STEPTRACKERHEMATOLOGY | PATHOLOGY | HIGH-YIELD REVIEW

DIC & Fibrinolysis

Clotting everywhere uses up the clotting system, so the patient bleeds — always secondary to something else.

FOCUS ON
DIC labs: ↓ platelets, ↑ PT, ↑ PTT, ↓ fibrinogen, ↑ D-dimer, schistocytes. Know the triggers (sepsis, obstetric emergencies, APL, trauma). Contrast DIC with primary fibrinolysis, where there is no D-dimer because no fibrin forms. Factor VIII separates DIC from liver disease.
TOPIC
MECHANISM
LABS · FINDINGS
CLUE · MANAGEMENT
DIC — definition
consumptive coagulopathy
Systemic thrombin generation → microthrombi everywhere → platelets and factors used up → bleeding.
↓ platelets, ↑ PT, ↑ PTT, ↓ fibrinogen, ↑ D-dimer, schistocytes
Always secondary — find the trigger
Sepsis
most common trigger
Endotoxin and cytokines → endothelial tissue factor expression.
Gram-negative sepsis, meningococcemia
Purpura fulminans (skin necrosis)
Obstetric
tissue factor from placenta
Placental tissue factor enters maternal blood.
Placental abruption, amniotic fluid embolism, retained dead fetus, HELLP
Sudden bleeding around delivery
Malignancy
acute or chronic
APL granules contain procoagulants; adenocarcinomas release mucin and tissue factor.
APL (AML-M3): acute DIC · pancreatic/gastric/lung adenocarcinoma: chronic DIC
APL → all-trans retinoic acid; chronic DIC → migratory thromboses
Other triggers
Tissue factor release or direct activation.
Major trauma, burns, acute pancreatitis, snake venom, acute hemolytic transfusion reaction, liver failure
—
Clinical picture
Bleeding and ischemia at the same time.
Oozing from IV sites and mucosa; organ failure from microthrombi (kidney, lung, brain, skin)
Treat the cause; give platelets, FFP, cryoprecipitate (fibrinogen) as needed
Primary fibrinolysis
plasmin overload
Excess plasmin without clotting — urokinase from prostate surgery, or ↓ α₂-antiplasmin in cirrhosis. Plasmin destroys fibrinogen.
↑ PT, ↑ PTT, ↓ fibrinogen, normal platelet count, no D-dimer
Bleeding after radical prostatectomy · aminocaproic acid, tranexamic acid
Thrombolytic therapy
iatrogenic
tPA (alteplase) converts plasminogen → plasmin.
Bleeding risk, including intracranial
Reverse with aminocaproic acid, cryoprecipitate

Mechanism — clot and bleed at once

TriggerTF, endotoxin, venom
→
Thrombin everywhereMicrothrombi
→
ConsumptionPlatelets, fibrinogen, factors
→
Fibrinolysis ↑D-dimer ↑
→
Bleeding + ischemiaOrgan failure

RBCs shear on the fibrin strands → schistocytes (microangiopathic hemolytic anemia).

Telling bleeders apart

FEATURE
DIC
FIBRINOLYSIS
LIVER DISEASE
Platelets
↓
Normal
Normal or ↓
PT / PTT
↑ / ↑
↑ / ↑
↑ / ↑
Fibrinogen
↓
↓
Normal or ↓
D-dimer
↑↑
Normal
Normal or mildly ↑
Factor VIII
↓ (consumed)
↓
Normal or ↑
Schistocytes
Yes
No
No

How it's tested

COMMON CONFUSIOND-dimer comes only from fibrin that was formed and cross-linked. That is why it is high in DIC and normal in primary fibrinolysis.
THE TRAPBleeding with prolonged clotting times in a cirrhotic patient might be liver disease or DIC. A normal or high factor VIII points to liver disease, because endothelium still makes it.
YOUR APPROACHFind the trigger in the stem, confirm consumption (platelets + fibrinogen ↓, D-dimer ↑), then treat the cause.

If you see… think…

Septic patient oozing from IV sites, ↓ platelets, ↑ PT/PTT, ↑ D-dimer → DIC
Placental abruption with falling fibrinogen → obstetric DIC
Promyelocytes with many Auer rods + DIC → APL — ATRA
Bleeding after prostatectomy, normal platelets, no D-dimer → primary fibrinolysis
Meningococcemia with spreading skin necrosis → purpura fulminans (DIC)
Sudden dyspnea and shock in labor, then DIC → amniotic fluid embolism
Best single screening test for DIC → D-dimer
Rattlesnake bite with uncontrolled bleeding → venom-induced consumption
Pancreatic cancer with recurrent migratory clots → chronic DIC / Trousseau