Disseminated Intravascular Coagulation (Dic)

DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

By

Dr.Nusrum Iqbal

Diplomate American Board of Internal Medicine

Assisstant Professor of Medicine

LahoreMedical & DentalCollege, Lahore

INRODUCTION

•An explosive and life threatening disorder

•Acute, subacute, or chronic thrombohemorrhagic disorder occurring as a secondary complication

•Widespread endothelial damage releases a protein known as tissue factor(tissue thromboplastin) that activates the endogenous coagulation cascade and the fibrinolytic system

•Results in a severe coagulopathy characterized by widespread microvascularthrombosis accompanied by depletion of circulating platelets and procoagulant proteins

Physiology of the coagulation cascade

•Extrinsic pathway-triggered by the release of tissue factor

•Intrinsic pathway-involves the activation of factor XII by surface contact with collagen or other negatively charged substances

•Clot-inhibiting influences- involves activation of the fibrinolysis

*DIC mainly results from pathologic activation of the intrinsic / extrinsic pathways or impairment of the clot-inhibiting influences

Pathology

•Two major mechanisms trigger DIC

–Release of tissue factor into the circulation

–Widespread injury to the endothelium

PATHOGENESIS

•Activation of leucocytes, particularly monocytes causing the release of tissue factor and cytokines

•Accleration of the coagulation reactions

•Early thrombotic phase

•Phase of procoagulant consumption

•Secondary Fibrinolysis

•Continued fibrin formation and fibrinolysis lead to hemorrhage from the depletion of coagulation proteins and platelets and the antihemostatic response of FDPs

Tissue factor sources

•Placenta

•Grannules of leukemic cells in AML

•mucus of adenocarcinomas

•Endothelial injury

•Bacterial endotoxin-- increased synthesis in monocytes---release of TNF-alpha & IL-1

•TNF-alpha is the most important mediator in DIC

•Suppression of the thrombomodulin

ETIOLOGIC FACTORS & DISORDERS

•Liberation of tissue factors

Obstetrical syndromes- abruptio placentae, amniotic fluid embolism , retained dead fetus 2nd trimester abortion

Hemolysis

Neoplasmsadenocarcinomas(mucinous) acute promyelocytic leukemia

Intravascular hemolysis

Fat embolism

Tissue damage- burns, frostbite, head injury, gunshot wounds

•Endothelial damage

•Vascular malformations & decreased blood flow

•Infections

Aortic aneurysm

Hemolytic uremic syndrome

Acute glomerulonephritis

Rocky Mountain spotted fever

Kasabach-Merritt syndrome

Bacterial: staphylococci, streptococci, meningiococci, gram negative bacilli

Viral: adenovirus, varicella, variola, rubella

Parasitic: malaria, kala-azar

Rickettsial: RMSF

Mycotic: acute histoplasmosis

Snake bite

CLINICAL PRESENTATION

•Presentation varies with the stage and severity of the syndrome

•Underlying problem is usually obvious

•Acutely ill and shocked

•Extensive skin & mucous membrane bleeding and hemorrahge from multiple sites

•Peripheral acrocyanosis, thrombosis and pregangrenous changes in digits, genetilia, and nose

•Patients with chronic DIC secondary to malignancy, have laboratory abnormalities without any evidence of thrombosis or hemorrhage

INVESTIGATIONS

The diagnosis is often suggested by the underlying condition of the patient and laboratory evidence

Severe cases with hemorrhage

•PT, PTT and TT(thrombin time)- prolonged

•Fibrinogen level- markedly reduced

•FDPs- very high levels

•D dimer immunoassay- crosslinked fibrin derivatives, more specific

•Thrombocytopenia-- severe

•Blood film- shistocytes or fragmented RBCs

Cotinued

Mild cases without bleeding

•Increased synthesis of coagulation factors and platelets results in normal PT, PTT, TT and Platlets

•FDPs will be raised

MANAGEMENT

•Emergency treatment- acute, fulminant DIC often has a fatal outcome

•Treatment of the underlying condition is the most important and may be all that is necessary in patients who are not bleeding

•Measures to control bleeding /thrombosis

•Prophylactic regimen to prevent recurrence in cases of chronic DIC

Management of Obstetric Complications

•Abruptio placentae or acute bacterial sepsis

–the underlying disorder is easy to correct

–prompt delivery of the fetus and placenta

–treatment with appropriate antibiotics

Metastatic tumors

control of primary disease is not possible

long-term prophylaxis is necessary

Symptomatic Management

Bleeding as a major symptom

Fresh frozen plasma

Platelet concentrates

Acrocyanosis/ Incipient gangrene

Intravenous heparin (use of heparin is controversial)

reserved for patients who continue to bleed or thrombosis

Management of Mild DIC cases

•Mild DIC cases may begin to bleed during surgery or chemotherapy

•Mild DIC, without clinical bleeding--saline or prostaglandin induced midtrimester abortions/ Acute promyelocytic leukemia

•Prophylactic heparin is required during surgical extraction of the retained dead fetus

•Chronic DIC doesnot respond to warfarin