Let's talk about Swimming Induced Pulmonary Edema.
A very specific disease you will see if you cover as a medic a triathlon or any other open water swimming event in the cold.
We will review its cause, presentation and management.
Hope this satisfies you, please send me comments and questions.
Speaker 1:
Hello everyone, welcome back to another episode of the Frozen Duck where we talk about wilderness medicine. I am your host, eric. Today we're going to talk about SIPE Swimming Induced Pulmonary Edema but before that I would like to do a few apologies. First of all, I haven't produced any episode in almost two years due to many changes in my life. The biggest one is having a second child, which is more exponential than additional, I would say, and the second reason is that it's a transatlantic move and starting two new jobs. So now I'm broadcasting from La Belle Province, quebec, in Canada, after five extremely beautiful years in Iceland. Yeah, we decided to move back. So to my dear Icelandic friends, I miss you dearly.
Speaker 1:
Second apology is for the pronunciation of sype in the previous episode, where I said sip, which I guess is a French deformation. So why another episode on sype? Well, I revisited my last episode with Jörgen Malao on sype and cold water immersion Super interesting podcast if you haven't listened to it and I got a bit excited to have such a nose. So we tap in on many things. But I really felt we needed to go a bit deeper on the subject of SIPE. So I wanted to take a step back and do, yeah, like a deeper dive on it, no pun intended. So the aim of the podcast today would be, by the end of this episode, listeners will have a clear understanding of what it is the pathophysiology, its presentation, its treatment and all A one-stopper if you're in a healthcare professional covering a sporting event where you might see it.
Speaker 1:
So, sipe, swimming Induced Pulmonary Edema quite a mouthful. Swimming-induced pulmonary edema quite a mouthful what it is. So, in short, it is a non-cardiogenic pulmonary edema that happens in people who swim in cold water, most often with a wetsuit. Basically, it's having too much fluid in your lungs, but instead of coming from your heart, from heart failure, it is coming, we think, from too much pressure in your thorax. What it is coming, we think from too much pressure in your thorax. What it is? Well, a few proposed mechanism. Basically, when people enter the water, it is cold and there is a peripheral vasoconstriction that redistributes the water from the limbs to its core, and an additional force would be its pressure. The pressure from the water on the body, what we would call the hydrostatic pressure, would also redistribute this water into your core. There's also, most of the time, people are wearing tight-fitting wetsuits. That would increase all this redistribution and its preload and afterload. So there would be basically a central pooling of blood up to 600 milliliters in physiological studies, and all of this would increase the left ventricular afterload in the heart due to immersion in cold water, increase pulmonary capillary pressure during physical exercise. So I mean quite a few things, but at the end all these forces will accumulate fluid and blood in the thorax and this will increase the pressure in the capillaries of the small vessels and will force fluid in the lungs. At least this is how I understand it.
Speaker 1:
So who's at risk? Mostly it's swimmers in cold water, typically wearing wetsuits. That would be triathletes, open water swimmer, military personnel, recruits, scuba divers. Interestingly, it's also more common in women and older individuals. So what does it look like?
Speaker 1:
How do you diagnose this? What's the presentation? I would say the classical way that you will diagnose this is that if you see a patient during or after a swimming in open water or cold water, they would have cough, shortness of breath, dyspnea, they would cough, they can have a bit of dysphorathia sputum, a bit of blood mixed to it, a bit of like blood mixed to it, and I would say what would really nail it is that when you examine them. They would have a saturation below 95 and also some crackles in the in the long auscultation. Most of them would need to stop the swim or you would see them right after uh the swim. But there's also been some cases in the norseman triathlon where some of them were diagnosed almost like 120 kilometer further in the in the cycling leg of the uh of the um long distance triathlon. When you see them they kind of a bit of like blue lips, a bit of central cyanosis, also just from the cold and the mix with the hypoxia. Most of the cases I've seen um they would have a saturation 88 to 95% and then a bit of like a bit of crackles in their lung. The rest of the exam should be normal and this is also just kind of like make sure that there's nothing else going on. They shouldn't have necessarily like a hurt, murmur or leg edema or fever. It's mostly the hypoxemia and the crackles that would nail the diagnosis.
Speaker 1:
For this investigation and diagnosis I mean this is mostly a clinical diagnosis I would say the only thing that would reinforce your diagnosis would be a portable ultrasound device where this is really common, also in sporting events. Most of the people will have it you will have the ultrasound findings of having, uh, basically b profiles, so three or more b lines in at least two intercostal space. Most of the time it's bilateral, but it can also be on one side, only more common on the right side in the studies, interestingly enough. And then some people can ask also for chest x-ray scan, ecg labs. But this would be if you're more worried about something else going on, like a p, like a pneumonia, like a myocardial infarction, pneumothorax. Um, yeah, so this would be also the differential diagnosis.
Speaker 1:
So how would you manage it? The immediate steps would be, if you suspect, would be to get the person off the water, remove the wetsuit, dry and rewarm them, examine them, get a story, get an oxygen level. If their oxygen level is above 95%, you can observe them for a while. If it's 92 to 95% saturation, this is where you could consider oxygen for comfort, unless there's any other thing going on. And then, if the saturation is below 92%, this would be where would be my personal cutoff, where I would provide supplemental oxygens. And from the few cases I've seen, it's what impressed me the most was not necessarily how low their saturation was, but more clinically how short of breath they were and how they were working for it. So it's very impressive. You would see these people and they would be really catching their breath, having a hard time finishing a sentence. Their SAT might be low but you would expect like a much lower SAT at least that's my personal experience since they're so short of breath.
Speaker 1:
Usually what we do is we just start them on on oxygen, most of the time on non-invasive ventilation like a CPAP or a BPAP. A lot of pre-hospital system have a CPAP like a bussingak valve that they can use, and what is very interesting is that this CPAP and this BiPAP, it really makes sense also to treat the disease physiologically Because, as we were saying earlier, we think there's a bit of fluid in the lungs and by applying a PEEP, a positive and expiratory pressure with a CPAP and a BiPAP, you will really open these alveoli and reduce the preload and the afterload. Some of the machines that they have in the pre-hospital system are not very expensive and they're fast to set up. There's been a few other medication or intervention suggested or tried, mostly betagonis for wheezing, or some people have tried furosemide or diuretics, steroids, but all of these are not necessarily recommended for SIPE, but if you're thinking you're treating something else, or asthma or bronchospasm, these might be end-fold Antibiotics or nitroglycerin, same thing. If you're worried about a pneumonia or myocardial infarction, you can use them, but not necessarily for SIPE. And, like I said earlier, one of the biggest challenges with SIPE is just to make sure you only deal with this, not with an MI, not with a PE, a pneumothorax pneumonia and that most of the time. With a bit of non-invasive ventilation, rewarming and a bit of time, most of them will just resolve and evolve favorably.
Speaker 1:
By the way, if you want to see something pretty cool that I've seen during my research, it's a very famous swim in Sweden where a lot of the studies on SIPE comes from. It's called FANSPROJET simningen. Sorry for my swedish. I speak a bit of icelandic but not swedish, so yeah, I probably got this wrong. Um. So it's the largest open water um event in sweden. It's in fans pro sweden. If you look at google map, it looks like a very uh yeah, like a small, lovely place and they have this event where they have 11 000 swimmers a this is a lot of people. The water is about 15 to 20 degrees Celsius and they say that 98% wear wetsuits. So this huge, massive event open water swimming and they've basically published a lot of studies from these events in the last few years. So check this out.
Speaker 1:
So how do SIPE evolve? What's their prognosis? Well, if recognized and treated early, it is a disease that evolves well. Its resolution is usually within 24 to 48 hours. Most of the cases are managed without hospital admission and they can, yeah, just be treated on site. If there's a medical tent and from a very large Swedish study, yeah, only one required intubation in thousands of patients. No recorded deaths from SIPE. But sometimes you would wonder if there's maybe a few drowning that happened because of SIPE. So I mean, you can just imagine being in an open lake in the middle of nowhere, having SIPE desaturating at 85%, panicking and basically drowned. But we never know. So when you would see them, if you're in a medical tent, you've seen a patient, you've put them on a non-invasive. They evolve well.
Speaker 1:
A follow-up with a pulmonologist or cardiologist is recommended if something is off or if you find something in your physical exam. But we have studies with a quite low rate of missing something and there are usually athletes that strain their body and heart pretty well. So if the symptoms persist, yeah, yeah, they would need to consult and, yeah, discharge instructions need to be pretty clear when you discharge them. This is where you might catch up something and also the evidence suggests that, yeah, symptoms resolve quickly post episode with no long-term effects in a study up to 14 weeks. So you could reassure them that people, yeah, shouldn't have any complications from it. But there is about a 20 to 25 percent risk of recurrence.
Speaker 1:
So people going back in the water, cold water, with a wetsuit and having an episode of sype. So to conclude, swimming induced pulmonary edema is something you will see in swimmers in cold water who exercise a lot. They would present with cough, shortness of breath, they might have crackles and a low SAT. When you examine them At least in my experience, they look quite disney compared to their low SAT. You need to get them out of the water, remove the wetsuit, dry them, warm them, give them a bit of oxygen and non-invasive I would say that would be my go-to Observe and see how they do. Most of them will do fine within an hour or two with non-invasive, but yeah, you would need to transfer them, depending on the resources and the location and the severity of the disease.
Speaker 1:
So that's a wrap for today. I'm very happy to be back again. My year resolution was to, yeah, reanimate this podcast, so you should expect more episodes in the next few months and weeks, hopefully. So, yeah, I hope this podcast satisfies you and please don't hesitate to contact me for comments or suggestions. And thank you for listening to the Frozen Duck and please subscribe and stay tuned for further episodes. I'm saying bless, bless.
