Anaesthesia for Laparoscopy
Anaesthesia for Laparoscopy
Dr. Ramachandra
Consultant Anaesthesiologist
A.V. Hospital
Bangalore
Introduction
Surgical procedures have been improved to reduce trauma to the patient, morbidity, mortality, and hospital stay and thereby to diminish health care costs. The development of better equipment and facilities, along with increased knowledge and understanding of anatomy and pathology, have allowed the development of endoscopy for diagnostic and operative procedures. Since about 1970, various pathologic gynecologic conditions have been diagnosed and treated by use of laparoscopy. This endoscopic approach has now been extended to gastrointestinal surgical procedures such as appendectomy, peritoneal adhesiolysis, and cholecystectomy as well as to inguinal hernia repair.
The pneumoperitoneum and the patient positions required for laparoscopy,induce pathophysiologic changes that complicate anesthetic management. The limited expertise and experience of some surgeons with these new procedures also contribute to the magnitude of these changes and increase the rate of complications. Finally, the duration of some operative laparoscopies, the risk of unsuspected visceral injury, and the difficulty in evaluating the amount of blood loss are other factors that make anesthesia for laparoscopy a potentially high risk procedure.
Although laparoscopy was introduced early in the 20th century and developed in the 1970s for gynecologic procedures, the recent extension of laparoscopy to gastrointestinal surgical procedures creates new interest in and considerations for the anesthetic management of laparoscopy. Several elements explain this growing interest. Young, healthy women are generally involved in gynecologic laparoscopy, in which minor or modest cardiorespiratory changes are of little concern. For instance, before the systematic use of capnometry, unsuspected hypercapnia frequently developed but was well tolerated by most of these young patients. With the development of laparoscopy for gastrointestinal surgery, we now must care for older patients who are more likely to have known or latent diseases. Furthermore, because of the multiple benefits reported after laparoscopy, the laparoscopic approach tends to be readily proposed for ill patients. Finally, many surgeons starting laparoscopy for gastrointestinal surgery are still inexperienced, which increases the risk of morbidity and mortality. Knowledge of the pathophysiologic consequences of increased intra-abdominal pressure is important for the anesthesiologist, who not only must prevent and adequately respond to these changes but also must evaluate and prepare the patient preoperatively in the light of these disturbances. Therefore, the pathophysiologic changes and the complications of laparoscopy are first reviewed. Then, the postoperative period is examined, with consideration of the benefits of laparoscopy as well as some specific postoperative problems (pain, nausea). Finally, practical consequences for the anesthetic management of laparoscopy are presented.
Ventilatory Problems during Laparoscopy
Three main ventilatory problems may occur during laparoscopy: increase in PaCO2, pneumothorax, and gas embolism.
Increase in PaCO2
The effects of CO2 insufflation have been studied primarily during gynecologic laparoscopy in the Trendelenburg position. This has led to some contradictory results, which may be accounted for by the choice of anesthetic technique, the duration of CO2 pneumoperitoneum, and patient characteristics. Indeed, during intraperitoneal insufflation of CO2, an increase in PaCO2 was observed both in animals and humans when ventilation was controlled at a constant minute volume. Indeed, duration of pneumoperitoneum influences the extent of the increase in PaCO2. It takes 15 to 25 minutes for PaCO2 to plateau and therefore anesthesia with spontaneous breathing should be limited to short procedures. The increase in PaCO2 also depends on the intra-abdominal pressure. Finally, patients with preoperative cardiopulmonary disease demonstrate significantly larger increases in PaCO2 than patients without underlying diseases. This important observation deserves further detailed studies.
The mechanism of the increase of PaCO2 is controversial. During CO2 pneumoperitoneum, absorption of CO2 from the peritoneal cavity, impairment of ventilation by mechanical factors such as abdominal distension, position of the patient, volume-controlled mechanical ventilation, and depression of ventilation by premedicants and anesthetics in the case of spontaneous breathing are all factors. The contribution of each factor depends on the anesthetic technique, steepness of patient tilt, and patient characteristics (underlying disease, obesity) and may therefore vary from patient to patient. The observation of an increase in PaCO2, when CO2 but not nitrous oxide was used as peritoneal insufflating gas, suggests absorption of CO2 from the peritoneal cavity as a potential mechanism for the PaCO2 increase. This hypothesis was further supported by the increased production of CO2 (etCO2) reported when CO2 but not nitrous oxide was the inflating gas. etCO2 increases slowly during the first 20 minutes and then reaches a plateau approximately 25 percent above the preinsufflation value. The maximum rate of diffusion of CO2 into the body was calculated to be 14 ml/min, suggesting that peritoneal absorption of CO2 is minimal and would produce less than a 10 percent increase in PaCO2.
The absorption of a gas from the peritoneal cavity depends on its diffusibility and the perfusion of the walls of that cavity. Since CO2 diffusibility is large, absorption of large quantities of CO2 into the blood, and consequently marked increases in PaCO2, would be expected to occur. The limited increase in PaCO2 actually observed can be explained by the capacity of the body to store CO2 and by impaired local perfusion. Several observations support the hypothesis of reduced peritoneal perfusion during pneumoperitoneum. The increased intra-abdominal pressure can constrict the peritoneal capillary bed but may also produce an increase in systemic vascular resistance (SVR), leading to a reduction of local blood flow, particularly in the intra-abdominal viscera. CO2 is absorbed much more quickly from the pleural cavity than from the peritoneal cavity. When CO2 subcutaneous emphysema occurs during extraperitoneal CO2 insufflation, a much more pronounced increase in PaCO2 and expired end-tidal PCO2 (PETCO2), sometimes difficult to control despite a 70 to 80 percent increase in minute ventilation, is observed. In this circumstance ETCO2 markedly increases. Finally, improvement of cardiac output after exsufflation may explain the increase in PaCO2 sometimes seen on release of intra-abdominal pressure.
Respiratory changes during the laparoscopic procedure also contribute to increasing CO2 tension. Ventilation is impaired by the position of the patient and abdominal distension. The elevation of the diaphragm results in mismatching of ventilation and pulmonary perfusion. An augmentation of the arterioalveolar CO2 difference [D (a-A) CO2], reflecting an increase in the physiologic dead space has been reported. This would indicate that if controlled ventilation is not adjusted in response to the increased dead space, PaCO2 will increase. However other authors failed to demonstrate any significant changes in d (a-A) CO2 due to pneumoperitoneum. It should be noted that the effect of pneumoperitoneum on ventilation is influenced by patient physical status. D (a-A) CO2 increased significantly more in American Society of Anesthesiologists (ASA) II and III patients and in obese patients than in ASA I patients PaO2 and intrapulmonary shunt do not change significantly during laparoscopy. Increase in PaCO2 and the ensuing arterial and tissue acidosis may cause dysfunction in several organs. However, current trends are more permissive with regard to hypercapnia than was the practice in the early 1970s. In the treatment of certain situations, such as the adult respiratory distress syndrome (ARDS) and status asthmaticus, marked hypercapnia is even accepted. Although increased PaCO2 may be well tolerated by young, healthy patients, the extent to which hypercapnia is acceptable has not been determined and probably varies according to patient physical status. Therefore, it is wise to maintain PaCO2 within physiologic values by adjusting controlled mechanical ventilation. Except in special circumstances, such as CO2 subcutaneous emphysema, correction of increased PaCO2 can be easily achieved by a 10 to 25 percent increase in minute ventilation. Monitoring of PaCO2 by capnometry and capnography is of great help for prevention of hypercapnia. PETCO2 is generally considered to provide reliable information on PaCO2 during laparoscopy. However, two points need to be emphasized. First, the D (a-A) CO2 varies from patient to patient. Second, although mean D(a-A)CO2 did not change significantly during peritoneal insufflation of CO2 in some studies, individual patient data regularly show an increase of this difference during pneumoperitoneum .
Pneumothorax, Pneumomediastinum, and Pneumopericardium
Movement of gas during the creation of a pneumoperitoneum can produce subcutaneous emphysema, pneumodiastinum, unilateral and bilateral pneumothorax, and pneumopericardium. Gas may dissect retroperitoneally through congenital foramina and produce a pneumomediastinum. There are potential channels of communication, embryonic remnants, between the peritoneal cavity and the pleural and pericardial sacs, and these can open when intraperitoneal pressure increases. Defects in the diaphragm or weak points in the aortic and esophageal hiatus may allow gas diffusion into the thorax. In case of pneumomediastinum, gas can also diffuse cephalad and produce subcutaneous emphysema of the neck and the face, particularly during long laparoscopies with the patient in the head-up position (as for gastrointestinal laparoscopic procedures). Pneumothorax may also develop secondary to pleural tears during laparoscopic surgical procedures at the level of the gastroesophageal junction (fundoplication for hiatal hernia). Finally, because of the increased alveolar inflation secondary to increased minute ventilation during pneumoperitoneum, pre-existing pulmonary bullae can rupture, leading to pneumothorax.
These complications are potentially serious and may lead to respiratory and hemodynamic disturbances. Pneumothorax should be suspected in the presence of cyanosis and a decrease of capillary oxygen saturation, subcutaneous emphysema and increases in peak airway pressure. Hemodynamic changes are not constant. The observation by the laparoscopist of abnormal motion of one hemidiaphragm is also helpful for the diagnosis. Diagnosis must be confirmed by auscultation of the chest and radiology. It should be noted that cervical and upper thoracic subcutaneous emphysema can develop without pneumothorax.
Pneumothorax during laparoscopy creates several specific issues and problems. Insufflated CO2 for the pneumoperitoneum can supply the pneumothorax and possibly lead to tension pneumothorax with cardiorespiratory alterations. Drainage of the pneumothorax by a chest tube can compromise the maintenance of the pneumoperitoneum and therefore the laparoscopy. In case of pneumothorax from highly diffusible gas such as nitrous oxide or CO2 without associated pulmonary trauma, spontaneous resolution of the pneumothorax occurs within 30 to 60 minutes after exsufflation. Therefore, when pneumothorax develops during laparoscopy, we recommend the following guidelines:
1 Stop nitrous oxide administration.
2 Adjust ventilator setting to correct hypoxemia.
3 Apply positive end-expiratory pressure (PEEP).
4 Reduce intra-abdominal pressure as much as possible.
5 Maintain close communication with the surgeon.
6 Avoid thoracocentesis unless necessary, since pneumothorax will spontaneously disappear after exsufflation.
Postoperative resolution of the pneumothorax can be hastened by single needle drainage. These guidelines have allowed us to successfully manage the 5 (of 120) patients who developed pneumothorax during laparoscopy for fundoplication. Correction of hypoxemia was easily achieved by temporarily (for 10 to 20 minutes) increasing the inspiratory fraction in O2 to 70 to 80 percent and using 5 cmH2O PEEP in two of these patients. The anesthesiologist must be aware of this complication, which can occur even without pulmonary or pleural trauma.
Gas Embolism
Although rare, gas embolism is the most feared and fatal complication of laparoscopy and may occur more frequently when laparoscopy is associated with hysteroscopy . Intravascular injection of gas may follow direct needle or trocar placement into a vessel or as a consequence of gas insufflation into an abdominal organ. This complication develops mainly during the induction of pneumoperitoneum. Indeed, early recognition and treatment of gas embolism reduces the size of the embolism and thus the severity of its effects and sequelae. Gas embolism may also occur later during surgery or even may be delayed after laparoscopy by trapping in portal circulation. CO2 is used most frequently for laparoscopy because it is more soluble in blood than air, oxygen, or even nitrous oxide. The capacity for CO2 carriage in the blood is high owing to bicarbonate buffering and combination with hemoglobin and plasma proteins. 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. A dose equivalent to 1 L of CO2 in humans can be given intravenously to dogs before cardiac output is altered profoundly. Therefore, peritoneal insufflation with CO2 should be started slowly at a rate not higher than 1 L/min to allow early recognition of gas embolism.
The pathophysiology of gas embolism is also determined by the size of the bubbles and the rate of intravenous entry of the gas. During neurosurgery the slow entrainment of small bubbles of air is more likely to result in air entrapment in the pulmonary vessels, whereas 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, will result. For example, acute right ventricular hypertension may open the foramen ovale, which is patent in 20 to 30 percent of the population, allowing for example, and arterial embolism to travel into the cerebral and coronary beds. Paradoxical embolism may, however, occur without patent foramen ovale. Systemic CO2 embolism may cause an acute reduction in the peripheral resistance and may account for the observation of more sudden hypotension with CO2 embolism than with air or O2 embolism. Ventilation/perfusion mismatches develop, with increases in physiologic dead space and hypoxemia. CO2 embolism does not produce bronchoconstriction or the changes in pulmonary compliance that accompany air embolism. Increased airway pressure has, however, been reported during CO2 embolism.
The diagnosis of gas embolism depends on the detection of gas emboli in the right side of the heart or recognition of physiologic changes secondary to emboli. Early changes, occurring with 0.5 ml/kg of air or less, include changes in Doppler sounds and increased mean pulmonary artery pressure when these monitors are available. When the size of the embolus increases (e.g., 2 ml/kg of air), tachycardia, cardiac arrhythmias, hypotension, increased central venous pressure, alteration in heart tones (e.g., millwheel murmur), cyanosis, and electrocardiographic (ECG) changes of right heart strain can develop; all these changes are rarely consistently positive. Pulmonary edema can also be an early sign of gas embolism. Although esophageal or precordial Doppler probes, or pulmonary artery catheters are the most sensitive means of detecting small quantities of gas prior to physiologic changes, the low incidence of gas embolism during laparoscopy precludes the routine use of such invasive or expensive monitors. Whereas pulse oximetry is helpful in recognizing hypoxemia, capnometry and capnography are more valuable in providing early diagnosis of gas embolism and determining the extent of the embolism. PETCO2 decreases in the case of embolism because of the decrease in cardiac output and the enlargement of the physiologic dead space. D (a-A) CO2 will consequently increase. The response time with capnometry is longer than that with Doppler ultrasound. Interestingly, CO2 embolization causes a biphasic change in PETCO2. The decrease in PETCO2 is preceded by an initial increase secondary to pulmonary excretion of CO2 that has been absorbed into the blood. Aspiration of gas or foamy blood from the central venous line will definitively establish the diagnosis. Routine preoperative insertion of a central venous line does not, however, appear justified for these minor procedures. Finally, blood on aspiration from the Verres needle, pulsation of the flowmeter pressure gauge, and/or absence or disappearance of abdominal distension despite a sufficient volume of gas should warn the anesthesiologist of a potential gas embolism.
Treatment of CO2 embolism consists of immediate cessation of the insufflation and release of pneumoperitoneum. The patient is placed in a steep head-down and left lateral decubitus (Durant's) position. Indeed, the amount of gas that will advance through the right heart to the pulmonary circulation is less if the patient is in this position, as the buoyant foam will be displaced laterally and inferiorly away from the right ventricular outflow tract. Discontinuing nitrous oxide will allow 100 percent O2 ventilation to correct hypoxemia but will not result in reducing the size of a CO2 embolus, as is the case with air embolus, since CO2 and nitrous oxide have similar solubilities in blood. 54 Hyperventilation increases CO2 excretion and is necessary because of the enlargement of the physiologic dead space. If these simple measures are not effective, a central venous or pulmonary artery catheter may be introduced for aspiration of the gas. Cardiopulmonary resuscitation must be initiated if necessary. The high solubility in blood of CO2, resulting in rapid absorption from the blood stream, accounts for the rapid reversal of the clinical signs of CO2 embolism with treatment. CO2 embolism may, however, be fatal. Cardiopulmonary bypass has been used successfully to treat a massive CO2 embolism. Hyperbaric oxygen treatment should be strongly considered if cerebral gas embolism is suspected.
Finally, air emboli have been reported during operative endoscopy using the neodymium: yttrium-aluminum-garnet (Nd: YAG) laser. The Nd: YAG laser is used with an artificial sapphire scalpel, which is protected from laser-induced thermal damage by cooling with a continuous flow of air, CO2, or nitrogen. Therefore inadvertent penetration of the sapphire tip into an abdominal viscus can result in air embolism. The anesthesiologist should therefore be aware of this possibility.
Risk of Aspiration of Gastric Contents
Patients undergoing laparoscopy are usually considered at risk of developing the acid aspiration syndrome. Risk factors include the fact that regurgitation may be facilitated by the increased intra-abdominal pressure but also the fact that the volume and acidity of the gastric juice of patients undergoing laparoscopy are routinely sufficient to produce the Mendelson syndrome (personal observation). However, the increased intra-abdominal pressure results in changes of the lower esophageal sphincter, which allow maintenance of the pressure gradient at the level of the gastroesophageal junction and which might therefore reduce the risk of regurgitation. Furthermore, the head-down position should help to prevent regurgitated fluid from entering the airway.
Hemodynamic Problems during Laparoscopy
Hemodynamic changes observed during laparoscopy result from the combined effects of pneumoperitoneum and patient position. Besides these pathophysiologic changes, reflex increase of vagal tone and arrhythmias can also develop.
Hemodynamic Repercussions of Pneumoperitoneum
Peritoneal insufflation to intra-abdominal pressures higher than 10 mmHg induces significant alterations of hemodynamics. These disturbances are characterized by decreases of cardiac output, elevation of arterial pressure, and increase of systemic and pulmonary vascular resistances. The decrease in cardiac output is proportional to the increase in intra-abdominal pressure. Cardiac output has also been reported to be increased or unchanged during pneumoperitoneum. These discrepancies might be due to differing rates of CO2 insufflation, intra-abdominal pressure, steepness of the tilt, time intervals between insufflation and collection of data, and techniques to assess hemodynamics. However, all recent studies showed a decrease of cardiac output (25 to 35 percent) during peritoneal insufflation regardless of whether the patient was placed in the head-down or head-up position. These adverse hemodynamic effects of pneumoperitoneum were confirmed by studies using transesophageal echocardiography. The combined effect of anesthesia, patient position (10 degrees head-up) and increased intra-abdominal pressure (14 mmHg) can reduce the cardiac output to as much as 50 percent of preoperative values. During laparoscopy, cardiac output remains significantly lower (30 to 35 percent) than prior to induction of anesthesia despite surgical stimulation. 28 Interestingly, McKenzie et al. 86 suggest that laparoscopy reduces cardiac output to a greater extent than does laparotomy.
The mechanism of the decrease of cardiac output is probably multifactorial. Increase of intra-abdominal pressure (IAP) results in pooling of blood in the legs and reduces the inferior vena caval flow. The subsequent decline in venous return parallels the decrease in cardiac output. Cardiac filling pressures, however, increase during peritoneal insufflation. Since intrathoracic pressure also increases consequent to the pneumoperitoneum, transmural right atrial pressure, an indicator of venous return, actually decreases. From a practical point of view, these changes in intrathoracic pressure, most often not measured, complicate the interpretation of the hydrostatic central venous and pulmonary artery pressures. The increase in SVR also contributes to the decrease in cardiac output. The SVR increase is not only related to mechanical factors (increased IAP, increased venous resistance), since it outlasts the end of the pneumoperitoneum. The release of humoral factors is therefore likely; catecholamines, prostaglandins, the renin-angiotensin system, and especially vasopressin are potential mediators. The increase in SVR also explains why the arterial pressure increases whereas the cardiac output falls. All these hemodynamic changes are similar whether CO2 or nitrous oxide is the insufflating gas.
Intra-abdominal organs appear to be particularly sensitive to the increased IAP. When IAP is increased to 20 mmHg, renal vascular resistance increases by more than 500 percent and renal blood flow and glomerular filtration decrease to less than 25 percent of normal. Therefore, adverse effects of pneumoperitoneum in patients with impaired renal function, although not yet reported, are theoretically possible. Four cases of anuric renal failure associated with increased IAP from postoperative hemorrhage have been reported. Resolution of the acute renal failure occurred in response to surgical decompression of the abdomen. Increased IAP significantly decreases organ blood flow (OBF) in all intra-abdominal organs except the adrenal gland. These changes in OBF are more marked than changes in cardiac output, which suggests a contribution of local control mechanisms to changes in OBF. An IAP of 20 mmHg results in a significant decrease of mesenteric artery blood flow and intestinal mucosal blood flow.
Whether these hemodynamic changes are well tolerated is poorly documented. Joris and Lamy 36 studied O2 transport during laparoscopic cholecystectomy in ASA I patients. Whereas the fall in cardiac output reduced O2 delivery, O2 consumption also decreased secondary to a reduction of metabolism by anesthesia. Consequently, venous O2 saturation (SvO2) and plasma concentrations of lactate remained within normal values during pneumoperitoneum, suggesting satisfactory tolerance in healthy patients. The decrease in preload and the increase in afterload resulting from peritoneal insufflation might induce deleterious effects in patients with impaired cardiac function, anemia, or hypovolemia. Unfortunately, this has never been investigated but indirect data suggest more pronounced alterations of hemodynamics in patients with cardiac disease. Rises more in these patients than in healthy patients, and the D (a-A) CO2 also increases much more in cardiac patients, reflecting a greater enlargement of the physiologic dead space. Finally, the cardiovascular monitoring routinely used during anesthesia (blood pressure, heart rate, capnography, pulse oximetry) gives no accurate information on the changes in SVR and cardiac output.
Cardiac Arrhythmias during Laparoscopy
In the early 1970s a high incidence of cardiac arrhythmias was reported during halothane anesthesia and spontaneous ventilation. Attention was focused on hypercapnia developing during peritoneal insufflation of CO2, known to precipitate arrhythmias during halothane anesthesia. The use of controlled hyperventilation was therefore recommended. However, questioned the responsibility of the increased PaCO2 for the arrhythmias occurring during laparoscopy. Indeed, arrhythmias are not correlated with PaCO2 and develop early in the insufflation, when a high PaCO2 is unlikely. Enflurane and isoflurane are less arrhythmogenic than halothane in the presence of increased circulating catecholamines and have been used safely in patients breathing spontaneously.
Reflex increase of vagal tone may result from sudden stretching of the peritoneum. Bradycardia, cardiac arrhythmias, and even asystole can develop. This vagal stimulation will be accentuated if the level of anesthesia is too superficial or if the patient is taking b-adrenergic blocking drugs. Electrocoagulation of the fallopian tubes can stimulate a vagal reaction. These events are easily and quickly reversible. Treatment consists of interruption of insufflation, administration of atropine, and deepening of anesthesia after recovery of heart rate.
Cardiac irregularities occur most often early in the insufflation, when the pathophysiologic hemodynamic changes are the most intense. Therefore, arrhythmias may also reflect intolerance of these hemodynamic disturbances in patients with known or latent cardiac disease.
Finally, gas embolism can also result in cardiac arrhythmias.
Problems Related To Patient Position
Patient positioning depends on the site of surgery: whereas the head-down tilt is used for pelvic and submesocolic surgery, the head-up position is preferred for supramesocolic surgery. In addition, 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 requested directly affects the magnitude of these changes and usually depends on the experience of the surgeon. 5
Cardiovascular Effects
In normotensive subjects, the head-down position results in an increase in central venous pressure and cardiac output. In fact, the baroreceptor reflex responds to the increased hydrostatic pressure with systemic vasodilation and bradycardia, keeping stable the cardiovascular status.In the 15-degree head-down position, the volume shift to the central circulation is small and does not seem sufficient to cause significant hemodynamic effects. Although these different reflexes may be impaired during general anesthesia, the hemodynamic changes induced by this position during laparoscopy remain insignificant. However, central blood volume and blood pressure changes are greater in patients with coronary artery disease, particularly in cases of compromised ejection fraction, leading to a potentially deleterious increased myocardial O2 demand. The Trendelenburg position may also affect the cerebral circulation, particularly in case of high intracranial pressure, and result in elevation of the intraocular venous pressure, which can worsen acute glaucoma. 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.
In the case of the head-up position, a decrease in cardiac output and mean arterial blood pressure is observed secondary to the reduction in venous return. This decrease in cardiac output compounds the hemodynamic changes induced by pneumoperitoneum. The steeper the tilt, the larger the decrease in cardiac output.
Venous stasis in the legs occurs in the head-up position and may be aggravated by the lithotomy position with the lower legs in flexion. Pneumoperitoneum further increases blood pooling in the legs. Venous stasis can lead to venous thrombosis and pulmonary embolism, particularly during long laparoscopic procedures. Any additional factor contributing to circulatory dysfunction should be avoided: the legs must be freely supported and not tightly strapped, and pressure on the popliteal space must be prevented.
Respiratory Effects
The head-down position facilitates the development of atelectasis. A PEEP of 5 cmH2O may minimize this complication. Steep head-down tilt results in decreased functional residual capacity, total lung volume, and pulmonary compliance. It should be noted that these changes are more marked in obese, elderly, or debilitated patients, who may not tolerate these changes. In healthy patients no major changes are seen.
During head-down tilting the endotracheal tube (ETT) can move into the right mainstem bronchus. Therefore, the cuff of the ETT must be positioned just below the cords and the correct position of the ETT must be verified after any change in patient position.
The head-up position is usually considered to be more favorable to respiration. The actual effect of head-up tilt on ŒA/‹ when the patient is receiving mechanical ventilation and general anesthesia has not been investigated.
Nerve Injury
Nerve compression is a potential complication in the head-down position. Overextension of the arm must be avoided. Shoulder braces should be used with great caution and must not impinge on the brachial plexus. Lower extremity neuropathies (peroneal neuropathy, meralgia paresthetica, femoral neuropathy) have been reported after laparoscopy. The common peroneal nerve is vulnerable and must be protected when the patient is placed in the lithotomy position. Prolonged maintenance of the lithotomy position, as is required for some operative laparoscopies, can result in lower extremity compartment syndrome.
Postoperative Benefits and Consequences of Laparoscopy
The intraoperative consequences of pneumoperitoneum described in the previous sections are hopefully counterbalanced by multiple postoperative benefits. In contrast to laparotomy, improved and earlier recovery and a heightened feeling of well-being are commonly reported and reflect better maintenance of homeostasis. In patients undergoing cholecystectomy, we demonstrated that 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 less after laparoscopy than after laparotomy.
Laparoscopy avoids prolonged exposure and manipulation of the intestines and decreases the need for peritoneal incision and trauma. Consequently, postoperative fasting, duration of intravenous infusion, and hospital stay are significantly reduced after laparoscopy. Economic implications are self-evident and represent an important benefit.
Surprisingly, whereas laparoscopy allows for a reduction of surgical trauma, the stress responses during laparoscopic and open cholecystectomy do not differ significantly: plasma concentrations of cortisol and catecholamines, cortisol and catecholamine breakdown products, and anesthetic requirements are similar. Combined general and epidural anesthesia for laparoscopic cholecystectomy does not result in a decreased stress response as compared with general anesthesia alone. Several hypotheses might be invoked to explain these observations. Pain and discomfort secondary to stretching of the peritoneum, hemodynamic disturbances, and ventilatory changes induced by pneumoperitoneum might contribute to the stress response of laparoscopy. The intraoperative stress response, however, can be reduced by preoperative administration of a2-adrenergic agonists.
Surgical trauma contributes to pain and pulmonary dysfunction. Although pain reported after laparoscopic cholecystectomy is not always less than after laparotomy, analgesic consumption is significantly reduced. The nature of the pain varies depending on the surgical technique: after laparotomy, patients complain more of parietal (abdominal wall) pain, whereas after laparoscopic cholecystectomy patients report visceral pain similar to that of biliary colic and shoulder-tip pain resulting from diaphragmatic irritation. Neck and shoulder pain is reported by 80 percent of patients at 24 hours and by as many as 50 percent at 48 hours. CO2 as insufflating gas induces more discomfort than does nitrous oxide. Different treatments have been proposed to provide pain relief. Topical anesthesia or infiltration of the fallopian tubes decreases postoperative pain and analgesic consumption after laparoscopic sterilization. Intraperitoneal administration of local anesthetic (80 ml of 0.5 percent lidocaine or 0.125 percent bupivacaine with epinephrine) in the right sub diaphragmatic area reduces shoulder pain and analgesic requirements. The use of an abdominal drain left for 6 hours to completely release residual CO2 has also been shown to be efficient. Thoracic epidural analgesia significantly decreases postoperative pain but only during the first 24 hours. The performance of bilateral rectus sheath block for diagnostic laparoscopy leads to the same benefits. Decreased pain and opiate consumption have also been reported after preoperative administration of nonsteroidal anti-inflammatory drug (NSAIDs), although some investigations have failed to demonstrate any significant effect of preoperative NSAIDs.
Upper abdominal surgery results in postoperative changes in pulmonary function. Respiratory dysfunction is less and recovery is quicker after laparoscopy. The recovery of pulmonary function is slower in patients older than 50 years. Thoracic epidural analgesia does not improve lung function after laparoscopic cholecystectomy. Together, these data suggest that the laparoscopic approach might decrease risk (relative to laparotomy) for patients with chronic obstructive pulmonary disease. Nevertheless, diaphragmatic function is still significantly impaired.
Laparoscopy also carries a high incidence of minor postoperative sequelae, which can persist for more than 48 hours and which can significantly delay discharge for outpatients. Nevertheless, these side effects are usually well tolerated and accepted by the majority (70 percent) of patients, who would be happy to have another laparoscopy as an outpatient if necessary. Besides postoperative pain of various types, the most frequent complaints are headache, sore throat in case of endotracheal intubation, and, more particularly, nausea and vomiting (in 40 to 75 percent of patients). Whereas an alfentanil infusion worsens the incidence of nausea and vomiting, propofol anesthesia can markedly reduce the high incidence of these side effects. The effect of nitrous oxide on the incidence of nausea is still controversial. Drainage of gastric contents also reduces nausea and vomiting. Intraoperative administration of droperidol and, more recently, the use of ondansetron appear to be very helpful in the prevention and treatment of these side effects. Transdermal scopolamine reduces nausea and vomiting after outpatient laparoscopy. Finally, analgesic techniques that allow reduction of opiate consumption can contribute to decreasing these symptoms.
Complications
Despite the low morbidity and mortality associated with laparoscopy, the occasional catastrophic complication indicates that the procedure is not without risk.
Most of the large surveys available were conducted in the 1970s and concerned gynecologic laparoscopy. The mortality rate substantially decreased during the 1970s-between 1 and 2 per 10,000 in the early 1970s, it became less than 1 in 100,000 by the end of the decade. One-quarter of the reported cardiac arrests resulted in death. It should be noted that most of these cardiac arrests occurred during the induction of pneumoperitoneum. The possible etiologies of these cardiac problems (e.g., gas embolism) have already been discussed. The improvement of anesthetic techniques, a better understanding of the pathophysiologic changes induced by laparoscopy, and also the improved training and experience of surgeons explain the decline in the mortality rate. It is stated that laparoscopists are dangerous, not laparoscopy. This statement is sadly illustrated by a medicolegal report that points out that one-third of the laparoscopists involved in law suits for severe or fatal mishaps are incompetent and inexperienced. Laparoscopy is new in the fieldof gastrointestinal surgery, and surgeons are still gaining experience. However, the mortality rate (0.15 to 0.2 percent) is similar after open and laparoscopic cholecystectomy, and post-operative morbidity is decreased after laparoscopic cholecystectomy. The rate of major complications is usually between 1 and 2 percent in most large series, with vascular injuries accounting for one-third of these complications. Large-vessel injury (aorta, inferior vena cava, iliac vessels) can lead to emergency situations. Retroperitoneal hematoma can develop insidiously and result in large blood loss without major intraperitoneal effusion, leading to delayed diagnosis. Finally, parietal hematoma can develop consequent to vessel injury during trocarplacement.
The second major traumatic complication consists of visceral injury, mainly gastrointestinal perforation, which may require conversion to laparotomy for adequate treatment. During gynecologic laparoscopy complications apparently occur more frequently during the creation of pneumoperitoneum and the introduction of trocars, whereas during gastrointestinal surgery they are more often related to the surgical procedure itself. Greater risk is usually observed with diagnostic procedures than with laparoscopic sterilization. However, a recent large survey of gynecologic laparoscopy in France reports that rates of complications are directly related to the extent of the laparoscopic surgical procedure. Injuries provoked by the Verres needle are usually less severe than those caused by trocars and may remain undiagnosed. Unrecognized gastrointestinal tract injury and subhepatic abscess formation can generate septic complications and lead to death. Once again, many of these complications can be attributed to lack of experience. 5 Other complications, such as pneumothorax, pneumomediastinum, and subcutaneous emphysema, have been described in a previous section. Although all these events are surgery-related, the anesthesiologist must be aware of both the complications and the timing of their occurrence and must be ready to respond promptly and adequately to these mishaps and to help the surgeon diagnose a complication.
Pneumoperitoneum and laparoscopy are contraindicated in patients with increased intracranial pressure, ventriculoperitoneal shunt, peritoneojugular shunt, hypovolemia, or congestive heart failure (CHF).
In patients with heart disease, cardiac function should be evaluated in the light of the hemodynamic changes induced by pneumoperitoneum and patient position, particularly in case of compromised ejection fraction. Patients with CHF are certainly more prone to develop cardiac complications than patients with ischemic cardiac disease during laparoscopy. Indeed, cardiac output remains significantly depressed during pneumoperitoneum as compared with values prior to surgery despite surgical stress, whereas increases in arterial blood pressure and heart rate, potentially deleterious in patients with coronary artery disease, are not very marked, at least in healthy patients. Whether laparoscopy 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. Laparoscopy using suspension of the abdominal wall instead of pneumoperitoneum may result in less hemodynamic changes and represent an alternative for these patients.
In patients with respiratory disease, laparoscopy appears preferable to laparotomy because of reduced postoperative respiratory dysfunction. This positive effect counterbalances the risk of pneumothorax during pneumoperitoneum and the risk of inadequate gas exchange secondary to ŒA/‹ mismatching.
Because of venous stasis in the legs during laparoscopy, 95 prophylaxis of deep vein thrombosis should be initiated prior to surgery, as for laparotomy. In my hospital all patients scheduled for laparoscopy wear antistasis stockings.
Premedication should be adapted to the duration of the laparoscopy and to the necessity of quick recovery after outpatient procedures. Because of the potential risk of regurgitation and aspiration, antacids, H2-receptor antagonists, and gastroprokinetic drugs are sometimes recommended. Preoperative administration of NSAIDs may be helpful in reducing postoperative pain and opiate requirements. Finally, preoperative clonidine and dexmedetomidine decrease the intraoperative stress response and improve hemodynamic stability.
Patient Positioning and Monitoring
Patients must be positioned with great care to prevent nerve injuries. Padding should protect from nerve compression, and shoulder braces, if needed, should be placed facing the coracoid process. Patient tilt should be reduced as much as possible and should not exceed 15 degrees, 5 and tilting must be slow and progressive to avoid sudden hemodynamic and respiratory changes. The position of the ETT must be checked after any change in patient position. Induction and release of the pneumoperitoneum must also be smooth and progressive. Mask ventilation before intubation can inflate the stomach with gas, which must be aspirated before trocar placement to avoid gastric perforation, particularly for supramesocolic laparoscopy. The bladder should be emptied prior to pelvic laparoscopy or prolonged procedures.
During laparoscopy, continuous arterial blood pressure, heart rate, ECG, capnometric, and pulse oximetric must be continuously monitored. Although this level of monitoring is valuable for detection of cardiac arrhythmias, gas embolism, and pneumothorax, it only poorly reflects 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 the measured central venous and pulmonary artery pressures. Use of transesophageal echocardiography might be more helpful in patients with severe cardiac disease. PETCO2 and oximetric oxygen saturation (SpO2) reliably reflect PaCO2 and arterial O2 saturation (SaO2). However, we must keep in mind that the D (a-A) CO2 may differ from patient to patient and during laparoscopy in the same patient. PETCO2 must be monitored carefully to avoid hypercapnia and to detect gas embolism. Since D (a-A) CO2 may increase more in patients with cardiac and pulmonary diseases, cannulation of a radial artery is helpful to allow direct measurement of PaCO2 on an arterial blood sample. Monitoring of muscle relaxation and body temperature 181 are useful during long surgical laparoscopy. Finally, esophageal stethoscope and precordial Doppler ultrasound, allowing early recognition of gas embolism, are recommended only by some authors.
Anesthetic Techniques
General, local, and regional anesthesia have been used successfully and safely for laparoscopy.
General Anesthesia
General anesthesia with endotracheal intubation and controlled ventilation must be used for long laparoscopic procedures especially when the surgeon is inexperienced. This technique provides good muscle relaxation, the ability to control ventilation, protection from aspiration of gastric contents, complete analgesia, and a still operative field. During the pneumoperitoneum, controlled ventilation must be adjusted to maintain PETCO2 at about 35 mmHg. In my experience, this requires no more than a 15 to 25 percent increase of minute ventilation except in cases of CO2 subcutaneous emphysema. Increase of respiratory rate rather than of tidal volume might be preferable in patients with obstructive airway disease and in patients with a history of spontaneous pneumothorax or bullous emphysema to avoid increased alveolar inflation and reduce the risk of pneumothorax. Anesthetics that directly depress the heart should be avoided in patients with compromised cardiac function in favor of anesthetics with vasodilating properties such as isoflurane. The latter allows partial correction of the hemodynamic changes induced by the pneumoperitoneum. Infusion of vasodilating drugs, such as nicardipine (a calcium channel blocker), reduces the hemodynamic repercussions of a pneumoperitoneum. Nitrous oxide has been suspected to affect oocyte function; however, the success rate of in vitro fertilization is not decreased by its use. The contribution of nitrous oxide to nausea and vomiting is still controversial. Total intravenous anesthesia (propofol, ketamine, etomidate) provides stable anesthetic conditions. Propofol results in fewer postoperative side effects and quicker recovery. IAP should be monitored, kept as low as possible to reduce hemodynamic and respiratory changes, and not allowed to exceed 20 mmHg. Increase in IAP can be avoided by ensuring a deep plane of anesthesia and paralysis. Because of potential reflex increase of vagal tone during laparoscopy, atropine should be administered before the induction of anesthesia or it should be available for injection if necessary.
The laryngeal mask airway results in less sore throat and might be proposed as an alternative to endotracheal intubation, even if this device does not protect the airway from aspiration of gastric contents. Indeed, it allows controlled ventilation and accurate monitoring of PetCO2, while the risk of regurgitation can be minimized by continuous drainage of gastric contents with a nasogastric tube. However, decreased thoracopulmonary compliance during the pneumoperitoneum frequently results in airway pressure exceeding 20 cmH2O. Since the laryngeal mask airway cannot guarantee an airway seal above this pressure, its use for controlled ventilation should be limited to healthy, thin patients.
Although it is prudent to recommend general anesthesia with endotracheal intubation and controlled ventilation, controversy still exists whether to intubate the tracheas of all patients undergoing laparoscopic procedures. General anesthesia in patients breathing spontaneously without intubation can be performed safely and avoids tracheal irritation as well as administration of muscle relaxant. However, Peterson et al. revealed that almost one-third of the deaths associated with laparoscopic procedures were related to anesthetic complications during general anesthesia without intubation. This anesthetic technique should thus be restricted to short procedures performed by an experienced surgeon using low IAP and low degrees of tilt. In these cases the laryngeal mask airway might improve the safety of anesthesia for laparoscopy in patients breathing spontaneously and is therefore recommended.
Local and Regional Anesthesia
Local anesthesia offers several advantages: reduced anesthesia time, quicker recovery, decreased postoperative nausea and vomiting, early awareness of complications, and less hemodynamic changes. Sequelae of general anesthesia, such as sore throat, muscle pain, and airway trauma, can be avoided. However, this anesthetic approach requires a 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 regularly supplemented with intravenous sedation. The combined effect of pneumoperitoneum and sedation can lead to hypoventilation and arterial oxygen desaturation. Success with local anesthesia requires a relaxed and cooperative patient, a supportive operating room staff, and a skilled surgeon. IAP should be as low as possible to reduce pain and ventilatory disturbances. Although laparoscopic tubal ligation is a good indication for local anesthesia, the multiple constraints explain the lack of enthusiasm of some gynecologic laparoscopists for this anesthetic technique. 41 Any other laparoscopic procedure that requires multiple puncture sites, considerable organ manipulation, steep tilt, and large pneumoperitoneum makes spontaneous breathing difficult for the patient, results in discomfort, and must not be managed with local anesthesia.
Regional anesthesia, such as an epidural technique, combined with the head-down position, can be used for gynecologic laparoscopy without major impairment of ventilation. The metabolic response is reduced by regional anesthesia. Globally, epidural and local anesthesia shares the same benefits and disadvantages. Regional anesthesia has the advantages of reducing the need for sedatives and narcotics, produces better muscle relaxation, and can be proposed for laparoscopic procedures other than sterilization. Since shoulder-tip pain secondary to diaphragmatic irritation is mediated by the phrenic nerve, it is difficult to provide complete analgesia by using epidural anesthesia alone. Extensive sensitive block (T4 to L5) is therefore necessary for surgical laparoscopy, leading to some discomfort. The epidural administration of opiate or/and clonidine might help to provide adequate analgesia. The hemodynamic effects of pneumoperitoneum under epidural anesthesia have not been studied. Although the sympathetic block may facilitate the development of vagal reflexes, vasodilation and the avoidance of positive pressure ventilation may reduce the cardiovascular changes described during pneumoperitoneum. Once again, patient collaboration, an experienced and skilled laparoscopist, reduced IAP, and tilt position are necessary to guarantee the success of epidural anesthesia, which should be avoided for long procedures.
Recovery and Postoperative Monitoring
Hemodynamic monitoring should be prolonged in the post-anesthesia care unit. Indeed, hemodynamic changes induced by the pneumoperitoneum, and more particularly the increased SVR, outlast the release of the pneumoperitoneum. Hypertension of short duration is not uncommon after recovery from anesthesia. After laparoscopic cholecystectomy in ASA I patients, Joris and Lamy measured an increase in cardiac output accompanied by a significant decrease in venous O2 saturation (SvO2) and an increase in plasma concentration of lactate. This increase in O2 extraction might be related to the high incidence of postoperative shivering (about 50 percent) that we observe after laparoscopy.
Despite the reduction in postoperative pulmonary dysfunction, PaO2 still decreases after laparoscopic cholecystectomy. Furthermore, an increased demand in O2 is observed after laparoscopy. 36 Although laparoscopy tends to be considered a minor surgical procedure, O2 should be administered postoperatively even in healthy patients. Hypercapnia can also develop immediately after release of the pneumoperitoneum. Indeed, improvement of cardiac output may increase absorption of CO2.
Finally, prevention and treatment of nausea, vomiting, and pain are very important, particularly after outpatient laparoscopic procedures
Summary
Laparoscopy results in multiple postoperative benefits including less trauma, less pain, less pulmonary dysfunction, quicker recovery, and shorter hospital stay. These advantages are regularly emphasized and explain the increasing success of laparoscopy, now proposed for many surgical procedures. This contrasts with the silence surrounding the incidence of complications, which vary from minor to major and sometimes result in fatalities. Intraoperative cardio respiratory changes occur during pneumoperitoneum. Although these repercussions were studied in the 1970s, they have been neglected until now, mainly because laparoscopy was proposed for young healthy women who tolerate well these pathophysiologic changes. Older patients with known or latent diseases are now undergoing surgical laparoscopy. Tolerance of pneumoperitoneum by those patients has not been investigated and deserves further study. Furthermore, the changes produced by the increased IAP have been explored mostly in normal subjects. Whether the results of these studies can be extended to older patients is unknown.
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Raja Kishore commented, on August 14, 2009 at 6:28 p.m.:
good article.