Sei sulla pagina 1di 3

DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

 a disorder characterized by systemic activation of the clotting cascade with microthrombi formation,
platelet consumption, and subsequent exhaustion of all clotting factors, which causes hemorrhagic
manifestations.
 The most common causes are sepsis, trauma, and malignancy. Patients present with bleeding
manifestations (e.g., purpura), and/or signs of multiorgan failure.
 Laboratory studies show thrombocytopenia, prolonged PT and aPTT, decreased fibrinogen levels,
and increased D-dimer.
 Treatment of DIC involves treatment of the underlying cause, and supportive therapy with
transfusions of platelet concentrates, FFP, and/or cryoprecipitate.

ETIOLOGY

 Sepsis (more commonly with gram-negative organisms)


 Malignancies
o Acute promyelocytic leukemia
o Pancreatic, ovarian, or gastric adenocarcinomas
 Acute traumatic coagulopathy
 Acute hemolytic transfusion reaction (AHTR)
 Traumatic brain injury
 Obstetric complications
o Amniotic fluid embolism
o Pre-eclampsia
o Abruptio placenta
o Retained products of conception
 Acute pancreatitis
 Heat stroke
 Intravascular hemolysis (e.g., acute transfusion reaction)
 Extracorporeal procedures (e.g. dialysis)
o Due to contact of blood with an exogenous surface
 Toxins: snake bites, amphetamine overdose
 Vascular malformations: aortic aneurysms

PATHOPHYSIOLOGY

Types of DIC Bleeding Organ- Massive Non-


(hyperfibrinolytic failure (thrombotic) bleeding symptomatic DI
) type type (consumptive) C
type
Pathophysiolo  ↑ Cytokines →
 Hyperfibrinolysis  Hyperfibrinolysis Mild fibrinolysis a
gy hypercoagulation with and nd mild
hypofibrinolysis hypercoagulation hypercoagulation
→microthrombi → → consumption
impaired perfusion and of platelets and
tissue necrosis all coagulation
factors
Common   Sepsis
Leukemia (e.g., ac  Post-  Any cause of
causes ute promyelocytic operative DIC DIC
leukemia)  Obstetric
 Obstetric complications
complications  Pancreatic,
 Aortic aneurysms ovarian,
 Acute traumatic gastric, brain
coagulopathy tumors
Clinical  Bleeding  Multi-organ failure  Massive  Asymptomatic
manifestation  Microangiopathic hemol hemorrhage
ytic anemia

Note: DIC is an acquired coagulopathy that is frequently seen in hospitalized individuals!


CLINICAL FEATURES

 Bleeding manifestations
o Petechiae, purpura, ecchymoses
o Oozing of blood from surgical wounds,intravenous lines
o Hematuria
o Hematemesis, hematochezia
o Collection of blood in body cavities: features of hemoperitoneum, hemothorax
 Thrombotic manifestations
o Acute renal failure: oliguria
o Hepatic dysfunction: jaundice
o ARDS: dyspnea, rales
o Pulmonary thromboembolism: dyspnea, chest pain, hemoptysis
o Deep vein thrombosis: lower limb edema
o Neurological dysfunction: altered mental status, stroke
o Purpura fulminans: DIC with extensive skin necrosis
o Waterhouse Friderichsen syndrome: adrenal infarcts → adrenal insufficiency
 Note: The clinical features of DIC may appear acutely (e.g., following trauma, sepsis), or may appear
subacutely (e.g., DIC following malignancy)!

DIAGNOSTICS

The diagnosis of DIC is not based on a single marker but on a combination of laboratory findings!
Thrombocytopenia, elevated D-dimer, increased PT and aPTT, and low fibrinogen should immediately
raise suspicion for DIC!

Finding Type of DIC


Bleeding Organ Consumptive Non-
type failure type symptomatic
type type
Thrombocytopenia → ↑ bleeding time ✓ ✓ ✓ ✓
(Thrombocytopenia is an early, sensitive
finding of DIC!)
↑ Markers of fibrin breakdown ✓ ✓ ✓ ✓
(D-dimer, or FDP)
↑ PT and APTT ✓ ✓ ✓ ×
↓ Fibrinogen levels ✓ × ✓ ×
↓ Antithrombin × ✓ × ×

↓ Hematocrit × × ✓ ×
Schistocytes × ✓ ✓ ×
(In the case of DIC, schistocytes
(fragmented erythrocytes) are seen in
association with microangiopathic
hemolytic anemia.)

DIFFERENTIAL DIAGNOSIS

 Severe hepatic dysfunction: clinical features, and/or laboratory findings of liver injury, normal factor
VIII assay
 Thrombotic thrombocytopenic purpura/immune thrombocytopenic purpura: no consumption
coagulopathy → normal PT, aPTT
 Heparin-induced thrombocytopenia: history of heparin use, heparin-PF4 (HIT) antibodies in serum

Note: All coagulation factors would be decreased in patients with DIC!


TREATMENT

 Treatment of the underlying illness (e.g., antibiotics for infectious diseases, chemotherapy or
surgery for malignant disease)
 Bleeding and consumptive types
o Transfusion of blood products
 Platelet concentrate if:
 Platelet count < 10,000 in asymptomatic individuals
 Platelet count < 50,000 in patients with active bleeding or if a surgical procedure
is planned
 Fresh frozen plasma if PT or APTT > 1.5 times the normal value
 Cryoprecipitate if fibrinogen < 150 mg/dL
 Packed RBCs if:
 Massive hemorrhage without hemodynamic response to fluid therapy
 Hb < 7 g/dL
 If acute traumatic coagulopathy → transfuse packed RBC, FFP, and platelet
concentrate in a 1:1:1 ratio
o Synthetic protease inhibitor (e.g., Gabexate mesilate®, nafamostat®)
o Antifibrinolytic therapy (e.g., tranexemic acid)
 Organ failure type: natural protease inhibitor (e.g., antithrombin, or rhTM administration)
 Non-symptomatic type: heparin

Note: Treatment of the underlying disease forms the cornerstone of the management of DIC!

Potrebbero piacerti anche