial pressure (MAP) and ICP, is the pressure that contributes to aneurysm rupture. Cerebral perfusion pressure (CPP), which determines brain tissue perfusion, is governed by the same equation. Although TMP and CPP are derived from the same variables and share the same equation, they represent opposing physiological goals (Fig. 3). The aim of anaesthesia for surgical clipping of intracranial aneurysms is to minimise the change in TMP of the aneurysm while maintaining adequate CPP and providing optimal brain relaxation.

Fig 3.

Interplay between ICP and MAP in an intracranial aneurysm.

CPP, cerebral perfusion pressure; ICP, intracranial pressure; MAP, mean arterial pressure; TMP, transmural pressure.

Intraoperative monitoring

In addition to standard monitoring, invasive arterial pressure monitoring should be sited before induction of anaesthesia. A central venous catheter and wide-bore venous access are preferable. Processed EEG monitoring aids in titrating anaesthetic agent.

Induction and maintenance of anaesthesia

The primary goal during induction of anaesthesia is to maintain haemodynamic stability and minimise rapid changes in arterial pressure. This typically involves giving judicious doses of an opioid, hypnotic agent and a neuromuscular blocking drug. Laryngoscopy should be performed with care and supplementation with additional anaesthetic agents, opioids, or both may be necessary to avoid a hypertensive response.

In patients with an unruptured aneurysm or a good-grade SAH, where ICP often remains normal, increasing MAP can raise TMP and increase the risk of rupture or rerupture, respectively. In contrast, in patients with poor-grade SAH with intracranial hypertension, a higher MAP target is often required to maintain adequate CPP because of increased ICP. Management of carbon dioxide concentrations follows a similar principle: although hyperventilation can lower ICP, it may also increase TMP and the risk of rupture, whereas hypercapnia should be avoided to prevent swelling of brain tissue. For unruptured aneurysms and ruptured aneurysms with normal ICP, it is recommended to aim for systolic BP less than or equal to the patient's normal systolic BP.¹⁸ For ruptured aneurysms with suspected or known intracranial hypertension, avoid treating passive hypertension and manage hypertension caused by stimuli or vasopressors carefully.¹⁸ The techniques of induced and permissive hypotension were once commonplace for neurovascular surgery with the aim of reducing intraoperative blood loss and improving the surgical field. Improvements in microsurgical access and concerns over cerebral ischaemia and postoperative organ dysfunction have led to a decline in the practice of both induced and permissive hypotension.¹⁹

Application of cranial pins to immobilise the patient's head is highly noxious and can provoke a hypertensive response. This can be blunted through local anaesthetic infiltration at pin sites, scalp blocks or with additional doses of anaesthetic agent or opioid.

The effects of anaesthetic agents on cerebral physiology are outlined in Table 3. Although there is no strong evidence to favour volatile anaesthetic agents or total intravenous anaesthesia (TIVA) for intracranial aneurysm surgeries, TIVA is often considered ideal because of its superior cerebral haemodynamics, minimal interference with intraoperative neurophysiological monitoring (IONM) and more efficient burst suppression.²¹

Table 3.

Effects of anaesthetic agents on cerebral physiology.²⁰

↑ = increase; ↑↑ = significant increase; ↔ = unchanged; ↓ = decrease; ↓↓ = significant decrease.

	Cerebral metabolic rate	Cerebral blood flow	Intracranial pressure
Sevoflurane	↓ to ↓↓	Variable	↔ to ↑
Isoflurane	↓↓	↔ or ↑	↔ to ↑
Desflurane	↓↓	Variable	↔ or ↑
Nitrous oxide	↔ to ↑	↑↑	↑↑
Propofol	↓↓	↓↓	↓↓
Barbiturates	↓↓	↓↓	↓↓
Ketamine	↔ or ↑	↑↑	↑ to ↑↑
Etomidate	↓↓	↓↓	↓↓

Provision of a ‘relaxed brain’ helps to protect the brain from retraction injury and compression-induced ischaemia. Various strategies can be used to achieve this, including 30° head-up positioning, careful management of fluids and avoiding excessive concentrations of volatile agents because of their inherent vasodilatory effects. Controlled hyperventilation can be used to reduce cerebral blood volume and improve the surgical field. However, there is a risk is that cerebral perfusion may be compromised by this strategy.²² Osmotic agents such as hypertonic saline and mannitol may also be used.

Both hyperglycaemia and hypoglycaemia are linked to an increased risk of vasospasm and poor outcomes.²³ The IHAST study showed that intraoperative hypothermia did not improve the neurologic outcome after craniotomy among patients with good-grade aneurysmal SAH.²⁴

Surgical approaches

Positioning the patient for aneurysm clipping varies, depending on the surgical approach and the location of the aneurysm, each associated with distinct risks. A pterional (fronto–temporo–sphenoidal) craniotomy is frequently used for anterior circulation aneurysms, and for aneurysms at the basilar apex and superior cerebellar artery. This may involve modified orbitozygomatic osteotomies for deep-seated aneurysms. The patient is positioned supine for this approach, with the ipsilateral shoulder raised and the head turned to the opposite side.²⁵

For posterior circulation aneurysms, a retrosigmoid craniotomy is often preferred. This approach may be augmented with C1 laminectomy and occipital condylectomy to facilitate a ‘far-lateral’ approach to complex or deeply located aneurysms. The patient is typically positioned in the ‘park bench’ lateral position, with the head rotated towards the opposite shoulder.²⁵

Minimally invasive neurosurgery, using intracranial keyhole approaches, can also be used for surgical clipping of aneurysms. The term ‘keyhole’ is a misnomer, as it refers to reducing the craniotomy to a mini-craniotomy, typically up to 3 cm in diameter, rather than an actual keyhole size. It involves approaching the aneurysm through a reverse cone-shaped surgical corridor using an endoscopic technique. Commonly used approaches include supraorbital, lateral supraorbital and pterional mini-craniotomies.²⁶ With a minimal skull window, it reduces surgical contusion and neurological damage by using natural sulcus fissure and cistern as the surgical channel. The primary challenge lies in the reduced visualisation of the surgical field and restricted manoeuvrability when placing clips. While keyhole approaches are associated with shorter operative times, less blood loss and shorter hospital stays, long-term outcomes are still not well established.²⁷

Temporary clipping

Temporary clips are a crucial part of a neurosurgeon's armamentarium, often used for large, complex aneurysms with fragile walls. These clips are placed on the parent artery proximal to the aneurysm with the aim of inducing temporary vessel occlusion. Unlike permanent clips, temporary clips have a much lower closing pressure, typically ranging from 0.88 to 1.01 N, which minimises trauma to the vessel.²⁸ Temporary clips have a range of indications and can be applied either as an intended step or in the event of intraoperative rupture to control bleeding. Elective application of temporary clips aids in the dissection of complex aneurysms, allowing for better delineation of their morphology. It reduces chances of rerupture and reduces aneurysm turgor before a permanent clip is applied. Temporary clips are also useful in suction decompression techniques, sac remodelling and during the readjustment of permanent clips.²⁸ Prolonged temporary clip applications can result in ischaemia of the corresponding arterial territory and worse neurological outcome. The maximal permissible duration for temporary clip application remains undefined, as different studies report durations ranging from 0 to 93 min.²⁹ A safe limit is generally considered to be <7 min, beyond which the risk of ischaemia increases.³⁰

Several strategies can be used during temporary clipping to reduce the risk of focal ischaemia and ensure adequate collateral circulation. One approach is induced hypertension, where MAP is increased by 20–30% above baseline to increase collateral blood flow. The brain can also be protected against ischaemia by the reduction of cerebral metabolic rate of oxygen consumption (CMRO₂), with burst suppression often used for prolonged temporary clipping. Thiopental is commonly used, but other agents, including propofol, etomidate and sevoflurane, can also achieve an isoelectric EEG.²⁹ It is crucial that if this technique is used that the drugs used are given before the application of temporary clips. There is currently no evidence that giving supplemental drugs during temporary clipping improves outcomes.³¹ Intermittent application of temporary clips, with intervals between clippings to allow reperfusion, has been shown to be safer than a single continuous prolonged clipping.²⁹ Removing the temporary clip also exposes the unsecured aneurysm to significant shear stress risking rupture.¹¹ The optimal reperfusion time between clippings is unknown. However, when neurophysiological monitoring such as somatosensory evoked potentials (SSEPs) or motor evoked potentials (MEPs) is used, subsequent clip application typically waits until these variables return to baseline.²⁹ During the removal of temporary clips, intermittent reperfusion with intermittent occlusion of the artery—achieved by releasing the clips in a staggered manner—creates ischaemic post-conditioning, which helps reduce the risk of reperfusion injury.

Intraoperative neurophysiological monitoring

Intraoperative neurophysiological monitoring can be used to aid the prompt detection of cerebral ischaemia, particularly during temporary clip application. The most commonly used techniques include SSEPs, MEPs and brainstem auditory evoked potentials.^11,23

Somatosensory evoked potentials monitor the integrity of the dorsal column medial lemniscal pathway by assessing cortical electrical activity in response to peripheral nerve stimulation. This technique is useful for aneurysms located in both anterior and posterior circulation as the somatosensory cortex and internal capsule lie within the supply distribution of the anterior cerebral artery and MCA.^11,23 Thalamic subcortical activity, which lies within the territory of posterior cerebral artery, can also be monitored using median nerve SSEPs.

Motor evoked potentials monitor the integrity of the corticospinal tract by stimulating the motor cortex and recording the resulting electrical potential in corresponding peripheral muscles. It is helpful in detecting subcortical ischaemia, as any disruptions in the corticospinal tract at the level of the corona radiata or internal capsule resulting from inadequate perfusion by perforating arteries can be detected. Subdermal recording electrodes are typically placed in the muscles of the face and limbs contralateral to the surgical site to capture these potentials. Stimulation can be performed either as direct cortical stimulation on the exposed cortex, or through transcranial electrical stimulation via scalp electrode.

Brainstem auditory evoked potentials monitor the integrity of brainstem auditory pathways and are useful in monitoring aneurysmal surgery in the posterior circulation.^11,23 An acoustic stimulus is delivered via an ear insert device and recorded by electrodes placed near the mastoid process or earlobe. Disruption in the auditory pathways within the brainstem caused by posterior circulation ischaemia typically leads to detectable reduction in evoked potential recorded.

The detection of cerebral ischaemia through IONM can facilitate corrective actions, such as augmentation of MAP, retractor adjustment and clip manipulation to restore blood flow.¹¹

All anaesthetic agents interfere with SSEPs to varying degrees. Volatile agents can cause a dose-dependent reduction in SSEP amplitude and an increase in latency. Total intravenous anaesthesia is usually preferred because propofol has minimal effects on SSEPs.³² Etomidate and ketamine have the opposite effect of increasing the amplitude of cortical SSEPs.³² Neuromuscular blocking drugs have no effect on SSEPs but do disrupt MEPs.³² If MEPs are used, dexmedetomidine should also be avoided because of its inhibitory effects. Brainstem auditory evoked potential is minimally affected by all anaesthetic drugs.

Indocyanine green videoangiography

Indocyanine green (ICG) videoangiography is an imaging technique used to confirm the placement of surgical clips and ensure the complete obliteration of the aneurysm sac. It uses infrared imaging to provide real-time visualisation of blood flow during surgery. During the procedure ICG is injected through a peripheral vein and a surgical microscope equipped with an integrated near-infrared camera is used to visualise the fluorescence of the dye. The recommended dose of ICG for angiography is 0.2–0.5 mg kg⁻¹ (maximum 5 mg kg⁻¹).³³ While digital subtraction angiography (DSA) remains the gold standard for intraoperative evaluation of aneurysm clip placement, ICG videoangiography offers notable advantages, such as faster timeframe and the ability to be performed without requiring extensive logistical support. It has limitations in visualising thrombosed and calcified vessels or aneurysms.³³ Transient oxygen desaturation is common after injection of ICG.

Intraoperative ruptures

Intracranial aneurysms are at risk of rupture during surgical manipulation, with a rupture rate of 1.1% during exposure, 15.2% during aneurysm dissection and 6.7% during clip application or manipulation.³⁴ Inadvertent intraoperative aneurysm ruptures significantly increase mortality and morbidity, with mortality rates up to 40% if not managed swiftly.³⁵ Risk factors for intraoperative rupture include hypertension, pre-existing rupture of the aneurysm, location in the anterior communicating artery and larger sac size.³⁶ A rupture simulation during the preoperative briefing helps ensure team members are prepared for prompt, coordinated action. Close communication with the surgical team during an intraoperative rupture is important and arterial pressure targets should be clearly communicated. During an intraoperative rupture, a brief period of controlled hypotension, with a 10–20% reduction in MAP may be necessary to improve aneurysm visualisation to facilitate temporary clipping. A bolus dose of an anaesthetic agent (propofol or thiopental) is useful in this instance, as it can not only lower arterial pressure but also further reduce CMRO₂.

Circulatory arrest

Adenosine-induced temporary flow arrest is a technique to induce a brief cardiac standstill, creating a global reduction in CBF and cessation of flow to the aneurysm. It is useful during intraoperative ruptures as it provides a bloodless surgical field. It can also be used in unruptured aneurysms to improve visualisation and dissection, especially those located at the skull base where temporary clipping is challenging. Adenosine has a rapid onset and offset of action; its action on A1 receptors leads to depressed sinoatrial node activity, slowed atrioventricular (AV) nodal conduction and reduced ventricular automaticity. It also has vasodilatory effects and can cause a range of cardiovascular effects, from AV nodal blockade, bradycardia and profound hypotension, to brief sinus arrest followed by the spontaneous return of rhythm.³⁷ There is currently no consensus or established guideline on the exact dosage or method of delivery (infusion or bolus) and practices vary across institutions. A bolus dose of 0.3–0.6 mg kg⁻¹ is commonly used and may induce up to 40 s of flow arrest.^18,36,38 Adenosine should be avoided in patients with asthma, coronary artery disease or conduction abnormalities.

Sodium nitroprusside and glyceryl trinitrate are among other drugs that can be used to induce cardiac standstill, but they carry adverse effects such as rebound hypertension and increased ICP. Other than pharmacological means, rapid ventricular pacing can also be used to achieve cardiac standstill but it requires advanced planning and the placement of pacing wires before the start of surgery.³⁷ Cardiopulmonary bypass for clipping of complex or giant cerebral aneurysms is also feasible but is infrequently used.

Ruptures during endovascular therapy

While aneurysm rupture during endovascular therapy is rare, the increasing reliance on this technique has led to an increase in the incidence of ruptures occurring during the procedure. In many cases, rescue endovascular techniques can be used to manage the rupture. However, some situations still require emergency conversion to surgical clipping. This life-threatening event requires an urgent transfer to the operating theatre, posing significant logistical and clinical challenges.

In the majority of cases the patient will already be anaesthetised with tracheal intubation and if not, this needs to be done expeditiously and in a neuroprotective manner. Induction of anaesthesia should aim to minimise acute changes in arterial pressure, and sedation should be maintained during transfer. There will be a surge in ICP at this time and 30° head-up positioning, osmotherapy and a normal Paco₂ may help. Assessment of the pupils is often the most useful indicator of impending uncal and transtentorial herniation. Unlike intraoperative rupture during surgical clipping—where controlled hypotension may be used to enhance visualisation—rupture during endovascular therapy necessitates an augmented arterial pressure to preserve adequate CPP. Continuous communication between teams is essential to avoid delays and ensure the patient remains as stable as possible during transfer to the operating theatre.

Postoperative care and postoperative neurological deterioration

Patients who undergo surgical clipping of aneurysms are typically admitted to a neurointensive care or high dependency area after surgery for close neuro-observation. There are numerous reasons for neurological deterioration after clipping of a ruptured or unruptured intracranial aneurysm, the most common being hydrocephalus, cerebral oedema, delayed cerebral ischaemia (DCI) and seizures.

Hydrocephalus

Hydrocephalus affects ∼20–30% of patients with aneurysmal SAH.³⁹ It occurs when blood in the ventricles obstructs CSF flow and impairs CSF reabsorption. Neurological deterioration in the postoperative period should prompt a CT brain scan. Treatment options include the insertion of an external ventricular drain, lumbar drain or permanent CSF shunt.

Cerebral oedema

Cerebral oedema after aneurysmal SAH follows a biphasic pattern. It involves a complex pathophysiological process involving direct ischaemic insult at initial haemorrhage and failure of the blood-brain barrier.⁴⁰ It may present as late neurological decline and is associated with a poor prognosis. Diagnosis is made through imaging (CT, MRI) of the brain or via ICP monitoring. There is no specific treatment for cerebral oedema beyond the implementation of strict neuroprotective strategies. In cases of refractory raised ICP, decompressive craniectomy may be necessary.

Delayed cerebral ischaemia and vasospasm

Delayed cerebral ischaemia and vasospasm are closely related but are two distinct entities. Delayed cerebral ischaemia is defined as focal neurological impairment (e.g. hemiparesis or aphasia), or a decrease of at least two points on the GCS, lasting for at least 1 h, which is not apparent immediately after aneurysm occlusion, and cannot be attributed to other causes.⁴¹ Vasospasm is an angiographic diagnosis, identified by the radiological evidence of arterial narrowing. While vasospasm can lead to DCI, clinical symptoms or signs are only apparent in ∼30% of patients with vasospasm.⁴² DCI can occur without vasospasm and up to 25% of delayed cerebral infarcts do not correspond with areas of arterial narrowing.⁴³ The pathophysiology of DCI in patients with aneurysmal SAH involves the release of cytokines such as endothelin-1, interleukin (IL)-6 and IL-1B activated by oxyhaemoglobin in the subarachnoid space, causing vasoconstriction. It affects up to 70% of patients with aneurysmal SAH and can also occur in those who have undergone clipping of unruptured aneurysms.²³ The incidence of vasospasm typically peaks between days 3 and 14 after aneurysmal SAH and carries a mortality rate of around 21%.^43,44 The ‘gold standard’ for diagnosing vasospasm is through DSA, although other modalities such as CTA, CT perfusion imaging and transcranial Doppler ultrasound are also used. Treatment for DCI includes induced hypertension, endovascular therapy and an infusion of milrinone.

Induced hypertension involves increasing MAP by titrating vasoactive agents in order to enhance CBF and CPP. Euvolaemic hypertensive therapy is commonly the first line of therapy for DCI. Although ‘triple-H’ therapy (hypertension, haemodilution and hypervolaemia) was once the cornerstone of managing DCI, it is no longer recommended in current guidelines because of increased cardiovascular morbidity associated with hypervolaemia, lung injury and haemodilution.¹⁷ Notably, prophylactic induced hypertension for patients at risk of DCI is also not recommended.

Endovascular angioplasty can be performed either pharmacologically or mechanically (balloon angioplasty). Pharmacological endovascular dilation involves injecting a vasodilator drug (e.g. nifedipine or milrinone) into the artery via a catheter to directly target the affected vessels. Balloon angioplasty is more effective for vasospasm in proximal vessels but carries risks of vascular complications, such as thrombosis or rupture.

The phosphodiesterase III inhibitor milrinone is emerging as a therapeutic option for DCI. When used to treat DCI, milrinone is given at doses higher than those typically used for cardiovascular indications (between 0.5 and 2 μg kg⁻¹ min⁻¹).⁴⁵

Seizures

Prophylactic antiseizure medications are not routinely recommended but may be reasonable for patients at high risk of developing seizures (e.g. ruptured MCA aneurysm, high-grade SAH, or raised ICP).¹⁷ Levetiracetam is often preferred because of its favourable safety profile. Phenytoin should not be used, as its use in conjunction with nimodipine increases the metabolism of nimodipine and is associated with higher morbidity and mortality in patients with SAH.

Conclusions

Clipping of intracranial aneurysms, whether unruptured (elective) or ruptured (emergency), presents many challenges to the anaesthetist. Understanding cerebral anatomy and physiology and communication with the neurosurgical team, particularly during application of temporary clips, are required.

MCQs

The associated MCQs (to support CME/CPD activity) is accessible at www.bjaed.org/cme/home by subscribers to BJA Education.

Declaration of interests

The authors declare that they have no conflicts of interest.

Biographies

Jun Hui Ng MD FCAI DPMCAI is a neuroanaesthesia and neurocritical care fellow in the National Neuroscience Centre, Beaumont Hospital, Dublin, Ireland.

Caroline Larkin MD FCAI FJFICMI MRCPI is an anaesthesiologist and intensivist in the National Neuroscience Centre, Beaumont Hospital, Dublin, Ireland. Her particular areas of interest are neuroanaesthesia and neurocritical care.

Matrix codes: 2A07