DIC DNB obg Theory Question Dec 2007

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DNB OBS AND GYN THEORY QUESTION DEC 2007 -

DISSEMINATED INTRAVASCULAR COAGULATION – DESCRIBE ITS CAUSES, PATHOGENESIS AND

MANAGEMENT ( 10 MARKS )

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• DEFINITION• ETIOLOGY• PATHOPHYSIOLOGY• CLINICAL MANIFESTATIONS• LABORATORY FINDINGS• DIFFERENTIAL DIAGNOSIS• TREATMENT

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DEFINITIONIT IS AN ACQUIRED CONDITION IN WHICH

NORMAL PHYSIOLOGY OF COAGULATION IS DISTURBED LEADING TO WIDESPREAD INTRAVASCULAR COAGULATION PROCESS ASSOCIATED WITH INJURY TO MICROVASCULATURE WHICH RESULTS IN ORGAN DYSFUNCTION, CAPILLARY LEAK & SHOCK.

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MECHANISMSOccurs due to simultaneous action of the following 4 mechanisms

1) Increased thrombin generation2) Suppressed physiological anticoagulant pathways3) Activation & subsequent impairment of fibrinolysis4) Activation of inflammatory pathways

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ETIOLOGY INFECTIOUS:

Meningococcemia- purpura fulminans

Bacterial sepsis- staphylococcal, streptococcal, E coli Rickettsia- Rocky Mountain spotted fever

Viral- CMV, varicella, arboviruses

Malaria, Candida, Aspergillus TISSUE INJURY:

Multiple fractures with fat emboli, crush injury, head injury MALIGNANCY:

Acute promyelocytic leukemia, acute myeloid leukemia, neuroblastoma

VENOM OR TOXIN:

Snake bites, insect bites

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CONTD… MICROANGIOPATHIC DISORDERS:

TTP, HUS, Kasabach-Meritt syndrome GI DISORDERS:

Fulminant hepatitis, Inflammatory bowel disease, Pancreatitis HEREDITARY THROMBOTIC DISORDERS:

Antithrombin III deficiency, Homozygous protein C deficiency NEWBORN:

Maternal toxemia, Abruptio placentae, Necrotizing enterocolitis, Erythroblastosis fetalis

MISCELLANEOUS:

Acute graft rejection, Acute hemolytic transfusion reaction, Collagen vascular disorders, Heparin induced thrombosis, hyperpyrexia

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PATHOPHYSIOLOGY

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CLINICAL MANIFESTATIONS

DIC

NON OVERT DIC OVERT DIC ACUTE DIC CHRONIC DIC

CONTROLLED UNCONTROLLED

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Non overt DIC:

Stressed & compensated hemostatic system. Lab tests- abnormal but no clinical manifestations.

Overt DIC:

Stressed and decompensated hemostatic system. Lab tests- abnormal with clinical bleeding or micro vascular thrombosis and organ dysfunction.

Further divided into controlled and uncontrolled based on whether the process will resolve when the underlying condition is removed.


Acute DIC:

• Bleeding from vein puncture site, surgical wound.• Grayish discoloration of tips of fingers, toes &

ears in a symmetrical distribution.• Meningococcemia(PURPURA FULMINANS)-

bleeding from GI tract, gingival bleeding, epistaxis, pulmonary hemorrhage, hematuria.

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Chronic DIC:

• Superficial and extensive ecchymosis of extremities without petechiae which may be intermittent or can persist.

• Recurrent episodes of epistaxis or internal mucosal bleeding.

• Trousseau sign- Recurrent migratory thrombophlebitis in association with cancer.

• Impairment of renal function, confusion, repeated episodes of cerebral thrombosis.

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PURPURA FULMINANS OF A CHILD'S LEG


Specific features of DIC in neonates and infants

CAUSES:

• Transplacental passage of thromboplastin or other procoagulant substances in neonates born of mothers affected with DIC owing to abruptio placenta, eclampsia or septicemia

• Development of DIC in a twin fetus may be due to feto-fetal passage of thromboplastin.

• DIC secondary to hemangioma . PRECIPITATING FACTOR:

Asphyxia, septicemia, eclampsia


CLINICAL FEATURES: Symmetric ecchymosis of lower extremities and

buttocks. Later these lesions become necrotic ultimately forming blood filled bullae.

Sharply circumscribed infarcts of skin and genitalia Gangrene of extremities involves digits symmetrically. Fever and prostration Mortality 40-70% TREATMENT: Heparin. Relapse common after cessation.


BULLAE SEEN IN DIC


LABORATORY FINDINGS

COMPLETE BLOOD COUNT:

Severe thrombocytopenia(50000-100000/µl) with or without anemia

PERIPHERAL BLOOD SMEAR:

Schistocytes- Microangiopathic hemolysis

PROTHROMBIN TIME & aPTT:

Prolonged in early cases but may be normal or short in chronic cases

FIBRINOGEN LEVEL:

Low


SCHISTOCYTES IN PERIPHERAL BLOOD SMEAR


D dimer, FIBRINOGEN / FIBRIN DEGRADATION PRODUCTS:

Increased >25µg fibrinogen equivalents/ml

PROTEIN C & S, ANTITHROMBIN:

decreased

MARKERS OF ENDOGENOUS THROMBIN GENERATION:

Prothrombin fragment 1.2 and

Thrombin-Antithrombin complexes(TATs) are elevated


Overt DIC Scoring System


DIFFERENTIAL DIAGNOSIS

Primary fibrinogenolysis or Pathologic fibrinolysis:

Platelet count is normal

D dimer may be normal or minimally increased

No hypoprothombinemia & No deficiency of coagulation factors (VII, IX, X, XI)

Severe liver disease:

D dimer test is normal


TREATMENT

BLOOD COMPONENT THERAPY:

INDICATIONS:Active bleedingInvasive procedureRisk of bleeding complication

GOALS: To maintainPlatelet count >50000/µlFibrinogen concentration >1g/LProthrombin values less than double the normal range


FRESH FROZEN PLASMA(FFP):

Constituents:

0.7-1.0 U/ml of factors II,V, VII, VIII, X, XI, XII, XIII and2.5mg/ml fibrinogen.

Dosage: 15ml/kg

CRYOPRECIPITATE: Constituents;

fibrinogen 150mg/bagfactor VIII 80-120units/bagfactor XIII & vWB

Dosage: 1 bag/5kg body wt.


PLATELETS:

Random donor platelets(RDP):

• Constituents:

5.5×10¹° platelets

• Dosage:

1 unit/ 10 kg Single donor platelets:

• Constituents:

3×10¹¹ platelets

FRESH BLOOD:

Indicated in severe trauma to replace acute massive blood loss.


ANTICOAGULANT THERAPY: Heparin and other anticoagulant therapy to inhibit thrombin.

Indicated in patients with clinically overt thromboembolism , chronic DIC and extensive fibrin deposition.

Dosage:

Weight < 30kg – 10U/kg/hr

Weight > 30kg – 4U/kg/hr


REPLACEMENT OF NATURAL ANTICOAGULANT PATHWAYRecombinant human activated protein c 24µg/kg/hr.

Adverse effects include bleeding.

ANTI-THROMBIN INDEPENDENT INHIBITORS desirudin

gabexate mesylate


COMPLICATIONS

Respiratory failureRenal failureStrokeCardiac tamponadeHemothorax


PROGNOSIS

• Since DIC is a result of an acute medical illness, prognoses depends almost entirely upon the speed of the intensivist in handing the bleeding emergency, as well as the ability to treat the underling disorder

• The underlying disease that causes the disorder will usually predict the probable outcome.


Thank you

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DIC DNB obg Theory Question Dec 2007

Health & Medicine

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