Case

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Impromptu

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Case

A 76 year old female with NASH is scheduled for a TIPS procedure. NASH has resulted in endstage liver disease with some associated chronic kidney disease. She is currently undergoing semi-weekly percutaneous pericentesis. She is unable to take diuretics because of low blood pressures. She has a strong heart and walked 2 miles to the hospital that morning for the procedure. Today's EKG shows possible left anterior fascicle block. Echo 1 month prior 70% EF, mild MR/TR. No tobacco/alcohol/drugs.

BP 86/62. HR 93. SpO2 100% on RA. These are her normal vitals.

Physical shows grossly distended belly with fluid wave. No edema in legs. No jaundice. Lungs are clear. Heart sounds normal. Airway looks decent. She is a very pleasant lady with great family there to support her.

Today's Hgb 12.5, platelets 150, INR 1.2, Na 130. Creatinine 1.3.

Is there anything else you would like to know?

What is your plan? What would you be watching out for.

(There are several more parts to this story)

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old ekg's? any new cardiac symptoms?

the rest of the metabolic panel?

last pericentesis? ideally this procedure would be done a cuppla days after her last pericentesis.

otherwise she gets a pregnant lady induction - bicitra, ranitidine, good preO2, then RSI with cricoid (etomidate, sux (if K is ok), tube). induce in reverse T at least 30 deg with suction handy.

start snake oil gtt prior to induction (neo, ephedrine). cycle cuff q2min. sevo, whiffs of alfentanil to keep her still, extubate wide awake again in reverse T at least 30 deg.

curious her legs aren't swollen.

the fact that she's a nice person with a great family is an independent prognosticator for disaster, I would roll on my toes.
 
obviously shes vasoplegic and that wont get better after induction. i would hate to break out octreotide for this radiologic procedure but i dont think your first line vasoactives will be much help. have octreotide in line, norepi available. very possible LAFB is ominous, eval of heart is clouded by hyperdynamic circulation, high EF secondary to almost no afterload. pulmonary hypertension likely, could be severe, although her presumed METS make that less likely. i agree with the induction plan, although would probably use remifentanil, possibly nitrous/remi with no/minimal halogenated volatile anesthetic.

would love to know how much volume was taken off during last PC. high risk for acute hepatorenal syndrome without anesthesia, probably much higher with.
 
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very unlikely i know but i wonder about intraabdominal process such as bleed/abscess secondary to multiple interventions. def a zebra but needles are poky things...
 
I thought TIPS were mostly done by IR under local. Why involve us on this one?

Procedure can take a long time, patients get fidgety and need to be still, may be encepholopathic, radiologists and nurses probably don't like sedating patients who may be an aspiration risk.
 
Head up some, ketamine/roc/tube, whatever flavor of RSI you prefer. Use etomidate if you want, I prefer K with maybe a whiff of propofol. If she walked to the hospital, she's not living on the edge of her sypmathetic drive, and you won't worry about bagging her adrenals.

Doubt significant pulm htn with mild TR, even moreso having walked 2 miles to hospital for procedure.

Would probably place a-line, would probably do so awake to get a room air gas and to monitor vitals during induction.

Have stuff to increase SVR around, in order of use neo->vasopressin->norepi.

Agree that nice lady with nice family is a bad prognostic sign. Case seems fairly straightforward so far, wonder what trouble lurks around the corner...
 
No prior EKG available in our hospital to compare. No new cardiac symptoms. Rest of the metabolic panel is pretty normal, though chloride is low at 96. Last pericentesis was done a couple days before at a different facility, not sure how much fluid was removed.

IR doc thought this might be a tricky one that could last longer than normal, so he wanted us involved.

Case continued.

18 G IV. Premedicated with reglan and pepcid. RSI with etomidate and sux. Placed A-line. Intra-op rocuronium, sevoflurane at 0.3-0.4 MAC, and 1 mg of midazolam.

Pt starts out stable, HR around 100-110. BP needs occasional 50 mcg phenylephrine to stay near baseline. We open up the fluids because she is likely intravascularly depleted.

IR cannot get TIPS placed on first attempt, so will now do pericentesis to see if that makes the angles a little better. He pulls off 4 Liters. The last bottle has a slight pinkish tinge to it, but nothing overtly bloody. Belly is now much softer. We run some albumin because large volume pericentesis is notorious for dropping blood pressure. Give albumin 500 mL X3.

Except for initial 150 mL, urine has been about 30 mL/hour.

Case takes a little longer than anticipated, but IR is able to successfully place their shunt. By this time I am giving 100-200 mcg phenylephrine every 3-4 minutes. I consider a phenylephrine drip, but they are done, so figure that waking the pt up and getting off the volatile anesthetics will help with blood pressure more.

With 2 strong ulnar twitches we give full reversal. Extubate when pt appears ready. Pt is communicating with us for several minutes, but blood pressures continue to decline (SBP 60s-70s) and start becoming refractory to phenylephrine. Soon the patient is becoming more unresponsive. Pupils are normal and reactive. Lungs still sound clear. We start another 500 mL albumin (2000 mL total) and call for the blood that had been typed and crossed to be brought to the room.

We decide to reintubate the patient. Send an ABG with lytes, PT/PTT/fibrinogen, and CBC. The first blood sample I drew from the A-line looked diluted, like I hadn't fully drawn off all the saline from my pressure tubing, so I draw back a second sample and send it to the lab.

Belly still feels soft. EKG shows no ST segment or T-wave changes. Now tachycardic in 110s-120s. SpO2 100%.

Thoughts? (more to follow)
 
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Most likely some sort of vascular injury from the TIPS procedure itself based on the timing of events. Less likely hepatorenal syndrome, pericentesis injury(how radiology could f@ck that up I don't know), intraoperative MI, PE etc etc
 
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Vascular injury highly suspicious, maybe they bagged an epigastric artery during the paracentesis. If TEE available, would be useful to confirm inadequate filling vs less likely further drop in SVR vs even less likely PE as evidenced by R heart strain. Work on getting bigger access as well, probably would throw a cordis in there while waiting on labs. Would think about get that levophed running to temporize things while you get your resuscitation going and search for the cause of injury. Wouldn't give a ton of fluid while you search for a cause, would wait for the blood you sent for and would work on getting some FFP as well.

Would start the process of finding a surgeon to take pt for ex-lap and getting an OR ready. Hope for the best and plan for the worst.
 
I would make sure radiology attempted some sort of embolization before opening her belly because you're looking at a blood bath if you do, aka liver transplant type bleeding.
 
they took off 4L - her belly's a big floppy bag with a 6-8L capacity. her abdomen's gonna feel benign/soft until she has her whole life blood in there. wouldn't put much stock in belly exam.

PE, MI, post-pericentesis hypotension are in the differential.

but, with pinkish stuff coming out of her belly, dilute looking abg, tachycardia, and hypotension, the money's on exsanguination. likely a venous injury, and given the volume of ascites this lady has in her belly not surprising that the fluid only looks pink.

you should get your crit back in 1 minute or less. in that 1 minute, open the fluids, get your blood and order FFP, platelets. agree with starting norepi gtt to temporize things. you need more than that 18 - place 14 or RIC while calling surgeon friend.

crit should be back by now - if it looks visibly dilute it's gonna be less than 20 - unleash the transfusion that should be locked and loaded by now. get thee to the OR.
 
Where did I leave off? Oh yes. Much of the following happens very quickly and my order may be off slightly. We had other attendings and residents assisting us for most of the rest of our care for her.

Get blood going, call blood bank for more blood and some fresh frozen plasma. Place another IV. Get norepinephrine gtt. Place cordis in IJ.

ABG comes back with pH of 7.11, BE -11, bicarb around 12, and hemoglobin of 3.0. I think that is unbelievable, so send another ABG (which subsequently confirms low hemoglobin). In the meantime the IR doc pulls in ultrasound, sees some fluid in the abdomen, but does not think the volume he is able to see would cause such a drop in hemoglobin. To me the belly is beginning to look and feel more distended.

The INR comes back a few minutes later at 7.3. PTT also massively prolonged. Fibrinogen is low. Platelets are 52 (down from 150 in holding area that morning).

Now this is making sense to me and I am starting to think of acute and severe DIC (though it could possibly be other things). We set up rapid infuser and resuscitate with 10 pRBC, 6 ffp and 2 units platelets. Also bicarb and Calcium. Pt opens her eyes and communicates with us, able to follow commands and move all extremities. Blood pressure still low. Now on 3 pressor gtts.

My attending did pull in a TEE and saw inadequate filling.

Resuscitation doesn't last and pt needs more pRBCs, ffp, platlets. Also give some cryoprecipitate.

Also went to radiology to get abdomen/pelvis. We saw a lot of fluid in the belly, though the radiologist said that the color of it was closer to ascites than to blood (though I guess it might be consistent with a hemoglobin of 3). IR doc also checked with angiography to see if there was arterial bleeding, which he would have embolized if he had seen it.

Belly is now very distended and tight. She is oozing around all the IV sites, including the cordis distending her neck a bit.

She is sent to the ICU to continue resuscitation efforts.

This ends the acute phase of my interactions (summarized and simplified).

I'm not big on follow-up, but I'd like to know how she does, so I check back during the next several days and she is still alive, still intubated with some sedation, and still on pressor drips, though lower doses. They perform pericentesis on occasion to prevent abdominal ischemic events from high pressures. They continue giving her blood and plasma and fluids as needed. With the sedation off she will communicate and follow commands.

Further scans are unable to find a single source of bleeding. TIPS placement itself was successful.

Long term prognosis is yet to be determined. I'm leaning towards walking out of the hospital (though we wouldn't let her walk home). But there is always the chance of her going back into DIC or the liver failing further or any number of bad things.
 
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What were the d-dimer and fibirn split products. If those are off the chart, yeah you can make a case for dic, but don't forget you are giving lots of volume in a patient who's bleeding and consuming what little clotting reserve she has which can give you the same picture you presented. Not saying you can't have dic but that wouldn't be the first thing on my mind.
 
Does DIC even exist? i've never seen it, just dilution coagulopathy.
Only thing you can be sure of is that some form of bleeding must have occurred for her to drop to those values.
 
she walked into the IR suite.

DIC doesn't happen spontaneously - they musta nicked something with their pericentesis. her distance to coagulopathy was obviously much shorter than a healthy patient - small to moderate venous bleed led to vicious cycle of consumptive coagulopathy - more bleeding. angio usually won't reveal a venous source of bleeding.

sounds like she was well managed and will do ok - good case.
 
You are right. Traumatic/surgical blood loss is also likely, which can result in a consumptive coagulopathy, especially in someone with end stage liver disease. I'll have to go back and see if it was ever figured out.
 
You are right. Traumatic/surgical blood loss is also likely, which can result in a consumptive coagulopathy, especially in someone with end stage liver disease. I'll have to go back and see if it was ever figured out.

I think it's easy (in retrospect) to see how this pt went into DIC.
1) baseline abnormal coagulation system
2) surgical bleeding (could be quite small) consuming what factors ARE around
3) dilutional coagulopathy from a large volume of clotting-factor- and hemoglobin-devoid colloid

Nice case, and you guys did well.
 
I think it's easy (in retrospect) to see how this pt went into DIC.
1) baseline abnormal coagulation system
2) surgical bleeding (could be quite small) consuming what factors ARE around
3) dilutional coagulopathy from a large volume of clotting-factor- and hemoglobin-devoid colloid

Nice case, and you guys did well.

DIC is actually disseminated intravascular coagulation meaning that you're whole clotting and fibrinolytic system has been actived throughout your body in your vasculature. This is usually caused by some sort of inflammatory process such as occurs with amniotic fluid emboli, cancer, sepsis, etc. Did this patient have a coagulopathy, definitely. Was it DIC, I doubt it.
 
DIC is actually disseminated intravascular coagulation meaning that you're whole clotting and fibrinolytic system has been actived throughout your body in your vasculature. This is usually caused by some sort of inflammatory process such as occurs with amniotic fluid emboli, cancer, sepsis, etc. Did this patient have a coagulopathy, definitely. Was it DIC, I doubt it.

if DIC and consumptive coagulopathy are not the same thing, they are on the same continuum.

you're splittin hairs...
 
I'm not big on follow-up,


You need to work on this. The case was nicely handled and you did a good job, but you should really want to follow up on your patients, like every other real doctor. Patients and their families love it and the surgeons respect you for it.

Some points:

1) The patient was likely quite hemoconcentrated. Those lab values were falsely reassuring because of it.
2) In patients undergoing large volume paracentesis, most gastroenterologists will give albumin (mostly to prevent decrease renal function). Although there is debate about the utility of routine albumin, the correct kind to give is concentrated. This is usually 25% or 20%, not 5%. 5% will not provide oncotic replacement in reasonable volumes. 25% + crystalloid/fluid of choice does.
3) As others have stated, this sounds more like a consumptive coagulopathy rather than traditional DIC. Remember that to fix a low fibrinogen, you should give cryoprecipitate vs FFP. The FFP was also clearly indicated given the massive transfusion and abnormal PT. FFP, because of the associated volume, has a dilutional effect on clotting factor concentration (a point that surgeons rarely understand). Factor 7a could have also been useful.
4) A rare form of DIC in ESLD, particularly after something like TIPS, can be a peritoneal-venous shunt. I'm sure that is as awful as it sounds.
 
yeah these patients are grossly volume overloaded but so much of it is in third and fourth spaces, ive actually never given an OR patient 2 liters of albumin and you essentially replaced half her blood volume (im assuming she got some crystalloid as well) with clear fluids. i probably would have used concentrated albumin and pressors rather than large volumes, and may have considered a switch to blood products when my hypotension became refractory, REGARDLESS OF WHETHER YOU ARE WAKING THE PATIENT UP. ive gotten burned before on a situation like this, hypotensive at the end of the case but we are waking up, transport to ICU extubated, immediately gets two pressors started in the unit. i now refuse to rely on emergence to temporize hypotension in the critically ill.

i think you did a great job and the fact that she survived this simple radiologic procedure is testament to it.

presence of a surgeon would have ended this story pretty quickly
 
Our trasnsplant surgeons came in and evaluated the patient during the resuscitation. They didn't want to go to the OR right away with an INR so high, but they did accept the patient onto their service and took care of her in the ICU.

I was debating 5% or 25% albumin. Liver failure patients definitely need oncotic pressure. That is good to know. Thanks.
 
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