Hi! I am a SICU/CVICU nurse in TX.
Case Review: 23 yo GSW to abdomen s/p nephrectomy, bowel resection, GI procedures. Post-op day 3 or 4 patient develop hypotension MAP 40’s, baseline HR 130-140’s Fever 102 started non-rebreather at 100% with saturation at 93%. He was intubated with pO2 95 and pressor requirements increasing and at enormous doses. Epinephrine 40 mcg/min, Levophed 70 mcg/min, Vasopressin 0.04 units/hr and even gave Methylene blue bolus 2 mcg/kg and a drip. Urine output is blue 20 ml for 12 hours. 5% Albumin total of 2L given including infusions via drip. Resident and surgeon thinks it’s sepsis of unknown cause. Just wondering if it is PE segmental turned into a full PE death after 12 hours. MAP has been absurd between 50-65 but lactate downtrend from 16 to14 then back up. Attending and resident decided not to start SLED (dialysis) without ultrafiltration because of MAP and give sodium bicarb pushes and drip (pH never below 7.2). Patient saturation most of the time is between 94-100% until the last 2 hours before death. Bedside TTE by resident said that LV appears systolic function OK good? and RV is not dilated. No heparin drip started because no confirmation of PE and patient is too unstable to go to VQ scan.
My question is does MAP below 60 accompanied by hyperlactenemia and oxygenation pO2 >95 with saturation 94-100% on this case due to sepsis or PE with RV strain? or heart failure? anything?.
I don't know if the hyperlactatenemia due to sepsis from decrease O2 in the microcirculation or most likely due to aerobic glycolysis in the skeletal muscle by epinephrine? or it's a good thing as metabolic fuel for the heart.
I know its too much but I always brainstorm with all this type of cases on what else could we have done differently. I just wonder how a 23 yo patient die if his injuries have been repaired.
Thank you and I would appreciate any feedback!
