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Venous air embolism (VAE)

Venous air embolism (VAE)

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Venous air embolism (VAE)

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  1. 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

  2. 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

  3. 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

  4. 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

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

  6. 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.

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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 10-80 % • Reports of venous air embolism in the setting of severe lung trauma have been estimated between 4-14%.

  13. 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

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

  15. Why it is great?? It is iatrogenic

  16. 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

  17. 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

  18. 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"

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

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

  21. 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

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

  23. 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

  24. 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.

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

  26. Various investigations • Doppler, • TEE, • ETCO2 • ETN2 • Pulse oximetry, • CT scan • CxR

  27. Friends – Don’t sleep !!

  28. 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

  29. Doppler

  30. CT slice showing air

  31. TEE

  32. Westermark sign-

  33. Oligemia

  34. Fluoroscopy

  35. tachycardia, right ventricular strain pattern, and ST depression

  36. Coronary embolus

  37. 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.

  38. 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

  39. 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 ??

  40. 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

  41. 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.

  42. 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.

  43. 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

  44. 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

  45. 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)

  46. (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

  47. 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

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

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