quick lecture about DIC, I used textbook sources and some online references hope you find what you are looking for. in this presentation, you will find practical guidance for DIC management which you can depend on in managing your patients

1. Disseminated intravascular
coagulation

2. DIC
 Widespread inappropriate intravascular deposition of
fibrin with consumption of coagulation factors and
platelets occurs as a consequence of many disorders
that release procoagulant material into the circulation or
cause widespread endothelial damage or platelet
aggregation.

3. Overview
 DIC never occurs in isolation and recognition that a patient has a clinical
disorder which may result in the development of DIC is the key to
appropriate investigation and management. DIC may arise in patients with
a wide spectrum of disorders including sepsis, malignancy, trauma, liver
disease and vascular anomalies. It is also seen when pregnancy is
complicated by placental abruption or amniotic fluid embolism and may
complicate poisoning, envenomation and major transfusion reactions. All of
these conditions share the ability to induce systemic activation of
coagulation either by activating cytokines as part of a systemic
inflammatory response or by causing the release of, or exposure to,
procoagulant substances.

5. Pathogenesis
 The key event underlying DIC is increased activity of thrombin in the
circulation that overwhelms its normal rate of removal by natural
anticoagulants. This can come from tissue factor (TF) release into the
circulation from damaged tissues or from up‐regulation of TF on circulating
monocytes or endothelial cells in response to proinflammatory cytokines
(e.g. interleukin‐1, tumor necrosis factor, endotoxin).

7. Clinical features
 These are usually dominated by bleeding, particularly from venipuncture
sites or wounds. There may be generalized bleeding in the gastrointestinal
tract, the oropharynx, into the lungs, urogenital tract and in obstetric cases,
vaginal bleeding may be particularly severe. Less frequently, micro thrombi
may cause skin lesions, renal failure, gangrene of the fingers or toes or
cerebral ischemia.

8. Investigations
1-Platelet count
 A reduction in the platelet count is a sensitive (though not specific) sign of DIC.
 Thrombocytopenia is a feature in up to 98% of DIC cases with the platelet count
<50×109/l in approximately 50%. A single determination of the platelet count is not
very helpful as the original platelet count may remain in the ‘normal’ range of 150–
400×109/l. At the same time, a continuous drop even within a normal range may
indicate the active generation of thrombin.

9.  2- The PT and APTT are prolonged in the acute syndromes.
 Compensation by the liver may render some of the coagulation tests
normal.
 In nearly half of patients who have DIC, the PT and aPTT are normal or
even shortened. The reasons for normal or shorter times are the presence of
circulating activated clotting factors, such as thrombin or Xa, which can
accelerate the formation of thrombin .Thus, normal clotting times for either
the PT or aPTT do not exclude activation of the hemostatic system and
repeat monitoring is required. It should also be emphasized that the PT, not
the International Normalized Ratio (INR), that is to be monitored; the latter
being validated only for oral anticoagulant monitoring.

10.  3- High levels of fibrin degradation products and D‐dimers are found in
serum and urine.
 it is important to remember that many conditions other than DIC, such as
trauma, recent surgery or venous thromboembolism, are associated with
elevated FDPs including D‐dimer. Also, because FDPs are metabolized by
the liver and secreted by the kidneys, liver and kidney impairment can
influence levels.

11.  3- Fibrinogen concentration is low.
 the sensitivity of a low fibrinogen level for the diagnosis of DIC was only 28%
and hypofibrinogenemia was detected in very severe cases of DIC only.

12. 4-Blood film examination
 In many patients there is a hemolytic anemia (‘microangiopathic’) and the
red cells show prominent fragmentation because of damage caused when
passing through fibrin strands in small vessels .
 fragmented RBCS neither sensitive nor specific to DIC however some cases
of chronic DIC with elevated D‐dimers but normal coagulation screening
assay results, the presence of fragmented red cells can provide
confirmatory evidence.

14. ISTH Diagnostic Scoring System for DIC
Scoring system for overt DIC
Risk assessment: Does the patient have an underlying disorder known to be associated with overt
DIC?
If yes: proceed
If no: do not use this algorithm
Order global coagulation tests (PT, platelet count, fibrinogen, fibrin related marker)
Score the test results
• Platelet count (>100 × 10
9
/l = 0, <100 × 10
9
/l = 1, <50 × 10
9
/l = 2)
• Elevated fibrin marker (e.g. D‐dimer, fibrin degradation products) (no increase = 0,
moderate increase = 2, strong increase = 3)
• Prolonged PT (<3 s = 0, >3 but <6 s = 1, >6 s = 2)
• Fibrinogen level (>1 g/l = 0, <1 g/l = 1)
Calculate score:
≥5 compatible with overt DIC: repeat score daily
<5 suggestive for non‐overt DIC: repeat next 1–2 d

15.  Prospective validation studies show this scoring system to be highly
accurate for the diagnosis of DIC. The sensitivity of the DIC score for a
diagnosis of DIC is 91-93%, and the specificity is 97-98%.

16. Treatment
 Treatment of the underlying cause is most important. The management of
patients who are bleeding differs from that of patients with thrombotic
problems.
 Management of the DIC itself has the following basic features:
-Monitor vital signs
-Assess and document the extent of hemorrhage and thrombosis
-Correct hypovolemia
-Administer basic hemostatic procedures when indicated

17. Bleeding
 Plasma and platelets

18. Recommendations
 Transfusion of platelets or plasma (components) in patients with DIC should
not primarily be based on laboratory results and should in general be
reserved for patients that present with bleeding.
 In patients with DIC and bleeding or at high risk of bleeding (e.g.
postoperative patients or patients due to undergo an invasive procedure)
and a platelet count of <50×109/l, transfusion of platelets should be
considered.
 In non‐bleeding patients with DIC, prophylactic platelet transfusion is not
given unless it is perceived that there is a high risk of bleeding.

19.  In bleeding patients with DIC and prolonged PT and aPTT administration of
FFP may be useful in those with active bleeding and in those requiring an
invasive procedure. The suggested starting dose is 15 mg/kg.
 Severe hypofibrinogenaemia (<1 g/l) that persists despite FFP
replacement may be treated with fibrinogen concentrate or
cryoprecipitate.
 If transfusion of FFP is not possible in patients with bleeding because of fluid
overload, consider using factor concentrates such as prothrombin complex
concentrate, recognizing that these will only partially correct the defect
because they contain only selected factors, whereas in DIC there is a
global deficiency of coagulation factors.

21. Thrombosis
Anticoagulation

22.  In cases of DIC where thrombosis predominates, such as arterial or venous
thromboembolism therapeutic doses of heparin should be considered. The use
of heparin in chronic DIC where there is preponderance of coagulation without
consumption coagulopathy is well established.
 Antithrombin, the primary target of heparin activity, is markedly decreased in
DIC, which means that the effectiveness of heparin therapy will be limited
without concomitant replacement of antithrombin.
 In patients where there is perceived to be a co‐existing high risk of bleeding
there may be benefits in using continuous infusion UFH due to its short half‐life
and reversibility
 In critically ill, non‐bleeding patients with DIC, prophylaxis for venous
thromboembolism with prophylactic doses of heparin or low molecular weight
heparin is recommended
 A dose of 4-5 U/kg constant infusion without a 80-U/kg bolus is a safe means to
deliver heparin to the DIC without increasing the bleeding risk.

23. Chronic (Compensated) DIC
 Patients with chronic DIC can have either bleeding or thrombotic disorders.
The thrombotic disorders range from migratory chronic thrombophlebitis
(Trousseau syndrome) to pulmonary emboli.
 Chronic DIC virtually always occurs in association with solid tumors.
 With chronic DIC, a slower consumption of coagulation factors is
compensated by increased synthesis of these same coagulation factors.
Because of this, the lab results vary from acute DIC and all may be normal
except FDP/ D-dimer (elevated).
 In the setting of an underlying malignancy, diagnosis of chronic DIC can be
made with the finding of microangiopathic hemolytic anemia on
peripheral smear and increased FDP/D-dimer.