Linking To, Embedding, and Excerpting From “The Failing Liver” From CriticalCareNow

Today, I review, link to, embed, and excerpt from The Failing Liver from CriticalCareNow.

All that follows is from the above resource.

What do you do when a patient’s liver is failing and time is running out? In this lecture from the ResusX: Reset conference (see the link below for more lectures), Dr. Alice Gallo de Moraes walks you through the critical steps to resuscitate a failing liver. From managing coagulopathy to addressing multi-organ dysfunction, Dr. Gallo de Moraes provides a systematic approach to stabilizing these complex cases. Learn how early diagnosis, targeted treatment, and timely transplant referral can make all the difference in patient outcomes. This is a must-watch for anyone in critical care or emergency medicine! To watch more videos from the ResusX conference, check out https://www.resusx.com/offers/bwjtxAHf

  • 00:00 Introduction
  • 00:40 Case Presentation: A 32-Year-Old with Liver Failure
  • 01:25 Initial Examination and History
  • 02:30 Laboratory Findings and Further Investigations
  • 05:04 Diagnosis and Initial Management Steps
  • 05:35 The Ten Commandments of Liver Resuscitation
  • 07:14 Stabilization and Identifying the Cause
  • 11:21 Fluid Management in Liver Failure
  • 14:25 Organ-Specific Considerations
  • 18:45 Liver Transplantation and Secondary Survey
  • 20:28 Conclusion

0:15

0:45

1:49

2:39

3:41

4:41 Heart POCUS was performed showed the heart was hyperdynamic.

5:05

5:17

5:49

6:33

7:51

8:41

10:33

11:38

15:30 – 19:58

So again, for cardiovascular think about splenic vasodilation, early pressors.

For GI and attrition, think about variceal bleeding.

So, if they had varices in the past, be mindful, be in the

lookout for any GI bleeding.

Start them on PPI early.

If they had, if they have GI bleed and you think they, it’s from variceal

bleeding – start octreotide early.

You call your colleagues in endoscopy early so they can address this.

Make sure that they are receiving thiamine and folate because they are again

chronically malnourished, very likely.

Be on the lookout for refeeding syndrome when they are ready to get nutrition.

Endocrine.

Remember, these patients with chronic liver failure are potentially in a very

low state of adrenal insufficiency.

So if they are in shock, consider early stress dose steroids.

This patient also might present with hypoglycemia because their

liver is so sick that they cannot, can no longer do glyconeogenesis.

So, be on the lookout if you have a patient with acute or chronic

liver failure or acute liver failure and they are persistently

hypoglycemic, you run to their bedside.

You don’t walk.

Because that means that their liver is really sick and really failing.

Coagulation.

Like I mentioned before, they will have impairment of all their procoagulable

proteins and they might be procoagulable despite the fact that they have an INR of

more than 20, in this case, for example.

Tags are still controversial.

Even in the liver literature, tags are approved currently for

liver transplant, intraoperative.

Coagulation, evaluation, and trauma coagulation evaluation, but for a patient

who is in the ED or needing only the medical ICU, very controversial, the

use of tag to guide blood resuscitation, blood products resuscitation, but if a

patient with liver failure is bleeding, always try to do one to one pRBCs and

FFPs in addition to platelets and cryo.

Because again, these patients are very, their coagulation is very disturbed.

Infection, again, address early.

These patients have immunodeficiency just because they have liver disease.

Think about clostridium difficile.

This patient’s liver failure patients usually have toxic megacolon

from C-diff instead of diarrhea.

So, be mindful of that if a patient is taking their lactulose

and they’re not pooping for a whole day, think about C-diff.

And, like I mentioned before, think about drug resistant organisms because

these patients are immunodeficient.

Think about kidneys ascites can cause renal dysfunction because of extrinsic

compression to the blood flow to the kidneys and also splenctic vasodilation,

the kidneys won’t get as much flow.

And good old pulmonary, they can have infections, they can have pancreatitis,

they can develop ARDS pretty quickly.

In neurology, most common cause for brain dysfunction is gonna

be hepatic encephalopathy.

So, early lactulose when they come in, even if you have to put an angiotube

to give them lactulose as well.

And rifaximin in the last two years has become a great adjunct for the

treatment of hepatic encephalopathy.

But it’s very expensive, so be mindful of that.

Liver transplantation evaluation.

Call your friends and liver transplant as early as possible.

Again, nowadays, there’s not a formal cutoff for age in

terms of liver transplant.

If a patient who is still drinking or still using drugs can show that

they can have an excellent support from family post transplant, they

might be considered for transplant.

And if it’s an acute, so less than a week of acute liver failure that

we can pinpoint to the timing, these patients do better also.

So, don’t forget to call your liver transplant colleagues soon.

And secondary survey.

Almost like trauma, you go back and you re-evaluate all those organs again to make

sure that we have the right antibiotics.

The kidneys are being perfused.

We have drain ascites to look for SVP and to give the kidneys a break as well

in terms of intra-abdominal pressure.

We have them on lung protective ventilation if they needed.

They’re airway protected.

We have lactulose plus or minus rifaximin going.

We are giving them appropriate nutrition with a little bit of

protein and all the vitamins that they need for again, secondary survey.

Don’t forget your prophylaxis in terms of antifungals and SPP prophylaxis if

they didn’t have SPP this time around.

This entry was posted in Hepatology, Liver, Liver Failure (Acute On Chronic), Liver Failure (Acute), Liver Transplantation. Bookmark the permalink.