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Year : 2003  |  Volume : 51  |  Issue : 3  |  Page : 370--372

Venous air embolism: Does the site of embolism influence the hemodynamic changes?

P Bithal, HH Dash, N Vishnoi, A Chaturvedi 
 Department of Neuroanesthesia, All India Institute of Medical Sciences, New Delhi - 110029, India

Correspondence Address:
P Bithal
Department of Neuroanaesthesiology Neurosciences Centre, All India Institute of Medical Sciences New Delhi - 110029


Three hundred and ninety-seven patients undergoing posterior cranial fossa surgery in the sitting position were prospectively studied to evaluate the incidence of venous air embolism (VAE) and its effects on hemodynamics. End-tidal carbon dioxide (ETC02) tension was monitored to diagnose VAE. A sudden and sustained decrease in ETC02 of more than 5 mmHg, in the absence of sudden hypovolemia, was presumed to be the result of VAE. The site of probable air entrainment (whether muscle, bone or tumor) was noted. Hemodynamic consequences were managed symptomatically. ETC02 monitoring detected VAE in 22% of the patients. The highest incidence of embolism resulted from muscles and tumor (40% in each case). Forty-two per cent of patients developed hypotension during the embolic episode (systolic BP less than 100 mmHg). Ten per cent of patients developed ventricular arrhythmias during the embolic episode. Air aspiration was successful in 4.8%. There were no statistically significant differences in the frequency of VAE among the different groups (P>0.05). Also, the frequency of hypotension and ventricular arrhythmias were not significantly different, irrespective of the source of VAE (P>0.05). The general condition of the patients in the preoperative stage had no influence on the incidence of embolism, hypotension or ventricular arrhythmias.

How to cite this article:
Bithal P, Dash H H, Vishnoi N, Chaturvedi A. Venous air embolism: Does the site of embolism influence the hemodynamic changes?.Neurol India 2003;51:370-372

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Bithal P, Dash H H, Vishnoi N, Chaturvedi A. Venous air embolism: Does the site of embolism influence the hemodynamic changes?. Neurol India [serial online] 2003 [cited 2021 Dec 5 ];51:370-372
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Full Text



The use of the sitting posture in patients who undergo posterior cranial fossa (PCF) surgeries is controversial. Its various benefits, related to the ease of surgery, are negated by the potential of the position to result in venous air embolism (VAE). However, many neurosurgeons in different parts of the world still use and recommend this position for posterior cranial fossa surgery.[1],[2],[3],[4],[5],[6],[7],[8]

In our center, the use of the sitting position has diminished over the years, but some surgeons still prefer it. In the present study we examined the stage of surgery at which VAE is most likely to occur, with the help of ETC02 and invasive blood pressure monitoring.


   Material and Methods

Three hundred and ninety-seven consecutive patients (men = 215, women = 182) of all age groups and either sex, who underwent PCF exploration from January 1990 to December 1994 for tumor excision in the sitting posture were included in the study. The project was cleared by the Ethics Committee of our hospital. The technique of anesthesia was similar in all of them, and consisted of thiopentone-induction (halothane in small children), tracheal intubation following pancuronium, and maintenance with 67% nitrous oxide in oxygen, halothane 0.5%, pancuronium and a narcotic. Lungs were mechanically ventilated using Bain circuit. The volume of ventilation and fresh gas flow was adjusted to maintain an ETC02 tension of approximately 30 mmHg. A single orifice central venous catheter was inserted into the right atrium either via the right basilic vein or via the right internal jugular vein in all patients except small children. A pin-type holder was used to stabilize the head in the sitting posture.

Monitoring during the surgery consisted of ECG, heart rate, intra-arterial blood pressure (by cannulating a peripheral artery and keeping the transducer at the level of the forehead), ETC02 tension (Datex multicap), nasopharyngeal temperature (in children), arterial blood gas analysis (whenever feasible), and blood loss and urine output.

Intraoperatively, VAE was assumed to have taken place when there was a sudden and sustained decrease in ETCO2 tension of more than 5 mmHg, in the absence of sudden hypovolemia or any change in the volume of ventilation. The site of embolism (muscle, bone or tumor) was noted. General therapeutic measures were instituted promptly in the form of switching off nitrous oxide, ventilation with 100% oxygen (without altering the volume of ventilation), informing the surgeon who flushed the surgical field with saline, coagulated any visible bleeding vessel, smeared the bone edges with bone wax, and packed the wound with a wet sponge. Air retrieval was attempted from the central venous catheter. Cardiac sounds were monitored by a precordial stethoscope for any murmur. Premature ventricular contractions (PVCs) were treated with xylocaine.

The VAE episode was considered to have resulted in only mild hypotension when the systolic blood pressure (SBP) decreased by 20% of the pre-episode value but remained above 100 mmHg. Hypotension was graded as moderate when SBP decreased to less than 100 mmHg but remained above 70 mmHg. However, hypotension was labeled as severe whenever SBP decreased to less than 70 mmHg. Mild hypotension was managed with the general therapeutic measures outlined above. Patients with mild hypotension were excluded from the total incidence of hypotension. In case of moderate hypotension, crystalloids were infused at a faster rate along with the general therapeutic measures. However, in severe hypotension, patients were administered mephentramine in divided doses of 5 mg each, in addition to other measures. The head end of the table was lowered or the table was made horizontal if deemed necessary, to manage severe hypotension. With the improvement in the hemodynamic status of the patient and a rise in ETC02 tension towards normal, nitrous oxide was reintroduced in a step-wise manner, keeping a close watch on the ETC02 tension (maintaining a constant volume of ventilation throughout). When the ETC02 tension as well as hemodynamics remained stable in the presence of 67% nitrous oxide, surgery was resumed and completed in the sitting posture. However, the procedure was abandoned if all these measures failed to restore hemodynamic stability. Postoperatively, the patients were either extubated or electively ventilated, depending on the discretion of the attending anesthesiologist.

Chi square test was used for statistical comparison and P value of less than 0.05 was taken as significant.



The majority of the patients (87.9%) were in ASA physical status II and I. The age range in the series was from 11 months to 72 years. There were 76 children (age 14 or below). VAE was observed in 89(22.4%) patients. The youngest patient to get VAE was a two-year-old male. The male to female ratio among those who developed VAE was 64:25. Though VAE resulted more frequently from muscle and tumor (36 patients in each group), and less commonly from bone (17 patients), its frequency among these groups was not statistically different (P>0.05).

Hypotension (moderate as well as severe) was observed in 37 patients out of 89 who had VAE episode (42%). Moderate and severe hypotension was observed in 54% (20 of 37) and 46% (17 of 37) patients, respectively [Table:1]. Though the frequency of hypotension was more in the case of VAE from tumor than in the other groups, it was statistically non-significant (P>0.05). The head end of the table had to be lowered to treat hypotension in 4 patients, 2 each in the muscle and the tumor groups. Surgery had to be abandoned in 1 patient in the tumor group.

VAE resulted in PVCs in 9 patients (5 in the tumor group, 3 in the muscle group and 1 in the bone group). The incidence of VAE, PVCs as well as hypotension did not bear any relation with the ASA physical status of the patients (P>0.05) [Table:2]. Air retrieval from the central venous catheter was successful in only 4.8% of the patients; the maximum volume of air aspirated was approximately 15 cc. Cardiac murmur was present in 5% of the patients and its character varied from tinkling sounds to harsh quality murmur.



VAE, a potential complication of surgery performed in the sitting posture, has also been described during laminectomy performed in prone positions[9] and even after closure of craniotomy in the immediate postoperative period.[10] Various methods, including the use of PEEP, have been tried to prevent the occurrence of VAE during PCF exploration in the sitting posture, without any success.[11] If left untreated, VAE carries a very high mortality.[12] At times, air may even traverse from the venous side into the arterial circulation resulting in highly dangerous paradoxical air embolism. Therefore, in order to prevent potentially serious complications, the ability to detect and treat VAE promptly assumes a significant aspect of anesthetic care. A battery of monitors is in use for its early detection before hemodynamic changes occur. Of there monitoring tools transesophageal echocardiography and Doppler ultrasound are highly sensitive.[13] However, both have their own drawbacks.

ETC02 tension monitoring, though intermediate in sensitivity, has the advantages of being non-invasive and semi-quantitative, and is positively decreased by air embolism once its threshold sensitivity (0.4 ml/Kg/min) is reached prior to alteration in BP.[14] But ETCO2 tension monitoring is not specific to air embolism alone. Its sudden decrease can also result from pulmonary embolism resulting from any pathology. However, the most common cause of intraoperative pulmonary embolism apart from VAE is fat embolism. The latter is usually seen after trauma to long bones. None of our patients had history of trauma, thus ruling out fat as the cause of pulmonary embolism. Another clinical situation where one may come across a decrease in ETC02 is acute hypotension but decrease in ETC02 during hypotension is a very slow process unlike VAE. The fall was no more than 1-6 mmHg even where mean arterial pressure was deliberately decreased by 43%.[16] Similar observations have also been reported during hypotension of various etiologies.[15]

We observed 22% incidence of VAE in the present series. By monitoring ETCO2, other authors have described the frequency of VAE from 7% to 40% in patients undergoing PCF surgery in an upright posture.[16],[17] Such variability in incidence could be ascribed to the different states of preoperative hydration of the patients in these different studies, including our study. That the adequacy of hydration is important in the prevention of VAE, was conclusively demonstrated by Gottdiener et al.[18] They often detected the presence of air from the echocardiogram whenever the surgeon commented on the lack of venous bleeding at the surgical site, indirectly implying a low central venous pressure.

In the absence of ETC02 monitoring, VAE could have been missed in a large proportion of our patients if we relied solely on BP and ECG monitoring. Unexplained hypotension and unexplained PVCs in our study could be assumed as the consequence of VAE episodes. However, moderate as well as severe hypotension was observed only in 9% (37 patients out of 397), whereas unexplained PVCs were observed in only 2% of the patients (9 of 397). That BP and ECG changes are not sensitive indicators of VAE has been stressed in previous studies.[19] The low incidence of air retrieval (5%) from the single-orifice central venous catheter may have been due to aberrant location of the catheter tip.[20],[21] Moreover, even with the Swan Ganz catheter, it is often difficult to aspirate a signigicant quantity of air.[22] In this context, the efficacy and superiority of the multi-orifice catheter for air aspiration has been noted.[23],[24] VAE can occur any time during the surgery when the surgical field is above the heart level. Any laxity on the part of the operating surgeon while dealing with the opened veins is the most important predisposing factor for VAE. In our study, both these factors together, could have resulted in VAE during various stages of the surgery. VAE from the tumor and muscle group resulted in 41% and 35% incidence of hypotension, respectively. Whereas, in the tumor group, hypotension was severe in 47% of the patients, in the muscle group it was severe in 41% of the patients. Hypotension in these groups was accompanied by PVCs (5 patients in the tumor group and 3 in the muscle group). In the bone group, though the incidence of hypotension (moderate as well as severe) was 24%, only 2 patients (12%) developed severe hypotension. Air passes through the right heart and subsequently lodges in the pulmonary arterioles. A small amount of air can be excreted through the lungs, but when the capacity of the pulmonary vasculature is exceeded, air bubbles back up into the right heart, decreasing the cardiac output. This decrease in the cardiac output, which culminates in hypotension is directly proportional to the volume of air inside the right heart, which in turn, may be determined by the size of the offending vein.

Statistically insignificant differences in the frequencies of hypotension (moderate as well as severe) in our study, suggest that the site of air entrainment is not a determinant of the severity of hemodynamic disturbances. Hypotension following VAE episode is solely influenced by the volume of air ingressed into the circulation, independent of the anatomic site.

In conclusion, VAE may result from various sites during PCF surgery performed in the sitting posture and the ensuing severity of hemodynamic disturbances are not determined by the site of air entrainment.


1Bedel AE, Berge KH, Losasso TJ. Paradoxical air embolism during venous air embolism. Transesophageal echocardiographic evidence of transpulmonary air passage. Anesthesiology 1994;80:947-50.
2Tommasino C, Bretta L, Dellacqua A, et al. Use of intracranial Doppler for venous air embolism monitoring in sitting position. Technical note. Minerva Anestisiol 1992;58:1131-4.
3Tommasino C, Rizzardi R, Bretta L, et al. Cerebral ischemia after venous air embolism in the absence of intracardiac defect. J Neurosurg Anesthesiol 1996;8:30-4.
4Schaffranietz L, Gunther L. Neurosurgical operations in sitting position: Result of a survey in Germany. Anaesthetist 1997;46:91-5.
5Schaffranietz L, Grothe A, Olthoff D. Use of sitting position in neurosurgery Results of a 1998 survey in Germany. Anaesthetist 2000;49:269-74.
6Elton RJ, Howell RSC. The sitting position in neurosurgical anaesthesia: a survey of British practice in 1991. Br J Anaesth 1994;73:247-8.
7Matijasko J, Petrozza P, Cohen M, et al. Anaesthesia and surgery in the seated position: Analysis of 554 cases. Neurosurgery 1985;17:695-702.
8Standefer M, Bay JW, Trusso R. The sitting position in neurosurgery: A retrospective analysis of 488 cases. Neurosurgery 1984;14:649-58.
9Albin MS, Ritter RR, Pruett CE, et al. Venous air embolism during lumbar laminectomy in the prone position: Report of three cases. Anesth Analg 1991;73:346-9.
10Olympio MA, Bell WO. Venous air embolism after craniotomy closure: tension pneumocephalus implicated. J Neurosurg Anesthesiol 1994;6:35-9.
11Giebler R, Kollenberg B, Pohlen G, et al. Effect of positive pressure on the incidence of venous air embolism and on the cardiovascular response to sitting position during neurosurgery. Br J Anaesth 1998;80:30-5.
12Gottlieb JD, Ericsson JA, Sweet RB. Venous air embolism: a review. Anesth Analg 1965;44:773-9.
13Muzzi DA, Losasso TJ, Black S, et al. Comparison of transesophageal and precordial ultrasonic Doppler sensor in the detection of venous air emboli in dogs. Anesth Analg 1990;70:103-4.
14English JB, Westenskow D, Hodges MR, et al. Comparison of venous air embolism monitoring methods in supine dogs. Anesthesiology 1978;48:425-9.
15Hatle L, Rokseth R. The arterial to end tidal carbon dioxide tension gradient in acute pulmonary embolism and other cardiopulmonary diseases. Chest 1974;66:352-7.
16Brechner VL, Bethune RWM. Recent advances in monitoring pulmonary air embolism. Anesth Analg 1971;50:255-61.
17Tateishi H. Prospective study of air embolism. Br J Anaesth 1972;44:1306-10.
18Gottdiener JS, Papademetrior V, Notargiacomo A, et al. Incidence and cardiac evidence of arterial embolization via noncardiac shunt. Arch Int Med 1988;148:795-800.
19Buckland RW, Manners JM. Venous air embolism during neurosurgery; a comparison of various methods of detection in man. Anaesthesia 1976;31:633-43.
20Bithal P, Dash HH, Vishnoi N. Comparative evaluation on proper placement of central venous catheters with and without stillete. Ind J Med Res (B) 1991;94:238-40.
21Kellner GA, Smart JF. Percutaneous placement of catheters to monitor central venous pressure. Anesthesiology 1972;36:515-6.
22Anderson KH. Air aspiration from the venous system during total hip replacement. Anesthesiology 1983;38:1175-8.
23Colley PS, Artu AA. Bunegin-Albin catheter improves air retrieval and resuscitation from lethal venous air embolism in dogs. Anesth Analg 1987;66:991-4.
24Artu AA. Modification of a new catheter for air retrieval and resuscitation from lethal venous air embolism. Effect of nitrous oxide on air retrieval. Anesth Analg 1992;75:226-31.