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Departments of
*Anesthesiology and
Surgery, University of Maryland School of Medicine, Baltimore, Maryland
Address correspondence and reprint requests to Brenda G. Fahy, MD, Department of Anesthesiology, University of Maryland School of Medicine, 22 S. Greene St., Baltimore, MD 21201-1595.
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Abstract |
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Implications: Laparoscopic surgery has gained popularity as a procedure for the removal of donated kidneys. Although the insufflation of gas necessary for this relatively simple approach poses a low risk of venous air embolism, it may increase the risk of changes in valvular competency.
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Introduction |
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One potentially lethal complication of laparoscopic surgery is gas embolism (3). The incidence of gas embolism associated with procedures that do not entail manipulation of major vessels has been well documented. Clinically significant gas embolism is rare during gynecologic procedures performed via laparoscopy (4). In contrast, emboli have been observed in 69% of patients undergoing laparoscopic cholecystectomy (5), and the risk of embolism may be even higher during laparoscopic procedures involving large vessels (6), such as nephrectomy. In addition, the risk of venous thromboembolism may be increased during laparoscopic nephrectomy by impairment of venous return caused by pneumoperitoneum, dependent positioning of the lower extremities, and lengthy surgery.
The objective of this study was to document the incidence of embolic events and associated hemodynamic and end-tidal CO2 changes during laparoscopic nephrectomy in healthy donors. Cardiac function was monitored with transesophageal echocardiography (TEE). In addition, cardiac and valvular function were analyzed in relation to changes in patients’ position and to induction of pneumoperitoneum.
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Methods |
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Patients received 2 mg of midazolam preoperatively. With patients in the supine position, anesthesia was induced with thiopental (5 mg/kg) and sufentanil (0.3 µg/kg). Neuromuscular relaxation was achieved with 0.5 mg/kg atracurium or 0.2 mg/kg cisatracurium followed by a continuous infusion of 2–5 µg · kg-1 · min-1 or 1–3 µg · kg-1 · min-1, respectively. Patients received 30% O2/70% N2O, with end-tidal isoflurane concentration maintained below 0.6%. A sufentanil infusion of 0.2 µg · kg-1 · min-1 was adjusted according to hemodynamic indications. Intraoperative medications administered included papaverine (30 mg), heparin (5000 U), and protamine (25 mg). Medications and fluids were administered through a peripheral IV catheter.
End-tidal CO2 partial pressure was maintained at 30–35 mm Hg. All patients received 5 cm H2O positive end-expiratory pressure (PEEP). A precordial Doppler was used to monitor heart sounds. A liter of crystalloid solution was given preoperatively, and intraoperative fluid administration was adjusted to maintain urine output 
-1 mL · kg-1 · h-1. Intermittent sequential pneumatic lower extremity compression devices were in place during surgery.
Stomach air and contents were aspirated via a gastric tube after tracheal intubation to enhance TEE visualization. A 5.0 -MHz biplane TEE probe (Hewlett-Packard) view was monitored continuously for chamber size, wall motion, gas entry, and valvular regurgitation with the patients in both supine and lateral decubitus positions, except during the periods when a complete TEE examination was performed. Complete TEE examination included a four-chamber view for valvular function and intracardiac gas entry; transverse superior vena cava (SVC) and inferior vena cava (IVC) view for intracardiac gas; short-axis view for left ventricular end-diastolic area (LVEDA); and left ventricular end-systolic area (LVESA).
A complete TEE examination was performed preoperatively with the patient in the supine position after surgery. All other complete TEE examinations were performed with the patient in the lateral decubitus position at the following points: before surgery, during establishment of CO2 pneumoperitoneum to 15 mm Hg, every 30 min during insufflation, during abdominal deflation for kidney removal and reinsufflation to 15 mm Hg to obtain hemostasis, and after subsequent deflation. TEE monitoring continued for at least 30 min after abdominal deflation to allow detection of venous thromboemboli. A variable-flow insufflator maintained 15 mm Hg intraabdominal pressure throughout surgery.
If gas entered the heart, a longitudinal view of the SVC and IVC was obtained to document its pathway. Cardiovascular instability during gas entry was defined as a sudden decrease in mean arterial pressure >10 mm Hg or an acute episode of pulse oximetric saturation (Spo2 < 90%). Using statXact 3 and exact binomial estimation, a 95% confidence interval on the estimate of the population rate (p) was calculated for gas embolism and venous thromboembolism.
LVEDA and LVESA were calculated by on-line analysis of end-systolic and end-diastolic endocardial manual tracings. Three tracings were averaged. Ejection fraction (EF) was calculated as follows: ([LVEDA - LVESA]/LVEDA) x 100. Simultaneous electrocardiographic monitoring permitted precise cardiac cycle timing. TEE studies were recorded on VHS tape for further analysis. To avoid interpersonal variability, calculations were performed by one registered sonographer. An independent cardiac anesthesiologist certified in echocardiography reviewed the tapes for gas embolism and TEE interpretation. A second observer reviewed all tapes. Both were blinded to changes in patients’ positions and the state of abdominal insufflation.
Systolic, diastolic, and mean arterial blood pressure and Spo2 were recorded during gas entry, Doppler tone changes, and TEE examinations. Analysis of variance for repeated measures was used to compare hemodynamic values and EF between different positions and in the presence or absence of pneumoperitoneum. EF and hemodynamic values were analyzed by using one-way repeated-measures analysis of variance. A P value <0.05 was considered significant.
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Results |
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Discussion |
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The heart may shift after induction of pneumoperitoneum, altering its position relative to the transducer and making visualization difficult (7). In that circumstance, the biplane probe used in our study permits better visualization compared with a single-plane probe. With the biplane TEE probe, fluid microbubbles entering from the SVC are also distinguishable from gas emboli entering from the IVC.
There are several possible explanations for the unexpectedly low incidence of gas embolism that we observed during laparoscopic nephrectomy. Increasing central venous pressure may decrease the risk of embolism (8). The central venous pressure was probably high in our patients because they received 1 L of fluid preoperatively and an average of 4.5 L of fluid replacement intraoperatively. During laparoscopic nephrectomy, pneumoperitoneum increases central venous pressure when the patient is in head-down position, whereas, during laparoscopic cholecystectomy, pneumoperitoneum decreases central venous pressure when the patient is in the head-up position (9). Head-down positioning may also reduce gas embolism to the head because the bubbles are buoyant. The patients undergoing laparoscopic nephrectomy received 5 cm H2O PEEP, which may have decreased the pressure gradient between a vessel opening and the heart, thus reducing the likelihood of gas entry.
We expected a higher risk of venous thromboembolism related to increased venous stasis during laparoscopic nephrectomy. Venous stasis may be increased by dependent positioning of the lower extremities and increased intraabdominal venous pressures during pneumoperitoneum. No venous thromboemboli were seen after abdominal deflation, when thromboembolic events most likely occur. Possible explanations include intraoperative heparin administration and lower pressures on the venous system during laparoscopic nephrectomy. In addition, calf-length intermittent sequential pneumatic compression devices were worn by all patients during laparoscopy. These devices prevent the decrease in blood velocity in the common femoral vein during pneumoperitoneum and head-up positioning (10) and thus may have decreased thromboembolic risk.
Although TEE has been performed in a number of studies during laparoscopic surgery (5,11,12), there have been no reports of valvular regurgitation associated with pneumoperitoneum (13–15). Some of the TEE studies used single-plane TEE probes, which cannot visualize the full extent of valvular regurgitation (5,11,16). One proposed mechanism for valvular regurgitation is an increased systemic vascular resistance during pneumoperitoneum (16,17). Preoperative hydration and head-down positioning may also contribute to valvular regurgitation.
If preoperative valvular disease exists, an increase in or onset of valvular regurgitation during laparoscopic nephrectomy could cause hemodynamic compromise. Existing MR could increase during pneumoperitoneum and precipitate pulmonary edema. With preexisting mitral valve prolapse, acute MR could develop after pneumoperitoneum.
To decrease the risk of MR during pneumoperitoneum, a vasodilator could be used to decrease systemic vascular resistance. Nitroglycerine has been used successfully to decrease systemic vascular resistance during laparoscopy in patients with known heart disease (18,19). Valvular regurgitation during laparoscopy could have implications for patients with other cardiac diseases. The decrease in forward flow with MR could precipitate myocardial ischemia.
EF remained unchanged during changes in patients’ positions and induction of pneumoperitoneum. There are no other published data concerning EF during laparoscopic nephrectomy. During laparoscopic cholecystectomy, studies have shown conflicting results, ranging from no change in EF (11,12) to significant decreases after insufflation (5). These differences may have arisen because of different anesthetic techniques and varying CO2 levels.
Studies have shown variations in blood pressure and HR caused by abdominal insufflation for laparoscopic surgery with the patient in the Trendelenburg position (9,20). The changes we observed for lateral decubitus positioning agree with one of these reports (21). Other postures, such as reverse Trendelenburg, have yielded results similar to our findings related to the Trendelenburg position (22), whereas still others have shown conflicting results (12,23). These differences could be at least partially related to the varying postures and anesthetic techniques used (9,20). In addition, arterial CO2 partial pressure values vary widely among studies: some patients remained normocapnic, whereas others exhibit hypercarbia, which increases hemodynamic variability.
Our study had a low incidence of embolic events during laparoscopic nephrectomy. However, we documented a surprisingly high incidence of regurgitation at the mitral, tricuspid, pulmonic, and aortic valves after CO2 insufflation. Our study group, consisting of healthy donors, suffered no compromise of hemodynamic or cardiac function during the laparoscopic procedures. The consequences of these challenges in patients with preexisting valvular or cardiac disease are unknown and warrant further study.
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Acknowledgments |
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This article has been cited by other articles:
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  P. Lindstrom, J. Wadstrom, A. Ollerstam, C. Johnsson, and A. E. G. Persson Effects of increased intra-abdominal pressure and volume expansion on renal function in the rat Nephrol. Dial. Transplant., November 1, 2003; 18(11): 2269 - 2277. [Abstract] [Full Text] [PDF]
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