Imperial College School of Medicine, Hammersmith Hospital, London W12 0HS, UK
Keywords: hormones, glucagon; hormones, insulin; hormones, somatostatin; gastrointestinal tract; cancer; surgery
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Introduction |
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The heterogeneous hormones produced by the gastrointestinal tract control digestion. They are secreted from cells that line the lumen of the gut, that is, in the mucosa as well as in endocrine organs such as the pancreas. The major secretory and motor functions of the peptide hormones of the gut are listed in Table 1. Gut hormones also regulate cell growth. A few peptides, such as substance P and pancreatic polypeptide, are recognized as gut hormones but their function is uncertain. However, they can be secreted by endocrine tumour cells and may be responsible for some of their systemic manifestations.
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The anaesthetic management of patients with abnormalities of gut hormone function induced by such tumours broadly requires an assessment of endocrine dysfunction (which may complicate anaesthesia and drug therapies), preferably with a standardized battery of tests for gut hormones. The spread of tumour growth by direct invasion or metastases also needs to be assessed in order to quantify organ dysfunction. For example, pancreatic endocrine tumours secrete vasoactive substances, leading to haemodynamic instability, and block the biliary system, resulting in obstructive jaundice. Recent developments in imaging technologies, such as the placement of biliary stents, hepatic artery embolization, radioisotopes of somatostatin for precise imaging of tumour location by scintigraphy and medical therapies to restrict tumour growth with targeted chemotherapy, enable improvements in organ function and symptomatic control to be achieved before anaesthesia and allows surgical targets to be identified in advance. Tumours limited to one part of the gastrointestinal tract can potentially be completely removed by surgery and even palliative surgery can provide an improved quality of life by reducing hormone secretion, thus potentiating the use of somatostatin analogues. If the tumour shows no somatostatin receptors on imaging, histological confirmation of this can limit the side-effects of somatostatin analogue therapies, which would otherwise be administered. However, not all patients have these types of tumours diagnosed before surgery. Anaesthetists should therefore be alert for the rare causes of bronchospasm, such as carcinoid tumours.
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Multiple endocrine neoplasia |
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Pancreatic endocrine tumours |
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Tumours of the pancreatic islet cells secrete one or more hormones and are termed apudomas. These hormones can be ones that are normally secreted by the pancreas, or they can be non-pancreatic hormones, such as adrenocorticotrophic hormone. Approximately 75% of apudomas are insulinomas (incidence of one to four cases per million people). About 20% of apudoma patients will have MEN1 and the pancreatic endocrine tumours listed in Table 3 in order of frequency, with, in addition, tumours of the parathyroid, pituitary and rarely adrenal cortex.
Non-functioning neuroendocrine tumours of the pancreas may be silent because they produce hormones without specific clinical signs or because they produce peptides in insignificant amounts, or none at all. They are large in size and vascular.5 Resection, even if incomplete, is often associated with prolonged survival and, since these tumours respond poorly to chemotherapy, surgery is the treatment of choice.
Strategies to control tumour growth are required if the tumour is growing quickly or if symptoms are severe. The number of ways of treating such tumours has increased rapidly over the past decade. Tumour debulking makes symptoms easier to manage and allows further treatment to reduce tumour mass by chemotherapy. Other therapies include hepatic artery embolization, treatment with somatostatin analogues, IFN, combination therapies with somatostatin and IFN
, or occasionally systemic chemotherapy or liver transplantation. The rarity and variety of endocrine syndromes have necessitated the development of multicentre clinical trials in tertiary referral centres to support evidence-based treatments.
Gastrinoma
ZollingerEllison syndrome was described as intractable, painful, peptic ulcer disease that recurs after surgery unless total gastrectomy is performed. Duodenal, pancreatic or rarely ovarian cystadenocarcinoma cells releasing gastrin cause the clinical syndrome. In the pancreas it is the islet cells which produce gastrin. Diarrhoea and steatorrhoea leading to weight loss often occur as a result of excess acid production, which inactivates pancreatic enzymes. Less frequently, dysphagia presents secondary to oesophagitis. A concentration of gastrin of >100 pg ml1 in a fasting basal state is diagnostic of a gastrinoma. However, anything that decreases gastric acid production can lead to high circulating concentrations of gastrin; this includes drug treatment with H2 receptor antagonists (such as cimetidine) and hydrogen ion (proton) pump blockers (such as omeprazole), as well as diseases such as pernicious anaemia. Thus, to prevent confusion, this type of drug treatment should be withdrawn before diagnostic tests for gastrinoma. If there is any uncertainty, provocative tests with calcium or secretin may be required.
Although medical treatment can control acid secretion, tumour excision for sporadic tumours has a high overall survival rate.34 The role of surgery in ZollingerEllison syndrome associated with MEN1 is less clear. Measurement of serum calcium concentrations and plasma parathyroid hormone or pituitary hormone studies may confirm the diagnosis of MEN1. In the future, specific genetic screening may be required because of the difference in prognosis between sporadic and MEN1 gastrinomas.
Preparation for surgery requires titration of the dose of proton-pump inhibitors, such as omeprazole or lansoprazole, to achieve normal basal gastric acid secretion. Oral medications are preferred rather than somatostatin, which has to be administered subcutaneously. Antacid prophylaxis with proton-pump inhibitors and H2 receptor antagonists should be maintained until surgery. The possibility of anaemia from bleeding gastric ulceration must be investigated. A full coagulation screen and liver function tests are required because alterations in fat absorption may influence clotting factors and hepatic function may be disturbed by liver metastases. Immediately before and after operation, intravenous ranitidine is useful to prevent gastric acid hypersecretion from the hypertrophied acid-producing gastric mucosa. A nasogastric tube will be required perioperatively; it should be placed and its position confirmed at induction of anaesthesia. At exploratory laparotomy, further localization of pancreatic or duodenal gastrinomas may be required using palpation, transillumination, ultrasound and endoscopy. These processes may increase the surgical exposure required to mobilize these structures and hence may increase the duration of surgery. Anaesthetic planning should include preparations to reduce heat loss during prolonged surgery.
Insulinoma
Tumours of the ß cells of the pancreas secrete insulin; patients with such tumours present with episodic symptoms of fasting hypoglycaemia, such as dizziness, blurred vision, confusion, irritability, tremors and occasionally coma. Compensatory sympathetic mechanisms lead to sweating and tachycardia. The differential diagnosis is broad; the causes of hypoglycaemia listed in Table 4 should be excluded, together with other aetiologies such as cerebrovascular disorders. About 8% of insulinomas are associated with MEN1. The diagnosis is made by Whipples triad:49 (i) symptoms of hypoglycaemia; (ii) a low plasma glucose; and (iii) relief of symptoms when glucose is administered and normal glucose levels restored. The diagnosis is made by a fasting plasma glucose of <2.2 mmol litre1, increased insulin (6 µunits ml1; >40 pmol litre1), increased C-peptide (
0.2 nmol ml1) and an absence of sulphonylurea in the plasma.11 25 The high insulin and C-peptide concentrations confirm the diagnosis. These two compounds are formed in equimolar amounts by enzymatic cleavage of proinsulin. Measurable C-peptide therefore indicates an endogenous source of insulin, in contrast with the use of a pharmaceutical preparation of insulin that may be used to mimic the symptoms of an insulinoma.
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Diazoxide is a non-diuretic benzothiazide which inhibits the release of insulin from secretory granules of ß cells. It may be a therapeutic option in preoperative preparation. Its use is usually restricted to situations where surgery has failed because it may not block secretion from abnormal (i.e. non-ß) cells. It can also suppress the release of glucagon and exacerbate symptoms. Besides its unpredictable efficacy, diazoxide also has serious dose-dependent side-effects, causing oedema, sodium retention, hypotension, cardiac disturbances, weight gain and hirsutism. Verapamil, a calcium channel blocker, has been successfully used in long-term therapy when surgery was refused.45
Although most tumours are enucleated, the head or tail of the pancreas has to be exposed. Resection may sometimes be required, especially with MEN1, where the head of the pancreas often needs to be removed. The spleen is preserved whenever possible but splenectomy may be unavoidable. Planning for this will include vaccination against meningococcus and Haemophilus influenzae with Pneumovax and having blood cross-matched for transfusion. Prophylactic therapies include antibiotics and possibly somatostatin. In one of the largest studies of insulinomas, although no direct deaths were reported, complications of surgery included acute myocardial infarction, congestive cardiac failure and paroxysmal atrial tachycardia.13 Assessment of cardiac function preoperatively and monitoring and maintenance of cardiac stability perioperatively are prerequisites for anaesthetic care.
It is essential that close monitoring of glucose intake and blood glucose is started the evening before surgery and continued throughout the perioperative period. During this period of starvation and at operation when the tumour is handled, glucose 50% solution should be available. Intravenous glucose with potassium should be infused and blood glucose, electrolytes and fluid input and output monitored at least hourly in order to avoid hypoglycaemia, water load and hyponatraemia. On tumour excision, a progressive increase in blood glucose has been described within minutes. Repeated measures of blood glucose and maintenance of normal values are more important than the observation of rebound hyperglycaemia which used to be a marker of complete tumour resection.31
The choice of anaesthetic agents for removal of an insulinoma has focused on their effects on blood glucose. Methoxyflurane has been used4 because it tends to increase blood glucose concentrations. More recently, sevoflurane has been recommended because it is considered to suppress the spontaneous release of insulin.29 However, the metabolic profile of isoflurane should be considered an advantage, particularly if liver blood flow or liver function is disturbed. Another technique that has been reported not to interfere with blood glucose control is general anaesthesia, using propofol, combined with epidural analgesia.40
Postoperative complications that may alter blood glucose homeostasis include diabetes mellitus as a result of pancreatic insufficiency, acute pancreatitis and intra-abdominal abscesses. Pancreatic fistula is a serious complication because it can lead to electrolyte imbalance and the need for further surgery.
Glucagonomas
The cells of the pancreas release glucagon. The two clinical diagnostic features of glucagonomas are an erythematous rash and diabetes mellitus. The rash, presenting in the groin and perineum and then migrating to the distal extremities, is known as necrotizing migratory erythema; it may be treated with zinc ointments. Stimulation of hepatic glycogenolysis and gluconeogenesis results in the metabolic production of glucose and symptoms of diabetes mellitus. However, ketoacidosis is rare because insulin concentrations are also increased. Tumours are associated with weight loss, glossitis, stomatitis, anaemia (probably from bone marrow suppression), reduced blood amino acid concentrations and diarrhoea. If the cachexia is severe and the patient is malnourished, nutritional support and supplements for several weeks before surgery should be given, otherwise infection and poor wound healing are likely to occur postoperatively.
A blood glucagon concentration of 50 pg ml1 and a demonstrable tumour are diagnostic of glucagonoma. The increase in glucagon should be differentiated from the increases measured in prolonged fasting or renal and hepatic failure. The tumour may be primary, in an elderly population, or associated with other syndromes such as ZollingerEllison and MEN1 and present in younger patients. The majority of patients have liver metastases at presentation. Treatment is by debulking and somatostatin analogues, which give rapid relief at first but increased dosage may be necessary later. There is an increased incidence of venous thromboses in this disease and prophylactic antithrombotic therapy is appropriate. Once the tumour is excised, symptomatic relief is achieved.
Somatostatinomas
Tumours of the cells may release somatostatin and are often misdiagnosed as adenocarcinomas. Patients with such tumours present commonly with obstructive biliary disease because many pancreatic tumours are large. Obstructive jaundice should be relieved by stenting before surgery so that complications, such as coagulopathies and postoperative renal failure, are avoided. Other symptoms are usually mild. These include diabetes, from a reduction in insulin release, steatorrhoea from decreased pancreatic enzyme secretion and gallstones resulting from stasis within the gall bladder. Somatostatinomas can present in association with phaeochromocytomas and von Recklinghausens disease in the MEN2 syndrome.
VIPoma
VernerMorrison or WDHA (watery diarrhoea, hypokalaemia, achlorhydria) syndrome is characterized by profuse watery diarrhoea, intestinal ileus, abdominal distension, confusion, drowsiness, hypokalaemia, achlorhydria, hypomagnesaemia, metabolic alkalosis and tetany (Table 5). It is very rare. The mediator is vasoactive intestinal peptide (VIP), which should be measured accurately in order to establish the diagnosis. VIP inhibits gastrin release. Pancreatic VIPomas are commonly located in the body and tail of the organ while extra-pancreatic VIPomas occur in the autonomic nervous system. The rate of malignancy warrants resection because 40% of VIPomas are benign and the others are slow growing, commonly with liver metastases. The tumours are vascular and are usually localized on routine imaging. Care should be taken when injecting contrast media because VIP may be released. Medical treatment includes somatostatin analogues, which inhibit both VIP release and the secretion of water and electrolytes from the gastrointestinal tract.
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Carcinoid tumours |
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Carcinoid cells secrete a variety of amine and peptide hormones, which may be identified biochemically using a standard battery of tests including high-pressure liquid chromatography for 5-hydroxyindole acetic acid (5-HIAA) and radioimmunoassay for glycogen, VIP, calcitonin, gastrin, pancreatic peptide and insulin. Bronchial carcinoids can produce an excess of adrenocorticotrophic hormone and growth hormone-releasing factor and may present as Cushings syndrome or acromegaly. The secretory pattern of gut tumours can change over time; an anaesthetist should be aware of this preoperatively in order to interpret investigations. Tumour location is identified by non-specific investigations such as computerized tomography, magnetic resonance and ultrasound imaging; and somatostatin receptor scintigraphy or positron emission tomography with 11C-labelled 5-hydroxytryptophan (the precursor of serotonin) are used for more specific localization. Symptomatic tumours are treated with surgery and drug therapy. Further diagnostic tests with histology and immunocytochemistry can determine the peptide profile of the tumour.
Gastric carcinoid tumours are divided into various types, which have different prognoses. Benign tumours arise from mucosal cells that synthesize and store histamine. They occur as multiple tumours in the fundus or body of the stomach and have been associated with 29% of patients with pernicious anaemia, and atrophic gastritis, situations in which gastrin concentrations are high. Tumours associated with MEN1 have a higher rate of malignancy. Those composed of a mixture of cell types are solitary and metastasize. They produce various hormones including neuroendocrine and exocrine pancreatic secretions.
Small bowel carcinoid tumours grow slowly. They can present with bowel obstruction from mesenteric fibrotic stricture, carcinoid syndrome, gastrointestinal bleeding, diarrhoea and weight loss. Arterial or venous obstruction by the tumour can lead to abdominal pain (angina) precipitated by food. Since carcinoid tumours are the commonest small bowel neoplasms, any small bowel obstruction should alert an anaesthetist to consider this diagnosis. The anaesthetist must prepare for emergency anaesthesia with precautions to prevent aspiration of stomach contents. During surgery the tumour site should be observed (for bleeding or manipulations) and cardiovascular instability treated with therapies, such as octreotide. Gross pathology may reveal a yellow nodule and frozen section histology may confirm the diagnosis.
Bronchial carcinoid tumours can present as a mass, atelectasis, unilateral lung hyperinflation (from a ball-valve action) and with filling defects in the airways.32 When major airways are affected, flow-volume and ventilation-perfusion abnormalities can be detected. At thoracotomy, surgery may be limited to a bronchial wedge resection or extend to a lobectomy, especially if suppuration has proceeded distal to the tumour or to a tracheal resection for tracheal obstruction. Airway maintenance during anaesthesia for these procedures can be a challenge.21
Carcinoid syndrome occurs secondary to the systemic release of secretions either as a result of metastasis in the liver or from the lung. Bronchial carcinoids can liberate substances directly into the circulation. It has been postulated23 that when a carcinoid tumour releases active substances into the portal vein, the liver destroys them until either liver function deteriorates, or shunts between the portal and hepatic veins, or metastases developed. Thus general release of secretory products from the gastrointestinal tract is usually prevented until the portal system is bypassed. Substances released by carcinoid tumours include: serotonin (5-hydroxytryptamine), which is synthesized from 5-hydroxytryptophan and metabolized to 5-HIAA, which can be measured in urine; histamine, which is metabolized and excreted in the urine as tele-methylimidazoleacetic acid; tachykinins, such as substance P, neurokinin A and neuropeptide K, which causes flush and may be an early indicator of carcinoid disease;33 bradykinins; and prostaglandins. Table 6 lists these mediators, their clinical effects and management.28
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Common features of carcinoid syndrome are diarrhoea, from gastrointestinal hypermotility, and flushing, but neither usually requires resuscitative treatment. Diarrhoea may persist after surgery for resection of the terminal ileum because of a loss of bile acids. Thus when the patient is assessed preoperatively for any complications of surgery, this secondary complication should be considered and long-term electrolyte abnormalities sought.
It is the respiratory and cardiovascular effects of carcinoid syndrome with which an anaesthetist should be familiar because of their severity. Bronchoconstriction, which presents as wheezing and paroxysmal coughing, can be life-threatening and requires prophylactic treatment. Dyspnoea may be present but an underlying cardiac problem should be considered in addition to bronchoconstriction. Right ventricular failure, resulting from endocardial fibrosis, is a major cause of death in carcinoid syndrome. It is slow in onset and although cardiac oedema is reported, underdiagnosis occurs in clinical practice.23 Echocardiography can confirm the presence of right ventricular dysfunction and tricuspid and pulmonary valve lesions. These abnormalities are thought to result from the episodic circulatory crises associated with liberation of active substances from the tumour. 5-Hydroxytryptamine increases pulmonary artery pressure and intestinal peristalsis together with bronchoconstriction.47 Intravenous substance P in humans causes flushing, tachycardia and hypotension9 10 but is not considered to be the main active chemical responsible for carcinoid syndrome. Endocardial fibroelastosis has been linked to growth factors.48 Such activity is part of the function of gut hormones. Sclerosis and partial fusion of cusps is the pathological result. It leads to tricuspid and pulmonary valve incompetence and stenosis and may even recur in bioprosthetic valves39 used for valve replacement. Rarely, ascites and pleural effusion have been described. When considering anaesthetic monitoring, such valve damage may predispose to endocarditis, so pulmonary artery catheter insertion may be contraindicated.
Left-sided heart disease has also been described.19 Carcinoid syndrome can therefore present as a critical crisis in addition to structural heart disease, with bronchoconstriction, tachycardia and hypotension or hypertension leading to cerebral hypoxia with confusion and coma. These acute cardiorespiratory events are most common during laparotomies and during or after embolization of liver metastases; in their differential diagnosis, acute anaphylaxis should be considered.1 Unfortunately, there is no predictor of cardiovascular instability, such as peptide concentrations, so vigilance and early intervention are advised.
Therapeutic management, as shown in Table 6, targets symptoms or more specific mechanisms. Methylsergide in the past was used as a non-selective vasoactive agent, but it can cause fibrotic heart lesions. Codeine phosphate can be used to treat the diarrhoea, but fluid, electrolyte and nutritional deficiencies require replacement. Antibrady kinin agents, such as aprotonin, used to be administered acutely during carcinoid tumour surgery. In vitro, aprotinin effectively inhibits kallikrein22 26 but clinically it is not so effective.28 46 Antiserotonin antagonists, including non-specific drugs, such as cyproheptadine41 and parachlorophenylalanine,35 and more specific antagonists, such as ketanserin (a 5HT2 antagonist15 16 46) and ondansetron (a 5HT3 antagonist), have been used to relieve symptoms.51 However, the approach based on antagonizing released hormones has been largely superseded by a preference to inhibit hormone release.38 Steroids have been used successfully to block substance release but more specific drugs based on somatostatin have been developed. Steroids may be indicated in asthmatic patients.46 Generally, it is only when these somatostatin analogues fail to reduce symptoms adequately that antagonists are used in medical treatment. However, H1 and H2 receptor antagonists may be considered for preoperative prophylaxis and during surgery; where there is the potential for release of large quantities of hormones on tumour handling, judicious use of hormone antagonists should be considered.
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Principles of management of gastrointestinal endocrine tumours |
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Somatostatin
The development of synthetic somatostatin analogues, such as octreotide (Table 7), that are long-acting and inhibit hormone release rather than block their action has revolutionized anaesthetic management, particularly for carcinoid, glucagonoma and VIPoma tumours. Somatostatin binds to cell surface receptors, inhibits adenylyl cyclase and enhances potassium conductance, thus decreasing intracellular calcium ion availability and cellular secretion.44 Somatostatin analogues do not bind to all somatostatin receptor subtypes; this limits their diagnostic and therapeutic use. In addition, long-term efficiency may be reduced by receptor down-regulation. Octreotide has to be given parenterally, for example as 100 µg subcutaneously every 8 h, or 100 µg h1 during surgery. In an emergency a single dose of 50 µg i.v. before surgical manipulation may suffice if no preoperative prophylaxis has been given. Another beneficial preoperative effect of somatostatin is an indirect anti-angiogenesis activity that can reduce the size of metastases. The success of such specific therapies has enabled more aggressive surgery combined with medical treatments to improve survival rates.42 There is no evidence to support the postoperative use of octreotide to prevent gastrointestinal complications,24 but it may have a role in maintaining cardiovascular stability.
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Specific types of surgery may be required. The development of right-sided heart failure in carcinoid syndrome is an indication for tricuspid and pulmonary valve replacement. Significant morbidity and mortality in older patients has been described in valvular replacement in carcinoid syndrome.6 Haemodynamic instability can be the result of endocrine secretion or treatment with somatostatin, which is a negative inotrope.55 Treatment of hepatic metastases may be surgical. However, hepatic artery ligature and devascularization have a high mortality and survival from hepatic transplantation is disappointing. Occasionally, if metastases are well localized to a lobe, cytoreductive surgery is an acceptable option. Selective hepatic artery embolization is preferred for symptom relief. The acute tumour lysis that follows can generate severe systemic dysfunction for which intensive care management is the preferred option. Abnormalities of liver function are common and accompanied by fever, nausea, vomiting (ileus) and abdominal pain. Vasoactive peptides can be released and renal failure results from contrast load, fluid loss and cardiovascular disturbances such as hypotension. Prophylactic octreotide and broad-spectrum antibiotics are essential and secondary infection or infarction of gastrointestinal structures must be excluded.
Anaesthesia
Preoperative medical therapy with octreotide or a similar somatostatin analogue will provide prophylaxis against the risk of a carcinoid crisis. It may not prevent an overwhelming release of bronchoconstrictors or vasoactive substances during handling of the tumour at surgery. Preparations for anaesthesia, as summarized in Table 8, involve correction of fluid abnormalities and hypovolaemia, maximizing and quantifying cardiac and respiratory function with electrocardiography, echocardiography, lung function tests and chest radiography, assessing liver function and clotting abnormalities (particularly if there are liver metastases) and minimizing any medical complication. Surgical assessment should have defined the type of endocrine dysfunction and the site of the tumour and predicted the magnitude of the surgical intervention and the need for prophylactic immunization before splenectomy.53
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A review of anaesthetic drugs for carcinoid syndrome has suggested that the hypertensive response to intubation should be prevented by using a short-acting opioid and etomidate or propofol.47 Succinylcholine has been used safely for rapid sequence induction although hormone release theoretically could be stimulated by fasciculations increasing intra-abdominal pressure. Non-depolarizing neuromuscular blocking drugs should be selected on the basis of their lack of histamine release and ease of reversal. Vecuronium is the drug of choice, although in hepatic failure, atracurium should be considered. Agents for maintenance of anaesthesia primarily should be non-hepatoxic and cardiostable. In addition, where high concentrations of serotonin can cause drowsiness, agents with a short elimination time should be considered for safe postoperative recovery.28 The choice of regional anaesthesia, particularly in carcinoid syndrome, is controversial because treatment of hypotension with catecholamines is contraindicated.17 However, epidural nerve blocks using incremental or infusions of local anaesthetics without epinephrine have been administered effectively in a number of patients. They provide good pain relief to reduce the stress response and allow mobilization.30 47
Blood loss during surgery depends on specific pathology. For example, carcinoid tumours induce an intense mesenteric reaction which may not have a focal point of bleeding; metastatic involvement of major vessels, such as the hepatic and portal vessels, can lead to a blood loss of 12 litres min1; the large incision will ooze blood over time and if portal hypertension is present blood loss occurs from the time of skin incision. These problems can be compounded if there are coagulation abnormalities. Average blood loss is 2 litres.50 Blood loss can be assessed by weighing swabs and suction volume can but often this is not accurate because of fluid losses. A urinary catheter and half-hourly measures of urine output supported by blood gas, acid base and haemoglobin concentration measurements at hourly intervals provide the more detailed information required to make decisions on the amount of non-acute continuing bleeding. Adequate amounts of cross-matched blood with facilities to infuse and maintain blood volume and renal blood flow even in cardiovascularly compromised patients are basic requirements which can be supplemented by indirect measures of cardiac function, such as an oesophageal Doppler probe or transoesophageal echocardiography.
If therapies to reduce or antagonize hormone secretions have been administered perioperatively, slow withdrawal with close monitoring is advised.46 Postoperative complications are common, and range from minor morbidity to death. A recent surgical review37 reports a 3% hospital mortality. At operation, haemorrhage has been the major cause of death, especially in the elderly where cardiovascular and hepatic reserve is limited. After surgery, generalized or localized infections, for example intra-abdominal or pulmonary infections, can lead to septicaemia. Sepsis is common and poor nutrition and cachexia predispose to it. Thus nutritional assessment and treatment should be prioritized preoperatively and prophylactic antibiotics given perioperatively. Postoperatively, the appropriate antibiotic should be sought for any specific infection.
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Conclusions |
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References |
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