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Prothrombin time (PT) and partial thromboplastin time (PTT) tests are commonly ordered for hospitalized patients. A significant reduction in laboratory workload and expense can be achieved if these tests are ordered appropriately. The likelihood that the patient will benefit from these tests is small.
Activated partial thromboplastin time (APTT) and prothrombin time (PT) were performed in four groups of studies in order to evaluate the influences of time, temperature, and different forms of plasma storage to the result. Different designs for storage of the plasmas were studied, including the plasmas stored either with or without packed cells, the plasmas stored in the cuvette with exact volume for performing the test or in the test tube. The temperatures for store of the plasma were at room temperature, at 4 degrees C and at -70 degrees C. The time for store of the plasma was from 1 hour up to 7 hours. The plasmas included normal pooled plasmas and diseased plasmas. From this study, it is found that the PT test was not easily affected by the temperature, storage time and the form of storage in comparison with the APTT test which was much easily affected by the above conditions. APTT should be done within 2 hours after sampling and the plasma should be stored with the packed cells at 4 degrees C in order to obtain a reliable result. PT could be done within 7 hours without influence to the result if the plasma was stored with the packed cells at 4 degrees C. No significant cold-induced shortening of PT could be noted when the plasma was incubated at 4 degrees C up to 7 hours. In either PT or APTT, the most suitable condition for storing the plasma should be with the packed cells at 4 degrees C.
Effect of ingestion of 50 g of glucose on euglobulin clot lysis time and prothrombin time was studied in 14 diabetic and 12 non-diabetic persons. There was no significant change in euglobulin clot lysis time and prothrombin time after ingestion of glucose in the non-diabetic group. In the diabetic group, ingestion of glucose resulted in significant increase in euglobulin clot lysis time at the end of one hr which returned to initial level at the end of two hours even though blood glucose level at two hrs was still higher than fasting level. Increase in clot lysis time has no correlation to the blood glucose level. There was no significant change in prothrombin time after glucose ingestion.
Echis carinatus venom contains proteases capable of activating both normal and descarboxy prothrombin. We showed this venom (Sigma) principally activates prothrombin with almost no factor X activation. Echis time in combination with prothrombin time can predict vitamin K responsiveness since the Echis time is usually normal in the presence of descarboxy prothrombin associated with vitamin K deficiency. 38 patients with abnormal routine prothrombin times (PT) had both coagulant and immunogenic factor II assays along with Echis times done before and after vitamin K. Of 22 patients responding to vitamin K, based on correction of PT, 21 had normal initial Echis times and of 16 not responding, 11 had abnormal Echis times, giving a sensitivity of 95.4% and specificity of 68.8% for vitamin K responsiveness. 90% of patients with a PT/Echis time ratio less than 1.3 and a prolonged Echis time did not correct their PTs with vitamin K therapy. The 5 non-responders with normal Echis times all showed normal initial coagulant and antigenic prothrombin, but 3 had low F V and/or F VII.
Determinations of prothrombin time with the semiautomatic fibrometer and with a more automated machine (Electra 600) were compared in regard to reproducibility, accuracy, and speed. Prothrombin times determined for replicate samples with the two machines showed a correlation coefficient of 0.98, but the Electra 600 sensed the clot 0.5 seconds before the fibrometer. The overall coefficients of variation for multiple tests in the normal therapeutic and elevated ranges of prothrombin time were 3.5% for the fibrometer and 2.0% for the Electra 600. The average technician working time was 60% shorter with the fully automated machine than with fibrometer. It is concluded that the automated machine was more accurate and more rapid in determining prothrombin time.
Five abnormal prothrombin time pooled patient plasma samples and seven commercially prepared abnormal prothrombin time control plasmas were compared. A fibrometer was used to run prothrombin time tests from 8 to 51 days on individual aliquots of the pooled patient plasmas and individual vials of the commercial products. Pooled patient plasmas exhibited greater reproducibility with generally lower coefficients of variation than did the commercial products, with the added advantage that they reflected the patient population more directly. Almost all samples displayed a significant rise in mean clotting times during the testing period. However, the reasons for this rise are not entirely clear.
Treatment with warfarin using a target International Normalized Ratio (INR) range of 1.7 to 2.5 is efficacious for many clinical indications, but the minimal intensity of anticoagulation required for antithrombotic protection has yet to be determined. To evaluate whether patients could be reliably monitored with a less intense regimen, we anticoagulated patients with warfarin for several months using a target INR range of 1.3 to 1.6 as determined by prothrombin time (PT) using a sensitive thromboplastin (Dade IS, International Sensitivity Index [ISI] = 1.3). Plasma measurements of F1+2, a marker of factor Xa action on prothrombin in vivo, were also obtained to determine the suppressive effect of warfarin on hemostatic system activity. Overall, 20 of 21 patients with a history of cerebrovascular events (mean age, 61 years) could be reliably regulated with warfarin in the target INR range. F1+2 levels were significantly suppressed from baseline in all patients, with a mean reduction of 49% (range, 28% to 78%). We found a significant relationship between the extent of suppression of prothrombin activation levels and the baseline measurements. A mean reduction of 65% was observed for those patients with baseline F1+2 greater than or equal to 1.5 nmol/L, but only 38% for baseline F1+2 less than or equal to 0.5 nmol/L. Overall, 68% of plasma samples obtained during stable anticoagulation were within the target INR range. PTs were also determined on all plasma samples with two thromboplastins of lower sensitivity (C+, ISI = 2.09; and automated simplastin, ISI = 2.10). Only 47% and 35% of PT determinations, respectively, were within the target range with these reagents. We conclude that prothrombin activation can be significantly suppressed in vivo with use of warfarin in an INR range of 1.3 to 1.6. This level of anticoagulation can be reliably achieved by monitoring PTs with a thromboplastin of high sensitivity.
The incidence and type of pathology causing a prolonged prothrombin time and clinical bleeding episodes were assessed in a multicentre study of 1109 patients receiving cefotetan, a N-methyl-thiotetrazole (NMTT), or equivalent antibiotics. There was no significant difference in the incidence of a prolonged prothrombin time (9.9% with cefotetan, 8.0% with comparable antibiotics) of clinical bleeding episodes. However, prothrombin time increases of greater than 12 seconds were significantly (p = 0.002) greater with cefotetan (3.8%) than with comparators (0.8%). In both antibiotic groups increases in prothrombin time were more likely following surgery and in patients who were older, with a high platelet count, low albumin, or higher urea and creatinine concentrations. All antibiotic treatment can be associated with prolonged prothrombin times and new agents should always be assessed in a large multicentre study before the practical, clinical importance of haemostatic defects can be defined.
Accurate prothrombin time tests are important because they are frequently performed on presurgical patients to evaluate their blood-clotting status. We studied the effect of temperature (27-47 degrees C) on PTs obtained with eight different brands of thromboplastin. We also compared the sensitivities of two types of coagulation timers to changes in blood viscosities between 1 and 16 mPa/s. Viscosities were measured with the Brookfield Digital Viscometer. The MLA Eletra 800 and the BBL fibrometer were used to measure PTs. All eight thromboplastins gave convex curves of PT versus temperature, with optimum values lying between 38 and 39 degrees C. The curves were fitted to 4th-degree polynomials which showed that a mean temperature bias of 2 degrees C can increase PTs. Ortho Brain (7.8% change) was affected the most, while thromboplastin C (4.4% change) was affected the least. Plots of PT versus viscosity showed that the BBL fibrometer, which uses an electromechanical sensor, was more affected by viscosity than the MLA Electra 800, with an optical detector. However, above 8.2 mPa/s, all PTs were significantly elevated. Hence, patients with macroglobulinemia, whose plasma viscosities sometimes exceed 8.2 mPa/s, may have falsely elevated PTs. We conclude that temperature and viscosity are critical factors in the test and significantly contribute to within and between laboratory variations in PT measurements.
The authors assessed the cost effectiveness of monitoring warfarin therapy guided by standard plasma prothrombin times performed on blood samples obtained by venipuncture versus prothrombin times performed on capillary whole blood samples obtained by fingerstick. Twenty patients receiving long-term oral anticoagulation had either standard or capillary prothrombin times determined every other week for eight weeks in a cross-over design. All time intervals were monitored, including receptionist, secretarial, nursing, phlebotomy, etc., and costs for all materials, procedures, and labor were calculated. The total cost per test by the capillary whole blood prothrombin time method was significantly less than by standard prothrombin time methods ($7.55 vs. $15.64) even though the nurse-patient encounter time was greater per test for the capillary method (12.4 minutes vs. 8.3 minutes). The management of oral anticoagulation guided by prothrombin times performed on instrumentation designed to sample capillary whole blood should result in a significant cost savings, and because of the immediate availability of results, provide the potential for improved health care.
Prothrombin time monitoring of oral anticoagulation is highly dependent on the tissue thromboplastin used. In the United States, patients have received a higher level of anticoagulation because of the use of a less sensitive thromboplastin. Many advocate the use of an International Normalized Ratio to rectify this problem. Laboratory supervisors from all acute care hospitals in Massachusetts were surveyed to determine the disparity in thromboplastin use and reporting practices for prothrombin time testing. Eighty-eight of 103 (86%) hospitals responded. Fifty-eight lots from six manufacturers of thromboplastin were in use. The International Sensitivity Index of these lots ranged from 1.89 to 2.74. Ninety-nine percent of hospitals reported prothrombin times in raw seconds. Only 5% reported an International Normalized Ratio. Sixteen different coagulation instruments were in use. Close to 70% of laboratory supervisors had little or no understanding of the significance of an International Sensitivity Index or an International Normalized Ratio. The management of oral anticoagulation appears far less precise than had been believed. Prothrombin times in the same individual from different laboratories may have poor correlation. Based on the level of understanding of laboratory supervisors, extensive education will be necessary to change practices and improve accuracy and comparability of prothrombin time testing.
The effect of lipid emulsions on prothrombin time in blood from anticoagulated patients was determined. Blood samples were obtained from 23 patients therapeutically anticoagulated with warfarin (prothrombin time 1.3-2.0 x control). Varying amounts of an intravenous lipid emulsion (Intra-lipid) were added to the blood to simulate concentrations seen in vivo with a constant lipid infusion. The prothrombin time was measured on the plasma from these samples and compared to the prothrombin time of the plasma samples without lipid. The mean decrease in prothrombin times were: 0.29 sec at 50 micrograms/ml, 0.23 sec at 100 micrograms/ml, and 0.29 sec at 200 micrograms/ml. All concentrations showed a statistically significant decrease (p less than 0.05) when compared to the control by the Scheffe test. Lipid emulsions appear to decrease the prothrombin times in anti-coagulated patients. The differences however, were small and not of clinical significance at the concentrations tested.
An acquired inhibitor of blood coagulation, similar to that described in patients with Systemic Lupus Erythematosus (SLE), was detected during routine coagulation screening in 10 patients who did not meet the criteria for a diagnosis of SLE. The lupus-like anticoagulant (LLAC) was diagnosed on the basis of prolonged activated partial thromboplastin time (APTT) and/or prothrombin time (PT) which failed to correct when patient plasma was added to normal plasma; an additional criterion was an abnormal tissue thromboplastin inhibition test. No patient had a specific inhibitor directed against factors VIII and IX. Demonstration of LLAC was highly dependent upon the type of reagents adopted in the APTT and PT: the abnormality was detected consistently by one reagent only. One-stage assays of factors VIII and IX were characteristic of the presence of an inhibitor, showing non-parellel dose-response curves or decreased activity at low dilutions which were partially corrected at higher dilutions. Although 7 patients were free of abnormal bleeding, unequivocal signs of haemorrhagic tendency after a surgery were present in the remaining 3 patients. The findings suggest that LLAC is a non-exceptional cause of prolonged coagulation screening tests, and that it may sometimes be associated with impaired haemostasis.
PURPOSE: To determine the relation of bleeding to prothrombin times and important remediable lesions in outpatients treated with warfarin. PATIENTS AND METHODS: An inception cohort of 565 patients starting outpatient therapy with warfarin on discharge from a university hospital was assembled. Detailed records of outpatient prothrombin times were obtained for 103 of 130 case subjects with major or minor bleeding and for 117 control patients without bleeding. A nested case-control design was used to evaluate the association of bleeding with temporally related prothrombin times; odds ratios were estimated using multivariate logistic regression analysis to control for known predictors of major bleeding. The relation of bleeding to important remediable lesions was determined in all 130 cases of bleeding. RESULTS: For each 1.0 increase in the prothrombin time-to-control ratio, the odds ratio for major bleeding during the week after a prothrombin time measurement increased 80%; the odds ratio for minor bleeding increased 50%. These odds ratios were lower during the first month of therapy and higher thereafter. Bleeding was related to important remediable lesions in 49 of 130 cases (38%), but these lesions were unknown before bleeding in only 22 cases (17%). The mean prothrombin time rose sharply at the time of bleeding in patients without important remediable lesions, but not in patients with lesions. New, previously unknown lesions (including nine malignancies) were discovered in 20 of 59 case subjects (34%) with gastrointestinal bleeding or hematuria, but in only two of 71 case subjects (3%) with other bleeding (p less than 0.001). CONCLUSION: Our results provide a valid quantitative basis for estimating the odds of bleeding in relation to the prothrombin time and the yield of diagnostic evaluation in patients with bleeding.
Prothrombin time, serum albumin, aminotransferases and liver size were evaluated in 40 consecutive cases of kwashiorkor. Eleven (27.5%) of the 40 patients died. Eight out of the 11 patients who died had a prolonged prothrombin time of more than 3 s above the control compared to only 4 out of the 29 who survived (p = 0.005). Mean serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) albumin, globulin and liver size were abnormal but similar in both groups. These results may indicate a predictive mortality value of prothrombin time in kwashiorkor.
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A method for the comparison of prothrombin time systems using single large lots of lyophilized plasma in the College of American Pathologists Surveys is presented. Systematic biases for prothrombin time methods as well as for thromboplastins have been measured, and their use allows a very accurate (within 2.25%) prediction of the prothrombin time for the great number of prothrombin time systems presently being used in the United States.