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diagram from Life in the Fast Lane Blog<\/p>\n
Autoimmune thrombocytopenia, other cell lines not effected<\/p>\n
Seen in kids as a acute, usually post-viral disease.\u00a0 In adults, chronic form often seen in women.<\/p>\n
Mucosal or skin bleeding, ptechiae, purpura<\/p>\n
May See spherocytes but no fraged cells<\/p>\n
Steroids (Solumedrol 1 gm over 30 minutes), IgG (1 gm\/kg over 6 hours), plasmapheresis, splenectomy.\u00a0 Can administer platelets if bleeding (6 to 8 units Q8 if CNS\/GI bleeds), but usually patients can tolerate levels as low as 1000 without needing transfusion<\/p>\n
group of three disorders with low platelets and organ failure<\/p>\n
endotheliopathy caused by infection, CP bypass, transplant, radiation, chemotherapy, auto-immune disease, or medications<\/p>\n
Review Article (Crit Care 2006;10:235)<\/p>\n
In differential:\u00a0 DIC (coag path affected,) SLE, Ehrlichiosis, Hemolytic Uremic Syndrome (HUS)<\/p>\n
think TTP whenver there is a combination of renal insufficiency, thrombocytopenia and CNS dysfunction<\/p>\n
\u25cfFever, thrombocytopenia, microangiopathic hemolysis (elevated LDH), renal dysfunction<\/p>\n
Acute form from antibody against vWF cleaving protein; pts have <10% ADAMTS 13 activity<\/p>\n
large vWF multimers can not be cleaved so cause massive amounts of PLT aggregation. SHear stress is greatest in brain and kidney, so largest amounts of thrombi deposition occurs there.<\/p>\n
Thrombotic Microangiopathy<\/p>\n
Always associated c hemolysis, Coag path is spared<\/p>\n
Fever, signs of hemolysis<\/p>\n
PENTAD:\u00a0 fever, Microangiopathic Hemolytic Anemia (MAHA), Thrombocytopenia,\u00a0 Renal Dysfunction, Neuro Sx.\u00a0 (present in less than 50%)<\/p>\n
Reticulocytosis, Shistocytes\/Helmut Cells<\/p>\n
Increased LDH, BUN and Cr, Indirect hyperbillirubinemia,<\/p>\n
Excellent Review Article (Blood 2015;125(25):3860)<\/p>\n
Steroids-b\/c vWF problems can be antibody mediated<\/p>\n
Emergent Plasmapheresis (FFP 2 units Q6) and continued daily<\/p>\n
Vincristine\u00a0as a last resort medication<\/p>\n
No rapid platelet infusion<\/p>\n
Resolution when PLT>150,000<\/p>\n
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Not in the beginning – only when the process has already triggered a certain degree of fibrinolysis. D-dimers are much higher in DIC than in TTP. FDP too. Neoplasia more often causes DIC than TTP…I BET her protein C activity is low…these coagulopathies seen in cancer usually respond well to heparin in small and carefully titrated dosage and antithrombin III reposition. Perhaps some corticosteroids could be a good idea in this case, after you proper address the diagnosis of the lesions…corticosteroids do control some paraneoplastic syndromes and can ameliorate coagulopathies in neoplasic patients for a limited time. If plasma exchange does not improve it, I would try corticosteroids and vincristine…but would try to obtain a biopsy specimen before doing it… Do you think it can be breast cancer??Plasmacytoma?? Uterus\/ovary?? VERY interesting case. I have seen a similar one two years ago that was the first manifestation of an uterine carcinoma. The patient had predominantly thrombosis and low platelet numbers with microangiopathy…we started LMWH and antithrombin and it improved…she was discharged from the ICU. The assistant internist started coumadin to the patient, and it precipitated skin necrosis and finger ischemia – for the protein C levels were too low, and he called me. I asked him to stop coumadin immediately and restart LMWH – we don\u00b4t have thrombin inhibitors easily available here… The patient had to live on enoxaparin since then. One month later, transvaginal US detected endometrial inspissation, and they diagnosed the carcinoma. She received radiotherapy and the coagulation disturbance greatly improved for some time.<\/p>\n
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Micro-angiopathic Hemolytic Anemia (MAHA) thrombocytopenia and neuro findings are often presentLow grade temp maybe kidney rare Inhibitor of protease of vegFFP okPlasma exchange is much better Protease in that is missing is present in FFPExchange gets rid of inhibitor and multimersCryosupperent FTP???????Steroids inhibit inhibitorNo evidence ofr IVIGNo plateletsHUS plt fibrin clotsHUS shiga urine test<\/p>\n
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July 2000 Closure Time Platelet Function Screening Andrea Cortese Hassett, Ph.D. and Franklin A. Bontempo, M.D. BACKGROUND Platelet dysfunction may be acquired, inherited, or induced by platelet inhibiting agents. It is clinically important to assess platelet function as a potential cause of a bleeding diathesis, especially in critically ill patients who may develop life-threatening hemorrhages. The most common causes of platelet dysfunction are related to uremia, liver disease, von Willebrand\u0092s disease (vWD) and exposure to agents such as acetyl salicylic acid (ASA, aspirin). Current methods to assess platelet function include bleeding time (BT), aggregation studies and whole blood in vitro test systems such as the closure time (CT). CLOSURE TIME TESTING Closure times are performed on a PFA-100, an instrument and test cartridge system in which the process of platelet adhesion and aggregation following a vascular injury is simulated in vitro. This system allows for rapid evaluation of platelet function on samples of anticoagulated whole blood. Membranes consisting of Collagen\/Epinephrine (CEPI) and Collagen\/Adenosine-5\u0092-diphosphate CADP and the high shear rates generated under standardized flow conditions, result in platelet attachment, activation and aggregation, building a stable platelet plug at the aperture. The time required to obtain full occlusion of the aperture is reported as the closure time (CT) in seconds. The test is sensitive to platelet adherence and aggregation abnormalities and allows the discrimination of aspirin-like defects and intrinsic platelet disorder. The CEPI membrane is used to detect platelet dysfunction induced by intrinsic platelet defects (vWD, drug effects etc.). Abnormalities result in prolongations of CT >175 seconds. Follow-up testing using the CADP membrane enables the discrimination of aspirin effects. The following table shows expected patterns observed with CT on normal subjects and subjects with various disorders. Normal ASA vWD Glanzmann’s Thrombasthenia CEPI normal abnormal abnormal abnormal CADP normal normal abnormal abnormal CLOSURE TIMES vs. BLEEDING TIMES While thrombocytopenias are accurately assessed by automated platelet counters, qualitative platelet defects are presently difficult to diagnose. The only global screening test for platelet and vascular functions is the BT. BT is a bedside procedure, is labor intensive, expensive and its accuracy is heavily dependent on operator skills. A critical review of BT concluded that the utility of BT is not enhanced by recent standardization attempts; that in individual patients there is no relationship between BT and platelet counts; that the BT is not a specific indicator of platelet function and that the BT is a poor indicator of surgical bleeding risk. As a consequence many clinicians no longer use BT. The noted deficiencies of BT lead to the development of an in vitro device that globally measures platelet-related primary hemostasis. Closure time is sensitive to platelet adherence and aggregation abnormalities and therefore has increased sensitivity for von Willebrand\u0092s screening when compared to bleeding time. Comparative studies at our facility support these findings: CT was abnormal in 64% of patients diagnosed with vWD as compared to 43% by BT. INDICATIONS Closure times are indicated when a disorder of platelet function is suspected by a personal or family history of easy bruising, nose bleeds, menorrhagia, or post-operative bleeding, especially following dental extractions or tonsillectomy. It is not recommended as a screen for potential bleeding risk. Closure times may be prolonged when the platelet count is < 100,000\/mm3 even if platelet function is normal. In addition the CT will be prolonged when hematocrit levels are < 35%, due to the contributory effect of red blood cells on platelet behavior. These restrictions should be considered prior to performing a closure time. Suspected von Willebrand\u0092s disease, inherited platelet disorders and evaluation of acquired disorders of platelet function (hepatic disease, renal disease, drug effects) are appropriate clinical reasons for closure time screening. It may also be useful to monitor the response of therapeutics, such as DDAVP infusions, renal dialysis, platelet and antiplatelet drug therapy. Abnormal closure times, indicating possible defective platelet function, should be further investigated with standard platelet aggregation tests. SUMMARY Closure time is a test system to assess platelet-related primary hemostasis with improved accuracy and reliability in comparison to bleeding time. This assay is an important aid in the assessment of platelet dysfunction and bleeding risk caused by uremia, von Willebrand\u0092s disease, congenital platelet disorders and exposure to agents such as aspirin. REFERENCES 1. Rogers, RPC., Levin J., \u0093A critical reappraisal of the bleeding time.\u0094 Semin. Thromb. Hemost. 1990; 16: 1-20. 2. Cattaneo, M., Federici, AB., et. al. \u0093Evaluation of the PFA-100 system in the diagnosis and therapeutic monitoring of patients with von Willebrand\u0092s disease.\u0094 Thromb. Hemost. 1999; 82: 35-39. 3. Mammen, EF., Comp, PC., et. al. \u0093PFA-100 System: A new method for assessment of platelet dysfunction. Semin. Thromb. Hemost. 1998; 24: 195-202. 4. Fressinaud, E., Veyradier, A., et. al. \u0093Screening for von Willebrand\u0092s disease with a new analyzer using high shear stress: a study of 60 cases.\u0094 Blood 1998; 91: 1325-1331.<\/p>\n
Systemic inflammation results in systemic coagulation. Thrombotic thrombocytopenuc purpura (TTP) is a microangiopathy phenotype characterized by ADAMTS 13 deficiency. Left: Platelets attach to ultra large vWF multimers. Because vWF-CP (ADAMTS 13) is inhibited this leads to massive vWF:platelet thrombosis (right). Ab, antibody; CP, cleaving protease; vWF, von Willebrand factor.<\/p>\n Secondary thrombotic microangiopathy (TMA) has a phenotype characterized by decreased ADAMTS 13, and increased plasminogen activator inhibitor type I (PAI-1) and von Willebrand factor (vWF) levels with normal or high fibrinogen levels. Platelets attach to increased large vWF multimers and form thrombi in the presence of decreased PAI-I activity (left), leading to systemic platelet thrombi with delayed fibrinolysis (right). CP, cleaving protease; TF, tissue factor; TFPI, tissue factor pathway inhibitor; vWF-CP, ADAMTS 13.<\/p>\n Disseminated intravascular coagulation (DIC) is a microangiopathy phenotype characterized by increased tissue factor (TF) and plasminogen activator inhibitor type I (PAI-1), unopposed by the anticoagulant proteins TFPI, protein C, antithrombin III, and prostacyclin. The severest forms also have an ADAMTS 13 deficiency. Tissue factor activates factor VII (left), leading to massive consumptive fibrin thrombosis (right). VII, factor VII; vWF, von Willebrand factor.<\/p>\n <\/p>\n Specific therapies used to reverse or promote thrombosis and promote or stop fibrinolysis. Therapies used to reverse thrombosis include protein C concentrate (prot C), activated protein C (APC), tissue factor pathway inhibitor (TFPI), antithrombin III, heparin, and thrombin inhibitors such as argatroban and hyarudin. Therapies used to promote thrombosis include activated factor VII. Therapies used to promote fibrinolysis include tissue plasminogen activator (TPA), streptokinase, urokinase, and defibrinopeptide. Therapies used to stop fibrinolysis include aminocaproic acid, tranexamine, and aprotinin. PAI, plasminogen activator inhibitor type I.<\/p>\n <\/p>\n thrombocytopenia with decreased fibrinogen and increased d-dimer. Depletion of factors V and X causes increased pt\/ptt. Increased intravascular coagulation despite increasing pt\/ptt<\/p>\n <\/p>\n hits CNS and kidney hardest.<\/p>\n Dx<\/p>\n 1.\u00a0\u00a0\u00a0\u00a0\u00a0 Risk assessment:\u00a0 Does the pt have an underlying disorder known to be associated with DIC?\u00a0 If yes, proceed<\/p>\n 2.\u00a0\u00a0\u00a0\u00a0 Order global coag tests (CBC, PT, fibrinogen, FDP, D-Dimer)<\/p>\n 3.\u00a0\u00a0\u00a0\u00a0 Score by test results<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Platelets (>100=0, <100=1, <50=2)<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Elevated FDP (no icrease=0, mod. Increase=1, strong increase=2)<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Prolonged PT (<3 sec=0, >3 sec but <6 sec=1, >6 sec=2)<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Fibrinogen (>1 gram\/l=0, <1 gram\/l=1)<\/p>\n 4.\u00a0\u00a0\u00a0\u00a0 Greater than or equal to 5 is DIC, <5 may be non-overt DIC or another diagnosis<\/p>\n Validated in Crit Care Med (Volume 32(12) December 2004 pp 2416-2421)<\/p>\n Replace plasma until pt\/ptt is corrected, but only if infusing heparin as well<\/p>\n In places where ATIII or Protein C concentrate are available, these may be used instead or in combination with plasma<\/p>\n May be a role for xigris at some point<\/p>\n May be a role for infusions of prostacyclin (nitroglycerin or nitroprusside as well) all for microcirculatory flow<\/p>\n <\/p>\n <\/p>\n Bleeding<\/p>\n give plts<\/p>\n prbcs<\/p>\n ffp<\/p>\n if fibrinogen is <100, give cryoprecipitate<\/p>\n may need low dose heparin to block consumptive coagulopathy<\/p>\n 20-30 units\/kg then 5-10 units\/kg\/hour<\/p>\n Fibrin deposition-heparin.\u00a0 Treat underlying cause.<\/p>\n <\/p>\n The activity of plasma antithrombin is reduced in sepsis and DIC, indicating defective anticoagulation [12, 21]. In this study the lowest plasma antithrombin activity distinguished well the patients with overt DIC, as did the lowest platelet count and the highest plasma D-dimer. Antithrombin has been suggested to be included as a part of the score for nonovert DIC [6]. Our results suggest that antithrombin could have a role in the diagnosis of overt DIC as well. Furthermore, in an earlier study on septic patients we found higher levels of plasma antithrombin in survivors than in nonsurvivors, although antithrombin did not independently affect mortality [22]. Availability of the plasma antithrombin test may limit its use, however. (Inten Care Med Intensive Care Medicine 2005;31(9))<\/p>\n <\/p>\n secondary TTP or Hemolytic Uremic Syndrome<\/p>\n normal or mildly elevated pt\/ptt<\/p>\n only small amounts of hemolysis<\/p>\n increased d-dimer, but increased <\/strong>\u00a0fibrinogen<\/p>\n Probably benefit from same plasma-exchange therapies as TTP<\/p>\n <\/p>\n Test of vascular integrity and platelet function; independent of the clotting cascade<\/p>\n Increase is seen in thrombocytopenia, qualitative platelet dysfunction, vWD, Vascular disorders<\/p>\n Ask about ASA and NSAIDs as they cause platelet dysfunction<\/p>\n Spontaneous hemorrhage when count falls below 10-20,000<\/p>\n test of the extrinisic pathway (VII) and common pathway (X,V,II, and I)<\/p>\n Normally 10-12 seconds<\/p>\n Deficiencies of Factor VII can be seen with Vit K deficiency, Coumadin, Liver Disease<\/p>\n Test of all factors except VII and XIII, used to evaluate the intrinsic pathway<\/p>\n Normally 25-35 seconds<\/p>\n Increase seen with Factor VIII, IX, or XI and Heparin<\/p>\n Heparin and Coumadin can raise both PT and PTT<\/p>\n Tests fibrinogen to fibrin<\/p>\n Increased with Heparin, LMH, DIC, Liver disease<\/p>\n Increase seen with increased clot burden or consumptive coagulopathy<\/p>\n DIC in association with symmetric limb ecchymosis and necrosis of the skin<\/p>\n seen after viral syndromes or secondarily from meningococcal infections or most other severe infections.<\/p>\n there may be a role for activated protein c.<\/p>\n Thrombolytics<\/p>\n To reverse, use 6 units FFP and 10 units cryoprecipitate<\/p>\n Obtain CBC, fibrinogen level, thrombin time, PT\/APTT, Type and Screen Most cases need no further care. Goal FBG is 100 mg\/dL. If life-threatening bleeding, transfuse 10 units of CRYO (FBG source), 2 FFP (procoagulant source), and PLAT if thrombocytopenic. Protamine sulfate 1 mg\/100 units of heparin may be used if heparin given within the previous 4 hours. Anti-fibrinolytic, e.g., EACA can be given if life-threatening bleeding continues after CRYO\/FFP.<\/p>\n Mild forms can remain undiagnosed until adulthood<\/p>\n Hemostasis is reliant on three mechanisms:\u00a0 platelet activation, coagulation activation, and fibrinolysis<\/p>\n The platelets form a plug at the site of a vascular defect which is then stabilized by fibrin, plasmin then breaks down the fibrin.<\/p>\n Defects in plt adhesion cause immediate bleeding of the mucosal<\/strong> surfaces.\u00a0 Caused by vWF deficiency, NSAIDS, ASA, and Ganzman’s thrombasthenia (IIbIIIa deficiency)<\/p>\n Impaired coagulation causes immediate bleeding in the soft tissue and joints<\/strong>.\u00a0 Caused by VIII, IX deficiency or warfarin\/heparin.<\/p>\n Accelerated fibrinolysis causes delayed, mucosal or GU<\/strong> bleeding.\u00a0 Caused by liver dysfunction, Factor VIII deficiency or thrombolytics.<\/p>\n <\/p>\n The intrinsic pathway is so named b\/c everything needed for activation is already in the plasma.\u00a0 The extrinsic needs inflammatory cytokines.\u00a0 PT=extrinsic, PTT=intrinsic.\u00a0 If both are altered then consider X, V, Fibrinogen, or Thrombin defects.<\/p>\n Get history of minor\/major surgeries, dental work, hepatic, kidney, cancer, drugs<\/p>\n Type of bleeding:\u00a0 Purpura=decreased platelets, Mucosal or Soft Tissue=Coag, hemarthroses=hemophilia<\/p>\n Labs:\u00a0 CBC, Coag, DIC Panel (Fibrinogen, FSP\/D-Dimer, Thrombin Reptilase)<\/p>\n Rx:<\/p>\n Liver-FFP, if fibrinogen<100 give cryoprecipitate<\/p>\n Uremia-dDAVP .3 mcg\/kg IVPB over 15-30 minutes QD, Estrogens 3mg\/kg IV, Blood transfusion<\/p>\n <\/p>\n PT\/PTT may be inaccurate with crits<20 or >50 b\/c of imbalance between plasma and sodium citrate.<\/p>\n If patient is clinically normal, look at smear for platelet clumps and giant platelets<\/p>\n Bleeding secondary to anti-thrombotics<\/p>\n Bleeding and thromboses<\/p>\n Acute Leukemia<\/p>\n Sickle Cell Chest Syndrome<\/p>\n <\/p>\n Br J Anesthaes 1992;69:307<\/p>\n <\/p>\n <\/p>\n Figure 1. A normal thromboelastograph tracing. R = reaction time (the time from placing the sample in the cuvette until the tracing amplitude reaches 2 mm (normal range = 19\u009628 mm). R denotes the rate of initial fibrin formation and is functionally related to plasma clotting factors. K = clot formation time (normal range = 8\u009613 mm). K measured from R to the point where the amplitude of the tracing reaches 20 mm. K represents the time it takes for a fixed degree of viscoelasticity to be achieved by the forming clot. It is effected by the activity of the intrinsic clotting factors, fibrinogen, and platelets. Alpha angle ([alpha]\u00b0) (normal range = 29\u009643\u00b0) is the angle formed by the slope of the thromboelastograph tracing from the R to the K value. It denotes the rate at which a clot is formed. Maximum amplitude (MA) (normal range = 48\u009660 mm) is the greatest amplitude on the thromboelastograph tracing. MA is a reflection of the absolute strength of the fibrin clot and can be altered by both qualitative and quantitative platelet abnormalities (11<\/a>).<\/p>\n <\/p>\n TEG does not monitor platelet adhesion\/release in abnormalities such as low dose aspiring use or renal failure<\/p>\n <\/p>\n The time from the start of the curve until it reaches 1 mm wide This is the time taken to form fibrin. Prolonged with clotting factor deficiencies, anticoagulants and thrombocytopaenia.<\/p>\n The time taken for the graph to widen from 1 mm to 20 mm. This is dependent on fibrinogen and platelets.<\/p>\n This is the width of the curve at the widest point. This is affected by platelet function and number and fibrinogen.<\/p>\n This is the angle measured between the midline of the tracing and a line drawn from the 1 mm point tangential to the curve. The alpha value and CFT indicate the rate of increase of elastic shear modulus in the sample \u0096 i.e. how fast the clot structure is forming. This is abnormal in the presence of clotting factor deficiencies, platelet dysfunction, thrombocytopenia and hypofibrinogenaemia.<\/p>\n This is measured as a decrease in amplitude from the maximum. If there is a substantial decrease \u0096 i.e. more than 15% \u0096 then this is an indication of fibrinolysis taking place.<\/p>\n <\/p>\n <\/p>\n <\/p>\n Dr Mattox, Two hours ago I was called by the hospital\u00b4s transfusional team to discuss an interesting clinical case. A 78 yo patient with abdominal sepsis (an infected gastrostomy) on the vent. Yesterday his platelets, antithrombin and protein C levels dropped, and thrombin-antithrombin (TAT) complexes , PF 1+2, plasminogen activator inhibitor (PAI) raised, with low fibrinogen and low levels of all coag factors except VIII (which is an acute phase protein…). Some hours later he developed a purpuric rash. He was in norepi and terlipressin, and received antithrombin to compensate for extremely low ATIII plama levels. ANti PF 4 test was performed to exclude HIT too, since the patient has received lots of heparin before. They performed a ROTEM in him with reagents for the intrinsic pathway (INTEM), extrinsic pathway tissue factor- activated (EXTEM), fibrinogen polymerization &fibrin formation pathway (FIBTEM) and a test with a fibrinolysis inhibitor (APTEM. EXTEM curve was not that bad…. INTEM curve had a reduced maximum amplitude and all the signs of fibrinolysis, and the same with FIBTEM curve which was flat.HEPTEM demonstrated there was no reversal of the problem with heparin neutralization. Fibrinogen levels were 280, platelets were 20000. Aprotinin was administrated. Despite improvement of fibrinolysis in the APTEM (EXTEM with an in-vitro fibrinolysis inhibitor) the INTEM and FIBTEM worsened. So we decided to administer platelets, cryo and FFP together with aprotinin and later perform another TEG.Why not to use r VIIa? Low coag factor and fibrinogen levels. Fibrinolysis on course. Bad timing for VIIa but good timing for factor concentrates…why we didn\u00b4t do it? their protein C content is not enough to make sure thrombosis won\u00b4t happen. This patient had previously a prothrombotic state in his complex coag profile.So we decide to treat the guy conventionally, blocking fibrinolysis and administrating coag factors and platelets first. Later another ROTEM will be performed with the same reagents. Coagulation complex tests interact with ROTEM to provide a better bedside decision-making tool. There is already literature on these tests, written mainly by French authors (DHAINAUT, RUGERI, LEVRAT). I think ROTEM does not substitute the tests, but rather, they go together very well. This is a wonderful way of DIC management, and there is some literature coming on TRAUMA too.ROTEM cannot make the specific diagnosis among the several platelet disorders, acquired or congenital, nor several kinds of acquired dysfibrinogenemia – like abnormal fibrinogens, lack of factor XIII, etc.ROTEM is also not accurate for platelet function. For this purpose, PFA-100 and Accumetrics are better. Also, it cannot address prognosis and phase of endothelitis and microvasculature coagulation status in sepsis like the complex tests like TAT, PAP, PAI, PF 1+2, etc. Common sense and deep knowledge of the pathophysiology of coagulation derangements are important to address properly the indicated tests according to the patient\u00b4s moment. My 2 brazilian cents, since Dr Rubens Costa, once more, decided to shut up. claudia Usefulness of Thromboelastography (ROTEM\u00ae) in Coagulation Management in Trauma Patient Abstract number: P0696 Rugeri1 L, Levrat2 A, Gros2 A, Floccard2 B, Scherrer1 F, Delecroix1 E, Allaouchiche2 B, Negrier1 C 11Laboratoire H\u00e9mostase, H\u00f4pital E. Herriot, Chu-lyon, France 11Laboratoire H\u00e9mostase, H\u00f4pital E. Herriot, Chu-lyon, France 22Service R\u00e9animation Chirurgicale, H\u00f4pital E. Herriot, Chu-lyon, France The purpose of this study was to investigate thromboelastography in assessment of trauma patient coagulation. ROTEM\u00ae was performed on 268 samples from 71 men and 20 women with a mean of age 34 \u00b1 16 years (mean \u00b1 SD) admitted to our intensive care. Normal values were established on 42 male and 18 female controls with a mean age of 39\u00b112 years. The ROTEM\u00ae parameters were performed for EXTEM (tissue factor activated test), FIBTEM (assessment of fibrinogen status) and APTEM (in-vitro fibrinolysis inhibition) at H0, 6, 12 and H24 comparatively to standard assays. Results: EXTEM parameters FIBTEM N PT Fibrinogen Platelets CT normal (56 \u00b1 7) A15 normal (55 \u00b1 5) A10 normal (12 \u00b1 4) 181 72 \u00b1 12 2.8 \u00b1 0.9 197 \u00b1 61 CT increased (85 \u00b1 18) A15 normal (55 \u00b1 5) A10 normal (11 \u00b1 4) 27 71 \u00b1 11 2.4 \u00b1 0.9 196 \u00b1 69 CT normal (56 \u00b1 7) A15 decreased (39 \u00b1 5) A10 decreased (7 \u00b1 2) 28 55 \u00b1 13 1.7 \u00b1 0.6 110 \u00b1 65 CT increased (120 \u00b1 69) A15 decreased (33 \u00b1 13) A10 decreased (4 \u00b1 3) 32 46 \u00b1 22 1 \u00b1 0.6 123 \u00b1 53 Subgroup (219 \u00b1 91) (15 \u00b1 12) (0 \u00b1 0) 8 18 \u00b1 12 0.2 \u00b1 0.2 112 \u00b1 62 Mean \u00b1 SD, CT = Clotting Time (sec), A15 or A10 = Clot firmness in mm at 10 or 15 min. In 1 case, we observed a correction of APTEM parameters evocating a hyperfibrinolysis. These results showed that a normal A15 of EXTEM was always associated with normal A10 of FIBTEM and coagulation parameters over transfusional threshold. When abnormal A15 of EXTEM was found, A10 of FIBTEM would be studied to be helpful for monitoring of hemostatic therapy. In the last 8 samples, the results indicated a very severe hypocoagulability requiring rapid therapy management. In conclusion, ROTEM\u00ae is a rapid test that could be helpful in coagulation monitoring in trauma patients. To cite this abstract use the following format: Journal of Thrombosis and Haemostasis 2005; Volume 3, Supplement 1: abstract number Session Details<\/p>\n <\/p>\n ROTEG is involved in some transfusion algorhythms and it\u00b4s supposed to reduce excessive blood transfusions. Dr Plinio Gomes, Dr Jo\u00e3o Luiz, Dr Rubens Costa, Dr Edimilson Silva and Dr Erica Tavora are starting to validate this method in Procardiaco Hospital ICU, Rio de Janeiro. There are several algorhythms involving TEG-guided blood transfusions published, and it seems a very good application of the method. Hyperfibrinolysis is much more common in general ICU than one might suppose. Despite many papers advocating it, and one DBMC showing benefit in blunt trauma, I seriously fear administering rVIIa in trauma without the help of a TEG or a fast TEG or a ROTEM at bedside. Many of these patients are hypercoagulable and a disaster might happen. In others hyperfibrinolysis will just “eat” r VII a, unless you administer some antifibrinolytic that helps to stop the fibrin degradation. while you start factor reposition with factor concentrates and rVII a. My 2 cents.<\/p>\n <\/p>\n An increased CFT or MA in thromboelastography, is by no means a rare finding – those who are used to this method can endorse my words. And many patients who are supposed to have bleeding tendencies because of aspirin use before CABG procedures are actually HYPERCOAGULABLE when you check their MA in TEG and test their coagulation profile. I BET that if you administer aprotinin to this kind of patient the drug will probably be detrimental to the microvascular coagulation status. Only for curiosity, aprotinin use during CABG causes PAI-1 to increase in plasma and there was a trend to a greater incidence of Non-Q wave myocardial infarction in the people who received this drug, as shown by an RCT done with 54 patients.PAI-1 is a predictor of bad prognosis in septic patients with acute renal failure. Take a good look in the two papers which abstracts I send below, and take your own conclusions. That means that WE ARE YET to discover who will benefit from these drugs, and the way to discover it is through complex coagulation monitoring. All of this said, and apologizing for the BIG post, I leave the scenario wondering what the OTHER coagulation buffs in the list are thinking about all that. claudia Clotting and Bleeding: Ouchie, Mommy! We know that when Johnnie or Susie cut their finger on the playground, that they bleed, get a bandage, and then clot. But why, when a child is in the ICU, does he or she clot and then bleed. The secrets of the paradox have now been revealed. When vasculature is focally injured by a laceration on the playground, the focal endothelium at the point of injury, normally antithrombotic and profibrinolytic, becomes prothrombotic and antifibrinolytic, allowing the bandage to get all the credit. In critical illness, systemic inflammation\u0096induced endotheliopathy causes all the endothelium to become prothrombotic and antifibrinolytic. Systemic antithrombotic factors (protein C and antithrombin III) are consumed until they become low enough that prothrombotic factors take over and are systemically consumed in clots. When enough prothrombotic factors are consumed in this manner, then spontaneous hemorrhage occurs. An armamentarium of anticoagulants (e.g., heparin, antithrombin III, protein C, argatroban), procoagulants (e.g., activated factor VII), fibrinolytics (e.g., tissue plasminogen activator, activated protein C), and antifibrinolytics (e.g., Amicar, tranexamic acid) are now available to the physician. Unfortunately, clinical tests that might guide the clinician as to which specific therapy to use are not readily available in most clinical laboratories. One can sometimes see bleeding, but how does one know if the patient may have systemic thrombosis precedent to bleeding? You should think about it in any patient who develops new-onset thrombocytopenia and multiple organ failure. These patients are likely to be consuming platelets in microvascular fibrin or platelet clots. If the child has a prolonged prothrombin time\/partial thromboplastin time and low fibrinogen, then it is likely to be disseminated intravascular coagulation pathophysiology, and if the child has a normal or high fibrinogen, then it is likely to be thrombotic thrombocytopenic purpura pathophysiology. Plasma exchange is an effective therapy for reversal of coagulopathy from either condition because it corrects any and all abnormalities (21).<\/p>\n <\/p>\n Coag Abnormalities in the Crit Ill (Crit Care 2006;10:222)<\/p>\n <\/p>\n Differential diagnosis of thrombocytopenia in the intensive care unit<\/strong>\u00a0 Differential diagnosis \u00a0 Approximate relative incidence \u00a0 Additional diagnostic clues \u00a0 Sepsis \u00a0 52% \u00a0 Positive (blood) cultures, positive sepsis criteria, hematophagocytosis in bone marrow aspirate \u00a0 DICa \u00a0 25% \u00a0 Prolonged aPTT and PT, increased fibrin split products, low levels of physiological anticoagulant factors (antithrombin, protein C) \u00a0 Massive blood loss \u00a0 8% \u00a0 Major bleeding, low hemoglobin, prolonged aPTT and PT \u00a0 Thrombotic microangiopathy \u00a0 1% \u00a0 Schistocytes in blood smear, Coombs-negative hemolysis, fever, neurological symptoms, renal insufficiency \u00a0 Heparin-induced thrombocytopenia \u00a0 1% \u00a0 Use of heparin, venous or arterial thrombosis, positive HIT test (usually ELISA for heparin-platelet factor IV antibodies), rebound of platelets after cessation of heparin \u00a0 Immune thrombocytopenia \u00a0 3% \u00a0 Anti-platelet antibodies, normal or increased number of megakaryocytes in bone marrow aspirate, thrombopoeitin decreased \u00a0 Drug-induced thrombocytopenia \u00a0 10% \u00a0 Decreased number of megakaryocytes in bone marrow aspirate or detection of drug-induced anti-platelet antibodies, rebound of platelet count after cessation of drug \u00a0 Seven major causes of thrombocytopenia (platelet count <150 \u00d7 109\/l) are listed. Relative incidences are based on two studies in consecutive intensive care unit patients [1,6] but may vary depending on the population studied. Patients with hematological malignancies were excluded.aPatients with sepsis and disseminated intravascular coagulation (DIC) are classified as DIC. aPTT, activated partial thromboplastin time; ELISA, enzyme-linked immunosorbent assay; HIT, heparin-induced thrombocytopenia; PT, prothrombin time.<\/p>\n <\/p>\n![\"\"](\"\/wp-content\/images\/part1\/TTP%20diagram.jpg\")
<\/a>TTP<\/p>\n<\/a>TMA<\/p>\n<\/a>DIC<\/p>\n<\/a><\/p>\n<\/span>DIC<\/span><\/h3>\n
<\/a><\/a><\/p>\n<\/h4>\n
Treatment<\/h4>\n
Rarely will fibrinogen get to cutoff in crit care patients, consider ATIII instead<\/h4>\n
<\/span>Non-Consumptive secondary thrombotic micro-angiopathy (TMA)<\/span><\/h3>\n
<\/span>\u00a0
<\/span><\/h3>\n<\/span>Coagulation Pathway Disorders<\/span><\/h2>\n
<\/a><\/a><\/a><\/a><\/a><\/h3>\nBleeding Time<\/h4>\n
Platelet Count<\/h4>\n
Prothrombin Time (PT)<\/h4>\n
Partial Thromboplastin Time (PTT)<\/h4>\n
Thrombin Time<\/h4>\n
D-Dimer<\/h4>\n
<\/h3>\n
<\/span>Purpura Fulminans<\/span><\/h2>\n
<\/span>Hematologic Emergencies:<\/span><\/h2>\n
Bleeding Diatheses<\/h4>\n
Severe Thrombocytopenia<\/h4>\n
<\/span>Thromboelastography (TEG)<\/span><\/h2>\n
<\/a><\/a><\/a><\/a><\/a><\/p>\n<\/a>Clotting time (CT) or reaction time( R time)<\/h4>\n
Clot formation time (CFT) or K time<\/h4>\n
Maximum clot firmness (MCF )or maximum amplitude<\/h4>\n
Alpha angle<\/h4>\n
Fibrinolysis<\/h4>\n