A 52-year-old man presented to the ED via ambulance from his home with altered mental status. His wife had called the ambulance when he was unable to get out of bed in the morning and was moaning in pain. The patient had been in the hospital one week prior for septic arthritis of the right knee and MSSA bacteremia. He was still being treated with Nafcillin through a PICC line. When medics arrived, he had a systolic blood pressure in the 60’s and was transported to the ED with presumed sepsis.
Initial VS: HR 123, BP 65/42, RR 30, Sp02 100% on RA
The patient was lying on the bed, moaning with his eyes closed. He would open his eyes when asked and would answer questions appropriately. He reported that he was having severe left-sided back pain. His wife reported that when he went to bed, he was his normal self, but in the morning, he seemed confused and in severe pain.
Given that the patient appeared to be in profound shock, the physician taking care of the patient reached for the bedside ultrasound to assess his shock state. Here is the parasternal long view:
What do you think?
It appears that the LV is hyperdynamic. Look how the walls of the LV completely come together during systole. The physician taking care of the patient also thought that the RV looked enlarged.
Here is a parasternal short view:
What do you notice?
The RV is huge. The LV appears small and under-filled. Here is an outline of the RV and LV that may help to point things out better as the lung is moving in and out of view in the clip:
Here are the apical views:
Again, the RV appears larger than the LV.
Bilateral lung windows were obtained (we will only show one side, but they appeared the same):
You can see that there is sliding present, and there is an a-line predominance. This is consistent with the lungs being dry.
A clip of his IVC was not saved, but it was about 2 cm in diameter with about 50% collapse with respirations.
After doing the ultrasound, the patient was asked if he was short of breath, and he answered, “No, I don’t think so.” He also denied chest pain.
These ultrasound findings were concerning for an obstructive cause of shock, such as pulmonary embolism. This information was confusing to the physician taking care of the patient because he had every reason to have septic shock and was not hypoxic or short of breath. Sepsis and PE remained in the differential, but the physician also considered aortic dissection and AAA given the patients severe back pain.
After IV access was obtained, labs were drawn, and a liter of LR was hung, the physician prepared for RSI given his AMS, unstable hemodynamics, and expected clinical course. Before RSI, the patient was given 20 mcg of push dose epinephrine. RSI was completed with succinylcholine and etomidate.
After intubation, the first BP obtained was 100/50. The next cycled BP minutes later registered in the 30’s systolic. No pulses were felt but there was electrical activity on the cardiac monitor. BSUS showed very poor cardiac contractility, and instead of initiating compressions, 1 amp of epinephrine was administered. Within seconds, cardiac contractility improved on ultrasound and pulses returned. Compression of the bilateral common femoral veins revealed no evidence of DVT.
An arterial line and a central line were placed. Broad-spectrum antibiotics were started. A FAST exam was completed and was negative for free fluid in the abdomen. The patient was subsequently started on levophed and vasopressin before being transported to the CT scanner for a CT-PA of the chest and a CT of the abdomen and pelvis because of the severe left back pain. Upon transfer the CT scanner, the BP was in the 110’s systolic.
Here are the images from the CT-PA:
You can see that there is large clot burden in the bilateral pulmonary arteries.
After this finding, he was moved back to the stabilization bay, and a bolus of 10 mg of tPA was administered followed by an infusion of 90 mg over 2 hours. He was then transferred to the ICU.
He was weaned from pressors and extubated 2 days after admission and had no neurologic deficits. He was started on Lovenox with plans to bridge to Coumadin. He did undergo an MRI of his back because of persistent pain, which showed osteomyelitis/discitis that was thought to have developed secondary to seeding from the MSSA bacteremia.
Bottom Line: Ultrasound in an invaluable tool in cases of undifferentiated shock. The patient presented above had every reason to have septic shock, and only with the aid of ultrasound did PE move up the differential.
It almost seems like there is hyper-echoic material swirling around in the RA/RV (especially in #2/#3 of the A4C views). In hindsight do you think that is some of the clot burden itself or just artifact?
Great case
Great question! I do not think that is clot. The echogenic swirls that you are seeing are bubbles (and the artifact created by the air) from the saline that was infusing. I think it is more pronounced in this patient because there is RV failure from the large clot burden, and the contents of the right side of the heart are not moving forward well.
What do you make of the pericardial effusion (best seen in the apical 4 chamber?) Bacteremia seeding the pericardium? Underlying oncotic process leading to a false diagnosis of the “septic” knee and now pericardial effusion? blood? Would be interesting to know how the guy did in the long run. Effusions always give me pause when I’m thinking thrombolytics…
The gain appears appropriate considering the anechoic LV, so I don’t think its all fat pad.
Pericardial effusion is not something I usually see in my PEs. Is this a common finding for anyone else?
I am not sure what to make of the pericardial effusion. I did take note of it initially, however, in the sub-xiphoid views which were not saved, it appeared insignificant. In my opinion, pericardial effusions can look much more significant in certain views and insignificant in other views. The follow-up formal TTE by cardiology noted a “very small” pericardial effusion. I think that this effusion was unrelated to the PE.
I left out some of the history: he had septic arthritis of the same knee 20 years prior. A week or so before developing the septic knee the second time around, he had a steroid injection for arthritis. The hypothesis was that a dormant infection was reactivated. The septic knee was aspirated and grew out MSSA, which eventually grew out in the blood.
I think seeing a large pericardial effusion would give me pause too when pushing thrombolytics, however, this patient was clearly dying of a massive PE (needing 2 pressors to maintain BP). The effusion seemed small, and in the clinical context, it was not blood in the pericardium. Luckily, things turned out well for this patient, as he survived to hospital discharge.
Thanks for reading! I am interested to hear what others have to say.
Best,
Andie
Completely agree! Would have done the same (tPA) considering the case. And thanks for the extra case history.