DIC is not a disease entity but an event that can accompany various disease processes. It is an “Acquired” Pathological process. Widespread activation of the clotting cascade lead to formation of blood clots in small blood vessels throughout the body causing a compromise of tissue blood flow leading to multiple organ damage MOD. The coagulation process consumes clotting factors and platelets,normal clotting is disrupted and severe bleeding can occur from various sites. Patients with DIC should be treated at hospitals with appropriate critical care units (ICU) with available Subspecialty expertise, such as hematology, blood bank, or surgery. Patients who present to hospitals without those capabilities and who are stable enough for transfer should be referred expeditiously to a hospital that has those resources. Treatment of DIC includes the underlying disorder, supportive treatment and hemostatic Therapy.
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Polytrauma part 6 (DIC)
1. Dr. Fathi Neana, MD
Chief of Orthopaedics
Dr. Fakhry & Dr. A. Al-Garzaie Hospital
January, 24- 2019
Polytrauma
Part 6
Disseminated intravascular
coagulation
(DIC)
5. Disorders causing obstruction of the Microvascular Circulation
1- Thrombotic microangiopathy (TMA)
2- Disseminated intravascular coagulation (DIC)
DIC
Increased fibrin
formation
Obstruction of the Microvascular
Circulation
6. Other Terms:
Disseminated intravascular coagulopathy
Consumptive coagulopathy
Disseminated intravascular
coagulation (DIC)
• DIC is an alteration in the blood clotting mechanism
• Abnormal acceleration of the coagulation cascade
-> Thrombosis
• As a result of the depletion of clotting factors
• Hemorrhage occurs simultaneously
• DIC is s a paradoxical clinical presentation “Clotting
and Hemorrhage”
Porth, C.M. (2004) Essentials of Pathophysiology) & (Otto, S. (2001).
Oncology Nursing
7. Disseminated intravascular coagulation
(DIC) Definition
DIC is an acquired syndrome
characterized by:
• The intravascular activation of coagulation with
loss of localization
• Arising from different causes
• It can originate from and cause damage to
microvasculature
• Which if sufficiently severe, can produce Organ
dysfunction and Bleeding disorder
ISTH´s Scientific Subcommittee on DIC, July 2001
8. DIC is an “Acquired” Bleeding
Disorder
• DIC is not a disease entity but an event that can
accompany various disease processes
• It is an “Acquired” Pathological process
• Widespread activation of the clotting cascade ->
formation of blood clots in small blood vessels
throughout the body
• Compromise of tissue blood flow lead to multiple
organ damage MOD
• The coagulation process consumes clotting factors
and platelets,
• Normal clotting is disrupted and severe bleeding can
occur from various sites
acute thrombotic microangiopathy,
abbreviated TMA. Kidney biopsy. PAS stain.
The differential diagnosis of TMA includes:
[1] Hemolytic uremic syndrome (HUS).
Thrombotic thrombocytopenic purpura
(TTP). HIV associated TTP. Disseminated
intravascular coagulation (DIC). Malignant
hypertension. Scleroderma renal crisis.
Antiphospholipid antibody syndrome
(APLA). Drug toxicity, e.g. calcineurin
inhibitor t
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Global dimming” can it counter Global warming? - Earth
Wolfs - Russia
Eagles - USA
Osteoblast vs. Osteoclast - Bone
Microbiota non pathogenic vs. pathogenic – Intestine
Immunological Response
Inflammatory vs. Ant inflammatory mediators
Haemostatic Response
Coaulatory vs. Anticoagulatory mediators
Balance & Equilibrium every where
from Galaxy to Atom
10.
11.
12. SIRS
Injurious stimulus -Tissue Trauma – Sepsis
Especially with sepsis the immunologic and haemostatic response
amplify each other
MODS
DIC
Circulating
mediators
Circulating
mediators
Haemostatic
Response
Immunological
Response
ModificationModification
AmplificationAmplification
Ischaemia -Ischaemia - BleedingBleeding DestructionDestruction
13. 1- TF (Tissue Factor) - mediated thrombin
generation
2- Dysfunctional physiologic anticoagulant
mechanisms (depression of Antithrombin and
protein C system)
3- Impaired fibrin removal due to depression of the
(impaired Fibrinolytic system )
however, in exceptional forms of DIC, Fibrinolytic
activity may be increased and contribute to
bleeding
4- Inflammatory activation (Hypercoagulability)
Pathophysiology
The hematologic derangements in DIC results from
4 simultaneously occurring mechanisms
TF
14. Pathophysiology
The hematologic derangements in DIC results from
4 simultaneously occurring mechanisms
2- Dysfunctional physiologic
Anticoagulant mechanisms
3- Impaired fibrin removal
Fibrinolytic system
1- TF- mediated
Thrombin generation
4- Inflammatory activation
Hypercoagulability
17. The combination of widespread tissue ischemia and simultaneous bleeding
carry an increased risk of death
In addition to that posed by the underlying disease
DIC can be overt and severe in some cases, but milder and insidious in
others
The diagnosis of DIC depends on the findings of characteristic laboratory
tests and clinical background
Treatment is mainly geared towards the underlying condition
DIC does not occur by itself
A complication from another underlying condition
Usually in critical illness
18. • Extrinsic ( tissue)
– Shock or trauma
– Infections
gram positive & gram
negative sepsis, aspergillosis
– Obstetric complications
(eclampsia, placenta
abruptio, fetal death
syndrome)
– Malignancies
APML, AML, cancers of the
lung, colon, breast, prostate)
• Intrinsic (blood vessel)
– Infectious vasculitis (certain
viral infections, rocky
mountain spotted fever)
– Vascular disorders
– Intravascular hemolysis
(hemolytic transfusion
reactions)
– Miscellaneous snakebite
pancreatitis
liver disease
Risk factors and etiology of DIC
(Porth, 2004) & (Otto, 2001)
Almost always a secondary event from activation of one of the coagulation
pathways. Underlying pathology creates a triggering event either 1- Tissue injury
(Extrinsic) or 2- Blood vessel injury (Intrinsic)
28. 1- The underlying cause
2- Thrombosis
3- Dysfunction of multiple organs MODS
4- The most common sign of DIC is Bleeding
Signs and symptoms
29. Signs and symptoms
The underlying cause
• The underlying cause usually leads to symptoms and signs, and
DIC is discovered on laboratory testing
• The onset of DIC can be sudden, as in endotoxic shock or
amniotic fluid embolism
• or it may be insidious and chronic, as in cases of malignancy
• Overt DIC can further lead to, multiorgan failure and widespread
hemorrhage from various sites
31. • Microvascular clot formation is the primary event
• Signs of Organ dysfunction Indistinguishable from SIRS,
Sepsis and MODS
• Lung dysfunction
i. Acute pulmonary micro embolism syndrome
ii. Late pulmonary micro embolism syndrome → ARDS ,
Microatelectasis and capillary leakage
• Acute renal failure
i. Oliguria or anuria
ii. Microscopic or macroscopic haematuria
Signs and symptoms
Dysfunction of multiple organs (MODS)
32. • Cerebral dysfunction
i. Confusion & Blurring of consciousness
• Dermal changes :micro thrombosis / bleedings
i. Focal hemorrhagic necroses : face & peripheral extremities
ii. Petechiae and/or Ecchymoses
• Additional symptoms
i. from dysfunction of the liver, endocrine glands and other organs
Signs and symptoms
Dysfunction of multiple organs (MODS)
33. • Ecchymoses, petechiae, and purpura
• Cool and or mottled extremities
• Bleeding from multiple sites either oozing or frank bleeding
(hematemesis)
• Dyspnea and chest pain if pleura and pericardium involvement
• Haematuria
(Porth, 2004) & (Otto, 2001)
Signs and symptoms
Most common sign of DIC is Bleeding
37. Pathophysiology
Thrombosis
Hypercoagulability
1) Coagulation cascade is
initiated, -> widespread fibrin
formation
2) Micro thrombi throughout the
microcirculatory system
3) Fibrin deposits result in tissue
ischemia, hypoxia, necrosis
4) Leads to multi organ
dysfunction MODS
5) Exhaustion of platelets and
coagulation factors (results in
Hemorrhage) consumption
coagulopathy
(Porth, 2004) & Otto, 2001
Fibrinolysis
Hypocoagulability
1) Activates the Complement
system
2) Byproducts of fibrinolysis
(fibrin/fibrin degradation
products(FDP)) further
enhance bleeding by
interfering with platelet
aggregation, fibrin
polymerization, & thrombin
activity
3) Leads to Hemorrhage
38.
39.
40. Laboratory Diagnosis
Analysis Early changes Late changes
Platelets /
APTT
Fibrinogen
D-dimer
F:II,VII,X
Protein C
Anti-thrombin
TAT complex
Soluble fibrin
41. Blood tests
when DIC is suspected
Simple screening
Platelet count
Activated partial
thromboplastintime (APTT)
Prothrombin time (PT)
Extended screening
Fibrin D-dimer fragment
Antithrombin (AT)
Fibrinogen
Supplementary tests
Further evidence for activation of
coagulation & fibrinolysis
*Prothrombin fragment 1.2
*Thrombin-antithrombin complexes (TAT)
(↑ procoagulation)
*Fibrinopeptid A (FPA) or soluble fibrin
*Protein C
*Fibrinolytic activity (Clot lysis time)
*Thrombin time
*Plasmin-antiplasmin complexes (PAP)
43. Treatment of DIC
General Guidelines
Patients with DIC should be treated at hospitals with appropriate
critical care units (ICU)
Available Subspecialty expertise, such as hematology, blood
bank, or surgery.
Patients who present to hospitals without those capabilities and
who are stable enough for transfer should be referred
expeditiously to a hospital that has those resources.
45. Treatment of DIC
Treatment of underlying disorder
• Antibiotic treatment of infections
• Surgical debridement and drainage of infected foci
• Immobilization of fractures
• Evacuation of uterus in obstetric DIC
47. Treatment of DIC
Hemostatic Therapy
• Antithrombotic treatment
• Antithrombin concentrate (AT concentrate)
• Concurrent treatment with heparin should be avoided, heparin
worsens thrombocytopenia
• Fresh frozen plasma (FFP) When bleeding; administer after
antithrombin
• Platelets : severe thrombocytopenia + bleeding
antifibrinolytic treatment Should be avoided
48.
49. Management of DIC
Medication Summary
Anticoagulants, Hematologic
• Heparin
• extensive fibrin deposition without evidence of substantial hemorrhage, reserved for cases
of chronic DIC.. limited use in acute hemorrhagic DIC acral cyanosis and digital ischemia
• Antithrombin(Atryn, Thrombate III)
• Recombinant Human Activated Protein C
• Withdrawn from the worldwide market on October 25, 2011.was approved for the reduction
of mortality in patients who have severe sepsis
• Tissue factor pathway inhibitor (Recombinant thrombomodulin)
Blood Components
• Packed red blood cells (PRBCs; washed)
• Platelets
• Fresh frozen plasma (FFP)
• Cryoprecipitate or fibrinogen concentrates
Antifibrinolytic Agents
• Aminocaproic acid (Amicar)
• Tranexamic acid (Cyklokapron, Lysteda)
51. Prognosis of DIC
•Prognosis varies depending on
The underlying disorder
The extent of the intravascular thrombosis
•The mortality rate with DIC, regardless
of cause is 10% to 50%
•DIC with Sepsis has a significantly
higher rate of death compared to DIC
associated with Trauma
Notas do Editor
The most common symptoms are those described for SIRS (Systemic Inflammatory Response Syndrome) and MODS (Multiple Organ Dysfunction Syndrome) and cerebral dysfunction.
As Microvascular clot formation is the primary event, signs of organ dysfunction determine the clinical symptoms in most DIC patients. Thus making the presentation of DIC rather indistinguishable from SIRS/Sepsis and MODS.
Characteristic changes in skin :micro thrombosis / bleedings
because heparin increases the degradation of antithrombin, worsens thrombocytopenia and increases bleeding complications.