Textbook of Neuroanaesthesia and Critical Care - part 7 pptx

Experimental cervical spine injury model: evaluation of airway management techniques.. Cervical spine movement during airway management: cinefluoroscopic appraisal in human cadavers.. Or

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31 Bohlman HH Acute fractures and dislocations of the cervical spine: an analysis of three hundred hospitalised patients and review

of the literature J Bone Joint Surg 1979; 61: 1119–1142

32 Aprahamian C, Thompson DM, Finger WA, Darin JC Experimental cervical spine injury model: evaluation of airway

management techniques Ann Emerg Med 1984; 13: 584–587

33 Graham JJ Complications of cervical spine surgery: a five year report on a survey of the membership of the Cervical Spine Research Society by the Morbidity and Mortality Committee Spine 1989; 14: 1046–1050

34 Meschino A, Devitt JH, Koch JP, Szalai JP, Schwartz ML The safety of awake intubation in cervical spine injury Can J Anaesth 1992; 39: 114–117

35 Sawin PD, Todd MM, Traynelis VC et al Cervical spine motion with direct laryngoscopy and orotracheal intubation: an in vivo cinefluoroscopic study of subjects without cervical abnormality Anesthesiology 1996; 85: 26–36

36 Horton WA, Fahy L, Charters P Disposition of the cervical vertebrae, atlanto-axial joint, hyoid and mandible during X-ray laryngoscopy Br J Anaesth 1989; 63: 435–438

37 Hauswald M, Sklar DP, Tandberg D, Garcia JF Cervical spine movement during airway management: cinefluoroscopic appraisal

in human cadavers Am J Emerg Med 1991; 9: 535–538

38 Johnson RM, Hart, DL, Simmons EF Cervical orthoses J Bone Joint Surg 1977; 59A: 332–339

39 Chandler DR, Nemejc C, Adkins RH, Waters RL Emergency cervical spine immobilisation Ann Emerg Med 1992; 21: 1185–1188

40 Podolsky S, Baraff LJ, Simon RR, Hoffman JR, Larmon B, Ablon W Efficacy of cervical spine immobilisation methods J Trauma 1983; 23: 461–465

41 Heath KJ The effect on laryngosocoy of different cervical spine immobilisation techniques Anaesthesia 1994; 49: 843–845

42 Hastings RH, Wood PR Head extension and laryngeal view during laryngoscopy with cervical spine stabilisation manoeuvres Anesthesiology 1994; 81: 1081–1082

43 Majernick TG, Bieniek R, Houston JB, Hughes HG Cervical spine movements during orotracheal intubation Ann Emerg Med 1986; 15: 417–420

44 Nolan JP, Wilson ME Orotracheal intubation in patients with potential cervical spine injuries An indication for the gum elastic bougie Anaesthesia 1993; 48: 630–633

45 Bogdonoff DL, Stone DJ Emergency management of the airway outside the operating room Can J Anaesth 1992; 39: 1069–1089

46 Hastings RH, Marks JD Airway management for trauma patients with potential cervical spine injuries Anesth Analg 1991; 73: 471–482

47 Nolan JP Resuscitation of the trauma patient Care of the Critically Ill 1995; 11: 222–226

48 Redan JA, Livingston DH, Tortella BJ, Rush BF The value of intubating and paralysing patients with suspected head injury in the emergency department J Trauma 1991; 31: 371–375

49 Talucci RC, Shaikh KA, Schwab CW Rapid sequence induction with oral endotracheal intubation in the multiple injured patient

52 Doolan LA, O'Brien JF Safe intubation in cervical spine injury Anaesth Intens Care 1985; 13: 319–324

53 Narrod JA, Moore EE, Rosen P Emergency cricothyrostomy – technique and anatomical considerations J Emerg Med 1985; 2: 443–446

54 DeLaurier GA, Hawkins ML, Treat RC, Mansberger AR Jr Acute airway management: the role of cricothyroidotomy Am Surg 1990; 56: 12–15

55 Salvino CK, Dries D, Gamelli R, Murphy-Macabobby M, Marshall W Emergency cricothyroidotomy in trauma victims J Trauma 1993; 34: 503–505

56 McGill J, Clinton JE, Ruiz E Cricothyrotomy in the emergency department Ann Emerg Med 1982; 11: 361–364

57 Esses B, Jafek BW Cricothyroidotomy: a decade of experience in Denver Ann Otol Rhinol Laryngol 1987; 96: 519–524

58 Wood PR, Lawler PGP Managing the airway in cervical spine injury: a review of the Advanced Trauma Life Support protocol Anaesthesia 1992; 47: 792–797

59 McHale SP, Brydon CW, Wood MLB, Liban JB A survey of nasotracheal intubating skills among Advanced Trauma Life Support course graduates Br J Anaesth 1994; 72: 195–197

60 Logan AStC Use of the laryngeal mask in a patient with an unstable fracture of the cervical spine Anaesthesia 1991; 46: 987

61 Calder I, Ordman AJ, Jackowski A, Crockard HA The Brain laryngeal mask An alternative to emergency tracheal intubation Anaesthesia 1990; 45: 137–139

62 Benumof JL Management of the difficult adult airway Anesthesiology 1991; 75: 1087–1110

63 Ovassapian A Fiberoptic tracheal intubation In: Ovassapian A (ed) Fiberoptic airway endoscopy in anesthesia and critical care.

Raven Press, NewYork, 1990

64 Sidhu VS, Whitehead EM, Ainsworth QP, Smith M, Calder I A technique of awake fiberoptic intubation Anaesthesia 1993; 48: 910–913

65 Ovassapian A, Krejcie TC, Yelich SJ, Dykes MHM Awake fiberoptic intubation in the patient at high risk of aspiration Br J Anaesth 1989; 62: 13–16

69 McNamara RM Retrograde intubation of the trachea Ann Emerg Med 1987; 16: 680–682.

70 Barriot P, Riou B Retrograde technique for tracheal intubation in trauma patients Crit Care Med 1988; 16: 712–713

71 Fox DJ, Castro T, Rastrelli AJ Comparison of intubation techniques in the awake patient: the Flexi-lum surgical light

(lightwand) versus blind nasal approach Anesthesiology 1987; 66: 69–71

72 Mallampati SR, Gatt SP, Gugino LD et al A clinical sign to predict difficult tracheal intubation: a prospective study Can Anaesth Soc J 1985; 32: 429–434

73 Wilson ME, Spiegelhalter D, Robertson JA, Lesser P Predicting intubation Br J Anaesth 1988; 61: 211–216

74 Frerk CM Predicting difficult intubation Anaesthesia 1991; 46: 1005–1008

75 Calder I Predicting difficult intubation Anaesthesia 1992; 47: 528–529

76 Wilson ME, John R Problems with the Mallampati sign Anaesthesia 1990; 45: 486–487

77 Oates JDL, Macleod AD, Oates PD, Pearsall FJ, Howie JC, Murray GD Comparison of two methods for predicting difficult intubation Br J Anaesth 1991; 66: 305–310

78 Laurent SC, De Melo AE, Alexander-Williams JM The use of the McCoy laryngoscope in patients with simulated cervical spine injuries Anaesthesia 1996; 51: 74–75

79 Hastings RH, Vigil AC, Hanna R, Yang BY, Sartoris DJ Cervical spine movement during laryngoscopy with the Bullard, Macintosh and Miller laryngoscopes Anesthesiology 1995; 82: 859–869

80 Marks RJ, Forrester PC, Calder I, Crockard HA Anaesthesia for transoral craniocervical surgery Anaesthesia 1986; 41: 1049–1052

81 Bland JH Rheumatoid arthrits subluxation of the cervical spine (editorial) J Rheumatol 1990; 17: 134–137

82 Macather A, Kleinman S Rheumatoid cervical joint disease: a challenge to the anaesthetist Can J Anaesth 1993; 40: 154–159

83 Sherk H Atlanto/axial instability and acquired basilar invagination in rheumatoid arthritis Orthop Clin North Am 1978; 9: 1053–1063

84 Foley-Nolan D, Stack JP, Ryan M Magnetic resonance imaging in the evaluation of patients with rheumatoid arthritis: a

comparison with plain film radiographs Br J Rheumatol 1991; 30: 101–106

85 Crockard HA, Calder I, Ransford AO One-stage transoral decompression and posterior fixation in rheumatoid atlanto-axial subluxation J Bone Joint Surg (Br) 1990; 72: 682–685

86 Calder I, Calder J, Crockard HA Difficult direct laryngoscopy in patients with cervical spine disease Anaesthesia 1995; 50: 756–763

87 Cormack RS, Lehane J Difficult tracheal intubation in obstetrics Anaesthesia 1984; 39: 1105–1111

88 Skues MA, Welchew EA Anaesthesia and rheumatoid arthritis Anaesthesia 1993; 48: 989–997

89 Morton RE, Khan MA, Murray-Leslie C, Elliott S Atlanto-axial instability in Down's syndrome: a five year follow up study Arch Dis Child 1995; 72: 115–119

90 Powell JF, Woodcock T, Luscombe FE Atlanto-axial subluxation in Down's syndrome Anaesthesia 1990; 45: 1049–1051

91 Kadis LB Neurological disorders In: Katz J, Berumof J, Kadis LB (eds) Anaesthesia and uncommon diseases: pathophysiologic and clinical correlations, 2nd edn WB Saunders, Philadelphia, 1981, pp 485–508

92 Highland T, Salciccioli G, Wilson RF Spinal cord injuries In: Wilson RF, Walt AJ (eds) Management of trauma: pitfalls and

practice, 2nd edn Williams and Wilkins, Baltimore, 1996, pp 212–213

93 Braken MB, Shepard MJ, Collins WF et al A randomised, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury Results of the second National Acute Spinal Cord Injury Study N Engl J Med 1990; 322: 1405–1411

94 Prendergast MR, Saxe JM, Ledgerwood AM, Lucas CE, Lucas WF Massive steroids do not reduce the zone of injury after penetrating spinal cord injury J Trauma 1994; 37: 576–580

95 Theodore J, Robin ED Speculations on neurogenic pulmonary edema Am Rev Respir Dis 1976; 113: 405–411

96 John DA, Tobey RE, Homer L, Rice CL Onset of succinylcholine-induced hyperkalaemia Anesthesiology 1976; 45: 294–299

97 Tobey RE Paraplegia, succinylcholine and cardiac arrest Anesthesiology 1970; 32: 359

98 Stone WA, Beach TP, Hamilberg W Succinylcholine – danger in the spinal-cord injured patient Anesthesiology 1970; 32: 168

99 Raeder JC, Gisvold SE Perioperative autonomic hyperreflexia in high spinal cord lesion: a case report Acta Anaesthesiol Scand 1986; 30: 672–673

100 Erickson RP Autonomic hyperreflexia; pathophysiology and medical management Acta Physiol Med Rehab 1980; 61: 431–440

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18—

Anaesthesia for Neurosurgery Without Craniotomy

Andrew C Summors & Richard E Erskine

Page 256eventually to the empty sella syndrome The sphenoid bone surrounds it bilaterally and inferiorly

The pituitary is close to several structures affected by its enlargement

• The lateral walls of the sella are close to the cavernous sinus containing the internal carotid artery, oculomotor nerve, trochlear and abducens nerve and the first two divisions of the trigeminal nerve

• Tumour can spread into the sphenoid sinus lying anteriorly and inferiorly below the thin inferior sella

• The optic chiasm lies directly above the sella diaphragma in front of the hypophyseal stalk and is easily compressed by suprasellar extension

• The hypothalamus and third ventricle of the brain lie above the roof of the sella Compression by space-occupying lesions may give rise to hypothalamic abnormalities

The circulation of the pituitary gland is complex Arterial supply arises from two paired arteries, the superior and inferior

hypophyseal arteries arising from the internal carotid arteries A portal circulation provides 80–90% of the blood supply to the anterior lobe from the infundibulum of the posterior lobe and pituitary stalk This contains high concentrations of hypothalamic neuroregulatory hormones controlling anterior hormone synthesis and release The posterior pituitary receives blood from the inferior hypophyseal artery and some branches of the superior hypophyseal artery and has a rich nerve supply of unmyelinated fibres from the supraoptic and paraventricular nuclei and other areas of the hypothalamus ADH and oxytocin are synthesized in the

hypothalamus and transported via neurones to the posterior pituitary From here, they are released into the peripheral circulation.1,2

Acromegaly

Acromegaly occurs as a result of an increase in growth hormone produced by a pituitary adenoma Growth hormone (GH), a 191 amino acid polypeptide, is produced by the anterior pituitary in a pulsatile fashion The temporal pattern of these pulses is determined

by a hypothalamic pulse-generating mechanism, influenced in turn by other areas of the brain such as the limbic system, the

amygdaloid nucleus and the brainstem The pulsatile release of hormone into the blood results from the influence of GH-releasing factor, which stimulates, and somatostatin, which inhibits release of the hormone from the anterior pituitary The most important of these influences is the sleep-stage cycle Slow-wave sleep stimulates and REM sleep inhibits release

Like ACTH and prolactin, GH is produced as part of the stress response In addition, GH secretion is influenced by metabolism Hypoglycaemia and fasting stimulate its release while hyperglycaemia and food inhibit its release This is the basis of the oral glucose tolerance test (OGTT) utilized to test GH secretion Blood is taken half-hourly for 2 hours after administration of 100 g glucose GH should remain below its nadir of 1 μg/l In the liver and at the growth plate of longitudinal bones, activation of GH receptors results in the production of insulin-like growth factor 1 (IGF-1) It is produced in the liver under the influence of GH but also other influences and thus has to be considered a hormone in its own right IGF-1 is transported in the blood bound to a protein, insulin-like growth factor binding protein 3 (IGFBP-3) The concentration of this binding protein is regulated by GH Unlike GH, IGFBP-3 levels in the blood are fairly constant and can be used as an index of GH activity

Physical Findings

The head is elongated due to growth of the mandible with resultant malocclusion of the teeth The tongue is enlarged, making intubation difficult In addition, there is an increase of the lymphoid tissue mass in the upper airway These patients are prone to develop a nocturnal oxygen deficit which may be compounded by a central sleep apneoa.3 Kyphoscoliosis may be present, leading to restrictive lung disease

Hypertension is a feature and may be the result of the direct antinaturetic effect of GH, leading to the activation of the

renin-angiotensin system and an increase in blood volume.4,5 Patients with long-standing acromegaly develop cardiomegaly Thickening of the left ventricle is the most consistent finding.6 This hypertrophy is reversible when the GH returns to normal.7

An excess of GH prior to closure of the epiphyseal plates leads to gigantism After the plates have fused, the bony growth is by apposition, i.e thickening of the cortices The muscles are paradoxically weak as a result of both a specific acromegalic myopathy and a peripheral neuropathy resulting from endo- and perineural connective tissue thickening

GH plays a pivotal role in intermediate metabolism It acts with insulin to encourage protein production and, in insulin-depleted states, as a fat-mobilizing agent It increases amino acid uptake into muscle In excess, it causes glucose intolerance and a third of acromegalics present with diabetes mellitus which reverts to normal after the acromegaly is successfully treated Lean body mass is increased as protein is laid down at the expense

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of fat This is accompanied by an increase in total body water, possibly resulting from the antinaturetic effect of GH Acromegaly is diagnosed by the demonstration of autonomous GH production which is not inhibited by oral glucose However, some response to oral glucose load may persist Because IGF-1 has a longer half-life it does not exhibit the same pulsatility in the blood and hence its blood level is used as a diagnostic test It is also used to measure the response of acromegalic patients to treatment PRL is raised in a third of acromegalic patients In some cases this is because both hormones are produced in the same cell (mammosomatotroph cell)

or because a GH-producing macroadenoma has expanded to compress the pituitary stalk and reduce the hypothalamic dopaminergic inhibition of PRL production As with other pituitary adenomas, the expanding GH-secreting tumour may compress the normal areas

of the gland and inhibit the production of, in ascending order of occurrence: gonadotrophins, prolactin, ACTH and, rarely, TSH This results in secondary inhibition of the peripheral glands After treatment, either medical or by surgery or irradiation, the response is measured by oral glucose tolerance or by estimation of IGF-1 in the blood

Anaesthetic Considerations

The patient with acromegaly, or gigantism if excess growth hormone is secreted prior to pubertal closure of bony epiphyses, presents

a variety of challenges to the anaesthetist Acromegalic symptoms are present before surgery on average for 6–7 years This means most patients have anatomical and physiological changes when they present for anaesthesia Anatomical distortions of the face, tongue, vocal cords and pharyngeal and glottic structures, cardiovascular disease including hypertension and idiopathic

cardiomyopathy, pulmonary disease and endocrine dysfunction such as diabetes mellitus are not uncommon.8 The airway probably presents the most significant problem Difficulty may be experienced with intubation due to both the longjaw and the connective tissue disturbances of the vocal cords A fibreoptic bronchoscope may be needed to facilitate intubation Problems with the upper airway may be suspected with exertional dyspnoea, hoarseness, stridor, macroglossia and decreased mobility of the neck and

temporomandibular joints Hypertrophy of pharyngeal and laryngeal soft tissue obscures the glottis Thyroid enlargement may distort the airway and cause glottic stenosis Elective tracheostomy has been suggested for the severe grades of airway involvement but fibreoptic-guided intubation has also been used.9 Indirect laryngoscopy, soft tissue X-ray assessment of the neck and inspiratory or expiratory flow volume studies may also be helpful.10

The heart needs to be carefully assessed for involvement as described above The commonly present diabetic state needs to be recognized and treated This usually reverts back to normal when GH levels return to more physiological levels in the postoperative period

Muscle relaxants should be used with caution and each increment monitored with a peripheral nerve stimulator As for any

transsphenoidal pituitary operation, the patient needs to be observed carefully for any signs of generalized hypopituitarism and specifically for the development of diabetes insipidus (DI)

Close attention to the use of narcotic analgesics during anaesthesia and supervision in the postoperative period is required

Postoperatively, these patients are prone to airway obstruction due to both their preoperative anatomy and nasal packing and a sleep apnoea caused by the central disturbance of ventilation that occurs with elevated growth hormone Nasal airway catheters through the nasal packing have been used to overcome this and provide a means of positive pressure ventilation if required.8 Their use has been well described and advantages include: suctioning and airway toilet; bypassing the tongue with a high FiO2; avoiding unnecessary and complex tracheostomies; and avoiding the problems of mechanical ventilation.11,12

Large respiratory volumes may be necessary to maintain PaCO2, especially in the patient with gigantism These patients pose special problems with moving and positioning.10 Raised intracranial pressure may be a problem if extrasellar extension is present but it is likely a transcranial route would be used for large extrasellar extensions

Surgical Treatment of Acromegaly

Acromegaly almost always results from an adenoma of the pituitary The treatment is surgical in the first instance Surgery is

additionally indicated for those patients in whom upward pressure on the optic chiasm above has resulted in visual field defects Fifty percent of patients will be cured by surgery alone, as tested by a GH level persistently below 2 μg/l on OGTT A further half of the remainder will respond satisfactorily to additional measures These include medical treatment with the dopaminergic agent

bromocriptine or the somatostatin analogue octreotide, or radiotherapy applied to the gland Factors which predispose to a less favourable surgical result include tumour involvement of the dura lining the pituitary cavity, extention out of the sella and younger patients in whom gigantism may be a factor

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Cushing's Disease

Cushing's disease, first described by Harvey Cushing in 1912, is an adenoma of corticotrophic cells of the anterior pituitary

Physiologically, corticotrophin-releasing hormone (CRH) from the hypothalamus stimulates the synthesis and release of ACTH and other pro-opiomelanocortin (POMC)-derived peptides in the pituitary ACTH in turn induces secretion of cortisol and adrenal androgens by the adrenal gland with complex feedback mechanisms regulating plasma cortisol Normal levels of urine free cortisol are under 250 nmol/day13 and this can be used as a basis for screening Total plasma cortisol levels vary widely as most is protein bound to cortisol-binding globulin (80%) or albumin (10%) and protein levels change with various disease states

Most ACTH-secreting tumours are microadenomas, less than 1 cm diameter, lying centrally in the anterior pituitary;14 10% are large enough to produce changes in the sella turcica Most tumours are basophilic Immunochemical stains detect ACTH and POMC-related peptides A minority are chromophobic or mixed basophilic/chromophobic with minimal ACTH These are often larger, faster growing and less hormonally active.15 Diagnosis of adenoma can be confirmed with a low-dose overnight dexamethasone

suppression test causing feedback decrease in ACTH secretion and subsequent cortisol release A plasma cortisol level <140 nmol/l

is normal after 0.5 mg dexamethasone every 6 h for two days or 1mg dexamethasone the night before and blood sampled at 8.00 am the following morning High-dose dexamethasone can still partly suppress ACTH from adenomas and is used to distinguish pituitary adenomas from ectopic ACTH sources.15,16

Physical Findings

Symptoms and signs depend on the degree and duration of disease and are caused by:

• endocrine effects of ACTH on cortisol, adrenal androgens and aldosterone, to a lesser degree;

• mass effects

Patient appearance is one of generalized obesity of face, neck, trunk and abdomen with atrophic limb muscles The neck appears short and thick from the dorsocervical fat pad that may cause difficulty with intubation Changes in cellular glucose transport may result in steroid-induced diabetes mellitus.17 Mild hypertension is common and hypertension is severe in 10% with diastolic BP >130 mmHg due to both low renin and an elevated response to vasoactive substances.18

Congestive cardiac failure is common The skin is atrophic, thin and very fragile with loss of connective tissue Osteoporosis and bone fractures are common and care is needed when gaining vascular access and positioning the patient Wound healing is slow and the immune response is suppressed by glucocorticoids Psychiatric symptoms occur in over half of patients

Hypokalaemia is rare in contrast to other causes of hypercortisolism Peptic ulcers usually occur if NSAIDS have been given Mass effects usually produce headaches and visual field defects.15

Treatment and Outcomes

The preferred treatment is surgical in most instances Remission rates of 85–95% can be expected following surgery in experienced hands Determination of ACTH levels in the inferior petrosal veins has helped to identify the position of the microadenoma in the pituitary gland

Prolactinoma

Prolactinoma is the most common pituitary disorder Symptoms relate to central decrease in gonadotrophin secretion, giving

menstrual disturbances in females and loss of libido in men, and to stimulation of the mammary gland, giving galactorrhoea (Table 18.2) Over half are microadenomas, sometimes occurring as part of the multiple endocrine neoplasia syndrome type 1 Their small size means adequate functioning pituitary gland often remains after surgery.19

Table 18.2 Symptoms and signs of prolactinoma

(reproduced in part from reference 21 )

Space occupation

Visual field defects

Hydrocephalus (blockage of foramen of Monro)

Anterior pituitary insufficiency

Page 259PRL is the only anterior pituitary hormone under the dominant tonic inhibitory control of dopamine from the hypothalamus Stress or suckling has a stimulatory effect on PRL secretion via hypothalamic TSH release Prolactin levels correlate well with adenoma size,

in contrast to other pituitary adenomas Normal levels in males are <15 μg/l and in non-pregnant females 5–20 μg/l.20,21

Treatment and Outcomes

Prolactinomas tend to be very slow growing and remain stable in size and the amount they secrete over many years Most

prolactinomas are treated with the dopamine agonist bromocriptine which is successful in reducing PRL levels to normal in 60–90%

of patients Treatment needs to be continued for a very long time, often for life Surgery is successful mainly when the tumour is small and is thus considered when patients do not tolerate medical treatment or for a small tumour that does not respond adequately

to bromocriptine

Endocrine Inactive Adenomas

Up to 30% of patients with pituitary adenomas have endocrinologically silent tumours and present with symptoms secondary to mass effects (headache, visual field disturbance) or pituitary hypofunction secondary to destruction of normal gland Compression of the optic chiasm often results in visual field defects and extension into the cavernous sinus may cause cranial nerve palsies Headache is the most frequent presenting symptom of mass effect (Table 18.2)

The absence of specific hormone markers makes it difficult to distinguish these tumours from other intrasellar and suprasellar lesions such as meningiomas, craniopharyngiomas or metastases.22

Pituitary Apoplexy

Pituitary apoplexy is a clinical syndrome characterized by a sudden onset of headache, accompanied by a loss of vision and

impairment of ocular mobility due to the rapid enlargement of a pituitary adenoma subsequent to a vascular event The rise in pressure within the pituitary fossa constitutes a neurosurgical emergency to reduce this pressure, usually by operation via the

transnasal route Enlargement upwards compresses the optic pathways and may produce effects on the function of the midbrain and hypothalamus This may result in altered levels of autonomic function and a deterioration in conscious level The

hypothalamicpituitary axis (HPA) is nearly always compromised and systemic steroid replacement should be immediately

commenced in the diagnosis of pituitary apoplexy.23

Other Sella Masses

Craniopharyngiomas

These histologically benign tumours are formed of epithelial remnants in the region of the pituitary stalk and may represent a persistent form of Rathke's pouch They are mostly suprasellar but present for surgery via the transseptal route if intrasellar and require biopsy or cyst decompression The anaesthetist should be aware that they are usually adherent to critical vascular, endocrine and cerebral structures, making surgery difficult Stereotactic irradiation under local anaesthesia may be an option for some.19,24

Empty Sella Syndrome

This is a dynamic process due to prolapse of arachnoid through an incomplete diaphragmatic sella or from previous pituitary surgery

or irradiation The sella is enlarged by CSF and pituitary tissue is compressed against the posterior floor of the sella.19

Surgery

Transseptal pitiuitary surgery is a safe and effective method of management of pitiutary adenomas and related parasellar anomalies The extracranial approach to the hypophysis was first described by Schloffer in 1906, who reported the removal of a pituitary tumour through the nose.19

Four transseptal approaches to the pitiuitary fossa are described (direct transnasal transsphenoidal, transethmoidal, sublabial

transseptal and transantral), the most common approach today being the direct transnasal transsphenoidal route.25 Since the 1970s the transsphenoidal has been the preferred route for removal of pituitary tumours, even those with suprasellar extensions.26 In

comparison with a transcranial approach, a transsphenoidal approach is faster and less traumatic There is a better cosmetic outcome afterward and less frequent panhypopituitarism The posterior pituitary often remains intact, decreasing the incidence of DI There is

a faster recovery and shorter hospitalization and no external scarring Transfusion requirements are also less A more selective resection of tumour avoids injury to the frontal lobes, olfactory tracts, pituitary stalk and optic chiasm.1,26 However, all the

transsphenoidal operations are liable to have complications relating to damage within and adjacent to the pituitary fossa, e.g CSF leak, meningitis, diabetes insipidis, carotid and cavernous sinus injury and optic chiasm injury It is not the best route to use if spread

is extensive There are also complications due to the route of access to the fossa, e.g hypertensive responses and dental or septal complications.1,25,27

Anaesthetic Management

Anaesthetic management of patients for transsphenoidal surgery is similar to that for transcranial surgery The patient should undergo appropriate preoperative investigation and preparation, including baseline endocrine function tests and investigation of anatomical manifestations (e.g changes in airway) The patient should receive appropriate premedication and explanation, a smooth induction, stable maintenance and recovery with appropriate monitoring and fluid management with control of intracranial pressure

A number of investigations may be required to assess endocrine dysfunction, including:

• baseline glucose, cortisol, ACTH, GH, FSH, LH, TSH, PRL and testosterone in males, with repeat levels after stimulation;

• thyroid function tests;

• water deprivation tests for DI (measurement of serum electrolytes and plasma and urine osmolalities)

Coagulopathy is a rare problem with primary brain tumours but has been reported with chronic activation of the coagulation system during episodes of chronic DIC The risk of DIC often worsens with surgery with the risk extending to several days

postoperatively.28 An explanation of the operative risk should be given A 1% mortality has been reported.19 The patient should also

be given an explanation of packing of the nose and nasopharyngeal space that will require mouth breathing postoperatively

Admission to the intensive care unit may also be required after surgery

Evidence suggests that the current amount of peroperative glucocorticoid coverage is excessive and based on anecdotal information New recommendations based on preoperative glucocorticoid dose, preoperative glucocorticoid duration and the nature and duration

of surgery have been proposed Transsphenoidal hypophysectomy may equate to minor or moderate surgical stress with targets of 25–50 mg hydrocortisone equivalents per day for 1–2 days based on daily cortisol secretion rates and static plasma cortisol

measurements There is no information suggesting that these new recommended equivalent doses need to be exceeded, so a patient receiving maintenance glucocorticoid therapy exceeding the estimated stress requirement will not need more steroid cover during the stress period After uncomplicated surgery, circulating cortisol concentration returns to normal by 24–48 h in most patients.29

Premedication

Our practice is to administer a small dose of benzodiazepine orally to reduce anxiety Assessment of the HPA axis will establish the requirement for glucocorticoid replacement Thyroid function should be controlled and diabetes stabilized Antibiotic prophylaxis is commonly given

Explanations are given for mouth breathing postoperatively, intensive care admission or awake fibreoptic intubation if required

Maintenance of Anaesthesia

Vascular access is established with a 16G peripheral intravenous cannula Invasive arterial monitoring can be achieved with

cannulation of a radial artery or dorsalis pedis if collateral flow is inadequate.30

Capnography is used to ensure adequate ventilation and a moderate reduction in PaCO2 to 4–4.5 kPa

Page 261Hypocapnoea is induced before adding a volatile anaesthetic agent but it is rare to have raised intracranial pressure without

suprasellar extension Surgical access may be aided by normalization of PaCO2 to induce descent of the gland as CO2 rises to normal The surgeon may request a Valsalva manoeuvre at the end of surgery to check for CSF leaks

Anaesthesia and Choice of Drugs

Techniques and agents are chosen based on their effects on CMR, CBF and intracranial blood volume Thus, thiopentone, propofol and fentanyl are used frequently Volatile agents can be used after modest hyperventilation, with isoflurane being safer than enflurane

or halothane, but care should still be exercised with midline shift on CT scan Sevoflurane also has advantages in maintaining cerebral autoregulation.31–33 A TIVA technique with propofol is favoured by some neuroanaesthetists

Generally, CPP is controlled and cerebral vasodilatation avoided with hypocapnia One study with a large number of patients showed

no major untoward effect of nitrous oxide in transsphenoidal hypophysectomy but isoflurane requirements decreased Nitrous oxide increases cerebral blood flow and intracranial pressure and, unlike other inhaled agents, gives no brain protection by decreasing cerebral metabolic rate A trend toward a higher incidence of early postoperative nausea and vomiting may be seen with nitrous oxide after transsphenoidal hypophysectomy.34 The same authors found an association with an increased incidence of atrioventricular dissociation and a trend toward more premature ventricular contractions in these same patients receiving infiltrations of lignocaine with adrenaline for haemostasis.35

Blood pressure control is important for haemostasis, enabling the surgeon to perform an optimal resection Blood pressure should be maintained at least at preoperative levels Bleeding is more likely in Cushing's disease and acromegaly, with hypertension and fragile blood vessels, and in metastatic cancer, with thrombocytopaenia due to bone marrow invasion These problems can be exacerbated with the severe cardiovascular reactions that have been reported with transsphenoidal surgery Hypertension can be severe and uncontrollable, obscuring the operative field Use of at least 1% lignocaine with the adrenaline has been shown to minimize

hypertensive responses.27

Cocaine and adrenaline combinations may sometimes be used to help achieve haemostasis Cocaine provides topical anaesthesia and vasoconstriction and adrenaline increases vasoconstriction further and decreases cocaine absorption However, life-threatening complications with arrhythmias and hypertension have occurred when maximum recommended doses are exceeded, especially with the high-concentration solutions and pastes used to shorten the onset time and improve duration The value of adding cocaine to adrenaline has recently been called into question.36

Moderate hypotension has been used to improve the surgical view by reducing bleeding However, hypotension may be best avoided,

as one study of intrasellar pressures suggests that the blood supply to the pituitary is mixed arterial and venous with the arterial supply pressure lower than normal arterial pressure Hence a small decrease in mean blood pressure or an increase in intrasellar pressure may give rise to pituitary apoplexy.37

Small amounts of vasopressors may be required to support the circulation but hypertension is frequently seen initially

A mean blood pressure between 60 and 80 mmHg at the highest point of the skull maintains cerebral perfusion pressure and

minimizes blood in the surgical field At the conclusion of the operation, a piece of muscle or fascia taken from the the thigh may be used to seal the operation site and reduce the risk of CSF leak The muscle relaxant is reversed, the pack removed and the oropharynx suctioned under direct vision The patient is extubated when responsive to command with adequate ventilation, given humidified oxygen and reminded to mouth breathe.38 The patient is positioned 30° head up to minimize CSF leakage and a mini neuroexam may

be performed

Intravenous Fluids and Blood Loss

Blood loss is usually less than 100 ml and a normal perioperative fluid regimen includes 11 of Hartmann's solution intraoperatively and for the first 8 h thereafter followed by a further 1 l over the next 16 h Most patients have resumed normal oral intake by then Blood transfusion is rare and occurs in 1–2%.38

Postoperative Course and Complications

As the transcranial route is avoided, neurological complications are rare and the postoperative course is generally smooth The patient

is closely monitored in the recovery area for 1–2 h for assessment of vital signs, neurologic examination and fluid monitoring Most patients are ambulatory and resuming normal oral intake in 48 h Hypertension lasting more than 12 h is common, especially in Cushing's syndrome, and may

Page 262only resolve after nasal packs are removed on the fifth or sixth postoperative day.

Particular care with ventilation may be required depending on the level of consciousness Problems with acromegaly and gigantism have been detailed above Ventilation may also be required postoperatively in the patient with advanced Cushing's disease who has a reduced chest wall compliance

Antibiotic prophylaxis is continued for at-risk patients including those with nasal or sinus infections, previous pituitary surgery and Cushing's syndrome Corticosteroid substitution is continued for 24 h (e.g 25–50 mg hydrocortisone/day) and decreased to a maintenance dose depending on preoperative adrenal function and the amount of pituitary tissue remaining

Complications of Sellar Region Surgery

Cranial DI is a well-recognized cause of fluid balance disturbance after pituitary surgery and can occur in up to 20% of patients A greater than 90% destruction of the paraventricular and supraoptic nuclei is usually associated with permanent DI Most patients tend

to retain fluids on the day of surgery followed by a slight diuresis therafter but without the signs of DI Transient DI from

manipulation of the posterior lobe or irritation of the pituitary stalk resolves after several days and a urine output of up to 2.5 l/day may be normal DI is suspected when dilute urine is excreted in volumes greater than the fluid intake Most cases have polyuria (UO

> 30 ml/kg/h), hypernatraemia and elevated plasma osmolality Patients with a complete DI have urine volumes in excess of 10 l/day with urine osmolality 50–200 mosmol/kg and specific gravity of 1.001–1.005 They are sensitive to exogenous ADH Partial DI patients have smaller urine volumes and urine osmolalities between 290 and 600 mosmol/kg The diagnosis can be confirmed with the ADH synthetic analogue desmopressin (DDAVP) which causes the urine output to fall and urine osmolality to increase Other causes of polyuria include osmotic diuretics (e.g mannitol, radiocontrast agents), severe hyperglycaemia and fluid overload

Comparison of plasma and urine osmolalities may help (Figure 18.1)

Treatment consists of adequate fluid resuscitation and correction of electrolytes with regular monitoring of intake and output Severe polyuria can be treated with IV desmopressin 1–4 μg/day The duration of DDAVP is dose dependent and ranges from 8 to 12 h SIADH due to inappropriate release of ADH from damaged posterior pituiary cells is much more rare but has also been reported, usually in the late postoperative period after discharge.39

Figure 18.1 Plasma and urine osmolalities (redrawn from Moses AM, Blumenthal SA, Streeten DH

Acid–base and electrolyte disorders associated with endocrine disease: pituitary and thyroid

In: Arief AI, Defronzo RA (eds) Fluid, electrolyte and acid–base disorders Churchill Livingstone, New York, 1985, pp 851–892)

CSF rhinorrhoea associated with diaphragmatic lesions may occur and be complicated by bacterial meningitis from nasal flora Some centres routinely continue antibiotic prophylaxis

Vision changes are rare and cranial nerve palsies affecting the third, fourth and sixth cranial nerves are usually transient if they occur.Anterior pituitary function after surgery depends on the size of the tumour.40

Lesions to adjacent anatomical structures occur, including bleeding from the carotid artery and cavernous sinus or hypothalamic lesions leading to hyperthermia, electrolyte disturbance and cerebral coma.41Venous air embolism is rare with the supine patient.Sinusitis, fractures from surgical instruments, deviated nasal septum with obstruction of nasal ventilation and dental problems have all been described

Stereotactic Biopsy

Image-guided stereotactic surgery allows the biopsy or destruction of intracranial lesions without the need for craniotomy It gives greater accuracy and diagnostic yield in tissue sampling and may be of great benefit in deciding the question of histology prior to a major surgical undertaking.42 It is most commonly used for biopsy of lesions seen on CT and to locate small lesions difficult to find visually, especially lesions deep to the brain's surface It also enables the surgeon to

Page 263biopsy lesions adjacent to vital centres more safely, thereby avoiding the risks of freehand techniques

Stereotaxis is also used for radiotherapy with radioactive wires placed through plastic cannulae or sheaths

Method

A mechanical frame is attached to the patient's head and a scan obtained as usual The scanner's computer calculates the 3D

coordinates of points in the brain and relates them to the stereotactic space outlined by the frame Simple calculations then convert these radiographic coordinates to the coordinate system used by the frame These coordinates are set on the micrometers on the frame through which biopsy instruments can be directed with an accuracy of 1 mm.43

Many of these procedures can be carried out under local anaesthesia (together with supplementation by IV sedation) This has the advantage of continuous patient evaluation during biopsy General anaesthesia is used for patient comfort in prolonged procedures and particularly in children

A potential complication of the technique is intracerebral haemorrhage from accidental puncture of major arteries, sinuses and bridging veins This may require urgent transfer of the patient for CT or even urgent craniotomy.43

Anaesthesia

Anaesthetic technique aimed at cardiovascular and respiratory stability throughout will maintain a stable CBF and thus ICP and CPP Localized or general oedema is thus minimized and therefore lesion movement with respect to the skull Bone and Bristow44describe results from a year's experience with total intravenous anaesthesia for stereotactic surgery The technique consists of a combination

of propofol, fentanyl, vecuronium and O2 in air It provides good cardiovascular stability and adequate depth of anaesthesia for all stages in stereotaxis and a reliable rapid recovery Furthermore, it can also be useful for transferring head-injured patients from the ICU to the CT scanner Propofol is also believed to be the ideal agent for easing the discomfort of siting the stereotactic frame if the procedure to follow requires the patient to be awake, e.g thalamotomy.45

After careful preoperative assessment, a short-acting benzodiazepine premed is given and large-bore IV access is established A level

of monitoring is chosen that maintains patient care in transit, commonly NIBP, SpO2, EGG, EtCO2 All monitors, pumps, O2 cylinder and ventilator are fixed to the trolley securely if transported and arranged for easy observation from outside the CT scanner

Bone and Bristow44 used IV lignocaine 1 mg/kg, fentanyl 2 μg/kg, propofol 1–2 mg/kg over 30 s, vecuronium 0.1 mg/kg followed by intubation and positive pressure ventilation with a portable ventilator with fresh gas flow titrated against EtCO2 Anaesthesia was then maintained by a propofol infusion according to Roberts et al,46 i.e 10 mg/kg/h for the first 10 min, followed by 8 mg/kg/h for the next 10 min and 6 mg/kg/h thereafter and adjusted according to depth of anaesthesia A volatile agent is not required This has the advantage of avoiding the need for an anaesthetic machine during transfer and avoiding the adverse effects of a volatile agent on the cerebral vasculature The problem of pollution and scavenging requirements is also overcome Muscle relaxant was provided with boluses or infusion of vecuronium

After skin preparation, a minimum of four cranial fixation pins are applied to the skull This stimulus requires careful attention to anaesthetic technique to avoid increases in ICP (a bolus of propofol or opiate is commonly used at this point to deepen anaesthesia quickly and overcome any sympathetic response) The propofol infusion is stopped just prior to reversal with neostigmine and glycopyrrolate The patient usually remains supine throughout

The advantages of this total intravenous technique are the haemodynamic and respiratory stability during the stereotactic procedures, patient transfer between CT and operating theatre and after use of radiocontrast in CT It is a simple technique and the same

anaesthetic technique can be continued in the operating room

Postoperative patient care includes frequent neurological monitoring There is a potential risk of air embolism through transgressed venous channels in bone

Overall, there is a low incidence of nausea and vomiting and morbidity and mortality are very low.44

Ventriculoperitoneal Shunts

Hydrocephalus is usually due to obstruction of CSF flow giving rise to increases in volume and thus intracranial pressure Surgical treatment aims are to provide a shunt through which excess fluid can drain to a site to be absorbed The most common drains are to the peritoneal cavity but the right atrium, cisterna magna and pleural cavity are also sometimes used

Page 264

VP shunts drain CSF from the fourth or lateral ventricles to the peritoneal cavity Systems usually involve three components: a ventricular catheter, a one-way valve and a distal catheter Other devices may also be used (on–off valves, siphon control devices and chambers for flushing the system) The ventricular catheter is inserted through a burr hole (usually on the right), connected to the one-way valve that determines the draining pressure from the ventricle and then connected to the peritoneal catheter, passed over the chest wall and inserted into the peritoneal cavity through a small incision

Position

Children

For VP shunts the child is placed supine with the head turned to the opposite side for the occipital insertion of the ventricular

catheter A towel is placed under the nape of the neck so the head, neck and abdomen are in one plane for the passage of the

subcutaneous tunneller for shunt placement (Fig 18.2) Children are usually positioned with towels, rolls and pillows rather than table adjustment The tunneller theoretically reduces chest wall compliance and may cause underventilation or dangerous increases in airway pressures

Figure 18.2 The shunt is passed subcutaneously from the cranial end to the peritoneal incisions through a shunt-passing device (redrawn from reference47)

Anaesthetic Management

The child presenting for insertion of VP shunt or shunt revision must be considered to have overt or potentially raised intracranial pressure Anaesthetic technique should be tailored to minimize sympathetic responses and steps taken to reduce intracranial pressure.Preoperative respiratory depressant drugs are avoided in the presence of a raised ICP A smooth induction is desirable as crying will further increase the ICP An inhalation induction is acceptable if the fontanelle and sutures are opened, otherwise an intravenous induction is preferred EMLA cream is used over the venepuncture site For induction, thiopentone and propofol have the advantage

of decreasing cerebral metabolic rate and cerebral blood flow

Vecuronium has the fewest cardiovascular effects during induction but the other muscle relaxants have also been used satisfactorily Other measures may be used to limit the pressor responses to laryngoscopy and intubation, such as the use of a bolus of lignocaine or fentanyl This, however, seems less of a problem in children with open sutures than in adults A RAE tube or armoured tube is used either orally or nasally and fixed well to prevent movement The chest is auscultated for breath sounds bilaterally after the patient is placed in their final position The breathing circuit is secured firmly to prevent dragging on the endotracheal tube The eyes and limbs are protected from injury

Anaesthesia is maintained with a total intravenous technique using propofol or with volatile agents and IV analgesics such as

fentanyl or alfentanil or with combinations of these

TIVA with propofol decreases CMRO2, may give neuroprotection, reduces relaxant needs and gives rapid wakening postoperatively Isoflurane also decreases CMRO2 and relaxant requirements and gives easy control of blood pressure if required Opioids are

adjusted to avoid postoperative respiratory depression Their use increases the incidence of postoperative nausea and vomiting.Moderate hypocapnia using capnography to monitor ventilation reduces brain mass by cerebral vasoconstriction

Surgical infiltration with adrenaline reduces bleeding but the addition of at least 1% lignocaine provides scalp analgesia and helps reduces any hypertensive response.27

Page 265Intravenous fluids without glucose are used as elevated levels of glucose worsen outcome.

At the conclusion of surgery, the pharynx is cleared of secretions under direct vision, muscle relaxants reversed and the patient extubated, avoiding coughing if possible

3 Ho KY, Sullivan CE Sleep apnea in acromegaly Ann Intern Med 1991; 115: 527–532

4 Ho HI, Weissberger JA The antinaturetic effect of biosynthetic human growth hormone in man invoves activation of the angiotensin mechanism Metabolism 1990; 39: 133–137

renin-5 Hirsch EZ, Sloman JG, Martin FIR Cardiac function in acromegaly Am J Med Sci 1969; 257: 1–8

6 Savage DD, Henry WL, Eastman RC Echocardiographic assessment of cardiac anatomy and function in acromegalic patients Am

11 Singelyn FJ, Scholtes JL Airway obstruction in acromegaly: a method of prevention Anaesth Inten Care 1988; 16: 491–492

12 Perks WH, Horricks PM, Cooper RA et al Sleep apnoea in acromegaly BMJ 1980; 280: 894–897

13 Burke CW, Beardwell CG Cushing's syndrome: an elevation of the clinical usefulness of urinary free cortisol and other urinary steroid measurements in diagnosis Quart J Med 1973; 42: 175–204

14 Hardy J Cushing's disease: 50 years later Can J Neurol Sci 1982; 9: 375–380

15 Schulte HM, Petersenn S Cushing's disease – clinical findings and endocrinology In: Landolt AM, Vance ML, Reilly PL (eds) Pituitary adenomas Churchill Livingstone, NewYork, 1996, pp 101–110

16 Liddle GW Test of pituitary-adrenal suppressibility in the diagnosis of Cushing's syndrome J Clin Endocrinol Metab 1960; 20: 1539–1560

17 Murray DK, Hill ME, Nelson DH Inhibitory action of sphigosine, sphinganine and dexamethasone on glucose uptake: studies with hydrogen peroxidase and phorbol esters Life Sci 1990; 46: 1843–1849

18 Ritchie CM, Sheridan B, Fraser R et al Studies on the pathogenesis of hypertension in Cushing's disease and acromegaly Quart J Med 1990; 76: 855–867

19 Kern EB, Pearson BW, McDonald TJ, Laws ER The transseptal approach to lesions of the pituitary and parasellar regions Laryngoscope 1979; 89 (5 pt 2 suppl 15): 1–34

20 Vance ML, Thorner OM Prolactin and hyperprolactinaemic syndromes and management In: DeGroot L (ed) Endocrinology

WB Saunders, Philadelphia, 1989, pp 408

21 Von Werder K Prolactinoma: clinical findings and endocrinology In: Landolt AM, Vance ML, Reilly PL (eds) Pituitary

adenomas Churchill Livingstone, New York, 1996, pp 111–126

22 Katznelson L, Klibanski A Endocrine-inactive, FSH, LH and -subunit adenomas: clinical findings and endocrinology In: Landolt AM, Vance ML, Reilly PL (eds) Pituitary adenomas Churchill Livingstone, New York, 1996, pp 127–131

26 Peter M, DeTribolet N Visual outcome after transsphenoidal surgery for pituitary adenomas Br J Neurosurg 1995; 9: 151–157.

27 Abou-Madi MN, Trop D, Barnes J Aetiology and control of cardiovascular reactions during transsphenoidal resection of pituitary microadenomas Can Anaesth Soc J 1980; 27: 491–495

28 Weinberg S, Phillips L, Twersky R, Cottrell JE, Braunstein KM Hypercoagulability in a patient with a brain tumor

Anesthesiology 1984; 61: 200–202

29 Salem M, Tainsh RE Jr, Bromberg J, Loriaux DL, Chernow B Perioperative glucocorticoid coverage A reassessment 42 years after emergence of a problem Ann Surg 1994; 219: 416–425

30 Campkin TV: Radial artery cannulation Potential hazard in patients with acromegaly Anaesthesia 1980; 35: 1008–1009

31 Grosslight K, Foster R, Colohan AR, Bedford RF Isoflurane for neuroanesthesia: risk factors for increases in intracranial pressure Anesthesiology 1985; 63: 533–536

Page 266

32 Messick JM Jr, Newberg LA, Nugent M, Faust RJ Principles of neuroanesthesia for the neurosurgical patient with CNS

pathophysiology Anesth Analg 1985; 64: 143–174

33 Gupta S, Heath K, Matta BF The effect of incremental doses of sevoflurane on cerebral pressure autoregulation in humans: a transcranial doppler study Br J Anaesth 1997; 79: 469–472

34 Eger EI II, Lampe GH, Wauk LZ, Whitendale P, Calahan MK, Donegan JH Clinical pharmacology of nitrous oxide: an

argument for its continued use Anesth Analg 1990; 71: 575–585

35 Lampe GH, Donegan JH, Rupp SM et al Nitrous oxide and epinephrine induced arrythmias Anesth Analg 1990; 71: 602–605

36 Nicholson KEA, Rogers JEG Cocaine and adrenaline paste: a fatal complication BMJ 1995; 311: 250–251

37 Kruse A, Astrup J, Cold GE, Hansen HH Pressure and blood flow in pituitary adenomas measured during transsphenoidal surgery Br J Neurosurg 1992; 6: 333–342

38 Landolt AM, Schiller Z Surgical technique – transsphenoidal approach In: Landolt AM, Vance ML, Reilly PL (eds) Pituitary adenomas Churchill Livingstone, New York, 1996, pp 315–331

39 Tymms J, Griffith HB, Hartog M, Clark JDA, Reckless JPD Pituitary surgery and inappropriate antidiuretic hormone secretion J Roy Soc Med 1992; 85: 302

40 Maclanahan CS, Christy JH, Tindall GT Anterior pituitary function before and after transsphenoidal microsurgical resection of pituitary tumors Neurosurgery 1978; 3: 142–144

41 Fahlbusch R, Buchfelder M Surgical complications In: Landolt AM, Vance ML, Reilly PL (eds) Pituitary adenomas Churchill Livingstone, NewYork, 1996, pp 394–408

42 Apuzzo MJL, Chandrasoma PT, Cohen D, Zee CJ, Zelman V Computed imaging stereotaxy: experience and perspective related

to 500 procedures applied to brain masses Neurosurgery 1987; 20: 930–937

43 Salcman M The surgical management of gliomas In: Tindall GT, Cooper PR, Barrow PL (eds) The practice of neurosurgery Williams & Wilkins, Baltimore, 1996, pp 649–670

44 Bone ME, Bristow A Total intravenous anaesthesia in stereotactic surgery – one years clinical experience Eur J Anaesthesiol 1991; 8: 47–54

45 Anderson BJ, Marks PV, Futter ME Propofol – contrasting effects in movement disorders Br J Neurosurg 1994; 8: 387–388

46 Roberts FL, Dixon J, Lewis GTR, Tackley RM, PrysRoberts C Induction and maintenance of propofol anaesthesia Anaesthesia 1988; 43(suppl): 14–17

47 Roth PA, Cohen AR Management of hydrocephalus in children In: Tindall GT, Cooper PR, Barrow PL (eds) The practice of neurosurgery Williams & Wilkins, Baltimore, 1996, pp 2707–2728

48 Trouillas J, Girod C Pathology of pituitary adenomas In: Landolt AM, Vance ML, Reilly PL (eds) Pituitary adenomas

Churchill Livingstone, New York, 1996, pp 27–46

Page 269The posterior fossa is a small, rigid compartment which houses the cerebellum, pons, medulla oblongata and fourth ventricle Life-threatening symptoms can result from compression of these vital structures Because of the narrow outflow of cerebrospinal fluid (CSF), intracranial hypertension can develop suddenly The common goal of the anaesthetist and surgeon is an operation in which the need for retraction, with consequent tissue damage, is minimized This is achieved by optimizing the surgical approach and patient position and by minimizing congestion of cerebral vasculature.

Figure 19.1 Acute hydrocephalus in a child with medulloblastoma

Signs and Symptoms

Headache and vomiting are the most common symptoms in patients with posterior fossa tumours Hemicerebellar lesions are

characterized by unilateral ataxia, dysmetria, intention tremor and hypotonia Vermian lesions tend to present with a wide-based gait, truncal ataxia and abnormal extraocular movements Brainstem tumours present with bulbar palsies, secondary to cranial nerve dysfunction, and contralateral motor and sensory deficits Depending on the level of the lesion, respiratory changes may occur.When a posterior fossa lesion is complicated by obstructive hydrocephalus, headache and vomiting are exacerbated The patient develops an unsteady gait, mental state changes, diplopia, incontinence and signs of meningism

These account for 12–28% of childhood brain tumours They are relatively benign lesions with very good long-term survival

following surgical resection

Brainstem Glioma

These represent 25–30% of posterior fossa tumours in childhood Most are low-grade astrocytomas They tend to be slow growing with insidious onset of symptoms The exception is pontine gliomas which are malignant and present with a short and aggressive history

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Ependymoma

These lesions tend to occur in childhood and adolescence, with 50% occurring in children less than three years old They arise from the floor of the fourth ventricle Treatment involves surgical removal and adjuvant irradiation Complete removal may not always be possible if there is brainstem involvement

Choroid Plexus Papilloma/Carcinoma

These are rare lesions arising from the fourth ventricle They account for only 3% of paediatric intracranial tumours They

hypersecrete CSF and are associated with communicating hydrocephalus

Schwannomas may also affect cranial nerves V, VII, IX, X and XII

Meningioma

Ten percent of all meningiomas are in the posterior fossa They may arise from the petrous ridge of the temporal bone and extend into the cerebellopontine angle Other possible sites are the clivus, tentorium cerebelli, fourth ventricle and, rarely, foramen magnum Because they are vascular lesions, preoperative embolization is usually attempted

Clival Tumour

These are rare tumours and comprise chordomas, chondrosarcomas and carcinomas Surgery is technically difficult and local

recurrence rates are high

Arachnoid Cyst

These are common congenital lesions affecting sites throughout the central nervous system In the posterior fossa, they are found around the foramen magnum, the cerebellopontine angle and in the pineal region They are often asymptomatic Should a mass effect occur, surgical treatment involves marsipualization of the cyst

Glomus Jugulare Tumour

These are tumours of the extraadrenal paraganglion system They arise in the region of the middle ear and may extend through the jugular foramen or through the petrous bone to the cerebellopontine angle

Epidermoid Cyst

These are benign tumours arising from epithelial cells They are usually found in the cerebellopontine angle where they may enlarge

to cause cranial nerve or brainstem dysfunction

Because of the proximity of the skull base to perinasal sinuses, the mouth and upper respiratory tract, carcinomas originating in these regions can readily invade the posterior fossa In recent years, combined surgical approaches involving neurosurgery, ear, nose and throat and plastic surgery have been utilized to treat these tumours aggressively