Class Presentation on DIC

1. Disseminated Intravascular Coagulation
Presented by,
Sumona Ghosh
M.Sc.Nursing Final Year Student
College of Nursing, Medical College and Hospital, Kolkata

2. Introduction
Disseminated intravascular coagulation (DIC) is an acquired
dysregulation of homeostasis. The presentation ranges from an
isolated derangement of laboratory parameters to severe bleeding
from multiple sites, associated with high mortality. DIC may be
triggered by a variety of conditions that result in activation of the
clotting cascade, deposition of fibrin in the microcirculation and
consumption of platelets and clotting factors. The diagnosis of DIC
is clinical; laboratory tests provide confirmatory evidence.

3. Incidence
Very rare (less than 1 lakh cases per year in India)

4. Definition
Disseminated intravascular coagulation (DIC) is an acquired
haemorrhagic disorder in which there is an unregulated thrombin
explosion leading to release of free thrombin in the circulation
resulting in widespread micro vascular thrombosis.

5. Types
Acute or decompensated DIC
Where there is a sudden massive exposure of tissue factor over a
brief time period, the control mechanisms are overwhelmed and there is
no time for regeneration of coagulation factors, is referred as acute or
decompensated DIC.
Chronic or compensated DIC
When the control mechanisms in the body replenish the factors by
augmented production, it is referred to as chronic or compensated DIC.

6. Etiology
Acute DIC
 Infection
 Septicaemia
 viral or other infections
 Trauma
 Crush injury
 Burns
 Multiple fractures
 Major surgery
 Allograft rejection

7. Continue
 Systemic condition
 Fulminant hepatic failure
 Heat stroke
 Acute promyelocytic leukaemia
 Neuroblastoma
 Haemolytic uremic syndrome
 Collagen vascular disease and snake bite
 Iatrogenic
 Haemolytic transfusion reaction
 Heparin induced thrombosis.

8. Continue
 Malignancies
 Monocytic leukaemia
 Neuroblastoma
 Cardiovascular
 Shock,
 Cyanotic congenital heart disease,
 Giant haemangioma,
 Aortic aneurysm

9. Continue
 Haemolytic anaemia’s
 Thalassemia
 Sickle cell anaemia
 Collagen vascular diseases
 Liver cirrhosis

10. Pathophysiology
Due to trigger factors such as hypoxia, tissue necrosis, acidosis, shock and endothelial damage
activates clotting mechanism (The process of coagulation follows either intrinsic or extrinsic
pathway)
Thrombin generation results due to activated platelets by extrinsic pathway
Rapid depletion of platelets, prothrombin and fibrinogen
Formation of fibrin
Vascular occlusion & platelet dysfunction
Increased, uncontrolled bleeding resulting
from the
platelet and clotting factors depletion
Anaemia caused by
excessive bleeding
Organ damage resulting
from the formation of
emboli
Tissue hypoxia
leading to tissue
necrosis

11. Three main pathological process
1. Initiation of fibrin deposition Thrombin generation in DIC is mediated
by the extrinsic (tissue factor) pathway. The tissue factor accumulates
on activated platelets by binding to platelet P-selectin which results in
thrombin generation.
2. Amplification role of thrombin Thrombin generated amplifies
inflammation and clotting by activating platelets and factors V, VIII
and 1X, which lead to more thrombin production. Activated factor XIII
leads to it cross-linking with fibrin clots making them insoluble, while
thrombin activates the fibrinolysis inhibitor, making the clot resistant
to fibrinolysis.

12. Continue
3. Propagation of fibrin deposition There is suppression of fibrinolysis
secondary to sustained increase in plasma levels of plasminogen-activator
inhibitor. Following injury, infection or other precipitating factors, there is
release of cytokines (tumour necrosis factor alpha, IL-1 and IL-6) which
change the endothelium from an anticoagulant to a procoagulant surface and
interfere with fibrinolysis.
As DIC continues, fibrinogen, prothrombin, platelets and other clotting
factors are consumed beyond the capacity of the body to compensate and
bleeding ensues. Activated protein C has an anti-inflammatory effect: it
down regulates the tissue factor and decreases calcium ion flux.

13. Clinical Features
 Bleeding:
 Petechiae
 Purpura
 Haemorrhagic bullae
 Surgical or traumatic wound bleeding
 Oozing from puncture site
 Subcutaneous hematoma
 Epistaxis,
 Sub-conjuntival haemorrhages
 Haematuria

14. Continue
 Micro vascular thrombosis in skin, subcutaneous tissue and
other organs
 End organ damage
 Intracranial bleed
 Pulmonary oedema
 Acute renal failure
 Peripheral cyanosis and gangrene
 Purpura fulminance may occur leading sharply demarcated large
patches of ecchymosis and skin infarction.

15. Diagnostic evaluation
Algorithm for diagnosis of disseminated intravascular coagulation
(DIC) using the DIC score
 Risk assessment
Does the patient have an underlying disorder known to be associated
with disseminated intravascular coagulopathy? (If yes, proceed. If
no, do not use this algorithm).
 Order global coagulation tests
Platelet count; prothrombin time, fibrinogen, soluble fibrin
monomers or fibrin degradation products

16. Continue
Score test results
(a) Platelet count
 >100,000/mm3 0
 50,000-100,000 / mm3 1
 <50,000 / mm3 2
(b) Elevated fibrin-related marker (soluble fibrin monomers or fibrin degradation products)*
 No increase 0
 Mild increase 1
 Moderate increase 2
 Strong increase 3
(c) Prothrombin time
 <3 sec 0
 >3 but <6 sec 1
 >6 sec 2
(d) Fibrinogen level
 >1 g/l 0
 <1 g / l 1
Calculate score
Score >5: Compatible with overt DIC; repeat
daily
Score <5: Suggestive of non-overt DIC; repeat in
1-2 days

17. Continue
 Screening tests Peripheral blood film examination and hemogram show
schistocytes and thrombocytopenia. Prothrombin time, activated partial
thromboplastin time and thrombin time are prolonged.
 Supportive tests Increase in fibrin degradation products or D-d isomer is
characteristic. No single test is diagnostic of DIC. The presence of
thrombocytopenia and low levels of fibrinogen (50% drop in either value)
are most sensitive in making a laboratory diagnosis. A DIC scoring
system has been established based on the recommendations of the
Scientific Standardization Committee of the International Society on
Thrombosis and Haemostasis; an underlying predisposing disorder is a
prerequisite for the use of this algorithm. A score of 25 is diagnostic.

18. Treatment
 Treatment of the triggering disease: Early use of antibiotics in sepsis, optimizing
hemodynamic stability, maintaining adequate oxygenation and acid-base balance.
 Heparin therapy: Heparin to inhibit thrombin formation and function
administered at a dose of 15 U/kg/hr. as a continuous infusion.
 Blood component therapy: Packed red cells, platelet concentrates and non-clotting
protein containing volume expanders such as albumin.
 Inhibitor therapy: Inhibitors of coagulation such as activated protein C and tissue
factor pathway inhibitor (TFPI)
 Antifibrinolytic agents: Epsilon-aminocaproic acid and tranexamic acid.

19. Continue
 Supportive nursing care should include:
 Continuous monitoring of signs of vascular occlusions and patient's
general condition
 Maintenance of IV fluid, oxygen therapy
 Precautions to prevent injury and bleeding
 Administration of prescribed medications avoiding vasoconstriction
and dislodging clot
 Bed rest, change of position
 Range of motion exercises and maintenance of warmth
 Pressure to be applied for 20 minutes at the site of bleeding and
topical haemostatic agents to be used to minimize bleeding. Features
of internal bleeding should to be assessed for prompt management.

20. Nursing Diagnosis
 Impaired Gas Exchange related to altered oxygenation and/or carbon
dioxide elimination at the alveolar- capillary membrane or altered
oxygen- carrying capacity of blood.
 Ineffective tissue perfusion decreased in the oxygen resulting in the
failure to nourish the tissues at the capillary level may be related to
blood circulation disruption/ micro thrombi.
 Deficient knowledge or deficiency of cognitive information related
to specific topic may be related complexity of treatment/ emotional
state affecting learning/ new condition and/or treatment/ unfamiliar
environment.
 Risk for bleeding related to abnormal blood profile ( depleted
coagulation factors)/ drug therapy (adverse effects of heparin)

21. Complications
 Pulmonary embolism
 Acute renal failure
 Cerebral haemorrhage (most common causes of death) and
infarction in cerebrum, myocardium and spleen.
 Haemolytic anaemia
 GI ulcerations
 Tissue necrosis and gangrene may also develop.

22. Prognosis
Mortality rate is high in acute DIC, i.e. about 50 to 85%. Highest
mortality is found in neonates. Prolonged prothrombin time (more than
1.5 times) and activated partial thromboplastin time indicate poor
prognosis.

23. Conclusion
DIC is serious life threatening condition secondary to any underlying
pathology. There is spontaneous resolution of DIC after correction of
pathology.

24. Thank you