Textbook of Neuroanaesthesia and Critical Care - part 10 ppt

Table 27.4 Typical cardiovascular and ECG changes associated with BSD Cerebral ischaemia Vagal activation Increased heart rate, cardiac output and blood pressure Sinus bradycardia and br

Table 27.4 Typical cardiovascular and ECG changes associated with BSD

Cerebral ischaemia Vagal activation Increased heart rate, cardiac

output and blood pressure

Sinus bradycardia and bradyarrhythmiasIschaemia in the pons

Sinus bradycardia,

Medullary ischaemia Ischaemic vagal cardiomotor

nucleus Unopposed sympathetic stimulation – 'storm'

Increased heart rate, cardiac output, blood pressure, vascular resistance and left atrial pressure(pulmonary oedema)

Sinus tachycardia, multifocal ventricular ectopics, marked ischaemia

Spinal cord ischaemia Ischaemic sympathetic

nuclei

Decreased heart rate, cardiac output, blood pressure and vascular resistance (spinal shock)

Sinus rhythm, reduced wave size, persistent ischaemic changes

R-The classic rostrocaudal progression of events may not develop in the clinical setting

Following BSD, catecholamine levels fall Together with relative hypovolaemia, hypothermia, autonomic dysfunction and the myocardial changes described above, this leads to a fall in cardiac output, systemic vascular resistance and mean arterial pressure.Asystole usually occurs within 48 h without cardiovascular support but there is evidence that infusions of epinephrine and

vasopressin can delay this for several weeks,24 information that may be of relevance if organ donation is being considered

Pulmonary Changes

During the sympathetic storm, the rapid rise in left atrial pressure (LAP) which may even exceed pulmonary artery pressure, in combination with an expanded lung blood volume (from an enhanced venous return and subsequent increased right ventricular output), may result in capillary disruption, protein-rich pulmonary oedema and interstitial haemorrhage.20 This may lead to a

deterioration in gas exchange and hypoxaemia

Endocrine Changes

Hypothalamic-Pituitary Axis

The discovery that BSD in animals is often followed by a decrease in plasma levels of T3, insulin and cortisol20 has stimulated research on the hypothalamicpituitary axis (HPA) during and after BSD, with mixed results.12,13,17,25–28 Ill-defined hormone reference ranges in acutely ill patients, the use of free-standing hormone levels rather than their dynamic axis function and poor understanding

of the interactions between various hormones probably accounts for the inconsistency of the results

Posterior Pituitary Function

Neurogenic diabetes insipidus (DI) occurs in up to 84% of patients with BSD.14 Polyuria >200 ml/h should alert the clinician to the possibility of DI The serum osmolality is usually >310 mosmol/l with a urine osmolality of <200 mosmol/l Electrolyte disturbances such as hypernatraemia, hypokalaemia, hypocalcaemia, hypophosphataemia and hypomagnesaemia occur rapidly without treatment.Antidiuretic hormone (ADH) has intrinsic vasoconstrictive properties Therefore, decreased levels of ADH may contribute to the cardiovascular instability associated with BSD Replacement therapy has been shown to attenuate some of this instability in BSD patients.32 Prolactin levels may be normal or low The use of dopamine infusions in BSD patients may account for some of the low values that have been reported.29

Anterior Pituitary Function

There are conflicting reports regarding changes in anterior pituitary hormones following BSD.14,29,30 Follicule stimulating hormone (FSH) and luteinizing hormone (LH) remain relatively unchanged Circadian release of growth hormone (GH) and its

Page 387

Figure 27.1 Cardiovascular effects of brainstem deathrole in the stress response complicate interpretation of the changes seen in its levels after BSD.12,14,29 Levels of adrenocorticotrophic hormone (ACTH) remain within the normal laboratory range after BSD.12,14,30 Cortisol levels may also be 'normal' for non-stressed patients but this may indicate a relative deficiency, which might be uncovered with stress testing (short synacthen test) No

relationship between cortisol levels and severe hypotension has been demonstrated.14

Thyroid Hormones

Changes in thyroid hormone levels after BSD are similar to those found in patients with sick euthyroid syndrome (Table 27.5).12–14,29The syndrome, often associated with acute illness, results in impaired peripheral conversion of thyroxine (T4) to triiodothyronine (T3) and a rise in reverse T3 (rT3)

Table 27.5 Thyroid hormones levels in the

sick euthyroid syndrome

T4 = thyroxine; T3 = triiodothyronine; TSH = thyroid-stimulating hormone

Although the exact significance of a reduced T3 level is unknown, experimental work suggests an association with reduced

myocardial function and an alteration in cellular mitochondrial metabolism from aerobic to anaerobic producing a lactic acidosis.20

Page 388

Hepatic and Coagulation Changes

In an animal model of BSD, hepatic function remained unaffected by profound hypotension.34 The arterial ketone body ratio did not change significantly, suggesting an adequate oxygen supply

Fibrinolytic agents and plasminogen activators are released from damaged brain tissue into the circulation in patients with BSD and can cause coagulation defects, including disseminated intravascular coagulopathy These defects may be aggravated by hypothermia

Metabolic Changes

Changes in oxidative processes have been demonstrated after BSD.20 Reductions in plasma glucose, pyruvate and palmitate with parallel rises in lactate and fatty acids may indicate a shift from aerobic to anaerobic mitochondrial metabolism This change could lead to reductions in cellular high-energy phosphates and thus cellular and organ function Delivery-dependent oxygen consumption and high plasma lactate levels have been reported in BSD patients It is not clear whether this is due to a reduction in tissue oxygen extraction or mitochondrial impairment.21,35

The possible complications of BSD are highlighted in Tables 27.6 and 27.7 and Figure 27.1 and 27.2

Diagnosis of Brain Death

The criteria for the diagnosis of brain death published by the Honorary Secretary of the Royal Colleges and their faculties in the United Kingdom,7 and the Harvard Report in the United States, became the basis for the confirmation of brain death in many other countries.7 However, the exact criteria upon which brain death is diagnosed vary between countries, with

Table 27.6 Complications associated with BSD

Complication Frequency Contributing factors

Haemodynamic instability Very common Autonomic dysfunction

Myocardial damageβ-receptor dysfunctionHypovolaemiaHypothermiaHypoxia Common Pulmonary oedema, retained secretions, atelectasis

Hypovolaemia Common Diabetes insipidus

Endothelial damageDiuretics

HyperglycaemiaFluid restrictionHaemorrhageHyperosmolality Common Diabetes insipidus

Hyperglycaemia Common Insulin resistance

AcidosisIntravenous dextroseEndogenous and exogenous steroidsEndogenous and exogenous catecholaminesHypothermia Common Hypothalamic ischaemia

VasodilatationReduced basal metabolic rateCoagulation defects Uncommon Fibrinolytic agents

Cytokines

Transfused blood products

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Table 27.7 Electrolyte disturbances associated with BSD

Electrolyte disturbances Contributing factors

InsulinDiureticsCatecholaminesHyperventilationEndogenous andexogenous steroids

some but not all countries requiring confirmatory tests of absent brain function, such as EEG or cerebral angiography The diagnosis

of BSD in the United Kingdom will be described in detail A revision of the Code of Practice for the Diagnosis of Brainstem Death was published in 1998.36

There are three sequential steps in making the diagnosis of BSD To avoid unnecessary testing and to eliminate the chance of making

an incorrect diagnosis, it is essential that steps 1 and 2 are completed before beginning step 3.

End-organ effects of brainstem death

• hypothermia, < 35°C;

• depressant drugs, both therapeutic and non-therapeutic;

• metabolic disorders, e.g hyponatraemia;

• endocrine abnormalities, e.g myxoedema

Altered drug metabolism due to concurrent pathology or, less commonly, enzyme variants should be borne in mind at this stage In the absence of toxicological screening, it has been suggested that three days is a reasonable time to allow potential drug effects to disappear.37,38 Metabolic and endocrine abnormalities may be suspected from the history, examination and routine blood tests, i.e full blood count, arterial blood gas, electrolytes and blood glucose measurements,

Page 390although more sophisticated tests may be necessary Certain abnormalities accompanying BSD (e.g hypernatraemia) do not preclude the diagnosis of BSD.38

Specific conditions, such as the 'locked-in' syndrome and brainstem encephalitis (Bickerstatt's encephalitis or the Miller Fisher syndrome), may produce a clinical picture similar to that seen in BSD When such conditions are suspected, BSD tests should not be undertaken as the patient does not comply with the precondition 'there should be no doubt that the patient's condition is due to irremediable brain damage of known aetiology.37 The 'locked-in' syndrome is produced by a lesion in the pons which paralyses the limbs, respiratory muscles and lower cranial nerves Patients are conscious and able to blink and produce vertical eye movements Brainstem encephalitis may produce a comatose, areflexic, apnoeic patient, with motor and central nerve paralysis including internal and external ophthalmoplegia Full recovery from brain encephalitis is possible.39Therefore, the importance of obtaining an adequate history consistent with the clinical picture together with strict adherence to the preconditions and exclusions before BSD testing cannot be overemphasized If any doubt exists as to the cause of the patient's condition, BSD tests should not be performed

Step 3—

The Tests

The tests should not be performed unless steps 1 and 2 have been fulfilled

Who and When?

BSD tests should be performed by two medical practitioners who have been registered for more than five years and are competent in this field At least one of the practitioners should be a consultant and neither practitioner should be a member of the transplant team Two sets of tests should be performed; the two practitioners may perform the tests separately or together The tests should be

repeated to ensure no observer error has occurred The timing of this second set of tests is a matter for the doctors involved but should be adequate for the reassurance of all those directly concerned.40 The interval between the two sets of tests can be used to discuss the possibility of organ donation with the relatives if they have not already raised the subject

How?

For confirmation of BSD, five tests of the brainstem reflexes and testing for apnoea are required (Table 27.8) The tests are easily performed at the bedside and have unambiguous endpoints In the United Kingdom there is no requirement to perform cerebral angiography or electroencephalography for the confirmation of BSD

Testing for Apnoea

This test is considered positive if the patient does not exhibit any respiratory movements whilst disconnected from the ventilator despite a PaCO2 of at least 6.65 kPa

Table 27.8 The five tests of reflexes

1 A bright light is shone into both

pupils

No reaction in either pupil II and III

2 A strong stimulus is applied to

the corneas

No blinking V and VII

3 20 ml of iced water is injected

into both external auditory

meatae

No eye movement III, VI and VIII

4 painful stimulus is applied –

No coughing or gagging IX and X

*The tympanic membranes should first be visualized and seen to

be intact

**Spinal reflexes may be present

(50 mmHg) The lungs are normally hypoventilated with 100% O2 for 10 min prior to disconnection to achieve a PaCO2>6.6 kPa and

to prevent hypoxaemia Insufflation of oxygen at 6 l/min via a catheter passed into the trachea during disconnection will further reduce the risk of hypoxaemia during disconnection

Common Difficulties Encountered When Performing Tests for BSD

The difficulties commonly encountered during BSD testing are summarized in Table 27.9

Death is pronounced after the second set of tests but the legal time of death is recorded when the patient fulfils the first set of BSD criteria When BSD has been diagnosed the relatives should be informed and the clinician should ensure that the relatives fully understand that death has occurred If there is no absolute contraindication to organ donation, management of the patient should now

be directed to preservation of organ function (Tables 27.10, 27.11)

The completion of the first set of BSD tests is a suitable time to discuss organ donation with the patient's relatives In the United Kingdom, refusal by relatives accounts for the failure to donate organs in about 30% of potential organ donors The local transplant coordinator should be contacted as soon as possible after the first set of BSD criteria have been fulfilled as they are experienced in dealing with bereaved relatives who are considering organ donation

Management of Patients with Brainstem Death

After permission for organ donation has been obtained from the patient's relatives, the intensivist in charge of the patient's care should contact the local transplant coordinator to discuss specific treatments which may be requested by the transplant team, e.g hormone therapy A continued high standard of nursing care, the use of invasive monitoring and prompt treatment to preserve organ function will increase the chances of successful organ donation The patient management goals are similar to those before the diagnosis of BSD with the exception of specific measures to maintain cerebral perfusion pressure and oxygen delivery

Optimize Cardiac Output and Tissue Oxygen Delivery

Cardiac output is optimized by volume loading guided by central venous and/or pulmonary artery wedge pressures Blood, colloid and crystalloid solutions are used as appropriate to maintain the circulating volume A combination of inotropes and peripheral vasoconstrictors is usually required to improve cardiac

Table 27.9 Common difficulties encountered when performing the tests for BSD

Patients with cataract(s)/false eye(s) and or

disrupted tympanic membrane(s)

The published criteria are 'guidelines rather than rigid rules' 'It is for the doctors at the bedside to decide when the patient is dead'.40The patient is now hypothermic and/or has a

metabolic disturbance, e.g hypernatraemia

Abnormalities accompanying BSD do not preclude the diagnosis

of BSD.37 Although the exact temperature below which hypothermia is likely to be the cause of coma is uncertain, we do not perform BSD tests in patients whose core temperature is <35°

Does the patient have other conditions that can

account for the symptoms? (differential

diagnosis)

Ensure the preconditions and exclusions have been strictly adhered to

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Table 27.10 Absolute contraindications to organ donation

Moral Patient directive, relative(s) refusal

Transmissible disease Active bacterial, fungal, protozoan or viral

infection

Includes patients in high-risk groups for HIV infection Hepatitis

C is not an absolute contraindicationMalignancy Past or current diagnosis of malignancy including

the following primary CNS tumours: Anaplastic astrocytoma (Grade III), glioblastoma

multiforme, medulloblastoma, anaplastic oligodendroglioma, malignant ependymoma, pineoblastoma, anaplastic and malignant meningioma, intracerebral sarcoma, chordoma, primary cerebral lymphoma*

Exceptions: Low grade skin tumours e.g basal cell carcinoma Carcinoma in situ of the uterine cervix

Primary brain tumours that exceptionally spread outside the central nervous system

Hormone

replacement

Treatment with human pituitary extract

co-ordinator

*Council of Europe International Consensus Document: 'Standardization of Organ Donor Screening to Prevent

Transmission of Neoplastic Disease' 1997

Table 27.11 Referral to the coroner in the UK The coroner should be informed if:

death is the result of an accident

death occurred intraoperatively or before recovery from anaesthesia

death is of unknown cause

death is the result of suicide

death is from violent or unnatural or suspicious cause

death is due to self-neglect or neglect by others

death is due to an abortion

the deceased was not seen by the certifying doctor either after death or within the 14 days before death

death occured during or shortly after detention in police or prison custody

death may have been due to an industrial disease or related to the deceased's employment

Table 27.12 Physiological goals for heart or heart-lung donation

Mean arterial pressure >60 mmHg

Left ventricular stroke work index >15 g/m2

Pulmonary artery wedge pressure 12 mmHg

Central venous pressure 12 mmHg

contractility and to increase organ perfusion pressure Although dopamine is the most commonly used agent, dobutamine,

epinephrine and norepinephrine may be required depending on the cardiac index and systemic vascular resistance at the time The transplant team may specify their most favoured regimen for organ preservation, as shown in Table 27.12.28

The 'rule of 100s' has been suggested as a guide to treatment (Table 27.13)

Adequate Oxygenation

As these patients are intubated and ventilated they are at risk of atelectasis, retained secretions and nosocomial pneumonia

Physiotherapy, aseptic tracheobronchial suction and low levels of positive end-expiratory pressure (PEEP) of 5 cmH2O may be used

to prevent basal atelectasis and improve gas exchange Bronchoscopy may be necessary to facilitate clearance of secretions but care must be taken to avoid damaging the lungs if lung donation is being considered To minimize the risk of barotrauma and volutrauma, the peak inspiratory ventilatory pressure should be kept below 35 cmH2O and tidal volume less than 10 ml/kg The lowest

concentrations of inspired oxygen that give adequate haemoglobin saturation should be used to reduce the risk of oxygen toxicity The end-tidal CO2 should be kept within normal limits However, this may be difficult as CO2 production is low in brain-dead patients and dead space may have to be added to the ventilator circuit

Maintenance of Homeostasis with Failing Autonomic and Hormonal Systems

Diabetes insipidus is treated with intravenous or subcutaneous boluses of desmopressin (DDAVP) 0.5–4.0 μg or, if the patient is hypotensive, intravenous vasopressin (AVP, Pitressin) 5–20 units Repeat doses should be given to keep the urine output <200 ml/h Rapid treatment is essential to prevent the development of electrolyte abnormalities and hypotension Urine losses should be replaced with the appropriate crystalloid solution according to plasma and urine electrolyte measurements Infusions of insulin should be used

to maintain blood glucose concentrations within normal limits By using a combination of hormone replacements, it is possible to increase the number of suitable donors (Table 27.14)

Table 27.14 Hormone replacement combination (adapted from reference 29 )

Methylprednisolone 15 mg/kg bolus

Triiodothyronine 4 μg bolus + 3 μg/h infusion

Antidiuretic hormone (pitressin) 1 IU bolus + 1.5 IU/h infusion

Insulin Minimum 1 IU/h – to maintain blood glucose of 6–11 mmol/l

Epinephrine 1–5 μg/min – to maintain SVR 800–1200 dyne/s/cm–5

Hypothermia should be prevented by keeping the patient covered, the use of a warm air blanket, warmed fluids and humidification of the breathing circuit

Conclusion

The change from the idea of a cardiovascular death to the concept of brain death arose as a result of advances in medical technology Death of the brainstem, which can be reliably diagnosed by clinical tests, implies death of the whole brain and thus death of the individual The preconditions that must be fulfilled before

a diagnosis of brainstem death can be considered are essential to prevent any errors in the diagnosis Brainstem death results in a loss

of homeostasis and therefore successful organ transplantation is only possible after careful management of the organ donor.41

References

1 Cushing H Some experimental and clinical observations concerning states of increased intracranial tension Am J Med Sci 1902; 124: 375–400

2 Mollaret P, Goulon M Le coma dépassé (mémoire preliminaire) Rev Neurol (Paris) 1959; 101: 3–15

3 Wertheimer P, Jouvet M, Descotes J A propos du diagnostic de la mort du système nerveux — dans les comas avec arrêt

respiratoire traités par respiration artificielle Presse Med 1959; 67: 87–88

4 Ad Hoc Committee of the Harvard Medical School A definition of irreversible coma JAMA 1968; 281: 1070–1071

5 Mohandas A, Chou SN Brain death – a clinical and pathological study J Neurosurg 1971; 35: 211–218

6 Jennett B, Gleave J, Wilson P Brain deaths in three neurosurgical units BMJ 1981; 28: 2533–2539

7 Working Group of Conference of Medical Royal Colleges and their Faculties in the United Kingdom Diagnosis of death BMJ 1976; ii: 1187–1188

8 Working Group of Conference of Medical Royal Colleges and their Faculties in the United Kingdom Diagnosis of death BMJ 1979; i: 3320

9 Working Group of Conference of Medical Royal Colleges and their Faculties in the United Kingdom The criteria for the

diagnosis of brainstem death J Roy Coll Physicians Lond 1995; 29: 381–382

10 Fisher CM Brain herniation: a revision of classical concepts Can J Neuro Sci 1995; 22: 83–91

11 Black PM Brain death (first of two parts) N Engl J Med 1978; 299: 338–344

12 Gramm HJ, Meinhold H, Bickel U et al Acute endocrine failure after brain death? Transplantation 1992; 54: 851–857

13 Powner DJ, Hendrich A, Lagler RG, Ng RH, Madden RL Hormonal changes in brain dead patients Crit Care Med 1990; 18: 702–708

14 Howlett TA, Keogh AM, Perry L, Touzel R, Rees LH Anterior and posterior pituitary function in brain-stemdead donors Transplantation 1989; 47: 828–834

15 Kolin A, Norris JW Myocardial damage from acute cerebral lesions Stroke 1984; 15: 990–995

16 Shivalkar B, Van Loon J, Wieland W et al Variable effects of explosive or gradual increase of intracranial pressure on

myocardial structure and function Circulation 1993; 87: 230–239

17 Chen EP, Bittner HB, Kendall SWH, Van Trigt P Hormonal and haemodynamic changes in a validated animal model of brain death Crit Care Med 1996; 24: 1352–1359

18 Powner DJ, Hendrich A, Nyhuis A, Strate R Changes in catecholamine levels in patients who are brain dead J Heart Lung Transplant 1992; 11: 1046–1053

19 Mertes PM, CarteauxJP, Taboin Y et al Estimation of myocardial interstitial norepinephrine release after brain death using cardiac microdialysis Transplantation 1994; 57: 371–377

20 Cooper DKC, Novitzky D, Wicomb WN The pathophysiological effects of brain death on potential donor organs, with particular reference to the heart Ann Roy Coll Surg Engl 1989; 71: 261–266

21 Depret J, Teboul J-L, Benort G, Mercat A, Richard C Global energetic failure in brain-dead patients Transplantation 1995; 60: 966–971

22 White M, Wiechmann RJ, Roden RL et al Cardiac β-adrenergic neuroeffector systems in acute myocardial dysfunction related to brain injury Circulation 1995; 92: 2183–2189

23 Cruickshank JM, Neil-Dwyer G, Degaute JP et al Reduction of stress/catecholamine-induced cardiac necrosis by β1-selctive blockade Lancet 1987; 2: 585–589

24 Yoshioka T, Sugimoto H, Uenishi M et al Prolonged hemodynamic maintenance by the combined administration of vasopressin

and epinepherine in brain death: a clinical study Neurosurgery 1986; 18: 565–567

25 Novitzky D, Cooper DKC, Reichart B Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors Transplantation 1987; 43: 852–854

26 Goarin J-P, Cohen S, Riou B et al The effects of triiodothyronine on haemodynamic status and cardiac function in potential heart donors Anesth Analg 1996; 83: 41–47

27 Randell TT, Hockerstedt KA Triiodothyronine treatment in brain-dead multiorgan donors – a controlled study Transplantation 1992; 54: 736–738

28 Wheeldon DR, Potter CDO, Oduro A, Wallwork J, Large SR Transforming the 'unacceptable' donor: outcomes from the

adoption of a standardized donor management technique J Heart Lung Transplant 1995; 14: 734–742

29 Harms J, Isemer FE, Kolenda H Hormonal alteration and pituitary function during course of brain-stem death in potential organ donors Transplant Proc 1991; 23: 2614–2616

30 Power BM, Van Heerden PV The physiological changes associated with brain death – current concepts and implications for the treatment of the brain dead organ donor Anaesth Intens Care 1995; 23: 26–36

31 Galinanes M, Smolenski RT, Hearse DJ Brain death-induced cardiac contractile dysfunction and long-term cardiac preservation Rat heart studies of the effects of

hypophysectomy Circulation 1993; 88(part 2): II–270–280

32 Bensadoun H, Blanchet P, Richard C et al Kidney graft quality: 490 kidneys procured from brain dead donors in one center Transplant Proc 1995; 27: 1647–1648

33 Wicomb WN, Cooper DKC, Novitzky D Impairment of renal slice function following brain death, with reversibility of injury by hormonal therapy Transplantation 1986; 41: 29–33

34 Lin H, Okamoto R, Yamamoto Y et al Hepatic tolerance to hypotension as assessed by the changes in arterial ketone body ratio

in the state of brain death Transplantation 1989; 47: 444–448

35 Langeron O, Couture P, Mateo J Riou B, Pansard J-L, Coriat P Oxygen consumption and delivery relationship in brain-dead organ donors Br J Anaesth 1996; 76: 783–789

36 Cadaveric organs for transplantation A code of practice including the diagnosis of brainstem death HMSO, London, 1998

37 Working Group of the Royal College of Physicians and the Conference of Medical Royal Colleges and their Faculties in the United Kingdom Criteria for the diagnosis of brainstem death J Roy Coll Physicians Lond 1995; 29: 381–382

38 Pallis C ABC of brainstem death Diagnosis of brainstem death – I BMJ 1982; 285: 1558–1560

39 Al-Din ASN, Adnan JS, Shakir R Coma and brain stem areflexia in brain stem encephalitis (Fisher's syndrome) BMJ 1985; 291: 535–536

40 Robson JG Brain death (letter) BMJ 1981; 283: 505

41 The organ donor Intensive Care Society, London, 1994

Page 401The investigation of neurosurgical conditions by radiology began surprisingly early Dandy (1918)1 injected air into a lateral

ventricle to allow its visualization by X-rays Angiography followed in 1927 when Moniz2 reported the injection of sodium iodide into a surgically exposed carotid artery, demonstrating the cerebral vessels The technique was improved subsequently by

percutaneous injection and the development of less toxic contrast agents and remains a mainstay of neuroradiology Contrast studies

of the ventricular system have lessened in number following the improvement of imaging techniques and the introduction of

computed tomographic (CT) scans3 and magnetic resonance imaging (MRI)

The demands made of anaesthetists in the X-ray department have changed considerably over the last 10 years as the techniques of imaging have changed and expanded Improvement in imaging techniques and equipment has meant that very few neurosurgical patients require anaesthesia for diagnostic neuroradiology, but the continued development of interventional radiology, where some neurosurgical conditions may be treated in the X-ray department, makes new demands of the anaesthetist The new procedures pose their own problems but usually share the dangers of anaesthesia and surgery in the operating theatre.4,5,6

Problems of Anaesthesia in the X-ray Department

Neuroradiological procedures are associated with a significant morbidity and mortality.7,8,9 Anaesthesia constitutes an additional hazard There are a number of factors that add to the difficulties of the anaesthetist in the neuroradiological department:

• strange environment;

• hostile environment;

• bulky X-ray equipment;

• reduced lighting;

Strange Environment

The neuroradiology department is best situated close to the neurosurgical operating theatre It is, however, frequently part of the radiology department, so that expensive imaging equipment may be best used This physical separation means that the X-ray staff may not be familiar with operating theatre disciplines and patient care The anaesthetist must ensure that there is adequate, skilled help available and that the X-ray department staff are familiar with the requirements of anaesthesia All the facilities available to the anaesthetist

Bulky X-ray Equipment

The equipment required for X-ray is frequently expensive and bulky In the neuroradiology room, surrounding the couch on which the patient lies, there will be the X-ray tube on its support (usually a balanced, motor-driven assembly), several monitors and

computer controls There may be automatic injectors Careful planning is needed in setting up the room so that the X-ray equipment and the anaesthetic equipment do not impede each other In particular, the X-ray tube, on its gantry, must be swung out of the way for induction of anaesthesia and at the end of the anaesthetic It should be possible to move the tube assembly out of the way without delay in case of an emergency during a radiological procedure Particular thought must be given to the likely movement required in the X-ray equipment (tube and couch) during an examination, so that such movement does not imperil the patient's life support systems

breathing tubes, monitoring cables, infusions) must not only be secure but arranged in such a way as not to impede the couch

movement Wherever possible, we mount equipment on the X-ray couch; if this is not possible, we ensure that there is adequate slack

in cables, infusion lines or breathing tubes

No Skull Decompression

In the operating theatre, the fact that the surgeon will be performing a craniotomy means that the brain is being decompressed and probably that CSF will be aspirated, so that the patient is to a certain extent protected from high ICP In the X-ray room, the skull remains intact, so great care must be taken by the anaesthetist to avoid an increase in ICP in patients with space occupation

Angiography

In Interventional procedures a complex arrangement of catheters and guidewires may be used.6,10 A large sheath (7.5 Fr gauge) is placed in the femoral artery and through it another catheter is passed into one of the major vessels, such as a carotid or vertebral artery Finer catheters or guidewires, passed through main catheter, are used to access the vessel or lesion requiring treatment Recent development of small catheters and guidewires has made the catheterization of small vessels a practical proposition

The process is aided by modern digital radiographic techniques, where the bone and other non-vascular structures can be subtracted from the image Another aid is the ability to make a 'road map' image In this technique, the radiologist makes an injection of contrast into a major vessel, so outlining the vascular anatomy This image is saved and computer techniques allow the live image obtained from screening to be superimposed on the saved image, so that the radiologist can see the position of the catheter relative to the vasculature This facility helps the radiologist to advance the catheter along the cerebral vessels It requires that no movement of the patient take place once the vessel anatomy has been visualized and stored; though, of course, repeated 'road map' injections may be made

Interventional Procedures

Interventional neuroradiology has advanced dramatically in recent years as improved imaging techniques

and new tools for intervention have been developed A wide variety of conditions, both intracranial and spinal, can be treated and sometimes the procedure is complete in itself On other occasions, the procedure may be an adjunct to other forms of treatment Intracranial aneurysms may be occluded completely (Fig 28.1) A vascular tumour may be partially embolized before surgery in an attempt to reduce operative blood loss It may be possible to obliterate an arteriovenous malformation (AVM), but commonly the AVM will be incompletely embolized to reduce its size and make it more amenable to surgery or radiotherapy Dural venous malformations may also be completely embolized.

The tools and materials for interventional procedures are under rapid development The treatment of intracranial aneurysms has recently been advanced by the development of the Guglielmi detachable coils (GDC).11,12 These are coils of platinum wire attached

to a stainless steel guidewire The coil is manoeuvred into the aneurysm sac through a fine catheter and opens to hold itself in position The position of the coil is checked, as it is important to ensure that there is no tendency for the coil to prolapse into the feeding vessel or to interrupt blood flow past the aneurysm If the position is unsatisfactory, the coil can be removed When the position is satisfactory, the connection between the guidewire and the platinum coil is fused (by passing an electrical current through the joint) so that the guidewire can be removed, leaving the coil in place Several coils may be needed before the aneurysm is completely occluded but partial occlusion may allow recurrence of the subarachnoid haemorrhage Giant aneurysms may be

obliterated by coiling but occlusion of the feeding vessel by balloons is possible and may be combined with a subsequent

extracranial-to-intracranial vascular anastomosis.13

Obliteration by coiling is not possible for all aneurysms It may be impossible to reach the aneurysm with the catheter and the shape

of the aneurysm must be such as to retain the coil within the aneurysmal sac

Arteriovenous malformations can be treated in a number of ways, the main problems being presented by the morphology of the AVM The AVM may have a dramatic appearance on angiography (Fig 28.2), with many feeding vessels, multiple fistulae and large arterialized draining veins, through all of which the blood flow is extremely rapid The high flow may be associated with the

concomitant formation of an aneurysm.14 Treatment is aimed at obliterating the fistulae in turn and because manipulating the catheter into each part of the AVM can be difficult, the

Figure 28.1 (A) Radiograph showing an aneurysm of the bifurcation between middle and anterior cerebral arteries (B) Radiograph showing the obliteration of the aneurysm by Guglielmi detachable coils Six coils were placed in all