[The preparation of platelet-rich plasma for platelet counts and tests of platelet function (author's transl)].
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Blood Cell Count↗
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[Fragmented red cells are the major cause of spuriously high platelet counts in patients with fragmented red cells when counts are obtained by automated blood cell counter].
Platelet counts measured by automated blood cell counter often show spuriously high values when measuring samples contain particles of equal size to platelets. The major cause of spuriously high platelet counts in samples with fragmented red cells (FRC) is thought to be the FRC themselves. We studied the correlation between FRC and spuriously high platelet counts in 40 patients demonstrating FRC on blood smears. FRC were measured by manual hemocytometry and by flow cytometry using a monoclonal antibody against glycophorin A (GPA method). There was a significant correlation between spuriously high platelet counts and FRC by manual hemocytometry (r=0.60, p<0.001) or FRC by the GPA method (r=0.45, p<0.005). These data suggest that FRC are the major cause of spuriously high platelet counts in samples with FRC.
Adolescent↗
The timing of a positive test result for heparin-induced thrombocytopenia relative to the platelet count and anticoagulant therapy in 43 consecutive cases.
We studied the timing of a positive heparin-induced thrombocytopenia (HIT) test result relative to changes in platelet count and anticoagulant use. We obtained platelet counts in 100 consecutive HIT+ cases before, during, and after heparin therapy; 43 cases met study criteria and were included in study part 1. In part 2, platelet counts at the time of the HIT test in 2 groups (100 each HIT+ and HIT- cases) were compared. In part 1, cases could be divided into 4 groups based on the diagnosis of HIT relative to platelet counts (1, within 1-2 days of a major drop in platelet count [11.6%]; 2, after > 2 days of a major fall in platelet count [41.9%]; 3, in patients with already low platelet counts [27.9%]; 4, after platelet count was rising [18.6%]). In study part 2, the mean platelet counts for the HIT+ and HIT- groups were almost identical. HIT should be suspected in any thrombotic patient who had a previous decline in platelet count, has a low platelet count, or has a rising platelet count after a previous decline in association with heparin exposure. In study part 2, 1 platelet count value at the time of the HIT test did not provide useful information.
Anticoagulants↗
Platelet count.
An estimate of the platelet count is usually given as part of the complete blood count (CBC). It should not be neglected when reviewing CBC results as it is a fair screening test and satisfactory for most purposes in the emergency department. It is a quantitative study, and the functional status of the platelet must always be considered in interpretation of clinical significance. Patients presenting with abnormal bleeding histories, particularly women with mucosal origin bleeding, should have an evaluation of platelet quantity by an accurate method and functional quality by a bleeding time. Though rarely used, the emergency physician should be familiar with the indication and mechanics of platelet transfusions. The laboratory charge for the platelet count is $17.00 to 18.00, whether it is automated or hand counted.
Adult↗
Platelet counts in children with iron deficiency anemia.
Platelet count was evaluated in 30 children with iron deficiency anemia. It was found elevated when compared with 40 normal controls. No significant difference was found between the platelet counts in patients with hemoglobin levels higher or lower than 7 g/dl. Although no relation was observed between platelet count and transferrin saturation, it was correlated with serum iron values. After oral and/or parenteral iron therapy platelet count decreased insignificantly, while reticulocytes were found to be increased.
Adolescent↗
Effect on platelet counts and fever of platelet transfusion in leukemia.
The efficacy of platelet transfusions in pretransfused HL-1 sensitized patients has been doubtful, particularly where repeated platelet transfusions were required. The efficacy of one hundred and nine ABO-compatible, cross match negative platelet transfusions in 26 adult patients with acute leukemia was therefore studied. Although most of the patientswere old and pretransfused and although no HL-A typing could be made, a statistically significant average increase of about 11 000 platelets/mul was seen not only after the first but also after subsequent (up to 8) platelet transfusions. Moreover, significant reduction in temperature followed platelet transfusions. However, platelet recoveries were worse in severely infected patients.
Acute Disease↗
Effect of acute uncomplicated malaria on platelet counts.
OBJECTIVE: To determine the effect of uncomplicated malaria on platelet count. PATIENTS AND METHODS: Adult Nigerians (residing in the Lagos metropolis) who were diagnosed as having uncomplicated malaria were treated with a standard regime of chloroquine. Platelet counts were obtained before treatment, Day 0, and again on day 14 when parasitaemia had been cleared in the patients. There were 40 (21 males, 19 females) patients enrolled for the study. Their ages ranged from 15 years to 56 years with a mean +/- SEM of 27. 4 +/- 1.8 years. 28 (14 males, 14 females) patients had both day 0 and 14 platelet counts. RESULTS: The malaria parasite counts ranged from 1020 /mm(3) to 72,000 /mm(3) at day 0 with a mean +/-SEM of 15,638.0 +/- 3,727.0/mm(3) and zero on day 14. The mean platelet count on day 0 was 137.0 +/- 58.4x 10(9)/L while the day 14 mean platelet count was 234.0 +/- 96.9 x 10(9)/L. Comparison of mean platelet counts on day 0 with those on day 14 showed a highly statistically significant difference (p < 0.001). The degree of malaria parasitaemia was not significantly related to the level of platelet count. Transient thrombocytopenia is very common in uncomplicated malaria in semi -immune adults. The mechanism, aetiology, and clinical relevance of the phenomenon deserve further studies.
Adolescent↗
Relationship between platelet count and bleeding risk in thrombocytopenic patients.
Platelets are lost from circulation by 2 mechanisms: senescence and random loss. Approximately 7.1 x 10(3) platelets/microL/d are postulated to be randomly used in maintaining vascular integrity. Thus, in clinically stable patients, major bleeding is unusual unless the platelet count is </=5 x 10(3)/microL. Risk factors for bleeding at higher platelet counts are disseminated intravascular coagulation with contributory clotting factor deficiencies, structural lesions with loss of vascular integrity, and refractoriness to platelet transfusions. Several large studies have documented the safety of lowering the prophylactic platelet transfusion trigger from the previously used 20 x 10(3)/microL to 10 x 10(3)/microL. A few studies have even suggested that a 5 x 10(3)/microL trigger is acceptable. Based on these results, the next step of giving just therapeutic platelet transfusions is being evaluated. In a large retrospective study, the most significant predictor of bleeding was not the patient's platelet count but a history of bleeding in the prior 5 days. These data suggest that attention should be focused on providing aggressive platelet therapy for active bleeding rather than transfusing platelets prophylactically. Therapeutic platelet transfusions have been documented to control bleeding, and mortality rates are not increased when comparing patients receiving therapeutic to that seen in patients receiving prophylactic platelet transfusions.
Clinical Trials as Topic↗
A statistical model for estimating donor postdonation platelet counts after plateletpheresis.
BACKGROUND: To avoid the need, in serial apheresis donors, either to delay plateletpheresis until a predonation platelet count is completed or to obtain a postdonation count after each procedure, a statistical model has been developed to predict the postdonation platelet count from the donor predonation platelet count, weight, and hematocrit. STUDY DESIGN AND METHODS: Predonation and postdonation platelet counts were measured in two groups of approximately 100 consecutive donors (Group A to test the model and Group B to validate it), and the postdonation counts were calculated with the model. Using stepwise multiple linear regression from donor data, estimated postdonation platelet counts were found to be comparable to the postdonation platelet counts actually measured. RESULTS: Estimated postdonation platelet counts x 10(9) per L (mean +/- SD) for each group, respectively, were Group A, 195 +/- 35, versus actual platelet counts of 195 +/- 39 (p = 0.43), and Group B, 183 +/- 36, versus actual platelet counts of 189 +/- 34 (p = 0.14). Sensitivity and specificity, respectively, were Group A, 57 and 99 percent and Group B, 62 and 99 percent. CONCLUSION: For most serial apheresis donors, application of this predictor model should preclude the need to obtain an extra postdonation platelet count.
Blood Donors↗
Electronic platelet counts with the Coulter counter. Reassessment of a correction factor.
Platelet counts are determined on the Coulter electronic counter by counting the diluted platelet-rich plasma obtained by sedimentation or centrifugation of whole blood. In calculating the whole-blood platelet count, an empirical correction factor for platelet-free plasma trapped by sedimented erythrocytes has been recommended, and a widely-distributed circular slide rule calculator incorporates the correction factor. In this study, visual and electronic platelet counts were compared in 100 specimens with counts ranging from 10 to 1,100 X 10(3) per mul and hematocrits ranging from 17.5 to 48.5%. Platelet-rich plasma samples prepared by a centrifugation method (Plateletfuge) gave machine counts in close agreement with those of samples prepared by sedimentation. Whole-blood platelet counts determined with the circular calculator were consistently lower than visual counts, with an average difference of -17%. The electronic counts were recalculated after elimination of the correction factor, and agreement then improved to an average difference of only +1.6%. The correction factor for trapped platelet-free plasma leads to erroneously low values and should not be used.
Blood Cell Count↗
An evaluation of the Haema-Count MK-4S platelet counting system.
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Blood Cell Count↗
Association of platelet counts on presentation and clinical outcomes in ST-elevation myocardial infarction (from the TIMI Trials).
Platelet activation and aggregation play pivotal roles in the thrombotic process of acute coronary syndromes. However, data regarding platelet count and its association with clinical outcomes in the setting of ST-elevation myocardial infarction (STEMI) are limited. We hypothesized that higher platelet counts on presentation would be associated with poorer clinical outcomes. Data from 10,793 patients with STEMI in the Thrombolysis In Myocardial Infarction (TIMI) trials database were analyzed. Mean platelet count on presentation was 254.8 x 10(3)/microl. Higher platelet counts were associated with higher rates of adverse clinical outcomes at 30 days. In a multivariable analysis that adjusted for confounders of platelet counts (age, gender, weight, diabetes, and smoking), higher platelet counts remained associated with an increased risk of the combined end point of death, reinfarction, and congestive heart failure. With a reference group of platelet counts <200 x 10(3)/microl, the multivariable odds ratios were 1.22 (95% confidence interval 1.05 to 1.42, p = 0.009) for platelet counts of 201 to 300 x 10(3)/microl, 1.37 (95% confidence interval 1.11 to 1.68, p = 0.002) for counts of 301 to 400 x 10(3)/microl, and 1.71 (95% confidence interval 1.16 to 2.51, p = 0.005) for counts >400 x 10(3)/microl. Further, a greater decrease in follow-up platelet counts (compared with baseline values) was independently associated with an increased risk of reinfarction at 30 days (odds ratio 1.44 for every decrease of 100 x 10(3)/microl unit of platelets, 95% confidence interval 1.13 to 1.82, p = 0.03). In conclusion, in STEMI, a higher platelet count on presentation was independently associated with adverse clinical outcomes, whereas a greater subsequent platelet count decrease was associated with an increased risk of reinfarction.
Aged↗
Quantitative changes in platelet counts following major urological pelvic surgery.
Postperative quantitative changes in platelet counts have been reported following various extensive surgical procedures. It is generally accepted that reactive thrombocytosis at levels less than 1,000,000/mm3 is a benign condition and is not associated with increased risk of postoperative thrombohemorrhagic complications. The role of prophylactic treatment with platelet inhibitors in these situations is controversial. We assessed retrospectively the timing and the extent of postoperative thrombocytosis in 85 consecutive patients following major urological pelvic surgery and evaluated its possible clinical significance to hemorrhagic and thromboembolic complications, in view of the coincidence of multiple potential risk factors for thromboembolism in these patients. 73 (85.9%) patients demonstrated marked postoperative changes of platelet counts. In 12 patients (14.1%) we found only minor fluctuations in platelet counts throughout the postoperative period. Two distinct groups of 26 and 47 patients respectively could be identified among these 73 patients, who differed in the rate and extent of changes in platelet counts. Those fluctuations were characterized by an early decrease in platelet levels (mean percentage change of 40 and 60% in groups I and II respectively). This was followed by a gradual increase leading to delayed thrombocytosis (mean percentage change of 225 and 305% in groups I and II respectively). Thromboembolic complications were diagnosed in 5 patients. The occurrence of thromboembolism preceded any significant increase in platelet counts in all 5 patients. There was no correlation between the timing of thromboembolic complications and timing and extent of the change in platelet count. We conclude that reactive thrombocytosis following major urological pelvic surgery is a frequent innocuous finding and is not associated with hemorrhagic or thromboembolic complications.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Improved platelet counting using two-dimensional laser light scatter.
Clinical management of platelet disorders depends on accurate platelet counts. We evaluated a new analytic approach for platelet counting based on improved platelet discrimination. Current automated counting methods provide accurate platelet counts for most samples but often are unable to discriminate platelets accurately from nonplatelet particles such as microcytic RBCs, RBC fragments, and cellular debris that may falsely elevate platelet counts. The new approach measures 2 light-scatter angles of platelets and nonplatelet particles as they pass through a laser beam. The volume and refractive index of each platelet and particle are derived from the light-scatter measurements using the Mie scattering theory. Together, these 2 measurements provide improved platelet discrimination compared with 1-dimensional methods. With its improved discrimination, 2-dimensional platelet analysis provides more accurate platelet counts in samples containing interfering particles and may contribute to more effective clinical management of patients with platelet disorders.
Blood Platelet Disorders↗
Platelet counts during rapid massive transfusion.
The effect of rapid massive transfusion upon platelet counts has been studied retrospectively in 24 patients treated for severe trauma. Multiple linear regression analysis showed that a platelet dilution model with an exponential form described the quantitative relationship between the pre- and posttransfusion platelet counts and the volumes of blood products administered. Intravenous salt solutions had very little effect upon the platelet count even when large volumes were infused. Red blood cell transfusions decreased the platelet count to an extent two and one-half times greater than that of colloid infusions. The differences in the magnitudes of the dilution effects are attributable to the different physiologic volumes of distribution of the various classes of infusates. If only red blood cells (RBC) and fresh frozen plasma (FFP) are transfused, two useful equations obtain. First, the current platelet count (Pt) can be predicted knowing the initial platelet count (Po) and the number (#) of units of RBC and FFP administered: Pt = Po (0.634) e-0.046 [#RBC + #FFP/8]. Second, the point during massive transfusion when platelet transfusions will be necessary can be predicted knowing the initial platelet count.
Colloids↗
Effect of altitude on thrombopoietin and the platelet count in healthy volunteers.
Although there is evidence that altitude increases the platelet count, its effect on the platelet precursor stimulating factor, thrombopoietin (TPO), is unclear. Unlike erythropoietin, TPO appears largely unresponsive to exogenous signals. In a study in 16 healthy volunteers, we report the effects of altitude exposure at between 1000 and 1822 m for 1 or 2 weeks on TPO, the platelet count (+ indices), erythropoietin, hemoglobin, hematocrit and erythrocytes (+ indices). There were significant post-exposure increases in TPO (57.9 vs 37.1 U/l; P=0.0006), platelet count (219.1 vs 208.0 x 10(3)/ml; P=0.031) and erythropoietin (16.1 vs 9.9 U/l; P=0.0032). There was a positive correlation between the increases in TPO and platelet count (r=0.52, P=0.043). Hemoglobin and hematocrit remained unchanged. Our results provide clear evidence for a relationship, presumably driven by hypoxia, between altitude exposure, TPO production and the platelet count.
Adult↗
Plasma fibrinogen levels, leucocyte and platelet counts in male Zimbabwean hypertensives.
Plasma fibrinogen levels, leucocytes and platelets are among the many factors known to influence haemostasis. Impaired haemostatic processes in hypertension are thought to contribute to the other cardiovascular diseases seen in this condition. This study compares the level of plasma fibrinogen, and leucocyte and platelet counts between 17 male hypertensives and 24 male normotensives. The results for the hypertensives were: leucocyte count mean 5.45 x 10(9)/L, platelet count mean 234.7 x 10(9)/L, and plasma fibrinogen 4.13 g/L. The results for the normotensives were: leucocyte count mean 4.83 x 10(9)/L, platelet count mean 222.9 x 10(9)/L, and plasma fibrinogen 3.27 g/L. The hypertensives had higher plasma fibrinogen levels, and leucocyte and platelet counts compared to the normotensives, but this only reached statistical significance for the plasma fibrinogen levels (p < 0.025).
Adult↗
[Usefulness of immunoplatelet measurement using the flow cytometric method for accurate platelet counting in hematological patients with severe thrombocytopenia].
We measured platelet counts in 95 patients with hematological disorders accompanied by thrombocytopenia (platelet counts < 5.0 x 10(4)/microliter) including 35 patients with severe thrombocytopenia(platelet counts < 2.0 x 10(4)/microliter). We used four methods based on different principles and compared the results, i.e., the flow cytometric method (BEADS method) utilizing platelet-specific monoclonal antibody (SZ2, antiGPIb) in conjunction with fluorescent reference beads (Flow-Count Fluorospheres), manual hemocytometry, and two automated blood cell counters, the NE-8000 (impedance method) and the Technicon H-2 (optical method). The BEADS method was superior to the other methods in linearity of serial dilutions, and the coefficient variations of the BEADS method(2.5-5.2%) were superior to the other methods. The platelet counts measured by the automated blood cell counters were higher(0.6-0.9 x 10(4)/microliter) than those by the BEADS method and manual hemocytometry. Furthermore, the BEADS method was able to measure accurate platelet counts in samples containing red blood cell fragments. The BEADS method may be an accurate and useful method for measuring samples with severe thrombocytopenia, and, especially, samples containing red blood cell fragments.
Adult↗