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High Scvo2 an sepsis

Discussion in 'Critical Care' started by Hayduke, Sep 28, 2008.

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  1. Hayduke

    Hayduke Member

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    I have a fairly complex guy in the SICU.
    He has hepatic failure from his EtOH career and Hep C. He was admitted for a hernia repair that revealed ~10 cm dead bowel. He had a normal 3 day post op course then crashed in a big way. Intubated, swanned, worked like sepsis etc. His initial picture was shock liver. He was treated and progressed well over the next five days.
    A long term HTN pt., as his insult resolved he became hypertensive. He actually was on nipride for 48 hours. Unable to extubate due to mentation. Encephalopathic vs. hypoxic injury vs. vascular accident vs. hypernatremia.
    He eventually got trached and is a TPN guy.
    I am new on the service and inherited him 3 days ago.
    In the last 48hours he spiked a temp, his UOP decreased, he got started on levophed for maps of 55. Today, blood cxs grew MRSA. I started Abs, steroids, have kept his pressure at goal with fluid and a whisper of norepi. He has had a climbing creatinine with a FENA that indicates pre-renal. The picture looked like classic sepsis, but this guy's evolution has me considering hepato-renal in the setting of infection.
    I'm an EM resident that felt foolish considering re-swanning this pt. after his other line got pulled just 5 days prior.
    I drew a scvo2 off his cvc and it came back 84%. His Hgb is 7.5 and he has a massive O2 requirement. Bucks the vent at any bilevel and barely tolerates APRV at 30mm with a FiO2 of 90%. (yep I said 90)

    I recognize this is a single data point in a big picture, but I believe I am misunderstanding the pathophys. of the scvo2 and could use some help.

    My questions are-
    Why am I seeing such a high percentage when this guy is looking sicker?
    How can I use Scvo2 in the long term maintenace of the septic pt? I am comfortable with EGDT and the use of the number on presentation and early mgt., but what about when all goals are met and I need something to guide therapy?
    Any suggestions for articles, or chapters are welcome.
    Thanks.
  2. HomerSD

    HomerSD

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    While a decrease in the SVO2 is associated with a drop in CO, this is not an absolute relationship. In certain conditions such as cirrhosis, shunt, or cyanide posioning, the SVO2 can still be above 80%. The SVO2 can still be above 80% in sepsis as well, requiring clinical context for interpretation.

    You didn't mention a lactate; was it elevated in this patient? I agree with you that this patient sounds septic, although it would be hard to argue this with a normal SVO2 and normal lactate.


    See:
    Question 16 on an ATS quiz on PA cathethers and
    A short article on SVO2 and high cardiac output
  3. souljah1

    souljah1 Attending

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    A high SvO2 is common in cirrhosis b/c of peripheral vasodilation and a compensatory increase in cardiac output. A high lactate is also quite common in cirrhosis b/c conversion of lactate to pyruvate occurs in the liver and that capacity is limited in ESLD.

    Given the Pt's fever, tachycardia and postive blood cultures with MRSA along with his hypotension and end organ damage - you make a great case for severe septic shock. The SvO2 in the setting of cirrhosis should not be your main variable in your decisoin making tree. Ensure he is adequately volume resuscitated (what is his CVP?) and that his MAP is over 60-65. Did his blood cultures clear? Echo? Does he have ascites? tappend and sent for cx? Does he have more dead bowel

    What does his CXR show? That is quite a high FiO2. Is he overresuscitated? Does he have ARDS from sepsis? Could he have endocarditis and septic emboli? Could he have been profoundly encephalopathic and aspirated? If he does have ARDS, his cirrhosis makes it even more of a morbid situation. Did he have preexisting hypoxia? Any hepatopulmonary syndrome or portopulmonary hypertension? If PA pressures were thought to be elevated, he may benefit from a sprinkle of Flolan...

    The other thing that I'm curious about is his MELD score at the time of surgery. Surgery is associated with morbitity and mortality in ESLD/cirrhosis and the MELD score is linearly associated with increased mortality.

    To diagnosis hepatorenal (type 1) you need to double your creatinine to greater than 2.5 in less than two weeks, have no improvement in your creatinine after 1.5L bolus, have a negative renal US and have a UNa less than 10 with no evidence of nephritis or nephrosis. You need to provide more information, but infection is the most common cause of HRS in cirrhotics.

    Interesting case.
  4. proman

    proman Member Moderator

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    Don't forget that in sepsis you have adequate delivery of oxygen but inadequate utilization, likely due to mitochondrial dysfunction. One reason why lactate and other surrogates of end organ perfusion should be part of the picture.

    When were antibiotics started? Ideally, broad spectrum coverage should be initiated as soon as possible, and tailored based on cultures. The way I read your post, it seems that abx weren't started for 48 hours (which I doubt).
  5. KGUNNER1

    KGUNNER1 Senior Member

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    Proman, not necessarily. This was the "classical" view for patients that had been in the ICU for days before they were enrolled in the trials that initially described their physiology (Gattinoni, Hayes, etc...)http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
    http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

    "Early" severe sepsis and septic shock is commonly one that is hypodynamic with components of both hypovolemia AND myocardial depression http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=153435.

    As you know, both of these will decrease oxygen delivery by affecting the cardiac output, and if it is profound enough, global tissue hypoxia will follow reflected by the low SvO2 and elevated lactate (as seen in the EGDT paper by Rivers) http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

    In later stages (assumed) or in completely different presentations for unknown reasons, you may see the classic picture of cytopathic hypoxia as you described. http://www.ncbi.nlm.nih.gov/pubmed/11219231

    KG
  6. proman

    proman Member Moderator

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    I think that's where EGDT comes into play. To generalize the studies above, restoring hemodynamics with volume, pressors/inotropes, and transfusions to a normal level helps, but supranormal levels has no impact. There is evidence that norepinephrine improves mitochondrial respiration PubID: 18625036. There is also evidence that TNF-a directly inhibits cytochrome c PubID: 18534980.

    I imagine that impaired cellular respiration is central to the pathophysiology of sepsis.
  7. DarthNeurology

    DarthNeurology

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    Basically, SCVO2 can be increased in severe (late) sepsis. From Marino (Third Edition 2007),

    ". . . the tissue PO2 is increased in the septic patients, indicating that tissue oxygenation is not impaired in sepsis. Similar results have been reported in the bowel mucosa of animals injected with endotoxin (13). Despite the improved tisseu oxygenation, aerobic metabolism is challenged in sepsis because there is apparent defect in oxygen utilization in mitochondria (14). Nevertheless, because tissue oxygen levels are not impaired in sepsis, therapy designed to improve tissue oxygenation does not seem warranted in patients with severe sepsis or septic shock."

    In early sepsis the SCVO2 can be decreased secondary to increased tissue demands for oxygen and it helps to know if enough oxygen is given. Your patient is ventillated and getting enough oxygen, but likely has severe sepsis and it is thought that mitochondria are basically poisoned by endotoxin such that cells are oxygen starved but can't use the oxygen, so the underlying sepsis must be addressed. Actually, a high SCVO2 is very concerning compared to a normal SCVO2, it means the body is "rejecting oxygen" or there is decreased oxygen consumption. The 2008 surviving sepsis guidelines recommend that mixed venous oxygen saturation greater than 65 and central venous oxygen saturation greater than 70.

    http://www.survivingsepsis.org


    A low SCVO2 means that the body is oxygen starved in a way, such that supply is not meeting consumption and the body is trying to suck up as much oxygen as it can from the blood so venous blood comes back to the heart extra starved of oxygen. This could be secondary to various cardiac and pulmonary causes.

    Usually with hepatorenal syndrome a patient has ascites and portalhypertension (which this patient may or may not have had) in association with chronic or acute hepatic failure. But, really I think that since we are pretty sure that the patient has septic shock/severe sepsis that much more likely this patient has renal failure as part of a multiorgan failure secondary to severe sepsis/septic shock.

    This patient's shock liver, which usually occurs in the setting of chronic liver failure (no surprises here) is likely secondary to septic shock, or perhaps even a hypotensive episode during surgery could have contributed as well. 50% of patients with shock liver also develope a hepatopulmonary syndrome which produces pulmonary dilatation and effectively shunts deoxygenated blood around the lungs. This can be diagnosed by cardiac echo with bubbles. I don't know if this is feasible in this patient. Mostly shock liver is treated supportively as the underlying etiology of the patient's shock liver, i.e. etiology of hypotension (rarely hypoxemia) causes the patient to be gravely ill, not necessarily the shock liver. However, somatostatin may have small efficacy and could possibly be tried cautiously in this patient, as it may act to decrease pulmonary vasodilatation in hepatopulmonary syndrome.

    However, this patient may also have an ARDS like picture secondary to sepsis.

    I would:

    1. Stabilize the blood pressure. Is a MAP of 60 a reasonable goal? Perhaps for a normal person, but this patient is a known hypertensive and when the MAP fell below 75 to 80 this should have been a warning sign. I feel it was a big mistake to start a drip to treat hypertension here, unless it was well above the patient's baseline, as this lowering could have been accomplished more slowly as an outpatient. Is this patient third spacing fluid? I would consider increasing fluids. If you are thinking hepatorenal, then colloid, i.e. albumin might be warranted. I would consult renal about this.

    2. Where is the source of infection? Post-op infection? I would call the surgery team to re-evaluate for possible post-op infection or complication, i.e. did they perhaps miss some dead bowel? The patient is not in any condition to return to the OR, but I would plan for this at some point and have surgery re-evaluate, if not already. ID and pulmonary have to see this patient daily. I would pan culture everything every 24 hours, i.e. blood culture, sputum, urin, surgical wound site if possible. And I would consider expanding the spectrum of coverage of antibiotics and would talk with ID directly as soon as possible.

    3. Anemia, i.e. hemoglobin around 7, . . . if he has cardiac issues then 10 might be a more reasonable goal, I would transfuse very slowly. Why is he anemic? Is he bleeding out from his surgery? How much of a drop over how long? If any imaging procedure is done an abdominal CT might be most helpful.

    4. Encephalopathy. The etiology is on the backburner right now, no doubt neuro wants a head CT which might not be feasible now, and probably not a head MRI, but an EEG could be done as well as a neuroeval, but don't expect a lot of answers. I would guess encephalopathy secondary to sepsis/multiorgan failure vs. secondary to shock liver vs. secondary to an hypoxic event.

    Guidelines:

    In terms of guidelines I recommend printing/reading the guidelines for medical professionals on http://www.survivingsepsis.org Basically, this patient has not met guidelines, i.e. MAP > or equal to 65, and possibly his urine output is below guidelines, . . . either the patient will survive this septic shock or they will not. It all depends on how meticulous and rapid the treatment is. You could also consider calculating the APACHE score and consider giving APC which is in the guidelines, if appropriate. Remember that things change quickly in the ICU and this patient is very sick, . . . likely when the guidelines are met the patient will be a lot better.

    Say the central venous oxygen saturation falls below 70%. Guidelines are that you can use a combination of blood transfusions, ionotropic support etc . . . to get that central venous saturation above 70%. Beyond the guidelines are patient specific things like hunting down consults and keeping on top of supportive care which is paramount at this stage of the game.
    Last edited: Oct 1, 2008
  8. souljah1

    souljah1 Attending

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    While a high SvO2 can represent severe sepsis with impaired oxygenation consumption, this case is confounded by the presence of a cirrhotic liver. It is quite normal to have a very high cardiac output in cirrhotics, which will drive up the SvO2. Regardless, it doesn't change your management in this case.

    His source appears to have been stated above -> MRSA bacteremia - a common nosocomial bug especially in trached individuals. MRSA bacteremia in individuals with indwelling central venous catheters and ventilated patients can be very morbid. What's this guys CXR look like? New murmur? Neuro exam the same? Dopplered for clots? Did he clear his cultures?

    The more difficult question based on this original posters description is in regards to the severity of his liver disease. If this guy has ETOH/HCV with decompensated cirrhosis and goes to the OR for a bowel resection, he has a SIGNIFICANT mortality risk with this that is largely based on his MELD score: Gastroenterology, Volume 132, Issue 4, April 2007, Pages 1261-1269

    If he's a cirrhotic, he has the recipe for post-op decompensation including the development of ascites w/ possible SBP, hepatic encephalopathy, hepatorenal syndrome and worsening V/Q mismath from HPS. If he's not really a cirrhotic and just has a strong h/o EtOH and HCV, then all the thoughts about post op liver dysfunction are of less value.

    For his anemia, any GI bleeds? NGL negative for coffee grounds? If coagulopathic, peripheral smear negative for schistocytes? Right now, I would not transfuse him.

    There isn't much data for stress dose steroids unless he's refractory to a couple pressors and you don't have much to lose

    A lot of people are throwing around EGDT algorhythms in a patient who has been hospitalized for weeks and who now looks like he may be receiving "Late goal directed therapy". The Rivers paper is notorious for extrapolation.

    I would:
    1. Volume resuscitate him and, in the absence of TR, follow his CVP
    2. Keep MAPS
    3. Fluid bolus, check UA, renal US to eval for HRS if he's cirrhotic
    4. Put an US on his belly and tap him if he has ascites (I've seen MRSA SBP a few times)
    5. Follow surveillance cultures while on antibiotics and if that MRSA doesn't clear in the next culture I'd aggressively look for seeding -> TTE w/ bubble, US extremities, follow neuro exam closely
    6. Sort out the process in the lungs. If he really has an FiO2 of 90% w/ adequate PEEP and is "bucking the vent", you need to try alternative modes of mechanical ventilation. If his CXR is c/f ARDS 2/2 ESLD w/ sepsis or TRALI or whatever, you need to micromanage his vent and if he's still hypoxic without the ability to ween his FiO2 it'll get interesting.
  9. bigtuna

    bigtuna Member

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    This is an interesting and useful discussion. I hope that this forum can become more active in the future.

    I would like to point out that it seems that EGDT has lead to an overreliance on CVP measurement as a predictor of hemodynamic response to volume loading.

    This is exactly the type of patient whose CVP may give you misleading information. As he has a PA catheter in place, it would be more useful to give a fluid bolus and see if this improves CO.

    See the following metaanalysis about the use of CVP in predicting hemodynamic response.

    Chest. 2008; 134:172-178
  10. needadvice

    needadvice Member

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    a couple observations...
    i have found scvo2 and svo2s to be high in early sepsis or even early infection without hemodynamic compromise. in fact, as infection is treated with antibiotics, i have seen the scvo2 fall to normal levels.

    remember, the scvo2 is a great trend monitor but is not a reliable surrogate for a svo2. multiple studies have proven this. in addition, it only represents the oxygen saturation of perfused tissues. if you're dude is not perfusing certain organs, the scvo2 doesn't capture those areas of regional compromise.

    you could get an echo to see if the heart is hyperdynamic, if its not, you dont have to wonder whether or not this is due to cirrhosis.

    if you truly are on 90%, i would guess your arterial saturation stinks, so in the context the scvo2 of 80% is that much worse. you aren't extracting!

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