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Anaesthesia for laparoscopic surgery
Current Anaesthesia & Critical Care (2001) 12, 159d165 ^ 2001 Harcourt Publishers Ltd doi:10.1054/cacc.2000.0309, available online at http://www.idealibrary.com on
ANAESTHESIA
Anaesthesia for laparoscopic surgery A. Kaba and J. Joris Department of Anaesthesia and Intensive Care Medicine, University Hospital of Lie` ge, Domaine du Sart Tilman - B35, B-4000 Lie` ge, Belgium
KEYWORDS surgery, laparoscopy, cholecystectomy, techniques; anaesthesia, general; anaesthesia, regional; pain, postoperative
Summary Laparoscopy results in multiple postoperative benefits allowing for quicker recovery, and shorter hospital stay. These advantages explain the increasing success of laparoscopy, which is now proposed for many surgical procedures. Intraoperative cardiorespiratory changes occur during pneumoperitoneum. PaCO2 increases due to carbon dioxide absorption from the peritoneal cavity. In compromized patients, cardiorespiratory disturbances aggravate this increase in PaCO2. Peritoneal insufflation induces alterations of haemodynamics, characterized by decreases of cardiac output, elevations of arterial pressure, and increases of systemic and pulmonary vascular resistances. Haemodynamic changes are accentuated in high-risk cardiac patients. Improved knowledge of the pathophysiologic haemodynamic changes in healthy patients allows for successful anaesthetic management of cardiac patients, by optimizing preload before pneumoperitoneum, and through judicious use of vasodilating agents. Gasless laparoscopy may be helpful to reduce pathophysiologic changes induced by carbon dioxide pneumoperitoneum, but unfortunately increases technical difficulty. Whereas no anaesthetic technique has proved to be clinically superior to any other, general anaesthesia with controlled ventilation seems to be the safest technique for operative laparoscopy. Improved knowledge of the intraoperative repercussions of laparoscopy permits safe management of patients with more and more severe cardiorespiratory disease, who may subsequently benefit from the multiple postoperative advantages offered by this technique. 䊚 2001 Harcourt Publishers Ltd
INTRODUCTION The many benefits reported after laparoscopy explain its success and the efforts to encourage its use.1,2 However, the pneumoperitoneum and the patient positions required for laparoscopy induce pathophysiologic changes that complicate anaesthetic management.3,4 Knowledge of the pathophysiologic consequences of increased intra-abdominal pressure is important for the anaesthesiologist, who must prevent at best and adequately respond at worst to these changes. In the early 1990s, several studies reported haemodynamic, respiratory and ventilatory changes and raised concern about the use of the laparoscopic approach in patients with cardiac and respiratory comorbidity. Other studies have since improved our understanding of these disturbances allowing safe management of complicated patients undergoing laparoscopy. This article summarizes the main pathophysiologic changes resulting from
Correspondence to: JJ. Fax: 32-4-3667636; E-mail: Jean.Joris@ chu.ulg.ac.be
a 12d14 mmHg CO2-pneumoperitoneum in adults and highlights practical aspects of the anaesthetic management of laparoscopy.
PATHOPHYSIOLOGIC CONSEQUENCES OF CO2-PNEUMOPERITONEUM Ventilatory and respiratory changes during laparoscopy Ventilatory changes Pneumoperitoneum decreases thoracopulmonary compliance.3,5 Compliance is reduced by 30d50% in healthy patients, those with obesity and patients with cardiopulmonary disease. The shape of the pressured volume loop does not, however, change. On-line compliance and pressuredvolume loop monitoring are therefore most helpful in diagnozing complications resulting in increased inspiratory airway pressure.
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Increase in PaCO2 Carbon dioxide is currently preferred to other gases to create the pneumoperitoneum. Its physico-chemical properties reduce the consequences of any potential gas embolism. However, its high solubility and the permeability of the peritoneum facilitate CO2 diffusion outside the peritoneal cavity, as well as its vascular absorption. Consequently, CO2-pneumoperitoneum results in a progressive increase in PaCO2 which reaches a plateau 20d30 min after the beginning of intraperitoneal insufflation in patients under controlled mechanical ventilation.3,6,7 The increase in PaCO2 depends on the intra-abdominal pressure and ranges between 15 and 30%.7 Larger change in PaCO2, or one occurring later than 30 min after the beginning of insufflation requires a search for a cause, either independent of or more often related to CO2 insufflation, such as CO2 subcutaneous emphysema.3,6 During laparoscopy with local anaesthesia, PaCO2 does not change but minute ventilation significantly increases.8 During general anaesthesia with spontaneous breathing, the compensatory hyperventilation is insufficient to avoid hypercapnia because of anaesthetic-induced respiratory depression. As it takes 15 to 30 min for PaCO2 to plateau, anaesthetic techniques using spontaneous breathing should be limited to short procedures with low intra-abdominal pressure. In patients without cardiorespiratory disease, the increased PaCO2 results mainly from CO2 absorption.3,6 Furthermore, a 12d15 mmHg pneumoperitoneum does not significantly modify either physiologic dead space or shunt. As a consequence, the gradient between PaCO2 and end-tidal PCO2 (PETCO2) does not change during pneumoperitoneum.9 In healthy patients, PETCO2 monitoring adequately reflects PaCO2 and can be used to guide adjustment of ventilation to prevent hypercapnia. Hypercapnia can be easily prevented by a 15d20% increase in minute ventilation. In patients with cardiorespiratory disease or in cases of acute cardiopulmonary disturbances, pneumoperitoneum impairs pulmonary ventilation and perfusion, resulting in increased physiologic dead space, reduced alveolar ventilation and increased PaCO2 to PETCO2 gradient. The combined effects of these impairments and of the systemic absorption of peritoneal CO2 explain why the increase in PaCO2 is proportionately greater and why more hyperventilation is required to prevent hypercapnia.9 In sick patients, capnometry no longer provides reliable monitoring of PaCO2.
Main respiratory complications10 CO2 subcutaneous emphysema Subcutaneous emphysema from carbon dioxide can develop as a complication of accidental extraperitoneal insufflation and may be an unavoidable side-effect of procedures requiring
CURRENT ANAESTHESIA & CRITICAL CARE intentional extraperitoneal insufflation (e.g. inguinal hernia repair, pelvic lymphadenectomy) and of surgery at the diaphragmatic hiatus. In the latter case, the opening of the peritoneum overlying the hiatus allows passage of CO2 under pressure through the mediastinum to the cervicocephalic region. As the subcutaneous emphysema extends, the absorption area of CO2 increases, causing a secondary increase in PaCO2 and PETCO2.6 This complication must be suspected and sought any time the PETCO2 increases abnormally either over time (see above) or in magnitude. The increase in CO2 absorption may be such that prevention of hypercapnia using hyperventilation becomes almost impossible. In this case, laparoscopy must be temporarily interrupted to allow CO2 elimination and can be resumed after correction of hypercapnia using a lower insufflating pressure, since this pressure determines the extent of the surgical emphysema. This complication does not contraindicate tracheal extubation at the end of surgery, since CO2emphysema readily resolves once insufflation has ceased. Nevertheless, we must keep in mind the increased work of breathing required to eliminate the excess of CO2, particularly in patients with chronic obstructive pulmonary disease.
Capnothorax11 During CO2-pneumoperitoneum gas can enter the pleural cavity, leading to CO2-pneumothorax (capnothorax). Embryonic remnants constitute potential channels of communication between the peritoneal cavity and the pleural spaces, which can open because of the increased intraperitoneal pressure. Opening of these ducts usually results in right-sided capnothorax. This complication can also develop secondary to pleural tears during laparoscopic surgical procedures at the gastroesophageal junction (fundoplication). In this case, capnothorax is more frequently located on the left. Capnothorax should be suspected whenever reduced thoracopulmonary compliance is associated with an increase in PETCO2.11 This is due to absorption of CO2 across the pleura. Haemodynamic changes and capillary oxygen desaturation are not always present. When actual pneumothorax occurs secondary to alveolar rupture, PETCO2 does not increase but instead decreases due to decreased cardiac output. Diagnosis is confirmed by auscultation of the chest and chest X-ray. It should be remembered that cervical and upper thoracic emphysema can develop without capnothorax. Treatment of capnothorax consists of discontinuation of nitrous oxide, adjustment of ventilator settings to correct hypoxaemia, and positive end-expiratory pressure.11 Thoracocentesis can usually be avoided as capnothorax will spontaneously resolve after exsufflation. In cases of ‘classical’ pneumothorax, positive end-expiratory pressure must not be applied and thoracocentesis is mandatory.
ANAESTHESIA FOR LAPAROSCOPIC SURGERGY
Endobronchial intubation During pneumoperitoneum, the cephalad movement of the carina can lead to endobronchial intubation. This complication has been reported in both head-down and head-up position, and results in a decrease in SpO2 associated with an increase in plateau airway pressure. Gas embolism3 The pathophysiologic consequences of gas embolism depend on the size of the bubbles and the rate of intravenous (i.v.) entry of the gas. This complication develops principally during the induction of pneumoperitoneum. The diagnosis of gas embolism depends on the detection of gas emboli in the right side of the heart or on the recognition of the physiologic changes secondary to embolization. Precordial Doppler probes are very sensitive means of detecting small quantities of gas before physiologic changes occur. Capnometry and capnography are valuable in providing early diagnosis of gas embolism and determining the extent of the embolism. PETCO2 decreases suddenly and markedly due to the fall of cardiac output and the enlargement of the physiologic dead space. This drop in PETCO2 is sometimes preceeded by an initial increase caused by pulmonary excretion of the CO2 absorbed in the blood. Treatment of CO2 embolism consists of immediate cessation of insufflation, release of the pneumoperitoneum, placement of the patient in a steep head-down and left lateral decubitus position, discontinuation of nitrous oxide, and hyperventilation with 100% oxygen. In case of severe haemodynamic disturbances, external cardiac massage may be helpful in fragmenting CO2 emboli into small bubbles. Hyperbaric oxygen treatment should be strongly considered if cerebral gas embolism is suspected. The best treatment remains prevention, assured by safe and careful technique during induction of the pneumoperitoneum.
Haemodynamic changes during laparoscopy Haemodynamic consequences of pneumoperitoneum Haemodynamic changes observed during laparoscopy result from the combined effects of pneumoperitoneum, patient position, anaesthesia, and, if present, hypercapnia. Peritoneal insufflation to an intra-abdominal pressure higher than 10 mmHg induces significant alterations of haemodynamics.12d14 These disturbances are characterized by elevations of arterial pressure, a decrease in cardiac output, and an increase in systemic and pulmonary vascular resistances.12,13 Heart rate either remains unchanged or increases only slightly. The decrease in cardiac output is proportional to the increase in intra-abdominal pressure. Haemodynamic deterioration occurs mainly at the beginning of peritoneal insufflation. Although most studies report
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a reduction of cardiac output at the beginning of peritoneal insufflation, cardiac output has also been shown to be unchanged or increased during pneumoperitoneum.14 These changes are well tolerated in healthy patients.13 In patients with moderate to severe cardiac disease, the haemodynamic repercussions of pneumoperitoneum are more marked.15,16 The mechanism of the decrease of cardiac output is multifactorial.12,13,17 Venous return decreases secondary to caval compression, pooling of blood in the legs, and an increase in venous resistance. Despite a decline in venous return, cardiac filling pressures increase during pneumoperitoneum. The paradoxical increase in these pressures can be explained by the increased intrathoracic pressure associated with pneumo peritoneum.13 Therefore, right atrial and pulmonary artery occlusion pressures can no longer be considered to be reliable indices of cardiac filling pressure during pneumoperitoneum. Any increase in afterload may also further decrease cardiac output in patients with cardiac diseases. The increase in systemic vascular resistance is mediated by mechanical as well as neurohumoral factors (vasopressin).13 The use of low intra-abdominal pressure and slow insufflation rates, increasing circulating volume before the pneumoperitoneum,13 treatment with clonidine13 or dexmedetomidine before insufflation, and administration of vasodilating anaesthetic agents or direct vasodilating drugs15 (nicardipine) attenuate these haemodynamic changes.
Effect of pneumoperitoneum on regional haemodynamics Increased intra-abdominal pressure results in lower limb venous stasis. Femoral vein blood flow decreases with increasing intra-abdominal pressure. Although these changes may predispose to the development of thromboembolic complications, their actual incidence does not seem to be increased after laparoscopy as compared with laparotomy.18 Urine output, renal plasma flow and glomerular filtration rate significantly decrease (to less than 50% of baseline) during laparoscopy and are lower than during laparotomy.19 Due to these renal effects the anaesthetist must pay particular attention to maintenance of intravascular volume and to avoid the use of nephrotoxic drugs in patients with compromized renal function. Controversy persists with regard to the effect of CO2-pneumoperitoneum on splanchnic blood flow. Blobner et al. suggested that the direct splanchnic vasodilating effect of CO2 counteracts the mechanical effect of increased intra-abdominal pressure on splanchnic blood flow.20 Accordingly, reports of mesenteric ischaemia after laparoscopy are rare. Intracranial pressure rises during pneumoperitoneum. The laparoscopic approach should probably be avoided
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in cases of intracranial hypertension, unless monitoring of intracranial pressure, and perhaps concomitant drainage of cerebrospinal fluid is provided.
Alternatives to CO2}pneumoperitoneum Two different approaches have been proposed to reduce these pathophysiologic consequences: the use of an inert gas instead of CO2 and gasless laparoscopy. Insufflation of an inert gas (helium, argon) avoids the increase in PaCO2. However, the ventilatory and haemodynamic consequences of increased intra-abdominal pressure persist. Gasless laparoscopy avoids the haemodynamic and respiratory consequences of increased intra-abdominal pressure as well as the consequences of the use of CO2.21 This technique also reduces the postoperative discomfort observed after CO2-pneumoperitoneum. Although gasless laparoscopy would appear to be particularly appealing for patients with severe cardiac or pulmonary disease, it compromizes surgical exposure and increases technical difficulty.
Laparoscopy during pregnancy22 Laparoscopy during pregnancy may increase the risk of miscarriage, premature labour, and damage to the gravid uterus. Open laparoscopy should be used to avoid damaging the uterus. Provided maternel PaCO2 is maintained at normal levels, physiology of the feto-placental unit seems unaffected by CO2-pneumoperitoneum. Mechanical ventilation must therefore be adjusted to maintain a physiologic maternal alkalosis. Capnometry remains adequate to guide ventilation during laparoscopy in pregnant patients. Respiratory acidosis does not occur when PETCO2 is maintained at 32 mm Hg. Gasless laparoscopy is an alternative which can sometimes be managed using epidural anaesthesia.
Postoperative benefits Soon after the development of laparoscopy for gastrointestinal surgical procedures, it became clear that the laparoscopic approach results in several benefits as compared with laparotomy. These benefits should be exploited to accelerate postoperative recovery. Nevertheless, postoperative side-effects persist and should be considered in the management of patients after surgery. The laparoscopic approach allows for reductions in surgical trauma to the abdominal wall and intra-abdominal viscera, as well as the stress response. This results in the shortening of postoperative ileus and subsequently the duration of postoperative fasting and hospital stay.1 Pain and analgesic consumption after laparoscopy are reduced as compared with open procedures.1,24 The pain characteristics also differ: visceral pain becomes
CURRENT ANAESTHESIA & CRITICAL CARE predominant and shouldertip pain appears as a consequence of pneumoperitoneum.23,24 Nevertheless, marked individual variability in pain scores is reported after operative laparoscopy, with some patients complaining of severe pain. Therefore, analgesia should not be neglected after laparoscopy. Laparoscopy for upper-abdominal procedures results in a postoperative pulmonary restrictive syndrome. This syndrome is less severe than after laparotomy;25 this explains why this approach is readily proposed in patients with respiratory disease. However, the problem does occur and is more marked in obese patients and those with chronic obstructive pulmonary disease than in healthy ones. Finally, the incidence of nausea and vomiting is high after laparoscopy, particularly laparoscopic gynaecologic procedures.
PRACTICAL IMPLICATIONS FOR THE ANAESTHETIC MANAGEMENT OF LAPAROSCOPY Patient positioning and monitoring3 Patients must be positioned with great care to prevent nerve injuries. Padding should be used to protect nerves from compression injury: peroneal nerve in the case of the lithotomy position, the ulnar nerve when the upper limbs are adducted against the body, the brachial plexus when using shoulder braces. Changes in patient position must be slow and progressive to avoid sudden haemodynamic and respiratory modifications. The position of the endotracheal tubes must be checked after any change in patient position, and again after insufflation. Arterial blood pressure, heart rate, electrocardiogram, capnometry and pulse oximetry must be continuously monitored. Capnometry is valuable to prevent hypercapnia and to diagnose gas embolism or CO2 subcutaneous emphysema as well as capnothorax. The use of real-time pressure volume measurement may be useful to monitor ventilatory changes secondary to pneumoperitoneum or capnothorax. The low incidence of gas embolism during laparoscopy precludes the routine use of expensive monitors. Changes of the cardiac electrical axis secondary to cephalad displacement of the diaphragm during pneumoperitoneum complicate the interpretation of continuous ST segment monitoring.
ANAESTHESIA3 Induction of anaesthesia The choice of anaesthetic technique does not seem to play a major role in patient outcome. Because of the
ANAESTHESIA FOR LAPAROSCOPIC SURGERGY
potential for reflex increases in vagal tone during laparoscopy, atropine should be administered before the induction of anaesthesia, or should be ready for injection if necessary. Increasing circulating volume by infusion of i.v. fluid and/or by tilting the patient to a slight headdown position before pneumoperitoneum both attenuate the haemodynamic changes secondary to increased intra-abdominal pressure.13 Clonidine given i.v. before pneumoperitoneum improves haemodynamic stability.13 This treatment should not be administered in patients undergoing ambulatory surgery procedures. The stomach must be aspirated before trocar placement to avoid gastric perforation. The bladder should be emptied before pelvic laparoscopy or prolonged procedures. Due to venous stasis in the legs during laparoscopy, deep vein thrombosis prophylaxis should be initiated before surgery, as for laparotomy.
Maintenance of anaesthesia Volatile anaesthetics are valuable because of their vasodilating properties. Propofol anaesthesia results in less postoperative nausea and vomiting. Omission of nitrous oxide improves surgical conditions for colonic and intestinal surgery, but does not seem to be contraindicated for laparoscopic cholecystectomy. Whether nitrous oxide contributes to nausea and vomiting is still controversial. Nevertheless, nitrous oxide must be interrupted as soon as a gas embolism is suspected. Haemodynamic stability can be improved by the administration of clonidine or by the infusion of nicardipine, a calcium-channel blocker. Whether profound muscle relaxation is necessary for laparoscopy is not clear. Rather, a constant level of muscle relaxation is desirable to provide adequate surgical conditions and to avoid abrupt changes in intra-abdominal pressure. Remifentanil infusion at a rate of 0.3d0.4 lg/kg/min allows almost complete avoidance of the hypertensive response at the beginning of intra-abdominal insufflation (personal observation).
Ventilation and management of the airway General anaesthesia with endotracheal intubation and controlled ventilation is certainly the safest technique, and is recommended for in-patients and for long laparoscopic procedures. This technique allows the best control of PaCO2. Prevention of hypercapnia requires an increase in minute ventilation of no more than 15d25%, except when CO2 subcutaneous emphysema develops. Airway control using a laryngeal mask (LM) might be proposed as an alternative to endotracheal intubation, since it allows controlled ventilation and accurate monitoring of PETCO2 . However, decreased thoracopulmonary compliance during pneumoperi-
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toneum frequently results in airway pressures exceeding 20 cm H2O, a pressure above which an airway seal cannot be guaranteed with this device. Therefore, its use should be limited to circumstances associated with airway pressures lower than 20 cm H2O: healthy, thin patients (with high thoracopulmonary compliance), low risk of regurgitation of gastric contents (because the LM affords no protection of the airway from aspiration), for surgical procedures not associated with subcutaneous emphysema which requires marked hyperventilation. General anaesthesia in patients breathing spontaneously with a LM should be restricted to short procedures (less than 15 min before CO2 peaks) using low intra-abdominal pressure and small degrees of tilt.
Regional anaesthesia3 The haemodynamic effects of pneumoperitoneum under epidural anesthesia have not been studied. However, the vasodilation induced by sympathectomy, and avoidance of positive pressure ventilation might reduce the cardiovascular changes induced by pneumoperitoneum. Regional techniques provide excellent postoperative analgesia. These potential advantages must be balanced against certain disadvantages. Indeed, shouldertip pain secondary to diaphragmatic irritation as well as discomfort secondary to abdominal distension are incompletely alleviated using epidural anaesthesia, and may require i.v. analgesics. The extensive sensory block necessary for surgical laparoscopy may also lead to patient discomfort. Use of sedatives and/or an extensive block can interfere with the increased work of breathing required by decreased thoracopulmonary compliance and the absorption of CO2. Regional anaesthesia must be proposed with caution any time CO2-subcutaneous emphysema (which further increases CO2 absorption) may develop, particularly in patients with chronic obstructive pulmonary disease. Regional anaesthesia has been used for gynaecologic laparoscopy in the head-down position and for laparoscopic cholecystectomy in COPD patients without impairment of ventilation.26 Patient collaboration, an experienced and skilled laparoscopist, reduced degrees of both intra-abdominal pressure and tilt are necessary to guarantee the success of epidural anaesthesia, which should be avoided for long procedures. Epidural or spinal anaesthesia can be used for gasless laparoscopy since it provides adequate relief of pain and discomfort in these circumstances.
Anaesthesia for the patient with heart disease Because of the haemodynamic consequences of CO2pneumoperitoneum, some concerns have been raised
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with regard to tolerance of these changes by cardiac patients. In the light of the haemodynamic consequences of laparoscopy, patients most at risk are those with compromised ventricular function (such as congestive heart failure), and those with severe valvular diseases which render them intolerant of increased afterload. The haemodynamic consequences of pneumoperitoneum are minor in heart transplant recipients. It is well established that peri-operative risk in cardiac patients undergoing non-cardiac surgery is higher during the postoperative period, when the patient is no longer protected by the close surveillance of the anaesthesiologist. This notion may be extended to laparoscopic surgery. Laparoscopy probably results in more haemodynamic changes than laparotomy. However, these changes occur mainly at the beginning of insufflation. Moreover, knowledge and understanding of the intraoperative changes, as well as the pathophysiology of the cardiac disease, allow them to be minimized. On the other hand, the postoperative benefits of laparoscopy are welcome in these ill patients. Anaesthetic management of cardiac patients comprises several measures: (1) patients with a profile suggesting depleted intravascular volume experience the most severe haemodynamic changes. Preload augmentation before peritoneal insufflation partially offsets haemodynamic deterioration; (2) insufflation must be slow, and intra-abdominal pressure must be kept as low as possible; (3) vasodilators can be used to correct or prevent the increase in afterload. Nicardipine, a calcium-channel blocker, presents an adequate profile: reduction of afterload, no effect on preload, no effect on contractility; (4) in case of poor ventricular function, an inotropic agent such as dobutamine may be necessary; (5) we routinely infuse a small intraoperative dose of clonidine (0.150 mg) to reduce the hyperdynamic state occurring after exsufflation; (6) a diuretic may be necessary to restore preoperative intravascular volume status. It should be kept in mind that pressures measured with a pulmonary artery catheter do not accurately reflect cardiac filling pressures during pneumoperitoneum due to the increase in intrathoracic pressure.
CURRENT ANAESTHESIA & CRITICAL CARE disease.1,4,25 It should be noted that, despite better preservation of pulmonary function after laparoscopy, the restrictive syndrome reported in these patients is more marked than in healthy patients; it must therefore be considered when caring for these patients. Preoperative optimization of respiratory function remains necessary even before minimally invasive surgery. In these patients, pneumoperitoneum alters the distribution of pulmonary ventilation and perfusion. This results in an enlargement of alveolar dead space. Therefore, the PaCO2 to PETCO2 gradient increases and PETCO2 no longer accurately reflects PaCO2.9 Due to decreased thoracopulmonary compliance secondary to pneumoperitoneum, airway pressures increase. To avoid excessive airway pressures, which could potentially lead to rupture of emphysematous bullae, the hyperventilation normally required during CO2-pneumoperitoneum can be limited. As a consequence, permissive hypercapnia develops. A reduction in airway pressures can be also achieved by increasing respiratory rate rather than tidal volume. Finally, we also administer clonidine to these patients because it reduces metabolism and attenuates the requirement for hyperventilation. Caution is required in case of CO2-subcutaneous emphysema, since it increases the body load of CO2 to be eliminated and consequently the work of breathing.
Postoperative analgesia Postoperative pain and analgesic requirements are less after laparoscopy than laparotomy.1,24 As a consequence, very good pain relief can be provided not only using epidural analgesia but also using ‘balanced’ analgesia with systemic analgesics.24,27 Indeed, because of pain characteristics, a combination of different non-opioid analgesics (paracetamol, non-steroidal anti-inflammatory drugs, tramadol) allows opioid-free analgesia, further accelerating recovery of intestinal function. Tramadol relieves visceral pain, which predominates after gynaecologic and gastro-intestinal laparoscopic procedures, whereas paracetamol and NSAIDs alleviate parietal and shouldertip pain. However, high individual variability in pain intensity is reported, and opioids still may be necessary in some patients. Finally, controversy remains regarding the efficacy of intraperitoneal instillation of local anaesthetics.23,27 Whereas this technique provides some pain relief after gynaecologic laparoscopy, no significant effects are reported after laparoscopic cholecystectomy.
Anaesthesia for the patient with chronic obstructive pulmonary disease3 The reduction in the postoperative pulmonary restrictive syndrome observed after laparoscopy as compared to laparotomy justifies efforts to use the laparoscopic approach in patients with respiratory
Prevention of postoperative nausea and vomiting The incidence of nausea and vomiting is high after laparoscopy, particularly gynaecologic procedures.
ANAESTHESIA FOR LAPAROSCOPIC SURGERGY
Several measures, used alone or in combination, can reduce the incidence of these side-effects: these measures include use of propofol, prophylactic administration of antiemetic medications, suction of gastric contents at the end of laparoscopy and intraoperative administration of a high oxygen concentration (80%).
CONCLUSION A better knowledge of the pathophysiologic changes induced by CO2-pneumoperitoneum allows the clinician to reduce their impact and to allow a greater number of patients to benefit from the postoperative advantages of laparoscopy. Increased surgeon experience is associated with decreased operative times and rates of minor or moderate surgical complications. At this time, the postoperative benefits largely outweigh intraoperative side effects, which can be corrected or prevented by an anaesthesiologist who is aware of the pathophysiology of pneumoperitoneum. This balance in favour of laparoscopy justifies efforts to apply the laparoscopic approach to other surgical procedures.
REFERENCES 1. Joris J, Cigarini I, Legrand M et al. Metabolic and respiratory changes after cholecystectomy performed via laparotomy or laparoscopy. Br J Anaesth 1992; 69: 341d345. 2. Kehlet H. Surgical stress response: does endoscopic surgery confer an advantage? World J Surg 1999; 23: 801d807. 3. Joris J. Anesthesia for laparoscopic surgery. In: R. Miller (ed) Anesthesia. New York: Churchill Livingstone, 1998. 4. Wahba R W, Beique F, Kleiman S J. Cardiopulmonary function and laparoscopic cholecystectomy. Can J Anaesth 1995; 42: 51d63. 5. Fahy B G, Barnas G M, Flowers J L, Nagle S E, Njoku M J. The effects of increased abdominal pressure on lung and chest wall mechanics during laparoscopic surgery. Anesth Analg 1995; 81: 744d750. 6. Mullet C E, Viale J P, Sagnard PE et al. Pulmonary CO2 elimination during surgical procedures using intra- or extraperitoneal CO2 insufflation. Anesth Analg 1993; 76: 622d626. 7. Lister D R, Rudston-Brown B, Warriner C B, McEwen J, Chan M, Walley K R. Carbon dioxide absorption is not linearly related to intraperitoneal carbon dioxide insufflation pressure in pigs. Anesthesiology 1994; 80: 129d136. 8. Ciofolo M J, Clergue F, Seebacher J, Lefebvre G, Viars P. Ventilatory effects of laparoscopy under epidural anesthesia. Anesth Analg 1990; 70: 357d361. 9. Wittgen C M, Andrus C H, Fitzgerald S D, Baudendistel L J, Dahms T E, Kaminski D L. Analysis of the hemodynamic and ventilatory effects of laparoscopic cholecystectomy. Arch Surg 1991; 126: 997d1001.
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10. Wahba R W, Tessler M J, Kleiman S J. Acute ventilatory complications during laparoscopic upper abdominal surgery. Can J Anaesth 1996; 43: 77d83. 11. Joris J, Chiche J D, Lamy M L. Pneumothorax during laparoscopic fundoplication: diagnosis and treatment with positive endexpiratory pressure. Anesth Analg 1995; 81: 993d1000. 12. Struthers A D, Cuschieri A. Cardiovascular consequences of laparoscopic surgery. Lancet 1998; 352: 568d570. 13. Joris J, Chiche J D, Canivet J L, Jacquet N, Legros J J, Lamy M L. Hemodynamic changes induced by laparoscopy and their endocrine correlates: effects of clonidine. J Am Coll Cardiol. 1998; 32: 1389d1396. 14. Andersson L, Wallin C J, Sollevi A, Odeberg-Wernerman J. Pneumoperitoneum in healthy humans does not affect central blood volume or cardiac output. Acta Anaesthesiol Scand 1999; 43: 809d814. 15. Feig B W, Berger D H, Dougherty T B, Dupuis J F, His B, Hickey R C et al. Pharmacologic intervention can reestablish baseline hemodynamic parameters during laparoscopy. Surgery 1994; 116: 733d741. 16. Hein H A, Joshi G P, Ramsay M A et al. Hemodynamic changes during laparoscopic cholecystectomy in patients with severe cardiac disease. J Clin Anesth 1997; 9: 261d265. 17. Kashtan J, Green J F, Parsons E Q, Holcroft J W. Hemodynamic effects of increased intraabdominal pressure. J Surg Res 1981; 30: 249d255. 18. Catheline J M, Turner R, Gaillard J L, Rizk N, Champault G. Thromboembolism in laparoscopic surgery: risk factors and preventive measures. Surg Laparosc Endosc 1999; 9: 135d139. 19. Iwase K, Takenaka H, Ishizaka T, Ohata T, Oshima S, Sakaguchi K. Serial changes in renal function during laparoscopic cholecystectomy. Eur Surg Res 1993; 25: 203d212. 20. Blobner M, Bogdanski R, Kochs E, Henke J, Finders A, JelenEsselborn S. Effects of intraabdominally insufflated carbon dioxide and elevated intraabdominal pressure on splanchnic circulation: an experimental study in pigs. Anesthesiology 1998; 89: 475d482. 21. Koivusalo A M, Kellokumpu I, Scheinin M, Tikkanen I, Makisalo H, Lindgren L. A comparison of gasless mechanical and conventional carbon dioxide pneumoperitoneum methods for laparoscopic cholecystectomy. Anesth Analg 1998; 86: 153d158. 22. Lemaire B, van Erp W F. Laparoscopic surgery during pregnancy. Surg Endosc 1997; 11: 15d18. 23. Joris J, Thiry E, Paris P, Weerts J, Lamy M. Pain after laparoscopic cholecystectomy: characteristics and effect of intraperitoneal bupivacaine. Anesth Analg 1995; 81: 379d384. 24. Alexander J I. Pain after laparoscopy. Br J Anaesth 1997; 79: 369d378. 25. Karayiannakis A J, Makri G G, Mantzioka A et al: Postoperative pulmonary function after laparoscopic and open cholecystectomy. Br J Anaesth 1996; 77: 448d452. 26. Pursnani K G, Bazza Y, Calleja M, Mughal M M. Laparoscopic cholecystectomy under epidural anesthesia in patients with chronic respiratory disease. Surg Endosc 1998; 12: 1082d1084. 27. Bisgaard T, Klarskov B, Kristiansen V B et al. Multi-regional local anesthetic infiltration during laparoscopic cholecystectomy in patients receiving prophylactic multi-modal analgesia: a randomi zed, double blinded, placebo-controlled study. Anesth Analg 1999; 89: 1017d1024.
ANAESTHESIA
Anaesthesia for laparoscopic surgery A. Kaba and J. Joris Department of Anaesthesia and Intensive Care Medicine, University Hospital of Lie` ge, Domaine du Sart Tilman - B35, B-4000 Lie` ge, Belgium
KEYWORDS surgery, laparoscopy, cholecystectomy, techniques; anaesthesia, general; anaesthesia, regional; pain, postoperative
Summary Laparoscopy results in multiple postoperative benefits allowing for quicker recovery, and shorter hospital stay. These advantages explain the increasing success of laparoscopy, which is now proposed for many surgical procedures. Intraoperative cardiorespiratory changes occur during pneumoperitoneum. PaCO2 increases due to carbon dioxide absorption from the peritoneal cavity. In compromized patients, cardiorespiratory disturbances aggravate this increase in PaCO2. Peritoneal insufflation induces alterations of haemodynamics, characterized by decreases of cardiac output, elevations of arterial pressure, and increases of systemic and pulmonary vascular resistances. Haemodynamic changes are accentuated in high-risk cardiac patients. Improved knowledge of the pathophysiologic haemodynamic changes in healthy patients allows for successful anaesthetic management of cardiac patients, by optimizing preload before pneumoperitoneum, and through judicious use of vasodilating agents. Gasless laparoscopy may be helpful to reduce pathophysiologic changes induced by carbon dioxide pneumoperitoneum, but unfortunately increases technical difficulty. Whereas no anaesthetic technique has proved to be clinically superior to any other, general anaesthesia with controlled ventilation seems to be the safest technique for operative laparoscopy. Improved knowledge of the intraoperative repercussions of laparoscopy permits safe management of patients with more and more severe cardiorespiratory disease, who may subsequently benefit from the multiple postoperative advantages offered by this technique. 䊚 2001 Harcourt Publishers Ltd
INTRODUCTION The many benefits reported after laparoscopy explain its success and the efforts to encourage its use.1,2 However, the pneumoperitoneum and the patient positions required for laparoscopy induce pathophysiologic changes that complicate anaesthetic management.3,4 Knowledge of the pathophysiologic consequences of increased intra-abdominal pressure is important for the anaesthesiologist, who must prevent at best and adequately respond at worst to these changes. In the early 1990s, several studies reported haemodynamic, respiratory and ventilatory changes and raised concern about the use of the laparoscopic approach in patients with cardiac and respiratory comorbidity. Other studies have since improved our understanding of these disturbances allowing safe management of complicated patients undergoing laparoscopy. This article summarizes the main pathophysiologic changes resulting from
Correspondence to: JJ. Fax: 32-4-3667636; E-mail: Jean.Joris@ chu.ulg.ac.be
a 12d14 mmHg CO2-pneumoperitoneum in adults and highlights practical aspects of the anaesthetic management of laparoscopy.
PATHOPHYSIOLOGIC CONSEQUENCES OF CO2-PNEUMOPERITONEUM Ventilatory and respiratory changes during laparoscopy Ventilatory changes Pneumoperitoneum decreases thoracopulmonary compliance.3,5 Compliance is reduced by 30d50% in healthy patients, those with obesity and patients with cardiopulmonary disease. The shape of the pressured volume loop does not, however, change. On-line compliance and pressuredvolume loop monitoring are therefore most helpful in diagnozing complications resulting in increased inspiratory airway pressure.
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Increase in PaCO2 Carbon dioxide is currently preferred to other gases to create the pneumoperitoneum. Its physico-chemical properties reduce the consequences of any potential gas embolism. However, its high solubility and the permeability of the peritoneum facilitate CO2 diffusion outside the peritoneal cavity, as well as its vascular absorption. Consequently, CO2-pneumoperitoneum results in a progressive increase in PaCO2 which reaches a plateau 20d30 min after the beginning of intraperitoneal insufflation in patients under controlled mechanical ventilation.3,6,7 The increase in PaCO2 depends on the intra-abdominal pressure and ranges between 15 and 30%.7 Larger change in PaCO2, or one occurring later than 30 min after the beginning of insufflation requires a search for a cause, either independent of or more often related to CO2 insufflation, such as CO2 subcutaneous emphysema.3,6 During laparoscopy with local anaesthesia, PaCO2 does not change but minute ventilation significantly increases.8 During general anaesthesia with spontaneous breathing, the compensatory hyperventilation is insufficient to avoid hypercapnia because of anaesthetic-induced respiratory depression. As it takes 15 to 30 min for PaCO2 to plateau, anaesthetic techniques using spontaneous breathing should be limited to short procedures with low intra-abdominal pressure. In patients without cardiorespiratory disease, the increased PaCO2 results mainly from CO2 absorption.3,6 Furthermore, a 12d15 mmHg pneumoperitoneum does not significantly modify either physiologic dead space or shunt. As a consequence, the gradient between PaCO2 and end-tidal PCO2 (PETCO2) does not change during pneumoperitoneum.9 In healthy patients, PETCO2 monitoring adequately reflects PaCO2 and can be used to guide adjustment of ventilation to prevent hypercapnia. Hypercapnia can be easily prevented by a 15d20% increase in minute ventilation. In patients with cardiorespiratory disease or in cases of acute cardiopulmonary disturbances, pneumoperitoneum impairs pulmonary ventilation and perfusion, resulting in increased physiologic dead space, reduced alveolar ventilation and increased PaCO2 to PETCO2 gradient. The combined effects of these impairments and of the systemic absorption of peritoneal CO2 explain why the increase in PaCO2 is proportionately greater and why more hyperventilation is required to prevent hypercapnia.9 In sick patients, capnometry no longer provides reliable monitoring of PaCO2.
Main respiratory complications10 CO2 subcutaneous emphysema Subcutaneous emphysema from carbon dioxide can develop as a complication of accidental extraperitoneal insufflation and may be an unavoidable side-effect of procedures requiring
CURRENT ANAESTHESIA & CRITICAL CARE intentional extraperitoneal insufflation (e.g. inguinal hernia repair, pelvic lymphadenectomy) and of surgery at the diaphragmatic hiatus. In the latter case, the opening of the peritoneum overlying the hiatus allows passage of CO2 under pressure through the mediastinum to the cervicocephalic region. As the subcutaneous emphysema extends, the absorption area of CO2 increases, causing a secondary increase in PaCO2 and PETCO2.6 This complication must be suspected and sought any time the PETCO2 increases abnormally either over time (see above) or in magnitude. The increase in CO2 absorption may be such that prevention of hypercapnia using hyperventilation becomes almost impossible. In this case, laparoscopy must be temporarily interrupted to allow CO2 elimination and can be resumed after correction of hypercapnia using a lower insufflating pressure, since this pressure determines the extent of the surgical emphysema. This complication does not contraindicate tracheal extubation at the end of surgery, since CO2emphysema readily resolves once insufflation has ceased. Nevertheless, we must keep in mind the increased work of breathing required to eliminate the excess of CO2, particularly in patients with chronic obstructive pulmonary disease.
Capnothorax11 During CO2-pneumoperitoneum gas can enter the pleural cavity, leading to CO2-pneumothorax (capnothorax). Embryonic remnants constitute potential channels of communication between the peritoneal cavity and the pleural spaces, which can open because of the increased intraperitoneal pressure. Opening of these ducts usually results in right-sided capnothorax. This complication can also develop secondary to pleural tears during laparoscopic surgical procedures at the gastroesophageal junction (fundoplication). In this case, capnothorax is more frequently located on the left. Capnothorax should be suspected whenever reduced thoracopulmonary compliance is associated with an increase in PETCO2.11 This is due to absorption of CO2 across the pleura. Haemodynamic changes and capillary oxygen desaturation are not always present. When actual pneumothorax occurs secondary to alveolar rupture, PETCO2 does not increase but instead decreases due to decreased cardiac output. Diagnosis is confirmed by auscultation of the chest and chest X-ray. It should be remembered that cervical and upper thoracic emphysema can develop without capnothorax. Treatment of capnothorax consists of discontinuation of nitrous oxide, adjustment of ventilator settings to correct hypoxaemia, and positive end-expiratory pressure.11 Thoracocentesis can usually be avoided as capnothorax will spontaneously resolve after exsufflation. In cases of ‘classical’ pneumothorax, positive end-expiratory pressure must not be applied and thoracocentesis is mandatory.
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Endobronchial intubation During pneumoperitoneum, the cephalad movement of the carina can lead to endobronchial intubation. This complication has been reported in both head-down and head-up position, and results in a decrease in SpO2 associated with an increase in plateau airway pressure. Gas embolism3 The pathophysiologic consequences of gas embolism depend on the size of the bubbles and the rate of intravenous (i.v.) entry of the gas. This complication develops principally during the induction of pneumoperitoneum. The diagnosis of gas embolism depends on the detection of gas emboli in the right side of the heart or on the recognition of the physiologic changes secondary to embolization. Precordial Doppler probes are very sensitive means of detecting small quantities of gas before physiologic changes occur. Capnometry and capnography are valuable in providing early diagnosis of gas embolism and determining the extent of the embolism. PETCO2 decreases suddenly and markedly due to the fall of cardiac output and the enlargement of the physiologic dead space. This drop in PETCO2 is sometimes preceeded by an initial increase caused by pulmonary excretion of the CO2 absorbed in the blood. Treatment of CO2 embolism consists of immediate cessation of insufflation, release of the pneumoperitoneum, placement of the patient in a steep head-down and left lateral decubitus position, discontinuation of nitrous oxide, and hyperventilation with 100% oxygen. In case of severe haemodynamic disturbances, external cardiac massage may be helpful in fragmenting CO2 emboli into small bubbles. Hyperbaric oxygen treatment should be strongly considered if cerebral gas embolism is suspected. The best treatment remains prevention, assured by safe and careful technique during induction of the pneumoperitoneum.
Haemodynamic changes during laparoscopy Haemodynamic consequences of pneumoperitoneum Haemodynamic changes observed during laparoscopy result from the combined effects of pneumoperitoneum, patient position, anaesthesia, and, if present, hypercapnia. Peritoneal insufflation to an intra-abdominal pressure higher than 10 mmHg induces significant alterations of haemodynamics.12d14 These disturbances are characterized by elevations of arterial pressure, a decrease in cardiac output, and an increase in systemic and pulmonary vascular resistances.12,13 Heart rate either remains unchanged or increases only slightly. The decrease in cardiac output is proportional to the increase in intra-abdominal pressure. Haemodynamic deterioration occurs mainly at the beginning of peritoneal insufflation. Although most studies report
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a reduction of cardiac output at the beginning of peritoneal insufflation, cardiac output has also been shown to be unchanged or increased during pneumoperitoneum.14 These changes are well tolerated in healthy patients.13 In patients with moderate to severe cardiac disease, the haemodynamic repercussions of pneumoperitoneum are more marked.15,16 The mechanism of the decrease of cardiac output is multifactorial.12,13,17 Venous return decreases secondary to caval compression, pooling of blood in the legs, and an increase in venous resistance. Despite a decline in venous return, cardiac filling pressures increase during pneumoperitoneum. The paradoxical increase in these pressures can be explained by the increased intrathoracic pressure associated with pneumo peritoneum.13 Therefore, right atrial and pulmonary artery occlusion pressures can no longer be considered to be reliable indices of cardiac filling pressure during pneumoperitoneum. Any increase in afterload may also further decrease cardiac output in patients with cardiac diseases. The increase in systemic vascular resistance is mediated by mechanical as well as neurohumoral factors (vasopressin).13 The use of low intra-abdominal pressure and slow insufflation rates, increasing circulating volume before the pneumoperitoneum,13 treatment with clonidine13 or dexmedetomidine before insufflation, and administration of vasodilating anaesthetic agents or direct vasodilating drugs15 (nicardipine) attenuate these haemodynamic changes.
Effect of pneumoperitoneum on regional haemodynamics Increased intra-abdominal pressure results in lower limb venous stasis. Femoral vein blood flow decreases with increasing intra-abdominal pressure. Although these changes may predispose to the development of thromboembolic complications, their actual incidence does not seem to be increased after laparoscopy as compared with laparotomy.18 Urine output, renal plasma flow and glomerular filtration rate significantly decrease (to less than 50% of baseline) during laparoscopy and are lower than during laparotomy.19 Due to these renal effects the anaesthetist must pay particular attention to maintenance of intravascular volume and to avoid the use of nephrotoxic drugs in patients with compromized renal function. Controversy persists with regard to the effect of CO2-pneumoperitoneum on splanchnic blood flow. Blobner et al. suggested that the direct splanchnic vasodilating effect of CO2 counteracts the mechanical effect of increased intra-abdominal pressure on splanchnic blood flow.20 Accordingly, reports of mesenteric ischaemia after laparoscopy are rare. Intracranial pressure rises during pneumoperitoneum. The laparoscopic approach should probably be avoided
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in cases of intracranial hypertension, unless monitoring of intracranial pressure, and perhaps concomitant drainage of cerebrospinal fluid is provided.
Alternatives to CO2}pneumoperitoneum Two different approaches have been proposed to reduce these pathophysiologic consequences: the use of an inert gas instead of CO2 and gasless laparoscopy. Insufflation of an inert gas (helium, argon) avoids the increase in PaCO2. However, the ventilatory and haemodynamic consequences of increased intra-abdominal pressure persist. Gasless laparoscopy avoids the haemodynamic and respiratory consequences of increased intra-abdominal pressure as well as the consequences of the use of CO2.21 This technique also reduces the postoperative discomfort observed after CO2-pneumoperitoneum. Although gasless laparoscopy would appear to be particularly appealing for patients with severe cardiac or pulmonary disease, it compromizes surgical exposure and increases technical difficulty.
Laparoscopy during pregnancy22 Laparoscopy during pregnancy may increase the risk of miscarriage, premature labour, and damage to the gravid uterus. Open laparoscopy should be used to avoid damaging the uterus. Provided maternel PaCO2 is maintained at normal levels, physiology of the feto-placental unit seems unaffected by CO2-pneumoperitoneum. Mechanical ventilation must therefore be adjusted to maintain a physiologic maternal alkalosis. Capnometry remains adequate to guide ventilation during laparoscopy in pregnant patients. Respiratory acidosis does not occur when PETCO2 is maintained at 32 mm Hg. Gasless laparoscopy is an alternative which can sometimes be managed using epidural anaesthesia.
Postoperative benefits Soon after the development of laparoscopy for gastrointestinal surgical procedures, it became clear that the laparoscopic approach results in several benefits as compared with laparotomy. These benefits should be exploited to accelerate postoperative recovery. Nevertheless, postoperative side-effects persist and should be considered in the management of patients after surgery. The laparoscopic approach allows for reductions in surgical trauma to the abdominal wall and intra-abdominal viscera, as well as the stress response. This results in the shortening of postoperative ileus and subsequently the duration of postoperative fasting and hospital stay.1 Pain and analgesic consumption after laparoscopy are reduced as compared with open procedures.1,24 The pain characteristics also differ: visceral pain becomes
CURRENT ANAESTHESIA & CRITICAL CARE predominant and shouldertip pain appears as a consequence of pneumoperitoneum.23,24 Nevertheless, marked individual variability in pain scores is reported after operative laparoscopy, with some patients complaining of severe pain. Therefore, analgesia should not be neglected after laparoscopy. Laparoscopy for upper-abdominal procedures results in a postoperative pulmonary restrictive syndrome. This syndrome is less severe than after laparotomy;25 this explains why this approach is readily proposed in patients with respiratory disease. However, the problem does occur and is more marked in obese patients and those with chronic obstructive pulmonary disease than in healthy ones. Finally, the incidence of nausea and vomiting is high after laparoscopy, particularly laparoscopic gynaecologic procedures.
PRACTICAL IMPLICATIONS FOR THE ANAESTHETIC MANAGEMENT OF LAPAROSCOPY Patient positioning and monitoring3 Patients must be positioned with great care to prevent nerve injuries. Padding should be used to protect nerves from compression injury: peroneal nerve in the case of the lithotomy position, the ulnar nerve when the upper limbs are adducted against the body, the brachial plexus when using shoulder braces. Changes in patient position must be slow and progressive to avoid sudden haemodynamic and respiratory modifications. The position of the endotracheal tubes must be checked after any change in patient position, and again after insufflation. Arterial blood pressure, heart rate, electrocardiogram, capnometry and pulse oximetry must be continuously monitored. Capnometry is valuable to prevent hypercapnia and to diagnose gas embolism or CO2 subcutaneous emphysema as well as capnothorax. The use of real-time pressure volume measurement may be useful to monitor ventilatory changes secondary to pneumoperitoneum or capnothorax. The low incidence of gas embolism during laparoscopy precludes the routine use of expensive monitors. Changes of the cardiac electrical axis secondary to cephalad displacement of the diaphragm during pneumoperitoneum complicate the interpretation of continuous ST segment monitoring.
ANAESTHESIA3 Induction of anaesthesia The choice of anaesthetic technique does not seem to play a major role in patient outcome. Because of the
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potential for reflex increases in vagal tone during laparoscopy, atropine should be administered before the induction of anaesthesia, or should be ready for injection if necessary. Increasing circulating volume by infusion of i.v. fluid and/or by tilting the patient to a slight headdown position before pneumoperitoneum both attenuate the haemodynamic changes secondary to increased intra-abdominal pressure.13 Clonidine given i.v. before pneumoperitoneum improves haemodynamic stability.13 This treatment should not be administered in patients undergoing ambulatory surgery procedures. The stomach must be aspirated before trocar placement to avoid gastric perforation. The bladder should be emptied before pelvic laparoscopy or prolonged procedures. Due to venous stasis in the legs during laparoscopy, deep vein thrombosis prophylaxis should be initiated before surgery, as for laparotomy.
Maintenance of anaesthesia Volatile anaesthetics are valuable because of their vasodilating properties. Propofol anaesthesia results in less postoperative nausea and vomiting. Omission of nitrous oxide improves surgical conditions for colonic and intestinal surgery, but does not seem to be contraindicated for laparoscopic cholecystectomy. Whether nitrous oxide contributes to nausea and vomiting is still controversial. Nevertheless, nitrous oxide must be interrupted as soon as a gas embolism is suspected. Haemodynamic stability can be improved by the administration of clonidine or by the infusion of nicardipine, a calcium-channel blocker. Whether profound muscle relaxation is necessary for laparoscopy is not clear. Rather, a constant level of muscle relaxation is desirable to provide adequate surgical conditions and to avoid abrupt changes in intra-abdominal pressure. Remifentanil infusion at a rate of 0.3d0.4 lg/kg/min allows almost complete avoidance of the hypertensive response at the beginning of intra-abdominal insufflation (personal observation).
Ventilation and management of the airway General anaesthesia with endotracheal intubation and controlled ventilation is certainly the safest technique, and is recommended for in-patients and for long laparoscopic procedures. This technique allows the best control of PaCO2. Prevention of hypercapnia requires an increase in minute ventilation of no more than 15d25%, except when CO2 subcutaneous emphysema develops. Airway control using a laryngeal mask (LM) might be proposed as an alternative to endotracheal intubation, since it allows controlled ventilation and accurate monitoring of PETCO2 . However, decreased thoracopulmonary compliance during pneumoperi-
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toneum frequently results in airway pressures exceeding 20 cm H2O, a pressure above which an airway seal cannot be guaranteed with this device. Therefore, its use should be limited to circumstances associated with airway pressures lower than 20 cm H2O: healthy, thin patients (with high thoracopulmonary compliance), low risk of regurgitation of gastric contents (because the LM affords no protection of the airway from aspiration), for surgical procedures not associated with subcutaneous emphysema which requires marked hyperventilation. General anaesthesia in patients breathing spontaneously with a LM should be restricted to short procedures (less than 15 min before CO2 peaks) using low intra-abdominal pressure and small degrees of tilt.
Regional anaesthesia3 The haemodynamic effects of pneumoperitoneum under epidural anesthesia have not been studied. However, the vasodilation induced by sympathectomy, and avoidance of positive pressure ventilation might reduce the cardiovascular changes induced by pneumoperitoneum. Regional techniques provide excellent postoperative analgesia. These potential advantages must be balanced against certain disadvantages. Indeed, shouldertip pain secondary to diaphragmatic irritation as well as discomfort secondary to abdominal distension are incompletely alleviated using epidural anaesthesia, and may require i.v. analgesics. The extensive sensory block necessary for surgical laparoscopy may also lead to patient discomfort. Use of sedatives and/or an extensive block can interfere with the increased work of breathing required by decreased thoracopulmonary compliance and the absorption of CO2. Regional anaesthesia must be proposed with caution any time CO2-subcutaneous emphysema (which further increases CO2 absorption) may develop, particularly in patients with chronic obstructive pulmonary disease. Regional anaesthesia has been used for gynaecologic laparoscopy in the head-down position and for laparoscopic cholecystectomy in COPD patients without impairment of ventilation.26 Patient collaboration, an experienced and skilled laparoscopist, reduced degrees of both intra-abdominal pressure and tilt are necessary to guarantee the success of epidural anaesthesia, which should be avoided for long procedures. Epidural or spinal anaesthesia can be used for gasless laparoscopy since it provides adequate relief of pain and discomfort in these circumstances.
Anaesthesia for the patient with heart disease Because of the haemodynamic consequences of CO2pneumoperitoneum, some concerns have been raised
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with regard to tolerance of these changes by cardiac patients. In the light of the haemodynamic consequences of laparoscopy, patients most at risk are those with compromised ventricular function (such as congestive heart failure), and those with severe valvular diseases which render them intolerant of increased afterload. The haemodynamic consequences of pneumoperitoneum are minor in heart transplant recipients. It is well established that peri-operative risk in cardiac patients undergoing non-cardiac surgery is higher during the postoperative period, when the patient is no longer protected by the close surveillance of the anaesthesiologist. This notion may be extended to laparoscopic surgery. Laparoscopy probably results in more haemodynamic changes than laparotomy. However, these changes occur mainly at the beginning of insufflation. Moreover, knowledge and understanding of the intraoperative changes, as well as the pathophysiology of the cardiac disease, allow them to be minimized. On the other hand, the postoperative benefits of laparoscopy are welcome in these ill patients. Anaesthetic management of cardiac patients comprises several measures: (1) patients with a profile suggesting depleted intravascular volume experience the most severe haemodynamic changes. Preload augmentation before peritoneal insufflation partially offsets haemodynamic deterioration; (2) insufflation must be slow, and intra-abdominal pressure must be kept as low as possible; (3) vasodilators can be used to correct or prevent the increase in afterload. Nicardipine, a calcium-channel blocker, presents an adequate profile: reduction of afterload, no effect on preload, no effect on contractility; (4) in case of poor ventricular function, an inotropic agent such as dobutamine may be necessary; (5) we routinely infuse a small intraoperative dose of clonidine (0.150 mg) to reduce the hyperdynamic state occurring after exsufflation; (6) a diuretic may be necessary to restore preoperative intravascular volume status. It should be kept in mind that pressures measured with a pulmonary artery catheter do not accurately reflect cardiac filling pressures during pneumoperitoneum due to the increase in intrathoracic pressure.
CURRENT ANAESTHESIA & CRITICAL CARE disease.1,4,25 It should be noted that, despite better preservation of pulmonary function after laparoscopy, the restrictive syndrome reported in these patients is more marked than in healthy patients; it must therefore be considered when caring for these patients. Preoperative optimization of respiratory function remains necessary even before minimally invasive surgery. In these patients, pneumoperitoneum alters the distribution of pulmonary ventilation and perfusion. This results in an enlargement of alveolar dead space. Therefore, the PaCO2 to PETCO2 gradient increases and PETCO2 no longer accurately reflects PaCO2.9 Due to decreased thoracopulmonary compliance secondary to pneumoperitoneum, airway pressures increase. To avoid excessive airway pressures, which could potentially lead to rupture of emphysematous bullae, the hyperventilation normally required during CO2-pneumoperitoneum can be limited. As a consequence, permissive hypercapnia develops. A reduction in airway pressures can be also achieved by increasing respiratory rate rather than tidal volume. Finally, we also administer clonidine to these patients because it reduces metabolism and attenuates the requirement for hyperventilation. Caution is required in case of CO2-subcutaneous emphysema, since it increases the body load of CO2 to be eliminated and consequently the work of breathing.
Postoperative analgesia Postoperative pain and analgesic requirements are less after laparoscopy than laparotomy.1,24 As a consequence, very good pain relief can be provided not only using epidural analgesia but also using ‘balanced’ analgesia with systemic analgesics.24,27 Indeed, because of pain characteristics, a combination of different non-opioid analgesics (paracetamol, non-steroidal anti-inflammatory drugs, tramadol) allows opioid-free analgesia, further accelerating recovery of intestinal function. Tramadol relieves visceral pain, which predominates after gynaecologic and gastro-intestinal laparoscopic procedures, whereas paracetamol and NSAIDs alleviate parietal and shouldertip pain. However, high individual variability in pain intensity is reported, and opioids still may be necessary in some patients. Finally, controversy remains regarding the efficacy of intraperitoneal instillation of local anaesthetics.23,27 Whereas this technique provides some pain relief after gynaecologic laparoscopy, no significant effects are reported after laparoscopic cholecystectomy.
Anaesthesia for the patient with chronic obstructive pulmonary disease3 The reduction in the postoperative pulmonary restrictive syndrome observed after laparoscopy as compared to laparotomy justifies efforts to use the laparoscopic approach in patients with respiratory
Prevention of postoperative nausea and vomiting The incidence of nausea and vomiting is high after laparoscopy, particularly gynaecologic procedures.
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Several measures, used alone or in combination, can reduce the incidence of these side-effects: these measures include use of propofol, prophylactic administration of antiemetic medications, suction of gastric contents at the end of laparoscopy and intraoperative administration of a high oxygen concentration (80%).
CONCLUSION A better knowledge of the pathophysiologic changes induced by CO2-pneumoperitoneum allows the clinician to reduce their impact and to allow a greater number of patients to benefit from the postoperative advantages of laparoscopy. Increased surgeon experience is associated with decreased operative times and rates of minor or moderate surgical complications. At this time, the postoperative benefits largely outweigh intraoperative side effects, which can be corrected or prevented by an anaesthesiologist who is aware of the pathophysiology of pneumoperitoneum. This balance in favour of laparoscopy justifies efforts to apply the laparoscopic approach to other surgical procedures.
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10. Wahba R W, Tessler M J, Kleiman S J. Acute ventilatory complications during laparoscopic upper abdominal surgery. Can J Anaesth 1996; 43: 77d83. 11. Joris J, Chiche J D, Lamy M L. Pneumothorax during laparoscopic fundoplication: diagnosis and treatment with positive endexpiratory pressure. Anesth Analg 1995; 81: 993d1000. 12. Struthers A D, Cuschieri A. Cardiovascular consequences of laparoscopic surgery. Lancet 1998; 352: 568d570. 13. Joris J, Chiche J D, Canivet J L, Jacquet N, Legros J J, Lamy M L. Hemodynamic changes induced by laparoscopy and their endocrine correlates: effects of clonidine. J Am Coll Cardiol. 1998; 32: 1389d1396. 14. Andersson L, Wallin C J, Sollevi A, Odeberg-Wernerman J. Pneumoperitoneum in healthy humans does not affect central blood volume or cardiac output. Acta Anaesthesiol Scand 1999; 43: 809d814. 15. Feig B W, Berger D H, Dougherty T B, Dupuis J F, His B, Hickey R C et al. Pharmacologic intervention can reestablish baseline hemodynamic parameters during laparoscopy. Surgery 1994; 116: 733d741. 16. Hein H A, Joshi G P, Ramsay M A et al. Hemodynamic changes during laparoscopic cholecystectomy in patients with severe cardiac disease. J Clin Anesth 1997; 9: 261d265. 17. Kashtan J, Green J F, Parsons E Q, Holcroft J W. Hemodynamic effects of increased intraabdominal pressure. J Surg Res 1981; 30: 249d255. 18. Catheline J M, Turner R, Gaillard J L, Rizk N, Champault G. Thromboembolism in laparoscopic surgery: risk factors and preventive measures. Surg Laparosc Endosc 1999; 9: 135d139. 19. Iwase K, Takenaka H, Ishizaka T, Ohata T, Oshima S, Sakaguchi K. Serial changes in renal function during laparoscopic cholecystectomy. Eur Surg Res 1993; 25: 203d212. 20. Blobner M, Bogdanski R, Kochs E, Henke J, Finders A, JelenEsselborn S. Effects of intraabdominally insufflated carbon dioxide and elevated intraabdominal pressure on splanchnic circulation: an experimental study in pigs. Anesthesiology 1998; 89: 475d482. 21. Koivusalo A M, Kellokumpu I, Scheinin M, Tikkanen I, Makisalo H, Lindgren L. A comparison of gasless mechanical and conventional carbon dioxide pneumoperitoneum methods for laparoscopic cholecystectomy. Anesth Analg 1998; 86: 153d158. 22. Lemaire B, van Erp W F. Laparoscopic surgery during pregnancy. Surg Endosc 1997; 11: 15d18. 23. Joris J, Thiry E, Paris P, Weerts J, Lamy M. Pain after laparoscopic cholecystectomy: characteristics and effect of intraperitoneal bupivacaine. Anesth Analg 1995; 81: 379d384. 24. Alexander J I. Pain after laparoscopy. Br J Anaesth 1997; 79: 369d378. 25. Karayiannakis A J, Makri G G, Mantzioka A et al: Postoperative pulmonary function after laparoscopic and open cholecystectomy. Br J Anaesth 1996; 77: 448d452. 26. Pursnani K G, Bazza Y, Calleja M, Mughal M M. Laparoscopic cholecystectomy under epidural anesthesia in patients with chronic respiratory disease. Surg Endosc 1998; 12: 1082d1084. 27. Bisgaard T, Klarskov B, Kristiansen V B et al. Multi-regional local anesthetic infiltration during laparoscopic cholecystectomy in patients receiving prophylactic multi-modal analgesia: a randomi zed, double blinded, placebo-controlled study. Anesth Analg 1999; 89: 1017d1024.