John H. Nguyen, MD, Pedro P. Tanaka, MD, PhD
Laparoscopic surgery is a principle technique for minimally invasive surgery of the abdomen, and it has been employed in procedures ranging across multiple surgical disciplines. Gynecologic surgeries were among its first applications. The advantages of laparoscopy in comparison to open abdominal surgery include reduced surgical trauma, less pain, fewer post-operative pulmonary complications, and shorter recovery times. The disadvantages include longer surgical times and higher equipment costs.1
Laparascopic surgery is most routinely performed with general anesthesia. It is furthermore facilitated by proper decompression of the gastrointestinal tract (GI), and by establishment of adequate muscle relaxation, pneumoperitoneum, and Trendelenburg position. These conditions collectively improve exposure of the abdominal organs and decrease the risk of operative mechanical injury to the patient. However, they also induce specific and potentially deleterious pathophysiologic changes to the patient. While the goal of the surgeon is to operate safely and efficaciously, the goal of the anesthesiologist is to help improve surgical conditions when possible, while also preventing (or mitigating) the side effects of these conditions and mantaining vital organ function. These goals must be achieved concurrently. Thus, it is critical for both the surgeon and the anesthesiologist to understand the physiologic consequences of laparascopy and to work in cooperation to achieve a good surgical outcome.
ESTABLISHMENT OF SURGICAL CONDITIONS
To provide optimal surgical conditions for laparascopy, the abdominal organs must be adequately exposed and the laparascopic ports and instruments must be inserted safely and in proper position. This is achieved with a multi-part approach that includes decompression of the GI tract followed by establishment of general anesthesia, muscle relaxation, pneumoperitoneum, and Trendelenburg position.
GI tract decompression starts preoperatively with a bowel preparation and continues intraoperatively with the placement of an oro- or naso-gastric tube immediately after induction of anesthesia. Both maneuvers decrease intraabdominal volume. The latter maneuver, in particular, decompresses the stomach of air that may have been insufflated from mask ventilation during induction of anesthesia and is important for reducing the risk of gastric injury from insertion of the Veress needle. With induction of anesthesia, neuromuscular blockade is established to relax the abdominal wall muscles, thereby facilitating placement of laparascopic ports and induction of the pneumoperitoneum. Neuromuscular blockade also prevents sudden patient movement that can lead to accidental injuries of intra-abdominal structures by laparascopic instruments. The pneumoperitoneum is then achieved by insufflating the abdomen, most commonly with carbon dioxide (CO2). Finally, the patient is positioned in Trendelenburg, so that the abdominal contents fall away from the lower abdomen to reveal the pelvic organs. These maneuvers induce a number of clinically relevant pathophysiologic effects during surgery. We will review these effects by organ system.
PHYSIOLOGIC EFFECTS OF LAPAROSCOPIC SURGERY
I. Cardiovascular System
A. Hemodynamic Effects of Pneumoperitoneum
Hemodynamic disturbances during laparascopy are primarily due to pneumoperitoneum. The pneumoperitoneum is established by insufflating the abdomen with pressures of 15 to 20 mm Hg. Normal intra-abdominal pressure (IAP) is 0 to 5 mm Hg. Increases in IAP above 10 mm Hg are clinically significant, and above 15mm Hg can result in an abdominal compartment syndrome, which affects multiple organ systems. The cardiovascular manifestations can be understood via the following simple relationship, which expresses the determinants of blood pressure:
Mean Arterial Pressure (MAP) = Cardiac Output (CO) x Systemic Vascular Resistance (SVR)
Pneumoperitoneum causes an increase in SVR while causing a decrease in CO. However, MAP is increased overall because increases in SVR exceed decreases in CO.2 These effects are proportional to the increase in IAP. The mechanism for increased SVR is compression of the abdominal organs and vessels. Resistance to flow through arterial beds is increased due to both mechanical and neurohumoral factors (e.g., release of catecholamines and vasopressin, and activation of the renin-angiotensin system). The decreases in CO are due to decreased venous return (i.e., decreased cardiac preload) from compression of the inferior vena cava, from increased resistance in the venous circulation, and from hypovolemia due to preoperative bowel preparation. CO typically decreases from 10 to 30%. However, despite a decrease in intracardiac blood volume, intracardiac filling pressures may be elevated due to pressure transmitted across the diaphragm to the heart. There are analagous effects in the pulmonary circulation that manifest as an increase in pulmonary vascular resistance (PVR) and decrease in CO to the lungs.
Healthy patients appear to tolerate these hemodynamic effects well. Several studies demonstrate that end organ perfusion is maintained in these patients despite a decrease in CO.3 However, patients with cardiac disease may be at increased risk for further cardiac compromise. Patients with intravascular volume depletion appear to tolerate these effects the least well.4 To minimize these effects, the lowest insufflation pressure required to achieve adequate surgical exposure should be used. Ideally, insufflation pressure should be less than 15 mm Hg. Increases in SVR may be treated with vasodilating agents, centrally acting alpha-2 agonists, or opioids. Decreases in venous return and CO may be attenuated by appropriate intravenous fluid loading prior to the induction of pneumoperitoneum.
B. Hemodynamic Effects of Positioning
Relative to the supine position and in the absence of a pneumoperitoneum, the Trendelenburg position generally increases venous return and CO. However, in the presence of a pneumoperitoneum, venous return and CO are decreased overall. If the patient is placed in extreme Trendelenburg, a decrease in venous return from the head may result, thus leading to increased intracranial and intraocular pressures. If this position is maintained for an extended duration, cerebral edema and retinal detachment may occur.5 Because of venous stagnation, cyanosis and edema in the face and neck may be expected. The head up (reverse Trendelendburg) position reduces venous return, which may lead to a fall in cardiac output and arterial pressure. The lithotomy position will induce auto-transfusion by redistributing blood from vessels of the lower extremities into the central body compartment, which thus will increase the preload of the heart.
C. Cardiovascular Complications
Bradyarrhythmias, dysrhythmias, and even asystole can occur during insertion of laparoscopic ports or during insufflation of the abdomen. Sudden stretching of the peritoneum can precipitate a sudden, reflexive, and sometimes profound increase in vagal tone. Slow insufflation of CO2 can decrease the risk of arrhythmias. Administration of anticholinergic medications may be appropriate in bradyarrhythmias. If the arrhythmia persists or results in hemodynamic compromise, prompt interruption of the surgery and release of the pneumoperitoneum is indicated.
II. Pulmonary and Respiratory System:
A. Pulmonary and Respiratory Effects of Pneumoperitneum
Pneumoperitoneum transmits pressure to the thorax. The upward pressure elevates the diaphragm, compresses the lungs, and impedes expansion of the lungs and chest cavity (i.e., decreases thoracopulmonary compliance). The pulmonary implications of this mechanical effect are two-fold. First, compression of the lungs leads to decreased functional residual capacity (FRC), i.e., the volume of gas remaining in the lungs after a normal exhalation. This circumstance exacerbates the decrease in FRC that normally occurs under general anesthesia. The decreased end-expiratory lung volume is insufficient to maintain patent alveoli, and thus atelectasis results. Atelectasis alters the normal relationship between ventilation and perfusion of the lungs. The atelectatic areas of lung are underventilated relative to their perfusion and therefore cause hypoxemia. Older patients are particularly at risk for atelectasis, because the minimum end-expiratory lung volume that is required to prevent atelectasis – known as the closing capacity – increases with age. Institution of positive end-expiratory pressure (PEEP) can mitigate the decreases in FRC by stenting alveoli open at end expiration. The second mechanical effect of pneumoperitoneum is that controlled mechanical ventilation is more difficult due to the decrease in thoracopulmonary compliance. Greater airway pressure is required to generate a given tidal volume. Conversely, a mechnically delivered tidal volume will result in higher airway pressures. As with hemodynamic effects, these effects are proportional to the increase in IAP. In addition, they may be further exacerbated by Trendelenburg position and by conditions resulting in restrictive lung disease (e.g., obesity). Thoracopulmonary compliance may be decreased by up to 50% during pneumoperitoneum.6,7
Pneumoperitoneum furthermore causes hypercapnea from systemic absorption of CO2.2 CO2 is the most commonly chosen gas for peritoneal insufflation. CO2 is a convenient choice because it is easily absorbed into the blood, is buffered by the principle physiologic buffer (bicarbonate), and is easily eliminated via the respiratory system. In uncomplicated laparoscopy, the partial pressure of arterial CO2 (PaCO2) rises on induction of pneumoperitoneum and plateaus from 15 to 30 minutes later, thus signifying CO2 equilibrium. PaCO2 can be reliably monitored via analysis of end-tidal gasses. The degree of hypercapnea depends on CO2 insufflation pressure, but in routine cases under general anesthesia and controlled mechanical ventilation, hypercapnea is easily managed by increasing alveolar ventilation by 10% to 25%.8 In cases where the degree of hypercapnea becomes unmanageable with hyperventilation alone, the pneumoperitoneum can be temporarily released to allow for CO2 elimination.
B. Pulmonary Effects of Positioning
The head-down position generally decreases FRC, overall lung volumes, and lung compliance. Morbidly obese patients will have greater peak airway pressures and often cannot sustain prolonged Trendelenburg position. Although laparoscopic surgery can be performed on the morbidly obese, each operation should be evaluated carefully for the feasibility of success and potential risk.
C. Pulmonary and Respiratory Complications
i. CO2 Subcutaneous Emphysema.
Subcutaneous emphysema is the most common respiratory complication during laparoscopy. It is suggested by an increase in end-tidal CO2 (etCO2) greater than 25% or an increase that occurs > 30 minutes after abdominal CO2 insufflation. Subcutaneous emphysema can often be palpated. The cause is extraperitoneal insufflation of CO2. Although in some cases this is unintentional, in other cases it is required to operate on extraperitoneal structures.9 The hypercapnea is managed by increasing mechanical ventilation. CO2 subcutaneous emphysema itself is not a contraindication to extubation at the end of surgery provided that other extubation criteria are satisfied.10
Movement of gas from the peritoneum into the thorax can occur under pressure through weak areas and defects in the diaphragm. The resulting pneumothorax may be asymptomatic, or it may manifest as increased peak airway pressure, decreased O2 saturation, and hypotension. In severe cases, there can be profound hypotension and cardiac arrest.9
Early diagnosis and treatment can be life saving. Surgery should be stopped and the pneumoperitoneum released. Supportive measures should be continued while confirming the diagnosis, either clinically or with chest radiography. Depending on the degree of cardiopulmonary compromise, the pneumothorax may be observed or treated with an intercostal cannula or a thoracostomy tube. After stabilization of the patient, conversion to an open procedure may be indicated.10
iii. Endobronchial intubation
Elevation of the diaphragm by the pneumoperitoneum can alter the position of the endotracheal (ET) tube within the trachea. In some cases, the lungs are pushed cephalad such that the ET tube is advanced past beyond the carina and into a mainstem bronchus. When this occurs, only one lung is ventilated. The non-ventilated lung still remains perfused, and as such becomes a large source of intrapulmonary shunt. Endobronchial intubation is suspected when there is a decrease in O2 saturation and pulmonary compliance. The decrease in compliance occurs because a given volume is being delivered into one lung rather than two. The diagnosis is often confirmed by the finding of unequal breath sounds when the lungs are auscultated. The ET tube should then be slightly withdrawn as needed to reestablish two-lung ventilation.
iv. Gas (CO2) Embolism
Gas embolism, although rare, has a mortality rate of nearly 30%. Profound hypotension, arrhythmias, or asystole can occur as a result of a “gas lock” in the vena cava or right ventricle (RV) that interrupts circulation. An increase in etCO2 is observed. This may be followed by an acute decrease in etCO2 if there is severe hypotension. The major cause is intravascular insufflation of gas from misplacement of the Veress needle or trocar either directly into a vessel or into a parenchymal organ. Risk factors include hysteroscopy, hypovolemia, and a history of prior abdominal surgeries. Gas embolism most frequently occurs on induction of pneumoperitoneum but can occur at any point during surgery.9
Initial steps include immediate deflation of the pneumoperitoneum, institution of 100% FiO2, placement of the patient in the left lateral head-down position to remove air from the RV outflow track, and hyperventilation to eliminate the increased PaCO2 caused by the sudden increase in pulmonary dead space. A central line may be required to aspirate gas from the RV. CPR may be required. Hyperbaric O2 treatment should be considered if there is suspicion of cerebral gas embolism.10
I. Patient Monitoring
Standard patient monitors for laparoscopy include electrocardiogram, noninvasive blood pressure monitor, pulse oximetry, capnography, and temperature monitor. Monitors of the neuromuscular junction can be used to ensure adequate muscle relaxation. An airway pressure monitor is routinely used during mechnical ventilation, and can aid detection of high IAP, endobronchial intubation, or even inadequate anesthesia. Invasive arterial blood pressure monitoring and arterial blood gas analysis should be considered in patients with advanced age or cardiopulmonary comorbidities.4
II. Anesthetic Technique
A wide variety of anesthetic techniques have been used for laparoscopic procedures. Although general anesthesia with endotracheal intubation is most routinely used and is considered to be the safest anethetic technique, local and regional anesthesia have also been used safely for laparascopic surgeries.
As more laparascopic procedures are performed on an outpatient basis, the choice of maintenance agents is likely to be reduced to short acting drugs such as sevoflurane, desflurane, and infusions of propofol. There is apparently no clinical advantage to omitting nitrous oxide, and any benefit from its elimination must be balanced against a greater risk of awareness. An Ultrashort-acting opioids analgesic such as remifentanil has allowed bypassing Phase I recovery in ambulatory setting. Because laparoscopic surgery has generally been performed with tracheal intubation and controlled ventilation short or intermediate-acting neuromuscular blockers should be administered based on surgical length. General anesthesia can be performed without intubation safely and effectively with ProSeal laryngeal mask airway in non-obese patients. Careful attention should be paid to patients with high airway pressures (>30 cmH2O) or where extreme head-down tilt will be applied. Reversal drugs such as neostigmine and glycopyrrolate have not been implicated in PONV. More important, it has been demonstrated that even minor degrees of residual neuromuscular block can produce distressing symptoms. Regional anesthesia (spinal, epidural) can be used in laparoscopic procedures (diagnostic, infertility, and tubal sterilization).4
III. Post-operative Recovery
A. Post-Operative Monitoring
Routine postoperative care should consist of adequate monitoring of vital organ functions. This includes continuous monitoring of peripheral oxygen saturation, respiratory rate, ECG, blood pressure measurement and heart rate and rhythm. Advanced postoperative monitoring may be required in cardiovascularly debilitated ASA III and IV patients.3
B. Post-Operative Nausea and Vomitting
Postoperative nausea and vomiting (PONV) is common after laparoscopic surgery, although its etiology is not quite clear. Ondansetron given at the end of surgery results in a significantly greater anti-emetic effect compared with preinduction dosing. Other 5-HT3 antagonists are effective as well. In addition, prophylactic dexamethasone decreases the incidence for nausea and vomiting after laparoscopic cholecystectomy relative to placebo and may decrease the severity of pain with no adverse effects noted from this single steroid dose.11
C. Post-operative Pain
Postoperative pain in laparoscopic surgery is less severe compared to an open procedure, but is still considerable. The most effective pain relief can be obtained by combining opioids, local anesthetics, and NSAIDS into balanced analgesia. This approach at least allows the opioids dose to be reduced by the use of other modalities, thereby limiting side effects, reducing postoperative pain and analgesics, and facilitating an earlier return to normal activities. Rectus sheath block, local infiltration of the laparoscopy portals and intraperitoneal local anesthesia can be used as regional techniques for pain relieve.4
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