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

Normal physiology:

*	Clot formationand Fibrinolysis is precise and localized to sites of vascular injury- process regulated by balance between procoagulants/anticoagulants and fibrinolytics/antifibrinolytics.

*	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

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

*	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

Mnemonic- TOMS

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
  *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)
  
  • INR and PTT
  • Fibrinogen
  • D-dimer

Question 10

D/Dx

Answer 10

2. HIT (Heparin-Induced Thrombocytopenia)

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.

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

*	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.

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.
5. Sepsis induced thrombocytopenia and coagulopathy-(SIC)
   -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.

Question 10

DIC INVx

Answer 10

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

⸻

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

⸻

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.

⸻

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.

⸻

Antithrombin III
* Consumed in DIC → reduced levels.
* May explain heparin resistance in DIC.
* Can indicate early (nonovert) DIC.

***Other causes of low AT III:
* ECMO, dialysis, IABP
* Heparin therapy
* Cirrhosis
* Nephrotic syndrome

⸻

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

⸻

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).

Question 11

Treatment

Answer 11

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.