So I was on call last weekend and got a call from one of the internists on the ward about a potential admission who may need dialysis. She was a woman in her 60’s, diabetic, hypertensive with minimal baseline renal dysfunction, who had been admitted with a hepatic abscess due to biliary obstruction. This had been stented and a pigtail catheter had been inserted to drain the abscess. However, over the last few days, her creatinine had risen to about 500 and she was becoming oliguric. Her O2 requirements had also increased and she was now on 15 liters by nasal prongs. This had been ascribed to pleural effusion and possible pneumonia.
When I saw this lady, she was visibly dyspneic at 30 with a heart rate 115-120 and a systolic BP of about 105-110, saturating 90% on 50% face mask.
So on physical examination, she had a soft abdomen (the first thing I feel just before I put probe to skin), her skin was cool, and the CUSE revealed a large (>20mm) IVC with no respiratory variation (despite the effort). I unfortunately forgot to hit the record clip button…and the parasternal long axis and apical 4 chamber are here:
Lung views showed “A” profiles except for the right base which had a small effusion and some consolidation/atelectasis and some B lines, but not very extensive.
So further assessment revealed she was not a smoker, previously quite active and easily able to go up and down several flights of stairs. She had noted dyspnea about 3 days ago, without chest pain. There were no leg symptoms, and she had been on LMWH for dot prophylaxis. The CXR was not very impressive – in a sense that there was not enough parenchymal disease to explain pulmonary hypertension.
This is PE until proven otherwise, and I would have been comfortable without further confirmation, but with the presence of some lung disease and an intrahepatic catheter, I preferred to have 100% confirmation before initiating thrombolysis.
After CT angiogram confirming bilateral and extensive embolism, I had a thorough discussion with her and her family and they all agreed to go ahead with TPA. She was quite concerned with cardiorespiratory limitation, given that she was quite active. She was comfortable with a quoted risk of intracerebral bleeding below 2%. I used the MOPETT half-dose of 50mg.
Overnight, her HR slowed to about 100, and sats increased to 93-94%.
When I rounded on her in the morning, she said “Doc, I can breathe!” with a big grin. Her HR was 95-100, she was not on 3 litters by NPs, BP 115-120 systolic, and CUSE showed:
So we can see that even though the RV is still quite impaired, it has decreased in size and the LV is now filling better. This was about 12-13h post thrombolysis. She was able to sit up without dyspnea and mobilize to the chair. Her IVC, although it remained around 18-19 mm, had clear respiratory variation.
So…success? Who really knows. It is concievable that, with heparin alone, she might have improved similarly. It is possible. I’m not putting this up to formally support the concept of thrombolysis in “submassive” PE but more to contribute to the #FOAMed discussion regarding the “grey zone” of thrombolysis, since she was technically not in shock (eg SBP>90, lactate normal), but the degree of impairment of the RV to me and the clinical picture, 3 days post, was concerning enough to warrant thrombolysis, but importantly to stress the following:
Point 1: the importance of bedside ultrasound, especially in acute cases. Without it, over a weekend, and with a patient in renal failure, how quickly would I have ordered a CT angio? Not without some hesitation…
I won’t review the MOPETT trial, these guys did a much better job than I could hope to, so definitely listen to this if this topic is of any interest to you (and it should!!!):
Great case debates in the RAGE podcast.
Keep in mind that morbidity, not mortality, is the main thing to focus on in sub-massive embolism and the MOPETT – even though I don’t really like the term, its quite vague – benefit in embolism with shock is quite clear.
Point 2: Equally interesting to me was the fact that the renal failure improved. In fact, overnight following thrombolysis, she had a urine output (without diuretic) over a litre, and over the next few days her creatinine normalized and renal replacement therapy was not needed. Interesting, since she even got a good blast of toxic dye with the CT. Some will feel that it is the improvement in CO that improved renal function, and this may be partly true, but in view of the lack of “systemic shock,” I think that venous decompression resolved the congestive renal failure, which I think was the main cause of her ARF. I posted about this topic a few months ago, so for more on this see:
so thanks for reading and love to hear anyone’s opinion!
QUESTION. IF SOMEONE DOES NOT HAVE A PALPABLE PULSE BUT HAS CARDIAC ACTIVITY ON THE ECHO AND RATE IS 90 AND BP IS 50. DO YOU CONSIDER THIS PEA AND INITIATE CPR?
Great question! There is a whole grey area in “PEA” and management is unclear. I don’t think there is a single answer to that, but physiologically and without further information about RV/LV, I would say your patient needs vasopressor/inotrope support, so I would probably give a small bolus of epi (maybe 100ug) and start an infusion. If I see little reaction (eg HR/BP doesn’t pick up in 30 seconds, I would probably give a short cycle of CPR to get the epi back to the heart. Of course, hopefully there is a reversible cause (MI/PE), that can be addressed.