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.
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.
