1. The man with multiple fractures shows signs of disseminated intravascular coagulation (DIC) including diffuse bleeding, prolonged prothrombin time and partial thromboplastin time, low platelet count, and positive D-dimer. 2. The postpartum woman experienced heavy bleeding after delivery of a stillborn fetus. Her symptoms progressed to include hypotension, tachycardia, ecchymosis, and laboratory findings consistent with DIC such as low platelet count and prolonged clotting times. 3. Both patients presented with clinical signs and laboratory abnormalities indicative of DIC, a coagulopathy that can develop as a complication of trauma, infection, cancer, or obstetric complications

1. Disseminated Intravascular
Coagulation
5

2. • DIC is an acquired syndrome characterized by the intravascular activation of
coagulation cascade. It can originate from and cause damage to the
microvasculature, which if sufficiently severe, can produce organ dysfunction.
• Several clots in some vessels  increase consumption of the blood clotting
factors and platelets deficiency, lack or destruction of those factors in other
body parts Several bleeding in other areas of the body.
• DIC is not a kind of independent disease, but a middle process or complication of
some diseases .
• Hence, a patient with disseminated intravascular coagulation (DIC) can present
with a simultaneously occurring thrombotic and bleeding problem.
DEFINITIONS

4. Pathogenesis
 Pathogenesis of this problem :-
1) Generation of a hyperthrombinemic state :-
• The exposing of the tissue factors thromboplastin and factor III during injury
causes a cascade activation of a factor pathway , as below :-
• The excessive thrombin formation in turn lead to :-

5. 2) decrease of the physiological anticoagulants levels:- (next page)
↓Antithrombin ↓Active Protein C
3)Impaired 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 , so their an excess levels of it decrease fibrinolysis
4)Activation and liberation of inflammatory cytokines:-
• Activation of Clotting sys.  Inflammatory cascade activation Induced pro-inflammatory
cytokines (thrombin and other serine proteases).
• Pro-inflammatory cytokines + Protease-activated receptors (of the cell surface of the
endothelial cells)  Inducing an inflammatory and clotting reaction

6. cccccccccccccccc

7. Disseminated Intravascular Coagulation
Coagulation Anticoagulation
Balance
Coagulation Fibrinolysis
Exposure of blood
to procoagulant
substances
Secondary fibrinolysis
（FDP formation）
widespread thrombosis systemic hemorrhagic syndrome
Clotting factors &
Platelet depletion
Coagulation Fibrinolysis

8. SYSTEMIC ACTIVATION
OF COAGULATION
Intravascular
deposition of
fibrin
Depletion of
platelets and
coagulation
factors
Thrombosis of
small and
midsize vessels
Bleeding
Organ failure DEATH

9. Pathophysiology :-

10. • DIC is not a primary disease, but a disorder secondary to numerous triggering events
such as serious illnesses.
infectious disease 31%~43%
cancer 24%~34%
obstetric complications 4%~12%
severe tissue injury 1%~5%
systemic disease
1)infectious disease 31%~43% :-
• (bacterial, viral, parasitic diseases and so on) Bacterial infection, in particular septicemia, is
commonly associated with DIC.
Etiology
ID
Cancer
OC
STI
SD

11. 2)cancer 24%~34%
(Acute leukemia,, disseminated prostatic carcinoma ,Lung, breast, gastrointestinal
malignancy)
3)Obstetric complications 4%~12%
(amniotic fluid embolus, septic abortion, and so on)
Continuo
4)severe tissue injury 1%~5%
(burn, heart shock, fracture and so on) ,Head trauma in particular is strongly associated with
DIC..
5)systemic disease
(malignant hypertension , Acute respiratory distress syndrome<ARDS>,
hemolytic transfusion reaction)

13. c
Classification :-
1) Acute DIC (non compensatory) :-
 It happened rapidly, the coagulopathy is dominant and major symptoms are bleeding and
shock, mainly seen in severe infection, amniotic fluid embolism.
 an explosive generation of thrombin depletes clotting factors and platelets and activates
the fibrinolytic system. Bleeding into the subcutaneous tissues, skin, and mucous
membranes occurs, along with occlusion of blood vessels caused by fibrin in the
microcirculation.
2) Chronic DIC (compensatory):-
 it happened slowly and last several weeks, thrombosis and clotting may predominate ,mainly seen in cancer.
 process is the same, but it is less explosive. Usually there is time for compensatory responses to take
place, which diminish the likelihood of bleeding but give rise to a hypercoagulable state.

14. Test
Platelet count
Fibrin degradation
product (FDP)
Factor assay
Prothrombin time (PT)
Activated PTT
Thrombin time
Fibrinogen
D-dimer
Antithrombin
Abnormality
Decreased
Increased
Decreased
Prolonged
Prolonged
Prolonged
Decreased
Increased
Decreased
DX based On laboratory TESTS:-

16. DX based on SIGNS AND SYMPTOMS :-
Bleeding(84%~95%) :-It may occur at any site, but spontaneous
bleeding and oozing at veni-puncture sites or wounds are important
clues to the diagnosis.
Thrombosis :-It is most commonly manifested by digital ischemia and
gangrene, renal cortical necrosis and hemorrhagic adrenal infarction
may occur.
Organs dysfunction :- due to micro vascular thrombi in various organs
and contributing to multiple organ dysfunction syndrome
Acute DIC present more with symptoms of hemorrhage .
Chronic DIC Present more with symptoms of thrombosis.

17. ORGAN ISCHEMIC HEMOR.
Skin Pur. Fulminans
Gangrene
Acral cyanosis
Petechiae
Echymosis
Oozing
CNS Delirium/Coma
Infarcts
Intracranial
bleeding
Renal Oliguria/Azotemia
Cortical Necrosis
Hematuria
Cardiovascular Myocardial
Dysfxn
Pulmonary Dyspnea/Hypoxia
Infarct
Hemorrhagic
lung
GI
Endocrine
Ulcers, Infarcts
Adrenal infarcts
Massive
hemorrhage.
Clinical Manifestations of DIC

20. Symptoms and Signs
COMPLICATION
Acute kidney injury
Change in mental status
Respiratory dysfunction
Hepatic dysfunction
Life-threatening thrombosis and
hemorrhage (in patients with moderately
severe–to–severe DIC)
Cardiac tamponade
Hemothorax
Intracerebral hematoma
Gangrene and loss of digits
Shock
Death

21. 1-liver disease.
2-Vitamin K deficiency.
3-Dysfibrinogenemia
4-Hemolytic-Uremic Syndrome
5-Heparin-Induced Thrombocytopenia
6-Idiopathic Thrombocytopenic Purpura
7-Thrombotic Thrombocytopenic Purpura (TTP)
Different Diagnosis

22. DIC SCORING SYSTEM :-
**The International Society on Thrombosis and Haemostasis (ISTH) developed a simple scoring
system for the diagnosis of overt DIC.
** This scoring system is only appropriate for patients with an underlying disorder that can be
associated with DIC.

23. Treatment Modalities
Treatment of the underlying
disorder .
Replacement therapy.
Heparin therapy.
Other Treatment.
TREATMENT

24. fff1-Treatment of the underlying disorder :-
 The primary focus should be the diagnosis and treatment of the underlying disorder that
has given rise to DIC.
2-Replacement therapy :-
 Coagulation factor deficiency require replacement with FFP
(fresh frozen plasma).
 Platelet transfusion should be used to maintain a platelet count greater than
30000/μl, and 50000/μl.
 Fibrinogen is replaced with cryoprecipitate. One unit of cryoprecipitate usually
raises the fibrinogen level by 6~8mg/dl,so that 15 units of cryoprecipitate will
raise the level from 50 to 150mg/dl.
3-Heparin therapy :- (esp. pt. with chronic DIC)
In some cases heparin therapy is contraindicated, but when DIC is producing serious
clinical consequences and the underlying cause is not rapidly reversible, heparin may be
necessary (Dose:500~750u/h is necessary).

25. Cont.
Attention:
Heparin therapy must be used in combination with
replacement therapy, it can lead to severe bleeding.
4) Other Treatment :- a)Aminocaproic acid
b)Tranexamic acid
 Those two drugs should be added to decrease the rate of
fibrinolysis, raise the fibrinogen level, and control
bleeding.

26. 1
1-Acute DIC:- (depend on the
case)
 Without bleeding or evidence of
ischemia:-
-No treatment
 With bleeding:-
1-Blood components as needed
2-Fresh frozen plasma
3-Cryoprecipitate
4-Platelet transfusions
 With ischemia:-
-Anticoagulants after bleeding
risk is corrected with blood
products
2-Chronic DIC :- (depend on
the case )
 Without thromboembolism:-
-No specific therapy needed, but
prophylactic drugs (eg, low-dose
heparin, low-molecular-weight
heparin) may be used for patients
at high risk for formation of
thrombosis.
 With thromboembolism:-
- Heparin or low-molecular-weight
heparin, trial of warfarin sodium
(Coumadin). (If warfarin is
unsuccessful, long-term use of low-
molecular-weight heparin may be
helpful.)

27. Prognosis
Since DIC is a result of an acute medical illness, prognosis
depends almost entirely upon the speed of the staff in handing
the bleeding emergency, as well as the ability to treat the
underling disorder.
The underlying disease that causes the disorder will usually
predict the probable outcome. .
An awareness of the clinical settings in which DIC can occur
and the diagnostic features that warn of its presence should
enable the physician to diagnose and treat DIC appropriately.
DIC may occur in 30-50% of patients with sepsis, and it
develops in an estimated 1% of all hospitalized patients
DIC occurs at all ages and in all races, and no particular sex
predisposition has been noted.

28. CASES :-
1-A 26 year old man with multiple fractures and soft tissue injuries from a motorcycle accident
has diffuse bleeding from all the needle puncture sites and open wounds on the second day of
his hospitalization. His prothrombin time (PT) is 20 seconds (11-15), his partial thromboplastin
time (PTT) is 100 seconds (60-85), and his platelet count is 45,000 (150K -450). His D-Dimer
assay is positive.
2-A 23yearold woman, induced abortion and delivered one dead fetus. Both lower
limbs were swollen when she was 17 weeks pregnant, without being obviously dizzy. The
fetal movement vanished when she was 34 weeks of pregnant. She delivered dead
fetus. The placenta was intact at 35 weeks of pregnant. During the 2 hours after
delivery, bleeding about 1000 ml. From then on, bleeding from vagina constantly.14 hours
after parturition, the woman had a convulsions. After being transfused, the
patient was conscious and was sent to the emergency room. The physical examination: BP
could not be detected, Pulse: 130 /min, Respiration: 26 /min. There were big
areas of ecchymosis on both upper extremities and abdomen, the breath sound was clear, ,
the abdomen was soft and flat, the rim of liver
and spleen could not be touched. The Gynecologic examination: There was a lacerated woun
d of 5 cm on the upper1/3 of right labium minus upper1/3 and the medial wall of vagina,
without active bleeding, no other abnormalities seen. Lab examination:
WBC: 7. 2 ×109/L, platelet: 7.0×109/L, PT:18s(5 s longer than the
control), Fibrinogen: 1.1 g/L