2. Disseminated intravascular coagulation
Disseminated intravascular coagulation (DIC) is a syndrome in
which either the
extrinsic or intrinsic or both pathways
are activated to produce multiple fibrin clots in small blood
vessels.
The resultant reduction of the coagulation factors and
platelets results in
Bleeding
3. Disseminated intravascular coagulation
It is essentially an imbalance between the
coagulation process and anticoagulation process.
It is a syndrome of coagulation proteins,
fibrinolytic proteins and platelets.
8. Fibrinolysis at the onset of
the DIC
Plasminogen activator inhibitor 1 (PAI-1) is a
neurohumoral compound released by the
endothelial cells at the effected site.
PAI-1 suppresses the normal fibrinolysis activity.
Some DIC individuals have shown a mutation in
the PAI-1 gene, leading to an increased plasma
PAI-1 levels.
9.
10. Etiology of DIC
DIC is not itself a specific illness
It is always secondary to an underlying disorder
and is associated with a number of clinical
conditions, generally involving activation of
systemic inflammation
16. Bleeding Manifestations
Bleeding from several sites of body
Ear nose throat
GI tract
Hematemesis
Melaena
Respiratory tract
Hemoptysis
Bleeding from intravenous (IV) lines and catheters
From surgical sites, drains.
17. Bleeding Manifestations
Skin may show various signs including
Petechiae.
Purpura.
Hemorrhagic bullae.
Acral cyanosis.
Skin necrosis of lower limbs (purpura fulminans).
Localize infarction and gangrene.
18. Organ Failure
Cardiovascular signs include the following:
1. Hypotension
2. Tachycardia
3. Circulatory collapse
Respiratory signs include the following:
Signs of acute respiratory distress syndrome
(ARDS)
19. Organ Failure
Genitourinary signs include the following:
Signs of azotemia and renal failure
Hematuria
Oliguria
Central nervous system signs include the
following:
Nonspecific altered consciousness or stupor
Transient focal or neurologic deficits
22. Investigations
CBC
Thrombocytopenia is usually present
Clotting times:
Prothrombin time (PT) – prolonged
Partial thromboplastin time (PTT) - prolonged
Thrombin time (TT) – may be increased due to
consumption of fibrinogen
23.
24. Investigations
Fibrin related markers important for the diagnosis
of DIC:
D-dimer – increased (best single test)
A normal d-dimer essentially rules out
DIC
Coagulation factors:
Fibrinogen is usually decreased
25.
26. Scoring systems
The International Society on Thrombosis and
Hemostasis (ISTH) developed a simple
scoring system for the diagnosis of overt DIC
that makes use of laboratory tests available in
almost all hospital laboratories.
27.
28. Management
• The cornerstone of the treatment of DIC is
treatment of the underlying condition
• If infection is the underlying etiology, the
appropriate administration of antibiotics and
source control is the first line of therapy
• In case of an obstetric catastrophe, the primary
approach is to deliver appropriate obstetric care, in
which case the DIC will rapidly subside.
29. Management of the DIC itself has the
following basic features
Monitor vital signs
Assess and document the extent of hemorrhage
and thrombosis
Correction of hypovolemia
Administer basic hemostatic procedures when
indicated
30. Transfusion of Platelet
Patients with
DIC and active bleeding
undergo an invasive procedure and
platelet count of <50k
then transfusion of platelets should be considered.
31. Transfusion of Platelet
In non-bleeding patients with DIC, prophylactic
platelet transfusion is not given unless it is
perceived that there is a high risk of bleeding
32. Transfusion of Fresh Frozen Plasma
Patient with
DIC with active bleeding or
Will undergo an invasive procedure
prolonged PT and aPTT,
administration of fresh frozen plasma (FFP) may be
useful.
Initial doses of 15-30 ml/kg are required
33. Transfusion of Fresh Frozen Plasma
Component
all coagulation factors
fibrinogen (400 to 900 mg/unit),
albumin, protein C, protein S, antithrombin,
tissue factor pathway inhibitor
Volume: 200-250ml
If FFP is not given immediately after thawing, it
should be stored at 1 to 6 C. If the thawed FFP is
not used in 24 hours, it should be discarded
34. Transfusion of cryoprecipitate
Severe hypofibrinogenemia (<1 g/L) that persists
despite FFP replacement, or specific fibrinogen
deficiencies may be treated with fibrinogen
concentrate or cryoprecipitate .
35. Cryoprecipitate
One unit of cryoprecipitate
Volume : 15 ml
Component :100unit clotting factor VIII, 250 mg of
fibrinogen, VWF.
Stored at – 18C.
Infusion within 6 hours of thawing
Dose: 1 unit / 10 kg.
36. Unfractionated Heparin
In cases of DIC where
thrombosis predominates, such as arterial or venous
thromboembolism,
severe purpura fulminans associated with acral
ischemia
vascular skin infarction,
therapeutic doses of heparin should be considered. If
there is a co-existing high risk of bleeding there may be
benefits in using continuous infusion of unfractionated
heparin (UFH) due to its short half-life and reversibility.
37. Heparin as a prophylaxis
In critically ill, non-bleeding patients with DIC,
prophylaxis for venous thromboembolism with
prophylactic doses of heparin or low molecular
weight heparin is recommended.
Dose 4-5 uint/kg constant infusion .
Observation for signs of bleeding is important
38.
39. Antithrombin
Antithrombin is used for
moderately severe–to–severe DIC or when levels
are depressed markedly.
It is an alpha2-globulin that inactivates thrombin,
plasmin, and other serine proteases of
coagulation, including factors IXa, Xa, XIa, XIIa,
and VIIa.
These effects inhibit coagulation
40. Recombinant human activated protein C
Consider treating patients with severe sepsis and
DIC with recombinant human activated protein C (
continuos infusion, 70U/kg/24h for 4 d)
Patients at high risk of bleeding should not be
given recombinant human activated protein
Current manufacturers guidance advises against
using this product in patients with platelet counts
of <30.
41. Recombinant thrombomodulin
Recently rTM shows significantly improved control
of DIC in comparison with unfractionated heparin,
In Japan, rTM is widely used for treatment of DIC
Thrombomodulin binds with thrombin> conversion
of thrombin procoagulant to anticoagulant .
42. Role of tranexamic acid
In general, patients with DIC should not be treated
with antifibrinolytic agents
Patients with DIC that is characterised by a primary
hyper fibrinolytic state and who present with severe
bleeding could be treated with lysine analogues, such
as tranexamic acid. (e.g. 1 gm in every 8 hour).
43. Summery of Treatment
Condition Treatment option
DIC with active bleeding + low platelet Transfusion of Platelet
DIC with active bleeding + raised PT
aPTT
Transfusion of FFP
Not respond to FFP Transfusion of Cryoprecipitate
DIC with no bleeding + sepsis recombinant human activated protein C
DIC with thrombosis Heparin
44. Complications of DIC
Two types of complication may occur
1. Due to hemorrhage
2. Due to intravascular thromboembolism .
A patient may die due to massive hemorrhage in
case of severe DIC.
45. Complications of DIC
DIC can rapidly lead to organ failure and it is often
fatal condition, especially when not identified and
treated early
Ischemic stroke
Myocardial infraction
Pulmonary embolism
Renal failure
Ischemia of extremities
46. Prognosis
Prognosis varies depending on the underlying
disorder, and the extent of the intravascular
thrombosis (clotting). The prognosis for those
with DIC, regardless of cause, is often grim:
Between 10% and50% of patients will die.
DIC with sepsis (infection) has a significantly
higher rate of death than DIC associated with
trauma.
