DISSEMINATED INTRAVASCULAR COAGULATION (DIC)



DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

By

Dr.Nusrum Iqbal

Diplomate American Board of Internal Medicine

Assisstant Professor of Medicine

Lahore Medical & Dental College, 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 microvascular thrombosis 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

Neoplasms adenocarcinomas(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

................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download