So a couple years ago I posted a discussion about HPVG around an interesting case, noting how, although traditionally felt to give a poor prognosis, this was extrapolated from early data when it was being detected by conventional radiographs. This simple fact, due to the relatively low sensitivity of radiographs for air in the portal system, meant that these cases had a lot of air, implying a worse underlying process that that detected by POCUS, which is exquisitely sensitive to the detection of air bubbles.
Had another interesting case today which I tweeted. This is an elderly patient, POD#3 for a subtotal colectomy for an obstruction, in the ICU with severe AKI. When scanning his RUQ for fluid tolerance assessment, here is what I see:
Impressive. Frank bubbles coming up the PV, and the liver parenchyma with extensive HPVG. He had some abdominal pain, but he was not in shock (at least not pressor or lactic acidosis shock). My first reflex, since he was in AKI (non pre-renal and non obstructive, and with new evidence of loss of integrity of the bowel mucosa, was to get the surgeons to go take a look.
We agreed to scan first and take it from there. Their view was that, given the absence of frank shock, they were not keen to go back in. I have to say I would have preferred that they did go take a look straightaway, but, as they pointed out, opening someone up is not entirely without drawbacks.
So the scan was equivocal, with some air noted in the mesenteric vessels and possible in the mucosa of a bowel loop. Clinically he had not deteriorated. In the meantime, we had stopped his early enteral feeds and put his NGT on suction.
So I took another POCUS look, figuring that if things looked worse, I might take another charge at the surgical team:
Lo and behold, things had resolved… Biochemically, not much change either, and hemodynamics still fine.
So clearly, at least today, the decision to not operate was the right one. Kudos to the surgical team. And it was a more risky decision than that to operate, since the consequences of missing something correctable are worse than those of an unnecessary “white” exploratory laparotomy…
So what did happen? In all likelihood, the post-op ileus on an ill bowel resulted in some dilation and “mucosal leak.” The NG suction likely decompressed the bowel and allowed the circulation to clear the HPVG.
So the lesson for all POCUS users is that we are using a highly sensitive tool for HPVG, such that this finding is certainly more common than commonly thought, and should be concerning but not necessarily ominous or requiring surgical intervention. Certainly close monitoring and repeat assessments, clinical, POCUS and biochemical are important.
The challenge will be discerning the cases that do need intervention, which is not simple, since waiting for shock or hemodynamic instability would represent a late intervention, likely with poorer outcomes – surgery on vasopressors is a bit suboptimal.
Love to hear comments and others’ experience!
Very interesting. So you’ve presented on this site two cases now where HPVG diagnosed by POCUS turned out to be not so bad. Importantly, in both these cases, the patient didn’t seem toxic.
As you point out, maybe POCUS is too sensitive and not specific for significant disease. With POCUS being still relatively young, I’m guessing there’s a lack of data on this issue.
The last time I saw HPVG, I noted it while Dopplering through a liver window looking at the kidney’s RRI. It was only 5 minutes within my first contact with the patient, so I probably would have gotten the CT scan otherwise, but there was disasterous ischemic bowel with HPVG on CT.
Maybe HPVG on POCUS is a “look further” rather than a “panic button” finding?