Anaesthetic management of posterior fossa surgery (Neuroanaesthesia) Part 1

Introduction

Anaesthesia for the posterior fossa provides a unique challenge for anaesthetists and neurosurgeons. he most common surgical procedures are excision of posterior fossa tumours, correction of congenital and acquired craniovertebral junction anomalies, and surgical procedures to relieve pressure on the brainstem.

Between 54 and 70% of all childhood brain tumours, and 15-20% of adult brain tumours, originate in the posterior fossa. In children <18 years, the majority of posterior fossa operations are for excision of tumours, of which the commonest are cerebellar astrocytomas, medulloblastomas and brainstem gliomas. he outlook for children with these tumours has improved since the advent of CT imaging of the brain, which enables early diagnosis and improved tumour excision during surgery. Improvements in mortality and morbidity following posterior cranial fossa surgery are also attributable to improved surgical and anaesthetic management.

Posterior cranial fossa anatomy

The base of the skull is divided into the anterior, middle and posterior cranial fossae. he posterior fossa is the largest and deepest and is densely packed with vital structures. he bony structures comprising the floor of the posterior fossa are the sphenoid, occipital and temporal bones, and the mastoid angles of the parietal bones. he occipital bone is separated superiorly from the parietal bone by the lambdoid suture, while the occipitomastoid suture separates the occipital bone and the mastoid part of the temporal bone. he posterior fossa is separated from the middle fossa centrally by the dorsum sellae of the sphenoid and laterally by the petrous temporal bones. It is limited posteriorly and inferiorly by the foramen magnum. he important structures occupying the posterior cranial fossa are the cerebellum, pons and medulla oblongata. here are two reflections of the dura in the posterior cranial fossa -the tentorium cerebelli and the falx cerebelli. he falx cerebelli is a reflection of dura below the tentorium cer-ebelli, which separates the cerebellar hemispheres.


Venous sinuses in the posterior cranial fossa are formed by dural indentations lined with endothelium. he important ones are the right and left transverse sinuses, which form grooves on the bones of the posterior cranial fossa, and join the superior sagittal sinus and the straight sinus to form the confluence of sinuses (which causes a concavity in the skull below the occipital protuberance, known as the torcular Herophili). he confluence of sinuses drains into the left and right sigmoid sinuses, which leave the posterior fossa to continue as the internal jugular veins.

Openings in the floor of the posterior fossa that transmit important structures are the foramen magnum, the internal acoustic meatus (transmits facial and vestibulocochlear nerves), the condylar canal (hypoglossal nerve and a meningeal branch from the ascending pharyngeal artery) and the jugular foramen (internal jugular vein and glossopharyngeal, vagus and accessory nerves) .

Types of posterior cranial fossa surgery

Excision of posterior fossa tumours

Posterior fossa tumours (Fig. 16.1) account for 20% of adult brain tumours, whereas the posterior fossa is the commonest location of brain tumours in children. Posterior fossa neoplastic lesions are often classified as arising from either the anterior or the posterior compartment. he reference point for this division is the fourth ventricle. Tumours of the anterior compartment are further subdivided into intra-axial and extra-axial (i.e. arising from within and without the pia, respectively). he commonest intra-axial anterior compartment tumours are gliomas, whereas the common extra-axial anterior compartment tumours arise mainly from the cerebello-pontine angle (acoustic schwannoma, meningioma, epidermoid tumours, cysts, glomus tumours and metastases). Tumours ofthe posterior compartment are predominantly intra-axial tumours – most commonly cerebellar astrocytoma (common in children), medulloblastoma (second most common tumour in children), ependymoma, haeman-gioblastoma, lymphoma and metastases.

(a) T2-weighted MRI image of a trigeminal neuroma; (b) T2-weighted MRI image of a cerebellar astrocytoma; (c) T1-weighted MRI of a vestibular schwannoma with gadolinium enhancement.

Fig. 16.1. (a) T2-weighted MRI image of a trigeminal neuroma; (b) T2-weighted MRI image of a cerebellar astrocytoma; (c) T1-weighted MRI of a vestibular schwannoma with gadolinium enhancement.

Histologically, all nervous system tumours can be broadly divided into three groups: primitive neuroectodermal tumours (PNETs, which occur in the brain, the sympathetic nervous system and the eye, e.g. medulloblastomas, pineoblastomas and ependymomas), glial tumours (which arise from the supportive tissue of the brain or glia, e.g. astrocytomas, ependy-momas and gliomas) and metastatic tumours.

Procedures for vascular lesions (including aneurysms and arteriovenous malformations) and procedures to relieve cranial nerve compression by vascular structures

Aneurysms in the posterior fossa are rare but can arise from the vertebrobasilar system and the arteries of the posterior inferior cerebellar system. hey can present with symptoms caused by general mass effects, or symptoms arising from direct compression of the cranial nerves.

Posterior fossa arteriovenous malformations (AVMs) are rare and are difficult to treat because of the proximity to vital brain structures. hey represent 5-7% of all intracranial AVMs. More than half present following a haemorrhage. Initial presentation with headache or seizures is rare. hey may be caused by congenital weakness of the vessel wall or an acquired lesion resulting from a head injury, or from closure of dural venous sinuses during surgery. he management options for posterior fossa AVMs are radiosurgery, surgical resection and endovascular obliteration.

Procedures for craniocervical abnormalities such as the Arnold-Chiari malformations

Craniovertebral junction anomalies are a group of unusual anomalies that include the occiput, atlas, axis and supporting ligaments that protect the medulla, spinal cord and lower cranial nerves. heir causes are numerous, the most common being Chiari anomalies, congenital bone diseases, metabolic diseases and genetic anomalies. Craniovertebral junction abnormalities are assessed by MRI of the brain and the spinal cord. he goal of surgical management is stabilization of the lesion. he surgical approach depends on the site of the lesion but is either transoral, transpalatopharyn-geal, lateral or posterior.

Arnold-Chiari malformations (Fig. 16.2) were originally described by Chiari based on his experience of a series of autopsies in children with hydrocephalus. he estimated incidence is 1:1000 live births. he malformations can be classified into various types. Type I is the commonest and involves herniation of the cere-bellar tonsils, but not the brainstem, into the foramen magnum. Some patients are asymptomatic in early life and present in later life with headache and cerebellar signs. he condition is often a chance finding during radiological imaging for another condition.

Tl-weighted MRI showing an Arnold-Chiari malformation and a large cervical spine syrinx.

Fig. 16.2. Tl-weighted MRI showing an Arnold-Chiari malformation and a large cervical spine syrinx.

Type II involves extension of the cerebellar tonsils and brainstem tissue into the foramen magnum and often is accompanied by a myelomeningocele, a form of spina bifida. In type III, part of the brain’s fourth ventricle also may be herniated and, in rare cases, an occipital encephalocele forms. Type IV involves cere-bellar hypoplasia, and parts of the skull and spinal cord may be exposed without any protection. he syndrome is caused by underdevelopment of the posterior fossa or an overgrowth of the supratentorial component. he commonest symptoms are headache, neck pain, weakness and paraesthesias of the hands, and fatigue. If the disease progresses, then management involves foramen magum decompression.

Evacuation of cerebellar haematomas, and decompressive craniectomy to relieve pressure on the brainstem

Haemorrhage (subarachnoid and intracerebellar), infarction and neoplasia in the posterior fossa can cause an acute obstruction of cerebrospinal fluid (CSF) drainage pathways causing acute hydrocephalus.

In our institution, severe cerebellar infarction causing hydrocephalus and depressed levels of consciousness is initially managed with external ventricular drain (EVD) insertion and then with decompressive craniectomy if further deterioration occurs.

Anaesthetic challenges for posterior fossa procedures

Optimal patient positioning should facilitate surgical access without compromising patient safety. he important considerations are surgical access, securing and maintaining the airway, maintenance of adequate anaesthetic depth, haemodynamic stability and oxy-genation. Also important are preservation of invasive monitors and intravenous catheters, and protecting the patient against pressure injuries to the skin, peripheral nerves and pressure sensitive organs such as eyes. Care should be taken to limit the ‘blackout state’ during which the patient is not monitored or connected to the breathing circuits during patient transfer or positioning on the operating table (current UK practice is to anaesthetize the patient in the anaesthetic room and then transfer to the theatre). he hazards during positioning can be reduced by meticulous planning, careful positioning and vigilance to facilitate early detection of complications.

The specific challenges in anaesthesia for posterior fossa procedures are caused by the following factors:

1. Die vital structures within the posterior fossa, particularly the brainstem, cranial nerves and cerebellum.

2. The confined space of the posterior fossa.

3. The ‘awkward’ position and anatomy of the lesions complicating surgical access.

4. Relatively longer duration of surgery in extreme positions.

5. The potential for the development of hydrocephalus .

Patient positioning

Supine position with maximal rotation to the contralateral side

This position is used for access to the lateral structures of the posterior fossa. Depending on the site of the lesion, maximal lateral rotation may be required. Up to 45° can be achieved by lateral rotation, and anything beyond can be achieved by elevation of the ipsilateral shoulder by a roll or a pillow. his might not be possible in patients with impaired neck movement. It is usual to provide head-up tilt or reverse Trendelenburg positioning to improve venous drainage from the brain, but it should be remembered that each 2.5 cm increase in vertical height of the head above the level of the heart leads to a 2 mmHg reduction in cerebral perfusion pressure .

Lateral rotation is associated with reduced venous return from the brain, thereby theoretically increasing the chances for raised intracranial pressure (ICP). Extreme lateral rotation for a prolonged period can cause macroglossia, so a soft block should be placed to avoid injury by the teeth. To reduce the risk of brachial plexus stretch and injury, the use of a supporting pad under the ipsilateral shoulder is advisable.

Lateral position

The lateral position is suitable for unilateral procedures of the posterior fossa, as it improves surgical access by gravitational retraction of the cerebellum, and drainage of CSF and blood from the operating field. Drainage can be improved further by placing the table in a head-up position. he incidence of venous air embolism (VAE) is lower than with the prone position, and haemodynamic stability is better when compared with the supine and sitting position. he main problems associated with this position are peripheral nerve injury (stretch injures of the bra-chial plexus and pressure injuries of the nerves) and gravitational ventilation perfusion mismatch in the dependent lung. he dependent arm should be positioned carefully to avoid pressure-induced nerve injuries. Our current practice is to confirm the safety of the pressure points by a visual check after ensuring optimal surgical access.

Park-bench position

This is a variation of the lateral position and is so called as it resembles the posture of a person reclining on a park bench. It gives better access to the midline structures when compared with the lateral position. he patient is placed semi-prone with the head rotated and the neck flexed, resulting in the brow facing the floor. Disadvantages include peripheral nerve injuries, venous engorgement and macroglossia. If the reverse Trendelenburg position is used to improve surgical access, then the resulting haemodynamic effects should be countered by careful volume loading and judicious use of vasopressors.

Prone position

The prone position facilitates access to the posterior fossa, craniocervical junction and the upper spinal cord. he advantage of this position is the low incidence of air embolism and the easy and optimal surgical access. his position may not provide optimal surgical access in patients with restricted neck movements, and the major disadvantages are diaphragmatic splinting in obese patients, restricted airway access and incompatibility with effective cardiopulmonary resuscitation.

Extreme care and meticulous planning are required, as prone positing is logistically difficult both in the operating theatre and the intensive care unit, with a risk of dislodging the airway, venous catheters and the invasive monitoring. Horseshoe frames can cause pressure on the face and the orbit. In our institution, three-point fixation using the Mayfield head holder is preferred for head support. Care should be taken to avoid diaphragmatic splinting by leaving the chest free and partially support the abdomen and the pelvis. In our institution, this is achieved with a Wilson frame. his position can be combined with head elevation to optimize surgical access and assist with venous drainage, but this may cause hypotension (poorly tolerated in the elderly), and increase the risk of VAE.

Sitting position

The sitting position was introduced into clinical practice by De Martel in 1973. It has been declining in popularity since the 1980s due to the high incidence of complications. In the UK during the period 1981-1991, the number of neurosurgical centres using the sitting position routinely decreased by >50%. his position provides optimal surgical access to the craniovertebral junction and the posterior fossa, particularly midline structures and the cerebellopontine angle. It promotes drainage of blood and CSF, provides easy access to the airway and promotes favourable changes in ven-tilatory mechanics. his position has several potential life-threatening complications, which include VAE, postural cardiovascular effects compounded by general anaesthesia, quadriplegia, pneumocepha-lus, macroglossia and peripheral nerve injuries. It is contraindicated in patients with a risk of right-to-left shunt (such as patent foramen ovale, which has an incidence of 27.3% in autopsy studies). he sitting position is also contraindicated in patient with ventriculoatrial CSF shunts, as any air entering the cerebral ventricles during surgery may migrate into the atrium.

Physiological effects of the sitting position

There are several physiological effects of the sitting position on the body:

• Cardiovascular system. Awake subjects placed in the sitting position partially compensate for hypotension with an increase in the heart rate and the peripheral vascular resistance, but the capacity for compensation is limited in patients who are anaesthetized. he effects of reduced venous return and hydrostatic pooling are accentuated by advancing age and associated comorbidities .

• Respiratory system. here is an increase in the functional residual capacity of the lung in the sitting position, but the reduction in perfusion negates the effects on oxygenation. here is no evidence of improvement in pulmonary function after the sitting position.

• Cerebral perfusion. here is a reduction in global cerebral perfusion after placing the patient in the sitting position, increasing the risk of ischaemic damage.

Complications associated with the sitting position

There are a number of complications associated with the sitting position:

1. Venous air embolism. his is the entry of air into the peripheral or central vasculature. It is a recognized hazard of surgery in the sitting position and is caused by gravity and the negative pressure in the venous sinuses and veins of the skull and brain.

The incidence of venous air embolism is high, approaching 100% in adults monitored by transoesophageal echocardiography. he incidence of VAE is thought to be lower in children because dural venous pressures are higher than in adults. In a large study, the incidence of VAE (defined by a fall in arterial carbon dioxide tension (PaCO2)) was 9.3%. he addition of positive end-expiratory pressure (PEEP) causes an increase in right atrial pressure when compared with left atrial pressure, and this predisposes the development of a paradoxical air embolism (PAE) after a VAE. hhe clinical consequences of VAE are dependent on the rate of accumulation and the volume of air entrained. In adults, the lethal volume is thought to be between 200 and 300 ml, or 3-5 ml kg-1. he air reaching the right atrium passes through the right ventricle and reaches the pulmonary vascular bed, causing an increase in the pulmonary vascular resistance, resulting in right heart strain and increased alveolar dead space (alveoli that are ventilated but not perfused), causing a reduction in end-tidal carbon dioxide (EtCO2). he other postulated mechanisms are increased microvascular permeability, pulmonary hypertension related to the release of endothelin 1, and turbulent flow causing platelet aggregation and toxic free-radical damage. If the embolism is large (approximately 5 ml kg-1), a gas air-lock scenario immediately occurs causing cardiac arrest.

The commonest signs of VAE are tachypnoea, tachyarrhythmias, hypoxaemia, hypotension, wheezes on auscultation and a decrease in EtCO2 with an increase in PaCO2. In awake patients, the signs are continuous coughing, breathlessness, light-headedness, chest pain and a sense of impending doom. Any unexplained hypotension or decrease in EtCO2 should trigger the suspicion of VAE. A PAE (5-10% of VAEs) usually produces signs and symptoms of myocardial and neurological symptoms of cerebral ischaemia. Monitoring for VAE relies on detecting the entrained air in the right heart using ultrasound techniques, or detecting the consequences of a pulmonary air embolism – appearance of nitrogen in the expired air in a nitrogen-free anaesthetic, a drop in PaCO2 or PaO2/oxygen saturation (SpO2) or a rise in pulmonary artery pressures. A particular issue is the risk of systemic air embolism in the presence of a patent foramen ovale (PFO), as the increase in pulmonary artery pressures associated with a VAE will increase right-sided pressures and promote a right-to-left shunt across an existing or potential atrial septal defect. he incidence of a PFO in patients with a posterior fossa lesion is up to 27%, so there is case for identifying it in advance. Contrast-enhanced transcranial Doppler ultrasound is very sensitive for the diagnosis of a PFO, detecting its presence with an overall accuracy of 92.8%.

The risk of VAE can be reduced by careful planning of the surgery, meticulous surgical technique and liberal use of bone wax, vigilance, avoidance of nitrous oxide (N2O) and maximization of intravascular pressure. he treatment of VAE should be directed towards the prevention of further air entrapment by flooding the field with saline, putting the patient in the Trendelenburg position if acceptable, and transient jugular venous compression. he treatment is high-concentration oxygen, placing the patient in the left lateral decubitus position to reduce the gas-lock effect, attempted aspiration of air from the right atrium, haemodynamic support (with intravenous fluids, inotropes and anti-arrhythmic drugs) and cardiopulmonary resuscitation .

2. Pneumocephalus. Pneumocephalus occurs when air enters the brain or spaces around the brain after dural incision. If the volume of air is large, and this is accompanied by other factors that cause cerebral oedema, then tension pneumocephalus may occur. he latter is a life-threatening neurosurgical emergency, as it may cause brain herniation. Precipitants include post-operative cerebral oedema, re-expansion of the brain following mannitol administration and use of N2O causing gas diffusion. he management is drainage of air via a burr hole, ventilation with 100% oxygen and avoidance of N2O. he investigation of choice is a CT brain scan (which may show air under tension) .

3. Macroglossia and airway swelling. his is caused by extreme neck flexion causing an obstruction of the lymphatic and venous drainage from the head. It can cause airway obstruction in children. Care should be taken to avoid trauma during oral airway and transoesophageal echo probe placement .

4. Other complications. hese include cardiac arrhythmias caused by damage or oedema of the vital centres, post-operative respiratory depression, aspiration caused by involvement of cranial nerves, peripheral nerve injuries and spinal cord injury. Spinal cord injury may be caused by extreme flexion, causing a stretch of the spinal cord or reduced cord blood supply during the sitting position. he commonly injured nerves are the common peroneal and recurrent laryngeal nerves. hese are caused by the stretch, compression or ischaemia of the nerve.

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