The document discusses disseminated intravascular coagulation (DIC), including its causes, clinical features, diagnostic testing, management, and complications. DIC results from excessive activation of coagulation pathways leading to microthrombi formation and bleeding. It is always secondary to an underlying condition like infection, malignancy, trauma, or obstetric complications. Management involves treating the underlying cause, monitoring for bleeding and organ dysfunction, and replacing clotting factors or administering anticoagulants depending on the clinical situation. Complications can be bleeding or thromboembolic in nature. The prognosis depends on the severity of DIC and underlying condition.

1. Disseminated
Intravascular Coagulation
and its Management
Dr. Noman
Phase A resident
Oncology BSMMU

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.

4. Disseminated intravascular coagulation
There are 3 most common natural Anticoagulants
in the body:
 Antithrombin,
 Active Protein C
 Tissue factor pathway inhibitor (TFPI).

5. Disseminated intravascular coagulation
In DIC:
 ↓Antithrombin
 ↓Active Protein C

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.

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

11. Etiology
Infection
 Bacterial (gram-negative sepsis, gram-positive
infections,
rickettsial )
 Viral (HIV, cytomegalovirus [CMV], varicella-zoster
virus [VZV], and hepatitis virus)
 Fungal (Histoplasma)
 Parasitic (malaria)

12. Etiology
Malignancy
 Hematologic
 Metastatic
Obstetric
 Placental abruption
 Amniotic fluid embolism
 Acute fatty liver of pregnancy
 Eclampsia

13. Etiology
 Trauma
 Burns
 Extensive surgery
 Snakebite,
 Heat stroke
 Vasculitis
 Liver disease
 Rejection of graft

14. Clinical Feature
 Feature of
bleeding manifestation
 Features of
organ failure

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

20. Feature Percentage
Bleeding 64%
Renal dysfunction 25%
Hepatic dysfunction 19%
Respiratory function 16%
shock 14%
Central nervous system 2%

21. Investigations
 CBC
 Clotting times
 Fibrin related markers important for the
diagnosis of DIC
 Coagulation factors

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

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

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.

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

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.