During a nighttime hostage rescue mission your team undertakes a strenuous swim in cold water. Shortly after climbing on board of a large watercraft one of your teammates becomes acutely ill. He is short of breath and he is coughing a lot. Thankfully, your team has successfully eliminated the threat and you can focus on helping your buddy.
At your initial assessment you note the following: HR 105 BPM, BP 145/95 mmHg, RR 30/min, SpO2 91% on room air, T 35.5 C (95.9 F)
This 41 yo male is in moderate respiratory distress and even without stethoscope you can hear him wheezing. He shakes his head, however, when you ask him about history of asthma. He doesn’t smoke either. Therefore, before attempting therapy you hook up a pocket-size ultrasound transducer to your smartphone.
- What specific diagnosis is likely and what suggestive findings are present in Figure 1 (as featured in JSOM)?
- What treatable risk factor (and likely in your patient) could contribute to this condition?
Whenever you hear a wheeze you should always remember this very important saying. Namely, “not everything that wheezes is asthma“.
So what else can possibly cause such sudden onset of respiratory distress and wheezing? Pulmonary edema surely can! The mechanism of wheezing in pulmonary edema is thought to be narrowing of the small airways because of bronchial wall edema and intraluminal fluid (rather than bronchial smooth muscle contraction as in asthma) .
Now why on earth would this healthy SOF operator, who was entirely asymptomatic prior to undertaking a strenuous swim in cold water, suddenly develop pulmonary edema?
This time we chose to skip the usual chit-chat about the differential diagnosis and the variety of possibilities. Without doubt, even a previously healthy, 41 yo male with sudden onset respiratory distress upon exertion (auto-stress test after all) must at least be considered to have an acute coronary syndrome. However, we picked this case to raise your awareness of a potentially life-threatening condition that many haven’t even heard of, i.e. SiPE = Swimming Induced Pulmonary Edema.
SiPE is of particular importance to athletes and military personnel performing strenuous exercise/missions in water – that surely includes you and your buddies! Cases range from young, healthy, fit, military swimmers, who have undergone careful medical screening, to older recreational athletes and divers with preexisting cardiopulmonary disease. It has been described in a variety of water-based sporting activities predominantly in scuba divers, military and recreational swimmers, and triathletes. However, there are also cases described during snorkeling and aqua jogging (e.g. BUD/S training 😉 right?). Cases are commonly but not exclusively seen in open water swimming/immersion. However, a scuba diver in a swimming pool can get it too .
SIPE presents as acute onset of breathing problems caused by accumulation of fluid in the lung extravascular space, induced by immersion and intense physical activity, usually but not always in cold water. Patients report shortness of breath and/or cough. Chest tightness, confusion and hemoptysis can also be present. On clinical exam their lungs always sound abnormal. You mostly hear crackles or wheezing. Throw a pulseOx on their finger and it’s quite likely you’ll note hypoxemia .
How exactly does it happen? The truth is we don’t really know for sure. Likely a perfect storm! Predominant theories suggest redistribution of blood from the extremities, which occurs with immersion, leading to central blood pooling. Peripheral vasoconstriction from cold water, prone position when swimming and/or a tight wetsuit further add to the problem. Ultimately it’s just like any horrible flood – there is too much pressure for the fluid to remain contained!
What to do?
- Get them out of water ASAP so they don’t drown and so that you reverse this hemodynamic fiasco caused by immersion – they generally show rapid improvement in symptoms as soon as you get them out of water (and most cases resolve entirely within 48 hrs with just supportive care).
- Keep them dry, warm them up – the least you can do.
- If they are hypoxic and you have access to supplemental oxygen – give it!
- Have albuterol (better known as salbutamol in Europe)? Try it! There is some rationale that such beta-2 agonists may accelerate resolution of pulmonary edema.
- Other therapies to trial if you have them: CPAP, diuretics, nitroglycerin.
- They need to be taken to a hospital for further evaluation, and because this condition tends to be recurrent they need to undergo a work-up before return to full duties.
- Some people get mild symptoms only. They attribute it to being a little out of shape! However, you should still consider it, if your buddy seems to get out breath on waterborne missions.
- Risk factor mitigation is recommended – hypertension treatment for our guy .
It is beyond the scope of this brief discussion to give you an in-depth description of SiPE, but follow the link to an open-access article published in 2018 and get the most current info on this topic.
To make a long story short – this is not a guy who can swim back on his own. He needs a ride!
SONOGRAPHiC MiSSiON SUPPORT
There is nothing easier than making a diagnosis of pulmonary edema with ultrasound. Even 5th-graders can do it – word! It’s ridiculously simple! In fact, if you plan on learning nothing more about lung ultrasonography, you should at the very least familiarize yourself with the concept of “wet lung” vs “dry lung” on your screen.
Extravascular fluid in the lung can obviously come from pulmonary edema, pneumonia, pulmonary contusion and a variety of other reasons. Just consider the clinical picture and the location (diffuse/bilateral vs focal/unilateral) when you see this very distinct pattern of vertical “B-lines” (“wet lung”) instead of normal horizontal “A-lines” (“dry lung”) . The great minds of lung ultrasonography are likely to curse me for this oversimplification, but the truth is it works for the majority of cases you are going to encounter in your operational environment.
Make sure to set your depth to at least 18 cm when looking for B-lines (a.k.a lung rockets). It must reach from pleura all the way down to the bottom of your screen to be called a B-line. Also, if you look between 2 ribs, there have to be at least 3 B-lines to consider them pathologic. Plenty more are seen in the video below – although technically it is not the best clip. It shows only 1 rib in the middle. However, if you look to the left and right of that rib, there are more than 3 B-lines on each side.
Upon placement of a phased array probe (could use curvilinear instead, because a linear probe won’t get you to 18 cm in depth!) on our patient’s chest you see bilateral B-lines all the way up to his upper lung fields. Pulmonary edema bingo!
Now, finish it off ninja-style and move your probe onto his left parasternal area to take a sneak preview of the heart. Parasternal long axis view (PLAX) will do the trick. It is pretty much to reassure yourself he doesn’t have some acute exacerbation of congestive heart failure (CHF). It wouldn’t be the first case of e.g. flu gone bad leading to cardiomyopathy/systolic heart failure. It is extremely unlikely this previously asymptomatic and healthy fit male has isolated diastolic heart failure, so no need to sweat that idea.
If you have looked at enough hearts on ultrasound, you can just eyeball the left ventricular (LV) systolic function and say it appears fairly normal. For our purposes we don’t care if the LV systolic function quantified as LVEF (left ventricular ejection fraction) is 51% or 57%. Just FYI, normal LV shoots out about 55-70% of its diastolic contents – it doesn’t go completely empty in systole. What matters is:
- LVEF looks alright
- LVEF sucks really bad
- LVEF is too crazy – beating fast and LV walls touching in systole
When in doubt, there is a quick and clean 😉 trick for getting this Q answered. Record a clip of a few beats (cardiac cycles) and hit pause. Then scroll slowly through it and watch the movement of the distal tip of the anterior mitral valve leaflet. If it bounces off the septum or comes very close to it, they surely don’t have significantly decreased systolic function (see clip below). There are only 2 major caveats to this story. If a patient has mitral valve stenosis, the leaflets don’t move so well, and if they have serious aortic valve regurgitation, the diastolic back flow jet from the aortic valve will prevent the anterior mitral valve leaflet from reaching the septum. Then again – how many SOF operators have either of the above?
What I describe in very SOFisticatED (simplifiED, betterED) terms comes from the concept of EPSS (E-point Septal Separation). You can actually measure it in a pretty simple way using M-mode, and use this measurement to calculate an estimation of the LVEF. We will surely cover it at some other point, but if you can’t wait to learn, here is a great summary on this topic.
- Barreiro TJ et al. Pulmonary Edema: A Clinical Overview.
- Smith R et al. Swimming-induced pulmonary edema: current perspectives. Open Access J Sports Med. 2018; 9: 131–137.
- Grunig H et al. Diagnosis of Swimming Induced Pulmonary Edema—A Review.Front Physiol. 2017; 8: 652.
- Lichtenstein DA et al. A-lines and B-lines: lung ultrasound as a bedside tool for predicting pulmonary artery occlusion pressure in the critically ill. Chest. 2009; 136: 1014-1020.