16 Neurosurgery

Craniotomy 408

Ventriculo-peritoneal shunt 410

Evacuation of traumatic intracranial haematoma 412

Pituitary surgery 416

Posterior fossa surgery 418

Awake craniotomy 422

Vascular lesions 424

Complications of aneurysmal subarachnoid haemorrhage (SAH)  426

Anaesthesia for vascular lesions 428

Interventional radiology 430

Venous air embolism (VAE)  432

Neurological determination of death 434

Organ retrieval from a beating heart donor 436

See also:

Increased CSF volume: hydrocephalus, benign intracranial hypertension, blocked shunt

Increased blood volume:

Increased extracellular fluid: cerebral oedema

Carbon dioxide tension: hypocapnia results in cerebral vasoconstriction and a reduction in CBF. The greatest effect is at normal PaCO₂, where a change of 1kPa (7.5mmHg) results in a 30% change in blood flow. MAP modifies the response of CBF to hyperventilation. High perfusion pressures increase the responsiveness to hyperventilation, whereas hypotension of 50mmHg abolishes the effect of PaCO₂ on CBF.

Oxygen tension: PaO₂ is not an important determinant of CBF, a value of <7kPa (53mmHg) being required before cerebral vasodilatation occurs.

Temperature: hypothermia reduces cerebral metabolism by ∼5% per degree centigrade, thereby reducing CBF.

Viscosity: there is no effect on CBF when the haematocrit is between 30 and 50%. CBF will increase with reduced viscosity outside this range.

Anaesthetic agents: see below.

Intraparenchymal: micro-miniature silicone strain gauge monitors can be inserted into the brain parenchyma to monitor ICP. They are accurate and relatively easy to insert even by non-neurosurgical staff. They are currently the most common technique used to measure ICP

Late: increasing blood pressure and bradycardia. Agitation, drowsiness, coma, Cheyne Stokes breathing, apnoea. Ipsilateral then bilateral pupillary dilatation, decorticate then decerebrate posturing.

Investigations: evaluate CT/MRI scans for the presence of generalised oedema, midline shift, acute hydrocephalus, and site/size of any lesion.

Avoid increasing venous pressure. Avoid coughing and straining, the head-down position, and obstructing neck veins with ET tube ties.

Prevent further cerebral oedema. While patients are generally fluid restricted, it is important to maintain intravascular volume and CPP. Do not use hypotonic solutions—fluid flux across the blood–brain barrier is determined mainly by plasma osmolality not oncotic pressure. Maintenance of a high normal plasma osmolality is essential.

Maintain CPP: hypotension will decrease CPP in the presence of a raised ICP. Control blood pressure using fluids and vasopressors as necessary. Aim for a CPP >70mmHg.

Avoid anaesthetic agents that increase ICP (see below).

Modest hyperventilation to PaCO₂ of 4.0–4.5kPa (30–34mmHg) has a transient effect in reducing ICP for 24hr. Excessive hyperventilation results in cerebral ischaemia and a loss of autoregulation. Note: ETCO₂ is lower than PaCO₂.

Corticosteroids reduce oedema surrounding tumours and abscesses but have no role in head injury. They take several hours to work. Dexamethasone 4mg 6-hourly is often given electively preoperatively.

CSF may be drained via a ventricular or lumbar drain.

Position the patient with a head-up tilt of 30° to reduce central venous pressure. Ensure that MAP is not significantly reduced as the overall result could be a reduction in CPP.

IV anaesthetic agents all decrease cerebral metabolism, CBF, and ICP with the exception of ketamine. Ketamine has some neuroprotective properties but is considered contraindicated in neurosurgery. CO₂ reactivity and autoregulation of the cerebral circulation are well maintained during propofol/thiopental anaesthesia.

Other drugs:

Intracranial tumours may be metastatic: primary sites include the lung, breast, thyroid, and bowel.

Check CT/MRI scans—the duration and complexity of the procedure are determined by the size, site, and vascularity of lesions being excised.

Patients receiving diuretics or who have been vomiting may have disordered electrolytes. Patients receiving dexamethasone may be hyperglycaemic.

Restrict IV fluids to 30ml/kg/d if cerebral oedema present. Avoid glucose-containing solutions. They may cause hyperglycaemia, which is associated with a worse outcome after brain injury. They also reduce osmolality, resulting in increased cerebral oedema.

Ensure graduated compression stockings are fitted to prevent DVT.

Prophylactic or therapeutic phenytoin may be required (a loading dose of 15mg/kg followed by a single daily dose of 3–4mg/kg).

Induce with thiopental 3–5mg/kg or propofol 2–3mg/kg combined with remifentanil (0.2–0.5µg/kg/min). Give IV induction agents slowly to avoid reducing BP and CPP. A non-depolarising relaxant is used to facilitate intubation. Remifentanil usually attenuates the hypertensive response to intubation—if not use additional agents such as lidocaine 1.5mg/kg or a β-blocker (labetalol 5mg increments). Use an armoured ETT to prevent kinking and secure in place with tapes as ties may cause venous obstruction. Protect the eyes.

Avoid N₂O. Maintain anaesthesia using either volatile agent (sevoflurane/isoflurane <1 MAC) or TCI propofol (3–6µg/ml). Remifentanil infusion is continued at a lower rate (0.15–0.25µg/kg/min) titrated to response. Top-up doses of muscle relaxants are rarely required when remifentanil is used. In the absence of remifentanil use fentanyl 5µg/kg at induction followed by top-up doses as required or an alfentanil infusion (25–50µg/kg/hr).

Patients may be placed in the supine or lateral position. Avoid extreme neck flexion or rotation, which may impair cerebral venous return, and maintain a head-up tilt. If the head is turned for surgery, support the shoulder to reduce the effect on neck veins.

Application of the Mayfield 3-point fixator to secure the head can cause a marked hypertensive response. Pin sites can be infiltrated with local anaesthetic and if necessary give a further dose of remifentanil (0.5–1µg/kg) or propofol (0.5–1mg/kg).

Aim for normotension during most procedures. Modest hypotension may infrequently be required to improve surgical field. Mild hypocapnia is used in tumour surgery. Aim for PaCO₂ of 4.0–4.5kPa (30–34mmHg).

Avoid hypotonic solutions for fluid maintenance. Replace blood loss with colloid or blood.

Maintain normothermia. Hypothermia is rarely indicated.

Use intermittent pneumatic compression device to the calves or feet.

Closure of the dura, bone flap, and scalp takes at least half an hour. Administer IV morphine at this stage to provide analgesia when the remifentanil is stopped. Sudden hypertension on awakening may be treated with small boluses of labetalol. Avoid coughing if possible.

Many routine craniotomies can be managed postoperatively on an adequately staffed neurosurgical ward. Continued monitoring of the patient's conscious level and neurological state is essential. Consider postoperative sedation and ventilation if there is continuing cerebral oedema or if the patient was severely obtunded preoperatively.

On return to the ward the majority of patients will experience pain in the mild to moderate range after craniotomy. At this stage codeine phosphate (60–90mg) combined with regular paracetamol is usually sufficient in >90% of patients. If not PCA with morphine may be used.

A central line is indicated for the majority of craniotomies to allow measurement of CVP, infusion of vasoactive drugs, and aspiration of air in the case of venous air embolism.

Many patients requiring shunts are children and the usual paediatric considerations apply.

Patients often have raised intracranial pressure.

Emergency cases may have a full stomach, requiring a rapid sequence induction.

Antibiotic treatment or prophylaxis is required and strict antisepsis protocols are normally followed to reduce the incidence of shunt infection.

Advancing the trocar to allow tunnelling of the shunt is particularly stimulating. Additional analgesia and/or muscle relaxation is often required at this stage.

Shunts often block or become infected, requiring revision.

Watch for signs of pneumothorax as the trocar is placed subcutaneously.

Subdural haematoma results from bleeding from the bridging veins between the cortex and dura. Early evacuation of acute subdural haematoma improves outcome. Chronic subdural haematomas may occur in the elderly, often after trivial injury. They present insidiously with headaches and confusion and can be evacuated via burr hole under local anaesthesia.

Intracerebral haematoma occurs in hypertensive individuals, as a complication of treatment with warfarin, or as a result of bleeding from an intracranial aneurysm.

Most patients will have a reduced or deteriorating GCS.

Intracranial pressure is usually raised.

Patients may have associated injuries to the chest, pelvis, or abdomen requiring resuscitation and treatment in their own right—see pp. 876–881. Protect C-spine if necessary.

Patients may have a full stomach, requiring rapid sequence induction. Insert an orogastric tube after intubation.

Check blood clotting profile and the availability of blood products prior to surgery.

Patients require standard monitoring, including invasive blood pressure and CVP monitoring.

Ensure smooth induction and normotension. Maintain CPP using fluids and vasopressors if necessary. Assume that the ICP is 20mmHg—the minimum acceptable MAP is therefore 80mmHg to achieve a CPP of 60mmHg.

Ensure head-up tilt; avoid nitrous oxide, ventilate to an ETCO₂ of 4.0kPa (30mmHg) and give mannitol (0.5–1g/kg) or 5% saline (100ml) and furosemide (0.25–1mg/kg) as required.

Once decompression has occurred there may be a decrease in systemic blood pressure, which can usually be treated with volume replacement.

Hypotension in a head-injured patient is a medical emergency and must be treated promptly and aggressively.

Causes of secondary insult are:

Steroids should not be administered to patients following severe head injury.

Hypertension and left ventricular hypertrophy

Sleep apnoea, diabetes mellitus

Electrolyte abnormalities (hypokalaemia, hyperglycaemia)

Steroid cover necessary pre- and postoperatively

A throat pack should be inserted following intubation. Moffett's solution ( p. 634) may be instilled into each nostril to improve surgical conditions.

Surgical access is via the sphenoidal air sinuses.

If there is suprasellar extension a lumbar drain is inserted into the CSF. The anaesthetist may be required to instil a volume of sterile saline to advance the tumour into the operative field.

Major haemorrhage may occur if there is disruption of the cavernous sinus/carotid arteries which lie lateral to the pituitary gland.

Diabetes insipidus may occur in up to 50% of patients. It is managed initially with IV desmopressin (0.25–1µg).

Cerebrospinal rhinorrhoea may occur. It is usually self-limiting, but, if persistent, intermittent CSF drainage via a lumbar drain may be required.

Assess intracranial pressure—may be raised. If hydrocephalus is present, ventricular drainage may be required before the definitive procedure.

Assess fluid status—may be dehydrated if vomiting. A reduced intravascular volume will result in hypotension on induction or if placed in the sitting position.

Check electrolytes and glucose, particularly if taking diuretics or steroids.

Assess cardiovascular function, particularly the presence of untreated hypertension, postural hypotension, and septal defects.

Insert an NG tube if risk of postoperative bulbar dysfunction.

Further specialised monitoring is required for posterior fossa surgery, including monitoring for venous air embolism ( p. 432) and nerve tract injury. The appropriate electrophysiological monitor used to detect nerve tract injury depends upon the neural pathway at risk during the procedure. Spontaneous or evoked electromyographic activity, somatosensory evoked potentials, or brainstem auditory evoked potentials are frequently monitored.

Lumbar CSF drainage is occasionally requested to improve surgical conditions and to reduce the incidence of postoperative CSF leaks.

Avoid N₂O—it increases cerebral metabolic rate and CBF and may worsen the outcome of air embolism. Finally, there is a risk that any residual intracranial air will increase in volume and cause postoperative pneumocephalus.

Surgical interference with vital centres may result in sudden and dramatic cardiovascular changes. Inform the surgeon—more gentle retraction or dissection usually resolves the problem. Use drugs such as atropine and β-blockers only if absolutely necessary as they make the interpretation of further changes difficult.

Prone position: allows good surgical access without the risks associated with the sitting position. Abdominal compression should be avoided as it results in increased cerebral venous pressure. This is achieved by adequately supporting the chest and pelvis.

Lateral position: the lateral or ‘park bench’ position is particularly suitable for lateral lesions such as acoustic neuroma and operations on a cerebellar hemisphere. The neck is flexed and the head rotated towards the floor ensuring that the jugular veins are not obstructed. Pressure points over the shoulder, greater trochanter, and peroneal nerves should be protected.

Airway obstruction can occur after posterior fossa surgery due to macroglossia, partial damage to the vagus, and excessive flexion of the cervical spine.

Surgery on medulla or high cervical lesions carries a significant risk of postoperative impairment of respiratory drive.

The patient should be admitted to ICU for ventilation if the preoperative state was poor, the surgical resection was extensive, there is significant cerebral oedema, or there are intraoperative complications.

Venous air embolism (see p. 432).

Postoperative analgesia is managed as for craniotomy.

Both the neurosurgeon and neuro-anaesthetist must be experienced in awake craniotomy. Appropriate patient selection is essential. The patient must be well informed, motivated, and able to tolerate lying still for the duration of surgery. Confusion, anxiety, and difficulty in communication are contraindications. Obesity, oesophageal reflux, and highly vascular tumours may also cause problems.

The patient should be given a full explanation of the procedures involved.

Premedication is generally avoided, but routine medication should be administered on the day of surgery. Anticonvulsant prophylaxis should be prescribed routinely for all patients and dexamethasone for those undergoing tumour surgery.

IV antiemetic prophylaxis is administered routinely (e.g. ondansetron 4mg IV). Anaesthesia is induced and maintained with a target- controlled infusion of propofol and a remifentanil infusion (0.05–1µg/kg/min). The propofol dose is titrated against the patient's responses, haemodynamics, and possibly bispectral index monitoring. The patient's lungs are ventilated using an LMA, allowing monitoring and control of ventilation/PaCO₂. This minimises the risks of hypoventilation and airway obstruction, providing good operative conditions. Adequate local anaesthetic infiltration of the Mayfield fixator pin sites and the operative field is essential.

When the tumour is exposed the remifentanil is reduced to 0.005–0.01µg/kg/min to allow return of spontaneous ventilation. When this occurs the LMA is removed and the propofol stopped. Once the resection is complete the patient is re-anaesthetised and the LMA reinserted until the end of the procedure.

Preoperative complications include: seizures, respiratory depression, restlessness, airway obstruction, air embolus, and brain swelling.

Other aspects of postoperative care are as for craniotomy ( p. 408).

Bispectral index monitoring may be useful in guiding the target- controlled infusion.

They are more common in females and 40–60yr olds, and in 25% of cases they are multiple. In the UK, the incidence is 10–28:100 000 per year. The prevalence of aneurysm is 6% of the population in prospective angiographic studies.

Aneurysms do not usually rupture until they are >5mm in diameter. They then present as a subarachnoid or intracerebral haemorrhage. Classic symptoms include sudden onset of severe headache with loss of consciousness, which may be transient in mild cases. Occasionally a patient presents with a focal neurological deficit due to the pressure of an enlarging aneurysm on surrounding structures.

Grading of subarachnoid haemorrhage (World Federation of Neurosurgeons): the grade of SAH influences morbidity and mortality. It is also of value in deciding whether to operate or coil early (grades 1–3) or to delay intervention (grades 4–5).

They may present clinically with subarachnoid haemorrhage or seizures.

High blood flow through such lesions may ‘steal’ blood from surrounding tissue leading to ischaemia.

There is a 60% risk of death with each episode of rebleeding. The main aim of management is to prevent rebleeding by securing the aneurysm either surgically by clipping it or angiographically by obliterating it endoluminally. (See ‘Interventional radiology’, p. 430.)

Surgery was previously delayed for up to 10d to avoid the peak of vasospasm.

The introduction of nimodipine has resulted in earlier surgery, ideally within 72hr. Grade 1–2 patients may be operated upon immediately.

Most aneurysms are now secured by coiling. Cranitomy and clipping are much less common.

It is associated with vasospasm caused by substances released as the subarachnoid blood undergoes haemolysis. The most likely spasmogenic agent is oxyhaemoglobin.

Although angiographic vasospasm occurs in up to 75% of studied patients, only half of these patients develop DND. Up to 20% of symptomatic patients will develop a stroke or die of vasospasm despite optimal management.

DND peaks 3–14d after the initial bleed. With increasingly early surgery for aneurysms, it is now commonly seen postoperatively.

Hypertensive, hypervolaemic therapy with or without haemodilution (‘Triple H’ therapy): this is based on the theory that vasospasm can be prevented or reversed by optimising cerebral blood flow. Goals are to increase cardiac output and blood pressure using volume expansion and then vasoactive drugs. The resulting haemodilution may improve cerebral blood flow by reducing viscosity. Disagreement exists as to the fluids/drugs that should be used and which haemodynamic goals to aim for. Suggested values are normal MAP + 15%, CVP >12mmHg, Hct 30–35%. Some centres advocate the use of PA catheters to monitor therapy. Noradrenaline (0.025–0.3µg/kg/min) and dobutamine (2–15µg/kg/min) are used to increase MAP.

In some centres balloon angioplasty or intra-arterial papaverine are also used.

ECG abnormalities: up to 27% of patients will have ECG changes— T wave inversion, ST segment abnormalities, and Q waves. Strongly associated with a poor neurological grade but not predictive of all causes of mortality.

Neurogenic pulmonary oedema: initially a hydrostatic pulmonary oedema resulting from an increase in pulmonary artery pressure, followed by damage to the pulmonary microvasculature and an increase in pulmonary capillary permeability.

Hyponatraemia: many patients are hypovolaemic and hyponatraemic as a result of excessive atrial natriuretic peptide release. Fluid restriction is inappropriate and it should be managed with sodium repletion.

Other complications include deep vein thrombosis, pneumonia, and hepatic, renal, and GI dysfunction.

Ensure adequate fluid intake, and that fluid is not being unnecessarily restricted.

Nimodipine treatment should be instituted.

Ensure graduated compression stockings are fitted.

Phenytoin (15mg/kg followed by a single daily dose of 3–4mg/kg) should be prescribed prophylactically for the majority of patients.

Discuss the anticipated difficulty of the surgical approach with the surgeon as it influences the decision to use induced hypothermia, barbiturates, and other forms of cerebral protection.

Ensure adequate venous access with large-bore cannulae.

Aim to avoid increases in arterial pressure that may result in aneurysm rupture, but maintain adequate cerebral perfusion pressure. Aim for the preinduction BP ± 10%.

Hypocapnia can result in cerebral ischaemia after SAH and must be avoided. Ventilate to a normal PaCO₂.

Maintain core temperature at 36–37^oC for all grade 1–3 patients.

Modern neurosurgical practice is to use temporary spring clips rather than induced hypotension. The latter may still be required in difficult cases or if rupture occurs. In this situation aim for a systolic BP of 60–80mmHg. Moderate hypotension may be achieved using isoflurane (up to 1.5MAC). Further hypotension is achieved using labetalol (5–10mg increments). Sodium nitroprusside is rarely used. Hypotension must not be induced in the presence of vasospasm.

If rupture occurs:

Other cerebral protection measures should be considered electively if temporary clipping of a major cerebral vessel is planned or in case of aneurysm rupture. This includes inducing the administration of thiopental (3–5mg/kg bolus followed by 3–5mg/kg/hr), in which case EEG monitoring should ideally be used to allow titration of the dose to burst suppression. It may be necessary to use a vasopressor to support MAP when infusing thiopental. Inducing hypothermia to a temperature of 32°C is reserved for complex surgical vascular procedures. The patient is cooled using surface devices and rewarmed once the cerebral circulation is restored.

Codeine phosphate and regular paracetamol may be prescribed for analgesia.

A decrease in the GCS may indicate vasospasm, intracranial haematoma, or hydrocephalus—perform a CT scan.

The procedure may be associated with significant blood loss—crossmatched blood and adequate IV access are essential.

Blood may be shunted through the AVM, resulting in relative ischaemia to the surrounding tissue. When the lesion is excised, a relative hyperperfusion of surrounding tissue may occur, resulting in cerebral oedema and increased ICP.

There is no risk of vasospasm and when indicated hypotension may be induced with relative safety. This is achieved using isoflurane ± labetalol as outlined for SAH (see above).

In children AVMs can cause high output failure due to intracerebral shunt. CCF may be precipitated by excision of the lesion.

A CVP line is not always necessary. It is preferable to monitor the arterial pressure before induction of anaesthesia, although the femoral artery introducer sheath inserted by the radiologist can be transduced. This provides a reliable mean but overestimates diastolic and underestimates systolic BP.

The patient will need a urinary catheter, temperature monitoring, and warming devices and a wide-bore IV cannula.

A baseline ACT should be measured before starting the procedure. After femoral cannulation an initial dose of heparin (5000IU) is administered followed by an infusion or intermittent doses to keep the ACT 2–3 times baseline. Reversal of heparin with protamine may be required at the end of the procedure.

It is important to maintain a normal MAP and PaCO₂. This may be difficult as coiling is not a particularly stimulating procedure.

The induction and maintenance of anaesthesia is the same as for clipping of an aneurysm, although a normal ETT tube or a ProSeal LMA may be used instead of an armoured tube.

Recovery should be smooth and rapid. An incompletely secured aneurysm may require control of MAP postoperatively. Patients who have had neurological complications need to be transferred to a neurological ITU for postoperative ventilation.

In patients with a high risk of a thrombotic event from a coil in the parent vessel, it may be necessary to administer aspirin (500mg IV) and to continue heparin into the postoperative period. Thrombotic events occurring during the procedure are often managed with abciximab.

Rupture of the aneurysm or haemorrhage is identified by extravasation of contrast. The intracranial haemorrhage may increase ICP and MAP with or without a bradycardia. Aim to reverse the heparin and reduce MAP to the level before the bleed. Measures to reduce ICP (see p. 406 and p. 414) may be required.

Patients with a reduced postoperative GCS should have a CT scan to exclude hydrocephalus or vascular complications. It may be necessary to insert an EVD and transfer to ICU for continued management.

If the nidus is suitable, the AVM may be treated by radiosurgery in a specialist centre.

Pulmonary embolus from systemic shunting of particulate materials.

Bleeding from incomplete embolisation, perforation of arterial feeders, or rupture of an associated aneurysm. Subtle changes in the dynamics of the fistula may also increase the risk of haemorrhage.

The sudden occlusion of the AVM can result in cerebral hyperperfusion, if the AVM and normal brain share venous drainage. This will result in cerebral oedema and increased ICP.

VAE causes pulmonary microvascular occlusion, resulting in increased physiological dead space. Bronchoconstriction may also develop. A large volume of air causes frothing within the right atrium, leading to obstruction of the right ventricular outflow tract and a reduction in cardiac output.

Signs of VAE include hypotension, arrhythmias, increased PA pressure, decreased ETCO2, and hypoxia.

N2O does not increase the risk of VAE but may worsen its outcome.

Doppler ultrasound is the most sensitive non-invasive monitor. It uses ultra-high-frequency sound waves to detect changes in blood flow velocity and density. Unfortunately, it is not quantitative and does not differentiate between a massive or physiologically insignificant air embolism. Positioning the probe and diathermy interference can prove problematic.

Trans-oesophageal echo allows determination of the amount of air aspirated but is more invasive, difficult to place, and needs expertise to interpret.

Pulmonary artery catheters are invasive but sensitive monitors for VAE. However, an increase in PA pressure is not specific for air.

The least sensitive monitor is a precordial or oesophageal stethoscope to detect a ‘millwheel’ murmur. This is apparent only after massive VAE, which is usually clinically obvious.

Elevate the head only as much as necessary.

Ensure adequate blood volume to maintain a positive CVP.

Small amounts of PEEP (5–10cmH2O) may reduce the risk of air entrainment.

A ‘G-suit’ or medical antishock trousers may be used to increase venous pressure and reduce hypotensive episodes in patients in the sitting position.

Inform the surgeon, who should flood the operative field with fluid. This stops further entrainment of air and allows the identification of open veins that can be cauterised or waxed if within bone.

Stop N2O if in use and increase the FiO2 to 1.0.

If possible position the operative site below the level of the heart to increase venous pressure.

Aspirate air from the CVP line. The tip should be placed close to the junction of the SVC and the right atrium.

Support the blood pressure with fluid and vasopressors.

If a large volume of air has been entrained and surgical conditions permit, turn the patient into the left lateral position to attempt to keep the air in the right atrium.

Commence CPR if necessary.

Small volumes of air in the systemic circulation can have disastrous consequences.

Intracardiac septal defects are an absolute contraindication to surgery in the sitting position.

The coma must be caused by a known and irreversible cause of brain injury.

Reversible causes for brainstem depression have been excluded: sedatives, muscle relaxants, alcohol, hypothermia, and metabolic or endocrine disturbances.

Corneal reflex is absent.

There is no motor response within the cranial nerve distribution to painful stimuli applied centrally or peripherally. Spinal reflexes may persist in brainstem-dead patients.

Oculo-vestibular reflex is absent. There is no eye movement in response to the injection of 50ml ice-cold water into the external auditory meatus—direct access to the tympanic membrane should be verified using an auroscope. The eyes should be observed for at least 1min after each injection.

There is no gag or cough reflex in response to a suction catheter passed into the pharynx or down the endotracheal tube.

Apnoea is present on disconnection from mechanical ventilation. This test is done last, to avoid unnecessary hypercarbia should any of the other reflexes be present. The patient should be preoxygenated by ventilating with 100% O2 and the minute ventilation reduced to achieve a PaCO2 of 6kPa (45mmHg). The patient is then disconnected and observed continuously for any respiratory movement for 5min. The PaCO2 should be measured and should be high enough to ensure an adequate stimulus to ventilation [>6.7kPa (50mmHg) in a previously normal individual]. Hypoxia is avoided during apnoea by passing a suction catheter down the endotracheal tube and supplying 5–10l/min of oxygen while monitoring the SaO₂.

The tests must be performed on two occasions separated by an adequate time interval to satisfy all concerned.

The diagnosis should not normally be considered until at least 6hr after the onset of apnoeic coma or 24hr after the restoration of circulation if the cause was cardiac arrest.

Death is confirmed after the second set of tests, but the time of death is recorded as the completion of the first set of brainstem death criteria.

No additional tests are required in the UK, but other countries may require EEG, carotid angiography, or brainstem evoked potentials.

The coroner (Procurator Fiscal in Scotland) needs to be informed of most of these patients due to the underlying diagnosis, and if organ donation is contemplated.

Care of the relatives is essential at this time irrespective of whether the patient is to be an organ donor or not.

Autonomic collapse results in a reduction in cardiac output, hypotension, and atropine-resistant bradycardia. Circulatory collapse follows if left untreated.

Deterioration in lung function is common due to neurogenic pulmonary oedema, acute lung injury, and pre-existing disease.

Reduced circulating T3 and T4 with increased peripheral conversion of T4 to reverse T3 causes depletion of myocardial energy stores, myocardial dysfunction, and a global shift to anaerobic metabolism.

Hyperglycaemia is due to reduced circulating insulin and insulin resistance.

Reduced ADH secretion leads to neurogenic diabetes insipidus with hypovolaemia and electrolyte disorders (hypernatraemia, hypermagnesaemia, hypokalaemia, hypophosphataemia, hypocalcaemia).

Release of tissue fibrinolytic agents and plasminogen activators from necrotic brain causes a coagulopathy.

Temperature regulation is lost due to hypothalamic dysfunction resulting in hypothermia.

Emphasis in management changes from cerebral resuscitation to optimal organ perfusion and oxygenation.

Ensure intravascular volume resuscitation using continuous CVP monitoring. Avoid overhydration in potential lung donors where a CVP >6mmHg may increase the A–a oxygen gradient and reduce the number of donor lungs that can be retrieved successfully. If hypotension persists despite fluid replacement then an infusion of vasopressin should be started as the first line vasopressor. PAFC and transoesophageal echocardiography are often requested for potential heart donors with high inotrope requirements. They allow assessment of cardiac structure and function, and prevent intravascular overload.

Continue regular chest physiotherapy and suctioning.

If desmopressin has been used to control diabetes insipidus it should be changed to vasopressin (ADH)—restores vascular tone and arterial pressure without a direct myocardial effect.

The use of hormone resuscitation using T3 replacement, methylprednisolone, and vasopressin varies amongst transplant centres. Their use should be guided by the local retrieval team or in-house protocols. High-dose methylprednisolone increases the successful retrieval of lungs for transplantation.

Correct hypernatraemia with 5% glucose (Na+ <155mmol/l). Glucose 4%/sodium chloride 0.18% with potassium chloride should be used to replace normal urinary water and electrolyte losses. Clotting abnormalities should be corrected with clotting factors and platelets.

Central venous access via the right internal jugular vein and left radial arterial access are preferred due to early ligation of the left innominate vein and right subclavian artery respectively.

Order CXR, ECG, echocardiography, and 4-hourly ABGs for potential heart/lung donors.

Need for general anaesthesia is controversial. Many use up to 1 MAC isoflurane or fentanyl (5–7µg/kg) to control reflex pressor responses during surgery. This can also be achieved using labetalol or GTN. Non-depolarising neuromuscular blocking agents are administered to obtund reflex muscular contractions due to the preserved spinal reflexes and improve surgical access. Pancuronium and vecuronium are cardiostable and preferred.

Large and frequent haemodynamic fluctuations occur due to compression of the inferior vena cava, manipulation of the adrenals, and blood/fluid loss. Hypotension is treated with colloid titrated to CVP, vasopressin infusion, and metaraminol (0.5mg increments).

Broad-spectrum antibiotics are given as per local transplant protocol.

Full heparinisation (300IU/kg) should be administered centrally prior to surgical cannulation of the major vessels.

Epoprostenol (5–20ng/kg/min) may be needed for 10min via pulmonary artery if lungs are to be harvested.

PAFC/CVC withdrawn before ligation of SVC.

Note time of aortic cross-clamp as beginning of organ ischaemic time.

At the end discontinue mechanical ventilation/monitoring and remove the ETT after lung inflation and trachea cross-clamp.

The abdominal surgical team continues to operate in circulatory arrest.

The quality of care afforded the multi-organ donor could affect the outcome of more than six recipients.

In the event of cardiac arrest CPR should be commenced, as procurement of liver and kidneys can still proceed rapidly with cross-clamping of the aorta at the diaphragm and infusion of cold preservation solution into the distal aorta and portal vein.