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Dilutions of 1: 600 and 1: 3000 of 1 mum diameter polystyrene latex suspensions are simple, inexpensive materials for quality control of Ortho ELT-8 platelet counts. The coefficient of variation (CV) for a 12-week period at the 350 X 10(9)/l level was 2.2%, comparable with that of a commercial control. The CV at the 70 X 10(9)/l level was 3.5%.
In a previous study we tried to assess the clinical usefulness of platelet count (PlC) to confirm whether postoperative pulmonary embolism could be suspected early. Unexpectedly, the 19 patients who subsequently developed pulmonary embolism had significantly lower mean PlC levels even before surgery. In an attempt to discover whether the preoperative PlC levels were associated with a different incidence of postoperative blood loss, we decided to retrospectively study the relationship between preoperative PlC levels and the consequences of blood loss. There were 459 consecutive patients undergoing hip surgery. After excluding 5 patients who died during the first 3 postoperative days, and 16 patients who bled from a definitive anatomic site, there were 438 patients. Blood loss was considered to be excessive when two or more of the following conditions were present: (1) total transfusion requirements exceeding 1,000 ml whole blood or 2 units of packed red cells; (2) a drop in hemoglobin level of 5 g/dl or more, and (3) a hemoglobin level below 8 g/dl at any moment during the first 8 postoperative days. Blood loss was considered to be excessive in 91 patients. Preoperative PlC levels were significantly lower in these patients as compared to patients without the condition (204 +/- 52 vs. 236 +/- 79 x 10(9) liter-1; p = 0.0002). When patients were classified according to the quartiles of preoperative PlC, the odds ratio of developing excessive blood loss was 0.69 (95% CI: 0.38-1.26) in patients in the second quartile; 0.57 (95% CI: 0.30-1.06) in the third quartile, and 0.27 (95% CI: 0.13-0.57) in patients in the highest quartile. After adjusting for age, sex, type of surgery and type of prophylaxis, the preoperative PlC levels maintained a statistically significant inverse correlation with postoperative blood loss.
The twin gestation in a patient with idiopathic thrombocytopenic purpura presents a unique problem if vaginal delivery is being considered. Scalp platelet sampling to exclude fetal thrombocytopenia only allows assessment of the presenting fetus. A case is described in which cordocentesis revealed discordant platelet counts in dizygotic twin fetuses.
A study was undertaken to evaluate a previous observation made in this laboratory that hyperoxic treadmill training is associated with a decrease in the circulating platelet count (PLT). The subjects studied breathed air containing 40% oxygen for 30 min/day, 5 days/week, for 6 weeks, while at rest in the seated position. Such exposure resulted in a consistent fall in PLT between day 1 and day 5 of each week (P less than .01). In addition, there was a progressive decline in PLT over the 6 weeks of exposure to the hyperoxic air, PLT being inversely correlated with the duration of hyperoxic exposure (rs = -0.886, P less than .02). The total decrease in PLT over the 6 weeks was 56 +/- 46 x 10(9) l(-1) (P less than .025). Not surprisingly, these changes were mirrored in the plateletcrit (Pct). The decrease in PLT did not appear to be secondary to either hemodilution or reduced erythropoietic stimulation. The mechanism of production and the biological significance of these changes remain to be elucidated.
PURPOSE: The purpose of this study was to determine the relationship between admission and postoperative platelet count (PC) and mortality and morbidity rates after emergency surgery for ruptured abdominal aortic aneurysm (AAA). METHODS: We performed a case record review of 65 consecutive patients admitted with ruptured AAA. RESULTS: Five patients did not undergo operation because of poor clinical condition, 12 patients died at operation, 13 patients died after operation, and 35 patients survived (operative mortality rate of 58%). Fifteen patients had an admission PC of less than 150 x 10(9)/L, of whom 14 (93%) died; 27 patients had an admission PC of 150 to 250 x 10(9)/L, of whom 8 (30%) died; and 18 patients had an admission PC of greater than 250 x 10(9)/L of whom 3 (17%) died. At the end of operation 29 patients had a PC of less than 100 x 10(9)/L, of whom 13 (45%) died, 20 (69%) had development of multiorgan failure (MOF), and 6 (21%) required relaparotomy for bleeding complications. By contrast, all 19 patients having a PC of 100 x 10(9)/L or greater at the end of the operation survived, three (16%) had development of MOF, and none required further surgery for bleeding. There was a significant inverse correlation between PC at the end of the operation and the number of postoperative days spent on a ventilator, in the intensive therapy unit, and in hospital. After operation, 15 patients had development of thrombocytosis (PC > 400 x 10(9)/L), of whom 10 had development of deep venous thrombosis and 8 had development of pulmonary embolism. There were no deep venous thromboses or pulmonary embolisms in patients who did not have development of a postoperative thrombocytosis. CONCLUSIONS: There is a direct correlation between PC on admission to the hospital and death after emergency repair of ruptured AAA. Thrombocytopenia at the end of the operation is associated with a high risk of morbidity from continuing hemorrhage or MOF. The development of postoperative thrombocytosis is associated with a high risk of thromboembolic complications. PC provides a simple marker of outcome in patients diagnosed with and undergoing operation for ruptured AAA.
The preeclampsia is the first cause of maternal morbility, with increase in the obstetric complications when it is associated to HELLP syndrome, for the low platelets that even involves to the neonate. This study was carried out in the patients accepted in the intensive Adults Cares Unit in the period of one year, surgical complications and the perinatal results were determined in women with low platelet count for HELLP syndrome in preeclampsia-eclampsia. Three groups were formed according to the platelets account and then were analyzed using chi square to determine association among these groups of patients, as well as mean and standard deviation (M +/- DE) to describe results. Forty patients were studied with low platelets by HELLP syndrome in preeclampsia-eclampsia, where the distribution for the group with platelets < 50,000 were 12 patients (30%), in the group among 51,000-100,000 of 18 cases (45%), and of 101,000-150,000 were of 10 cases (25%). The mean of gestas was of 2.3 +/- 1.2, more frequent delivery was for cesarean section in 39 cases (97.5%) and a single case for vaginal via (2.5%), a maternal death was presented (8.3%). The surgical reintervention was observed with more frequency in the group of < 50,000 platelets, the most frequent cause in these reinterventions was the hipovolemic shock. Also in this group the perinatal mortality was presented in 3 cases (25%) and the asphyxia at the birth with Apgar < 6 was presented in 5 cases (41.7%). A bigger morbility was observed inversely proportional to the account platelets, being the renal failure the cause most frequent of this morbility in the three groups. The low platelets account contribute in a direct way in the obstetric complications, since there are more surgical reinterventions, with bled in the transsurgical and increase in the days of intrahospitalary stay. Also with smaller account platelet, there are bigger prematural index, asphyxia and perinatal mortality in the newborn of mothers with HELLP syndrome.
A patient with the syndrome of hemolysis, elevated liver enzymes, and low platelet count and hyponatremia is described. Hyponatremia could explain the central nervous system symptoms sometimes seen in cases of toxemia.
A higher platelet count is independently associated with the presence of residual thrombus in the infarct-related artery after administration of fibrinolytic therapy, even after multivariate adjustment.
Studies in Southern Africa have shown that whites have significantly greater morbidity and mortality from coronary heart disease than blacks. This study investigated the distribution of some haemostatic variables known or suspected to be correlated with greater risk for coronary heart disease in healthy black and white Zimbabwean men. Factor VII, antithrombin III, leukocyte and platelet counts were measured in 56 blacks and 29 whites aged between 20 and 50 years. We found significantly greater factor VII and leukocyte counts in the whites compared to the blacks. The other variables measured were similar in the two ethnic groups. These results suggest that the greater prevalence of coronary heart disease in whites is consistent with high levels of factor VII and white blood cell counts previously identified as risk factors for this condition.
Activation of complement, neutrophils, and macrophages was studied in 14 women with severe preeclampsia, 11 of whom had the syndrome of hemolysis, elevated liver enzymes, and low platelet count; in 14 women with normal pregnancies; in seven normal pregnant women undergoing cesarean deliveries; and in 15 healthy nonpregnant women. Activation of complement, neutrophils, and macrophages was measured by plasma determinations of complement split products, polymorphonuclear (PMN) elastase, and neopterin, respectively. Women with severe preeclampsia had increased levels of C5a, terminal complement complex, PMN elastase, and neopterin at delivery and 1 day postpartum as compared with the normal pregnant group. One week postpartum, neopterin remained higher in preeclamptic women, whereas the complement components and PMN elastase had returned to normal. Cesarean delivery after normal pregnancy did not increase the levels of complement split products, PMN elastase (except for one value), or neopterin. The nonpregnant women had normal PMN elastase and neopterin levels. Accordingly, complement, neutrophils, and macrophages are activated in women with severe preeclampsia at delivery. The plasma levels of PMN elastase correlated positively to the formed terminal complement complexes in vivo. An in vitro study was performed to elucidate further the connection between complement and leukocyte activation. Recombinant C5a incubated in whole blood and in a neutrophil cell suspension gave a dose-dependent release of PMN elastase. Both the clinical and the in vitro results indicate that activation of the complement system may affect the function of neutrophils. This study supports the theory that the pathologic manifestations of severe preeclampsia may be explained by complement-induced release of biologically active substances from activated leukocytes.
In two patients suffering from post-transfusion purpura, anti-Zwa was demonstrated in either eluates from autologous platelets harvested during the remission phase and after normalization of the platelet count. In both patients, platelet-associated immunoglobulin (PAIg) was demonstrated during the acute phase. PAIg disappeared concomitantly with recovery and, thus, seems to be associated with the thrombocytopenia. These data support the assumption that immunocomplexes are adsorbed nonspecifically to the platelets and cause destruction of autologous platelets lacking the corresponding antigen. An association between the IgG3 subclass of anti-Zwa antibodies and the destruction of autologous platelets was also seen.
The activity of the c-Mpl ligand hematopoietic progenitors meets criteria expected for thrombopoietin (TPO). Bio-assays have shown that blood TPO levels are inversely related to platelet mass. We sought to identify the molecular basis for this regulation. To determine if TPO mRNA levels respond to platelet demand, RNA from selected organs of mice with high, normal or low platelet counts was subjected to semiquantitative reverse transcriptase-polymerase chain reaction. Although no differences in TPO mRNA levels between control and treated mice could be detected in liver or kidney, TPO-specific bands were more intense after 25 to 30 polymerase chain reaction cycles in marrow-derived mRNA from thrombocytopenic mice. The TPO-specific bands were less intense in thrombocytotic mouse marrow and spleen than control mouse marrow and spleen after 30 cycles. These data support the hypothesis that TPO levels are regulated, at least in part, by modulating mRNA levels in response to platelet demand.
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BACKGROUND: HELLP syndrome (a combination of hemolysis, elevated liver enzyme levels, and low platelet count) is a severe variant of preeclampsia that generally occurs before delivery but can occur post partum. This syndrome is more common than eclampsia and frequently leads to devastating neurological consequences such as intracerebral hemorrhage. OBJECTIVE: Although mentioned in the obstetric literature, there has been sparse reporting in the neurology literature specifically regarding intracerebral hemorrhage in HELLP syndrome. We illustrate such a case and review the existing literature regarding this severe complication. SETTING: Obstetric unit at an academic medical center. PATIENT: A 34-year-old primigravida experienced a pontine hemorrhage and subsequent respiratory arrest 22 hours after a normal delivery. This hemorrhage occurred 7 hours after the sudden onset of hypertension, severe headache, and intermittent abdominal pain. RESULTS: Laboratory and postmortem evidence suggested HELLP syndrome with disseminated intravascular coagulation as the cause of her intracerebral hemorrhage. CONCLUSIONS: Our case suggests the importance of the neurology consultant's familiarity with HELLP syndrome and the need for thorough laboratory testing and close monitoring in the puerperal patient with headache and hypertension.
Data are presented to define a unique group of preeclamptic/eclamptic patients with the finding of hemolysis (H), elevated liver enzymes (EL), and a low platelet count (LP). This entity has been termed the HELLP syndrome and may occur when the usual clinical findings to diagnose severe preeclampsia are absent. Often the patient is given a nonobstetric diagnosis and treatment is withheld or modified. The possible pathophysiology of this syndrome, the management of the patient, and the maternal and neonatal outcomes are presented. Recognition of the clinical and laboratory findings of the HELLP syndrome is important if early, aggressive therapy is to be initiated to prevent maternal and neonatal death. The practicing obstetrician must be knowledgeable about this severe consequence of hypertension in pregnancy.
OBJECTIVE: To evaluate the significance of reticulated platelets (RPs) in the diagnosis of thrombocytopenic disorders and the relationship between RPs and the proliferative degree of megakaryocyte (MK) in bone marrow. METHODS: With thiazole orange as a fluorescent dye, RPs were measured by analyzing the RNA content in platelets with flow cytometry and the percent and absolute counts of RPs were calculated. RESULTS: (1) The percent and absolute counts of the RPs in a normal group were (8.4 +/- 2.5)% and (16.8 +/- 6.8) x 10(9)/L respectively. (2) As compared with the normal group, the patients with idiopathic thrombocytopenic purpura (ITP) and hypersplenism had a significantly high percent and low absolute counts of RPs (P < 0.01). In patients with aplastic anemia, both the percent and absolute counts of RPs were at low levels (P < 0.05 and P < 0.01, respectively). There was no difference of RP percentage between the patients with acute leukemia or myelodysplastic syndromes and normal controls, but the absolute counts of RPs in the former was significantly lower than that in the latter. There was no difference between the percent and absolute counts of RPs among ITP patients with different proliferative degree of MK in bone marrow. (3) In all the diseases mentioned above, it was shown that RP percentage returned to normal in the effective cases after treatment, but no such change was found in the ineffective cases. CONCLUSIONS: Reticulated platelet counts contribute to the aetiology determination of the thrombocytopenia. It is also a valuable diagnostic method and a monitoring marker. There is no relationship between reticulated platelet counts and the counts of MK proliferation in bone marrow.