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Respiratory Complications

Carbon Dioxide Subcutaneous Emphysema

CO2 subcutaneous emphysema can develop as a complication of accidental extraperitoneal insufflation[41] but can


Figure 57-4 Diagnosis of respiratory complications during laparoscopy. ECG, electrocardiographic; Paw, airway pressure; PETCO2 , end-tidal carbon dioxide tension. (Data from Wahba RW, Tessler MJ, Kleiman SJ: Acute ventilatory complications during laparoscopic upper abdominal surgery. Can J Anaesth 43:77, 1996.)

also be considered as an unavoidable side effect of certain laparoscopic surgical procedures that require intentional extraperitoneal insufflation, such as inguinal hernia repair, renal surgery, and pelvic lymphadenectomy[19] [42] ( Fig. 57-4 ). During laparoscopic fundoplication for hiatal hernia repair, the opening of the peritoneum overlying the diaphragmatic hiatus allows passage of CO2 under pressure through the mediastinum to the cervicocephalic region. In these three circumstances, V̇CO2 , PaCO2 , and PETCO2 increase.[19] Any increase in PETCO2 occurring after PETCO2 has plateaued should suggest this complication. The increase in V̇CO2 may be such that prevention of hypercapnia by adjustment of ventilation becomes almost impossible. In this case, laparoscopy must be temporarily interrupted to allow CO2 elimination and can be resumed after correction of hypercapnia using a lower insufflation pressure. CO2 pressure determines the extent of the emphysema and the magnitude of CO2 absorption. CO2 subcutaneous emphysema readily resolves after insufflation has ceased. CO2 subcutaneous emphysema, even cervical, does not counterindicate tracheal extubation at the end of surgery.[43] We recommend keeping the patient under controlled mechanical ventilation until hypercapnia is corrected, particularly in COPD patients, to avoid excessive increases in the work of breathing.

Pneumothorax, Pneumomediastinum, and Pneumopericardium

Movement of gas during the creation of a pneumoperitoneum can produce pneumomediastinum,[44] unilateral and bilateral pneumothorax,[45] and pneumopericardium.[46] Embryonic remnants constitute potential channels of communication between the peritoneal cavity and the

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pleural and pericardial sacs, which can open when intraperitoneal pressure increases. Defects in the diaphragm or weak points in the aortic and esophageal hiatus may allow gas passage into the thorax. Pneumothorax may also develop from pleural tears during laparoscopic surgical procedures at the level of the gastroesophageal junction (e.g., fundoplication for hiatal hernia). Whereas opening of peritoneopleural ducts results mainly in right-sided pneumothorax (in the same way that ascites or peritoneal dialysis may be associated with right-sided pleural effusions),[47] pneumothorax during fundoplication is more frequently located on the left. Because of the increased alveolar inflation from increased minute ventilation during pneumoperitoneum, preexisting pulmonary bullae can rupture, leading to pneumothorax.

These complications are potentially serious and may lead to respiratory and hemodynamic disturbances. Capnothorax (i.e., CO2 pneumothorax) reduces thoracopulmonary compliance, and airway pressures increase. V̇CO2 , PaCO2 , and PETCO2 also increase.[48] In effect, the absorption surface of CO2 is increased, and the absorption from the pleural cavity is greater than from the peritoneal cavity. In case of pneumothorax from alveolar rupture, PETCO2 decreases because of decreased cardiac output. Hemodynamic changes and capillary oxygen desaturation are not constant, but tension pneumothorax with cardiorespiratory compromise can occur. 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 roentgenography. Cervical and upper thoracic subcutaneous emphysema can develop without pneumothorax.

When pneumothorax is caused by highly diffusible gas such as N2 O or CO2 without associated pulmonary trauma, spontaneous resolution of the pneumothorax occurs within 30 to 60 minutes after exsufflation.[49] When capnothorax develops during laparoscopy, we follow several guidelines[48] :

  1. Stop N2 O administration.
  2. Adjust ventilator settings to correct hypoxemia.
  3. Apply positive end-expiratory pressure (PEEP).
  4. Reduce IAP as much as possible.
  5. Maintain close communication with the surgeon.
  6. Avoid thoracocentesis unless necessary, because pneumothorax spontaneously resolves after exsufflation.

In case of pneumothorax from rupture of preexisting bullae, PEEP must not be applied and thoracocentesis is mandatory.

Endobronchial Intubation

Cephalad displacement of the diaphragm during pneumoperitoneum results in cephalad movement of the carina, potentially leading to endobronchial intubation[50] (see Chapter 42 ). Cases of endobronchial intubation associated with laparoscopy have been reported during gynecologic laparoscopy in the head-down position[51] and during laparoscopic cholecystectomy despite using the head-up position.[52] [53] [54] This complication results in a decrease in the oxygen saturation as measured by pulse oximetry (SpO2 ) associated with an increase in plateau airway pressure.

Gas Embolism

Although rare, gas embolism (see Chapter 53 ) is the most feared and dangerous complication of laparoscopy and may occur more frequently when laparoscopy is associated with hysteroscopy.[55] Intravascular injection of gas may follow direct needle or trocar placement into a vessel, or it may occur as a consequence of gas insufflation into an abdominal organ. This complication develops principally during the induction of pneumoperitoneum, [56] [57] particularly in patients with previous abdominal surgery.[58] Gas embolism may also occur later during surgery.[55] [59] [60] [61] CO2 is used most frequently for laparoscopy because it is more soluble in blood than air, oxygen, or N2 O. The capacity for CO2 carriage of the blood is high because of bicarbonate buffering and combination with hemoglobin and plasma proteins.[38] 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.

The pathophysiology of gas embolism is also determined by the size of the bubbles and the rate of intravenous entry of the gas.[62] [63] 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 decrease in cardiac output or even circulatory collapse can result. Acute right ventricular hypertension may open the foramen ovale, which is patent in 20% to 30% of the population, allowing paradoxical gas embolization of the cerebral and coronary beds.[55] [64] Paradoxical embolism, however, may occur without patent foramen ovale.[65] [66] Volume preload diminishes this embolic risk. [67] Ventilation-perfusion (V̇A/) mismatching develops with increases in physiologic dead space and hypoxemia.

The diagnosis of gas embolism depends on the detection of gas emboli in the right side of the heart or on recognition of the physiologic changes from embolization. Early events, 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 used. When the size of the embolus increases (2 mL/kg of air), tachycardia, cardiac arrhythmias, hypotension, increased central venous pressure, alteration in heart tones (i.e., millwheel murmur), cyanosis, and electrocardiographic changes of right heart strain can develop; all these changes are rarely consistently positive. [68] Pulmonary edema can also be an early sign of gas embolism.[64] Although transesophageal echocardiography, [62] esophageal or precordial Doppler probes, or pulmonary artery catheters are the most sensitive means of detecting small quantities of gas before 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 fall in cardiac output and the

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enlargement of the physiologic dead space. Consequently, Δa-ETCO2 increases. CO2 embolization may cause a biphasic change in PETCO2 . The decrease in PETCO2 is preceded by an initial increase from pulmonary excretion of the CO2 , which has been absorbed into the blood.[55] [63] Aspiration of gas or foamy blood from a central venous line definitively establishes the diagnosis. Routine preoperative insertion of a central venous line, however, does not appear justified for these procedures.

Treatment of CO2 embolism consists of immediate cessation of insufflation and release of pneumoperitoneum. The patient is placed in a steep head-down and left lateral decubitus (Durant) position. The amount of gas that advances through the right heart to the pulmonary circulation is less if the patient is in this position because the buoyant foam is displaced laterally and caudally away from the right ventricular outflow tract. Discontinuing N2 O allows ventilation with 100% oxygen to correct hypoxemia and reduces the size of the gas embolus and its consequences.[63] Hyperventilation increases CO2 excretion and is made necessary by 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. External cardiac massage may be helpful in fragmenting CO2 emboli into small bubbles. The high solubility of CO2 in blood, resulting in rapid absorption from the bloodstream, accounts for the rapid reversal of the clinical signs of CO2 embolism with treatment.[57] CO2 embolism, however, may be fatal. Cardiopulmonary bypass has been used successfully to treat massive CO2 embolism.[55] Hyperbaric oxygen treatment should be strongly considered if cerebral gas embolism is suspected.[64]

Risk of Aspiration of Gastric Contents

Patients undergoing laparoscopy may be considered to be at risk for acid aspiration syndrome. However, the increased IAP results in changes of the lower esophageal sphincter that allow maintenance of the pressure gradient across the gastroesophageal junction and that may therefore reduce the risk of regurgitation. [69] [70] The head-down position should help to prevent any regurgitated fluid from entering the airway.

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