A 62-year-old, 77-kg man with prostate cancer presented for robotic-assisted laparoscopic radical prostatectomy (RALP). Past medical history included hypertension and hyperlipidemia. The procedure went smoothly with the patient receiving 2500 mL of intravenous fluid and experiencing a surgical blood loss of 50 mL. The patient’s trachea was extubated, and he was transferred to the postanesthesia care unit (PACU). Shortly thereafter, he was noted to have difficulty breathing and decreasing oxygen saturation. It was decided to perform emergent reintubation, and on direct laryngoscopy, the patient was noted to have severe laryngeal edema.
What are the advantages of robotic-assisted laparoscopic radical prostatectomy over traditional open radical prostatectomy?
RALP is gradually supplanting open and laparoscopic techniques for the surgical treatment of prostate cancer. RALP offers the advantages of better visualization and increased precision manipulation of delicate nerves and vessels. RALP also provides enhanced ability to preserve the integrity of neurovascular bundles and reduced median recovery times for urinary continence and sexual function compared with open procedures. Other advantages are decreased intraoperative bleeding, reduced transfusion rates, less postoperative pain, shorter PACU stays, and shortened hospital stays.
Briefly describe the surgical procedure.
In RALP, after induction of general anesthesia, the patient is placed in lithotomy position, arms are carefully tucked at the side, and head-to-toe drapes are placed. Extensive draping limits the anesthesiologist’s view of the patient and inhibits further examination of the patient. All catheters, monitors, and patient protective devices have to be placed and secured before draping. At this point, carbon dioxide (CO 2 ) pneumoperitoneum is initiated, and the patient is placed in 30-degree to 45-degree Trendelenburg position. During positioning, care is taken to prevent kinking or dislodging of the endotracheal tube. The surgeon places additional ports in the abdomen, and the robotic arms are “docked” (attached) to the ports. With the robot positioned over the patient and its arms attached to the ports, the patient cannot be moved. If cardiopulmonary resuscitation is required, the robot must first be detached and moved away.
The surgeon sits at the robot console. An assistant at the patient’s side guides the robotic arms. Bladder neck, vas deferens, seminal vesicles, and prostate are dissected. As the prostate is dissected free, nerve-sparing is attempted when possible. When the prostate is freed up, it is placed elsewhere in the abdominal cavity, and the surgeon completes the vesicourethral anastomosis. Dissection of the pelvic lymph nodes is performed followed by placement of a perivesical drain. With the robotic phase of surgery completed, the robot is undocked and moved away from the patient.
The prostate is placed in a plastic specimen bag and removed from the patient through one of the port incisions. The patient is taken out of Trendelenburg position, the remaining ports are removed, incisions are closed, the patient’s legs are taken out of lithotomy position, and the patient is awakened. Depending on surgical experience and difficulty of the case, mean operative times range from 160–296 minutes with mean blood losses of 50–287 mL.
What are the primary anesthetic concerns for robotic-assisted laparoscopic radical prostatectomy?
The primary anesthetic concerns for RALP are as follows:
Physiologic effects of pneumoperitoneum in the Trendelenburg position
Restricted access to the patient because of the massive equipment placed over the patient
Prevention or treatment of complications secondary to inducing pneumoperitoneum and positioning the patient in exaggerated lithotomy and steep Trendelenburg
Describe the cerebrovascular, respiratory, and hemodynamic effects of pneumoperitoneum in steep trendelenburg position.
Significant cerebrovascular physiologic changes may occur with the use of pneumoperitoneum and the steep Trendelenburg position ( Box 38-1 ). Initiation of pneumoperitoneum increases intraabdominal pressure, which results in increased intracranial pressure (ICP). Placing patients in the Trendelenburg position also eventually increases ICP by elevating cerebral venous pressure, which hinders cerebral venous drainage and leads to increases in cerebral blood volume and potentially cerebrospinal fluid volume. Cerebral perfusion does not appear to be compromised during RALP. Disastrous consequences nevertheless may occur secondary to excessive increases in ICP, especially in patients with cerebral ischemia and cerebrovascular disorders.
cerebral venous drainage →↑ CBV and ↑ CSF
peak and plateau airway pressures
functional residual capacity
↓ mean arterial pressure
↓ or unchanged heart rate and cardiac output
central venous pressure and systemic vascular resistance
stroke work index
CBV, Cerebral blood volume; CSF, cerebrospinal fluid.
Regional cerebral oxygen saturation (rSO 2 ) employing near-infrared spectroscopy cerebral oximetry has been used to evaluate cerebrovascular effects during RALP. Increases in rSO 2 have been observed with the use of pneumoperitoneum and the steep Trendelenburg position suggesting that RALP does not induce cerebral ischemia. The use of near-infrared spectroscopy to monitor rSO 2 , a reflection of the balance between cerebral oxygen supply and demand, is limited because it measures only rSO 2 of the frontal cortex, not global cerebral oxygenation. rSO 2 was also found to increase with increases in arterial carbon dioxide (PaCO 2 ), but because hypercapnia also causes an increase in cerebral blood volume and eventually an increase in ICP, it is recommended that patients be maintained within normocapnic ranges.
Changes in respiratory homeostasis caused by pneumoperitoneum and steep Trendelenburg position are also significant. Pneumoperitoneum elevates intraabdominal pressure causing decreases in pulmonary compliance and tidal volumes along with increases in peak and plateau airway pressures. The addition of steep Trendelenburg position pushes abdominal contents against the diaphragm. The resulting pressure reduces functional reserve capacity, decreases pulmonary compliance, and predisposes to atelectasis. Further reductions in functional reserve capacity and pulmonary compliance are caused by increases in pulmonary blood volume and gravitational forces on mediastinal structures. To compensate for these effects, elevated peak airway pressures are required to maintain a constant minute volume. With ascending peak inspiratory pressures, the risk of barotrauma increases. This potential risk may be reduced by decreasing tidal volume, increasing the respiratory rate, and tolerating a minimal level of hypercarbia. Another potential concern of the steep Trendelenburg position is pulmonary interstitial edema, when much of the lung is below the left atrium.
Several observational studies have evaluated the hemodynamic effects of pneumoperitoneum in combination with the steep Trendelenburg position during RALP. In one large retrospective review comprising 1500 cases, mean arterial pressure, heart rate, and cardiac output all were noted to be decreased. Prospective studies with relatively small numbers of patients observed increases in mean arterial pressure, central venous pressure, and systemic vascular resistance with only the initiation of pneumoperitoneum. These changes are postulated to result from increased intraabdominal pressure compressing the aorta. Aortic compression results in increased afterload and may be enhanced further by humoral factors. Other studies found that central venous pressure did not change with insufflation but increased only with the addition of the steep Trendelenburg position.
Changes in heart rate and cardiac output have been variably reported as increased, no change, or decreased. Severe bradycardia, probably caused by vagal stimulation during peritoneal distention, has occurred on initiation of pneumoperitoneum in RALP cases. With the combination of pneumoperitoneum and steep Trendelenburg position, strain or workload on the heart, as measured by right-sided and left-sided stroke work index, is increased. The proposed mechanism for this phenomenon is increased filling pressures. In patients with sufficient cardiac reserve, these changes are probably well tolerated. Patients with compromised cardiac function could develop heart failure from increased preload.