 Hello, everyone. This is Steve Barker, and I'm going to talk to you for a few minutes about a very important patient safety topic, namely, air embolism. By way of introduction, I am an anesthesiologist with an original background in engineering, and I'm a board of directors member at the patient safety movement. So let's talk about air embolism and why it's important and what we can do about it. First of all, what is it? An air embolism occurs when air or some other gas is introduced into the vascular space. It gets into the bloodstream. This can happen in veins, arteries, in the lungs, or in the heart itself. Why is that bad? What's the big deal? Well, three ways it can be very bad. A venous air embolism, air embolism in the veins, can go to the lungs and block the pulmonary blood flow, the blood flow to the lungs, causing pulmonary hypertension and failure of the right side of the heart. Second mechanism, air embolism going into the heart in large amounts can cause what's called an air lock in the right side of the heart. The heart valves do not work properly and the heart cannot eject the air. Cardiac output falls very rapidly, in fact almost to zero. It's rapidly progressive to a cardiac arrest. It is fatal if not treated within a couple of minutes, literally. And the third mechanism is that air embolism from the right side of the heart, where it goes from the veins, and cross over and reach the left side of the heart from where it is pumped into the arterial circulation. And it can then cause infarction or a blockage of blood flow and oxygen delivery to the vital organs, including the heart and the brain. That obviously is very bad. How it gets from the right side of the heart to the left side is something we will talk about in a minute. How does this happen? Most often, air embolisms are iatrogenic, meaning that we cause them during our treatment in the hospital. Some procedure or something we were doing in the hospital that introduced the air. That means they can virtually all be prevented, and this should be considered a zero-tolerance event. We will look at some case report examples of how this happens to inpatients and what it resulted in. During surgery is a common setting for air embolism. It happens with an accidental exposure of open veins to air, especially when the surgical site is above the level of the heart. It is most common in trauma surgery, especially where you have an open chest or abdominal injuries resulting in an open abdomen. And it is also common in blast injuries, injuries from explosions. It can happen from mechanical ventilation, that is an artificial ventilator breathing for the patient. If the pressure supplied by the ventilator to the airway to the lungs gets too high, that can introduce air into the bloodstream in the lungs. And then finally, the old diver's decompression sickness. Divers get nitrogen dissolved in their blood when they go down deep. And if they come up too fast, that nitrogen comes out of solution and actually forms gas bubbles in the blood. And in other places, and that is classically called the bends, and it can be fatal. And it's basically the same disease as other air embolism. What are the signs and symptoms? What does it look like? What should be our clues? It can present with shortness of breath, especially if there's a large air embolism going to the lungs, coughing or wheezing or sneezing, or chest pain, joint or muscle pain if it's being pumped out to the body. A stroke or cerebral vascular accident, if it goes to the left side of the heart and gets pumped out to the brain, that will result in motor sensory or speech impairment, that is loss of sensation and partial or even complete paralysis. It can result in confusion or loss of consciousness, lowering of the blood pressure as the cardiac output is cut back by the air embolism in the heart. And a sudden decrease in the expired carbon dioxide, we'll talk about this more because that's one of the earliest signs that we can actually measure, is a change of decrease in the end-tidal carbon dioxide, which is something we can easily measure at least during surgery. Disrhythmias, meaning an irregular heartbeat instead of the normal sinus rhythm at a nice slow rate. We get rapid rhythm, we get irregular rhythm and that can be a clue of an air embolism. Finally, a blueness of the skin or what's called peripheral cyanosis. This is again due to the oxygen from the blood not being delivered to the organs and to the skin. How often does this occur and is it really a serious problem? Well according to the Centers for Medicare and Medicaid Services and the American Academy of Orthopedic Surgeons, air embolisms are the second most common preventable adverse event. The first most common preventable event being patient falls. Air embolisms happen many thousands of times per year. Most of them are asymptomatic and most of them we basically get away with. There's no harm done, but that does not mean we should tolerate it because as you have already seen some of them can be very harmful, including resulting in death and you see a list of the complications here, including stroke and cardiac arrest. One setting in which air embolism is very common is in neurosurgery, brain surgery performed in the sitting position or what we sometimes call, excuse me, the beach chair position. This clinical study of patients having cranial surgery found that in 100 or 400 patients having brain surgery in the sitting position, air embolism was detected by their very sophisticated mechanisms that they used in this study. That is one in four patients had a detectable air embolism during this surgery. Here is a clinical example that is more significant in my world of anesthesiology and this has happened a number of times. If you look at a bag of intravenous fluid, in this case lactated ringers, you notice that there is about 100 or 200 cc's of air in the top of that bag. Why is that air in the bag in the first place? Well, it's there so that you can read the level of the fluids here and tell how much liquid is left in the bag. That is the sole purpose for having air in the bag and that's what I call strike one. Let's suppose we need to give that fluid, maybe it's a trauma patient or someone who's lost a lot of blood. We need to give that fluid rapidly and we need to basically squeeze the bag to get it into the patient faster than it would be driven by gravity. Well, there are devices for doing exactly that. The level one is a particular device as shown here that basically you put the IV bag in these compartments and it pneumatically compresses the bag and squeezes it so that the fluid runs in faster. So the bag is under pressure, under excess pressure. This is what I call strike two. And strike three is what happens when the bag runs out of fluid and there's 200 cc's of air in the top of the bag. Well, you can guess the air is pumped into the patient and that is strike three. Let's look at some case reports of how this has happened. These are all true examples. A trauma patient is in the operating room for an open exploratory laparotomy. He's got an abdominal injury. Blood and fluids are being infused by pressurized fluid warmer. One of these devices, such as shown on the last slide. The normal saline IV bag emptied. All the saline was gone into the patient. But the bag, as I have shown, contains 200 cc's of air. The safety valve in the device did not stop the air infusion. The patient was infused 200 cc's of air under pressure into his veins and it resulted in death. There are actually several case reports of deaths in this exact circumstance. Here's a case that occurred at my institution that I was personally familiar with. A 19-year-old extremely healthy football player was involved in a motor vehicle accident. He had a central venous catheter that is a catheter placed in the right side of his heart for monitoring and for fluid management. Very common in severe trauma patients. He was taken from the intensive care unit to radiology for some x-ray studies. He did not have a bedside nurse accompanying him on that trip. His CVP central venous catheter became disconnected from the intravenous line and therefore was exposed to air. That is strike one in this case. The patient was left in the sitting position because he was actually more comfortable that way. That is strike two. And finally, he was observed to take a deep breath, strike three. When you take a deep breath, the pressure in your lungs actually goes below atmospheric and the pressure in the pulmonary veins can actually suck air into the veins if there is a pathway for air. And the pathway, of course, was this open CVP line. He had a massive air embolism, a right ventricular air lock, and immediate death. And the volume required for one of these air locks in the heart, by the way, is 200 to 300 cc's right up there in the amount contained in the IV bag. Another case, a posterior craniotomy for brain surgery was performed in the sitting position. During the dissection through the dura into the brain, the end tidal CO2 suddenly falls from its normal value of 35 to about 15 millimeters of mercury. At the same time, his blood pressure drops to 85 over 55. What happened? What happened is an air embolism, which I've already shown you is a high risk complication for sitting craniotomies. And it was detected, we were warned of it by the sudden fall in the end tidal CO2. What do you do? The first thing you do is put the patient's head down so that the head is actually below the heart so that no more air will be sucked in from the atmosphere. A couple more case reports. Here's a 68-year-old lady having a total hip replacement. The femoral prosthesis, which is a long steel rod, is hammered into place using a glue called methyl methacrylate. This is the cement to basically glue the rod into the femur. The anesthetist noted a sudden fall in the end tidal CO2, just like we discussed in the last case report. Followed by hypotension, bradycardia, slowing of the heart, and cardiac arrest. This was, in fact, a methyl methacrylate embolism. Not strictly speaking an air embolism, it was an embolism of the glue used to cement the hip. And the problem with that methyl methacrylate is it's not only a diffuse pulmonary embolism with all the problems that we've already discussed, but it is also a potent myocardial depressant. The methyl methacrylate itself depresses the heart and makes it contract not as well. Another case. A 23-year-old lady in labor, a parturian, has a long and stressful labor. She has a partial placental abruption, that is the placenta has torn off from the uterine wall. She finally reaches a cervical dilation of 10 centimeters, which is the full dilation and ready for delivery. So she's told to start pushing on her next contraction. She begins to push and suddenly starts panting and says, I can't get enough air, followed by hypotension, low blood pressure, and a cardiac arrest. What happened here? This was an amniotic fluid embolism, and this has been reported many times. Again, not strictly speaking an air embolism, but an embolism of something that doesn't belong in the blood, and in fact is not soluble in the blood and can cause cardiac arrest in the same manner. Last case. A 63-year-old is in the recovery room following a hernia repair, and he has an accidental infusion of 10 cc's of air. Just 10 cc's, that's very small volume. He has sudden onset of double vision, headache, nausea, and vomiting. He's taken to MRI Magnetic Resonance Imaging, where he's found to have a small stroke, a CVA, in his brainstem. What happened? 10 cc's of air as a pulmonary embolism is nothing. It should be very well tolerated. Well, here is the complication. Up to 30% of us have what's called a patent for Raymond O'Valley, or PFO. This is a pathway from the right atrium into the left atrium, and air emboli can follow this pathway, this shortcut, over to the left side of the heart, and then those air emboli are then pumped out as air bubbles from the left side of the heart, and they can infarct, or obstruct, vital organs, including the brain in this case. PFO can be detected by an echocardiogram, but it's not routinely done on most patients. Now, this is a personal interest to me, because I discovered that I am one of those 30% who have a PFO, and in fact, I got it repaired because of what happened. Here is a case of somebody who did not have it detected. He was having an interventional radiology procedure, a percutaneous lung biopsy. He suddenly became unresponsive, and you see on his CT scan of his brain, air bubbles in his brain, air bubbles that got from the left, from the right-sided circulation in the lungs, to the left side and went out and infarcted part of his brain. What are the procedures that are at risk for air embolism? Well, there are many non-surgical procedures that have a high risk, one we've already talked about, and that is the placement of a central venous catheter, which is a direct pathway into the right side of the heart. Other catheterizations, even parenteral nutrition that is intravenous feeding because it's often given through central catheters. Interventional radiology, I just showed you an example, and other procedures, I'm not going to read them all, but the point is you need to know which procedures that are being done in the hospital are at risk for air embolism and be wary of those. And then on the surgical side, the procedures that are done in the operating room, there are some that are known to be very high risk. We've already talked about setting position craniotomy, very high risk. Any operation, in fact, where the surgical site is well above the level of the heart, that is a risk factor. Posterior fossa neck surgery, laparoscopic procedures, total hip arth, which we talked about already, caesarean sections, etc. And you need to know which ones are the high risk going into the operating room, and here the list goes down to medium and low risk. I will not read them all. How do we detect air embolism? Well, it turns out that the best way, the most sensitive way, is something that we rarely do in routine surgical cases, and that is transesophageal echocardiogram, or TEE. It requires a specialized monitor that has to be placed down the esophagus of the patient. It requires an expertise of extra training. It's expensive, and it requires extra effort. So most of our patients do not have this available. Other Doppler and acoustic techniques are available. They are not quite as sensitive, but they're also easier to do. And notice you have to go quite a ways down the list to the moderate sensitivity before you get to N-Title CO2, which is the detection method that I've already told you about. A sudden drop in the expired carbon dioxide. Other routine monitors such as pulse oximetry, which measures oxygen saturation, are relatively low in their sensitivity. So the point is, we don't have high sensitivity monitoring for air embolism in most of our patients. Therefore, we have to maintain a relatively high index of suspicion and always be on guard. What is the treatment if you think you have an air embolism? The first thing is to get the head down, and at the same time the left side down. So you put the patient in what's called Trendelenberg position, head down, turn him with his left side down. That's called the Durant Maneuver. The second priority is to get the surgical site below the heart because that's where the air is getting into the patient's veins if this is happening during a surgery. So reposition patient. But wait a minute, you're probably already saying, aren't those two sometimes contradictory? For example, what if our operation is in the pelvis? Well, the only way to get the surgical site below the heart is to put the patient in just the opposite of Trendelenberg, or what we would call reverse Trendelenberg with the head up. And this in fact is a contradiction, and it's a decision that the clinician has to make in the heat of the moment. If the main goal is to stop the continued introduction of air at the surgical site, then get the surgical site below the heart. If the main priority is to stop the damage from the air that has already gotten into the system, but that source of air has been blocked, then put the patient in Trendelenberg. Stop the source of the air. Check the intravenous lines, make sure they are not introducing air, pressurized fluid warmers, et cetera. Flood the surgical field with normal saline. Increase the inspired oxygen concentration to 100%. Use a hyperbaric chamber or consider it if it's available. Remember, this is what's used in diving sickness in the bends. We put the divers in a hyperbaric chamber, typically for 24 hours or more, and gradually bring them back down to atmospheric pressure. Aspirate air directly from the right atrium of the heart. This is in the airlock situation that I described. That can either be done through a central venous catheter or percutaneously by sticking a needle and a catheter through the chest. This is a heroic maneuver. It has saved a number of lives. It's not that common, but if you have one of those airlock situations in the heart as I said, you've got literally seconds to do something to solve the problem and heroic measures may have to be tried. Try whatever you can do to maintain the hemodynamics. Maintain the blood pressure and the cardiac output within a normal range so that the patient's vital organs are getting needed oxygen. And last but not least, if the patient does go into an arrest, do not hesitate, do not wait, start CPR. CPR can save these patients, even if they are in an airlock situation. It may in fact help pump the air out of the heart. So you do CPR. An ounce of prevention as you can see, an ounce of prevention is worth a pound of cure in the situation of air embolism. So how do we prevent it? Well first, be sure that all central venous access catheters are securely attached. Use what's called lure lock fittings. These are screw-in fittings in the IV line that's connected to the central catheter. Not the old-fashioned push-in fittings that are not positively locked. Check the tightness of all these fittings. Some even suggest, and I agree, use tape over the fittings, connecting the central venous line to the tubing, especially if the patient's going to be transported like our football player. Eliminate all air from the IV bags if a pressurized device, fluid warmer with pressure such as a level one, will be used. And that is easy to do. It takes about 20 seconds to do to bleed the air out of the bag before you reconnect it to the IV and put it in the pressurized device. Check your drug syringes carefully for air. And check your IV tubing for air. My recommendation is be conservative. Assume that every one of your patients has a patent for Raymond O Valley unless proven otherwise. Which means unless you have an echocardiogram that shows that they do not have one. 10 cc's of air is not okay in someone with a PFO. Now how much is 10 cc's of air? It's actually quite a bit. If you put 10 cc's of air into your IV tubing, try this sometime, but not when it's connected to a patient obviously, you'll see that 10 cc's of air will fill your entire tubing from the bag of IV fluid down to almost down to the patient. So if you have enough air in your IV tubing that there's like a couple of inches of tubing with air in it, that's probably less than a cc and I would aspirate that out and get rid of it. On the other hand, tiny bubbles that you might see in the IV tubing are fractions of a percent of a cc and are not of concern. Consider new technologies for air removal. There are some in the market, air removal from the intravenous lines. Here is one I have no connection with this company, but it's an interesting product called Clearline. It detects air in the IV lines using ultrasound and then once it detects them, it actually diverts the air into a collection bag. It's been shown to be pretty effective and it can be used with one of these pressurized warmer devices such as the level one that I showed you already. So to conclude, air embolism is a serious risk to our hospital patients and the results can be serious problems up to and including death. With up to 30% of our patients including myself, having a patent for Amon O Valley, even small amounts of intravascular air are of concern. So assume that your patient has a PFO until proven otherwise and do not tolerate several ccs of air in your IV tubing and that amount of air is very visible in your IV tubing. Education is the key. Make sure everybody in the OR team knows the risk factors and the early signs and in any patient procedure where air embolism is a risk make sure everybody involved knows the situation and knows the early signs. Minimize those risk factors for example CVP lines are securely attached and taped, all air is removed from IV bags and have a rapid response plan for treatment in advance should this perhaps be part of the time out that we routinely conduct before we make the incision during surgery? I think so. In those high risk cases for example posterior fossa craniotomies yes I think it should be part of the time out. Finally last but not least review and report all cases. Let's learn from our mistakes. Publish them in literature as case reports whether they resulted in bad outcomes such as death or if you made a heroic save either one needs to be published so we can learn from one another's experience and mistakes that's how we prevent this. Our goal and this has to be a must-achieve goal is zero for air embolisms. Thank you very much for your attention I hope we have an opportunity to have some discussion and perhaps hear from you about any cases that you may have encountered. Thank you very much.