Textbook of Neuroanaesthesia and Critical Care - part 7 pptx

Pa g e 251 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 b ougie. 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. Am Surg 1988; 54: 185 – 187. 50. Grande CM, Barton CR, Stene JK. Appropriate techniques for airway management of emergency patients with suspected spinal cord injury. Anesth Analg 1988; 67: 714 – 715. 51. Lawes EG, Campbell I, Mercer D. Inflation pressure, gastric insufflation and rapid sequence induction. Br J Anaesth 1987; 59: 315 – 318. 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. Pa g e 252 66. Ovassapian A, Yelich SJ, Dykes MHM, Brunner EE. Fiberoptic nasotracheal intubation – incidence and causes of failure. Anesth Analg 1983; 62: 692 – 695. 67. Delaney KA, Hessler R. Emergency flexible fiberoptic nasotracheal intubation: a report of 60 cases. Ann Emerg Med 1988; 17: 919 – 926. 68. Mlineck EJ, Clinton JE, Plummer D, Ruiz E. Fiberoptic intubation in the emergency department. Ann Emerg Med 1990; 19: 359 – 362. 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 p ractice, 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 p enetrating 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. Pa g e 253 18— Anaesthesia for Neurosur g er y Without Craniotom y Andrew C. Summors & Richard E. Erskine Transsphenoidal Hypophysectomy 255 Surgery 259 Stereotactic Biopsy 262 Ventriculoperitoneal Shunts 263 References 265 Pa g e 256 eventually 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 A crome g al y 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. Ph y sical Findin g s 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 Pa g e 257 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 p eriod. 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 FiO 2 ; avoiding unnecessary and complex tracheostomies; and avoiding the problems of mechanical ventilation. 11,12 Large respiratory volumes may be necessary to maintain PaCO 2 , 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. Sur g ical Treatment of Acrome g al y 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 p atients in whom gigantism may be a factor. Pa g e 258 Cushin g '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/day 13 and this can be used as a basis for screening. Total plasma cortisol levels vary widely as most is protein b ound to cortisol- b inding 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 Ph y sical Findin g s 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 p ituitary gland. P rolactinoma 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 Ophthalmoplegia Endocrine disturbance Males Females Decreased libido Hypogonadism ( decreased andro g en- Amenorrhoea Oligomenorrhoea Anovulatory cycles Galactorrhoea dependent hair growth, testicular atrophy) Galactorrhoea G y naecomastia Virilization [...]... 50% of patients.33 Patients with functional or anatomical evidence of right-to-left shunt are clearly at risk of PAE in the event of venous air entrainment in the sitting position However, PAE does not always occur when these conditions exist Conversely, there have been reports of PAE in the absence of a cardiac septal defect.34,35 Indeed, transpulmonary passage of air in the absence of a right-to-left... 1991; 8: 47 54 45 Anderson BJ, Marks PV, Futter ME Propofol – contrasting effects in movement disorders Br J Neurosurg 1994; 8: 3 87 388 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... 1996, pp 270 7– 272 8 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 2 67 19— Anaesthesia for Posterior Fossa Surgery Catherine Duffy Anatomy 269 Posterior Fossa Lesions 269 Patient Positioning 272 Complications of the Sitting Position 273 Central Nervous System Monitoring 276 Anaesthetic... Management 277 Conclusion 278 References 278 Page 269 The posterior fossa is a small, rigid compartment which houses the cerebellum, pons, medulla oblongata and fourth ventricle Lifethreatening 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... approach and patient position and by minimizing congestion of cerebral vasculature Anatomy The anterior portion of the posterior fossa is the dorsum sellae and basilar portion, or clivus, of the occipital bone Laterally are the petrous portions of the temporal bones The roof is the tentorium cerebelli and the floor contains the foramen magnum Cranial nerve V arises from the pons and cranial nerves VI-XII... there is a risk of VAE A precordial Doppler should be used in conjunction with at least one other monitoring technique Prevention of VAE Reduction in the risk of VAE, and the potentially devastating complication of paradoxical air embolism (PAE), relies on careful surgical technique, vigilance on the part of the anaesthetist and clear communication between the anaesthetist and surgeon Page 275 Pin sites... 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... Acta Anaesth Scand 1 976 ; 20: 1 17 128 15 Marshall WK, Bedford RF, Miller ED Cardiovascular responses in the seated position – impact of four anesthetic techniques Anesth Analg 1983; 62 (7) : 648–653 16 Ganong W Dynamics of blood and lymph flow In: Lange (ed) Review of medical physiology, 15th edn Appleton and Lange, Norwalk, CA, 1991, pp 542–543 17 Papadopoulos G, Kuhly P, Brock M et al Venous and paradoxical... 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... documented an incidence of 76 %. 17 In a combined retrospective and prospective study, the incidence of VAE was found to be twice as high in the subpopulation of children compared with adults.10 Furthermore, children are more haemodynamically compromised by VAE.18 The adverse effects of VAE can be attributed to local endothelial reaction and to mechanical obstruction of blood flow At the level of the endothelium, . 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. 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. 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