So I admitted a patient to the ICU yesterday from the ED. He’s an 80-something gentleman from a nursing home with an indwelling catheter, and presented with stupor, hypotension, fever, leukocytosis and clearly infected urine. His labwork showed a lactate of 5.3, a double-normal creatinine and, after 3 liters or so of crystalloid, he was started on norpeinephrine and hence came to the ICU. His extremities were fairly warm, and his cerebral saturation was 62%.
Before seeing the POCUS info, however, consider a clearly septic patient with AKI and elevated lactate. He did get 3 liters of fluids, but i’ve seen these patients get more fluids, whether for hemodynamics, lactate, AKI or any combination of the aforementioned.
Below is the clip, a quick POCUS sequence going from IVC (with hepatic vein flows), subxiphoid cardiac views, both lung views.
So here, we see a plethoric and fixed IVC (sorry I didn’t include the short axis but it was round and full, so in this case the LAX is reliable) with biphasic hepatic flow. Cardiac views show normal ratios and a poor LV function. Chest views show bilateral effusions and consolidations.
So what did I do?
- stopped fluids (I do not believe in routine maintenance fluids any more than in maintenance antibiotics or vasopressors).
- gave lasix (given that he is on the flat part of FS curve, I was unconcerned with some diuresis decreasing his preload, vasopressors and lactate notwithstanding, and with the goal to decongest his kidneys, likely suffering from congestive insult on top of the septic one).
- did not try to chase his lactate with increasing cardiac output (lactate being a great alarm bell and prognosticator, but little else, and because he was worm and with a decent cerebral saturation, I did not feel that there was a major cardiogenic component to his shock).
So what happened?
This morning, after a negative balance of 1,500 cc in 24 hours, his levophed dose has dropped by half, his lactate is normal and his creatinine is decreasing. A decade ago, I would have chased down the last ounce of volume responsiveness with fluids, aggressively trying to drive down the lactate and creatinine, and maybe, 24 hours later, he would have developed “ARDS” because he was “so sick.” 😉
Just to clarify- hepatic flow is normally biphasic right? In normal individuals even there can be backwards flow towards end systole.
Absolutely, you have the small A wave, but what I am referring to is a large retrograde S wave which occurs with significant TR, which of course could be due to many causes. Good question, i should actually post a nuts and bolts on venous flow. Coming un in the next weeks!