scholarly journals Accuracy of platelet counting haematology analysers in severe thrombocytopenia and potential impact on platelet transfusion

2005 ◽  
Vol 128 (4) ◽  
pp. 520-525 ◽  
Author(s):  
H. C. Segal ◽  
C. Briggs ◽  
S. Kunka ◽  
A. Casbard ◽  
P. Harrison ◽  
...  
2021 ◽  
Vol 12 (7) ◽  
pp. 47-51
Author(s):  
Mamatha Tittamegalapalya Ramalingaiah ◽  
Jeetendra Kumar Jogihalli Mood ◽  
Satyanarayana Narayanashetty ◽  
Rashmi Madappa Bhuvaneshappa

Background: Dengue is an acute infectious febrile illness characterised by thrombocytopenia and platelet dysfunction leading to bleeding manifestations. Vitamin B12 is required for platelet production in the bone marrow. So, deficiency of vitamin B12 in dengue patients can have severe thrombocytopenia. Aims and Objective: Study was aimed to know the clinical profile of dengue fever patients and to correlate serum vitamin B12 level with severity of thrombocytopenia, platelet transfusion and duration of hospital stay. Materials and Methods: This observational study was done on dengue patients for period of 3 months January 2020 to March 2020. Confirmed cases of dengue fever with NS 1 Ag positive & Ig M antibody positive were included in the study. Patient with sepsis, underlying malignancy, autoimmune disorder, hematological disorder, drugs causing thrombocytopenia were excluded from the study. Appropriate statistical methods were applied. Results: Total 50 subjects were included. Majority of subjects were in the age group 31 to 40 years. 50% were males and females respectively. Most common clinical feature was fever and bleeding manifestations. Mean Vitamin B12 was significantly lower among those with severe thrombocytopenia and highest among those with no thrombocytopenia., there was significant difference in mean Platelet transfusion and duration of hospital stay with respect to severity of Platelet count. Conclusion: Dengue fever patients with vitamin B 12 deficiency had moderate to severe thrombocytopenia and more bleeding manifestations. Those patients required more platelet transfusion and increased duration of hospital stay.


Hematology ◽  
2020 ◽  
Vol 2020 (1) ◽  
pp. 518-522
Author(s):  
Darrell J. Triulzi

Abstract Prophylactic platelet transfusions are used to reduce the risk of spontaneous bleeding in patients with treatment- or disease-related severe thrombocytopenia. A prophylactic platelet-transfusion threshold of <10 × 103/µL has been shown to be safe in stable hematology/oncology patients. A higher threshold and/or larger or more frequent platelet doses may be appropriate for patients with clinical features associated with an increased risk of bleeding such as high fevers, sepsis, disseminated intravascular coagulation, anticoagulation therapy, or splenomegaly. Unique factors in the outpatient setting may support the use of a higher platelet-transfusion threshold and/or dose of platelets. A prophylactic platelet-transfusion strategy has been shown to be associated with a lower risk of bleeding compared with no prophylaxis in adult patients receiving chemotherapy but not for autologous transplant recipients. Despite the use of prophylactic platelet transfusions, a high incidence (50% to 70%) of spontaneous bleeding remains. Using a higher threshold or larger doses of platelets does not change this risk. New approaches to reduce the risk of spontaneous bleeding, including antifibrinolytic therapy, are currently under study.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Hiroaki Nomoto ◽  
Naoki Morimoto ◽  
Kouichi Miura ◽  
Shunji Watanabe ◽  
Yoshinari Takaoka ◽  
...  

Abstract Background Chronic liver disease (CLD) is often complicated by severe thrombocytopenia (platelet count < 50,000/µL). Platelet transfusion has been a gold standard for increasing the platelet count to prevent hemorrhagic events in such patients. Lusutrombopag, a thrombopoietin receptor agonist, can increase the platelet count in such patients when invasive procedures are scheduled. Former studies on lusutrombopag included patients with a platelet count of > 50,000/µL at baseline: the proportions of patients who did not require platelet transfusion were 84–96%, which might be overestimated. Methods The efficacy and safety of lusutrombopag were retrospectively investigated in CLD patients with platelet count of < 50,000/µL, a criterion for platelet transfusion, in real-world settings. We examined the proportion of patients who did not require platelet transfusion in 31 CLD patients, which exceeded a minimum required sample size (21 patients) calculated by 80% power at a significance level of 5%. Lusutrombopag, 3 mg once daily, was administered 8–18 days before scheduled invasive procedures. Results Among 31 patients who received lusutrombopag, 23 patients (74.2%) patients showed a platelet count of ≥ 50,000/µL (Group A) and did not require platelet transfusion. The remaining 8 patients (25.8%) did not reached platelet ≥ 50,000/µL (Group B). The means of platelet increase were 38,000/µL and 12,000/µL in groups A and B, respectively. A low platelet count at baseline was a characteristic of patients in group B. Among 13 patients who repeatedly used lusutrombopag, lusutrombopag significantly increased the platelet count as the initial treatment. When all repeated uses of lusutrombopag were counted among these 13 patients, platelet transfusion was not required in 82.1% (23/28) of treatments. Although one patient showed portal thrombosis after lusutrombopag treatment, the thrombosis was disappeared by anticoagulant treatment for 35 days. The degree of platelet increase with lusutrombopag was larger than that in their previous platelet transfusion. Conclusions The proportion of patients who did not require platelet transfusion was 74.2%, which is smaller than that in former studies which included CLD patients with a platelet count of > 50,000/µL. However, lusutrombopag is effective and safe for CLD patients with a platelet count of < 50,000/µL.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 961-961 ◽  
Author(s):  
Neil Murray ◽  
Sally Ballard ◽  
Angela Casbard ◽  
Mike Murphy ◽  
Irene Roberts ◽  
...  

Abstract Background: Platelet transfusion practice in neonates is not evidence-based and there is a lack of data relating transfusion to clinical outcome. To inform the design of clinical trials, we conducted a prospective multicentre observational study of platelet transfusion in thombocytopenic neonates to describe: transfusion practice, including reason for transfusion; clinically-related outcomes, including minor and major bleeding and mortality. Methods: Neonates with platelets &lt;60x109/l were studied at 7 UK neonatal intensive care units Mar 05-Jun 06. With parental consent, daily data were collected on minor bleeding (blood staining of oral/nasogastric/endotracheal secretions and stool; microscopic haematuria; petechial rash; oozing from puncture sites - scored 0–7), and major bleeding (intraventricular (IVH), intra-abdominal, pulmonary or renal). Surviving neonates were studied for 7 days or until platelets were ≥60x109/l. Blood counts and all transfusions were directed by the attending neonatologist, with reason for transfusion and its effect on bleeding prospectively documented. Results: 145 of 167 (87%) eligible neonates were enrolled; 123 (85%) were &lt; 37 weeks gestational age (GA), 89 (61%) were male. The study documented 186 episodes of thrombocytopenia (1606 study days) and 309 platelet transfusions given to 91 (63%) neonates. GA, birth weight and age at thrombocytopenic episode were: 27 (24–32) weeks; 825 (675–1370) grams; 5 (2–16) days, respectively [all data median (IQR)]. 21/145 babies (14%) had major IVH (Grade 3/4) at study entry. Platelets (x 109/l) at study entry, and at platelet nadir, and duration of count &lt;60x109/l were: 44 (33–54); 31 (19–42); 2 (1–5) days respectively. In transfused neonates, platelets (x109/l) pre- and post-transfusion, and number of transfusions were: 27 (19–36); 84 (46–138); 2 (1–4) respectively. The principal indications for transfusion were:- platelet count below threshold of unit guideline: 265/309 (86%); deteriorating clinical condition: 17/309 (6%); and significant bleeding: 7/309 (2%). At least 1 episode of minor bleeding was recorded on 622/1606 (39%) of study days. Minor bleeding scores recorded for 12 hours pre- and post each transfusion were [median (IQR)]: 1 (0–2) and 0 (0–1) respectively. New or extension of IVH bleeding to Grade 3/4 occurred in 7 neonates and other major haemorrhage in 9 neonates (4 pulmonary, 3 GI). A total of 20/145 (14%) neonates died, 13 with major IVH bleeding (of which 10 had Grade 3/4 IVH at study entry); all received platelet transfusions [total 87; median 3 (2 to 7). Conclusion: This study confirms that most neonates with severe thrombocytopenia are preterm, most episodes develop after 72 hours of life (median 5 days) and are of short duration (median 2 days). Minor haemorrhage is common and may be reduced by platelet transfusion. Major haemorrhage is uncommon (11%), is associated with mortality (82%) and affected patients receive a large number of platelet transfusions. There is a clear distinction between the majority of thrombocytopenic neonates who receive one or two transfusions as prophylaxis with a good outcome, and the minority who suffer adverse outcomes despite transfusion. Many neonates are transfused with platelets at thresholds below those suggested in guidelines without apparent clinical detriment. These data will be invaluable for planning the randomised trials necessary for rationalising platelet transfusion in these vulnerable patients.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4951-4951
Author(s):  
William R. Broderick ◽  
Amir A. Toor ◽  
Brian R. Curtis ◽  
Tulio E. Rodriguez ◽  
Scott E. Smith ◽  
...  

Abstract Platelet transfusion refractoriness following allogeneic bone marrow transplantation usually stems from HLA alloimmunization. However other platelet antigens may serve as targets of alloimmune reactivity. A 24-year-old Palestinian male with atypical CML in chronic phase underwent matched unrelated donor bone marrow transplant from a 39-year-old female, HLA-A, B, C and DR allele level matched donor. Conditioning was with busulfan 0.8mg/Kg IV q6 hours day -8 through -4, cyclophosphamide 60mg/Kg IV daily day -3 & -2 and rabbit anti-thymocyte globulin 1.5mg/Kg IV daily day -5 & -4. Graft versus host disease prophylaxis was with mini-dose methotrexate and tacrolimus, with filgrastim given for hematopoietic reconstitution. The cell dose was 1.86x106 CD34+ cells/Kg recipient body weight (3.66x108 mononuclear cells/Kg). Neutrophil engraftment occurred on day +14, and was complicated by a diffuse purpuric skin rash, with hypoxia and pulmonary infiltrates which resolved with corticosteroid therapy. His post-transplant course was also complicated by severe, transfusion refractory thrombocytopenia (to random donor pools, apheresis and crossmatched platelet units) starting on day +5 with platelet counts of <5x103/μL. He developed intra-retinal hemorrhage of the right eye, scleral hemorrhage bilaterally, epistaxis and muco-cutaneous bleeding. During the first 30 days following BMT he received 53 doses of platelets in addition to aminocaproic acid. He did not have DIC, splenomegaly or evidence of microangiopathy. HLA alloantibodies were not identified. Antigen Capture ELISA and flow cytometry for platelet specific antibody identification however demonstrated antibodies specific for CD36 in the patient’s serum (Fig). Platelets from the bone marrow donor typed positive for CD36. IVIG 0.5gm/Kg IV on d+13, 14, and 17 and Rituximab 375mg/m2 IV d + 17, 64, 72, and 82 were administered with no therapeutic response. The patient finally responded to transfusions of platelets collected from family members (parents, siblings and cousins) who were CD36negative. Bone marrow biopsies 2 months and 4 months following transplantation showed no evidence of residual disease with trilineage engraftment and adequate megakaryocytes, normal cytogenetics and >98% donor chimerism. As his immunosuppression has been tapered over time, the antibody titer has declined (Fig) as has his platelet transfusion requirement (41 doses transfused between day 31 and 120). However he remains dependent upon directed donor platelet transfusions from his CD36 negative family members at 120 days from transplant. The CD36 negative phenotype is rare in Caucasians, however, platelets from about 5% of individuals of Asian or African descent lack CD36. DNA sequencing to determine CD36 mutations in this patient is underway. We hypothesize that this patient developed a host vs. graft humoral response against donor derived and transfused platelets resulting in sustained severe thrombocytopenia. Patient serum CD36 antibody titers following transplant Patient serum CD36 antibody titers following transplant


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 93-93
Author(s):  
Binggang Xiang ◽  
Guoying Zhang ◽  
Xiang-An Li ◽  
Andrew J. Morris ◽  
Alan Daugherty ◽  
...  

Abstract Abstract 93 Sepsis is a tremendous burden for health-care systems. Patients with sepsis often have low platelet counts, and septic patients with severe thrombocytopenia have a poor prognosis and higher mortality. However, the role of platelets in the pathogenesis of sepsis has not been well elucidated. We investigated the role of platelets in septic shock using a mouse model of lipopolysaccharide (LPS)-induced endotoxemia. Depletion of platelets by intraperitoneal injection of a rat anti-mouse GPIb monoclonal antibody increased mortality and aggravated organ failure in endotoxemic mice as evident by increases in plasma aminotransferase (ALT), aspartate aminotransferase (AST), Lactate dehydrogenase (LDH), and Creatine kinase (CK) concentrations, while transfusion of platelets reduced mortality. Increases in mortality rate in thrombocytopenic mice by LPS challenge was not due to inflammatory hemorrhage, because there was no significantly hemorrhage observed in brains and lungs from mice pre-treated with either control IgG or the anti-GPIba antibody and blood RBC and Hb concentrations between IgG pre-treated mice and the anti-GPIba antibody pre-treated mice were similar. TNF-a, which is produced mainly by macrophages in vivo, plays critical roles in the development of disseminated intravascular coagulation, acute respiratory distress syndrome and shock in sepsis. Our data indicate that plasma concentrations of proinflammatory cytokines, TNF-a and IL-6, were markedly increased by platelet depletion and decreased by platelet transfusion in the mice challenged with LPS. Effects of platelet depletion on TNF-a production were eliminated in the mice that macrophages were pre-depleted. Furthermore, LPS- or thrombin-activated platelets or releasates from activated platelets inhibited TNF-a and IL-6 production in macrophages in vitro. Inhibition of TNF-a and IL-6 production in macrophages by activated platelets was prevented by pre-incubation of platelets with a COX1 inhibitor aspirin. Moreover, platelets from wild type mice but not COX1 deficient mice inhibited LPS-induced TNF-a and IL-6 production in macrophages. Transfusion of COX1 deficient platelets failed to protect against endotoxemia. Washed platelets from wild-type mice or platelet releasates from thrombin-activated wild-type mice inhibited LPS-induced TNF-a and IL-6 production in macrophages lacking TXA2 receptor, TP, suggesting that a metabolite other than TXA2 is responsible for platelet inhibition of macrophage function. We found that stimulation of platelets with thrombin or LPS induced PGE2 production and pre-incubation of macrophages with an antagonist of PGE2 receptor EP4 reversed platelet inhibition on TNF-a and IL-6 production in macrophages. Our results indicate that platelets protect against septic shock by inhibiting macrophage-dependent inflammatory response via the COX1/PGE2/EP4 dependent pathway. Thus, these findings demonstrate a previously unappreciated role for platelets in septic shock and suggest that platelet transfusion may be effective in treating septic patients. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 719-719
Author(s):  
Kathleen Pao Lynn Cheok ◽  
Rakchha Chhetri ◽  
Li Yan A Wee ◽  
Arabelle Salvi ◽  
Simon McRae ◽  
...  

Aim: Although 40-65% of myelodysplastic syndromes (MDS) patients are thrombocytopenic and require platelet transfusions, there is limited literature on the risk factors predictive of bleeding and the burden of immune mediated platelet refractoriness (PLT-R). Objectives: To evaluate the prevalence of thrombocytopenia, incidence of bleeding events, platelet transfusion dependency (PLT-TD) and immune-mediated platelet refractoriness (PLT-R) in MDS patients. Methods: A retrospective analysis of 754 MDS patients enrolled in the South Australian MDS (SA-MDS) registry was performed. Platelet counts &lt;100, &lt;50 and &lt;20 (x109/L) were used to define mild, moderate and severe thrombocytopenia respectively. The severity of bleeding events was classified according to the International Society of Thrombosis and Haemostasis (ISTH) classification. PLT-TD was defined as transfusion of at least one unit of platelets each month for four consecutive months. All other patients were classified as transfusion independent (PLT-TI). Immune mediated PLT-R was defined if a patient had HLA-class I or HPA antibodies, poor platelet increments and required HLA-matched platelets. Medication history with regards to anticoagulation and/or antiplatelet therapy was also collected. Results: At diagnosis, 332 (45%) patients had thrombocytopenia and 106 (14%) patients had moderate to severe thrombocytopenia. During the study period, 249 bleeding events were recorded in 162 (21%) patients with a cumulative incidence of 33% (Fig 1A). Of the 249 bleeding events, 85 (34%) were major and 164 (66%) were clinically relevant minor bleeding. Notably, 16, 90 and 5 bleeding events were intracranial, gastrointestinal, intraocular respectively. While 41% (96/235) bleeding events occurred in the setting of moderate to severe thrombocytopenia, 21% and 38% (Fig 1B) of bleeding events occurred at platelet counts of &gt;50-100 and &gt;100x109/L respectively. Twenty-eight percent (69/249) bleeding events were associated with concomitant anticoagulation and/or antiplatelet therapy and importantly, platelets counts were &gt;50x109/L and &gt;100 x109/L in 57 (83%) and 46 (67%) at the time of bleeding events, respectively. During the disease course, 393 (52%) patients required at least one unit of platelet transfusion. 106 (14%) patients were PLT-TD and had significantly poor overall survival (OS) compared to PLT-TI (26 vs 42 months, p&lt;0.0001). In total, 30/393 (7%) required HLA-matched platelet transfusions. 20/30 (66%) of PLT-R patients were female receiving disease modifying therapy (DMT). This was substantiated by cox regression analysis, demonstrating that females (HR=5.32, p=0.0006), older age (HR=0.97, p=0.028) and haemoglobin (Hb) at diagnosis (HR=1.03, p=0.009) were independent risk factors for PLT-R. Importantly, 20/76 (25%) female patients receiving platelets and DMT developed immune mediated PLT-R requiring HLA matched platelets. Conclusions: In our cohort of MDS patients, cumulative incidence of bleeding is 33% and 59% of the bleeding events occurred at platelet counts &gt;50X109/L. For all bleeding events that occurred while on anticoagulation and/or antiplatelet therapy, 83% events occurred with platelet counts &gt;50 x 109/L. Therefore, guidelines for anticoagulation and/or antiplatelet therapy are required for MDS patients. We also showed that development of PLT-TD is associated with poor OS. Importantly, 1 in 4 female MDS patients receiving platelets and DMT required HLA-matched platelets. Platelet transfusions practices should be optimised for these high-risk groups. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4293-4293
Author(s):  
Lakshminarayanan Nandagopal ◽  
Muthu Veeraputhiran ◽  
Tania Jain ◽  
Ayman Soubani ◽  
Charles A. Schiffer

Abstract Introduction Prophylactic platelet transfusions are often performed prior to bronchoscopy or broncho-alveolar lavage (BAL) to prevent bleeding in thrombocytopenic patients. There is a paucity of data to validate this approach, with a platelet transfusion threshold of <50,000/mm3 largely based on expert opinion. We conducted a retrospective study on the incidence of bleeding complications in thrombocytopenic patients undergoing bronchoscopy. Methods We identified 150 consecutive patients with platelet counts <100,000/mm3 who underwent bronchoscopy and/or BAL from January 2009 to May 2014 at our institution. Bronchoscopies performed in patients with frank hemoptysis and trans-bronchial lung biopsy procedures were excluded. Patient characteristics, underlying diagnosis, platelet count prior to bronchoscopy, administration of platelet transfusions and bronchoscopy details were recorded. Factors affecting bleeding risk including presence of renal dysfunction (defined as BUN >30 and/or Cr>2.0) and coagulation studies (PT, PTT, INR) were identified. The British Thoracic Society guidelines1 were used to categorize bleeding as a result of bronchoscopy. Data were analyzed using descriptive statistics. Results The median age was 59 years (range 27-90), with two-thirds of patients (63%) being male. One hundred and seventeen (78%) patients had underlying malignancy and 55 (37%) had thrombocytopenia related to malignancy. Fellows and residents under the supervision of a bronchoscopy certified attending performed all but 4 of the bronchoscopies. Infection (40%) was the primary indication for bronchoscopy with BAL performed in 127 (85%) patients. Fifty-eight of 89 (65%) patients with baseline platelet counts <50,000/mm3 received prophylactic transfusions compared to 8% of those with platelet counts >50,000/mm3. The platelet count did not rise to >50,000//mm3 in many transfused patients. Seventy patients (47%) had counts <50,000/mm3 and eighty patients (53%) had counts >50,000/mm3 at the time of bronchoscopy. 49% were receiving immunosuppressive medications, 45% had renal dysfunction and 8% had INR >1.5. Bloody lavage that resolved spontaneously without continuous suctioning (Grade 0) was observed in 9 (6%) patients. Bleeding that required continuous suctioning but then resolved spontaneously (Grade 1) was noted in 1 patient with a platelet count of 61,000/mm3. Of 10 total bleeding events, 7 occurred in patients who were intubated. Two additional patients with platelet counts of 30,000/mm3 and 53,000/mm3 had diffuse alveolar hemorrhage, which was present before bronchoscopy. “Old” blood and blood clots were observed in 6 patients. Discussion The low incidence of bleeding complications from bronchoscopy +/- BAL even in patients with platelet counts <30,000/mm3 (3 episodes in 31 patients, all grade 0) demonstrates that bronchoscopy can be safely done in severely thrombocytopenic patients. Adopting a lower threshold for prophylactic transfusions could save a considerable number of platelet units and translate into significant cost savings and decreased risk of transfusion-related complications. Table 1 Platelet count, transfusion history and bleeding complications during bronchoscopy Platelet count at the time of bronchoscopy Number (n) and percentage (%) of patients who underwent bronchoscopy Number of patients who received prior platelet transfusion Bleeding during bronchoscopy n % 0-15,000/mm3 9 6% (9/150) 5 Grade 0=1 pt 16-29 22 15% 16 Grade 0=2 pts 30-39 17 11% 9 Grade 0=1 pt 40-49 22 15% 9 Grade 0=3 pts 50-75 44 29% 14 Grade 1=1 pt 76-100 36 24% 10 Grade 0=2 pts Total 150 63 Grade 0=9 pts, Grade 1=1 pt. 1.Du Rand IA, Blaikley J, Booton R, et al. British Thoracic Society guideline for diagnostic flexible bronchoscopy in adults: accredited by NICE. Thorax. 2013:68 Suppl 1:i1-i44 Disclosures No relevant conflicts of interest to declare.


2021 ◽  
Author(s):  
Virginia Zarama ◽  
Jorge A. Revelo-Noguera ◽  
Jaime A. Quintero ◽  
Ramiro Manzano ◽  
Francisco L. Uribe-Buriticá ◽  
...  

Abstract Purpose: To study the occurrence of bleeding complications in patients with severe thrombocytopenia (platelet count <20x103/µL) subjected to ultrasound-guided central venous access (UG-CVA) while receiving or not routine prophylactic platelet transfusion (PPLT).Research Question: What is the frequency of bleeding complications related to the placement of ultrasound-guided central venous access in patients with severe thrombocytopenia between 2011 and 2019 at high complexity hospital?Methods: A total of 221 patients with severe thrombocytopenia subjected to UG-CVA from January 2.011 to November 2.019 were selected. They were classified as positive (P-PPLT) or negative (N-PPLT) recipients of PPLT. Then, P-PPLT (n=72) were 1:1 propensity matched to N-PPLT based on catheter diameter, anatomical insertion site, presence of hematologic malignancy, absolute platelet count and whether the health care provider performing the procedure was an attending or a trainee. Bleeding complications were graded according to the Common Terminology Criteria for Adverse Events (CTCAE) score and adapted to central venous catheter placement. A logistic regression analysis was then performed using “bleeding complications” as a binary compound outcome of major (Grades 3-4) and minor bleeding (Grades 1-2) vs. no bleeding.Results: Seventy-two patients were classified as P-PPLT, while 149 as N-PPLT. No grades 3-4 of bleeding events were identified in the entire population. No significant differences were observed between N-PPLT and P-PPLT for bleeding Grades 1-2 in both pre-matched (53[35.5%] vs. 26[36.1%], p=0.90) and propensity-matched populations (27[37.5%] vs. 26[36.1%], p=0.80). Logistic regression demonstrated that PPLT did not influence any bleeding complication (OR 0.9, 95%CI 0.42-1.92, p=0.791)Conclusions: Bleeding complications related to central venous catheterization in acutely ill patients with severe thrombocytopenia are not influenced by routine prophylactic platelet transfusion when catheter placement is performed under ultrasound guidance.


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