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

Thrombosis of small
and midsize vessels
with organ failure

Depletion of platelets
and coagulation factors

Bleeding

PROGRESSION OF SEPSIS

Monocytes
Cytokines
Tissue
factor

Non-adhesive
Adhesive
adhesive
surface
surface

Endothelial
cells

Platelets

Leukocytes

Accelerates
coagulation

Activation of coagulation Thrombin Fibrin

THE CLASSIC COAGULATION SYSTEM

SurfaceAPTT
contact
XII

Prothrombin
Tissue factor
time

XIIa
XI

XIa
IX

IXa

VIIa

VII

Ca++

Phospholipid, Ca++, VIII

X

Xa

Phospholipid, Ca++, V
II

IIa
I

Ia (fibrin)

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

Cerebral dysfunction

Oliguria, increasing serum creatinine, haematuria

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

D fragments
E fragments

Activation of coagulation
Prothrombin

Fibrinogen

Fragment 1+2

THROMBIN
Fibrinopeptide
A+B

Antithrombin

ThrombinAntithrombin
complex
(TAT)

FXIII

Fibrin

Plasmin

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

NO

continue

stop

Platelet count

(>100=0, <100=1, <50=2) ..............................

Soluble fibrin/D-dimer

(normal=0, =2, =3) .............................

Prolongation of PT

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

Fibrinogen

YES

(>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 ........................................

ISTHs Scientific Subcommittee on DIC, July 2001

NO
stop

SCORING SYSTEM FOR NON-OVERT DIC

Presence of underlying disorder

Platelet count + changes

(100=0, <100=1) + (=-1, stable=0, =1) .......

Sol.fibrin/D-dimer + changes

(normal=0, =1) + (=-1, stable=0, =1) ........

Prolongation of PT + changes

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

Antithrombin

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

Protein C

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

TAT complexes

(no=0, yes=2) ..........................................................

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

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

ISTHs Scientific Subcommittee on DIC, July 2001

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

Platelet

Fresh

with heparin

transfusion

frozen plasma

TREATMENT OF DIC
DIRECTED AGAINST ETIOLOGICAL FACTORS

Infections

Antibiotics

Trauma

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