Haematological emergencies

Question 1

What is Disseminated Intravascular Coagulation?

Answer 1

AKA consumptive coagulopathy, Defibrination syndrome

When coagulation and fibrinolysis both become abnormally and often massively activated

Question 2

What is the difference between acute (decompensated) and chronic (compensated) DIC?

Answer 2

Acute- Sudden exposure to large amounts of procagulant substance (ie tissue factor) leads to rapid activation and consumption of coagulation factors. This leads to a severe bleeding diathesis

Chronic- Prolonged exposure to small amounts of procoagulant leading to increased consumption but liver etc able to compensate. Typically thrombotic state and often asymptomatic, usually detected on blood tests

Question 3

What are the causes of acute DIC?

Answer 3

Severe trauma (especially CNS, fat embolism)
Severe sepsis (ie meningococcal) Acute promyeolcytic leukaemia
Obstetric complications (pre-eclampsia, retained dead fetus, acute fatty liver of pregnancy, amniotic embolism)
Intravascular haemolysis (particularly ABO incompatibility, also other forms ie plasmodium falciparum haemolysis)
Snake envenomation
Amphetamine overdose

Question 4

What are the causes of chronic DIC?

Answer 4

Typically chronic malignancy producing extra tissue factor, AKA “cancer associated hyper
- Pancreatic cancer
- Ovarian Cancer
- Brain tumours
- Gastric

Question 5

What are the lab coagulation abnormalities in acute DIC?

Answer 5

Thrombocytopaenia
Prolonged PT and APTT
Low fibrinogen
High D-Dimer

Question 6

What are the lab coagulation abnormalities in chronic DIC?

Answer 6

Mild thrombocytopaenia
Elevated D-Dimer
Mildly prolonged PT and APTT
Normal to slightly elevated Fibrinogen

Question 7

What are the acute treatments for the coagulopathy in DIC?

Answer 7

Severe bleeding +…
- Platelets <50,000 = 1 pool of platelets per 10kg
- Fib<0.5g/L, prolonged APTT/PT = FFP
- Fib <0.1g/L = Cryoprecipitate

Question 8

What is the reversal agent for Dabigatran?

Answer 8

Praxbind aka Idarucizumab
Dosing is 5gm for complete reversal

Question 9

What is the new reversal agent for the Factor Xa inhibitors?

Answer 9

Andexanet Alfa

Question 10

In life threatening bleeding how should Factor Xa inhibitors be reversed?

Answer 10

Andexanet Alfa now available in Australia
- Low dose 400mg IV then 4mg/min infusion for 120mins
- High dose 800mg IV then 8mg/min for 120mins (960mg)

If Andexanet Alfa not available
- Give antifibrinolytic agent ie 1gm TXA bolus then 1gm/8hrs
- Give 50 units/Kg 4 factor PCC (aka prothrombinex)
- Consider FEIBA (Factor eight inhibitor bypassing agent) 50IU/kg

• If the above unavailable then give FFP

Question 11

In life threatening bleeding how are antiplatelet agents reversed?

Answer 11

Desmopressin (DDAVP)
0.3mcg/kg IV

Can also be used in uraemia with uremic platelet dysfunction

Question 12

What can be done for Jehova’s Witnesses with life threatening bleeding who are anticoagulated?

Answer 12

• Reverse anticoagulation with non-blood products (ie andexanet alfa, praxabind, Vitamin K)
• TXA
• IV fluids to 1L
• Early vasopressors
• Recombinant factor VIIa
• Discuss with haematology

Question 13

What medications are used in the treatment of bleeding with Von Willebrands disease?

Answer 13

• vWF deficiency, leads to platelet dysfunction and relative lack of factor VIII (8)

Meds
- 15mg/kg IV TXA, max 1gm
- DDAVP (Desmopressin) 0.3mcg/kg max 20mcg (can cause seizures and hyponatraemia)
- 60/144 units/kg of VIII.vWF factor replacement IV

Question 14

How is a TEG interpreted and what do the different abnormalities require for treatment?

Answer 14

R-time >10
- Time to initial fibrin formation, looking at intrinsic pathway
- >10mins = FFP

K-time
- Time taken for fibrin cross linkage to reach 20mm of clot strength
- >3min = Cryoprecipitate

Alpha Angle
- Angle from baseline to slope of tracing, represents clot formation
- <53 degrees = Cryo +/- platelets

MA
- Maximum amplitude of tracing
- Represents platelet Number and function
- <50mm = platelets

LY30
- Clot lysis at 30mins following MA, a measure of fibrinolysis
- >3% = TXA

*TEG-ACT
- Time to initial fibrin formation, looking at mix of intrinsic/extrinsic pathway
- Not on all TEG’s
- >140 = FFP

Question 15

How are different TEG patterns interpreted?

Answer 15

Anticoagulants
- Long R time (fibrin formation)
- Long K time (cross linking)
- Reduced MA (platelet function)
- shallower a-angle (clot formation)
- LY30 +/- high

Platelet blockers
- Normal R time
- Long K time
- Shallower a-angle
- Reduced MA (platelets)
- LY 30 +/- high

Fibrinolysis
- Normal R time
- Short K time
- Steep a-angle
- Normal MA
- LY30 very high

Hypercoagulation
- Short R time
- Short K time
- Steep a-angle
- Large MA
- LY30 +/- low

DIC stage 1
- Initial pro-coagulant stage with factor consumption
- Short R time
- Short K time
- Steep a-angle
- Normal MA
- LY30 high

DIC stage 2
- After clotting factors depleted
- Very long R time
- Long K time
- Shallow a-angle
- Small MA
- LY30 very small (no TPA left to cause fibrinolysis when clots finally form)

Question 16

What is the treatment for major bleeding during or immediately post thrombolysis?

Answer 16

Initial
- Stop infusion (if alteplase)
- Take FBE, Coags and crossmatch
- Urgent imaging to confirm ie if ICH
- Large bore IV access, airway and respiratory support
- Pressure on any direct bleeding
- MTP as needed

Reversal General
- 10units cryoprecipitate, more as required aiming Fib 1.5-2
- TXA 1gm bolus then 1gm infusion

Reversal specific
- 8 units platelets if plats <100
- Protamine 1mg/100U if on unfractionated heparin
- FFP/Vit K/Prothrombinex if also on warfarin
- Consider urgent surgery for specific sites ie ICH