Had a Pt today who had a colectomy due to intestinal volvulus, was in surgery/PACU from about 1115, 1130, to about 3, 330 pm. Got back to my floor at 3:30, BP about 106/50, pulse 115, after he'd been SBP's 115-120, pulse 80's, all through surgery and PACU - by 5:30 pm, BP at 70/40, pulse 120, and we placed him in ICU with suspicion of septic shock-
There were a couple of other issues with this Pt (1) his lungs sounded terribly rhonchi-y, his external breathing was wet-sounding and since the PACU nurse stated, "He just started having that wet breathing now in the room, his respirations were normal-sounding before, " I thought maybe he'd aspirated during transfer or when we laid him flat briefly while turning him, and so I was thinking that high pulse was maybe 2' aspiration) - also, 2) he was poorly arousable, but he'd been drowsy before surgery, and a lot of post-op Pts are poorly arousable, and he'd gotten a lot of pain meds. Really, my main concern was his wet-sounding, labored breathing, and the continued high pulse (when we could pick up on his O2 Sat, it was 99, 100, although it was difficult, because he kept trembling/twitching his arms; was difficult even to get an O2 sat on his earlobe); - and I worked for a couple of hours, assessing, debating, and calling RT and MD, working with solumedrol, CXR (normal), albuterol, atrovent, tropi (normal), tele (sinus tach, 115 - 120's), ABG (showed partially compensated metabolic acidosis, - pH 7.34 or 7.35, CO2 25, O2 99, HCO3 15 - which flummoxed me, because I kept thinking "respiratory, respiratory" not metabolic - i.e., shock, and I couldn't figure out what would be causing a metabolic acidosis - I thought maybe it was some electrolyte imbalance after abdominal surgery), before calling a rapid response team when his BP dropped.
-but my question is, have you seen septic shock develop so quickly, and so quickly after surgery?? I guess maybe the germs were already there in his bloodstream pre-op, but, still, why'd he drop out like that on me, within 2 hours? (HGB did come down from 9.6 pre-op to 8 post-op, but colostomy dressing had only mild drainage, and this Pt had had multiple transfusions during his month-long stay, and I'm not seeing a 1.6 point drop in HGB causing that kind of low BP, so I guess everyone is right about the cause being septic shock - the MD and ICU nurses kept saying "sepsis") But I didn't know it could happen so quickly! Really, I would have thought that the only type of shock that could present so quickly would be from loss of fluid/hypovolemic, not septic. (And why did his pulse only spike when he hit my floor? From 80's to 115 within 15 minutes? I still think that that rapid pulse change there may have been 2' aspiration - he couldn't have just gotten compensatory tachycardia 2' sepsis in the duration of the elevator ride.)
Appreciate your help and wisdom.
Feb 23, '12
I would be interested in seeing his I&O intraop and in the PACU, as well as what he received in the way of pressors before getting to you. My guess is that he was receiving fairly aggressive fluid resuscitation and then was switched to his floor maintenance rate shortly before transfer. This would account partially for the timing of the onset of his symptoms, along with the typical progression of septic shock.
It can certainly happen that quickly. That is why early recognition of sepsis and aggressive treatment is so essential. The body can compensate pretty well for a while.
Given the ABG and your description of his breathing my bet is on septic shock. His breathing was a response to what was going on, not the cause of his problem. Textbook compensated metabolic acidosis. Sounds like this dude wasn't particularly healthy if he's been in the hospital for a month. I imagine his bowel was probably in pretty rough shape and a lot of toxins were released into his system. Remember that this wasn't an elective case where he went into the OR with a happy, relatively healthy bowel. He went in with a $h!%storm of bacteria and nastiness brewing in the affected area. These major bowel problem patients are at pretty high risk pre, intra, and post op.
I still think that that rapid pulse change there may have been 2' aspiration - he couldn't have just gotten compensatory tachycardia 2' sepsis in the duration of the elevator ride.)
You'd be surprised. Plus there's a little more to it than the elevator ride--the PACU nurse has to unhook the patient, prepare him for transfer, etc. Usually it's like 5-15 minutes off the monitor before the patient is settled into the room in my experience.
Honestly, I feel like the PACU RN dropped the ball a bit by not taking a moment to give you advice re: the tachycardia and probable causes and solutions. It's our job to be the experts on immediate post-op patient management. When I see BP drop and HR rise I get a little worried about my patient and take a hard look to see if there's something going on that I need to correct. I don't like dumping an iffy patient on some poor nurse without at least offering my honest SBAR including things to watch for. For example, if the patient is tachycardic but otherwise stable I would discuss possible reasons (including which findings support them or rule them out), what I would watch for, and my advice on how/when to intervene. In my experience the AR part of SBAR is the least addressed while it's the most important.
Feb 23, '12
Remember the old adage: everyone is stable, until they're not.
Feb 23, '12
Chances are, your patient was well into SIRS (systemic inflammatory response syndrome) prior to surgery due to the intestinal problem. This does not require any infection - can be triggered by any type of physical 'insult', including severe allergy or trauma.
If you add the effects of general anesthesia, plus the systemic introduction of bacteria via abdominal surgery, the cascade into frank sepsis can be very rapid.
One of the initial hallmarks of SIRS/sepsis is metabolic acidosis - resulting from lactic acidosis d/t out of control inflammatory response. This is exacerbated with infection, as micro-emboli cause dramatic decrease in peripheral circulation & the left shift (oxyhemoglobin dissassociation curve) which creates even more oxygen debt especially to vital organs. Initial response is tachypnea to blow off CO2.
Wet lungs d/t leaky capillaries (SIRS & sepsis) make oxygenation even worse.... and the drain circling begins.
Have you begun using a MEWS scoring system as part of your monitoring criteria? If not, you should begin to do so. It's basically a "Glasgow score" for sepsis - very nice way to set up your early warning system for sepsis.
Feb 23, '12
Yup, beware of sepsis. Our hospital is always campaining about sepsis. Part of our assesments every shift/prn are charting on sepsis screens. I work in ICU and rapid response so I guess I always have sepsis on my mind and am screening the patients on the floors for it. Its can happen fast. Your patients HR may have been lower in PACU and OR because of sedation, then when he was more alert and transfered, maybe it increased. The other posters said very good things so I wont repeat them. If if was you, when they did that ABG, did they do a lactate? If its elevated and it likely was then I would be really concerned. Despite have relatively OK vitals, apart from the HR, what did his color look like, how strong were his peripheral pulses, motteling, also his urine out put, thats something to always pay attention to on all your patients and I find often on a regular med/surg floor, the nurses often overlook it or dont really understand the importance of it.
Like someone else said, this patient is showing SIRS criteria and that ABG is concerning even though its somewhat compensated. Because of the SIRS, I would have wanted a CBC, lactate, coags, LFT's blood cultures. They would have likely needed fluids. With sepsis/severe sepsis they become extremely vasodilated and ususally needs multiple liters of fluids. For our sepsis bundle its 20ml/kg infused as fast as possible, 20 min if it will run in that fast. The key with sepsis is early recognition so you can start early resusitation. Once sepsis becomes severe, the risk of death increases dramatically.
Sepsis: Emergency - YouTube
a good video illustrating how fast it can overcome a patient, even if they are young and healthy.
The one patient I remember very well, was he had I think a cough, went to the ER, within less than 8 hours of him being normal, he was in our ICU in full blown sever sepsis, DIC, started on CRRT, maxed pressors, completely purple. He died in under 8 hrs.
So in a word, YES, it can happen fast. Educated yourself more on the mechansim of it, it pretty interesting (or im just a dork)
Feb 23, '12
I'm curious as to how the procedure was done, was it laproscopic or was he open for the procedure? Any complications during surgery, such as hypotensive intra op or spilling of gi contents into the abdomen? I&O's are key and also if they needed any hemodynamic support intraop.
Feb 23, '12
I love the video.. Thanks for sharing..
Feb 23, '12
Sepsis, Sepsis Syndrome, and Septic Shock - YouTube
At 3:40 they had a good explanation of how SIRS occur..
Feb 23, '12
THanks for your responses - it's late, so I'll review the links later, thank you - but I did go check out the Pt in ICU this morning, half-expecting him to have passed away, and, thankfully, he was awake, alert, oriented, pleasant, with NORMAL BP and pulse, O2 sat fine - wow, the wonders of levophed and fluid resuscitation! They gave him antibiotics, too.
Btw, in ICU, they had done a lactate, and it was elevated - 6 or something.
Will review this more in-depth tomorrow. Thanks for the input.
Feb 24, '12
Yup, a lactate of 6, yikes! When is see something like that, I know we gotta start things up ASAP. Glad he was doing better!
Feb 24, '12
Great advice, I concur..
. Just kidding. Really famiiarize yourself with sepsis as it can happen VERY fast.......great pick up and "gut feeling" on your part. Well done.
Feb 24, '12
SIRS can develop quite rapidly in some circumstances.
Admittedly my patients are hemo/onc and generally immunocompromised, but have seen where merely flushing a central line/access has sent a pt into decompensation within 15-30 minutes - the line was evidently infected.
Anything that can cause sudden severe cytokine release can cause rapid decompensation.