How Can You Tell There's an Air Bubble in Youre Veins
Int J Crit Illn Inj Sci. 2013 January-Mar; 3(1): 73–76.
Vascular air embolism
Stephanie Gordy
Department of Trauma Surgery, Oregon Health and Science Academy, Portland, Oregon, USA
Susan Rowell
Department of Trauma Surgery, Oregon Health and Science University, Portland, Oregon, Usa
Abstruse
Vascular air embolism is a rare just potentially fatal event. It may occur in a variety of procedures and surgeries but is most often associated equally an iatrogenic complication of central line catheter insertion. This commodity reviews the incidence, pathophysiology, diagnosis, treatment, and prevention of this phenomenon.
Keywords: Air embolism, air embolus, arterial air embolism, key line complications, chest trauma, complications of central catheterization, venous air embolism
INTRODUCTION
An air embolism occurs when air or gas is admitted into the vascular system. Information technology can occur iatrogenically via interventional procedures but has as well been described as a complication from a variety of circumstances ranging from blunt and penetrating trauma to diving and child nascency. The physiologic effects that consequence depend on the volume of air that has entered the arrangement. A patient's symptoms may range from asymptomatic to cardiovascular collapse and death. Physicians in all specialties should be aware of this as an iatrogenic complication and versed in its prevention and handling.
ETIOLOGY
Air embolism is a rare merely potentially fatal occurrence and may result from a diverseness of procedures and clinical scenarios. It tin occur in either the venous or arterial organization depending on where the air enters the systemic circulation. Venous air embolism occurs when gas enters a venous structure and travels through the right centre to the pulmonary circulation. Atmospheric condition for the entry of gas into the venous organization are the access of veins during the presence of negative force per unit area in these vessels. This is most usually associated with central venous catheterization, as the potential for negative force per unit area exists in the thoracic vessels due to respiration.[1] It tin can, notwithstanding, occur in numerous clinical scenarios. An arterial embolism occurs when air enters an artery and travels until it becomes trapped. For air to enter a closed arrangement, a connexion must occur between the gas and the vessel and a pressure slope must exist that enables flow of the air into the vessel.[2] This is not only due to negative pressure gradients but positive gas insufflations tin also cause air embolism. Moreover, a venous air embolism always has the potential to become an arterial embolism if a connection between the ii systems exists. If a right to left pressure gradient exists, the gas tin then travel from the venous to the arterial circulation. For example, if a patient has a patent foramen ovale, which is present in 30% of the general population, this can result in air traveling from the depression force per unit area right atrium to the arterial system if a pressure slope occurs. Additionally, air embolism most commonly occurs with ambient air just it has besides been reported to occur with a variety of gases including helium, nitrogen, and carbon dioxide.
EPIDEMIOLOGY
Air embolism was reported every bit early on as the 19th century, in both the pediatric and adult surgical exercise.[2] The nonspecific nature of the signs and symptoms of vascular air embolism besides as the difficulty in documenting the diagnosis does not permit the truthful incidence of it to be known. With primal line placement, it is estimated to occur in approximately 0.two% to 1% of patients. Treatment may bear witness futile if the air bolus is larger than fifty ml.[3] Interventional radiology literature reports an incidence of venous air embolism of 0.thirteen% during the insertion and removal of cardinal venous catheters despite using optimal positioning and techniques.[4] Furthermore, the incidence of massive air embolism in cardiac bypass procedures is between 0.003% and 0.007% with 50% having adverse outcomes.[5] The frequency of venous air embolism with placement of central venous catheters based on a reported case series varies and ranges from i in 47 to i in 3000.[2,six] It is near unremarkably associated with otolaryngology and neurosurgical procedures. This is due to the location of the surgical incision which is usually superior to the heart at a altitude that is greater than the central venous pressure. The sitting position in posterior craniotomies is deemed especially risky and procedure-related complications of venous air have been estimated to exist between x% and 80%.[7]
PATHOPHYSIOLOGY
The physiologic effects of venous air embolism are similar to that of pulmonary embolism of any etiology as evidenced by: (i) elevated pulmonary avenue and right ventricular pressures; (two) increased ventilation/perfusion mismatch; (iii) intrapulmonary shunting; and (4) increased alveolar expressionless infinite. Air aggregating in the left ventricle impedes diastolic filling, and during systole air is pumped into the coronary arteries, disrupting coronary perfusion.[8] The lodging of the air in the vasculature results in astute hypoxemia and hypercapnia. The astute changes in right ventricular force per unit area result in correct ventricular strain, which can lead to right heart failure, decreased cardiac output, right ventricular ischemia, and arrhythmia. This can be followed by systemic circulatory collapse, and even death. The degree of physiologic harm depends on the volume of air, charge per unit of air embolism, the type of gas (i.due east., room air, carbon dioxide or nitrous oxide), and the position of the patient when the embolism occurs.[9] The emboli not only cause a reduction in perfusion distal to the obstruction, but damage additionally results from an inflammatory response that the air bubble initiates.[10] These inflammatory changes can event in pulmonary edema, bronchospasm, and increased airway resistance.[11]
The severity of symptoms resulting from air embolism varies co-ordinate to the corporeality of air instilled and the end location of the air bubble. Patients may be asymptomatic or may have complete cardiovascular collapse. The lethal volumes of air in an acute bolus have been described and are approximately 0.v–0.75 ml/kg in rabbits and 7.v–xv.0 ml/kg in dogs. The lethal dose for humans has been theorized to be 3-5 ml/kg and it is estimated that 300-500 ml of gas introduced at a rate of 100 ml/sec is a fatal dose for humans. Furthermore, the charge per unit of accumulation and patient position likewise contributes to the lethality.[ii,12,thirteen] Moreover, air infusion rates of more than than 1.5 ml/kg/min are associated with bradycardia and cardiovascular decompensation. The true incidence of whatsoever vascular air embolism is uncertain due to presumed occurrences during procedures with subclinical responses. Additionally, it is difficult to document as a cause of death due to absorption of air prior to autopsy. Numerous case reports exist in the literature that depict air embolism from various causes. The occurrence is likely most familiar every bit a complication of fundamental venous catheterization. Multiple boosted clinical settings take reported the occurrence of air embolism. These include simply are not limited to disconnected central venous catheters, airline travel, ERCP, hemodialysis, trauma, laparoscopic insufflations, open heart surgery, lung biopsy, radiologic procedures, childbirth, head and cervix surgery, and diving.[two,6,xiv,15]
CLINICAL PRESENTATION AND DIAGNOSIS
The most important diagnostic criterion is the patient'south history, because the clinical suspicion of embolism is based on the initial neurologic symptoms and the direct temporal relationship between these symptoms and the performance of an invasive procedure. The procedures that carry the greatest risk of venous or arterial gas embolism are craniotomy performed with the patient in the sitting position, cesarean section, hip replacement, and cardiac surgery with cardiopulmonary bypass.[10]
The effects will vary according to the vessels afflicted just cardiovascular, pulmonary, and neurologic effects predominate the clinical flick. Occlusions of the cerebral and cardiac circulation are usually more than clinically significant equally these systems are highly vulnerable to hypoxia. Cardiovascular complications can upshot from either arterial or venous emboli. If a patient is conscious during the event, breast pain, dyspnea, headache, and confusion can all exist symptoms of air emboli. Additionally, electrocardiogram changes include ST depression and right center strain due to pulmonary avenue obstruction. Furthermore, clinical signs of correct heart failure and decreased cardiac filling can effect in jugular venous distention and pulmonary edema. If the embolus is severe, cardiac ischemia, arrhythmias, hypotension, and cardiac abort tin ensue. If embolization occurs to the cerebral arteries patients tin take symptoms of confusion, seizure, transient ischemic attack, and stroke.[xvi] When air goes to left ventricle and the aorta, it tin occlude any of the peripheral arteries and crusade ischemia.
To diagnose venous gas embolism, the physician should assess the clinical findings. A "millwheel" murmur can exist auscultated by a precordial or esophageal stethoscope. If a patient is intubated, an precipitous decrease in the end-tidal carbon dioxide levels, demonstrated past capnometry, can warning the anesthesiologist and is concerning for a change in the relation between ventilation and perfusion due to the obstacle of the pulmonary arteries. A massive air embolus can be seen occasionally on CXR. Figure 1 depicts a big embolism due to central line catheterization. Doppler ultrasonography is a sensitive and applied ways of detecting intracardiac air, and it is oftentimes used during neurosurgical procedures, procedures with the patient in the sitting position, and other procedures that entail a high gamble of gas embolism. An even more sensitive and definitive method for detecting intracardiac gas is transesophageal echocardiography is frequently utilized by anesthesiologists to monitor patients in loftier-risk procedures.[2,10,17–22]
Large air embolism due to left subclavian primal line placement with air evident in the main pulmonary avenue
TREATMENT
Awareness and prevention during high risk procedures is disquisitional for patient safety. If a venous air embolism is suspected, treatment includes stopping air entry into the organization, aspiration of the air from the correct ventricle if a central catheter is beingness used and placing the patient in Trendelenburg and left lateral decubitus position also known every bit Durant's maneuver.[7] This positioning allows the entrapped air in the heart to exist stabilized inside the apex of the ventricle. Previous studies have shown that left lateral decubitus positioning may be effective past allowing air to move toward the right ventricular noon, thereby relieving the obstacle of the pulmonary outflow tract. Aspiration via a central venous line accessing the heart may decrease the volume of gas in the right side of the heart, and minimize the corporeality traversing into the pulmonary apportionment. Subsequent recovery of intracardiac and intrapulmonary air may require open surgical or angiographic techniques.[iii]
In trauma, an air embolism should exist suspected in cases of penetrating breast trauma with cardiovascular collapse as this can occur if air gains access to the left heart. It so may reach the systemic circulation via communication between the alveoli and the pulmonary veins of the injured lung. This process is often accelerated with the establishment of endotracheal intubation and positive pressure ventilation. In the trauma scenario, emergency thoracotomy can exist life saving. This is followed past cross-clamping of the pulmonary hilum on the side of the injury to prevent further introduction of air. Intracardiac air tin be aspirated from the noon of the left ventricle and the aortic root with an 18-gauge needle and l-ml syringe. Vigorous massage tin can also exist used to force the air bubbling through the coronary arteries. Additionally, a tuberculin syringe may exist used to aspirate air bubbles from the right coronary artery if the massage efforts are unsuccessful. Once circulation is restored, the patient should exist kept in the Trendelenburg position with the pulmonary hilum clamped until the pulmonary venous injury is controlled operatively.[viii] If air progresses to the coronary apportionment, sudden cardiac plummet may ensue. If air were to travel and reach the cerebral apportionment, a new neurologic deficit may manifest itself as defoliation or cerebrovascular accident.[23]
If an air embolism were to be suspected while a patient is on cardiac bypass, the perfusionist should stop the automobile and cap all catheters. Air should and then be removed from the excursion and the patient placed in the Trendelenburg position. Transesophageal echo (TEE) can help with locating the air and it should so be aspirated. Consideration should be given to cooling the patient for neuroprotection purposes. Additionally, as soon equally possible, retrograde perfusion of the brain should be undertaken while the aortic arch is simultaneously aspirated with the patient in steep Trendelenburg position. Corticosteroids and/or barbiturates may exist considered too every bit hyperbaric oxygen therapy if it's bachelor.[5]
Gas bubbling in the tissue or systemic apportionment slowly resolve, but the rate at which they are removed can be enhanced profoundly by oxygen breathing and recompression. Recompression in cases of air embolism due to diving and hyperbaric oxygen (HBO) administration is master therapy. Additionally, ventilation with 100% Otwo helps correct hypoxemia and increases the diffusion gradient for nitrogen out of the bubbles, causing them to compress.[fifteen] Although there are no randomized controlled trials demonstrating the positive outcome of HBOT, in that location are numerous instance reports and case series that support its use. Moreover, in patients who survive the initial insult of a left-sided air embolism, hyperbaric oxygen therapy has shown some do good in reversing neurologic deficits.[23] The high oxygen tension promotes the assimilation of nitrogen from the bubble and the elevated ambient pressure reduces the size of the bubbles in accord with Boyle's law. At 282 kPa, a conventional HBOT treatment pressure, spherical gas bubble diameter will be reduced to 82% with a resulting 45% decrease in volume, such that bubble passage through the microcirculation and resolution of embolic phenomena may occur. In a review of a case series with 27 patients, substantial improvement in outcomes was shown in patients treated with HBOT. Three hundred and twoscore-half-dozen (78%) of the 441 who received HBOT fully recovered and 20 (four.5%) died. Of the 288 with no recompression therapy, 74 (26%) fully recovered and 151 (52%) died.[24] It must be performed at specialized centers and and so its availability is express. Care is largely supportive and goals should be to maintain end organ perfusion. Optimization of book status can be beneficial. Moreover, oxygen administration should be immediately initiated and hyperbaric oxygen may be of some benefit.[25]
CONCLUSION
In summary, vascular air embolism is a rare but potentially fatal complication of diverse procedures including key venous catheter admission. The severity of symptoms ranges but the worst example scenario is sudden cardiac death. A high degree of suspicion when doing high risk procedures should be nowadays in order to promote early recognition and potentially life-saving therapy.
Footnotes
Source of Support: Nil
Conflict of Interest: None declared.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665124/
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