DISSEMINATED INTRAVASCULAR

COAGULATION

(DIC)

Clinic Departement of Nursing Faculty UNPAD

DEFINITION

OF DISSEMINATED INTRAVASCULAR COAGULATION

DIC is an acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes. It can originate from and cause damage to the microvasculature, which if sufficiently severe, can produce organ dysfunction
ISTHs Scientific Subcommittee on DIC, July 2001

INCIDENCE / ETIOLOGY
DIC is reported to occur in 1% of hospitalized patients. Of those patients, the underlying cause was:

Generalized infection in ~30% of cases Malignancy in ~15% Surgery or trauma in ~20% Hepatic disease in ~10% Miscellaneous in ~25%

INFECTION
There are some mechanisms specific to infection in animals, there is evidence that Protein C is downregulated, as well as thrombomodulin. When shock develops, blood flow is reduced, which diminishes not only hemodilution, but to stasis as well. Tissue damage then occurs, which in itself causes thombin formation.

MALIGNANCY
Malignancy is a coagulopathic state. The features of malignancy most closely associated with DIC include: High levels of tissue factor expressed by tumor cells The expression by tumor cells of cancer procoagulant, a calcium-dependent cysteine protease which is not found in normal tissue (but is found in fetal tissue). It activates factor X directly.

TRAUMA
Trauma causes the release of tissue enzymes and phospholipids into the circulation in turn, these trigger the activation of cytokines and the coagulation system. The brain seems to have a higher proclivity to cause DIC than other body parts. Head trauma is associated with coagulopathy in twice as many patients with CT evidence of injury (41%) as in those without this evidence the coagulopathy was consistent with DIC by labs (more on labs later).

OBSTETRICAL
DIC occurs in a variety of obstetrical complications, including: Amniotic fluid embolization Abruptio placentae Eclampsia & severe pre-eclampsia Blah blah blah

DISSEMINATED INTRAVASCULAR COAGULATION (DIC) MECHANISM

Systemic activation of coagulation

Intravascular deposition of fibrin

Depletion of platelets and coagulation factors

Thrombosis of small and midsize vessels with organ failure

Bleeding

PROGRESSION OF SEPSIS
Non-adhesive Adhesive adhesive surface surface

Platelets

Monocytes
Cytokines Tissue factor

Endothelial cells

Leukocytes

Accelerates coagulation

Activation of coagulation Thrombin Fibrin

THE CLASSIC COAGULATION SYSTEM

Surface APTT contact XII XI IX XIIa XIa IXa

Prothrombin Tissue factor time

VIIa Ca++ Xa X IIa I Ia (fibrin)

VII

Phospholipid, Ca++, VIII X II Phospholipid, Ca++, V

CLINICAL
MANIFESTATIONS OF

DIC

SYMPTOMS OF DIC
Dysfunction of multiple organs
The pulmonary microembolism syndrome
Acute: vascular and bronchial constriction Late: ARDS

Acute renal failure

Oliguria, increasing serum creatinine, haematuria

Cerebral dysfunction
Confusion, blurred consciousness, coma

Cutane haemorrhagic Failure of liver.

DIAGNOSTIC
CRITERIA OF

DIC

BLOOD TESTS WHEN DIC IS SUSPECTED

Simple screening Platelet count Activated partial thromboplastin time (APTT) Prothrombin time (PT) Extended screening Fibrin D-dimer fragment Antithrombin Fibrinogen Supplementary tests Further evidence for activation of coagulation and fibrinolysis

Activation of coagulation Prothrombin

Fragment 1+2

D fragments E fragments

Fibrinogen

THROMBIN Antithrombin
Fibrinopeptide A+B

Fibrin

Plasmin

ThrombinAntithrombin complex (TAT)

FXIII

FXIIIa

Cross-linked fibrin
D dimer E fragments

SOLUBLE FIBRIN MONOMER AS PREDICTOR FOR DIC IN

NEONATAL SEPSIS
Healthy neonates: 24,5 6,09 mg/l Sepsis, no DIC: 33,7 11,9 mg/l Sepsis + DIC*: 73,2 31,6 mg/l *ISTH DIC score 5 Critical level: 48,5 mg/l Sensitivity: 100% Specificity: 93% Overall accuracy: 97,5%
Selim et al. Haematologica 2005;90:419-20

CONSIDERATIONS

IN PRACTICAL DIAGNOSTIC APPROACH TO DIC Presence of an underlying disorder The severity of haemostatic changes
Decompensated haemostatic system: Overt DIC Compensated haemostatic system: Non-overt DIC

The duration of activation

Temporary: e.g. Abruptio placentae, transfusion reaction Prolonged: e.g. Sepsis, malignancy, polytrauma

Laboratory tests
Global tests / Molecular markers Diagnostic value / Prognostic value

Use of scoring systems

DIC scoring system Other scoring systems
ISTHs Scientific Subcommittee on DIC, July 2001

SCORING SYSTEM FOR OVERT DIC

Underlying disorder known to be associated with overt DIC Platelet count
(>100=0, <100=1, <50=2) ..............................

YES
continue

NO
stop

Soluble fibrin/D-dimer
(normal=0, =2, =3) .............................

Prolongation of PT
(<3s=0, 3-6s=1, >6s=2) ................................

Fibrinogen
(>1g/l=0, <1g/l=1) ..........................................

Calculate sum ........................................

ISTHs Scientific Subcommittee on DIC, July 2001

SCORING SYSTEM FOR OVERT DIC

- Example Underlying disorder known to be YES associated with overt DIC Polytrauma continue Platelet count 85 1 (>100=0, <100=1, <50=2) .............................. Soluble fibrin/D-dimer 8 3 (normal=0, =2, =3) ............................. Prolongation of PT +3 1 (<3s=0, 3-6s=1, >6s=2) ................................ Fibrinogen 2,2 0 (>1g/l=0, <1g/l=1) .......................................... Calculate sum ........................................ 5 NO
stop

ISTHs Scientific Subcommittee on DIC, July 2001

SCORING SYSTEM FOR NON-OVERT DIC

Presence of underlying disorder Platelet count + changes
(normal=0, (100=0, <100=1) + ( =-1, stable=0, =1) + ( =-1, stable=0, (no=0, yes=2) .......................................................... =1) ....... =1) ........ =1) ...........

Sol.fibrin/D-dimer + changes Prolongation of PT + changes Antithrombin Protein C

(3s=0, >3s=1) + ( =-1, stable=0,

(normal=-1, low=1) ................................................. (normal=-1, low=1) ................................................. (normal=-1, high=1) .................................................

ISTHs Scientific Subcommittee on DIC, July 2001

TAT complexes

Calculate sum ................................................

SCORING SYSTEM FOR OVERT DIC

If the calculated score is

5: compatible with overt DIC repeat scoring daily <5: suggestive (not affirmative) for non-overt DIC repeat next 1-2 days.

ISTHs Scientific Subcommittee on DIC, July 2001

TREATMENT OF DIC

DIC TREATMENT APPROACHES

Treatment of underlying disorder Anticoagulation with heparin Platelet transfusion Fresh frozen plasma

TREATMENT OF DIC
DIRECTED AGAINST ETIOLOGICAL FACTORS

Infections Trauma

Antibiotics

Removal of damaged tissue stabilisation of fractures

Obstetric complications Evacuation of the uterus

ASSESMENT
abnormal bleeding from any or all body orifices bleeding into the skin (petechiae, ecchymoses, hematomas) bleeding from surgical or invasive procedure sites (incisions, venipuncture sites) mental status changes confusion dyspnea and tachycardia potential nausea, vomiting potential severe muscle, back and abdominal pain chest pain hemoptysis epistaxis seizures oliguria possible GI bleeding hematuria complicationsrenal failure hepatic damage, stroke, ischemic bowel,

LAB
Fibrinogen << Degradation fibrin product >> Platelet << PT, PTT prolonged

NX DIAGNOSE
Defisit fluid volume Ineffective tissue perfusion Impaired gas exchange: infant Anxiety

INTERVENTION
IV fluid with 16 0r 18 gauge cannula Folley catheter Intake out put monitoring Transfusion with red blood cell, fresh frozen plasmato replace fibrinogen and clothing factor Monitoring of transfusion reaction Asses client for abnormal bleeding: injection site, mucosa, etc

Posisi client of left side and monitori fetus well being Monitor laboratory values as obtained for improvement or worsening condition

THE FACE OF SEPSIS