Rigid Bronchoscopic Neodymium-Yttrium-Aluminum-Garnet (Nd:YAG) Laser Resection of Endobronchial Lesion: venous air embolism may occur due to coolant gas from the bronchoscope entering the systemic circulation through pulmonary venules
Laparoscopy (see Laparoscopy): venous air embolism
Colonoscopy (see Colonoscopy): venous air embolism
Neurosurgery
General Comments: common surgical precipitant of venous air embolism (as the surgical incision is usually superior to the heart at a distance that is greater than the central venous pressure)
Patients are especially at risk of air embolism in the sitting position (Fowler’s position)
Incidence of venous air embolism during neurosurgical procedures in the prone position: 10%
Incidence of venous air embolism during neurosurgical repair of cranial synostosis in Fowler’s Position: 80%
Arthroscopy (see Arthroscopy): venous air embolism
Endoprosthesis Placement
Total Joint Arthroplasty: venous air embolism
Otolaryngologic Surgery
General Comments: common surgical precipitant of venous air embolism (as the surgical incision is usually superior to the heart at a distance that is greater than the central venous pressure)
Venous Air Embolism Can Occur During Central Venous Catheter (CVC) Placement, During Use, or at Time of Catheter Removal (see Central Venous Catheter)
Risk Factors for Catheter-Related Air Embolism
Fracture or Detachment of Catheter Connections: accounts for 60-90% of episodes
Deep Inspiration During Catheter Insertion or Removal: increases the magnitude of negative pressure within the thorax
Dysfunction of Self-Sealing Valves in Cordis/Introducer Sheath
Failure to Occlude the Needle Nub and/or Catheter During Insertion or Removal
Hypovolemia: decreases central venous pressure
Presence of Persistent Catheter Tract After Central Venous Catheter Removal
Upright Positioning of Patient: decreases central venous pressure to below atmospheric pressure, increasing risk for entraining air rapidly into venous circulation
Penetrating/Blunt Chest Trauma: venous or arterial air embolism
Positive Pressure Ventilation
Positive Pressure Ventilation, Especially with High Levels of PEEP (see Invasive Mechanical Ventilation-General): gas may enter the circulation if the pulmonary vascular integrity is disrupted concomitantly with alveolar rupture from airspace overdistention
Occurs most commonly in adults with acute respiratory distress syndrome (ARDS) (see Acute Respiratory Distress Syndrome) or premature neonates with respiratory distress syndrome (hyaline membrane disease)
Decompression Sickness
Diving Ascent: breath hold (with closed glottis) with ascent leads to gas expansion within lungs, with rupture of alveoli into capillaries -> if the pulmonary veins tear as the alveoli rupture, air can return to the left heart with the oxygenated blood and then embolize through the arterial system (alternatively, air bubbles may form in the venous system during ascent and embolize to the systemic circulation via a patent foramen ovale)
Air embolism occurs in 7 out of every 100k dives
Physiology
Venous Air Embolism to Right Ventricle/Pulmonary Circulation
Venous Air Embolism Results in Right Ventricular Obstruction: leading to right ventricular failure and increased central venous pressure and hypotension
Venous Air Embolism Results in Obstruction to Pulmonary Artery Outflow: results in “air lock”
Venous Air Embolism Results in Abrupt Rise in Pulmonary Pressures: due to air bubble emboli to the pulmonary vasculature
Air Bubbles Occlude Pulmonary Capillaries and Induce Vasoconstriction and Formation of Platelet Microthrombi: results in local endothelial damage and accumulation of neutrophils, platelets, fibrin, and lipid droplets at the gas-fluid interface
Localized pulmonary hypoperfusion: may result in hypercapnia
Noncardiogenic pulmonary edema
Bronchoconstriction
Hypoxemia: due to alveolar flooding and ventilation-perfusion mismatching
Increased physiologic dead space: with a rise in PaCO2 if ventilation is held constant
Decreased lung compliance: due to pulmonary edema
Increased airway resistance: due to bronchoconstricting mediators (serotonin, histamine) released from damaged endothelium
Rate/Volume of Air Introduced into the Venous Circulation Determine the Clinical Effect of Venous Air Embolization: due to the fact that the capacity of the lung to filter microbubbles of air from the venous circulation can be exceeded
It is estimated that 300-500 mL of gas introduced at a rate of 100 mL/sec is a fatal dose for humans (his flow rate can be achieved through a 14-gauge catheter with a pressure gradient of only 5 cm H2O)
Arterial Air Embolism to Systemic Circulation
Mechanisms of Arterial Air Embolism
Direct Introduction of Air into Arterial System
Incomplete Filtration of Air by Pulmonary Capillary Bed: the capacity of the lung to filter microbubbles of air from the venous circulation can be exceeded (as noted above)
Paradoxical Air Embolization From Right->Left Side of Heart Via Intracardiac Shunt: in patients with a left-to-right shunt, venous air embolization into the pulmonary circulation can raise right heart pressures and reverse the direction of the shunt, allowing paradoxical embolism to occur
Air Traversal of Pulmonary Circulation Via Pulmonary Arteriovenous Malformation (AVM)
Destination of Arterial Air Emboli
Coronary Artery
Brain
Spinal Cord
Skin
Occlusion of Systemic Vessels: bubbles occlude systemic vessels and allow formation of associated platelet microthrombi, inducing the release of mediators and oxygen free radicals
Diving Ascent
Ascent with closed glottis or obstructive airways disease (like asthma) can cause alveolar rupture -> results in pneumothorax or arterial air embolism
Air bubble embolism to pulmonary vasculature (or coronary arteries or CNS vessels in case of patent foramen ovale)
Bubbles occlude vessels and allow formation of associated platelet microthrombi
Large amounts of air can traverse pulmonary circulation
Marked Discrepancy Between Arterial pCO2 and End-Tidal (Exhaled) CO2 May Occur in the Setting of Venous Air Embolism [MEDLINE]
Decreased End-Tidal CO2 Occurs Due to Increased Physiologic Dead Space and Worsening of Ventilation-Perfusion Matching
Intraoperative Echocardiography and End-Tidal CO2 Monitoring May Increase the Sensitivity of Detecting Early Air Emboli in High-Risk Patients During Surgery
Elevated Creatine Kinase May Occur in Divers with Air Embolism (Unclear if This Also Occurs in Other Patients with Air Embolism) (see Elevated Serum Creatine Kinase)
May detect air in the central venous system (especially the axillary and subclavian veins), right ventricle, or pulmonary artery
However, this finding is non-specific, as small (<1 mL), asymptomatic air emboli can be detected in 10-25% of contrast-enhanced CT scans if carefully sought: false positive CT studies may be more common when higher resolution or electron beam CT scanners are used
Acute Right Ventricular Dilation and Pulmonary Hypertension
Air within the Right Ventricle
Intraoperative Echocardiography or Transcranial Doppler Monitoring May Increase the Sensitivity of Detecting Early Air Emboli in High-Risk Patients During Surgery
This Position Places the Right Ventricular Outflow Tract Inferior to Right Ventricular Cavity, Causing Air to Migrate Superiorly into a Position within the Right Ventricle Where the Air is Less Likely to Embolize (and Which Prevents Foramen Ovale Crossover Which Might Result in Embolization to the Brain)
Durant’s Manuever: left lateral decubitus position (proven to decrease mortality in animal studies)
Due to the Force of Arterial Blood Flow, Air Bubbles Will Be Propelled Forward Even if the Patient is in Head Down Position: consequently, the above maneuvers are unlikely to trap air within the right ventricle
However, Head Down Positions Have the Potential to Exacerbate the Cerebral Edema Which is Generally Induced by Cerebral Air Embolism
Restoration of Circulation
Move Patient to Left Lateral Decubitus Position to Place the Right Ventricular Outflow Tract Inferior to Right Ventricular Cavity: these maneuvers (described above) may displace large bubbles from the right ventricular outflow tract, relieving the obstruction to blood flow
Chest Compressions (see Cardiopulmonary Resuscitation): force air out of the pulmonary outflow tract and into smaller pulmonary vessels, improving forward flow
Removal of Air Embolism
Percutaneous/Transcatheter Removal of Air from Right Ventricle: these have been used in studies, but the amount of air to be removed is usually small (<20 ml) and removal is generally limited
Percutaenous Needle Aspiration of Air
Removal of Air Via Central Venous Catheter: aspiration may be attempted in cases where a central venous catheter is already in place
Supplemental Oxygen Increases the Partial Pressure of Oxygen and Decreases the Partial Pressure of Nitrogen in the Blood, Resulting in a Positive Pressure Gradient for the Diffusion of Nitrogen from the Air Bubbles into the Blood, Accelerating Resorption of Air Emboli
High-Flow Supplemental Oxygen Increases the Partial Pressure of Oxygen in the Blood and Decreases the Partial Pressure of Nitrogen in the Blood (Undersea Hyperb Med, 1998) [MEDLINE]
This Results in Diffusion of Nitrogen from Inside of the Air Embolism Bubble (Which Has a High Nitrogen Content) into the Blood (Which Will Have a Low Nitrogen Content): decreases the size of the bubble, accelerating bubble resorption
In Contrast, Nitrous Oxide (N20) (Sometimes Given During General Anesthesia) Can Diffuse from the Blood into Air Emboli, Causing the Gas Bubbles to Enlarge and the Patient to Deteriorate (Anesth Analg, 1971) [MEDLINE] (Anesthesiology, 2007) [MEDLINE] (see Nitrous Oxide)
Therefore, Nitrous Oxide Should Be Discontinued if Air Embolism is Suspected
Rationale: decreases air bubble size and increases the arterial oxygen tension, potentially decreasing ischemia
May improve outcome even if it is delayed up to 30 hrs later
Indications
Cardiopulmonary Compromise
Neurologic Deficits
Other
Corticosteroids (see Corticosteroids): no proven role (in decreasing spinal cord or cerebral edema) in the treatment of air embolism or decompression sickness
This Position Places the Right Ventricular Outflow Tract Inferior to Right Ventricular Cavity, Causing Air to Migrate Superiorly into a Position within the Right Ventricle Where the Air is Less Likely to Embolize (and Which Prevents Foramen Ovale Crossover Which Might Result in Embolization to the Brain)
Not clear that this is actually effective though, as blood flow (rather than buoyancy) may be the main determinant of whether air embolizes
Increases the diffusion gradient for nitrogen out of any air bubbles (causing them to shrink)
Hyperbaric Recompression: procedure of choice for both decompression sickness and venous/arterial air embolism -> increases nitrogen diffusion from bubbles (causing them to shrink)
No randomized trials to establish efficacy though
May be useful even in cases where therapy is delayed for 24 hrs or more
Correction of Hypothermia: indicated
Prognosis
Mortality
Older studies cite a mortality rate of approximately 30%
Prognosis of Air Embolism in Patients Treated with Hyperbaric Oxygen (Intensive Care Med, 2010) [MEDLINE]
Intensive Care Unit Mortality Rate: 12%
Hospital Mortality Rate: 16%
6-Month Mortality Rate: 18%
1-Year Mortality Rate: 21%
Risk Factors for Death in ICU (Intensive Care Med, 2010) [MEDLINE]
Cardiac Arrest at Time of Air Embolization
Simplified Acute Physiology Score (SAPS II) of At Least 33 on Intensive Care Unit Admission
Risk Factors for Death Within 1 Year (Intensive Care Med, 2010) [MEDLINE]
Increasing Age
Presence of Babinski Sign at Intensive Care Unit Admission
Acute Kidney Injury
Predictors of Long-Term Neurologic Sequelae (Intensive Care Med, 2010) [MEDLINE]
Focal Motor Deficits or Babinski Sign at Intensive Care Unit Admission
Need for >5 Days of Mechanical Ventilation
References
General
Effect of nitrous oxide on the pulmonary circulation during venous air embolism. Anesth Analg. 1971;50(5):785 [MEDLINE]
Venous air embolism. Arch Intern Med 1982; 142:2173- 2176
Influence of hypothermia, barbiturate therapy and intracranial monitoring on morbidity and mortality after near drowning. Crit Care Med 1986; 14:529-534
Transient pulmonary perfusion scintigraphic abnormalities in pulmonary air embolism. Chest 1989;95(4):910 [MEDLINE]
Medical problems associated with underwater diving. N Engl J Med 1992; 326:30-35
Venous air embolism: Clinical and experimental considerations. Crit Care Med 1992; 20:1169-1177
Delayed hyperbaric treatment of cerebral air embolism. Is J Med Sci 1993; 29:22-26
Pulmonary embolism from amniotic fluid, fat, and air. Prog Cardiovasc Dis. 1994 May-Jun;36(6):447-74 [MEDLINE]
Body position does not affect hemodynamic response to venous air embolism in dogs. Anesth Analg 1994; 79:734-739
Effects of mechanical ventilation with normobaric oxygen therapy on the rate of air removal from cerebral arteries. Crit Care Med 1994; 22:851-857
Gas embolism. N Engl J Med 2000; 342:476-482
Pulmonary air embolism. J Clin Monit Comput. 2000;16(5-6):375-83 [MEDLINE]
Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007;106(1):164 [MEDLINE]
Long-term outcome of iatrogenic gas embolism. Intensive Care Med. 2010 Jul;36(7):1180-7. doi: 10.1007/s00134-010-1821-9 [MEDLINE]
Etiology
Retrograde cerebral air embolism. Am J Emerg Med. 2014 Dec;32(12):1562.e1-2. doi: 10.1016/j.ajem.2014.05.043 [MEDLINE]
