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Intravascular Coagulation

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Presentation on theme: "Intravascular Coagulation"— Presentation transcript:

1 Intravascular Coagulation
Disseminated Intravascular Coagulation Sidney F. Rhoades, M.D.

2 No off label usage of medications or products of any kind
NO disclosures No off label usage of medications or products of any kind

3 Objectives To attempt to not confuse you in regards to DIC
Define DIC and understand classification Understand the epidemiology, etiology and risk factors of DIC Describe signs and symptoms of DIC Understand the laboratory findings in DIC

4 Defining DIC Acquired Condition
Also known as consumption coagulopathy and defibrination syndrome Acquired Condition Systemically producing thrombosis and hemorrhage Initiated by several disorders or “illnesses” Consist of exposure of blood to procoagulants - tissue factor - cancer procoagulant

5 Defining DIC Formation of Fibrin within the circulation Fibrinolysis
Depletion of clotting factors End Organ Damage

6 Defining DIC A systemic disorder of clotting and bleeding after exposure to blood procoagulants thereby causing fibrin formation and degradation (FDP). Abnormal acceleration of the coagulation cascade, resulting in thrombosis Depletion of the clotting factors causing hemorrhage


8 DIC is a disorder of diffuse activation of the clotting cascade that results in depletion of clotting factors in the blood.

9 Epidemiology of DIC Incidence:
DIC is complication of underlying illness occurring in 1% of hospitalized patients

10 Classification: Acute or Chronic
Acute DIC -develops rapidly over a period of hours -presents with sudden bleeding from multiple sites -treated as a medical emergency Chronic DIC -develops over a period of months -maybe subclinical -eventually evolves into an acute DIC pattern (Otto, 2001)

11 Classification: Acute or Chronic
-blood is exposed to a large amount of tissue factor over a brief period of time -massive generation of thrombin -acutely triggers the coagulation cascade -overwhelming the inhibitory mechanisms

12 Classification: Acute or Chronic
Tissue factor : -integral membrane glycoprotein not normally expressed on the vascular cell surface -caused by vessel wall damage -circulates in the blood as a derivative of monocytes and macrophages -platelets also generate tissue factor in order to generate thrombin


14 Classification: Acute or Chronic
Secondary Fibrinolysis: -process of degrading fibrin creating FSP normally cleared from circulation -interrupts normal fibrin polymerization -binds to platelet surface glycoprotein Iib/IIIa -caused by tissue plasminogen activator plasminogen  plasmin -cleaves other proteins other than fibrin like fibrinogen -eats up other clotting factors


16 Classification: Acute or Chronic
-also known as compensated DIC -blood is continuously or intermittently exposed to small amounts of tissue factor -liver and bone marrow are able to replenish the depleted coagulation proteins and platelets

17 Etiology and Pathology of DIC
Extrinsic (endothelial) -Shock or trauma -Infection –gram positive and gram negative *bacterial and nonbacterial infection -Obstetric complications *eclampsia, placenta abruption, fetal death -Malignancies *Acute promyleocytic leukemia, AML, cancers of 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

18 Extrinsic (endothelial) continued…
Shock -reduced blood flow and tissue damage encourages thrombin formation Trauma -extensive surgery -release of tissue enzymes and phospholipids -head injury one study of 159 patients found coagulopathy in 41% of pt’s with CT evidence of brain injury and 25% of those without

19 Gunshot wound to the carotid artery

20 Extrinsic (endothelial) continued…
Trauma (cont.) -syndrome developed one to four hours after injry -studies show direct evidence of procoagulant release and thrombin formation in cerebrovenous blood within six hours of isolated head trauma -studies showed increased D-dimer and soluble fibrin concentrations indicating coagulation and fibrinolysis Infection –both gram positive and gram negative *bacterial and nonbacterial infection *Overt DIC reportedly occurs in 30-50% of Pt’s with gram negative sepsis *Activation of the endothelial pathway via endotoxin *Endotoxin also activates factor XII of the intrinsic pathway

21 Question: Are we missing out in regards to coding and increased severity/mortality?

22 Extrinsic (endothelial) continued…
Malignancies -3rd most frequent cause of DIC -accounts for 7 % of clinically evident cases -can cause acute DIC in Acute Promyelocytic Leukemia -pulmonary or cerebrovascular hemmorrhage in up to 40% patients -treat with rapid induction tumor cell differentiation with all-trans retinoic acid *down-regulates the receptor annexin II, a RC for plasminogen on the promyelocyte

23 DIC with microangiopathic hemocytic anemia in a 34 y/o female, Hb 8
DIC with microangiopathic hemocytic anemia in a 34 y/o female, Hb 8.6 g/dL, MCV fL, MCHC 32.8 g/dL, platelets 11,000/uL, WBC 59,000/uL. Patient had a history of disseminated non-small cell carcinoma of the lung. She presented to the ER in extremis and expired within a few hours of admission. (

24 Extrinsic (endothelial) continued…
Obstetric complications -seen in more than 50% of amniotic fluid embolism and abrupteoplacentae - the greater the abruption the higher the severity - thromboplastins integrated into mother’s blood system - peripartum hemorrhage may be spontaneous - 20% in women with HELLP - septic abortions - dead fetus syndrome


26 Clinical Manifestations
Bleeding (64%) Renal dysfunction (25%) Hepatic dysfunction (19%) Respiratory dysfunction (16%) Shock (14%) Thromboembolism (7%)

27 Clinical Manifestations
Bleeding -petechiae -ecchymoses -blood oozing from wound sites -intravenous lines -mucosal surfaces Acute Renal Failure -microthrombosis of afferent arterioles -cortical ischemia -necrosis -hypotension  ATN

28 Clinical Manifestations
Hepatic Dysfunction -jaundice (from liver disease and hemolysis) -hepatocellular injury (from sepsis/shock) Pulmonary Disease -hemorrhage with hemoptysis -ARDS -pulmonary microthrombosis

29 Clinical Manifestations
Central Nervous System -coma -delirium -transient focal neurologic symptoms -microthrombi, hemorrhage, and hypoperfusion are causes


31 Case Study Cc: chest pain, N/V
HPI: 67 y.o. female significant PMHx of rheumatoid arthritis on Enbrel, pericarditis presently on prednisone taper and known previous pleural effusion with a negative previous workup for tuberculosis. Pt. presented complaining of N/V and 7/10 sharp chest pain at her anterior chest wall radiating across the upper part of the chest, worsening with inspiration. She had productive green sputum and white count 42,000. Pt’s temp was

32 Case Study PMhx : GERD, depression, hypercholesterolemia, pericarditis, pleural Effusion, rheumatiod arthritis PSHhx: noncontributory Meds: Enbrel, Votaren, Ultram, Nexium, Zocor, Pristiq, tylenol#4, hydrocodone-apap, Melatonin, Erythromycin, prednisone, Gel eye drops Allergies:NKDA ROS: ten point review otherwise negative Social history: Patient lives with her family, no hx of tobacco or Etoh

33 Case Study Physical exam Vitals T 100.3 RR 20 P 128 BP 103/60 95% RA
WD WN Elderly female appearing ill no acute distress and oriented to person, place and time HEENT: AT, NC Anicteric…no conjuctival pallor mmm Neck Supple with no JVD and negative HJR Chest: Moderately good air entry bilaterally with few bibasilar crackles CVS: tachycardic, Regular S1:S2

34 Case Study Labs at 21:45 on 7/17/10 Na 137 CL101 BUN 23 glucose 158
K CO2 23 Cr0.57 Bilirubin total PT 13.7 INR 1.0 SGOT PTT 17.3 SGPT trp 0.04 Alk Phos BNP 79 WBC’s Hgb 14.7 plt 385 EKG sinus tachycardia, 114 no ST-T changes CXR: enlarged cardiac silhouette no infiltrates or pulmonary congestion

35 Case Study Pt. became more hypotensive , clammy and diaphoretic
She was transferred to the ICU and given fluid boluses as well as pressors Due to Pt’s immunocompromised state Pt. was placed on Imipenem and Vancomycin. Pt was ultimately intubated after ABG’s returned and were noted to be significantly worse.

36 Case Study Labs at 02:40 on 7/18/10 Na 137 CL106 BUN 24 glucose 168
K CO2 22 Cr 0.73 Bilirubin total 1.3 SGOT SGPT trp 0.16 Alk Phos WBC’s Hgb 11.8 plt 416

37 Case Study Labs at 07:10 on 7/18/10 Na 133 CL109 BUN 22 glucose 224
K CO2 15 Cr0.67 Bilirubin total 0.9 SGOT SGPT Alk Phos WBC’s Hgb 12.6 plt 438 U/A Nitrite negative, leukocyte est negative Bilirubin negative, Urobilinogen 0.2E. U/dl

38 Case Study Labs at 13:40 on 7/18/10 Na 134 CL105 BUN 22 glucose 279
K CO2 12 Cr1.13 Bilirubin total PT 39.7 INR 3.8 SGOT PTT 80.2 SGPT LDH 1261 Alk Phos amylase 126 Fibrinogen 157 ( mcg/dl) Fibrin Spit products (Less than 10) D.DIMER ( mcg/dl)


40 Case Study Risk Factors for Death 1. Increased age
2. Severity of organ dysfunction 3. Severity of hemostatic abnormalities

41 Treatment of DIC Patients bleed from thrombocytopenia and coagulation factor deficiency -transfuse platelets and coagulation factors in Pt’s bleeding or with high risk of bleeding -after surgery or those requiring invasive procedures -Patients with marked thrombocytopenia <20,000 -moderate thrombocytopenia <50,000/microL and bleeding -serious bleeding should have 1-2 units per 10kg per day

42 Treatment of DIC Actively bleeding patients
-with elevated prothrombin time/INR or Fibrinogen concentration < 50mg/dl -transfuse FFP -cyroprecipitate for fibrinogen replacement -preferable to keep fibrinogen level >100mg/dl

43 Treatment of DIC Heparin no controlled trials indicating benefit
little evident that it improves organ dysfunction use is limited to specific Patients with chronic DIC and mostly thrombotic manifestations -migratory thrombophlebitis used in retained dead fetus and hypofibrinogenemia prior to induction of labor excessive bleeding assoc with giant hemangioma aortic aneurysm prior to resection

44 Treatment of DIC

45 Treatment of DIC Xigris activated protein C
anticoagulant and anti-inflammatory activities direct anti-inflammatory effect on endothelial cells studies show modulation of gene expression inhibits TNF expression of cell adhesion molecules ICAM-1, VCAM-1, E-selectin by down regulation of Transcrition facor NF-kB enhances anti-apoptotic genes

46 Comparison of DIC to TTP/HUS
has normal coagulation components little or no prolongation of the PT or PTT will share microangiopathic blood smear TTP will have thrombocytopenia and schistocytes clinical settings are usually different than DIC associated sepsis, trauma, malignancy, OB

47 The End

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