Presentation on theme: "Intravascular Coagulation"— Presentation transcript:
1 Intravascular Coagulation DisseminatedIntravascular CoagulationSidney F. Rhoades, M.D.
2 No off label usage of medications or products of any kind NO disclosuresNo 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 classificationUnderstand the epidemiology, etiology and risk factors of DICDescribe signs and symptoms of DICUnderstand the laboratory findings in DIC
4 Defining DIC Acquired Condition Also known as consumption coagulopathy and defibrination syndromeAcquired ConditionSystemically producing thrombosis and hemorrhageInitiated 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 factorsEnd Organ Damage
6 Defining DICA 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 thrombosisDepletion 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 emergencyChronic 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 factorover 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 normallyexpressed 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 factorin order to generate thrombin
14 Classification: Acute or Chronic Secondary Fibrinolysis:-process of degrading fibrin creating FSPnormally cleared from circulation-interrupts normal fibrin polymerization-binds to platelet surface glycoprotein Iib/IIIa-caused by tissue plasminogen activatorplasminogen 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 thedepleted coagulation proteins and platelets
17 Etiology and Pathology of DIC Extrinsic (endothelial)-Shock or trauma-Infection –gram positiveand gram negative*bacterial and nonbacterial infection-Obstetric complications*eclampsia, placenta abruption, fetal death-Malignancies*Acute promyleocytic leukemia, AML, cancers of lung, colon, breast, &prostateIntrinsic (blood vessel)-Infectious vasculitis *certain viral infections*rocky mountain spotted fever-Vascular disorders-Intravascular hemolysis*hemolytic transfusion reactions-Miscellaneoussnakebite, pancreatitis, liver disease
18 Extrinsic (endothelial) continued… Shock-reduced blood flow and tissue damageencourages thrombin formationTrauma-extensive surgery-release of tissue enzymes and phospholipids-head injuryone study of 159 patients foundcoagulopathy in 41% of pt’s with CTevidence of brain injury and 25% of those without
20 Extrinsic (endothelial) continued… Trauma (cont.)-syndrome developed one to four hours after injry-studies show direct evidence of procoagulant releaseand thrombin formation in cerebrovenousblood within six hours of isolated head trauma-studies showed increased D-dimer and soluble fibrinconcentrations indicating coagulation and fibrinolysisInfection–both gram positive and gram negative*bacterial and nonbacterial infection*Overt DIC reportedly occurs in 30-50% of Pt’s withgram 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. (http://commons.wikimedia.org/wiki/File:DIC_With_Microangiopathic_Hemolytic_Anemia_( ).jpg)
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
31 Case Study Cc: chest pain, N/V HPI: 67 y.o. female significant PMHx of rheumatoid arthritison 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 StudyPMhx : GERD, depression, hypercholesterolemia, pericarditis, pleuralEffusion, rheumatiod arthritisPSHhx: noncontributoryMeds: Enbrel, Votaren, Ultram, Nexium, Zocor, Pristiq, tylenol#4,hydrocodone-apap, Melatonin, Erythromycin, prednisone,Gel eye dropsAllergies:NKDAROS: ten point review otherwise negativeSocial 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 distressand oriented to person, place and timeHEENT: AT, NC Anicteric…no conjuctival pallor mmmNeck Supple with no JVD and negative HJRChest: Moderately good air entry bilaterally with fewbibasilar cracklesCVS: 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 Cr0.57Bilirubin total PT 13.7 INR 1.0SGOT PTT 17.3SGPT trp 0.04Alk Phos BNP 79WBC’s Hgb 14.7 plt 385EKG sinus tachycardia, 114 no ST-T changesCXR: enlarged cardiac silhouette no infiltratesor 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 pressorsDue 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 0.73Bilirubin total 1.3SGOTSGPT trp 0.16Alk PhosWBC’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 Cr0.67Bilirubin total 0.9SGOTSGPTAlk PhosWBC’s Hgb 12.6 plt 438U/A Nitrite negative, leukocyte est negativeBilirubin 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 Cr1.13Bilirubin total PT 39.7 INR 3.8SGOT PTT 80.2SGPT LDH 1261Alk Phos amylase 126Fibrinogen 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 dysfunction3. Severity of hemostatic abnormalities
41 Treatment of DICPatients 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 dysfunctionuse is limited to specific Patients with chronic DIC andmostly thrombotic manifestations-migratory thrombophlebitisused in retained dead fetus and hypofibrinogenemiaprior to induction of laborexcessive bleeding assoc with giant hemangiomaaortic aneurysm prior to resection
45 Treatment of DIC Xigris activated protein C anticoagulant and anti-inflammatory activitiesdirect anti-inflammatory effect on endothelial cellsstudies show modulation of gene expressioninhibits TNF expression of cell adhesion moleculesICAM-1, VCAM-1, E-selectin by downregulation of Transcrition facor NF-kBenhances anti-apoptotic genes
46 Comparison of DIC to TTP/HUS has normal coagulation componentslittle or no prolongation of the PT or PTTwill share microangiopathic blood smearTTP will have thrombocytopenia and schistocytesclinical settings are usually different than DICassociated sepsis, trauma, malignancy, OB
Your consent to our cookies if you continue to use this website.