Arterial gas embolism is a rare, life-threatening entity, which requires prompt recognition and early intervention. The air in the arterial circulation can lead to ischemia of various organ systems (i.e., brain, spinal cord, heart, kidneys, spleen, and GI tract)). As a result, the complications arising from arterial gas embolism can be devastating. The clinical features can be an initial asymptomatic period to nonspecific signs and symptoms to complete cardiovascular collapse. However, there are many precautions and techniques medical professionals can undertake to prevent this lethal condition.
A myriad of etiologies can lead to arterial gas embolism. Typically it is associated with severe decompression sickness during the ascent phase of diving. However, ruptured alveoli from lung barotrauma and migration from venous circulation through a pre-existing right to left shunt (i.e., ventricular septal defect - VSD/atrial septal defect - ASD) can also lead to arterial gas embolisms. Outside of environmental factors, iatrogenic causes from medical and surgical procedures (ex: percutaneous lung biopsy & tumor ablation, and arterial catheterization) are also a culprit for arterial gas embolisms. During arterial catheterization, improperly flushed catheters and balloon rupture are potential causes. There have been cases reported in surgical literature caused by blunt and penetrating thoracic trauma. The suspected underlying mechanism is from bronchial injury with associated pulmonary vein injury leading to the emboli. There have also been some cases associated with catheter ablation procedures for atrial fibrillation.
The entry of air in arterial circulation is usually rare, as the high pressures of the arterial vascular system are usually protective from air entry. Surprisingly, reports of air embolism have been dated as early as the 19th century in both adult and pediatric surgical procedures. Given the varying clinical presentation, failure of recognization/documentation, and different etiologies of the disease, the true incidence is unknown. In scuba diving, the incidence of air gas embolism can be 7 per 100000 dives. In patients undergoing cardiac bypass, the prevalence can be as low as 0.003%, and 0.007% with 50% having serious adverse outcomes. Prospective cohort studies have reported the incidence to be 2.65 per 100000 hospitalizations.
The pathophysiological effects of an arterial gas embolism depend on the location of the embolism. Furthermore, the degree of impairment links with factors such as the type of gas (ex; room air, carbon dioxide, helium, or nitrous oxide), the volume of the gas, the rate of embolism, the presence of collateral circulation. Damage from an arterial gas embolism is not the only from the reduction of distal flow, but also from the inflammatory cascade that air bubbles instigate. A lethal volume of air embolism is theorized to be 3 to 5ml/kg. Estimates have also indicated that 300 ml to 500 ml of gas introduced at a rate of 100 ml/sec is considered a fatal dose.
Arterial gas embolism from diving results from a different process than the iatrogenic causes and be a covered topic below. During iatrogenic procedures, an air gas embolism migrates from venous to arterial circulation the presentation can be similar to the features of a pulmonary embolism. The air in the pulmonary artery will lead to an increased pulmonary artery and right ventricular pressure. Increased pressures in the right ventricle may lead to right-sided heart failure, reduction in cardiac output, and even arrhythmias. Additionally, the air in the pulmonary artery will cause a ventilation-perfusion mismatch, which leads to intrapulmonary shunting, and increased alveolar dead space. The air in the left ventricle will impede diastolic filling leading to complete cardiovascular compromise. Air can also be pumped from the left ventricle into the coronary vasculature, leading to myocardial ischemia.
In circumstances of diving-associated air gas embolism, numerous processes contribute to the formation of arterial gas embolism. Lung barotrauma during rapid ascent can cause alveoli to burst. During ascension, nitrogen gas, which may have dissolved during descent, now expands, and can for bubbles. If these bubbles form in the arterial circulation, they can cause end-organ damage. Finally, as mentioned earlier, venous gas forms embolisms.
The presumption is that bubbles directly injure the endothelium of postcapillary vessels, which results in the activation of cellular, and humoral responses.
The signs and symptoms of arterial gas embolism vary based on cause, and the initial organ inspected. Classically the presentation of the arterial gas embolism is usually catastrophic, with sudden collapse, neurologic symptoms mimicking stroke, apnea, and even cardiovascular collapse. If the affected individual does not die suddenly, the initial symptoms can be minor and easily missed. However, whenever the CNS is affected symptoms will be more exaggerated, presenting as hemiparesis and abnormal coordination. Typically, if divers develop loss of consciousness altered mental status, hemiparesis, seizures, or focal neurological deficits, within minutes of surfacing, then arterial gas embolism is the suspected to be the primary etiology.
The patient history should include questions about onset, location, and duration of symptoms. It should also elicit any inciting event, as well as exacerbating and relieving factors. History may be limited in patients with cerebral involvement. Most arterial air emboli of iatrogenic etiology, so a high index of suspicion is necessary during procedures. It should be a consideration in patients who suddenly develop signs of ischemia during procedures. In patients with delayed presentation, history should focus on determining if any recent procedures have been performed such as lung biopsy, tumor ablation, recent arterial catheterization, any recent lung or chest trauma which can lead to the formation of fistulas between airways and pulmonary vasculature. The clinician should also obtain information regarding symptoms that start following rapid ascent during diving during history.
The physical examination should be thorough but should not interfere with emergency intervention for any compromise of airway, breathing, or circulation. A complete cardiovascular examination is warranted to access for murmurs, signs of heart failure, bradycardia, hypotension, or pulse deficits. A pulmonary examination should focus on the assessment of respiratory status and signs or symptoms of pulmonary edema. A neurological examination should focus on any cranial nerve deficits, motor weakness, and sensory loss as well as GCS assessment in patients with altered mental status. GI exam should look for any signs of mesenteric ischemia, including peritoneal signs. Other examination components can be performed as deemed necessary by the patient's chief complaint.
Often the diagnosis is a clinical one. There is no specific lab test that will aid in the diagnosis of arterial air embolism. Laboratory testing should focus on the affected organ system or systems. Imaging studies can assist in the diagnosis with CT being the most helpful. It can be challenging to obtain CT in these patients as they can require extensive resuscitation and stabilization before definitive diagnosis. Bedside transthoracic echocardiography may reveal air within the cardiac chambers, and even in the great veins. A chest X-ray may be useful in cases involving invasive thoracic procedures to ensure symptoms are not related to lung collapse. The chest X-ray may show rare findings such as air in the cardiac chambers and air in hepatic circulation. MRI may be useful in patients with CVA symptoms or suspected spinal cord infarction. EKG may reveal signs of coronary infarction or ischemia, bradycardia, as well as ventricular arrhythmia.
The mainstay of arterial gas embolism treatment is trifold. Treatment goals should focus on maintaining hemodynamic stability, terminating the source of air, and decreasing the size of the gas bubble. The priority of focus for any unstable patient with arterial gas embolism should be stabilizing the airway, breathing, and circulation. Patients can be placed in the supine position as compared to the venous air embolism where patients in Trendelenburg or left lateral decubitus. The reasoning behind the positioning is secondary to the fact that unlike in venous circulation, the force of arterial circulation will propel air forward. Also, placing patients in Trendelenburg may exacerbate cerebral edema, the air embolus, and prevent transmission of air throughout the circulatory system. Managing hypotension may require IV fluids and vasopressors. For patients with cardiovascular collapse, the appropriate ATLS and ACLS protocols are necessary. The next goal of management should focus on the reduction in air emboli size and reabsorption of the air emboli. The clinician can accomplish this by early intervention with hyperbaric oxygen therapy (HBO). HBO is the preferred treatment method for patients when available and feasible. The hyperbaric therapy helps to reduce the size of the air emboli by facilitating the diffusion of nitrogen from the emboli back into the bloodstream. Unstable patients with a pulse may also benefit from closed cardiac massage, which is essential CPR, performed as a last resort. In patients with coronary artery involvement nitrates may be beneficial as well as an attempt at aspiration through thrombectomy catheters in cases occurring during coronary angiography.
The differential diagnosis for arterial air embolism is extensive as signs and symptoms are consistent with arterial occlusion, and the patient's presentation will depend on location and organ system involved.
Currently, the prognosis of arterial gas embolism is limited to studies using case series of patients selected for hyperbaric oxygen. Reports have shown better prognosis for patients with venous gas embolism who undergo hyperbaric oxygen within 6 hours of onset. However, for patients with arterial gas embolism, evidence for hyperbaric oxygen is still controversial. Some studies report no significant benefit in the time to initiation of hyperbaric oxygen to recovery sequelae or death. However, other retrospective case studies report patients with complete neurological recovery after hyperbaric oxygen. Factors that were predicted to carry a futile prognosis were: a positive Babinski test on presentation, focal neurological deficits, acute kidney failure, cardiac arrest on presentation, advanced age, or mechanical ventilation for greater than 5 days.
Complications for arterial gas embolisms are related to the respective organ systems involved. In a case series by Bessereau J, et al. 2010, 119 patients with venous or arterial gas embolism who received treatment with hyperbaric oxygen were followed from the time of diagnosis, at six months, and one year. Among those patients who survived, 43 percent had neurological sequelae at the time of discharge. From these patients, the most common complications included visual field deficits, motor deficits, cognitive issues, and seizures. However, at the end of six months, three-fourths of patients had mild or no disability.
Deterrence should focus on understanding which procedures or interventions lead to the highest risk of air embolism, and taking the appropriate steps needed to minimize them. For example, lung protective strategies are necessary when placing patients under mechanical ventilation to reduce the risk of pulmonary barotrauma. In patients with subclavian, and jugular central lines, care should be undertaken to put patients in Trendelenburg position and to ask them to Valsalva when removing the central line. Patients with femoral central lines, do not require Trendelenburg, and a supine position will suffice. In patients undergoing neurosurgical procedures, care should be taken to keep from placing patients the "sitting up" position, and instead put them in a "park bench" position.
Identifying and addressing the signs and symptoms of arterial gas embolism requires a high clinical index of suspicion and early intervention. To prevent iatrogenic causes of air embolisms, all clinicians should be aware of the risk, and causes of arterial gas embolism from the cases performed. Additional healthcare personnel, including nurses who deal with medical equipment used in interventional procedures, should receive training on the appropriate care of these devices to prevent the risk of arterial gas embolism.
Prevention is essential, as most cases of arterial air embolism are iatrogenic. Making sure coronary catheters are flushed during angiography may help in prevention during invasive cardiac procedures. When they encounter at-risk situations, nurses and other ancillary personnel should be ready to inform the surgeon or physician on duty regarding the potential risk. Nurses can also have training in hyperbaric oxygen administration and treatment so that they can assist the treating physician should there be a patient with emboli from any source. This type of interprofessional healthcare team approach can optimize results. [Level V]
Individuals undergoing recreational dives must understand the risk of vascular air embolism. In addition, dive computers, charts, or tables should be utilized to limit the depth and duration of dives' this, in turn, will reduce the risk of decompression sickness.
Healthcare entities should ensure that arrangements exist to readily gain access to a hyperbaric oxygen facility for timely early intervention.
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