Case 7.5

Posterior fossa craniectomy

Learning outcomes

1  Anaesthetic management of major craniectomy/craniotomy

2  Problems particularly associated with posterior fossa procedures

3  Analgesia after a craniotomy.

CPD matrix matches

2E01, 2F01

Case history

A 39-year-old man (83 kg, 1.84 m tall) presented with a 3-week history of headache and ataxia. An MRI demonstrated a cystic lesion in the right cerebellar hemisphere. There was a working diagnosis of a cerebellar haemangioblastoma.

What are the major features of an intracranial haemangioblastoma? How should this patient be worked up for theatre?

Cerebellar haemangioblastomas may be sporadic or present as part of a syndrome such as von Hippel–Lindau disease (vHLD) (in 20%). They are benign and may be solid or cystic, and the intracranial lesion is almost always in the posterior fossa. There is an association with polycythaemia.

vHLD may be associated with retinal angiomas, haemangioblastomas of the spinal cord or brain, renal cell carcinoma, and, in 10% of cases, phaeochromocytoma. Thus, screening for phaeochromocytoma may be undertaken. vHLD is an autosomal dominant inherited condition, with a 90% penetrance and an incidence of 1 in 36 000 live births. In appropriate cases, genetic counselling will be offered. Typical presenting complaints are similar to those in the patient (headache, nausea and vomiting, cerebellar signs).

Case update

The patient had an unremarkable previous medical and family history. Screening for phaeochromocytoma was negative.

◆  Preoperative medication included: paracetamol, omeprazole, dexamethasone (recently commenced to reduce swelling around the lesion)

◆  BP 110/74–135/70; pulse 75 regular.

Preoperative investigations included:

◆  Initial investigations: Na+ 141 mmol/L, K+ 4.3 mmol/L, urea 5.5 mmol/L, Cr 61 micromoles/L, eGFR >60 mL/min

◆  Hb 145 g/L, WCC 10.4 × 109/L, Plt 270 × 109/L

◆  Clotting: APTT ratio 1.0, INR 1.0, fibrinogen 2.7 g/L

◆  ECG: sinus rhythm.

What are the problems especially associated with posterior fossa procedures?

◆  Positioning which may include the prone position

◆  Vital structures in the posterior fossa

◆  Generally perceived as more painful than other approaches, as greater dissection through more muscle (trapezius) and more bone

◆  A high incidence of PONV.

How may a patient be kept comfortable after a craniotomy? What are the salient points for this?

Analgesic regimens between neurosurgical units are highly variable. This allows requirements to be tailored to those of the unit, but is not necessarily evidence-based. Patients must be kept comfortable, but without causing an altered consciousness or a respiratory depression (and hence a raised PaCO2 and all that means for ICP). Also the analgesic must not affect clotting, specifically the platelet function, and must not reduce the seizure threshold.

The means we use in our own unit are as follows:

◆  Regular paracetamol, starting with an IV administration perioperatively. That said, we review the requirement for regular paracetamol on a daily basis, changing to ‘as required’ use or discontinuing the paracetamol completely when a regular use is no longer deemed necessary

◆  Should the patient be sufficiently conscious to use a PCA, we give it, usually with morphine. As an intermediate between paracetamol and morphine, we usually prescribe dihydrocodeine, usually on an ‘as required’ basis

◆  We avoid tramadol, because it lowers the seizure threshold

◆  The use of NSAIDs after a craniotomy is highly contentious. Opinions range from the perioperative administration of drugs, such as parecoxib, after a dural closure, through the administration of NSAIDs after a period of between 6 and 24 hours, to an absolute abstention in a patient who has undergone an intracranial procedure. Our unit very rarely administers NSAIDs after a craniotomy, always after discussion with our neurosurgeons, and never within the first 24 hours. On the rare occasion when NSAIDS are used, it is when pain control has been problematic with other means

◆  We have been recently impressed by the use of clonidine IV (variable; slow IV bolus dose; when used, 30 micrograms is commonly the dose) as an adjunct to analgesia in patients who have difficulty in managing pain. Although mildly sedating, we find the patients easy to rouse and no appreciable effect on respiration. As the patients are usually catheterized, we find no problems with urinary retention

◆  A mixture of lidocaine and bupivacaine containing 1/400 000 adrenaline is usually administered by neurosurgical colleagues at the start of the procedure. We do not administer a local anaesthetic at the end of the procedure, as the dura has been opened, and there is a danger that the local anaesthetic may track beneath the dura. The bupivacaine may exert an effect for some hours after the procedure.

Some units use scalp blocks for craniotomies.

The old-fashioned prejudice was that the only safe opiate to give after intracranial surgery was codeine. This has been challenged. Now some colleagues prescribe morphine. Discuss this point.

Codeine is a prodrug, which is demethylated (to morphine) in the liver to its most active form. Some patients lack the enzyme to do this, and the intrinsic analgesic property of unaltered codeine is poor.

In doses used clinically, morphine was no more likely to cause side effects of respiratory depression and sedation than codeine. Morphine did, however, provide more predictable and persistent analgesia, as reported by Goldsack and colleagues.

Codeine is still used in many units, despite 50% of anaesthetists thinking it is poor analgesic, as described by Stoneham and Walters. Codeine should not be administered IV.

Case update

After 1 mg of IV midazolam, an arterial line was sited, followed by induction with propofol, remifentanil, and atracurium. Maintenance of anaesthesia was with a combination of oxygen/air/sevofluanne and an infusion of remifentanil and atracurium. A right internal jugular central line was sited, prior to preparation and prone positioning. Surgery, conducted under Brainlab® (neuronavigation) guidance, was uneventful, as was the post-operative course.

The patient was comfortable with the post-operative analgesia regimen of morphine PCA and regular paracetamol.

The patient went home 5 days post-operatively (GCS 15) and was doing well at the post-operative outpatient follow-up.

Summary

Posterior fossa procedures are especially challenging for a number of reasons, including positioning on the operating table and the close proximity of vital intracranial structures. They also tend to be more painful and to have a relatively high incidence of PONV. Analgesia regimens vary between units, and some of the agents used are highly controversial.

Some conditions associated with posterior fossa lesions (e.g. von Hippel–Lindau syndrome) may require screening for further associated medical conditions such as phaeochromocytoma or cysts.

Further reading

Greenberg MS (2006). Cerebellar haemangioblastoma. In: Handbook of neurosurgery, 6th edn, pp. 459–61. Thieme, New York.

NSAIDS and neurosurgery

Jones SJ,Cormack J,Murphy MA, and Scott DA (2009). Parecoxib for analgesia after craniotomy. British Journal of Anaesthesia, 102, 76–9.

Kelly KP,Janssens MC,Ross J, and Horn EH (2011). Controversy of non-steroidal anti-inflammatory drugs and intracranial surgery: et ne nos inducas in tentationem? British Journal of Anaesthesia, 107, 302–5.

Sebastian J and Hunt K (2006). United Kingdom and Ireland survey of the use of non-steroidal anti-inflammatory drugs after intracranial surgery. Journal of Neurosurgical Anesthesiology, 18, 267.

Shafer AI (1995). Effects of nonsteroidal antiinflammatory drugs on platelet function and systemic hemostasis. Journal of Clinical Pharmacology, 35, 209–19.

Umamaheswara Rao GS and Gelb AW (2009). To use or not to use: the dilemma of NSAIDs and craniotomy. European Journal of Anaesthesiology, 26, 625–6.

Haematoma after intracranial surgery

Palmer JD,Sparrow OC, and Iannotti F (1994). Postoperative hematoma: a 5-year survey and identification of avoidable risk factors. Neurosurgery, 35, 1061–4; discussion 64–5.

Taylor WAS,Thomas NW,Wellings JA, and Bell BA (1995). Timing of postoperative intracranial hematoma development and implications for the best use of neurosurgical intensive care. Journal of Neurosurgery, 82, 48–50.

Attitudes to pain control after neurosurgery

De Benedittis G, Lorenzetti A, Migliore M,Spagnoli D,Tiberio F, and Villani R (1996). Postoperative pain in neurosurgery: a pilot study in brain surgery. Neurosurgery, 38, 466–70.

Goldsack C,Scuplak SM, and Smith M (1996). A double-blind comparison of codeine and morphine for postoperative analgesia following intracranial surgery. Anaesthesia, 51, 1029–32.

Hockey B,Leslie K, and Williams D (2009). Dexamethasone for intracranial neurosurgery and anaesthesia. Journal of Clinical Neuroscience, 16, 1389–93.

Kahn LH,Alderfer RJ, and Graham DJ (1997). Seizures reported with tramadol. Journal of the American Medical Association, 278, 1661.

Kotak D,Cheserem B, and Solth A (2009). A survey of post-craniotomy analgesia in British neurosurgical centres: time for perceptions and prescribing to change? British Journal of Neurosurgery, 23, 538–42.

Oscier C and Milner Q (2009). Peri-operative use of paracetamol. Anaesthesia, 64, 65–72.

Stoneham MD and Walters FJM (1995). Post-operative analgesia for craniotomy patients: current attitudes among neuroanaesthetists. European Journal of Anaesthesiology, 12, 571–5.

Tramer MR (2000). Systematic reviews in PONV therapy. In: Tramer MR, ed. Evidence-based resource in anaesthesia and analgesia, pp. 157–78. BMJ Books, London.