| Management of Anesthesia for Outpatient Laparoscopy - II |
| POSTOPERATIVE MONITORING |
All patients should receive oxygen in the PACU. Although respiratory function may be less impaired after laparoscopic surgery as compared to an open procedure, increased oxygen demand and depressed PaO2 are still a problem which must be addressed. EKG, noninvasive blood pressure determination and Sp02 monitoring must be the standard. The hemodynamic changes resulting from pneumoperitoneum (particularly increased SVR) tend to continue beyond the release of the pneumoperitoneum.
Attention to restoring the patients temperature to normal speeds recovery and reduces oxygen consumption. The Bair Hugger has been very effective in restoring normothermia.
Choice of agents to treat postoperative pain and nausea should be made with outpatient discharge in mind.
| MANAGEMENT OF COMPLICATIONS |
Nausea and vomiting occur in a high proportion of patients (40 to 75%). Anesthetic techniques which minimize opiate consumption may reduce these symptoms. Some surgeons routinely inject local anesthetics (e.g. bupivacaine) subcutaneously around the trocar sites at the conclusion of surgery. The use of ketorolac (Toradol, Roche) may reduce opioid requirements. Nausea may be treated with metoclopramide (Reglan), small doses of droperidol (Inapsine) and the serotonin 5-HT3 blocker ondansetron (Zofran, Glaxo Wellcome). Transdermal scopolamine reduces nausea and vomiting after outpatient laparoscopy, but recently has been unavailable.
Headache, sore throat and shoulder pain are self limiting. Despite these side effects, one study showed that 70% of patients would be happy to have another laparoscopy as an outpatient if necessary.
Pneumothorax
Several mechanisms can result in the movement of gas from the pneumoperitoneum. Pneumothorax may result from pleural tears at the level of the gastroesophageal junction during fundoplication for hiatal hernia. Defects in the diaphragm or weak points in the esophageal or aortic hiatus may allow gas to diffuse into the thorax. The rupture of pre-existing pulmonary bullae may also lead to pneumothorax. Cyanosis, decreased oxygen saturation, subcutaneous emphysema and loss of breath sounds should promote a high suspicion of pneumothorax.
When a pneumothorax develops during laparoscopy, immediate attention must be given to correction of hypoxemia by adjusting inspired oxygen concentration and ventilation. Administration of nitrous oxide should be discontinued. In consultation with the surgeon, intraabdominal pressure should be reduced as much as possible. Since pneumothorax from carbon dioxide (without associated pulmonary trauma) will usually resolve spontaneously, thoracentesis should be avoided unless imperative.
The anesthesiologist should also be aware that insufflation gas may also move into the mediastinum and pericardium. Subcutaneous emphysema of the neck and face may be a consequence of pneumomediastinum.
Gas Embolism
Early recognition of gas embolism is essential to successful treatment. Aspiration of blood into the Verres needle or pulsation of the insufflation pressure gauge should alert the anesthesiologist to the possibility of a potential gas embolism. Although it most commonly occurs during induction of pneumoperitoneum, it may occur intraoperatively or even after the conclusion of the procedure (due to trapping of gas in the portal circulation). Because gas embolism is a rare complication, the usual methods of detection (e.g. precordial Doppler) will rarely be available. An unexplained decrease in end tidal CO2 (perhaps preceded by an initial increase), should give suspicion, especially if accompanied by hypotension, cyanosis and cardiac dysrhythmias.
On diagnosis, the pneumoperitoneum should be released and insufflation stopped. Hyperventilation with 100 % oxygen should be initiated. The patient should be placed in a steep head down and left lateral decubitus position. Because blood has a high capacity for CO2 carriage, as opposed to air, rapid reversal of clinical signs may occur. In the absence of recovery using these simple measures, aspiration of the gas with a central venous line or PA line may be necessary. Paradoxical embolization to the cerebral or coronary vessels is also a possibility (e.g. via the foramen ovale being opened due to right ventricular hypertension.)
Pulmonary Aspiration
Significant intraoperative aspiration is unlikely with the airway secured by an endotracheal tube. Because the laryngeal mask airway does not protect the airway, its use should be avoided as an alternative to intubation. In the event of significant aspiration, pulmonary consultation is advised.
Hemorrhage
Although uncommon with experienced laparoscopists, vascular injury leading to hemorrhage is a possibility. Injury to the aorta, vena cava and iliac vessels can result in rapid blood loss. It is important to have an IV access of reasonable size even though the procedure may be considered to have a low potential for blood loss. It should be remembered that a retroperitoneal hematoma may result in major blood loss without a great deal of blood being visible in the peritoneal cavity. Particular attention should be paid in the case of an inexperienced surgeon or in the case of a patient in whom difficulty in placement of needle or trocar is anticipated.
| PHYSIOLOGY |
PaCO2 increases with pneumoperitoneum and must be compensated for by increased ventilation. Ventilation is impaired by abdominal distention and patient position. In addition, carbon dioxide is absorbed from the abdominal cavity and may be absorbed from subcutaneous emphysema. Elevation of the diaphragm results in a mismatch of ventilation and pulmonary perfusion. An increase in the arterioalveolar CO2 difference results from increased physiological dead space. This difference is more pronounced in obese and ASA II and III as opposed to ASA I patients. End tidal CO2 measurement should be used to monitor PaCO2 keeping in mind that D(a-A)CO2 may vary from patient to patient.
Reduced FRC, total lung volume and pulmonary compliance result from a steep head down position, especially in obese or debilitated patients. The head down position may also result in the development of atelectasis.
Pneumoperitoneum results in decreased cardiac output, increased blood pressure and increased SVR and PVR. Increased intraabdominal pressure also causes reduced venous return leading to reduced cardiac output. Increased SVR is probably related to the release of humoral factors as it outlasts the pneumoperitoneum. Intraabdominal pressures of 20 mmHg result in a fall of renal blood flow and glomerular filtration to less than 25 percent of normal. In addition, such pressures may significantly affect blood flow to the intestines.
In the head up position, cardiac output decreases in proportion to the steepness of tilt. Compounded by blood pooling caused by the pneumoperitoneum, venous stasis in the legs can lead to venous thrombosis and pulmonary embolism, especially in long procedures.
The head down position results in increased central venous pressure which may affect cerebral circulation and cause increased intraocular venous pressure.
In patients with coronary artery disease, changes in central blood volume and blood pressure may be particularly deleterious.
Cardiac dysrhythmias may result from the reflex increase in vagal tone caused by peritoneal stretching or manipulation of the viscera. Bradycardia and even asystole may occur. Reduction in intraabdominal pressure followed by administration of atropine as necessary will result in recovery of heart rate. Deepening of anesthesia will usually blunt the effects of vagal stimulation.