I’d like to introduce everyone to our amazing Ultrasound Fellow, Dr. Viveta Lobo (otherwise known as “VLo” to our team – of course!). She came to us by way of Drexel, tolerates out antics, appreciates our quirks, and laughs at our jokes. We love her! Enjoy this post about a healthy guy who looked very sick, short of breath, and only bedside ultrasound, using the RADIUS protocol, could help diagnose it so quickly and get the patient what he needs and fast….
I’m about 4 months into my Ultrasound (US) Fellowship at Stanford, and while I am thrilled to have greatly improved my US skills, and image acquisition during a scanning shift, it is in no comparison to the thrill, and satisfaction I felt, after using my bedside US skills to navigate through the following case.
A 55-year-old healthy male, with no past medical history, presents with progressively worse shortness of breath over the past 2 weeks. Within 30 seconds of being in the room, he is getting more short of breath, dusky, diaphoretic, and requiring to now sit up and lean forward while speaking to me in 1 word sentences. He is on a 100% non re-breather, sating about 93%. The rest of his vitals – BP 124/84 RR 41 HR 124 Temp 97.8
Even as a new attending, I was pretty certain, that if I did not figure this out in the next few minutes, this once very healthy patient is going to decompensate, and likely end up with grave morbidity. However, given that he had no known history, I had nothing to go by, except…. I grabbed my US probe, and within 3 minutes, I gained a wealth of information. I first took a look at his chest by using the phased array low frequency probe on each side of his chest in 8 total areas (4 on each side). This is what I see throughout:
…. >2 large B lines bilaterally, rays from the pleural line on the top to the end of the screen.
When I switched to a RUQ and LUQ views, my suspicions were confirmed :
…Now, the US images are on cardiac presets so the resolution is a touch different than what we are used to, but the findings are obvious which heightened my concern for the patient even more: large pleural effusions noted bilaterally. Seen as a black (anechoic) area above the diaphragm. Black is fluid on ultrasound, and you can even see the lung trying to breathe on each of the images above.
Next, I quickly assessed his IVC, and saw a plump dilated IVC, consisted with fluid overload state, which prompted me to stop my nurse from hanging any IV fluids. I then performed a bedside echo:
Subxiphoid view: (placing the phased array low frequency probe in the subxiphoid area and pressing down while flattening the probe, using the liver as an acoustic window to see the heart):
Apical 4-chamber view: (placing the probe just underneath the nipple line, at the point of maximal impulse and angling toward the body center):
…. I was able to rule out a pericardial effusion and cardiac tamponade as well as any significant RV strain to suggest a hemodynamically unstable pulmonary embolism, but I appreciated significant left ventricle dysfunction, and hypokinesis.
I then took a look using the linear probe on the anterior chest wall at the 2nd intercostal space and saw:
So, there is great lung sliding but we see it almost too well! The reason is because fluid is the lover of ultrasound and will allow you to see tissue deep to it better due to enhancing of echoes. There is fluid between the parietal and pleural layers, more and more from superior to inferior chest – on both sides. That’s quite a bit of pleural effusion if it goes all the way up to the upper lung zones! While I was putting the pieces together and realizing the diagnosis, my nurse informs me that his istat troponin comes back elevated. His initial EKG:
…..showed sinus tachycardia with ischemic changes inferior and laterally, with t waves inversions. We also see multiple PVCs. No old one EKG for comparison. Ah, the evolution of an MI on EKG – love it!
So to recap, I have an otherwise healthy gentlemen, with progressive sob, no chest pain, but with positive family history of ACS, with confirmed LV dysfunction on US and bilateral pleural effusions and a positive troponin, and some possible ischemic changes on EKG. Sounds like a post ischemic cardiac event presenting with ventricular infarct! From door to diagnosis in 5 minutes! I placed him on BIPAP, gave him a big shot of Lasix IV, aspirin PO, and called my cardiologist! The patient started to improve after the medication, avoiding intubation. The Chest Xray was then done:
….showing bilateral diffuse opacities which could be typical for ARDS.
After a brief cardiology evaluation, my patient was admitted to the CCU and shortly after went to the Cath lab, and was found to have a complete LAD occlusion.
While I initially had a very broad differential including PE, new onset CHF, cardiac tamponade, myocarditis, pneumonia; my bedside ultrasound was quickly able to prioritize my differential, and consult the right service, with a specific question of – should this patient go to the cath lab? Without bedside US, this patient could have easily been a Medical ICU evaluation for respiratory distress, with an extensive work up, including CT Chest, intubation, and more time than the patient needed for a diagnosis to have bee made while we sorted through the differential.
This case is one of many that completely validates bedside ultrasound for me, and my decision to pursue this awesome fellowship!
As a follow up: Patient went on to get an LVAD, and is on the heart transplant list.