anestesia laparoscopia

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68 Anesthesia for Laparoscopic Surgery

Jean L. Joris

Key Points

1. CO2 pneumoperitoneum results in ventilatory and respiratory changes. Pneumoperitoneum decreases thoracopulmonary compliance. PaCO2 increases (15% to 25%) due to CO2 absorption from the peritoneal cavity. Capnography reliably reflects this increase, which plateaus after 20 to 30 minutes.

2. In compromised patients, cardiorespiratory disturbances aggravate the increase in PaCO2 and enlarge the gradient between PaCO2 and PETCO2.

3. Any increase in PETCO2 larger than 25% or occurring later than 30 minutes after the beginning of peritoneal CO2 insufflation should suggest CO2 subcutaneous emphysema, the most frequent respiratory complication during laparoscopy.

4. Peritoneal insufflation induces alterations of hemodynamics, characterized by decreases of cardiac output, elevations of arterial pressure, and increases of systemic and pulmonary vascular resistances. Hemodynamic changes are accentuated in high-risk cardiac patients.

5. The pathophysiologic hemodynamic changes can be attenuated or prevented by optimizing preload before pneumoperitoneum and by vasodilating agents, α2-adrenergic receptors agonists, high doses of opioids, and β-blocking agents.

6. Similar pathophysiologic changes occur during pregnancy and in children. Laparoscopy can be safely managed in pregnant women before the 23rd week of pregnancy provided that hypercarbia is prevented. The open laparoscopy approach should be considered to avoid damaging the uterus.

7. Gasless laparoscopy may be helpful to reduce pathophysiologic changes induced by CO2 pneumoperitoneum but unfortunately increases technical difficulty.

8. Laparoscopy results in multiple postoperative benefits, allowing for quicker recovery and shorter hospital stay. These advantages explain the increasing success of laparoscopy, which is proposed for many surgical procedures.

9. Although no anesthetic technique has proved to be clinically superior to any other, general anesthesia with controlled ventilation seems to be the safest technique for operative laparoscopy.

10. 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.

Surgical procedures have been improved to reduce trauma to the patient, morbidity, mortality, and hospital stay, with consequent reductions in health care costs. The provision of better equipment and facilities, along with increased knowledge and understanding of anatomy and pathology, has allowed the development of endo s-copy for diagnostic and operative procedures. Starting in the early 1970s, various pathologic gynecologic conditions were diagnosed and treated using laparoscopy. This endoscopic approach was extended to cholecystectomy in the late 1980s. Since the intro-duction of the first laparoscopic cholecystectomy procedures,1 laparoscopy has expanded impressively both in scope and volume. It quickly became apparent that laparoscopy results in multiple

benefits compared with open procedures2,3 and was characterized by better maintenance of homeostasis. Overenthusiasm ensued, which explains the effort to use the laparoscopic approach for gastrointestinal (e.g., colonic, gastric, splenic, hepatic surgery), gynecologic (e.g., hysterectomy), urologic (e.g., nephrectomy, prostatectomy), and vascular (e.g., aortic) procedures.

The pneumoperitoneum and the patient positions required for laparoscopy induce pathophysiologic changes that complicate anesthetic management. An understanding of the pathophysio-logic consequences of increased intra-abdominal pressure (IAP) is important for the anesthesiologist who must ideally prevent or, when prevention is not possible, adequately respond to these

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changes and who must evaluate and prepare the patient preopera-tively in light of these disturbances. The pathophysiologic changes and the complications of laparoscopy are reviewed first. The post-operative period is considered next, with examination of the ben-efits of laparoscopy and certain specific postoperative problems (e.g., pain, nausea). Practical consequences for the anesthetic management of laparoscopy are presented. Many animal and human studies of the consequences of laparoscopy have been published since the early 1970s. Because much higher IAPs (>20 mm Hg) were previously used and because of potential species differences, we have focused on the human literature published after 1990 using low IAP (<15 mm Hg) and modern anesthesia techniques.

Ventilatory and Respiratory Changes During Laparoscopy

Intraperitoneal insufflation of carbon dioxide (CO2), the cur-rently routine technique to create pneumoperitoneum for laparo s-copy, results in ventilatory and respiratory changes and can cause four principal respiratory complications: CO2 subcutaneous emphysema, pneumothorax, endobronchial intubation, and gas embolism.4

Ventilatory Changes

Pneumoperitoneum decreases thoracopulmonary compliance by 30% to 50% in healthy5-7 and obese patients.8,9 Reduction in functional residual capacity10 and development of atelectasis due to elevation of the diaphragm11 and changes in the distribu-tion of pulmonary ventilation and perfusion from increased airway pressure can be expected.11 However, increasing IAP to 14 mm Hg with the patient in a 10- to 20-degree head-up or head-down position does not significantly modify either physio-logic dead space or shunt in patients without cardiovascular problems.12,13

Increase in the Partial Pressure of Arterial Carbon Dioxide

During uneventful CO2 pneumoperitoneum, the partial pressure of arterial carbon dioxide (PaCO2) progressively increases to reach a plateau 15 to 30 minutes after the beginning of CO2 insufflation in patients under controlled mechanical ventilation during gyne-cologic laparoscopy in the Trendelenburg position14 or during laparoscopic cholecystectomy in the head-up position (Fig. 68-1).15,16 Any significant increase in PaCO2 after this period requires a search for a cause independent of or related to CO2 insufflation, such as CO2 subcutaneous emphysema. The increase in PaCO2 depends on the IAP.17 During laparoscopy with local anesthesia, PaCO2 remains unchanged but minute ventilation sig-nificantly increases.18

Capnography and pulse oximetry provide reliable monitor-ing of PaCO2 and arterial oxygen saturation in healthy patients and in the absence of acute intraoperative disturbances (see Figure 68-1).15,16 Although mean gradients (∆a-ETCO2) between PaCO2 and the end-tidal carbon dioxide tension (PETCO2) do not change significantly during peritoneal insufflation of CO2, individual patient data regularly show variations of this difference during pneumoperitoneum.19,20 PaCO2 and ∆a-ETCO2 increase more in ASA class II and III patients than in ASA class I patients (Fig. 68-2).21,22 These findings have been documented in patients with chronic obstructive pulmonary disease (COPD)23 and in children with cyanotic congenital heart disease.24 These data therefore highlight the lack of correlation between PaCO2 and PETCO2 in sick patients, particularly those with impaired CO2 excretion capacity, and in otherwise healthy patients with acute cardiopulmonary disturbances. Consequently, hypercapnia can develop, even in the absence of abnormal PETCO2. Postoperative intra-abdominal CO2 retention results in increased respiratory rate and PETCO2 of patients breathing spontaneously after laparoscopic cholecystec-tomy as compared with open cholecystectomy.25

During CO2 pneumoperitoneum, the increase of PaCO2 may be multifactorial: absorption of CO2 from the peritoneal cavity, impairment of pulmonary ventilation and perfusion by mechanical factors such as abdominal distention, patient posi-

Figure 68-1 Ventilatory changes (pH, PaCO2, and PETCO2) during CO2 pneumoperitoneum for laparoscopic cholecystectomy. For 13 American Society of Anesthesiologists (ASA) class I and II patients, minute ventilation was kept constant at 100 mL/kg/min with a respiratory rate of 12 breaths/min during the study. Intra-abdominal pressure was 14 mm Hg. Data are given as the mean ± SEM.*, P < .05 compared with time 0.***

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adjusted in response to the increased dead space, alveolar ventila-tion will decrease and PaCO2 will rise. In healthy patients, absorp-tion of CO2 from the abdominal cavity represents the main (or the only) mechanism responsible for increased PaCO2,13 but in patients with cardiorespiratory problems, ventilatory changes also significantly contribute to increasing PaCO2.21 PaO2 values and intrapulmonary shunt do not significantly change during laparoscopy.12,13

It is wise to maintain PaCO2 within a physiologic range by adjusting the mechanical ventilation. Except in special circum-stances, such as when CO2 subcutaneous emphysema occurs (see later), correction of increased PaCO2 can be easily achieved by a 10% to 25% increase in alveolar ventilation.

Respiratory Complications

CO2 Subcutaneous EmphysemaCO2 subcutaneous emphysema can develop as a complication of accidental extraperitoneal insufflation33 but can also be consid-ered as an unavoidable side effect of certain laparoscopic surgical procedures that require intentional extraperitoneal insufflation, such as inguinal hernia repair, renal surgery, and pelvic lym-phadenectomy (Fig. 68-3).14,34,35 During laparoscopic fundoplica-tion for hiatal hernia repair, the opening of the peritoneum overlying the diaphragmatic hiatus allows passage of CO2 under pressure through the mediastinum to the cervicocephalic region. In these circumstances, !VCO2, PaCO2, and PETCO2 increase.14 Any increase in PETCO2 occurring after PETCO2 has plateaued should suggest this complication. The increase in !VCO2 may be such that prevention of hypercapnia by adjustment of ventilation 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 insufflation pressure. Indeed, CO2 pressure determines the extent of the emphysema and the magnitude of CO2 absorption. CO2 subcutaneous emphy-sema readily resolves once insufflation has ceased. CO2 sub-cutaneous emphysema, even cervical, does not counterindicate tracheal extubation at the end of surgery.36 We recommend keeping the patient mechanically ventilated until hypercapnia is corrected, particularly in COPD patients, to avoid an excessive increase in the work of breathing.

Pneumothorax, Pneumomediastinum, PneumopericardiumMovement of gas during the creation of a pneumoperitoneum can produce pneumomediastinum,37 unilateral and bilateral pneumothoraces,38 and pneumopericardium.39 Embryonic rem-nants constitute potential channels of communication between the peritoneal cavity and the pleural and pericardial sacs, which can open when intraperitoneal pressure increases. Defects in the diaphragm or weak points in the aortic and esophageal hiatus may allow gas passage into the thorax. Pneumothoraces may also develop secondary to pleural tears during laparoscopic surgical procedures at the level of the gastroesophageal junction (e.g., fundoplication for hiatal hernia). Although opening of peritoneo-pleural ducts is associated with mainly right-sided pneumo-thoraces (in the same way that ascites or peritoneal dialysis may be associated with right-sided pleural effusions40), the pneumo-thorax associated with fundoplication is more frequently in the left side of the chest.

Figure 68-2 Ventilatory changes as a function of patient physical status. The PaCO2 and PETCO2 were measured before and during CO2 insufflation. Patients were grouped according to ASA classification: group 1 (green circles), ASA I (n = 20); group 2 (blue circles), ASA II-III (n = 10). (Data from Wittgen CM, Andrus CH, Fitzgerald SD, et al: Analysis of the hemodynamic and ventilatory effects of laparoscopic cholecystectomy. Arch Surg 126:997, 1991.)

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tion, and volume-controlled mechanical ventilation. The observa-tion of an increase in PaCO2 when CO2, but not nitrous oxide (N2O) or helium, was used as the insufflating gas suggests that the main mechanism of the increased PaCO2 during CO2 pneumo-peritoneum is absorption of CO2 rather than the mechanical ven-tilatory repercussions of increased IAP.26,27 Accordingly, direct measurement of CO2 elimination !VCO2( ) using a metabolic monitor combined with investigation of gas exchange showed a 20% to 30% increase of !VCO2 without significant changes in phy-siologic dead space in healthy patients undergoing pelvic lapar-oscopy (IAP of 12 to 14 mm Hg) in the head-down position14,28 or laparoscopic cholecystectomy in the head-up position.14,29 The time courses of the increase in !VCO2 and PaCO2 are similar. The absorption of a gas from the peritoneal cavity depends on its dif-fusibility, the absorption area, and the perfusion of the walls of that cavity. Because CO2 diffusibility is high, absorption of large quantities of CO2 into the blood and the subsequent marked increases in PaCO2 would be expected to occur. The limited rise of PaCO2 actually observed can be explained by the capacity of the body to store CO2

30 and by impaired local perfusion due to increased IAP.17 During deflation, CO2 that accumulated in col-lapsed peritoneal capillary vessels reaches the systemic circula-tion, leading to transient increases in PaCO2 and !VCO2.31

Respiratory changes during the laparoscopic procedure may contribute to increasing CO2 tension. Mismatched ventila-tion and pulmonary perfusion can result from the position of the patient and from the increased airway pressures associated with abdominal distention.18,32 Lister and colleagues17 investigated the relationship between !VCO2 and intraperitoneal CO2 insufflation pressure in pigs. For an IAP up to 10 mm Hg, increased !VCO2 accounts for the increased PaCO2. At higher IAPs, the continued rise of PaCO2 without a corresponding increase in !VCO2 results from an increase in respiratory dead space, as reflected by a wid-ening of the ∆a-ETCO2 gradient.17 If controlled ventilation is not

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These complications are potentially serious and may lead to respiratory and hemodynamic disturbances. Capnothorax (CO2 causing a pneumothorax) reduces thoracopulmonary compliance and increases airway pressures. !VCO2, PaCO2, and PETCO2 also increase.41 In effect, the absorption surface of CO2 is increased and the absorption from the pleural cavity is greater than from the peritoneal cavity. When a pneumothorax occurs secondary to alveolar rupture, the PETCO2 decreases because of decreased cardiac output. Hemodynamic changes and oxygen desaturation should suggest the presence of a tension pneumothorax. The laparoscopist may observe abnormal motion of one hemidiaphragm when a tension pneumothorax has occurred. It should be noted that cervical and upper thoracic subcutaneous emphysema can develop without the presence of a pneumothorax.

When a pneumothorax is caused by highly diffusible gas such as N2O or CO2 without associated pulmonary trauma, spon-taneous resolution of the pneumothorax occurs within 30 to 60 minutes without thoracocentesis.42 When capnothorax develops during laparoscopy, treatment with positive end-expiratory pres-sure (PEEP) is an alternative to chest tube placement.41 In con-trast, if the pneumothorax is secondary to rupture of preexisting bullae, PEEP must not be applied and thoracocentesis is mandatory.

Endobronchial IntubationCephalad displacement of the diaphragm during pneumoperito-neum results in cephalad movement of the carina in children43 and adults,44 potentially leading to an endobronchial intubation. Cases of endobronchial intubation associated with laparoscopy are reported during procedures in the head-down position45 and in the head-up position.44,46 This complication results in a decrease in the oxygen saturation as measured by pulse oximetry (SpO2) associated with an increase in plateau airway pressure (see Fig. 68-3).

Gas EmbolismAlthough rare, gas embolism is the most feared and dangerous complication of laparoscopy. Intravascular injection of gas may follow direct needle or trocar placement into a vessel, or it may occur as a consequence of gas insufflation into an abdominal organ. This complication develops principally during the induc-tion of pneumoperitoneum,47,48 particularly in patients with pre-vious abdominal surgery.49 Gas embolism may also occur later during surgery.50,51 CO2 is used most frequently for laparoscopy because it is more soluble in blood than either air, oxygen, or N2O.30 Rapid elimination also increases the margin of safety in case of intravenous injection of CO2. All these characteristics explain the rapid reversal of the clinical signs of CO2 embolism with treatment. Consequently, the lethal dose of embolized CO2 is approximately five times greater than that of air.

The pathophysiology of gas embolism is also determined by the size of the bubbles and the rate of intravenous entry of the gas.52,53 During laparoscopy, the rapid insufflation of gas under high pressure probably causes a “gas lock” in the vena cava and right atrium; obstruction to venous return with a fall in cardiac output or even circulatory collapse can result. Acute right ven-tricular hypertension may open the foramen ovale, allowing para-doxical gas embolization.50,54 Paradoxical embolism, however, may occur without patent foramen ovale.55 Volume preload diminishes the risk of gas embolism56 and of paradoxical embo-lism.57 Ventilation-perfusion ( ! !V Q) mismatching develops with increases in physiologic dead space and hypoxemia.

The diagnosis of gas embolism depends on the detection of gas emboli in the right side of the heart or on recognition of the physiologic changes from embolization. Early events, occur-ring with 0.5 mL/kg of air or less, include changes in Doppler sounds and increased mean pulmonary artery pressure. The low incidence of gas embolism during laparoscopy precludes the routine use of invasive or expensive monitors to detect emboliza-tion of small quantities of gas. When the size of the embolus

Figure 68-3 Diagnosis of respiratory complications during laparoscopy. ECG, electrocardiographic; Paw, airway pressure; PETCO2, end-tidal carbon dioxide tension. (Data from Wahba RW, Tessler MJ, Kleiman SJ: Acute ventilatory complications during laparoscopic upper abdominal surgery. Can J Anaesth 43:77, 1996.)

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a) Reduced air entry Yes Yes Yes MurmurNob) Hyperresonance Yes Yes HypotensionNoNoc) Swelling and crepitus

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increases (2 mL/kg of air), tachycardia, cardiac arrhythmias, hypotension, increased central venous pressure, alteration in heart tones (i.e., millwheel murmur), cyanosis, and electrocardiog-raphic changes of right-sided heart strain can develop; all these changes are rarely consistently positive.58 Pulmonary edema can also be an early sign of gas embolism.54 Although pulse oximetry is helpful in recognizing hypoxemia, capnometry and capno g-raphy are more valuable in providing early diagnosis of gas embo-lism and determining the extent of the embolism. PETCO2 decreases in the case of embolism owing to the fall in cardiac output and the enlargement of the physiologic dead space. Con-sequently, ∆a-ETCO2 increases. The decrease in PETCO2 may be preceded by an initial increase secondary to pulmonary excretion of the CO2, which has been absorbed into the blood.53 Aspiration of gas or foamy blood from a central venous line establishes the diagnosis. Routine preoperative insertion of a central venous line, however, does not appear justified for these procedures.

Treatment of CO2 embolism consists of immediate cessa-tion of insufflation and release of the pneumoperitoneum. The patient is placed in steep head-down and left lateral decubitus (Durant) position. The amount of gas that advances through the right side of the heart to the pulmonary circulation is less if the patient is in this position because the buoyant foam is displaced laterally and caudally away from the right ventricular outflow tract. Discontinuing N2O will allow ventilation with 100% O2 to correct hypoxemia and reduce the size of the gas embolus and its consequences.53 Hyperventilation increases CO2 excretion and is made necessary by the increase in the physiologic dead space. If these simple measures are not effective, a central venous or pul-monary artery catheter may be introduced for aspiration of the gas. Cardiopulmonary resuscitation must be initiated if necessary. External cardiac massage may be helpful in fragmenting CO2 emboli into small bubbles. The high solubility of CO2 in blood, resulting in rapid absorption from the bloodstream, accounts for the rapid reversal of the clinical signs of CO2 embolism with treatment.48 CO2 embolism, however, may be fatal. Cardiopul-monary bypass has been used successfully to treat massive CO2 embolism.50 Hyperbaric oxygen treatment should be strongly considered if cerebral gas embolism is suspected.54

Risk of Aspiration of Gastric ContentsPatients undergoing laparoscopy might be considered to be at risk for acid aspiration syndrome (see also Chapter 50). However, the increased IAP results in changes of the lower esophageal sphincter that allow maintenance of the pressure gradient across the gastroesophageal junction and that may therefore reduce the risk of regurgitation.59,60 Furthermore, the head-down position should help to prevent any regurgitated fluid from entering the airway.

Hemodynamic Problems During Laparoscopy

Hemodynamic changes observed during laparoscopy result from the combined effects of pneumoperitoneum, patient position, anesthesia, and hypercapnia from the absorbed CO2. In addition to these pathophysiologic changes, reflex increases of vagal tone and arrhythmias can also develop.

Hemodynamic Repercussions of Pneumoperitoneum in Healthy Patients

Peritoneal insufflation to IAPs higher than 10 mm Hg induces significant alterations of hemodynamics.61,62 These disturbances are characterized by decreases in cardiac output, increased arte-rial pressures, and elevation of systemic and pulmonary vascular resistances. Heart rates remain unchanged or increased only slightly. The decrease in cardiac output is proportional to the increase in IAP.63 Cardiac output has also been reported to be increased64 or unchanged during pneumoperitoneum.65,66 These discrepancies might be caused by differences in rates of CO2 insufflation, IAP,67 steepness of patient tilt, time intervals between insufflation and collection of data, techniques used to assess hemodynamics, and anesthetic techniques. However, most studies have shown a fall of cardiac output (10% to 30%) during perito-neal insufflation whether the patient was placed in the head-down68,69 or head-up position.70,71 These adverse hemodynamic effects of pneumoperitoneum have been confirmed by studies using pulmonary artery catheterization,69,71 thoracic electrical bioimpedance,68,70 esophageal echo-Doppler,72 and transesopha-geal echocardiography.73-75 Normal intraoperative values of venous oxygen saturation SvO2( ) and lactate concentrations suggest that changes in cardiac output occurring during pneu-moperitoneum are well tolerated by healthy patients.71,76 Cardiac outputs, which decrease shortly after the beginning of the perito-neal insufflation, subsequently increase, probably as a result of surgical stress.70,71 Hemodynamic perturbations occur mainly at the beginning of peritoneal insufflation.

The mechanism of the decrease of cardiac output is multi-factorial (Fig. 68-4). A decrease in venous return is observed after a transient increase in venous return at low IAPs (<10 mm Hg).77,78 Increased IAP results in caval compression,79 pooling of blood in the legs,80 and an increase in venous resistance.77,78 The decline in venous return, which parallels the decrease in cardiac output,63 is confirmed by a reduction in left ventricular end-diastolic volume measured using transesophageal echocardiography.74 Cardiac filling pressures, however, rise during peritoneal insufflation.69,71 The paradoxical increase of these pressures can be explained by the increased intrathoracic pressure associated with pneumoperi-toneum.70,81,82 Right atrial pressure and pulmonary artery occlu-sion pressure can no longer be considered reliable indices of cardiac filling pressures during pneumoperitoneum. The fact that atrial natriuretic peptide concentrations remain low despite increased pulmonary capillary occlusion pressure during pneu-moperitoneum further suggests that abdominal insufflation interferes with venous return.83 The reduction in venous return and cardiac output can be attenuated by increasing circulating volume before the pneumoperitoneum is produced (Fig. 68-5).77,84 Increased filling pressures can be achieved by fluid loading or tilting the patient to a slight head-down position before peritoneal insufflation, by preventing the pooling of blood with intermittent sequential pneumatic compression device,85 or by wrapping the legs with elastic bandages.86

The ejection fraction of the left ventricle, assessed by echocardiography, does not appear to decrease significantly when IAP increases to 15 mm Hg.73,74 However, all studies describe an increase in systemic vascular resistance during the existence of the pneumoperitoneum. This increase in afterload is not a reflex sympathetic response to the decreased cardiac output.73,82

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Systemic vascular resistance was reported to be increased in studies where no decrease in cardiac output was found.73,76 Although the normal heart tolerates increases in afterload under physiologic conditions, the increases in afterload produced by the presence of a pneumoperitoneum can be deleterious to patients with cardiac disease.87

The increase in systemic vascular resistance is affected by patient position. The Trendelenburg position attenuates this increase; the head-up position aggravates it.65,69,76,83 The increase in systemic vascular resistance can be corrected by the administration of vasodilating anesthetic agents, such as isoflu-rane,82 or direct vasodilating drugs, such as nitroglycerin88 or nicardipine.89

The increase in systemic vascular resistance is thought to be mediated by mechanical and neurohumoral factors.90 The return of hemodynamic parameters to baseline values is gradual, taking several minutes, suggesting the involvement of neuro-humoral factor(s).68,82,87 Catecholamines, the renin-angiotensin system, and especially vasopressin are all released during the pres-ence of the pneumoperitoneum and may contribute to increasing the afterload.70,71,81,83,91,92 However, only the time course of vaso-pressin release parallels that of the increase in systemic vascular resistance.70,71,92 Increases in plasma vasopressin concentrations correlate with changes in intrathoracic pressure and transmural right atrial pressure.81 Mechanical stimulation of peritoneal recep-tors also results in increased vasopressin release,93 systemic vas-

Figure 68-5 Changes in the cardiac index and systemic vascular resistance during laparoscopy in two groups of patients. For group 1 (controls, n = 10, yellow bars), pneumoperitoneum was induced with patients in a 10-degree head-up position. Group 2 (volume loaded, n = 10, blue bars) patients received 500 mL of lactated Ringer’s solution before anesthesia induction and were insufflated in the supine position. Data are presented as the mean ± SEM.

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Figure 68-4 Schematic representation of the different mechanisms leading to decreased cardiac output during pneumoperitoneum for laparoscopy.

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cular resistance, and arterial pressure.94 However, whether increasing IAP to 14 mm Hg is sufficient to stimulate these recep-tors is unknown. The increase in systemic vascular resistance also explains why the arterial pressure increases but the cardiac output falls.62,90 Use of α2-adrenergic agonists such as clonidine71,95 or dexmedetomidine96,97 and of β-blocking agents98 significantly reduces hemodynamic changes and anesthetic requirements. Use of high doses of remifentanil almost completely prevents the hemodynamic changes.66

Effect of Pneumoperitoneum on Regional Hemodynamics

Increased IAP and the head-up position result in lower limb venous stasis.80,85,99 Femoral vein blood flow decreases progres-sively with increasing IAP, and no adaptation to the reduced femoral venous outflow occurs, even during prolonged proce-dures.100 These changes may predispose to the development of thromboembolic complications. Although cases of thromboem-bolism have been reported in the literature, their actual incidence does not seem to be increased by laparoscopy.101-103

The effect of CO2 pneumoperitoneum on renal function has also been investigated.104-106 Urine output, renal plasma flow, and glomerular filtration rate decrease to less than 50% of base-line values during laparoscopic cholecystectomy and are signifi-cantly lower than those during open cholecystectomy.104 Urine output significantly increases after deflation.

Controversy exists regarding the effect of the CO2 pneu-moperitoneum on splanchnic and hepatic blood flow. A signifi-cant reduction was reported in animals107 and humans.108-110 However, others have not observed any significant changes.111-114 Blobner and coworkers,112 comparing CO2 pneumoperitoneum and air pneumoperitoneum in pigs, observed a reduction in splanchnic blood flow during air pneumoperitoneum but not during CO2 pneumoperitoneum. They suggest that the direct splanchnic vasodilating effect of CO2 may counteract the mechan-ical effect of increased IAP.

Cerebral blood flow velocity increases during CO2 pneu-moperitoneum in response to the increased PaCO2.115,116 When normocarbia is maintained, pneumoperitoneum combined with the head-down position does not induce harmful changes in intracranial dynamics.117 Intracranial pressure nevertheless rises during CO2 pneumoperitoneum, independently of changes in PaCO2, in pigs with preoperative induced intracranial hyperten-sion or normal intracranial pressure118,119 and in children with ventriculoperitoneal shunts.120 Intraocular pressure is not affected by pneumoperitoneum in women with no preexisting eye disease.121 In an animal model of glaucoma, pneumoperitoneum only slightly increases intraocular pressure.122

Hemodynamic Repercussions of Pneumoperitoneum in High-Risk Cardiac Patients

The demonstration of significant hemodynamic changes during pneumoperitoneum raises the question of tolerance of these changes in cardiac patients (see Chapters 35 and 60). In patients

with mild to severe cardiac disease, the pattern of change in mean arterial pressure, cardiac output, and systemic vascular resistance is qualitatively similar to that in healthy patients.87,88,123-126 Quan-titatively, these changes appear to be more marked. In a initial study including ASA class III or IV patients, SvO2 decreased in 50% of patients despite preoperative hemodynamic optimization using a pulmonary artery catheter.124 Patients who experienced the most severe hemodynamic changes with inadequate oxygen delivery were patients with low preoperative cardiac outputs and central venous pressures and high mean arterial pressures and systemic vascular resistances—a profile suggesting depleted intra-vascular volume. The investigators suggest preoperative preload augmentation to offset the hemodynamic effect of pneumoperi-toneum. Intravenous nitroglycerin, nicardipine, or dobutamine has been used to manage the hemodynamic changes induced by increased IAP in selected patients with heart disease.88,126 Nitro-glycerin was chosen to correct the reduction in cardiac output associated with increased pulmonary capillary occlusion pres-sures and systemic vascular resistance. The administration of nicardipine may be more appropriate than that of nitroglycerin. Right atrial and pulmonary capillary occlusion pressures are not reliable indices of cardiac filling pressure during pneumoperito-neum. Increased afterload is a major contributor to the altered hemodynamics seen during pneumoperitoneum in cardiac patients. Nicardipine acts selectively on arterial resistance vessels and does not compromise venous return.127 This drug is beneficial in case of congestive heart failure.128 Because normalization of hemodynamic variables does not occur for at least 1 hour post-operatively in certain patients,87,125 congestive heart failure can develop in the early postoperative period. Dhoste and associ-ates129 did not observe impaired hemodynamics in elderly ASA class III patients, but they used low IAP (10 mm Hg) and slow insufflation rates (1 L/min). The hemodynamic consequences of pneumoperitoneum are minor in heart transplant recipients who have good ventricular function.130,131 Laparoscopic adrenalectomy in patients with pheochromocytoma can be successfully managed using a continuous infusion of nicardipine.89,132 Several studies suggest that hemodynamic changes during pneumoperitoneum are well tolerated by morbidly obese patients.8,133,134

Cardiac Arrhythmias During Laparoscopy

Arrhythmias during laparoscopy have several causes. The increased PaCO2 may not be the cause of the arrhythmias occur-ring during laparoscopy. Arrhythmias do not correlate with the level of the PaCO2 and may develop early during insufflation, when high PaCO2 is not present.

Reflex increases of vagal tone may result from sudden stretching of the peritoneum and during electrocoagulation of the fallopian tubes.135 Bradycardia, cardiac arrhythmias, and asystole can develop. Vagal stimulation is accentuated if the level of anesthesia is too superficial or if the patient is taking β-blocking drugs. These events are easily and quickly reversible. Treatment consists of interruption of insufflation, atropine administration, and deepening of anesthesia after recovery of the heart rate.

Cardiac irregularities occur most often early, during insuf-flation, when pathophysiologic hemodynamic changes are the most intense. For this reason, arrhythmias may also reflect intol-erance of these hemodynamic disturbances in patients with

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known or latent cardiac disease. Gas embolism can also result in cardiac arrhythmias.

Problems Related to Patient Position

Patient positioning (see Chapter 36) depends on the site of surgery; whereas head-down tilt is used for pelvic and lower abdominal surgery, the head-up position is preferred for upper abdominal surgery. The patient is often placed in the lithotomy position. These positions may be responsible for, or contribute to, the development of pathophysiologic changes or injury during laparoscopy. The steepness of the tilt also affects the magnitude of these changes.

Cardiovascular Effects

In normotensive subjects, the head-down position results in an increase in central venous pressure and cardiac output. The baroreceptor reflex response to increased hydrostatic pressure consists of systemic vasodilation and bradycardia. Although these different reflexes may be impaired during general anesthesia, the hemodynamic changes induced by this position during laparo s-copy remain insignificant.69,76 However, central blood volume and pressure changes are greater in patients with coronary artery disease, particularly with poor ventricular function, leading to potentially deleterious increased myocardial oxygen demand.32 The Trendelenburg position may also affect the cerebral circula-tion, particularly in case of low intracranial compliance,136 and result in elevation of the intraocular venous pressure (which can worsen acute glaucoma).121 Although the intravascular pressure increases in the upper torso, the head-down position decreases transmural pressures in the pelvic viscera, reducing blood loss but increasing the risk of gas embolism.32,56

With the head-up position, a decrease in cardiac output and mean arterial pressure results from the reduction in venous return.69,76,82 This decrease in cardiac output compounds the hemodynamic changes induced by pneumoperitoneum. The steeper the tilt, the greater the fall in cardiac output.

Venous stasis in the legs occurs during the head-up posi-tion and may be aggravated by the lithotomy position with knees flexed.32 Because pneumoperitoneum further increases blood pooling in the legs,80,99 any additional factor contributing to cir-culatory dysfunction should be avoided. The legs must be freely supported and not tightly strapped, and pressure on the popliteal space must be prevented.

Respiratory Changes

The head-down position facilitates the development of atelectasis. Steep head-down tilt results in decreases in the functional resid-ual capacity, the total lung volume, and the pulmonary compli-ance. These changes are more marked in obese, elderly, and debilitated patients. In healthy patients no major changes are seen.32 The head-up position is usually considered to be more favorable to respiration.30,32

Nerve Injury

Nerve compression is a potential complication during the head-down position. Overextension of the arm must be avoided. Shoul-der braces should be used with great caution and must not impinge on the brachial plexus. Lower extremity neuropathies (e.g., peroneal neuropathy, meralgia paresthetica, femoral neu-ropathy) have been reported after laparoscopy.137,138 The common peroneal nerve is particularly vulnerable and must be protected when the patient is placed in the lithotomy position. Prolonged lithotomy position, such as required for some operative laparos-copies, can result in lower extremity compartment syndrome.

Postoperative Benefits and Consequences of Laparoscopy

Implicit in the decision to use the laparoscopic approach is the assumption that the intraoperative consequences of pneumoperi-toneum described in the previous sections are counterbalanced by multiple postoperative benefits. In contrast to laparotomy, improved and more rapid recovery, reduced postoperative fatigue,139,140 and a heightened feeling of well-being are commonly reported and reflect better maintenance of homeostasis.3,139

Stress Response

In patients undergoing cholecystectomy, the laparoscopic approach allows for a reduction of the acute phase reaction seen after open cholecystectomy. Plasma concentrations of C-reactive protein and interleukin-6, which reflect the extent of tissue damage, are significantly lower after laparoscopy as compared with laparotomy.3,139,141-143 The metabolic response (e.g., hypergly-cemia, leukocytosis) is also reduced after laparoscopy. As a con-sequence, nitrogen balance and immune function might be better preserved.144-147 Laparoscopy avoids prolonged exposure and manipulation of the intestines and decreases the need for perito-neal incision and trauma. Consequently, postoperative ileus and fasting, duration of intravenous infusion, and hospital stay are significantly reduced after laparoscopy.2,3,141,147-149 The duration of postoperative ileus is less shortened when compared with laparot-omy than previously reported.150 The economic implications of these factors are self-evident and beneficial.151-153

Surprisingly, whereas laparoscopy allows for a reduction of surgical trauma, the endocrine response to laparoscopic and open cholecystectomy does not differ significantly; plasma concentra-tions of cortisol and catecholamines,3,139,154,155 urinary concentra-tions of cortisol and catecholamine metabolites,141 and anesthetic requirements3 are similar after both procedures. Combined general and epidural anesthesia for laparoscopic cholecystectomy does not result in a decreased stress response compared with general anesthesia alone.154 Several hypotheses can be invoked to explain these observations. Pain and discomfort from peritoneal stretch-ing, hemodynamic disturbances, and ventilatory changes induced by pneumoperitoneum may contribute to the stress response of laparoscopy. Although parietal afference, which is markedly reduced by laparoscopy, appears to be an important stimulus for postoperative hyperglycemia, visceral nociception, which is less

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affected by laparoscopy, may contribute more to adrenocortical stimulation.139 The intraoperative stress response, however, can be reduced by preoperative administration of α2-agonists.71,96,97

Postoperative Pain

Surgical trauma contributes to pain and pulmonary dysfunction. Laparoscopy allows a significant reduction in postoperative pain and analgesic consumption (see Chapter 87).3,141,154,156-160 Never-theless, pain intensity may be significant.161-163 The nature of pain varies depending on the surgical technique; after laparotomy, patients complain more of parietal pain (e.g., abdominal wall), whereas after laparoscopic cholecystectomy, patients report also visceral pain (e.g., biliary colic [cholecystectomy], pelvic spasm [tubal ligation]), and shoulder-tip pain resulting from diaphrag-matic irritation.162,163 Pain after laparoscopy is multifactorial, and different treatments have been proposed to provide pain relief.164,165 Local anesthetic infiltration (e.g., intraperitoneal, port-site infil-tration) for postoperative pain relief after laparoscopic chole-cystectomy produces contradictory results.166-170 Benefits of intraperitoneal local anesthetic are greater after gynecologic laparoscopy.166,171 Mesosalpinx block decreases postoperative pain and analgesic consumption after laparoscopic sterilization.166 Residual CO2 pneumoperitoneum contributes to postoperative pain. Careful evacuation of residual CO2 after desufflation was shown to be effective.164,172,173 Preoperative administration of nonsteroidal anti-inflammatory drugs (NSAIDs) and of cyclooxygenase-2 inhibitors decreases pain, as does opiate con-sumption after gynecologic laparoscopy174-177 and laparoscopic cholecystectomy.178-182 However, others have failed to demonstrate any significant effect of preoperative NSAID on pain after laparo-scopic sterilization more severe than after diagnostic gynecologic laparoscopy.183-186 Dexamethasone is also effective in reducing postoperative pain.187 Multimodal analgesia is now recommended to prevent and treat post-laparoscopy pain.188-190

Pulmonary Dysfunction

Upper abdominal surgery results in postoperative changes in pulmonary function (see also Chapter 93). Respiratory dysfunc-tion is less severe and recovery is quicker after laparo-scopy.3,90,141,154,156,157,191-193 Nevertheless, diaphragmatic function remains significantly impaired after laparoscopy.194-196 Thoracic epidural analgesia does not improve lung function after laparo-scopic cholecystectomy.154 Greater reductions in expiratory volumes and slower recovery of pulmonary function after laparo-scopy are reported in older patients,197 obese patients,159,198 smokers, and patients with COPD198 than in healthy patients. Postoperative pulmonary function of these patients, however, is improved after laparoscopy as compared with laparotomy.159,160,198 Postoperative pulmonary function is less impaired after gyneco-logic laparoscopy than after upper abdominal laparoscopic surgery.199

Postoperative Nausea and Vomiting

Laparoscopy is frequently associated with minor postoperative sequelae that can persist more than 48 hours and that can signifi-

cantly delay discharge of outpatients.200 In addition to post-operative pain of various types, one of the main complaints is postoperative nausea and vomiting (PONV) (40% to 75% of patients).201-203 Whereas perioperative opioids increase the inci-dence of PONV,204-206 propofol anesthesia can markedly reduce the high incidence of these side effects.206,207 The effect of N2O on the incidence of nausea is still controversial.206,208,209 Intraoperative drainage of gastric contents also reduces PONV.210 Intraoperative administration of droperidol and a 5-hydroxytryptamine type 3 antagonist appears to be helpful in the prevention and treatment of these side effects.206,211-215 Transdermal scopolamine reduces nausea and vomiting after outpatient laparoscopy.201 Perioperative liberal intravenous fluid therapy can contribute to decreasing these symptoms and to improve postoperative recovery.216-218

Alternatives to CO2 Pneumoperitoneum

New approaches have been investigated to reduce pathophysio-logic consequences of CO2 pneumoperitoneum.

Inert Gases

Insufflation of inert gas (e.g., helium, argon) instead of CO2 avoids the increase in PaCO2 from absorption.219,220 Consequently, hyper-ventilation is not required.27,221-223 Also, the ventilatory conse-quences of the increased IAP persist. The hemodynamic changes produced by pneumoperitoneum using inert gas are similar to those observed with CO2. However, the use of these gases accen-tuates the decrease in cardiac output, whereas the increase in arterial pressure is attenuated.27,90,223,224 Unfortunately, the low blood solubility of the inert gases raises the issue of safety in the event of gas embolism.225,226

Gasless Laparoscopy

Another alternative is gasless laparoscopy. The peritoneal cavity is expanded using abdominal wall lift obtained with a fan retrac-tor. This technique avoids the hemodynamic and respiratory repercussions of increased IAP and the consequences of the use of CO2.227-231 Renal and splanchnic perfusion is not altered.108,232 Port-site metastases after laparoscopic surgery for cancer are reduced after gasless laparoscopy.233,234 This technique, therefore, is appealing for patients with severe cardiac or pulmonary disease. However, gasless laparoscopy compromises surgical exposure and increases technical difficulty.229,233,234 Combining abdominal wall lifting with low pressure CO2 pneumoperitoneum (5 mm Hg) may improve surgical conditions.

Laparoscopy During Pregnancy and in Children

The most common nonobstetric surgical procedures during preg-nancy are adnexal surgery, appendectomy, and cholecystectomy,

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and they are amenable to laparoscopic surgery (see Chapter 69).235 Laparoscopy during pregnancy raises several concerns. Abdomi-nal surgery increases the risk of miscarriage or premature labor. However, all the reports in the literature of laparoscopy carried out between 4 and 32 weeks of estimated gestational age have resulted in uncomplicated pregnancies.236-240 Another concern is the risk of damaging the gravid uterus. This can be avoided by alternative entry sites for the Veress needle and trocars. CO2 pneumoperitoneum induces significant fetal acidosis. Fetal heart rate and arterial pressure increase, but these changes are minimal.241 Provided maternal PaCO2 is maintained at normal levels, fetal placental perfusion pressure and blood flow, pH, and blood gas tensions are unaffected by insufflation or desufflation.242 Capnography is adequate to guide ventilation during laparoscopy in pregnant patients.243 Hemodynamic changes induced by pneu-moperitoneum are similar in pregnant and nonpregnant women.244 The following recommendations are for safe laparoscopy in preg-nant patients236:

1. The operation should occur during the second trimester, ideally before the 23rd week of pregnancy, to minimize the risk of preterm labor and to maintain adequate intra-abdominal working room.

2. Tocolytics are beneficial to arrest preterm labor, but their prophylactic use is debatable.

3. Open laparoscopy should be used for abdominal access to avoid damaging the uterus.

4. Fetal monitoring may be performed using transvaginal ultrasonography.

5. Mechanical ventilation must be adjusted to maintain a physiologic maternal alkalosis.

Gasless laparoscopy is an alternative to avoid the potential side effects of CO2 pneumoperitoneum and can sometimes be managed using epidural anesthesia.245,246

Laparoscopy is frequently performed in infants and chil-dren (see Chapter 82). Knowledge of the pathophysiologic changes induced by laparoscopy in children is necessary to adapt their monitoring and anesthetic technique.247 CO2 pneumoperi-toneum induces the same changes in respiratory mechanics to those reported in adults.248-250 PaCO2 and PETCO2 increase during pneumoperitoneum, but PETCO2 may sometimes overestimate PaCO2.251 The profile of CO2 absorption and the magnitude of CO2 absorption compared with metabolic !VCO2 are similar in infants and children to those recorded in adults.252 The hemodynamic changes observed in children are similar to those reported in adults.253-257 Pneumoperitoneum results in oliguria or anuria in children, reversible after desufflation.258 Controversy concerning the benefits (improved analgesia and postoperative recovery) of laparo scopy for appendectomy, the most frequent indication for laparoscopy in children, persists.259-261

Complications of Laparoscopy

With the development of more sophisticated endoscopic opera-tions, it is important to consider the risks and benefits of laparo s-copy. Although the benefits of the laparoscopic approach are well documented, knowledge of the incidence of complications is more imprecise and is frequently based on retrospective studies.

The experience of gynecologic laparoscopists extends over a relatively long time and, as a result, large surveys are availa-ble.262,263 Mortality rates have varied from 1 per 10,000 to 1 per 100,000 cases. The number of serious complications requiring laparotomy was 2 to 10 per 1000 cases. Intestinal injuries accounted for 30% to 50% of these and remained undiagnosed during laparoscopy in one half of the cases. Vascular complica-tions also accounted for 30% to 50%. Burns were responsible for 15% to 20% of the reported complications. Although the death rate decreased, the complication rate was slightly higher in the most recent surveys, probably because of the increased complex-ity of the laparoscopies performed over the past few years.

Large surveys of complications after laparoscopic cholecys-tectomy are available.152,264-268 The overall mortality rate is 0.1 to 1 per 1000 cases.268 Conversion to laparotomy was necessary in approximately 1% of patients. Bowel perforation occurred in about 2 per 1000 cases, common bile duct injury in 2 to 6 per 1000 cases, and significant hemorrhage in 2 to 9 per 1000 cases. Laparoscopic cholecystectomy was accompanied by a greater frequency of minor operative complications, whereas open cholecystectomy had a more frequent rate of minor general com-plications. A learning curve was demonstrated for laparoscopic cholecystectomy; experience was associated with decreased oper-ative times and rates of minor or moderate complications. Some of these complications might be prevented by open laparoscopy.269

Although large vessel injury (e.g., aorta, inferior vena cava, iliac vessels) caused emergency situations, retroperitoneal hematoma can develop insidiously and result in significant blood loss without major intraperitoneal effusion, leading to delayed diagnosis. During gynecologic laparoscopy, complications occur more frequently during the creation of pneumoperitoneum and the introduction of trocars, whereas during gastrointestinal surgery they are more closely related to the surgical procedure itself.152,270,271 Injuries provoked by the Veress needle are usually less severe than those by trocars and may even remain undiag-nosed. Unrecognized gastrointestinal tract injury and subhepatic abscess formation can lead to potentially lethal septic complica-tions.272 The rate of postoperative infections (e.g., surgical site, respiratory) seems to be significantly lower after laparoscopy than after laparotomy.273 Although all these events are surgery related, the anesthesiologist must be aware of the complications and timing of their occurrence. He or she must be ready to respond promptly and adequately to these mishaps and to help the surgeon diagnose a complication.

Anesthesia for Laparoscopy

Preoperative Evaluation of the Patient and Premedication

Without regard to surgical contraindications, absolute contrain-dications to laparoscopy and pneumoperitoneum are rare, and some still require characterization (see Chapter 34). Pneumoperi-toneum is undesirable in patients with increased intracranial pressure (e.g., tumor, hydrocephalus, head trauma) and hypovo-lemia. Laparoscopy can be performed safely in patients with ven-tricular peritoneal shunt and peritoneojugular shunt that are

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provided with unidirectional valve resistant to IAPs used during pneumoperitoneum. In case of glaucoma, the effects on intraocu-lar pressure do not seem to be clinically significant but deserve further confirmation.122

In patients with heart disease, cardiac function should be evaluated in light of the hemodynamic changes induced by pneu-moperitoneum and patient position, particularly in case of com-promised ventricular function (Table 68-1). Patients with severe congestive heart failure and terminal valvular insufficiency are more prone to develop cardiac complications than patients with ischemic cardiac disease during laparoscopy. Whether laparo s-copy is more dangerous than laparotomy in these patients has not yet been explored directly but deserves careful consideration. For these patients, the postoperative benefits of laparoscopy must be balanced against the intraoperative risks when the choice of laparoscopy versus laparotomy is discussed. Gasless laparoscopy may represent an alternative for these patients.

Because of the side effects of increased IAP on renal func-tion, patients with renal failure deserve special care to optimize hemodynamics during pneumoperitoneum, and the concomitant use of nephrotoxic drugs should be avoided.

In patients with respiratory disease, laparoscopy appears preferable to laparotomy because of reduced postoperative respi-ratory dysfunction. This positive effect counterbalances the risk of pneumothorax during pneumoperitoneum and the risk of inadequate gas exchange from ! !V Q mismatching.

Because of venous stasis in the legs during laparoscopy, prophylaxis of deep vein thrombosis should be the same as for laparotomy.

Premedication should be adapted to the duration of the laparoscopy and to the necessity for quick recovery in the outpatient setting. Preoperative administration of NSAIDs may be helpful in reducing postoperative pain and opiate require-ments. Preoperative clonidine and dexmedetomidine decrease

the intraoperative stress response and improve hemodynamic stability.71,95-97

Patient Positioning and Monitoring

Patients must be positioned (see Chapter 36) with great care to prevent nerve injuries; padding should protect from nerve com-pression, and shoulder braces, if needed, should be placed overly-ing the coracoid process. Patient tilt should be reduced as much as possible and should not exceed 15 to 20 degrees. Tilting must be slow and progressive to avoid sudden hemodynamic and res-piratory changes. The position of the endotracheal tube must be checked after any change in patient position. Induction and release of the pneumoperitoneum must be smooth and progres-sive. Mask ventilation before intubation can inflate the stomach with gas, which must be aspirated before trocar placement to avoid gastric perforation, particularly for supramesocolic laparo s-copy. The bladder should be emptied before pelvic laparoscopy or prolonged procedures.

During laparoscopy, arterial blood pressure, heart rate, electrocardiography, capnometry, and pulse oximetry must be continuously monitored. Although this level of monitoring is valuable for detection of cardiac arrhythmias, gas embolism, CO2 subcutaneous emphysema, and pneumothorax, it provides only indirect evidence of the hemodynamic changes induced by the pneumoperitoneum. Although more invasive hemodynamic monitoring may be necessary in patients with cardiac diseases, increased intrathoracic pressure complicates the interpretation of measured central venous and pulmonary artery pressures. Trans-esophageal echocardiography may be more helpful in patients with severe cardiac disease (see Table 68-1). PETCO2 and SpO2 reliably reflect PaCO2 and arterial oxygen saturation (SaO2). However, the ∆a-ETCO2 may vary from patient to patient and during the course of laparoscopy in the same patient. PETCO2 must be monitored carefully to avoid hypercapnia and to detect gas embolism. Because ∆a-ETCO2 may increase more in patients with cardiac and pulmonary diseases, cannulation of a radial artery may be helpful to allow direct measurement of PaCO2 from an arterial blood sample.

Anesthetic Techniques

General, local, and regional anesthesia have all been used success-fully and safely for laparoscopy.

General AnesthesiaGeneral anesthesia with endotracheal intubation and controlled ventilation is certainly the safest and most commonly used technique and therefore is recommended for inpatients and for long laparoscopic procedures. During pneumoperitoneum, con-trolled ventilation must be adjusted to maintain PETCO2 between 35 and 40 mm Hg. In our experience, this requires no more than a 15% to 25% increase of minute ventilation, except when CO2 subcutaneous emphysema develops. Increase of respiratory rate rather than of tidal volume may be preferable in patients with COPD and in patients with a history of spontaneous pneu-mothorax or bullous emphysema to avoid increased alveolar inflation and reduce the risk of pneumothorax. Infusion of vasodilating drugs, such as nicardipine,89,132 α2-adrenergic

Table 68-1 Management of Patients with Cardiac Disease for Laparoscopy

Preoperative Evaluation: Echocardiography

If left ventricular ejection fraction < 30%:

Intraoperative monitoring Intra-arterial line Pulmonary artery catheter? Transesophageal echocardiography Continuous ST-segment analysis? Gasless laparoscopy? Laparotomy?

Intraoperative Management

Slow insufflationLow intra-abdominal pressureHemodynamic optimization before pneumoperitoneum (preload augmentation)Patient tilt after insufflationAnesthesia: remifentanil, vasodilating anesthetic and drugs (nicardipine, nitroglycerin), cardiotonic agentsExperienced surgeon

Postoperative Care

Slow recovery from anesthesia (benefit of clonidine)

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receptor agonists,71,95-97 and remifentanil66 reduces the hemody-namic repercussions of pneumoperitoneum and may facilitate management of cardiac patients (see Table 68-1). The actual con-tribution of N2O to PONV is probably less than previously con-sidered.206 Although N2O does not seem to be contraindicated for laparoscopic cholecystectomy,208 omission of N2O improves sur-gical conditions for intestinal and colonic surgery.274 The choice of anesthetic technique does not seem to play a major role in patient outcome.275-277 Propofol, nevertheless, results in fewer postoperative side effects.278-280 Propofol anesthesia for laparo-scopic fertility procedures involving genetic material transfers, however, is associated with lower clinical and ongoing pregnancy rates compared with isoflurane.281 IAP should be monitored, kept as low as possible to reduce hemodynamic and respiratory changes, and not allowed to exceed 20 mm Hg. Increases in IAP can be avoided by ensuring a deep plane of anesthesia. Whether profound muscle relaxation is necessary for laparoscopy is not clear.282 Liberal perioperative intravenous fluid therapy decreases hemodynamic changes from pneumoperitoneum77,84 and PONV and improves postoperative recovery.216-218 Because of the poten-tial for reflex increases of vagal tone during laparoscopy, atropine should be available if necessary.

The laryngeal mask airway results in fewer cases of sore throat and may be proposed as an alternative to endotracheal intubation283-287 (also see Chapter 50) even if this device does not protect the airway from aspiration of gastric contents.288,289 It allows controlled ventilation and accurate monitoring of PETCO2. However, decreased thoracopulmonary compliance during pneumoperitoneum frequently results in airway pressures exceeding 20 cm H2O. The ProSeal laryngeal mask airway may be an alternative to guarantee an airway seal up to 30 cm H2O.290,291

General anesthesia in patients breathing spontaneously without intubation can be performed safely and avoids tracheal irritation as well as administration of muscle relaxant. This anes-thetic technique must be restricted to short procedures performed using low IAP and small degrees of tilt.292 In these conditions, the laryngeal mask airway might improve the safety of anesthe-sia283,286,293 and is therefore recommended.

Local and Regional AnesthesiaLocal anesthesia offers several advantages: quicker recovery, decreased PONV, early diagnosis of complications, and fewer hemodynamic changes (see Chapters 30, 51, and 52).294,295 However, this anesthetic approach requires precise and gentle surgical technique and may result in increased patient anxiety, pain, and discomfort during the manipulation of pelvic and abdominal organs. For these reasons, local anesthesia is routinely supplemented with intravenous sedation. The combined effect of pneumoperitoneum and sedation can lead to hypoventilation and arterial oxygen desaturation.296 Complex laparoscopic procedure must not be managed with local anesthesia.

Regional anesthesia, including epidural and spinal tech-niques, combined with the head-down position can be used for gynecologic laparoscopy without major impairment of ventila-tion.18,297,298 Laparoscopic cholecystectomy has been successfully performed using epidural anesthesia in COPD patients.299,300 The metabolic response is reduced by regional anesthesia.301 Globally, epidural and local anesthesia share the same benefits and disad-vantages. Regional anesthesia reduces the need for sedatives and

narcotics, produces better muscle relaxation, and can be proposed for laparoscopic procedures other than sterilization. Shoulder-tip pain from diaphragmatic irritation and discomfort from abdomi-nal distention are incompletely alleviated using epidural anesthe-sia alone.302 Extensive sensory block (T4-L5) is necessary for surgical laparoscopy and may also lead to discomfort. The epi-dural administration of opiates or clonidine, or both, may help to provide adequate analgesia.302 The hemodynamic effects of pneu-moperitoneum under epidural anesthesia have not been studied. Regional anesthesia can provide adequate relief of pain and dis-comfort in case of gasless laparo scopy, thus avoiding most of the side effects of CO2 pneumoperitoneum.246,303

Recovery and Postoperative Monitoring

Hemodynamic monitoring should be continued in the PACU (see Chapter 85). Hemodynamic changes induced by the pneumo-peritoneum, and more particularly the increased systemic vascu-lar resistance, outlast the release of the pneumoperitoneum. The hyperdynamic state developing after laparoscopy could conceiv-ably lead to a precarious hemodynamic situation in patients with cardiac disease.87,125

Despite the reduction in postoperative pulmonary dys-function, PaO2 still decreases after laparoscopic cholecystec-tomy.3,156,192 Increased oxygen demand is observed after laparoscopy. Although laparoscopy tends to be considered a minor surgical procedure, oxygen should be administered post-operatively, even to healthy patients.304

Finally, prevention and treatment of nausea, vomiting, and pain are important, particularly after outpatient laparoscopic procedures.

Summary

Laparoscopy results in multiple postoperative benefits including less trauma, less pain, less pulmonary dysfunction, quicker recov-ery, and shorter hospital stay. These advantages are regularly emphasized and explain the increasing success of laparoscopy, which is now proposed for many surgical procedures. Intraopera-tive cardiorespiratory changes occur during pneumoperitoneum. PaCO2 increases because of CO2 absorption from the peritoneal cavity. In compromised patients, cardiorespiratory disturbances aggravate this increase in PaCO2. Hemodynamic changes are accentuated in high-risk cardiac patients. Improved knowledge of the pathophysiologic hemodynamic changes in healthy patients allows for successful anesthetic management of cardiac patients, by optimizing preload before pneumoperitoneum and through judicious use of vasodilating agents. Alternative insufflating gases (e.g., He, Ar, N2O) do not seem to reduce the hemodynamic changes. Gasless laparoscopy may be more helpful but unfortu-nately increases technical difficulty. The incidence of complica-tions has now been reported in several large surveys and compares favorably with that of open surgery. The death rate during opera-tive laparoscopy is 0.1 to 1 per 1000 cases; the incidence of hem-orrhagic complications and visceral injury is 2 to 5 per 1000 cases. Whereas no anesthetic technique has proved to be clinically supe-rior to any other, general anesthesia with controlled ventilation

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seems to be the safest technique for operative laparoscopy. Improved knowledge of the intraoperative repercussions of lapar-oscopy permits safe management of patients with more and more

severe cardiorespiratory disease, who may subsequently benefit from the multiple postoperative advantages offered by this approach.

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