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Specializes in CCRN-CMC-CSC CVRN II-BC TNCC. Has 13 years experience.

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!

Caffeine Bolus, ADN, RN, EMT-P

Specializes in Critical Care, Pre-Hospital. Has 4 years experience.

This sounds like textbook onset septic shock. PE would be really low on my differential here; is there a reason you're looking for that as a problem outside of respiratory distress? Fever, hypotension and a few days post-op from trauma kinda paint the picture right there.

"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?." Heart failure is at play here, but probably 2/2 shock state decompensation. I assume some CXRs were done...did it look pulmonary edema wet? Is there other evidence of right heart failure...do you have filling pressure readings, Svo2 numbers? Or, more likely, did the CXR look more like diffuse opacitices suggesting endothelial insult 2/2 sepsis? ARDS would be an almost expected outcome in somebody that sick.

The use of pressors to the extent that this patient had could feasibly have been the root of the persistent elevated lactate levels; thinking about the damage done to microcirculation and probably end organ damage with that level of pressor use, it's not surprising to see the biomarkers of anaerobic metabolism that high. There's evidence that lactate levels aren't as useful in septic shock patients on pressors for that very reason.

I also question the use of albumin vs LR (or, heaven forbid, NSS) for resuscitation. Physicians sometimes love to jump right to pressors, but without any fluid in the pipes, squeezing them harder won't help much. If this patient only got 2L of colloid through all this mess, there were some balls dropped there.

Thanks for the opportunity to chime in on your case!

Edited by Caffeine Bolus

pbcerty, BSN, RN

Specializes in CCRN-CMC-CSC CVRN II-BC TNCC. Has 13 years experience.

My argument also is that I think they cannot rule out PE here also just because the patient is showing signs of septic shock. There were no obvious signs of infection or intra-abdominal abscess on CT if I remember, but noted to have extravasation/bleeding of L kidney that’s why Nephrectomy was performed <24 hrs prior. Fever can be a sign of PE also per PIOPED and PISAPED study. And a bedside TTE using bedside ultrasound not the formal TTE has a lot of limitations with imaging while looking for RV strain, RV systolic dysfunction and dilation and doing it for 5 mins is not convincing. With septic shock, heart failure/cardiomyopathy can happen and with PE respectively. But most patients in septic shock you won’t go that over board with pressors including meth blue with MAP’s barely at 60. But with PE submassive to massive you can go to severe R heart failure and die if not treated. CXR is acceptable no pneumo maybe some vascular congestion. No swan only CVC and a-line; CVP 24-28, SVV range from 12-20 but both unreliable. Severe ARDS just by looking at his FiO2:paO2 ratio of leas than 100. Lactate is important marker for mortality but the use of pressors specifically Epinephrines insane dose I believe is actually the most likely reason why the lactate is so high including hypoperfusion to organs. I forgot to mention 2-3 Liters of LR was also given including the enormous amount of fluid from the pressors and bicarb drip every hour. The use of albumin also has benefit in sepsis based on SAFE, Shock-2, Shock-3 , ALBIOS studies but in my experience LR and Albumin is acceptable for fluid resuscitation.

I just couldn’t understand and it is so unclear to me why a 23 year old healthy male would deteriorate that quick. I wished we placed him on ECMO to buy him more time while we figure out whats going on. I am still so sad and confused about what happened.

Thank you for the input caffeine bolus I really appreciate it.

Why was he not being fluid resuscitated? Just a question. We normally don’t start pressors on these people from the get go. A, he’s a trauma, and B he had an abdominal surgery. These people needs tons of fluid. Did you guys already try that?

It's a little difficult to follow some parts of your post, but it sounds like he was getting huge amounts of volume, plus huge amounts of pressors and still looked awful? Vent settings show hellacious ARDs, no pneumo and I presume crappy pulmonary compliance?

Was abdominal compartment syndrome considered? Was it considered again once or twice? Given his history, massive volume resuscitation and rapid collapse, this seems highly probable.

Edited by frozenmedic

pbcerty, BSN, RN

Specializes in CCRN-CMC-CSC CVRN II-BC TNCC. Has 13 years experience.

It could be abdominal compartment syndrome or an aggressive form of necrotizing fascitis.

Thank you guys!

Do you have any group to join to share knowledge and experience aside from allnurses?