Interesting Case

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SurferBoyMD

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Hey all. Had an good case earlier this week, thought I'd share.

Here's the case:

The patient is a 58 yo woman who states she does not know of any medical problems and has not seen a doctor for over 30 years. She presented to the Gyn-Onc team earlier in November stating over the course of 6 months she noticed increase weight gain and abdominal girth. During this time she also had worsening dyspnea on exertion, hypoxia with RA O2 in the low 90s needing O2 NC at night, increased bilateral lower extremity pitting edema. On CT scan shes found to have a huge abdominal pelvic mass measuring 16x20cm. Here metastatic scans were negative.

Other notable things on first clinic visit is that she is hypertensive (placed on labetalol), she's obese w/ BMI of 42, and significant bilateral edema (placed on lasix). She is sent back to her rural city to get worked up by a primary doctor (which she does not have). Her pshx significant for uterine rupture during pregnancy in the 80s needing ex lap. Social hx: No bad habits however works in a Bar and has significant 2nd hand smoke exposure.

The operative plan once all work up is complete is to perform an ex lap, removal of mass, b/l SPO, poss hysterectomy, lymph node dissection, omentectomy.

I'll stop here to open up discussion about what labs and studies you would want to perform.
 
bmi of 42 and no bad habits? heh

Probable malignancy and poor functional status, for a moderate risk surgery.
CBC, chemistry, lfts, coags, ekg, cxr to start. Because of her poor functional status she should have further cardiac eval (likely a TTE at minimum, and maybe more).
 
CBC, Chemistry, Coags, EKG
She should be seen by a cardiologist for an echo and possibly a stress test.
I would skip PFTs, because it wouldn't change my management.
 
Great. Exactly the workup she had. This is the data I had the day of surgery:

WBC 14 Hct 34 Plt 360; Chem panel Normal; 1 week old INR 1.4; AST/ALT normal. AlkPhos elevated, Tbili 2.4
CXR: Clear lung fields no effusion, cardiomegaly.
Ekg: NSR
She actually had a stress echo: Normal w/ no wall motion abnormalities, EF preserved 60-65%, no diastolic dysfunction, no valvulopathy
PFTs: Mild-moderate obstructive pattern, normal DLCO2, FVC, FEV1.

Proceed? Need more preop work up? Anesthetic plan?
 
I'd also like to know what her PASP is based on the otherwise normalish data we have so far....what is causing the hypoxia and 02 requirement at night? Perhaps her huge abdominal mass altering mechanics, but maybe not....
 
I can't remember when PFTs altered my anesthetic plan. In the elective situation perhaps it would point toward ensuring optimization by a pulmonologist but then again what they do is not rocket science. I can give bronchodilators and steroids as needed as much as they can, and we always have the anesthetic gas. Most of the time you can predict whether postop ventilation is an issue based on patient preop exam and type of surgery.
 
Despite having a preserved EF, I'm assuming that this woman probably has coronary (among other) vascular lesions. I'm guessing she spends most of her time on a couch eating Funyuns and not engaging in anything metabolically challenging.
She is also a pulmonary cripple. This is a huge mass that will likely require a large incision for removal. An epidural might help her take larger tidal volumes and stay off of the vent post op.

Provided that the INR is normal on the DOS, I would proceed with an epidural, central line, and art line. I'd also make sure to have blood crossed.
 
No PASP on echo report, no significant R changes on EKG.

Day of surgery: The patient has no significant changes from her last week's lab draw.
Nurses place and IV and do not draw any new coags for the case. Otherwise, no other studies are ordered and we proceed into OR for planned low thoracic epidural then GA, A line, 2 large IV's if not central line.

Question here: Would you proceed with epidural here given current coag status with no new coags? Would you go into room and draw coags and wait? Would you forego the epidural and straight GA (given her poor pulmonary mechanics)? Or cancel the case until further work up can be done?
 
I'm not sure I quite understand the thought process behind a thoracic epidural here. If you think her hypoxia and o2 requirement are 2/2 mechanics from the large mass, then this should improve after the case. If you think that its not the mass, then you haven't adequately worked her up yet/diagnosed the cause of hypoxia, which is worrisome.

We don't do many thoracic epidurals at my institution....mostly paravertebrals. Why not a TAP?
 
Random stab at the zebra --- carcinoid syndrome? Causing her mild obstructive pulmonary symptoms, her r sided heart symptoms, peripheral edema, and abdominal tumor.
 
Thought process of the thoracic epidural was for intraoperative and postoperative pain control. Decreasing the amount of systemic narcotics for a patient who is hypoxic at baseline and obese with probably sleep apnea. It may also help with pulmonary mechanics postoperatively for incision pain/splinting leading to atelectasis and worsening VQ mismatch. There's also some data on bowel surgery and epidurals with shortened length of return of bowel function and decreased risk of ileus (although a lidocaine infusion shows same benefit). For these reasons, we thought the benefits outweighed the risks.

That being said. Here is how the story unfolds: I place the epidural catheter and tape it in place. As the last piece is placed, the surgical resident states that they drew coags in the morning (and did not inform preop nurses or anesthesia). The INR comes back 1.7.

What would you do now that you have an epidural in place with a pt with worsened coagulopathy? Would you test dose? Run the epidural during the case? Pull the epidural out immediately? Give product? Cancel case now? Call a lawyer?
 
Give FFP. Keep epidural in place but do not use/test it until the INR decreases. Neuro checks until at least 24 hours after removal. There is also the question of the cause of the elevated INR, and whether the INR will be maintained after correction.

It's not the surgical resident's fault. I don't think any benefit could outweigh the risks of epidural hematoma. You guys should have rechecked the INR before inserting an epidural.
 
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You already placed the epidural... just use it as planned... nothing will happen, when time comes to remove the catheter, check the coags again and if coagulopathic you might need to correct that before removing the catheter.
I am curious though about the elevated alkphos and bilirubin that were known pre-op but ignored.
Something is pointing towards intra hepatic or biliary obstruction and could explain why the INR is rising but for some reason no one seemed to be interested in knowing why!
 
AST/ALT were normal, bili and alk phos were high. Biliary obstruction with probably vitamin K malabsorption.

Planktonmd, wouldn't you be afraid of busting a weak clot by using the epidural (increased fluid/pressure in the space)? In my mind, it's not the same thing as placing an epidural with normal coags, and then giving the patient heparin or whatever. Isn't this the reason we wait before/after giving heparin when placing the epidural?
 
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AST/ALT were normal, bili and alk phos were high. Biliary obstruction with probably vitamin K malabsorption.

Planktonmd, wouldn't you be afraid of busting a weak clot by using the epidural (increased fluid/pressure in the space)? In my mind, it's not the same thing as placing an epidural with normal coags, and then giving the patient heparin or whatever. Isn't this the reason we wait before/after giving heparin when placing the epidural?
This argument about dislodging a clot if you use the epidural is very strange in my opinion!
Do you know of any case reports where infusing medications through the already in place epidural catheter caused an epidural hematoma?
Also as far as I know we wait after giving heparin because we prefer to not insert a large tuohy needle in the epidural space if the coagulation is abnormal, not because we are concerned about a clot getting dislodged by the epidural infusion!
Epidural hematomas as you might already know are very rare and most of the times they are caused by catheter removal in the presence of coagulopathy and other comorbidity like advanced age and critically ill patients.
 
Thought process of the thoracic epidural was for intraoperative and postoperative pain control. Decreasing the amount of systemic narcotics for a patient who is hypoxic at baseline and obese with probably sleep apnea. It may also help with pulmonary mechanics postoperatively for incision pain/splinting leading to atelectasis and worsening VQ mismatch. There's also some data on bowel surgery and epidurals with shortened length of return of bowel function and decreased risk of ileus (although a lidocaine infusion shows same benefit). For these reasons, we thought the benefits outweighed the risks.

That being said. Here is how the story unfolds: I place the epidural catheter and tape it in place. As the last piece is placed, the surgical resident states that they drew coags in the morning (and did not inform preop nurses or anesthesia). The INR comes back 1.7.

What would you do now that you have an epidural in place with a pt with worsened coagulopathy? Would you test dose? Run the epidural during the case? Pull the epidural out immediately? Give product? Cancel case now? Call a lawyer?

so the issue here i think is what the stress of surgery is going to do, what kind of product she will require and how long it will be until you can perform a neuro exam. If this is going to be an 8+ hour blood bath, then with the volume shifts and possible need for resuscitation and subsequent coagulopathy you should at least think about what your plan for correction will be and how you will assess neuro status. id probably have her q1h neuro for at least 24 hours and definitely be cautious for several days longer.
 
If she develops a hematoma during her surgery you'd have no way to identify that so I think surgery needs to be delayed for 24 hours after correction of her coagulopathy and epidural removal.
 
Epidural hematomas as you might already know are very rare and most of the times they are caused by catheter removal in the presence of coagulopathy and other comorbidity like advanced age and critically ill patients.
Yes, they are very rare. However, I am not sure how rare they are at an INR of 1.7, otherwise ASRA would not advise inserting epidurals at a normal INR. I don't have experience in this area, just saying what I would or wouldn't do, based on my personal logic. I admit, I have always been extremely cautious with neuraxial blocks; primum non nocere.
 
Yes, they are very rare. However, I am not sure how rare they are at an INR of 1.7, otherwise ASRA would not advise inserting epidurals at a normal INR.
The other day you were saying that a stroke rate of 1/1000 is insignificant. Now you are making a big deal of the risk of an epidural hematoma with an 1.7 INR. Ironic, wouldn't you say?
 
What would you do now that you have an epidural in place with a pt with worsened coagulopathy? Would you test dose? Run the epidural during the case? Pull the epidural out immediately? Give product? Cancel case now? Call a lawyer?

I would proceed as planned. Repeat labs to confirm. Transfuse products if excessive surgical bleeding.
 
We continued to proceed with the case. Induced, Aline, big IVs. Attending did not want the epidural to be ran or bolused narcs until postop exam, as it may murky post op exam. Case was uneventful, mass removed. FFP was given throughout, no major improvement in INR, surgical field wet but no bleeding. Oxygenation improved after mass removed and with recruitment maneuver/increased PEEP. Able to wean off vent and extubate to facemask, then to ICU. Pt in ICU coherent, able to move lower extremity no sensation changes. Having significant amount of abdominal pain and splinting, with O2 sats in low 90s. Bolused and ran epidural with improvement of pain. No neurologic changes as of now. 2 days out, in ICU, still with poor O2. Epidural in running no neuro changes. Repeat TTE shows pulm HTN and RV mod/severe function with overload. Also with new AKI. Her INR still elevated in setting of congested hepatopathy. Her clinical course as of now is no bueno.

Thanks for the input. I learned and am learning a lot from this case. As there is only half a year until my residency is over, I'm taking the opportunity to learn from the attendings and continue to think what I would do differently/same in my practice. Hindsight is 20/20. I would have waited if I knew new coags were pending, and if not draw them myself. I would ? the surgeons if this case should be continued until her coagulopathy/liver and hypoxia was worked up; although, the case not being elective and urgent given the high likelihood of cancer, it probably would not stop me from doing the case. Opted to not do the epidural knowing she may have difficulty with postoperative pain and her pulmonary state postop. Run a lidocaine and ketamine infusion to limit opioids. And send her to the ICU for postop monitoring for pulm/pain issues. Any other learning points?
 
I think malignancy or not, bad pulmonary htn is something you should know about, because it will change management of the case. Would have been nice to know about that first....I'm surprised the echo didn't note that? Weird.
 
I think malignancy or not, bad pulmonary htn is something you should know about, because it will change management of the case.
How would it change management?
 
I'm not sure I quite understand the thought process behind a thoracic epidural here. If you think her hypoxia and o2 requirement are 2/2 mechanics from the large mass, then this should improve after the case. If you think that its not the mass, then you haven't adequately worked her up yet/diagnosed the cause of hypoxia, which is worrisome.

We don't do many thoracic epidurals at my institution....mostly paravertebrals. Why not a TAP?

impaired mechanics from a chronically occurring mass wont magically change immediately - they will be worse postop from fluid shifts/drugs.

TEP instead of TAP because u want days instead of hours of benefit.
 
How would it change management?

It may change management depending on its severity and whether it is precapillary vs venous. If hypoxia/hypercarbia could potentially make the pulm htn worse and lead to cor pulmonale leading into a death spiral at induction with rendering the patient apenic, it may change my induction; such as to have the pt continue spontaneous breathing. A line preinduction, sure why not. Central line, nah.
 
It may change management depending on its severity and whether it is precapillary vs venous. If hypoxia/hypercarbia could potentially make the pulm htn worse and lead to cor pulmonale leading into a death spiral at induction with rendering the patient apenic, it may change my induction; such as to have the pt continue spontaneous breathing. A line preinduction, sure why not. Central line, nah.

1 How does spontaneous versus positive pressure breathing make a difference in pulmonary hypertension?

2 How many people are doing asleep alines in burned out adults patients, bad heart or not? Just by looking at them from 20 feet away you can make that decision. Who needs an echo for such a "crucial" decision?
 
It may change management depending on its severity and whether it is precapillary vs venous. If hypoxia/hypercarbia could potentially make the pulm htn worse and lead to cor pulmonale leading into a death spiral at induction with rendering the patient apenic, it may change my induction; such as to have the pt continue spontaneous breathing. A line preinduction, sure why not. Central line, nah.

i think you are being pimped here, so im not adding to that, but pulmonary arterial and pulmonary venous hypertension both respond poorly to hypercapnia, hypoxia, acidosis and hypotension. there is a death spiral in someone with PTH that starts with induction agent, wait for apnea... and finishes with "call it" as you are still trying to get an art line in.

the right heart is a fickle mistress, it tolerates afterload to a point, whether from arterial hypertension (VERY rare) or venous hypertension (VERY common) or a mixes picture (between the two).

mechanicl ventilation is also very tough to optimize in pulmonary hypertension, as not enough causes worsening respiratory indices, too much increases PVR due to capillary compression. if your right heart is strong, it can overcome it, but you dont always know that - symptomatically, you could have predicted RV dysfunction in this patient preoperatively.

while you can do this case safely with adequate setup and management of suspected pulmonary HTN, i think a preop echo would have been warranted.
 
Yeah, mild hypoxia in the face of a clear chest film and her history, I'd like to see the RV/TVR, too.

If the pHTN is significant and has caused a lot of pre-capillary remodeling, giving a high FiO2 is unlikely to overcome the shunt in spite of voluntary recruitment maneuvers (to minimize atelectatic shunt). It's a crude but quick way to assess the significance of pHTN at the bedside.
 
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