Part II: Coagulation Laboratory: Methods, Standards & Cost Effective Testing. Donna D. Castellone ASCP Annual Meeting
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1 Part II: Coagulation Laboratory: Methods, Standards & Cost Effective Testing Donna D. Castellone
2 Understanding Coagulation Case Studies - clinical picture - analysis - diagnosis
3 Case Study A 15 yr old female presents with heavy periods Her HGB is 9.0 g/dl She has had intermittent periods of nose bleeding as a child An evaluation for a bleeding work-up was ordered PT= 12.1 sec APTT= 42.1 sec FVIII= 38% Mixing study: APTT 1:1 mix = 31.5 sec Correction
4 Additional Testing: Decreased Factor VIII, need to distinguish between vwd and Hemophilia vwd is autosomal dominant, 1/200 people, most common cause of bleeding This is a test of platelets- primary hemostasis Hemophilia is sex-linked recessive Mostly in males- secondary hemostasis
5 Hemophilia or vwd Second level testing: Ristocetin cofactor: 38% (nr %) vwf: antigen: 35% (nr %) Diagnosis: von Willebrand Disease Multimer analysis: all multimers decreased Type 1 VWD
6 Von Willebrand Disease Described in 1926 by Eric von Willebrand described a bleeding disorder that occurred in 24/66 families vw factor is a plasma protein that mediates the initial adhesion of platelets at the site of vascular injury It also stabilizes FVIII in circulation Caused by a deficiency or dysfunction of vwf
7 von Willebrand Disease: Affects 1-2% of general population, about 2.6 million people Autosomal dominant: 50% chance of passing the gene to a child Caused by a deficiency and/or qualitative abnormality of the VWF protein Can be acquired with certain malignancies, drugs or autoimmune disorders
8 Von Willebrand Factor vwf is a multimeric high molecular weight protein present in plasma and platelets In response to vascular injury it mediates platelet adhesion to the subendothelium and platelet aggregation Serves as a carrier protein and a stabilizer for FVIII- which is why FVIII is decreased in VWD Synthesized in endothelial cells and megakarocytes controlled by a gene on chromosome 7 Stored in the Weibel-Palade bodies
9 Types of von Willebrand Disease: Type 1: decreased vwf activity & antigen 70-80% of cases; mild bleeding symptoms, may be asymptomatic. Type 2: abnormal vwf protein, qualitative, 2:1 ratio of activity to antigen; deficiency of higher weight multimers; mild to severe bleeding Type 3: severely reduced or absent circulating vwf, rare & life threatening bleeding
10 Clinical Findings Mucosal bleeding (epistaxis, gingival bleeding. menorrhagia) Superficial ecchymosis: common Hemarthrosis, delayed bleeding, deep dissecting hematoma: rare Not one laboratory test can make the diagnosis Some screening tests may be normal, need specific vw laboratory tests.
11 How to test: PT, APTT, Fibrinogen, PLT FVIII measures the ability of vwf to bind and maintain the level of FVIII in circulation vwf Antigen measures the concentration of vwf protein in plasma vwf Ristocetin cofactor assay: functional assay of vwf measures its ability to interact with normal platelets the antibiotic ristocetin causes vwf to bind to platelets, resulting in clumps and remove from circulation
12 Additional testing: Collagen binding assay: ELISA assay Ristocetin Induced Platelet Aggregation (RIPA) vwf multimers: looks at the different molecular forms of vwf from dimer to high molecular weight multimers (HMWM). This is important in determining subtypes of vwd
13 Blood Typing: Different blood types have different normal ranges of vwf May be a consideration when classifying patients: Type O = % Type A = % Type B = % Type AB= % Technical Manual 9 th ed AABB
14 NHLB/NIH Guidelines TypeDescription R; vwf Ag FVIII CoF %% % NL NL > Partial quantitative vwf deficiency <30 <30 NL or 2A Decreased vwf dependent plt adhesion & selective deficiency of HMWM <30 < B Increased vwf affinity to GPib <30 < low NL or low NL or low NL or 2M Decreased vwf dependent platelet <30 <30- adhesion 200 low 2N Markedly decreased vwf binding Very affinity for FVIII low 3 Complete deficiency of vwf <3 <3 Very low R:CoF/A g >.5-.7 <.5-.7 <.5-.7 <.5-.7 >.5-.7 NA
15 Von Willebrand testing Sample integrity is important, antigen is more stable than activity Should freeze sample ASAP, but after thawing do not place on ice Thaw in water bath Mix, mix and mix Blood type is important
16 Case Study: A pregnant women has a routine OB visit This is her third pregnancy, no prior problems Upon taking a history, her only complaint is shortness of breath The physician orders a work-up
17 Thrombosis & Pregnancy: 6 times more thrombotic Recurrent rate: 1/71 Most prone 3 rd trimester Post-partum Can have micro vascular thrombosis 110 women with obstetrical complaints- 53 had thrombophilia-50% PE most common cause
18 Recommended Thrombosis Panel APC Resistance screen Protein C activity Protein S activity Antithrombin activity Prothrombin gene mutation Factor VIII Lupus Anticoagulant screening Homocysteine
19 c2 Laboratory Evaluation Must perform a panel of tests No global test available Must confirm plasma based assays before establishing diagnosis Many drugs and physiologic conditions may influence results Should consider evaluation of family
20 Slide 19 c2 castdo10, 12/17/2010
21 What happens? Increase in VII, VIII, IX, X and fibrinogen vwf Increased venous stasis Increased activation of platelets Increased PAI-1 Physiological resistance to APC
22 Why? Hemostatic changes: Physiological changes Congenital: Thrombophilia Mechanical: Change in Uterus 1600 women/day die in pregnancy
23 Additional risks: DVT 35 fold increased risk: 5/100 50% of women that have thrombotic Post partum ovarian DVT 1:500-1:2000 women High risk in thrombophilia patients 30-36% ATIII deficiency 3-10% Protein C deficiency 0-6% Protein S deficiency pre-partum 0-15% post-partum 46% APCR
24 Acquired Risk Factors: Cesarean delivery Maternal age>35 = 3 X risk; >40 =6 X risk Obesity >180 lbs Surgical procedure during pregnancy or post partum
25 How do you treat? Warfarin can cross the placenta, risk to the fetus Can use weeks, or post partum Heparin doesn t cross placenta, monitor with APTT Aspirin LMWH safe, 1/day, must remove 24 hours before labor
26 Advantages: Excessive blood loss is >600mls APCR + patients have a lower risk 14% of APCR patients will bleed Only 1% of APCR + patients bleed
27 Results: Fibrinogen= 485mg/dl ( ) Factor VIII=210% (50-150%) Factor V Leiden: negative Lupus anticoagulant: negative AT= 82% (80-120%) Protein C = 84% (70-130% Protein S= 50% (62-154%) What do we see?
28 Diagnosis: Physician tells the patient she was Protein S deficient Recommends a therapeutic abortion After much thought the patient agreed, since she had 2 small children at home What is wrong with this picture
29 Protein S: Protein S is a Vitamin K dependent factor It is an inherited disorder, occurring in about 3% of the thrombotic population However, protein S is normally decreased in pregnancy It also is decreased during the first few days of a women s cycle
30 How to test: This is a case where an abnormal result is normal Information is vital Not knowing can have consequences
31 Case Study A pediatric samples from a 3 month old sent to laboratory for testing Lupus work-up Pediatric samples: small volume, different ranges Transient? True LA? Many issues
32 Results PT= 16.1 APTT=54.7 1:1 mix = 15.9 & 52.1 Continue LAC work-up Drvvt screen= sec (abn) Drvvt confirm= ratio= 0.9; neg Hexagonal phase= positive (strongly 21.9 sec) Lupus, right?
33 Result Review Principle of DRVVT, is screen uses low concentration of ppl, prolongs result Confirm uses high concentration result should shorten Very prolonged results, confirm is longer than screen Different than APTT - suspicious...
34 Factor Assays also performed Factor 1:10 1:20 1:40 VIII 45% 65% 90% IX 32% 46% 62% XI 50% 71% 94%
35 Additional information Looked like an inhibitor, was heparin on board Thrombin time = 14.1 sec PNP=13.8 sec normal Running out of sample Techs were running out of patience
36 Additional Information HIT testing Positive for HIT Patient not on Heparin Patient was on Argatroban Baby had HIT, put on a DTI, laboratory not notified, caused abnormal results
37 Not just heparin and coumadin anymore: Large compendium of anticoagulation Newest are anti-thrombin's These direct inhibitors against IIa Cannot be monitored by an APTT, or a thrombin time
38 Direct Thrombin Inhibitors (DTI's) 1. Directly bind to and inhibit thrombin s interaction with its substrate 2. Action not mediated through antithrombin 3. Do not interact with other plasma proteins 4. Do not interact with PF4 5. Inactivate fibrin-bound thrombin and fluid-phase thrombin 6. Direct inhibitors 1. Lepirudin 2. Argatroban 3. Bivalirudin FDA approval for the treatment of HIT Alternative to heparin for the treatment of PCA 37
39 ARGATROBAN - Novastan Synthetic small molecule, derived from arginine Direct thrombin inhibitor 1/2 life of minutes Metabolized by the liver Approved for use in HIT
40 Assay Insensitivity: Many reagents are insensitive to DTI s The APTT reagent should be tested to determine where the insensitivity occurs For many reagent at 0,8mg/L the reagent is flat Leads to a potential to miss overdosing a patient Spike PNP with known concentrations of DTI and run the APTT Jensen, R., (2003), Novel Anticoagulants used in the Therapy of Thrombotic Disease, Clinical Hemostasis Review, 17 (8) 1-6.
41 APTT versus ARGATROBAN Argatroban spike versus APTT APTT: (seconds) Argatroban (ug/ml) Castellone, DD., Peerschke, EIB,(2006)A chromogenic method for quantitation of direct thrombin inhibitors: A case study, ISTH, abstract, Geneva,
42 Using the ACT to monitor levels Activated Clotting Time versus Bivalirudin Levels ACT (seconds) Time (minutes) ug/ml Castellone, DD., Peerschke, EIB,(2006)A chromogenic method for quantitation of direct thrombin inhibitors: A case study, ISTH, abstract, Geneva,
43 What do direct thrombin inhibitors do? PT/INR, APTT prolonged, remain prolonged in mix Acts like an inhibitor in clotting-time assays, under-estimating results Fibrinogen falsely low C & S, overestimated ATIII - has anti-thrombin activity, Increased- Heparin - anti-xa, is okay, unless IIa Walenga, J., (2006) Direct Thrombin Inhibitors & Laboratory Monitoring Issues, Coagulation Symposium, Indianpolis, May 5.
44 Argatroban Laboratory Monitoring aptt was recommended to be used: Baseline aptt performed 2 hours after infusion is started aptt range times baseline Further studies have demonstrated that this is reagent dependent, APTT can flatten out and not reflect an increased dose, can have dangerous outcomes Ecarin clotting time Linear, may be substituted when APTT is not usable Activated clotting time (ACT) Used during very high levels of Argatroban during percutaneous cardiac intervention Maintain ACT seconds We did not find this to be true, we also found a flattening of the results PT/INR cannot be used to monitor Argatroban therapy Thrombin time is not linear and can not be used to monitor Argatroban therapy When switching from Argatroban to Coumadin, the INR may not be reliable Therefore a chromogenic Factor X should be used until the patient of off of Argatroban 43
45 Ecarin Clotting Time Can be used to monitor DTI's Not affected by heparin or Warfarin therapy Superior responsiveness and specificity compared to the APTT Cannot be used to monitor UFH, LMWH, Fondaparinux Reagent poorly standardized with increased lot variability Limited availability; no kit available No manufactured calibrators or controls ShowPDF&ArtikelNr=81505&Ausgabe=230521&Produkt Nr=224034&filename=81505.pdf
46 Ecarin Clotting Time Ecarin is a thrombin-like snake venom Ecarin converts prothrombin to meizothrombin which forms 1:1 complexes with r-hirudin Meizothrombin is neutralized by DTI's but not affected by heparin or AVK Free meizoprothrombin stimulates the conversion of fibrinogen to fibrin Ecarin clotting time is prolonged with increasing amounts of r-hirudin
47 Anti IIa assay Thrombin is added in excess to the diluted patient plasma. Thrombin activity is neutralized in proportion to the amount of DTI contained in the sample. The remaining amount hydrolyses the chromogenic substrate. The pna used to promote a color reaction is released upon hydrolysis of the substrate and the released color is then measured photometrically at 405nm. The amount of residual thrombin activity is inversely proportional to the amount of DTI in the sample. Package inserts Chromogenix reagents
48 Transitioning Patients from Argatroban to Warfarin Used in treatement of HIT ARGATROBAN elevates the PT disproportionately; reasons unknown Treat concurrently until INR is therapeutic about 4-5 days However, true INR is not known Can use a conversion method provided in ARGATROBAN product labeling
49 Chromogenic X assay Chromogenic X assay measures the amount of factor X Levels of 11-42% inversely correlate with INRs of Levels <11% predict an INR of 3.5 and >42% predict and INR <2.0 Considered and INR value absent of argatroban if D/C 4 hours, and APTT decreased to 1.5 times baseline or < 40 seconds Demonstrates 93% sensitivity and 78% specificity Arpino,PA, Demirjian,Z., VanCott, EM, (2005) Use of the Chromogenic Factor X Assay to Predict the INR, Pharmacotherapy, 25(2):
50 Pentasaccharides Fondaparinux Plasma half-life hours 1X/day dosing via subcutaneous injection Contraindicated in patients with severe renal insufficiency Does not bind to platelets or PF4 No antidote Uncontrolled bleeding may be treated with recombinant Factor VIIa 2.5 mg SC daily 5-9 days Idraparinux* Plasma half-life 130 hours 1x/week via subcutaneous injection* Contraindicated in patients with severe renal insufficiency Does not bind to platelets or PF4 No antidote 50-fold higher binding affinity for Xa More highly sulfated derivative of Fondaparinux 49
51 Fondaparinux (Arixtra) Pentasaccharide Approved to DVT and PE Mechanism Contains the unique pentasaccharide sequence Binds to activated factor Xa Inhibits Factor Xa Indirect inhibitor of IIa NEJM 50
52 Pharmacology of the Pentasaccharides Predictable dose response Administered 1x/day Does not bind PF4 or plasma proteins Monitoring unnecessary Peak activity 3 hours No antidote, protamine ineffective Most common adverse reaction is bleeding Excreted by the kidneys Indications Orthopedic Perioperative DVT prophylaxis Hip Fracture Hip replacement Knee replacement 51
53 Pharmacology of the Pentasaccharides Contraindications (due to bleeding risk) Patients with severe renal impairment Patients weighing less than 110 pounds Complications Bleeding Similar safety to LMWH Spinal thrombosis with risk of paralysis Associated with concurrent spinal anesthetic procedures 52
54 Additional Contraindications with Pentasaccharides Patients with Renal disease Kidney only route of excretion Patients weighing less than 50 kg Patients over 75 years old Patients with any bleeding history Congenital or acquired coagulopathies Ulcerative gastrointestinal disease Hemorrhagic stroke Patients with history of HIT Despite no reaction with PF4* 53
55 Dosing and Laboratory Monitoring of Fondaparinux Chromogenic Heparin assay based on anti-xa activity Requires a calibration curve using Fondaparinux aptt is insensitive for monitoring Monitoring not needed in uncomplicated cases Collect blood 4 hours after administration Target range mg/l Consider monitoring Infants and children Obese and underweight patients Renal disease Long-term treatment Pregnancy Unexpected bleeding or thrombosis Exceptions 54
56 Dabigatran Etexilate OAC with several advantages over Warfarin and Enoxaparin Pro-drug Dabigatran is rapidly converted to its active form Specifically and selectively inhibits both free and clot bound thrombin Predictable and consistent pharmacokinetic profile Not significantly affected by interactions with food Eliminated mainly via the kidneys Not metabolized by cytochrome P450 system Does not affect the metabolism of other drugs that utilize this system Leads to a lower potential for drug interactions 55
57 Dabigatran Half-life is hours 12 hours after a dose ~ 50% of the drug is gone ~75% is excreted within 24 hours of the last dose Generally does not require monitoring INRs should not be used as a measure of the anticoagulant effect Modest elevation of INR, variable and cannot be predicted aptt can provide a qualitative indication of anticoagulant therapy aptt prolongation is linearly related to the square root of the plasma concentration which should not be used for a for precise quantification of effect Ecarin clotting time is a specific test that shows a close linear correlation with the plasma Has the potential to offer physicians and patients a simple and convenient alterative to the present anticoagulant options 56
58 Apixaban Oral, direct, selective factor Xa inhibitor Produces concentration-dependent anticoagulation No formation of reactive intermediates No organ toxicity Low likelihood of drug interactions Good oral bioavailability No food effect Balanced elimination (~25% renal) Half-life ~12 hrs He et al., ASH, 2006, Lassen, et al ASH,
59 Conclusion APTT Anti FXa Anti FIIa UFH Poor dose response Linear over Rx range Poorly standardized LMWH Fondaparinux Too insensitive Linear over Rx range Not applicable DTIs Plateau effect Not applicable Poorly responsive ECT Non reactive Non reactive Linear over Rx and interventional range PiCT Linear over prophylactic, Rx interventional ranges Linear over prophylactic, Rx interventional ranges Linear over prophylactic, Rx interventional ranges 58
60 Case Studies How to use the D-dimer assay
61 Clinical Utility of D-dimer Disseminated Intravascular Coagulation (DIC) Simultaneous formation of thrombin and plasmin Sensitive, but not specific marker for DIC Venous Thromboembolism (VTE) High negative predictive value for exclusion Potential positive predictive value Positive predictive of recurrent MI Independent predictor of ischemic heart disease Differentiate between a traumatic spinal tap or a subarachnoid bleed Predictor of VTE recurrence, elevated levels following discontinuation of anticoagulant therapy associated with recurrence
62 Diagnostic Utility If you have a D-dimer test that has been cleared by the FDA for exclusion, that test can be used to rule out DVT and PE for non-high clinical pre-test probability assessment model to exclude DVT and PE. Outpatient setting To achieve this claim the FDA requires: 1. To establish the cutoff study of the assay (0.500 mg/l) by testing samples against a predicate to verify sensitivity 2. To prospectively collect and enroll patients suspected with PE and or DVT (first time event) and compared standard of care results (imaging) versus the D-dimer result. 3. Negative D-dimer patients receive a 90 day follow up call to evaluate potential development of a PE or DVT 4. Sufficient patients must be enrolled have a >99% NPV to be approved as an exclusionary claim by the FDA.
63 Clinical Model to aid in assessment & diagnosis: Developed by Wells and colleagues Based on symptoms and signs for DVT and PE Presence or absence of an alternate diagnosis Presence and number of risk factors Patients are scored based on a series of criteria Scoring for DVT Scoring for PE High probability >/= 3 High probability >6 Moderate 1 or 2 Moderate 2-6 Low </=0 Low <2
64 Clinical Model for Predicting DVT Pre-Test Probability Questionnaire Score Active cancer 1 Paralysis, paresis or recent plaster immobilization of lower extremities Recently bedridden > 3d or major surgery w/in 4 wk 1 Localized tenderness along the distribution of deep venous 1 system Entire leg swollen 1 Calf swelling 3 cm > asymptomatic side (measured 10 cm below tibial tuberosity) Pitting edema confined to the symptomatic leg 1 Collateral superficial veins (nonvaricose) 1 Alternative diagnosis as likely or greater than that of DVT Wells, et al. Lancet, 1997;350:
65 Clinical Model for Predicting PE Pre-Test Probability Score Clinical symptoms and signs of DVT (leg swelling and pain) 3.0 No alternative diagnosis is more likely than PE 3.0 Heart rate > 100 beats/min 1.5 Immobilization or surgery previous 4 weeks 1.5 Previous DVT/PE 1.5 Hemoptysis 1.0 Malignancy (treated within previous 6 months) 1.0 Wells, PS, et al Ann Intern Med 2001;135:98
66 Case study A 52 year old male comes into the ED complaining of pain in the right calf Leg is slightly swollen, patient is concerned they may have a blood clot Otherwise healthy male, not on any medication, active Pain seems to have worsen through the night Wells scoring is a low PTP ED physician orders a D-dimer Result is negative (0.345 mg/l) Should this patient have imaging to rule out the possibility of a DVT?
67 Case Study Good subject to perform D-dimer for rule out claim. Healthy, not older population Low PTP D-dimer result not near the cutoff (result is.345 mg/l, cutoff mg/l) Even knowing the CV of the test (<5% at this level) would not bring the result into the positive range of > May suggest follow up with physician- if pain worsens Most likely a strain due to sliding into the bases while playing softball!
68 Case Study: A 76 year old male patient has been admitted into the ED for an infection After performing an APACHE assessment, it is determined that he is critically ill, possibly septic He has a history of DVT so a D-dimer is ordered Has a high PTP with the Wells score D-dimer is positive 6.4 mg/l Does the patient have a blood clot?
69 Clues: Older patient, septic, previous history of DVT Wells scoring results in a high PTP What is the utility of an elevated D-dimer? What are you looking for?
70 Case study This patient has all the reasons to have a positive D-dimer Older, septic with previous history of DVT We don t know specifically why it is increased There are many reasons Not the patient population to be using the D-dimer test to determine a DVT The patient may be in DIC
71 Case study 42 year old male enters the ED complaining of rapid onset, shortness of breath, pain in chest, numbness in arm Wells score is mod PTP Should this patient be imaged for a PE? D-dimer is normal 0.411mg/L Additionally testing included an elevated troponin and BNP Does this person have a PE?
72 Case study Patient test results appear to be more consistent with an MI, versus a PE Imaging doesn t seem to be indicated at this time Patient is then admitted Follow up with imaging if symptoms still persist several days post admission D-dimer will most likely be elevated as an inpatient, and imaging would be the more diagnostic approach.
73 Case Study A 25 year old pregnant female in her second trimester comes into the ED She is complaining of pains in her leg, leg is slightly swollen No history of DVT, Wells scoring is low- moderate PTP Run a D-dimer The D-dimer test is mg/dl (cut-off is mg/dl) They perform imaging and the imaging is negative
74 Case Study Why did the clinician choose to perform imaging? Patient is an outpatient, has a low PTP Why was the D-dimer positive? Positive D-dimer during pregnancy However, pregnancy is a hypercoagulable state, and pregnant patients are usually excluded from studies Best to perform imaging on this patient
75 Case Study A 40 year old male comes into the ED complaining of sudden onset of shortness of breath He has had a cold for 2 days, but now feels a heaviness in his chest He does have a history of asthma The clinician suspects that he might have pneumonia, but wants to make sure he doesn t have a PE Performs a D-dimer, which is negative Doesn t order a VQ scan, treats the patient, gives him medication with orders to follow up with his family physician next week. Did he do the right thing?
76 Case study The laboratory used an automated immunoturbidimetric D- dimer assay This assay has been FDA approved for exclusion for PE A prospectively collected clinic trial looking at over 1000 patients suspected of DVT and or PE were tested and imaged and their imaging results were compared to the D- dimer A negative predictive value of >99% was determined This results in being able to have patients with a lowmoderate pre test probability and a negative D-dimer not have to be imaged. This patient s diagnosis was asthmatic bronchitis, did not have to have expensive imaging, D-dimer was able to provide a diagnosis
77 Pearls for Practice: Understand the utilization of the D-Dimer in diagnosing patients with a low PTP for DVT or PE The value in having a test with an exclusion claim and the outcome for enhanced patient care: Less invasive testing Decreased risk to the patient Decreased time from testing to diagnosis
78 Thank you for your time any questions?
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