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

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Presentation on theme: "Disseminated Intravascular Coagulation Sidney F. Rhoades, M.D."— Presentation transcript:


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

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

4 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 Objectives

5 Defining DIC 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

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

7 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


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

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

11 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)

12 Classification: Acute or Chronic Acute -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

13 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 Classification: Acute or Chronic


15 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 Classification: Acute or Chronic


17 Chronic -also known as compensated DIC -blood is continuously or intermittently exposed to smallamounts of tissue factor -liver and bone marrow are able to replenish the depleted coagulation proteins and platelets

18 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

19 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 pts with CT evidence of brain injury and 25% of those without Extrinsic (endothelial) continued…

20 Gunshot wound to the carotid artery

21 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 Pts with gram negative sepsis *Activation of the endothelial pathway via endotoxin *Endotoxin also activates factor XII of the intrinsic pathway Extrinsic (endothelial) continued…

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

23 Malignancies -3 rd 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 Extrinsic (endothelial) continued…

24 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. ( _Anemia_( ).jpg)

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


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

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

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

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


32 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. Pts temp was 100.3

33 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

34 Case Study Physical exam Vitals T 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

35 Case Study Labs at 21:45 on 7/17/10 Na 137 CL101 BUN 23 glucose 158 K 4.2 CO2 23 Cr0.57 Bilirubin total 0.7 PT 13.7 INR 1.0 SGOT 60 PTT 17.3 SGPT 37 trp 0.04 Alk Phos 73 BNP 79 WBCs 42.1 Hgb 14.7 plt 385 EKG sinus tachycardia, 114 no ST-T changes CXR: enlarged cardiac silhouette no infiltrates or pulmonary congestion

36 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 Pts immunocompromised state Pt. was placed on Imipenem and Vancomycin. Pt was ultimately intubated after ABGs returned and were noted to be significantly worse.

37 Labs at 02:40 on 7/18/10 Na 137 CL106 BUN 24 glucose 168 K 3.5 CO2 22 Cr 0.73 Bilirubin total 1.3 SGOT 38 SGPT 29 trp 0.16 Alk Phos 46 WBCs 46.5 Hgb 11.8 plt 416 Case Study

38 Labs at 07:10 on 7/18/10 Na 133 CL109 BUN 22 glucose 224 K 4.2 CO2 15 Cr0.67 Bilirubin total 0.9 SGOT 30 SGPT 26 Alk Phos 45 WBCs 44.4 Hgb 12.6 plt 438 U/A Nitrite negative, leukocyte est negative Bilirubin negative, Urobilinogen 0.2E. U/dl Case Study

39 Labs at 13:40 on 7/18/10 Na 134 CL105 BUN 22 glucose 279 K 5.2 CO2 12 Cr1.13 Bilirubin total 2.0 PT 39.7 INR 3.8 SGOT 527 PTT 80.2 SGPT 724 LDH 1261 Alk Phos 39 amylase 126 Fibrinogen 157 ( mcg/dl) Fibrin Spit products (Less than 10) D.DIMER ( mcg/dl)


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

42 Treatment of DIC Patients bleed from thrombocytopenia and coagulation factor deficiency -transfuse platelets and coagulation factors in Pts 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

43 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

44 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

45 Treatment of DIC

46 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

47 Comparison of DIC to TTP/HUS 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

48 The End

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