DIC

Question 1

Definition

Answer 1

Widespread, uncontrolled clot formation and bleeding due to loss of coagulation regulation.

Question 2

Pathophysiology of DIC

Answer 2

->Widespread, uncontrolled clot formation throughout microvasculature.
Triggered by factors like:
* Bacterial endotoxins (e.g., LPS)
* Tissue factor from monocytes or placenta
* Endothelial glycocalyx damage

Wide spread coagulation results in depletion of procoagulant factors –> consumptive coagulopathy

BET by Mom leads to wide spread coagulation and as a result consumption coagulopathy
B- Bacterial endotoxin
E- Endothelial glycocalyx damage
T- Tissue factor release from monocytes or placenta

Question 3

Life threatening consequences of DIC

Answer 3

Life-Threatening Consequences of DIC
1. Disseminated microvascular thrombosis:
- tissue hypoperfusion and damage
2. Macrovascular thrombosis:
-May result in DVT or PE
3. Hemorrhage:
* Due to depletion of clotting factors (consumptive coagulopathy)

Question 4

Types of DIC

Answer 4

=> Acute DIC:
* Sudden trigger (e.g., sepsis)
* Rapid depletion of clotting proteins
* Prominent bleeding/thrombotic features
* Common in ICU/critical care

=> Chronic DIC:
* Ongoing low-level activation (e.g., adenocarcinomas)
* Slower consumption of coagulation factors
* Often clinically compensated, mild lab changes

Question 5

Clinical conditions causing DIC

Answer 5

• Sepsis (bacterial > gram-negative > gram-positive, rarely viral)
• Malignancy (especially hematological solid tumors)
• Trauma
• Obstetric complications
• Severe transfusion reactions

Trauma, Transfusion, Malignancy, Meningococcemia, Sepsi

Mnemonic- TTOMMS

Pts with solid tumors- greater risk of thrombosis than haemorrhage

Pts with haem malignancy eg- AML- greater risk of Bleeding because of hyperfibrinolytic state

Question 6

Causes in the young

Answer 6

• Pre-eclampsia/HELLP
• Sepsis
• Kawasaki disease
• Meningococcemia
• Massive transfusion

MSK(musculoskeletal)

Question 7

Causes of DIC in young females

Answer 7

• Amniotic fluid embolism
• PIH/Eclampsia
• Intra uterine Death
• HELLP
• Sepsis
• Massive transfusion
• Mismatched transfusion

Question 8

What are some clinical manifestations of DIC

Answer 8

=>May be asymptomatic or show signs of bleeding and/or thrombosis.

-> Microvascular thrombosis → organ failure:
* Renal failure.
* ARDS.
* Neurological: delirium, coma, seizure.
* Adrenal insufficiency (Waterhouse-Friedrichsen syndrome).
* Skin: Purpura fulminans (severe form requiring aggressive management).

-> Macrovascular thrombosis:
* Deep vein thrombosis (DVT).
* Pulmonary embolism (PE).

-> Bleeding:
* Petechiae, purpura.
* Oozing from catheters or mucosa.
* GI or intracranial hemorrhage (less common, but serious).

Question 9

DIC Screening Lab Panel

Answer 9

• Complete Blood Count (CBC)- platelets
• PBF - schistiocytes
• INR and PTT
• Fibrinogen
• D-dimer
• LDH

Question 10

D/Dx

Answer 10

• Cirrhosis
• HITS
• CAPS
• TTP/HUS
• SIC

=>DIC- is a clinical diagnosis with 3 major components:
*Underlying disorder known to cause DIC
*Constellation of characterstic lab anomalies
*Exclusion of alternative explanations.

Question 11

D/Dx

Cirrhosis

Answer 11

=>1. Cirrhosis:
* Risk factor for DIC.
* Liver disease: reduced synthesis of clotting factors, fibrinolytic proteins.
* Balance easily disrupted by insults.
* D Dimer: usually elevated in both DIC and advanced liver disease.
Factor VIII: produced by endothelium; normal in cirrhosis, reduced in DIC.

D/D of coagulopathy:
Dimple Hai Senior Critical Care Trainee
DIC, HITS, Cirrhosis, CAPS, SIC, TTP, HUS

Question 12

HIT

Answer 12

2. HIT

(Heparin-Induced Thrombocytopenia)
* Exposure to heparin essential.
* ELISA & serologic assay helps in diagnosis.
* Fibrinogen:
- Normal in HIT.
- Decreased in DIC.

Question 13

3. Primary Thrombotic Microangiopathies (TTP, HUS)

Answer 13

=>3. Primary Thrombotic Microangiopathies (TTP, HUS)
* Platelets < 30k suggests TTP > DIC.
* Schistocytes seen in both but TTP,HUS»DIC
* TTP: ADAMTS13 deficiency or autoantibodies.
* INR/PTT/Fibrinogen: typically normal in TTP because:
Coagulation factors not consumed in TTP(coagulation sys is not activated- clots composed of platelets only)

• TTP/HUS: LDH very high(sec to tissue ischemia).
• Key distinguishing features: thrombocytopenia, hemolysis, schistocytes, neuro symptoms.

Question 14

CAPS

Answer 14

=>4. CAPS (Catastrophic Antiphospholipid Syndrome)
* Can mimic DIC in ~25% of cases.
* Associated with SLE, APLA/pregnancy loss
* Skin Manifestations-eg- cutaneous necrosis
* Triggers: infection, anticoag withdrawal, surgery.

Question 15

SIC

Answer 15

5. Sepsis induced thrombocytopenia and coagulopathy-(SIC)

-Fibrinolysis suppressed–>impaired breakdown of microthrombi
-Fibrinogen levels- normal or high

Question 16

DIC INVx

Answer 16

1) D-dimer

• Almost always elevated in DIC (often >4,000 ng/mL).
• A normal D-dimer essentially excludes DIC.
• Non-specific

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2) Thrombocytopenia

• Common, but platelet count <30,000/uL is uncommon.
• A downward trend in platelet count often precedes other abnormalities.
• Not specific to DIC

⸻

3) INR and PTT
* Prolonged INR/PTT supports DIC but may be normal in >50% of cases.
* These tests measure clotting factor levels, not anticoagulant factor depletion.

⸻

4) Fibrinogen
* Least sensitive marker (only ~25% sensitivity).
* Low fibrinogen supports DIC, but levels may be normal or elevated in sepsis.
* Falling fibrinogen over time is more suggestive.
* Markedly low levels may suggest hyperfibrinolysis.

⸻

5) Antithrombin III
* Consumed in DIC → reduced levels.
* May explain heparin resistance in DIC.
* Can indicate early (non-overt) DIC.

=>Other causes of low AT III:
* ECMO, dialysis, IABP
* Heparin therapy
* Cirrhosis (not produced)
* Nephrotic syndrome(excess clearence)

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6) Microangiopathic Hemolytic Anemia (MAHA)
* Caused by microthrombi in capillaries.
* Leads to intravascular hemolysis and schistocytes on blood film.

⸻

7) Thromboelastography (TEG) in DIC
* TEG provides a whole-blood overview of coagulation.
* May reveal hypercoagulability early
* Later stages of DIC may show hypocoagulability.
* Most common TEG abnormality in DIC: reduced maximal amplitude (MA).

Heparin ⬇️es ATIII leves -mech- binds to ATIII and then is cleared rapidly- apparent deficiency, not actual.

Question 17

Treatment

Answer 17

=>Management of DIC
1. Treat the underlying disorder
* Sepsis: antibiotics + supportive care.
* APL (acute promyelocytic leukemia): ATRA.
* Purpura fulminans: aggressive supportive treatment.

2.	Platelet transfusion ->Generally avoided unless:
*	Platelets <10,000/µL.
*	Planned procedure or high bleeding risk.
*	Ongoing active bleeding.
*	Aim for platelets >50,000/µL in high-risk settings.

3.	Fibrinogen supplementation
*	If active bleeding: aim for fibrinogen 1.5–2 g/L.

4.	Clotting factor replacement
*	Based on TEG results, especially if bleeding is ongoing.

5.	Vitamin K administration
*	Can be given if deficiency suspected.

6.**	Heparin
*	Generally not beneficial in DIC due to already low antithrombin (AT) levels.**

7.	**Antithrombin III (ATIII) replacement**
*	May help in septic shock or DIC with low AT levels.

8.	Protein C concentrates
*	Considered for patients with meningococcemia or purpura fulminans–associated DIC.

Question 18

D/Dx

Cirrhosis

HITTS

TMAs (thrombotic microangiopathies)
CAPS

Sepsis

Answer 18

1. Cirrhosis:

*	Risk factor for DIC.
*	Liver disease: reduced synthesis of clotting factors, fibrinolytic proteins.
*	Balance easily disrupted by insults.
*	DDimer: usually elevated in both DIC and advanced liver disease. **Factor VIII:** produced by endothelium; normal in cirrhosis, reduced in DIC.

(Heparin-Induced Thrombocytopenia)
* Exposure to heparin essential.
* ELISA & serologic assay helps in diagnosis.
* Fibrinogen:
- Normal in HIT.
- Decreased in DIC.

Primary Thrombotic Microangiopathies
* Platelets < 30k suggests TTP > DIC.
* Schistocytes seen in both but TTP,HUS»DIC
* TTP: ADAMTS13 deficiency or autoantibodies.
* INR/PTT/Fibrinog
en: typically normal in TTP.

**Coagulation factors not consumed in TTP(coagulation sys is not activated- clots composed of platelets only)**.

*	TTP/HUS: LDH very high(sec to tissue ischemia).

*	Key distinguishing features: thrombocytopenia, hemolysis, schistocytes, neuro symptoms.

(Catastrophic Antiphospholipid Syndrome)
* Can mimic DIC in ~25% of cases.
* Associated with SLE, APLA/pregnancy loss
.Skin Manifestations-eg- cutaneous necrosis
* Triggers: infection, anticoag withdrawal, surgery.

Sepsis induced thrombocytopenia and coagulopathy
-Fibrinolysis suppressed–>impaired breakdown of microthrombi
-Fibrinogen levels- normal or high

***DIC- is a clinical diagnosis with 3 major components:
*Underlying disorder known to cause DIC
*Constellation of characterstic lab anomalies
*Exclusion of alternative explanations.