Venous Gas Embolism

A venous gas embolism is a gas bubble in the venous system. Clinically significant venous gas embolism passes into the heart and pulmonary circulation, blocking the pulmonary circulation with subsequent hypoxemia, hypercapnia, and depressed cardiac output. Several fatalities have been reported (119-121). If pressure in the right heart exceeds that in the left heart, a foramen ovale defect may allow gas to embolize into the arterial system (20,119,120). Symptomatic venous gas embolism is rare during laparoscopy, with an estimated incidence of 0.002% to 0.08% (122). Using careful surveillance with echocardiography, however, detectable venous gas embolism were noted in 0.59% of laparoscopic cases in one study (123).

Most venous gas embolisms occur during and within a few minutes of initial gas insufflation, but delayed cases have been reported (119).

The most useful indication of venous gas embolism is (i) a sudden fall in P(et)CO2 on capnometry if the CO2 embolus is large or (ii) its abrupt but transient increase if the CO2 embolus is small.

Venous gas embolism should be suspected in the presence of clinical indicators, especially if they occur suddenly or during initial insufflation. Swift response may be lifesaving.

Immediate desufflation prevents more gas from entering the venous system. Placing the patient in a steep head-down tilt position with the right side up tends to trap gas in the right ventricle and prevent passage into the pulmonary circulation. Rapid ventilation with 100% oxygen and general resusci-tative maneuvers are recommended to address hypoxemia, hypercapnia, and hypotension.

The moderate hypercapnia that occurs during most laparoscopic procedures using CO2 pneumoperitoneum is beneficial via a mild sympathetically mediated cardiostimulatory effect. However, the direct cardiodepressive effects of CO2 and the severe respiratory acidosis associated with hypercapnia of this magnitude can lead to cardiovascular collapse and/or fatal dysrhythmias if the level of PaCO2 exceeds 60 mmHg.

Venous gas embolism has also been produced experimentally in a bleeding vena cava model. In this setting, the risk is greatest when blood flow cephalad from the venotomy is reduced, owing to either mechanical occlusion of the vena cava or significant blood loss (124). At any point in the laparoscopic procedure, when a venotomy is created and flow past the injury is reduced, venous gas embolism must be considered. However, if the cavotomy is appropriately managed with attention to minimizing blood loss and potential for gas entering the proximal end, then venous gas embolism is unlikely (125).

The most useful indication of venous gas embolism is (i) a sudden fall in P(et)CO2 on capnometry if the CO2 embolus is large or (ii) its abrupt but transient increase if the CO2 embolus is small (121,126).

Other clinical signs of venous gas embolism include hypoxemia, pulmonary edema, increased airway pressure, hypotension, jugular venous distention, facial plethora, dysrhythmias, auscultation of a mill-wheel cardiac murmur, or the appearance of a widened QRS complex with right heart strain patterns on electrocardiography.

Venous gas embolism should be suspected in the presence of clinical indicators, especially if they occur suddenly or during initial insufflation. Swift response may be lifesaving.

The goal is to minimize further passage of gas into the pulmonary circulation, and to correct the ventilation problems.

Immediate desufflation prevents more gas from entering the venous system. Placing the patient in a steep head-down tilt position with the right side up tends to trap gas in the right ventricle and prevent passage into the pulmonary circulation. Rapid ventilation with 100% oxygen and general resuscitative maneuvers are recommended to address hypoxemia, hypercapnia, and hypotension.

If a central venous catheter is already in place, attempts to aspirate the gas are reasonable (127).

The nature of the gas that embolizes is an important determinant of the outcome of venous gas embolism (128). As outlined in Table 2, CO2 is 47 times more soluble than nitrogen. A venous gas embolism composed of CO2 would therefore be reabsorbed much more quickly than one composed of nitrogen. Comparing intravenous injection of air versus CO2 in a canine model, LD50 (lethal dose in 50% of subjects) of air (~80% nitrogen) was five times lesser than LD50 of CO2 (129). Helium, used as an alternative to CO2 for insufflation in some series (46,108-110), is even less soluble than nitrogen. In canine experiments, intravenous injection of helium was lethal on four of six occasions whereas injection of the same amount of CO2 was followed by hemodynamic recovery in all cases (Fig. 4) (130). Argon venous gas embolism during use of a laparoscopic argon beam coagulator has been reported (131).

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