This is a fascinating case demonstrating an extreme example of fairly common pathology. It helps illustrate some key principles of ultrasound interpretation: if you’re not sure what you’re seeing, start by finding your landmarks, describe what you’re seeing, and then come up with a list of possible explanations.
In the R flank view, we initially see some liver, and the screen is rapidly taken over by a large, well-circumscribed anechoic structure with evidence of complexity (hyperechoic debris) within its centre. In the L flank view, we see spleen and diaphragm screen left, and then several circular, well-circumscribed, anechoic cystic-like structures, this time without obvious debris within them. Finally, in the midline/peri-umbilical region, we see the screen once again taken up by what looks to be a large, fluid-filled, well-circumscribed structure with some complexity within the anechoic space.
To figure out what’s going on, we can start by ruling things out. This is not ascites, as the fluid collections are well-circumscribed and do not fill geometric spaces. It might be volvulus with bowel obstruction and severe dilation of bowel loops, although we don’t see typical haustra (though these can be lost in severe dilation). This also does not have a typical appearance for tumour or abscess.
The left flank image is probably the most revealing in the end, given the multiple anechoic spaces and position relative to the spleen. This is extremely severe hydronephrosis with a hugely distended bladder (that’s what you’re seeing in midline). POCUS findings led to a CT, which revealed a new diagnosis of metastatic small cell lung cancer. A couple impressive screenshots from the CT are shown below:
This is a transcranial doppler study done from a left transtemporal window (hint: we’re on the TCD preset as indicated on the top right of the screen). In the first clip we can see blood flow within the MCA with colour doppler that appears to have absent diastolic flow – there is a red flash only in systole. This is confirmed with a PW tracing through the vessel, which shows absent diastolic flow (only isolated spikes in systole, followed by a pause). A normal TCD tracing should, of course, demonstrate blood flow in both systole and diastole, as shown below.
As ICP increases and a patient progresses on a spectrum towards cerebral circulatory arrest, diastolic flow is at first blunted, then absent, and eventually reversed, as shown in the diagram below. We can use TCD to help us non-invasively monitor intracranial pathology in a population in whom neurologic examination is often very limited or confounded.
In our patient, TCD revealed pathologic absence of diastolic flow and increased ICP, with decreased CPP (cerebral perfusion pressure). These findings were confirmed with ancillary imaging, and, in conjunction with a consistent clinical exam, a declaration of brain death was made later that day.
The uses of TCD for POCUS providers include monitoring ICP, detecting vasospasm, evaluating for midline shift, and detecting progression towards cerebral circulatory arrest. The figures above are taken from an excellent attached paper from our very own Drs Vincent Lau and Robert Arntfield, for those who are interested in more details.