Brian Locke

Cirrhosis in the ICU

##Coagulopathy

  • Are patients with cirrhosis who have an increased INR at decreased risk of clot?

No

Patients with cirrhosis have increased risk of both arterial and venous thrombosis

Cirrhosis -> Stroke

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5710331/

1.6 million medicare beneficiaries who had cirrhosis were at increased risk of ICH (HR 1.9), SAH (HR 2.4) and ischemic stroke (HR 1.3) after controlling for stroke risk factors and demographic.

Cirrhosis -> VTE

https://pubmed.ncbi.nlm.nih.gov/19098856/

Danish nationwide case (cirrhosis, n=100,000) control (cohort matched on demographics and known clot risk factors, n=500,000): excluding cancer, trauma, surgery, pregnancy in 90d. RR of VTE = 1.74 higher in cirrhotics. DVT (and PVT) moreso than PE, but all increased

  • Are patients with a higher INR at increased risk of bleed? Does lowering their INR decrease their risk of bleed?

MELD-Na includes INR. Why?

alt

It is a marker of synthetic function -> high INR = deficiency in both pro- and anti-coagulant factors.

https://journals.lww.com/ajg/Abstract/2017/02000/Changing_Concepts_of_Cirrhotic_Coagulopathy.18.aspx

High INR = increased derangement of the clotting system.

INR = predictive of bleeding in patients who have decreased VKA function (e.g. warfarin) but FFP will low the INR but NOT lower the risk of bleed or improve the TEG

https://pubmed.ncbi.nlm.nih.gov/21298360/

Does NOT predict bleeding after liver biopsy: https://pubmed.ncbi.nlm.nih.gov/7249879/

alt Lowering the INR does NOT reduce this risk

Recommendations against procedural transfusion for low risk procedures (Para, Thora, non bleeding vatical banding) from all major organizations (SHM, AASLD, AGA)

https://www.journalofhospitalmedicine.com/jhospmed/article/228324/hospital-medicine/things-we-do-no-reasontm-routine-correction-elevated-inr

Less data for higher risk (e.g. central line)

alt

So why given IV Vitamin K?

Via K deficiency is comorbid with cirrhosis due to dysfunction of biliary function (cholestasis = less absorption). If INR elevation is due to vitamin K deficiency, correcting it will improving hemostasis.

High INR = hold DVT prophylaxis?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3551567/

No randomized evidence. Prospective cohort data after surgery = improvement to continuing.

  • What information does a TEG give you?

Spin a sample of blood around a needle and measure the clot as it forms.

alt

  • How do you interpret a TEG?

Traditional:

  • platelet < 50 -> tracryse platelets
  • Fibrinogen < 100 -> tranfuse cryo
  • INR > 1.5 -> transfuse FFP

TEG

  • R time > 10 minutes -> FFP
  • MA < 55m -> transfuse platelets
  • Alpha-angle < 45 degrees -> transfuse cryo (=fibrinogen, vhf, factor 13)
  • LY30 > 3-7% -> consider TXA

https://static1.squarespace.com/static/5e6d5df1ff954d5b7b139463/t/5e84984d130f6208e6b6d92a/1585748046029/ICU_one_pager_TEG.pdf

  1. What evidence is that TEG based transfusion improves outcomes?

RCTs, unblinded, ~50 patients in Cirrhotic: TEG vs Usual care. Less transfusion product, no signficant difference in outcomes though not powered to investigate that question

Guidelines:

AGA 2019 Coag in Cirrhosis:

https://pubmed.ncbi.nlm.nih.gov/30986390/