Venous Air Embolism

1. Venous Air Embolism Ravindra Prasad, M.D. UNC-CH School of Medicine Department of Anesthesiology April 18, 1997

2. Outline • Definition • History • Incidence • Pathophysiology • Complications • Detection • Treatment

3. Definition • Venous • Air • Embolism

4. History

5. Incidence • depends on method of detection • in sitting position, anywhere from 5 to 100% • may also occur from non-operative sites (e.g., headholder pins, burr holes, loose connections on venous lines)

6. Pathophysiology: overview • 2 types: slow or rapid entrainment • morbidity/mortality • risk factors • paradoxical air embolism • PEEP

7. Slow, continuous entrainment • Air enters venous system • peripheral pulmonary circulation • mechanical obstruction or local hypoxemia • release of endothelial mediators • complement activation, cytokine system, reactive O2 species • vasoconstriction

8. Rapid entrainment • “air lock” in right atrium/ventricle, or in pulmonary system  RV outflow, venous return • pulmonary arterial capacity estimated to be about 5cc/kg from animal studies • dysrhythmias,  CO, RV dilation/failure • myocardial and/or cerebral ischemia • cardiovascular collapse

9. Morbidity and mortality: main determinants • amount of air • rate of air entry • location air embolizes • dogs: tolerated 1000cc air given over 50-100 minutes, but 100cc bolus was fatal

10. Morbidity and mortality: other factors • baseline CV function, cardiopulmonary reserve • use of N2O inc. size of air pocket  inc morbidity • 50% N2O has been shown to have no effect on outcome if episodes of VAE are minor)

11. Risk factors: inc. incidence/severity • surgical site • patient position • age of patient • hypovolemia

12. Risk factors: dec. incidence/severity • careful surgeon • hemostasis • liberal use of bone wax

13. Paradoxical Air Embolism I • VAE + intracardiac defect • Patent Foramen Ovale: up to 50% of patients may have reversal of existing L->R shunt after one hour in sitting position • incidence of clinically detectable PAE is lower than predicted based on incidence of VAE and PFO (calculated risk = 5-10%)

14. Paradoxical Air Embolism II • ?via pulmonary vascular bed (not well characterized) • ?hypovolemia increases risk

15. PEEP • controversial • may inc CVP, therefore dec VAE • however, may decrease CO 15-50% • may increase chances of PAE by increasing right atrial pressure

16. Intraoperative complications: cardiovascular • dysrhythmias • hypotension/hypertension • change in heart sounds, murmurs • ECG evidence of ischemia • acute RV failure • cardiac arrest

17. Intraoperative complications: pulmonary • hypercarbia • hypoxemia • pulmonary hypertension • pulmonary edema

18. Intraoperative complications: CNS • hyperemia • brain swelling • morbidity and mortality are not correlated with volume of cerebral arterial air

19. Postoperative complications • Cardiovascular • myocardial ischemia • RV failure • Pulmonary • perfusion defects • pulmonary edema • CNS • neurologic deficits, coma • stroke

20. Detection: summary

21. Monitoring: precordial doppler • characteristic sound • very sensitive • positioned over right heart • may be difficult to place in some positions • crystallized mannitol sounds similar to VAE

22. Monitoring: TEE • very sensitive • can also detect air in left heart and aorta • qualitative, not quantitative • not specific for air: also detects fat emboli, blood microemboli • large probe size: difficult to place/use with head flexed

23. Monitoring: end tidal CO2 • ETCO2 decreases (increased A-a gradient) • valid only if CO and BP remain stable • large VAE can cause simultaneous decrease in BP and decrease in ETCO2 • affected by ventilation, COPD, decrease in CO due to other causes

24. Monitoring: end tidal N2 • specific for air • may not be sensitive enough to detect subclinical VAE • ETN2 decrease may reflect dec in BP rather than elimination of N2

25. Monitoring: CVC • useful to confirm diagnosis as well as to treat • multiorifice catheters are better • invasive • position may change during patient repositioning • may not be able to remove all air

26. Monitoring: PAC • increase in PAP • late sign • invasive • difficult to aspirate through small lumen single orifice in fixed position relative to tip • can follow improvement in PAP as sign of recovery from VAE

27. Monitoring: late signs • ABP decrease • EKG changes • esophageal stethoscope “mill-wheel murmur” • cardiovascular collapse

28. Monitoring: investigational • carotid duplex: not specific (also detects IJ air) • transcranial doppler of middle cerebral artery • emission spectroscopy (more sensitive than ETN2, lower cost; but halogenated anesthetics and hemodynamic changes effect accuracy)

29. Detection vs. clinical signs

30. Treatment • PREVENTION

31. Prevention • positive pressure ventilation • ensure adequate hydration • minimize head elevation • good surgical technique • avoidance of N2O in patients with known intracardiac defects • avoidance of drugs that increase venous capacitance (e.g. NTG)

32. Treatment: intraoperative • have surgeon flood field with fluids, pack wound, use bone wax • change patient position • give iv fluid • stop N2O; give 100% O2 • provide jugular vein compression • aspirate right atrial catheter • cardiovascular support

33. Treatment: postoperative • supplemental oxygen (hypoxemia) • check ECG (ischemia), chest x-ray (edema) • follow serial ABG’s • provide hyperbaric compression if arterial air emboli suspected (may dec. bubble volume, speed elimination of air)

34. VAE: Key Points • Most likely in sitting-position craniotomy • Pulmonary HTN/edema, myocardial ischemia, cardiovascular collapse, stroke • Prevention better than treatment • Precordial doppler excellent monitor • Multiorifice RAC for diagnosis/treatment

35. References • Anesthesia, 4th edition. Edited by Miller, R.D. pp. 1900-1907. • Anesthesia and Neurosurgery, 3rd edition. Edited by Cottrell, J.E. and Smith, D.S. pp. 348-357. • Lucas, W.J. “How to Manage Air Embolism.” Problems in Anesthesia, Vol. 1, No. 2, April/June 1987, pp. 288-303.