Venous Air Embolism Ravindra Prasad M D UNC-CH

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

Outline • • Definition History Incidence Pathophysiology Complications Detection Treatment

Definition • Venous • Air • Embolism

History

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)

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

Slow, continuous entrainment • • • Air enters venous system peripheral pulmonary circulation mechanical obstruction or local hypoxemia release of endothelial mediators complement activation, cytokine system, reactive O 2 species • vasoconstriction

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

Morbidity and mortality: main determinants • • amount of air rate of air entry location air embolizes dogs: tolerated 1000 cc air given over 50100 minutes, but 100 cc bolus was fatal

Morbidity and mortality: other factors • baseline CV function, cardiopulmonary reserve • use 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)

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

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

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%)

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

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

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

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

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

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

Detection: summary

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

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

Monitoring: end tidal CO 2 • ETCO 2 decreases (increased A-a gradient) • valid 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 causes

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

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

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

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

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

Detection vs. clinical signs

Treatment • PREVENTION

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

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

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)

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

References • Anesthesia, 4 th edition. Edited by Miller, R. D. pp. 1900 -1907. • Anesthesia and Neurosurgery, 3 rd 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.