scholarly journals Preoperative Thrombocytopenia and Postoperative Outcomes after Noncardiac Surgery

2014 ◽  
Vol 120 (1) ◽  
pp. 62-75 ◽  
Author(s):  
Laurent G. Glance ◽  
Neil Blumberg ◽  
Michael P. Eaton ◽  
Stewart J. Lustik ◽  
Turner M. Osler ◽  
...  

Abstract Background: Most studies examining the prognostic value of preoperative coagulation testing are too small to examine the predictive value of routine preoperative coagulation testing in patients having noncardiac surgery. Methods: Using data from the American College of Surgeons National Surgical Quality Improvement database, the authors performed a retrospective observational study on 316,644 patients having noncardiac surgery who did not have clinical indications for preoperative coagulation testing. The authors used multivariable logistic regression analysis to explore the association between platelet count abnormalities and red cell transfusion, mortality, and major complications. Results: Thrombocytopenia or thrombocytosis occurred in 1 in 14 patients without clinical indications for preoperative platelet testing. Patients with mild thrombocytopenia (101,000–150,000 µl−1), moderate-to-severe thrombocytopenia (<100,000 µl−1), and thrombocytosis (≥450,000 µl−1) were significantly more likely to be transfused (7.3%, 11.8%, 8.9%, 3.1%) and had significantly higher 30-day mortality rates (1.5%, 2.6%, 0.9%, 0.5%) compared with patients with a normal platelet count. In the multivariable analyses, mild thrombocytopenia (adjusted odds ratio [AOR], 1.28; 95% CI, 1.18–1.39) and moderate-to-severe thrombocytopenia (AOR, 1.76; 95% CI, 1.49–2.08), and thrombocytosis (AOR, 1.44; 95% CI, 1.30–1.60) were associated with increased risk of blood transfusion. Mild thrombocytopenia (AOR, 1.31; 95% CI, 1.11–1.56) and moderate-to-severe thrombocytopenia (AOR, 1.93; 95% CI, 1.43–2.61) were also associated with increased risk of 30-day mortality, whereas thrombocytosis was not (AOR, 0.94; 95% CI, 0.72–1.22). Conclusion: Platelet count abnormalities found in the course of routine preoperative screening are associated with a higher risk of blood transfusion and death.

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4834-4834 ◽  
Author(s):  
Fabiana Mendes Conti ◽  
Ana Paula Hitomi Yokoyama ◽  
Marcia R Dezan ◽  
Thiago H Costa ◽  
Maria Giselda Aravechia ◽  
...  

Abstract Background Post-transfusion purpura (PTP) is a rare yet serious disease characterized by severe thrombocytopenia occurring after a blood transfusion. It is caused by alloimmunization against platelet antigens, anti-HPA-1a being the most frequent antibody. We report two cases of PTP and discuss the clinical presentation, diagnosis and management of this serious condition. Case Report Case 1) Female patient, 90 years old, Caucasian, had a fracture in the umerus and head trauma in 2012, followed by upper GI bleeding. Four days after receiving two units of packed RBCs, she presented with a low platelet count (14.000/mm3), petechiae, gum bleeding and oozing from venipuncture sites. The platelet count further dropped to 2.000/mm3the following day. HPA genotyping and HPA antibody identification by MAIPA were performed to investigate post-transfusion purpura, which showed: HPA1bb, 3aa, 5aa and 15ab and presence of antibodies anti-HPA-1a. IVig 400 mg/kG was infused in two consecutive days, with normal platelet counts observed after a week. Two of her three children had the same HPA1bb genotype and performed a matched platelet and RBC donation by apheresis. One matched RBC unit was transfused to correct symptomatic anemia caused by bystander hemolysis seven days after the first transfusion. No platelet transfusions were needed. Case 2) Female patient, 29 years old, afrodescendant, had a hemorrhagic shock after an emergency hysterectomy due to placenta percreta in 2012. She received 14 RBC units, 10 fresh frozen plasmas and 10 units of cryoprecipitate. Two days later, another surgery was necessary to remove a retained coagulum, and she received 10 units of random platelets. Five days later, the platelet count dropped to 5.000/mm3, followed by sudden anemia (Hb=9--> 4,5 g/dL), without clinical or laboratory signs of hemolysis or evidence of bleeding, with normal coagulation times. HPA genotyping and antibody identification by MAIPA were performed and showed an HPA1bb genotype and presence of an anti-HPA-1a antibody. No platelet transfusions were administered and IVig 500mg/Kg was prescribed for 2 days. Only washed RBC units were transfused thereafter. The platelet count rose four days after starting IVig to 134.000/mm3, yet a second course of IVig was necessary a week later to reach normal platelet counts. Discussion Both reports illustrate severe thrombocytopenia in patients who presented with sudden thrombocytopenia up to a week after blood transfusion. Platelet alloimmunization happens after exposure to HPA antigens by transfusion or pregnancy, and severe thrombocytopenia occurs as an anamnestic response after reexposure to platelet antigens in any blood product that contains contaminating platelet membranes. The thrombocytopenia may evolve as an autoimmune process, which may also cause hemolytic anemia due toa bystander phenomenom. Diagnosis is based on the identification of the antibody in the serum of a patient who lacks the corresponding antigen, anti-HPA-1a being the most common. IVig 0,5-1g/Kg for 2 days is the treatment of choice. The RBC units must be washed to avoid exposure to platelet membranes and recurrence of thrombocytopenia. In future transfusions, washed RBCs or HPA1bb blood products should be used. Disclosures: No relevant conflicts of interest to declare.


2011 ◽  
Vol 114 (2) ◽  
pp. 283-292 ◽  
Author(s):  
Laurent G. Glance ◽  
Andrew W. Dick ◽  
Dana B. Mukamel ◽  
Fergal J. Fleming ◽  
Raymond A. Zollo ◽  
...  

Background The impact of intraoperative erythrocyte transfusion on outcomes of anemic patients undergoing noncardiac surgery has not been well characterized. The objective of this study was to examine the association between blood transfusion and mortality and morbidity in patients with severe anemia (hematocrit less than 30%) who are exposed to one or two units of erythrocytes intraoperatively. Methods This was a retrospective analysis of the association of blood transfusion and 30-day mortality and 30-day morbidity in 10,100 patients undergoing general, vascular, or orthopedic surgery. We estimated separate multivariate logistic regression models for 30-day mortality and for 30-day complications. Results Intraoperative blood transfusion was associated with an increased risk of death (odds ratio [OR], 1.29; 95% CI, 1.03-1.62). Patients receiving an intraoperative transfusion were more likely to have pulmonary, septic, wound, or thromboembolic complications, compared with patients not receiving an intraoperative transfusion. Compared with patients who were not transfused, patients receiving one or two units of erythrocytes were more likely to have pulmonary complications (OR, 1.76; 95% CI, 1.48-2.09), sepsis (OR, 1.43; 95% CI, 1.21-1.68), thromboembolic complications (OR, 1.77; 95% CI, 1.32-2.38), and wound complications (OR, 1.87; 95% CI, 1.47-2.37). Conclusions Intraoperative blood transfusion is associated with a higher risk of mortality and morbidity in surgical patients with severe anemia. It is unknown whether this association is due to the adverse effects of blood transfusion or is, instead, the result of increased blood loss in the patients receiving blood.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Tia C Kohs ◽  
Vikram Raghunathan ◽  
Patricia Liu ◽  
Ramin Amirsoltani ◽  
Michael Oakes ◽  
...  

Introduction: Extracorporeal membrane oxygenation (ECMO) is used to provide circulatory support and facilitate gas exchange via cardiopulmonary bypass. The relationship between ECMO and the incidence of severe thrombocytopenia (platelet count <50 x 10 9 /L) and subsequent clinical consequences are ill defined. We aimed to identify the risk factors for the development of thrombocytopenia and its clinical implications. Methods: This is a single-center retrospective cohort study of adults who received venoarterial (VA) ECMO. We examined consecutive platelet counts while on ECMO. Univariate logistic regression was used to determine if mean platelet count, platelet count range, or severe thrombocytopenia were predictors of overall survival, hemorrhage and thrombosis. A multivariate logistic regression model was used to identify factors that contribute to the development of the aforementioned patient outcomes. Results: In our cohort, 33 patients were included with a mean age of 55 years and duration of ECMO of 5.9 days. All patients received heparin, 33.3% received antiplatelet therapy and 45.5% developed severe thrombocytopenia. In univariate, analysis the development of severe thrombocytopenia increased the odds of major bleeding by 450% (OR 5.500, 95% CI 1.219 - 24.813, P -value 0.027), and the odds of surviving hospitalization decreased 84.1% (OR 0.159, 95% CI 0.033 - 0.773, P -value 0.023). Multivariate logistic regression controlling for additional clinical variables found no significant association between the development of severe thrombocytopenia and rates of thrombosis, hemorrhage, or overall survival. Platelet count decreased over time while on ECMO. Conclusions: Nearly half of the patients requiring VA-ECMO developed severe thrombocytopenia, which was associated with an increased risk of hemorrhage and in-hospital mortality. Additional studies are required to clarify the clinical implications of severe thrombocytopenia in ECMO patients.


Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 225-232 ◽  
Author(s):  
Thomas L. Ortel

Abstract Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of ~50 to 60 × 109 platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.


Blood ◽  
1998 ◽  
Vol 92 (2) ◽  
pp. 405-410 ◽  
Author(s):  
J.Y. Blay ◽  
A. Le Cesne ◽  
C. Mermet ◽  
C. Maugard ◽  
A. Ravaud ◽  
...  

Abstract Severe thrombocytopenia is a rare but life-threatening side effect of cytotoxic chemotherapy for which risk factors are not well known. Our objective was to delineate a risk model for chemotherapy-induced thrombocytopenia requiring platelet transfusions in cancer patients. Univariate and multivariate analysis of risk factors for chemotherapy-induced thrombocytopenia requiring platelet transfusions were performed on the cohort of the 1,051 patients (CLB 1996) treated with chemotherapy in the Department of Medicine of the Centre Léon Bérard (CLB) in 1996. In univariate analysis, performance status (PS) greater than 1, platelet count less than 150,000/μL at day 1 (d1) before the initiation of chemotherapy, d1 lymphocyte count ≤700/μL, d1 polymorphonuclear leukocyte count less than 1,500/μL, and the type of chemotherapy (high risk v others) were significantly associated (P &lt; .01) with an increased risk of severe thrombocytopenia requiring platelet transfusions. Using logistic regression, d1 platelet count less than 150,000/μL (odds ratio [OR], 4.3; 95% confidence interval [CI], 1.9 to 9.6), d1 lymphocyte counts ≤700/μL (OR, 3.37; 95% CI, 1.77 to 6.4), the type of chemotherapy (OR, 3.38; 95% CI, 1.77 to 6.4), and PS greater than 1 (OR, 2.23; 95% CI, 1.22 to 4.1) were identified as independent risk factors for platelet transfusions. The observed incidences of platelet transfusions were 45%, 13%, 7%, and 1.5% for patients with ≥3, 2, 1, or 0 risk factors, respectively. This model was then tested in 3 groups of patients treated with chemotherapy used as validation samples: (1) the series of 340 patients treated in the CLB in the first 6 months of 1997, (2) the prospective multicentric cohort of 321 patients of the ELYPSE 1 study, and (3) the series of 149 patients with non-Hodgkin's lymphoma treated in the CLB within prospective phase III trials (1987 to 1995). In these 3 groups, the observed incidences of platelet transfusions in the above-defined risk groups did not differ significantly (P &gt; .1) from those calculated in the model. This risk index could be useful to identify patients at high risk for chemotherapy-induced thrombocytopenia requiring platelet transfusions.


2019 ◽  
Vol 7 ◽  
pp. 2050313X1984052
Author(s):  
Dawid Ilnicki ◽  
Rafał Wyderka ◽  
Przemysław Nowicki ◽  
Alicja Sołtowska ◽  
Jakub Adamowicz ◽  
...  

The objective of this case report is to present how the chronic condition significantly complicates life-saving procedures and influences further treatment decisions. A 64-year-old man suffering from arterial hypertension and immune thrombocytopenic purpura presented to the Emergency Department with anterior ST-elevation myocardial infarction. An immediate coronary angiography was performed where critical stenosis of the proximal left anterior descending was found. It was followed by primary percutaneous intervention with bare metal stent. In first laboratory results, extremely low platelet count was found (13 × 109/L). Consulting haematologist advised the use of single antiplatelet therapy and from the second day of hospitalisation only clopidogrel was prescribed. On the sixth day of hospital stay, patient presented acute chest pain with ST elevation in anterior leads. Emergency coronary angiography confirmed acute stent thrombosis and aspiration thrombectomy was performed. It was therefore agreed to continue dual antiplatelet therapy for 4 weeks. As there are no clinical trials where patients with low platelet count are included, all therapeutic decisions must be made based on clinician’s experience and experts’ consensus. Both the risk of haemorrhagic complications and increased risk of thrombosis must be taken into consideration when deciding on patient’s treatment.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1106-1106
Author(s):  
Michael P. Marchetti ◽  
Francois Maignen ◽  
Herve Falet

Abstract Wiskott-Aldrich Syndrome (WAS) is an X-linked hematopoietic disorder that is characterized by immune deficiency, eczema and severe thrombocytopenia with small platelets. Platelets isolated from WAS patients are cleared rapidly from the circulation when transfused autologously. However, the role of WASp, the protein mutated or absent in WAS, is unclear since platelets isolated from WAS patients function normally. WASp knockout (KO) mice only have a mild thrombocytopenia. Because 1) human, but not mouse platelets express the Fc receptor for IgGs, FcγRIIA (CD32A), and 2) platelet-associated IgGs (PAIgGs) are often observed in WAS patients, we sought to determine whether FcγRIIA expression in humans was involved in the severe thrombocytopenia associated with WAS. WASp KO mice expressing human FcγRIIA on the surface of their platelets were generated by breeding female mice carriers for WASp deficiency with heterozygous FcγRIIA transgenic (TG) males. A total of 221 offsprings were obtained, of which only 97 were males. WASp KO / FcγRIIA TG males were a minority, with a total of 19 animals, compared to 24 WASp WT / FcγRIIA WT, 30 WASp WT / FcγRIIA TG and 24 WASp KO / FcγRIIA WT males. WASp KO / FcγRIIA WT and WASp KO / FcγRIIA TG males had about 70% of normal platelet count compared to WASp WT / FcγRIIA WT and WASp WT / FcγRIIA TG mice (Table 1). Thus, FcγRIIA expression did not affect the thrombocytopenia associated with WASp deficiency. PAIgGs were not detected on the surface of WASp KO / FcγRIIA TG platelets, as evaluated by flow cytometry using an anti-mouse IgG antibody. Spleen weight was increased in WASp KO / FcγRIIA TG compared to WASp WT / FcγRIIA WT and WASp WT / FcγRIIA TG males, but similar to that of WASp KO / FcγRIIA WT males (Table 1). Age of the mice was not involved since similar results were obtained with 6-, 12- or 24-weeks old mice. However, an increased population of macrophages appeared in the spleen of mice lacking WASp as they aged, as evidenced by flow cytometry using anti-mouse Mac-1 (CD11b) and Gr-1 (Ly-6G) antibodies. Our data indicate that expression of platelet FcγRIIA alone does not explain the difference observed between the severe thrombocytopenia of WAS patients and the mild thrombocytopenia of WASp KO mice. WASp deficiency may affect the surface organization of platelets such that clearance is accelerated by spleen macrophages. Table 1. Platelet count and spleen/body weight ratio in WASp KO / FcγRIIA TG mice relative to controls. WASp WT / FcγRIIA WT WASp WT / FcγRIIA TG WASp KO / FcγRIIA WT WASp KO / FcγRIIA TG Results represent mean ± SD. The statistical analysis was performed by analysis of covariance (ANCOVA) with an adjustment on the spleen/body weight ratio. The family error rate for the multiple comparisons was maintained below 0.05 (Sidak method). Platelet count (× 103/μl) 998 ± 145 963 ± 172 677 ± 147 682 ± 120 p &lt; 10−7 Spleen/body weight ratio (mg/g) 2.9 ± 0.6 2.9 ± 0.5 4.1 ± 1.6 3.8 ± 1.8 p &lt; 0.05 Number of males (adjusted) 31 35 30 30


2021 ◽  
Author(s):  
Bo Liu ◽  
Yue He ◽  
Junpeng Pan ◽  
Zhijie Wang

Abstract BackgroundThe purpose of our research is to explore the association between operation duration and the risk of blood transfusion in the patients undergoing TKA.MethodsThis study was a secondary analysis based on the data of a single-center retrospective cohort study in Singapore. The independent variable was the operation duration, and the dependent variable was the risk of blood transfusion events in the perioperation. we analyzed the risk factors of blood transfusion in the Perioperative period by univariate logistic regression, then, multivariable logistic regression analysis was performed adjusting for variables that might affect the operation duration of TKA and the risk of blood transfusion events. Additional analyses examined this association by the subgroup analysis by using stratified multivariate logistic regression models.ResultsAmong 2,622 patients, 153 (5.8%) had blood transfusion in perioperative period. The older (OR=1.051 ,95% CI:1.030, 1.073), the lower BMI (OR=0.939,95% CI: 0.903,0.976),the lower Hb (OR=0.603,95% CI: 0.541 6.132), the DM on insulin (OR=2.542,95%CI:1.054, 6.132), the Bilateral TKA(OR=3.202, 95%CI:2.087, 4.913), the within CHF (OR=4.600, 95% CI :1.685, 12.563), the Cr≥2mg/dl (OR=7.246, 95% CI:2.739, 19.166), the higher ASA status (OR=6.439, 95% CI:2.403, 17.249), the higher risk of blood transfusion (P<0.05).The operation duration was positively correlated with perioperative blood transfusion. We demonstrated that the risk of blood transfusion increased by 1.1% for 1-minute increase in operation duration (OR = 1.011,95% CI: 1.004,1.018). ConclusionOur research shows that the longer the TKA operation duration, the higher the incidence of blood transfusion. The risk of blood transfusion events increases by 66% for every 1-hour increase in operation duration. Compared with patients with operation duration<100 minutes, patients with operation duration more than 100 minutes have an increased risk of blood transfusion events by 56.8%.


Blood ◽  
1998 ◽  
Vol 92 (2) ◽  
pp. 405-410
Author(s):  
J.Y. Blay ◽  
A. Le Cesne ◽  
C. Mermet ◽  
C. Maugard ◽  
A. Ravaud ◽  
...  

Severe thrombocytopenia is a rare but life-threatening side effect of cytotoxic chemotherapy for which risk factors are not well known. Our objective was to delineate a risk model for chemotherapy-induced thrombocytopenia requiring platelet transfusions in cancer patients. Univariate and multivariate analysis of risk factors for chemotherapy-induced thrombocytopenia requiring platelet transfusions were performed on the cohort of the 1,051 patients (CLB 1996) treated with chemotherapy in the Department of Medicine of the Centre Léon Bérard (CLB) in 1996. In univariate analysis, performance status (PS) greater than 1, platelet count less than 150,000/μL at day 1 (d1) before the initiation of chemotherapy, d1 lymphocyte count ≤700/μL, d1 polymorphonuclear leukocyte count less than 1,500/μL, and the type of chemotherapy (high risk v others) were significantly associated (P < .01) with an increased risk of severe thrombocytopenia requiring platelet transfusions. Using logistic regression, d1 platelet count less than 150,000/μL (odds ratio [OR], 4.3; 95% confidence interval [CI], 1.9 to 9.6), d1 lymphocyte counts ≤700/μL (OR, 3.37; 95% CI, 1.77 to 6.4), the type of chemotherapy (OR, 3.38; 95% CI, 1.77 to 6.4), and PS greater than 1 (OR, 2.23; 95% CI, 1.22 to 4.1) were identified as independent risk factors for platelet transfusions. The observed incidences of platelet transfusions were 45%, 13%, 7%, and 1.5% for patients with ≥3, 2, 1, or 0 risk factors, respectively. This model was then tested in 3 groups of patients treated with chemotherapy used as validation samples: (1) the series of 340 patients treated in the CLB in the first 6 months of 1997, (2) the prospective multicentric cohort of 321 patients of the ELYPSE 1 study, and (3) the series of 149 patients with non-Hodgkin's lymphoma treated in the CLB within prospective phase III trials (1987 to 1995). In these 3 groups, the observed incidences of platelet transfusions in the above-defined risk groups did not differ significantly (P > .1) from those calculated in the model. This risk index could be useful to identify patients at high risk for chemotherapy-induced thrombocytopenia requiring platelet transfusions.


Hematology ◽  
2018 ◽  
Vol 2018 (1) ◽  
pp. 576-583 ◽  
Author(s):  
Tamam Bakchoul ◽  
Irene Marini

Abstract Many drugs have been implicated in drug-induced immune thrombocytopenia (DITP). Patients with DITP develop a drop in platelet count 5 to 10 days after drug administration with an increased risk of hemorrhage. The diagnosis of DITP is often challenging, because most hospitalized patients are taking multiple medications and have comorbidities that can also cause thrombocytopenia. Specialized laboratory diagnostic tests have been developed and are helpful to confirm the diagnosis. Treatment of DITP involves discontinuation of the offending drug. The platelet count usually starts to recover after 4 or 5 half-lives of the responsible drug or drug metabolite. High doses of intravenous immunoglobulin can be given to patients with severe thrombocytopenia and bleeding. Although in most cases, DITP is associated with bleeding, life-threatening thromboembolic complications are common in patients with heparin-induced thrombocytopenia (HIT). Binding of antiplatelet factor 4/heparin antibodies to Fc receptors on platelets and monocytes causes intravascular cellular activation, leading to an intensely prothrombotic state in HIT. The clinical symptoms include a decrease in platelet counts by >50% and/or new thromboembolic complications. Two approaches can help to confirm or rule out HIT: assessment of the clinical presentation using scoring systems and in vitro demonstration of antiplatelet factor 4/heparin antibodies. The cornerstone of HIT management is immediate discontinuation of heparin when the disease is suspected and anticoagulation using nonheparin anticoagulant. In this review, we will provide an update on the pathophysiology, diagnosis, and management of both DITP and HIT.


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