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

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Presentation on theme: "Venous Air Embolism Ravindra Prasad, M.D. UNC-CH School of Medicine Department of Anesthesiology April 18, 1997."— Presentation transcript:

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

2 Outline DefinitionDefinition HistoryHistory IncidenceIncidence PathophysiologyPathophysiology ComplicationsComplications DetectionDetection TreatmentTreatment

3 Definition VenousVenous AirAir EmbolismEmbolism

4 History

5 Incidence depends on method of detectiondepends on method of detection in sitting position, anywhere from 5 to 100%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)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 entrainment2 types: slow or rapid entrainment morbidity/mortalitymorbidity/mortality risk factorsrisk factors paradoxical air embolismparadoxical air embolism PEEPPEEP

7 Slow, continuous entrainment Air enters venous systemAir enters venous system peripheral pulmonary circulationperipheral pulmonary circulation mechanical obstruction or local hypoxemiamechanical obstruction or local hypoxemia release of endothelial mediatorsrelease of endothelial mediators complement activation, cytokine system, reactive O 2 speciescomplement activation, cytokine system, reactive O 2 species vasoconstrictionvasoconstriction

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

9 Morbidity and mortality: main determinants amount of airamount of air rate of air entryrate of air entry location air embolizeslocation air embolizes dogs: tolerated 1000cc air given over minutes, but 100cc bolus was fataldogs: tolerated 1000cc air given over minutes, but 100cc bolus was fatal

10 Morbidity and mortality: other factors baseline CV function, cardiopulmonary reservebaseline CV function, cardiopulmonary reserve use of N 2 O  inc. size of air pocket  inc morbidityuse of N 2 O  inc. size of air pocket  inc morbidity –50% N 2 O has been shown to have no effect on outcome if episodes of VAE are minor)

11 Risk factors: inc. incidence/severity surgical sitesurgical site patient positionpatient position age of patientage of patient hypovolemiahypovolemia

12 Risk factors: dec. incidence/severity careful surgeoncareful surgeon hemostasishemostasis liberal use of bone waxliberal use of bone wax

13 Paradoxical Air Embolism I VAE + intracardiac defectVAE + 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%)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)?via pulmonary vascular bed (not well characterized) ?hypovolemia increases risk?hypovolemia increases risk

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

16 Intraoperative complications: cardiovascular dysrhythmiasdysrhythmias hypotension/hypertensionhypotension/hypertension change in heart sounds, murmurschange in heart sounds, murmurs ECG evidence of ischemiaECG evidence of ischemia acute RV failureacute RV failure cardiac arrestcardiac arrest

17 Intraoperative complications: pulmonary hypercarbiahypercarbia hypoxemiahypoxemia pulmonary hypertensionpulmonary hypertension pulmonary edemapulmonary edema

18 Intraoperative complications: CNS hyperemiahyperemia brain swellingbrain swelling morbidity and mortality are not correlated with volume of cerebral arterial airmorbidity and mortality are not correlated with volume of cerebral arterial air

19 Postoperative complications CardiovascularCardiovascular –myocardial ischemia –RV failure PulmonaryPulmonary –perfusion defects –pulmonary edema CNSCNS –neurologic deficits, coma –stroke

20 Detection: summary

21 Monitoring: precordial doppler characteristic soundcharacteristic sound very sensitivevery sensitive positioned over right heartpositioned over right heart –may be difficult to place in some positions crystallized mannitol sounds similar to VAEcrystallized mannitol sounds similar to VAE

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

23 Monitoring: end tidal CO 2 ETCO 2 decreases (increased A-a gradient)ETCO 2 decreases (increased A-a gradient) valid only if CO and BP remain stablevalid only if CO and BP remain stable –large VAE can cause simultaneous decrease in BP and decrease in ETCO 2 affected by ventilation, COPD, decrease in CO due to other causesaffected by ventilation, COPD, decrease in CO due to other causes

24 Monitoring: end tidal N 2 specific for airspecific for air may not be sensitive enough to detect subclinical VAEmay not be sensitive enough to detect subclinical VAE ETN 2 decrease may reflect dec in BP rather than elimination of N 2ETN 2 decrease may reflect dec in BP rather than elimination of N 2

25 Monitoring: CVC useful to confirm diagnosis as well as to treatuseful to confirm diagnosis as well as to treat multiorifice catheters are bettermultiorifice catheters are better invasiveinvasive position may change during patient repositioningposition may change during patient repositioning may not be able to remove all airmay not be able to remove all air

26 Monitoring: PAC increase in PAPincrease in PAP late signlate sign invasiveinvasive difficult to aspirate through small lumen single orifice in fixed position relative to tipdifficult to aspirate through small lumen single orifice in fixed position relative to tip can follow improvement in PAP as sign of recovery from VAEcan follow improvement in PAP as sign of recovery from VAE

27 Monitoring: late signs ABP decreaseABP decrease EKG changesEKG changes esophageal stethoscope “mill-wheel murmur”esophageal stethoscope “mill-wheel murmur” cardiovascular collapsecardiovascular collapse

28 Monitoring: investigational carotid duplex: not specific (also detects IJ air)carotid duplex: not specific (also detects IJ air) transcranial doppler of middle cerebral arterytranscranial doppler of middle cerebral artery emission spectroscopy (more sensitive than ETN 2, lower cost; but halogenated anesthetics and hemodynamic changes effect accuracy)emission spectroscopy (more sensitive than ETN 2, lower cost; but halogenated anesthetics and hemodynamic changes effect accuracy)

29 Detection vs. clinical signs

30 Treatment PREVENTIONPREVENTION

31 Prevention positive pressure ventilationpositive pressure ventilation ensure adequate hydrationensure adequate hydration minimize head elevationminimize head elevation good surgical techniquegood surgical technique avoidance of N 2 O in patients with known intracardiac defectsavoidance of N 2 O in patients with known intracardiac defects avoidance of drugs that increase venous capacitance (e.g. NTG)avoidance of drugs that increase venous capacitance (e.g. NTG)

32 Treatment: intraoperative have surgeon flood field with fluids, pack wound, use bone waxhave surgeon flood field with fluids, pack wound, use bone wax change patient positionchange patient position give iv fluidgive iv fluid stop N 2 O; give 100% O 2stop N 2 O; give 100% O 2 provide jugular vein compressionprovide jugular vein compression aspirate right atrial catheteraspirate right atrial catheter cardiovascular supportcardiovascular support

33 Treatment: postoperative supplemental oxygen (hypoxemia)supplemental oxygen (hypoxemia) check ECG (ischemia), chest x-ray (edema)check ECG (ischemia), chest x-ray (edema) follow serial ABG’sfollow serial ABG’s provide hyperbaric compression if arterial air emboli suspected (may dec. bubble volume, speed elimination of air)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 craniotomyMost likely in sitting-position craniotomy Pulmonary HTN/edema, myocardial ischemia, cardiovascular collapse, strokePulmonary HTN/edema, myocardial ischemia, cardiovascular collapse, stroke Prevention better than treatmentPrevention better than treatment Precordial doppler excellent monitorPrecordial doppler excellent monitor Multiorifice RAC for diagnosis/treatmentMultiorifice RAC for diagnosis/treatment

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


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