Department of Neuroanaesthesia, The National Hospital for Neurology and Neurosurgery, University College London Hospitals, Queen Square, London WC1N 3BG, UK
Keywords: brain, pituitary; anaesthesia; pituitary surgery, neurological
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Introduction |
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The perioperative anaesthetic care of patients presenting for pituitary surgery requires careful preoperative assessment and meticulous per- and postoperative management using principles common to all intracranial procedures. Particular problems in such patients relate to primary hormonal hypersecretion and its complications, and to mass effects of the tumour. Knowledge of the normal anatomy and physiology of the pituitary gland is essential to allow an understanding of the pathophysiological effects relevant to anaesthesia and of the potential complications that might arise during and after surgery. The aim of this review is to present the issues which are crucial for the safe anaesthetic management of these challenging patients.
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Anatomy and physiology |
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Production and release of anterior pituitary hormones are under the control of the hypothalamus. Axons from hypothalamic neurones terminate on the median eminence where a system of fenestrated capillaries carries arterial blood down to the anterior pituitary through the hypophyseal portal system. Peptide hormones stimulate or inhibit release of the corresponding pituitary hormones. Prolactin release is stimulated by prolactin-releasing hormone (PRH) and inhibited by prolactin-inhibiting hormone, now known to be dopamine. These are secreted by medial regions of the hypothalamus. Growth hormone release is promoted by growth hormone releasing hormone (GRH) and inhibited by somatostatin; these are both produced in the ventromedial hypothalamus. Thyroid-releasing hormone (TRH), from ventral hypothalamic areas, stimulates the production and release of TSH. Similarly, corticotrophic hormone (CRH) stimulates ACTH release.
The anterior pituitary hormones affect specific target organs and tissues. In women, prolactin causes milk secretion from the breast after oestrogen and progesterone priming. In men, its role is unclear. Growth hormone acts on a wide variety of tissues, both directly and through release of insulin-like growth factor I (IGF-I). This is released principally from the liver in response to the presence of growth hormone. In addition to stimulating bone and cartilage growth, growth hormone and IGF-I increase protein synthesis and lipolysis whilst decreasing insulin sensitivity and causing Na+ retention. TSH stimulates iodine binding by the thyroid gland and increases synthesis and release of triiodothyronine (T3) and thyroxine (T4). Blood flow to the thyroid gland increases under the influence of TSH, and chronically elevated concentrations result in enlargement of the gland. ACTH acts on high-affinity membrane receptors of adrenocortical cells. Stimulation results in increased concentrations of intracellular cholesterol, which is converted to cortisol within the mitochondria before release into the circulation. FSH causes early maturation of ovarian follicles and both FSH and LH allow final maturation. Surges in LH are responsible for ovulation. In men, FSH stimulates spematogenesis and LH causes testosterone secretion.
Anterior pituitary hormones are under feedback control. Growth hormone increases circulating IGF-I which in turn directly inhibits growth hormone secretion from the pituitary. It also stimulates somatostatin secretion. Thyroid hormones feedback to inhibit TRH and TSH, and cortisol inhibits CRH and ACTH. Secretion of the gonadotrophic hormones FSH and LH is controlled by a single releasing factor, luteinizing hormone releasing factor (LHRH). The feedback from gonadal hormones at the pituitary and hypothalamus may be inhibitory or stimulatory. The significance of MSH in humans is unclear, but it is controlled by the hypothalamus through stimulatory and inhibitory factors.
In addition to the classic hormones described above, the pituitary secretes a number of other peptides, including vasoactive intestinal peptide, chorionic gonadotrophin, substance P and renin. Such diversity reflects the functional complexity of the gland.40
The posterior lobe of the pituitary is made up of pituicytes which, in keeping with its embryological origins, are similar to glial cells. The posterior pituitary is responsible for the storage and release of oxytocin and vasopressin, which are hormones synthesized in the paraventricular and supraoptic nuclei of the hypothalamus.
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Pituitary pathology |
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The prevalence of pituitary tumours is approximately 200 per million of the population20 but unselected post-mortem studies suggest an incidence of 1027%.8 The majority are therefore asymptomatic.
Presentation
Pituitary lesions may present in a variety of ways:39 41 (i) hormonal hypersecretion syndromes, such as hyperprolactinaemia, acromegaly and Cushings disease; (ii) mass effect, for example visual disturbance or raised intracranial pressure; (iii) non-specific, for example infertility, headache, epilepsy or pituitary hypofunction; (iv) incidental, such as those detected during imaging for other conditions.
Rarely, a patient may present with pituitary apoplexy following haemorrhage into an adenoma. Sudden and dramatic endocrine alterations are associated with headache, signs of meningism, visual impairment and ophthalmoplegia and other evidence of an intracranial mass lesion.
Hormonal hypersecretion syndromes
Hormonal hyperactivity usually occurs secondary to overproduction of hormones by a discrete adenoma. Prolactinomas occur most commonly. Adenomas producing acromegaly and Cushings disease are rarer. A non-functioning (i.e. non-hormone-secreting) adenoma can increase prolactin concentrations by compressing the pituitary stalk. This stalk effect in turn reduces transfer of prolactin-inhibiting factor (dopamine) from the hypothalamus to the pituitary.
Mass effect
Mass effect of a tumour on adjacent structures is more likely to occur with non-functioning macroadenomas (>1 cm in diameter). The structures most commonly affected lie adjacent to the pituitary and include optic nerves and chiasm (Fig. 2). Compression of the chiasm results characteristically in bitemporal hemianopia, although in the early stages upper quadrant defects only may be discernible. Occasionally, a third cranial nerve palsy may occur, especially in cases of pituitary apoplexy. Large tumours may also impede cerebrospinal fluid circulation, resulting in hydrocephalus and raised intracranial pressure.
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Incidentalomas
Pituitary tumours, often called incidentalomas, may present as an incidental finding during investigation of an unrelated condition;50 71 this is the result of the increased sensitivity of CT and MRI techniques. Incidental demonstration of a pituitary mass occurs in >10% of patients undergoing cranial imaging,39 an unsurprising finding as occult pituitary adenomas have been reported in up to 27% of post-mortem examinations of patients dying from unrelated causes.8
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Preoperative diagnosis and management of pituitary tumours |
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Prolactin-secreting tumours
Prolactin-secreting tumours account for more than half of functioning pituitary tumours. The majority are microadenomas (<1 cm) and 90% occur in women. Females present typically with secondary amenorrhoea and galactorrhoea, although the latter may be absent if oestrogen concentrations are low. Men with prolactin-secreting tumours can present with impotence and a decreased sperm count and such tumours may be diagnosed during investigation of infertility.
Prolactin-producing macroadenomas (>1 cm) are more common in men and may present with visual field defects secondary to pressure effects of the tumour, rather than with fertility problems.
Diagnosis
MRI of the pituitary fossa identifies the presence of a tumour and an elevated plasma prolactin concentration confirms the diagnosis.52 The upper limit of normal for basal circulating prolactin varies depending upon the assay but concentrations of >400 mU litre1 (20 ng ml1) are generally accepted to be elevated. Plasma concentrations correlate well with tumour size. Prolactin-secreting microadenomas generate prolactin concentrations of 10004000 mU litre1, whereas concentrations of >6000 mU litre1 are usually associated with macroadenomas. Large, non-functioning tumours can also increase prolactin concentrations by compressing the pituitary stalk (see above) but under such circumstances the prolactin concentration rarely exceeds 3000 mU litre1. As prolactin is a stress hormone, its plasma concentration may rise during venesection. If possible, an intravenous cannula should be placed and blood removed some hours later.
Treatment
The first-line treatment of prolactinomas is with a dopamine agonist, such as bromocriptine, titrated against plasma prolactin concentration.32 43 52 Bromocriptine should be introduced at a low dose (1 mg) with food and increased to 515 mg daily until optimum control is achieved. Cabergoline is an alternative to bromocriptine.32 Medical therapy is curative in <95% of patients, in whom prolactin concentrations are restored to normal.4 Surgical removal of the adenoma is indicated in the minority of patients who do not respond to dopamine agonists52 or in the rare cases when side-effects (nausea, lethargy or nasal stuffiness) limit their use.49 In patients with a macroadenoma, morning cortisol concentration should be checked if symptoms suggest hypopituitarism, although this is rare. If this concentration is borderline, a Synacthen test should be performed. Monitoring of visual field and acuity is vital. First-line therapy with bromocriptine should be reviewed after 1 week to check that field defects have not deteriorated. Many patients with large tumours do respond to medical treatment, and in 75% of such patients, visual defects are abolished.4 Although there is no evidence of teratogenicity, dopamine agonists are usually stopped during pregnancy. Symptomatic enlargement of treated microadenomas is extremely rare but monitoring of visual fields and sequential MRI will detect the 15% of macroadenomas that grow significantly during this time.51 In these patients drug therapy may be reintroduced as this does not affect the outcome of pregnancy.48
Growth hormone-secreting tumours
Excess secretion of growth hormone produces acromegaly in the adult and gigantism before epiphyseal closure. The annual incidence of acromegaly is six to eight cases per million of the population. The clinical syndrome is usually insidious in onset and is characterized by enlargement of the jaw, hands and feet and increased soft tissue growth secondary to elevation of growth hormone concentration (Fig. 3). Associated complications of the disease, such as diabetes mellitus and hypertension, are often the first medical indications of acromegaly. The common clinical signs and symptoms are shown in Table 1.
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Treatment
The primary treatment is surgery, with or without subsequent radiotherapy. A few patients respond to dopamine agonists and, in such cases, growth hormone and IGF-I concentrations can be normalized without surgery.3 Long-acting analogues of somatostatin (such as octreotide) may have a place in those who fail to respond to dopamine agonists but the need for parenteral administration and the high incidence of gallstones limits their use.35 Recently, a new slow-release preparation, somatuline, given by injection every 12 weeks has been investigated.30
ACTH-secreting tumours
The annual incidence of ACTH-producing pituitary tumours is two to four per million of the population. These tumours account for 4% of functioning pituitary adenomas and 80% occur in women. The majority are microadenomas. High concentrations of cortisol cause Cushings syndrome, which may occur secondary to treatment with glucocorticoid drugs (the most common cause), an adrenal tumour, ectopic production of ACTH associated with a neoplasm, or a pituitary tumour. The clinical condition resulting from excess ACTH production by a pituitary adenoma is called Cushings disease. Whatever the cause of the excess circulating cortisol, Cushings syndrome is characterized by widespread effects (Table 2).
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Treatment
Primary treatment is surgical, and is curative in <80% of patients. Pretreatment with metyrapone or betaconazole reverses the side-effects of increased concentrations of circulating cortisol, which used to cause significant peri-operative morbidity and mortality.15 If surgery is not possible or has failed, radiotherapy is a secondary option. This may be accompanied by bilateral adrenalectomy and mineralocorticoid and glucocorticoid replacement therapy. However, adrenalectomy carries the risk of Nelsons syndrome (hyperpigmentation as a result of MSH secretion and compression of parapituitary structures) in 20% of patients. Pituitary radiotherapy and adrenalectomy are highly effective in children.
Glycopeptide (TSH, FSH and LH)-secreting tumours
TSH-secreting pituitary adenomas are extremely rare, aggressive tumours whose first-line treatment is surgical. The diagnosis is confirmed by the presence of hyperthyroidism in association with elevated plasma concentrations of TSH. The diagnosis may be missed by the unwary if it is not appreciated that TSH concentrations within the normal range are inappropriately high in the presence of consistently elevated concentrations of circulating thyroid hormones.
Gonadotroph adenomas present usually as inactive adenomas but may present rarely with premature puberty or the resumption of menstrual bleeding in post-menopausal women. Elevated prolactin concentrations may occur in <80% of endocrinologically inactive adenomas because of compression of the pituitary stalk. Macroadenomas may present with compression of sella structures and secondary hypopituitarism. Again, first-line therapy is surgical.
Non-functioning tumours
Approximately 25% of pituitary tumours are non-functioning. They usually present with visual disturbance secondary to chiasmal compression or headache caused by increased intracranial pressure. Ophthalmological assessment is mandatory for all tumours extending into the suprasellar area. If there are no symptoms or signs of pressure effects, it is acceptable simply to review patients on a regular basis using measurements of visual fields and MRI. Increase in tumour size, deterioration in visual fields or onset of other symptoms requires surgical decompression, usually in combination with postoperative radiotherapy. Rarely, non-functioning tumours may present with panhypopituitarism or pituitary apoplexy. The latter is associated with abrupt onset of severe headache and may mimic subarachnoid haemorrhage. Hormone concentrations are usually normal, with the exception of raised prolactin concentrations resulting from the stalk effect. Cortisol status should be checked if there are signs of hypopituitarism.
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Preoperative assessment |
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Acromegaly
Growth hormone hypersecretion affects not only the extremities but also the soft tissues of the mouth, tongue and laryngeal cartilages. The anatomical changes that may result include prognathism and macroglossia. Thickening of the pharyngeal and laryngeal soft tissues and vocal cords, reduction in the size of the laryngeal aperture, hypertrophy of the periepiglottic folds and recurrent laryngeal nerve palsy also occur.19 About one-quarter of acromegalic patients have an enlarged thyroid, which may compress the trachea.53 Acromegaly is recognized as one of the causes of difficulty in airway management and tracheal intubation.7 9 28 34 55 60 72 Careful airway assessment using conventional criteria is essential and preoperative evaluation with indirect laryngoscopy has been recommended.34 54 Sleep apnoea is a rare complicating factor of acromegaly but is associated with a high risk of perioperative airway compromise.9 62 Upper airway obstruction is the major cause of sleep apnoea in acromegaly25 but central depression may also contribute.61 It is not surprising, therefore, that the risk of death from respiratory failure is threefold greater in acromegaly.54 81 A history of loud snoring and daytime hypersomnolence should alert the anaesthetist to the possibility of sleep apnoea. The response to resection of the underlying pituitary tumour is unclear,62 but vocal cord function reverts towards normal within 10 days of successful surgery.79
Hypertension occurs in 30% of patients with acromegaly but usually responds to therapy. Myocardial hypertrophy and interstitial fibrosis are common in acromegalic patients and may be associated with reduced left ventricular function.67 The impairment in left ventricular function may persist in those successfully treated by surgery if the disease has been longstanding. Left ventricular size often returns to near-normal after surgery and the failure of an associated return of normal function may reflect persistence of interstitial fibrosis.67 Glucose intolerance is encountered frequently and overt diabetes occurs in 25% of acromegalic patients.
Cushings syndrome
Increased reninangiotensin activity and elevated blood volume result in hypertension in 85% of these patients. This can be difficult to bring under control. ECG abnormalities (high voltage QRS complexes and inverted T waves) are common but revert to normal after curative pituitary surgery.74 Left ventricular hypertrophy and asymmetric septal hypertrophy are observed frequently in patients with Cushings syndrome. The aetiology of this hypertrophy is unknown but, because it occurs more commonly than in essential and other secondary hypertension syndromes, it is likely that excessive plasma cortisol is a contributing factor.74 Curative surgery results in improvement in left ventricular function in the majority of cases. Sleep apnoea is also a common finding in Cushings syndrome. In a recent investigation of Cushings patients using polysomnography, mild sleep apnoea was observed in 32% and severe sleep apnoea in 18%.68 Glucose intolerance or frank diabetes occurs in 60% of patients and is related to reduced insulin secretion and non-insulin-mediated glucose disposal in the presence of elevated insulin concentrations. Renal calculi are a common association. Obesity and gastroesophageal reflux are frequently encountered and prescription of H2 antagonists may be appropriate. High concentrations of glucocorticoids are immunosupressive and the presence of coexisting infection should be considered. Finally, the fragile skin and easy bruising typically found in these patients can make intravenous access problematic.
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Surgical approach |
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Anaesthetic management |
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Hormone replacement
Preoperative hormone replacement therapy should be continued into the operative period. In general, hydrocortisone 100 mg should be administered at induction of anaesthesia in all patients undergoing pituitary surgery; however, individual units with wide experience will have developed local protocols for perioperative hormone replacement, particularly for complex conditions such as Cushings disease.
Airway management
Careful preoperative assessment alerts the anaesthetist to the possibility of difficulties with airway management and tracheal intubation. Ventilation with a bag and mask is generally straightforward in acromegalic patients although an oral airway may be required.27 Four grades of airway involvement have been described in acromegaly: grade 1, no significant involvement; grade 2, nasal and pharyngeal mucosa hypertrophy but normal cords and glottis; grade 3, glottic involvement including glottic stenosis or vocal cord paresis; and grade 4, combination of grades 2 and 3, i.e. glottic and soft tissue abnormalities.72 Tracheostomy has been recommended for grades 3 and 4 but others have suggested that fibreoptic laryngoscopy is a safe alternative.60 However, difficulty with fibreoptic intubation in acromegalic patients has recently been described.27 In one patient in this study, the larynx could not be viewed with either a Macintosh laryngoscope or a fibreoptic laryngoscope but the trachea was intubated blindly with the help of an introducer. In the authors experience of >150 pituitary operations per annum at the National Hospital, airway management and tracheal intubation proceed uneventfully in the majority of patients if large face masks and long-bladed laryngoscopes are used. However, fibreoptic intubation should be considered in patients in whom difficult airway management is predicted.46 The intubating laryngeal mask airway has also been used successfully in a patient with acromegaly.69 Equipment for tracheostomy should be available if airway changes are advanced.72
Following intubation, the mouth and posterior pharynx should be packed before surgery begins. This will not only prevent bleeding into the glottic region during surgery, but also entry of blood and secretions into the stomach which may precipitate postoperative vomiting. The tracheal tube must be positioned to allow the neurosurgeon access to the chosen incision site.
Preparation of the nasal mucosa
Most surgeons prefer to introduce a vascoconstricting agent into each nostril before transsphenoidal surgery. Traditionally, mixtures of cocaine and epinephrine have been used.47 Although the addition of epinephrine limits systemic absorption,5 the use of cocaine-containing preparations continues to be associated with a risk of arrhythmias and myocardial infarction.16 57 Xylometazoline, a sympathomimetic amine acting at alpha adrenoreceptors, may be a safer alternative. It produces rapid and prolonged vasoconstriction lasting up to 8 h and, when combined with lidocaine, its effects are equivalent to those of cocaine.10
Lumbar drain
Some surgeons request insertion of a lumbar drain in patients with significant suprasellar tumour extension. This has two uses. Introduction of 10 ml aliquots of 0.9% saline will, during transsphenoidal surgery, produce prolapse of the suprasellar portion of the tumour into the operative field (see above). In addition, should the dura be breached during the procedure, the catheter can be left in place postoperatively to act as a CSF drain in an attempt to control any leak of CSF.63
Position
Transsphenoidal surgery is carried out with the patient supine with a moderate degree of head-up tilt. The head may be turned slightly to the side to facilitate surgical access. The surgeon may stand at the top of the table behind the head, or to the right or left. The tracheal tube and anaesthetic circuit should be placed away from the surgical field. As frequent radiography is required, the C-arm of the image intensifier is usually left in position throughout surgery. All theatre personnel should wear appropriate protection. Transcranial surgery to the pituitary area is also performed with the patient in the supine position. Subfrontal surgery is carried out with the head in the midline position but pterional approaches require the head to be turned. Care should be taken to ensure that the neck veins are not obstructed.
Maintenance of anaesthesia
Any anaesthetic technique suitable for intracranial procedures is acceptable, but the presence of increased intracranial pressure requires special attention. Choice of anaesthetic technique is usually determined by personal preference since attention to detail and a meticulous anaesthetic technique are generally more important than the use of specific drugs.36 The merits of inhalational and total intravenous techniques during neuroanaesthesia have been considered elsewhere.65 76 78 However, neither is superior to the other under most circumstances.75 In the presence of raised intracranial pressure, total intravenous anaesthesia and the avoidance of nitrous oxide has been recommended.44 76 Whichever technique is chosen, it is important that short-acting agents are used to allow rapid recovery at the end of surgery. Drugs such as propofol65 and sevoflurane70 clearly fall into this category. During transsphenoidal surgery, ventilation to normocapnia should be employed. Excessive hyperventilation will result in loss of brain bulk and make any suprasellar extension of the tumour less accessible from below. There are periods of intense stimulation during transsphenoidal access to the pituitary fossa. Short-acting opioids should be titrated against blood pressure. The ultra-short-acting opioid, remifentanil, allows maintenance of stable conditions in neurosurgical patients26 77 and is a useful adjunct during transsphenoidal surgery. Its short context-sensitive half-time ensures rapid offset of action when the infusion is discontinued. Although this will allow rapid emergence from anaesthesia, it is essential that longer-acting opioids are administered before the end of surgery so that patients do not awaken in pain. The administration of intravenous morphine or intramuscular codeine 2030 min before the end of surgery has been recommended.36 Bilateral maxillary nerve block with local anaesthesia has also been described as a method of preventing the hypertensive response to transsphenoidal surgery during general anaesthesia.13
Monitoring
Monitoring during pituitary surgery will include ECG, SpO2, endtidal carbon dioxide and direct arterial blood pressure. Co-morbidities, especially in Cushings patients, may require additional invasive cardiovascular monitoring. If cavernous sinus invasion is suspected, and the patient is positioned in a steep head-up tilt, monitoring for the possibility of venous air embolus should be considered.56 Visual evoked potential (VEP) recording has been recommended for tumour surgery in the region of the visual pathways. Although VEP recording is widely used in diagnosis, its use in the operating room has been limited by the high incidence of false-positive and false-negative results.21 Furthermore, the exquisite sensitivity of VEPs to anaesthetic agents has led some to suggest that, during anaesthesia, the waveforms are too unstable to be of much practical use.11 In a recent study, peroperative VEP monitoring resulted in greater improvement in field defects after transsphenoidal pituitary surgery although postoperative improvement in visual acuity was not affected.12
Prophylactic antibiotics
There remains debate over this issue. Although some neurosurgeons do not use prophylaxis and claim no problems, most units in the UK have adopted a consensus policy.1 This involves the administration of a cephalosporin (e.g. cefuroxime 1.5 g) at induction of anaesthesia and every 3 h thereafter during surgery. No further doses are given in the postoperative period, to minimize the development of resistant organisms.
Operative complications
Complications during transsphenoidal surgery are rare. Pituitary tumours are not usually vascular and the slight venous ooze that inevitably occurs can be controlled easily by gentle pressure. Other, more serious complications, occur if the neurosurgeon loses the anatomical landmarks of the fossa during transsphenoidal surgery. Deviation laterally may result in carotid damage, which is usually controllable by packing. Because of the risk of development of a false aneurysm in the postoperative period, carotid angiography should be performed. If an aneurysm is confirmed, it should be treated by endovascular radiological techniques or by clipping to prevent later rupture. If the surgeon misses the fossa altogether, damage to the pons may occur. This has serious consequences. The risk of these complications is minimized by frequent radiographic confirmation of the position during transsphenoidal surgery.
Transcranial pituitary surgery carries similar risks to other intracranial procedures. Frontal lobe ischaemic damage because of prolonged traction can be minimized by careful placement and intermittent release of retractors. Trauma to the carotid artery or optic chiasm can also occur. The incidence of postoperative seizures is higher after subfrontal surgery than after other approaches. Some recommend the use of prophylactic anticonvulsant therapy58 but others find the evidence unconvincing.22 Anosmia may also occur because of damage to the olfactory tract.
Emergence from anaesthesia
Smooth and rapid emergence from anaesthesia following neurosurgery is essential to allow early neurological assessment and maintenance of stable respiratory and cardiovascular variables.6 This is facilitated by the use of short-acting agents for maintenance of anaesthesia. At the end of transsphenoidal surgery, extubation is carried out after return of spontaneous ventilation, pharyngeal suction under direct vision, removal of the throat pack and return of laryngeal reflexes. Smooth emergence can be facilitated by placing the patient in a semi-seated position and ensuring that there is a response to verbal commands before extubation. Care should be taken to ensure that nasal packs or stents, put in place at the end of surgery, do not become dislodged during extubation.
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Postoperative care |
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Airway management
Maintenance of a clear airway can be difficult and requires careful attention. The presence of blood in the nasopharynx and oropharynx, nasal packs and the predisposition of acromegalic patients to airway obstruction all tend to compromise airway patency. All patients must, therefore, be closely observed after transsphenoidal surgery until fully awake. Airway management is particularly important in acromegalic patients, especially in those with a history of sleep apnoea. Such patients should be nursed in a high-dependency environment through the first postoperative night when hypoventilation and respiratory obstruction may occur. Usual treatment options such as nasal CPAP cannot be applied after transsphenoidal surgery. Acute pulmonary oedema secondary to airway obstruction has been reported in this patient group.23
Postoperative analgesia
Transsphenoidal surgery usually causes only moderate postoperative pain but the feeling of nasal congestion from the presence of nasal packs is frequently distressing to patients. Craniotomy is more painful and stronger analgesia is required.73 Codeine phosphate has been the mainstay of postoperative analgesia in neurosurgical patients for many years because it was considered to be relatively free from unwanted side-effects such as sedation, respiratory depression and pupillary changes. However, it is likely that this merely reflects underdosage and it is clear that pain after craniotomy can be more severe than previously appreciated.73 Attitudes to the management of postoperative pain in neurosurgical patients are changing. A recent double-blind study confirmed that intramuscular morphine is not associated with more side-effects after craniotomy and has a longer duration of action than codeine.24 Intravenous morphine administered via a PCA has been used successfully in neurosurgical patients.73
Hormone replacement
It is safest to assume that all patients will require cortisol replacement in the short term. Replacement should be tailed down to maintenance levels within a few days. A standard regimen recommends hydrocortisone 50 mg bd on the first postoperative day, 25 mg bd on the second, reducing to 20 mg in the morning and 10 mg in the evening by the third day.63 Patients usually leave hospital on this dose although it is higher than the normal replacement of 15 mg in the morning and 5 mg in the evening. The evening dose should be given between 17.00 and 18.00 h. Patients with prolactin-secreting microadenomas can be weaned off hydrocortisone safely within the first few days without risk if 20% of the pituitary gland has been left behind at surgery.63 In Cushings disease, normal corticotrophs are heavily suppressed and replacement will be required for many weeks or months. Preoperative replacement of other hormones should be continued into the postoperative period, until review by an endocrinologist. Postoperative management by a multidisciplinary team using locally developed protocols is crucial to successful endocrine management.
Postoperative hormone complications
These are rare but require careful and timely treatment.
Diabetes insipidus
This usually develops within the first 24 h and occurs when >80% of neurones synthesizing vasopressin are destroyed or become temporarily non-functional.66 It should be suspected if the patient is producing >1 litre of dilute urine in 12 h, associated with a plasma Na+ concentration of >143 mmol litre1. Urine output and specific gravity should be measured routinely after pituitary surgery. If problems develop, regular measurement of plasma and urinary osmolality is required.18 Modest polyuria in the early postoperative period may be related to delayed excretion of the fluid given during surgery or corticosteroid-induced hyperglycaemia. Patients may feel thirsty after transsphenoidal surgery, but this can be related to mouth breathing because of nasal packs rather than to diabetes insipidus. It is, therefore, essential that the diagnosis of diabetes insipidus is confirmed biochemically before treatment is instituted.18 A combination of increased plasma osmolality (>295 mosmol kg1), hypotonic urine (<300 mosmol kg1) and a high urine output (>2 ml kg1 h1) are the criteria on which the diagnosis should be based. Diabetes insipidus is easily treated with desmopressin acetate (DDAVP).18 However, if the patient is awake and has a normal thirst mechanism, it is safest to allow free access to fluid rather than attempt overzealous i.v. fluid and DDAVP replacement. Over-enthusiastic use of DDAVP may lead to hyponatraemia with its attendant problems of confusion, seizures and coma. Most borderline cases of diabetes insipidus resolve spontaneously over a few days, as posterior lobe function recovers. Comatose patients, those with no thirst response and the minority in whom urine volumes are excessively large are at particular risk, both from under-hydration as a consequence of the diabetes insipidus or of over-hydration as a consequence of therapy. Careful treatment with DDAVP will usually be required under such circumstances. The recommended iv/im dose of DDAVP is 0.1 µg repeated as required. In the acute phase, a smaller dose of 0.04 µg i.v. provides an adequate response with a shorter duration of action. An oral preparation and a metered dose nasal spray are also available. Plasma Na+ concentration and osmolality should be closely monitored until normal water balance has been re-established. Long-term DDAVP therapy is required in only a minority of cases.
Hyponatraemia
The commonest cause of hyponatraemia after pituitary surgery is over-enthusiastic use of DDAVP. Rarely, it may occur because of the syndrome of inappropriate ADH secretion (SIADH) caused by non-specific release of ADH from degenerating posterior pituitary neurosecretory terminals.33 This results in water retention and secondary loss of urinary Na+. It is usually transitory and rarely lasts for >710 days. It is managed by fluid restriction which should be carefully monitored by regular measurement of plasma electrolytes. Rarely, hyponatraemia after intracranial neurosurgery may be associated not only with natiuresis but also with a tendency to diuresis, leading to a significant contraction of circulating and extracellular volumes. This phenomenon is known as cerebral salt wasting syndrome (CSW) and may be difficult to differentiate from SIADH. However, it is crucial that the diagnosis is made correctly because the treatment regimens of the two conditions are diametrically opposed.42 In SIADH the problem is one of extracellular volume expansion caused by water retention, and the best approach is to limit water intake to 5001000 ml day1 depending upon the plasma Na+ concentration. In CSW, fluid restriction will not correct the hyponatraemia and will, in fact, be harmful because it will further reduce intravascular volume. Hypertonic saline is used to correct the hyponatraemia of CSW. Correction of low Na+ concentrations should always take place over 2448 h, at a rate to increase plasma Na+ concentration by <1 mmol h1. Too rapid correction may result in central pontine myelinolysis.2
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Acknowledgement |
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References |
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