Venous air embolism (VAE) Dr. S. Parthasarathy MD. DA. DNB., Dip.diab. MD(acu), DCA, Dip. PhD (physio) Mahatma Gandhi medical college and research institute, puducherry – India

What is it ?? Venous air embolism (VAE), a subset of gas embolism, is an entity with the potential for severe morbidity and mortality iatrogenic complication atmospheric gas is introduced into the systemic venous system

When will it occur ?? neurosurgical procedures conducted in the sitting position central venous catheterization, penetrating and blunt chest trauma high-pressure mechanical ventilation thoracocentesis, hemodialysis

Other causes diagnostic studies, such as during radiocontrast injection for computerized tomography carbon dioxide and nitrous oxide during medical procedures invasive vascular procedures Massive Air Embolism After Central Venous Catheter Removal

During LSCS The incidence of VAE during cesarean delivery ranges 10 % The risk factors operation in the Trendelenburg position, abruptio placentae, placenta previa, exteriorization of the uterus, extraction of the placenta, preeclampsia,

Two prerequisites (1) a direct communication between a source of air and the vasculature (2) a pressure gradient favoring the passage of air into the circulation.

Open vessels collapse usually When open vessels cannot collapse, which is the case with major venous sinuses as well as bridging and epidural veins, the risk of VAE increases substantially

What is important ?? The key factors determining the degree of morbidity and mortality volume of gas entrainment, the rate of accumulation, the patient’s position at the time of the event

Volume ?? 5 ml/kg is routine – but 20 ml (the length of an unprimed IV infusion tubing) 2 or 3 mL of air into the cerebral circulation 0.5 ml in coronaries

Rate ?? >0.30 mL/kg/min– 60 kg man – 18 ml/min. can overwhelm the air-filtering capacity of the pulmonary vessels, resulting in symptoms

Position Venous air emboli pose a risk anytime the surgical wound is elevated more than 5 cm above the right atrium Sitting !! A pressure gradient of 5 cm H2O between air and venous blood across a 14-gauge needle allows the entrance of air into the venous system at a rate of 100 mL per second

Incidence 0.13% during the insertion and removal of central venous catheters The neurosurgical procedure-related complications of venous air embolism have been estimated to be between % Reports of venous air embolism in the setting of severe lung trauma have been estimated between 4-14%.

Mortality Catheter-associated VAE mortality rates have reached 30%. In a case series of 61 patients with severe lung trauma, the mortality rate associated with concomitant VAE was 80% in the blunt trauma group and 48% in the penetrating trauma group

Why is it not great ?? Often it is asymptomatic Symptoms even present – trivial Are we diagnosing ??

Why it is great?? It is iatrogenic

Patho physiology large volumes of air Strain RV rise in pulmonary artery (PA) pressures. RV outflow obstruction decreased pulmonary venous return. Decreased LV preload decreased cardiac output systemic cardiovascular collapse

Air embolism and SIRS Air embolism has also been described as a potential cause of the systemic inflammatory response syndrome triggered by the release of endothelium derived cytokines

Symptoms Acute dyspnea, Continuous cough "Gasp" reflex (a classic gasp at times reported when a bolus of air enters the pulmonary circulation and causes acute hypoxemia) Dizziness/lightheadedness/vertigo Nausea, Substernal chest pain Agitation/disorientation/sense of "impeding doom"

Respiratory symptoms Adventitious sounds (rales, wheezing) Tachypnea Hemoptysis Cyanosis

CNS Acute altered mental status Seizures Transient/permanent focal deficits (weakness, paresthesias, paralysis of extremities) Loss of consciousness, collapse Coma (secondary to cerebral edema)

Position. Recumbent position, gas proceeds into the right ventricle and pulmonary circulation, subsequently causing pulmonary hypertension and systemic hypotension sitting position, gas will travel retrograde via the internal jugular vein to the cerebral circulation, leading to neurologic symptoms secondary to increased intracranial pressure

Factors spontaneously breathing (yielding negative thoracic pressure) or under controlled positive pressure ventilation

Cardiovascular Dysrhythmias "Mill wheel" murmur - A temporary loud, machinery like, churning sound due to blood mixing with air in the right ventricle, best heard over the precordium (a late sign Hypotension Circulatory shock/cardiovascular collapse

Paradoxical embolism Arterial embolism as a complication of venous air embolism (VAE) can occur through direct passage of air into the arterial system via anomalous structures such as an atrial or ventricular septal defect, a patent foramen ovale, pulmonary arterial-venous malformations.

Preop test for PFO?? a preoperative ‘‘bubble test’’ in conscious patients using TEE is advocated by some investigators if the sitting position is considered

Various investigations Doppler, TEE, ETCO2 ETN2 Pulse oxi metry, CT scan CxR

Friends – Don’t sleep !!

Doppler device can detect 1 mL of air or less The Doppler probe should be placed after the patient is in the operative position. The probe is usually positioned at the middle third of the sternum on the right side Can be confirmed with agitated saline

Doppler

CT slice showing air

TEE

Westermark sign-

Oligemia

Fluoroscopy

tachycardia, right ventricular strain pattern, and ST depression

Coronary embolus

Diagnosis Pulmonary artery catheter – Can detect increases in pulmonary artery pressures, which may be secondary to mechanical obstruction/vasoconstriction from the hypoxemia induced by the VAE Pulse oximetry – Changes in oxygen saturation are late findings with VAE.

End-tidal carbon dioxide (ETCO2) – VAE leads to V/Q mismatching and increases in physiologic dead space. This produces a fall in end-tidal CO2 (normal value is < 5). A change in 2 mm Hg ETCO2 can be an indicator of VAE. this finding is nonspecific, slow

End-tidal nitrogen (ETN2) Most sensitive gas-sensing VAE detection modality; usually less then 2%, measures increases in ETN2 as low as 0.04%. Response time is much faster than ETCO2 False positives ??

Management The optimal management of venous air embolism prevention. Avoid and treat hypovolemia prior to catheter placement. Occlude the needle hub during catheter insertion/removal. Maintain all connections to the central line closed/locked when not in use

Principles of therapy Management of venous air embolism (VAE), once is suspected, identification of the source of air, prevention of further air entry (by clamping or disconnecting the circuit), a reduction in the volume of air and hemodynamic support.

Useful measures N2O is used, it should be discontinued The surgeon should flood the surgical field with fluids while open veins are cauterized or exposed bone is waxed compress both jugular veins lightly to minimize air entrainment.

Catheter removal During catheter insertion/removal, place the patient in the supine position with head lowered). If the patient is awake he or she may assist by holding his or her breath or by doing a Valsalva maneuver, both of which can increase the central venous pressure

Management Central venous catheter – If in place, aspiration of air may help make the diagnosis. It is also helpful in monitoring central venous pressures, which may be increased in VAE. Any procedure posing a risk for venous air embolism (VAE), if in progress, should be aborted

Management Administer 100% O 2 and perform endotracheal intubation for severe respiratory distress or refractory hypoxemia or in a somnolent or comatose patient in order to maintain adequate oxygenation and ventilation. Institution of high flow (100%) O 2 will help reduce the bubble's nitrogen content and therefore size hyperbaric oxygen therapy (HBOT)

(Durant maneuver) left lateral decubitus and Trendelenburg position. CPR required – supine and Trendelenburg position. Direct removal of air from the venous circulation by aspiration from a central venous catheter

Special situations cross-clamping the aorta, cardiac massage, and aspirating air from the left ventricle, aortic roots, and pulmonary veins emergency thoracotomy with clamping of the hilum of the injured lung

Management Supportive therapy should include fluid resuscitation increase venous pressure and venous return. gas emboli may cause a relative haemo concentration

Vasopressors and ventilation The administration of vasopressors and mechanical ventilation are two other supportive measures that may necessary Usually ephedrine may be enough

Massive Air Embolus Treated with Rheolytic Thrombectomy- july 2007, Invasive cardiology

Summary Suspicion in possible situations Diagnosis Prevention Stop nitrous, flood fields 100 % O2, fluids, vasopressors, Ventilation SOS Aspirate if possible

Thank you all