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Summary There has been a significant surge in admissions to critical care during the coronavirus disease 2019 (COVID‐19) pandemic. At present, the demands on blood components have not been described. We reviewed their use during the first 6 weeks of the outbreak from 3 March 2020 in a tertiary‐level critical care department providing venovenous extracorporeal membrane oxygenation (vv‐ECMO). A total of 265 patients were reviewed, with 235 not requiring ECMO and 30 requiring vv‐ECMO. In total, 50 patients required blood components during their critical care admission. Red cell concentrates were the most frequently transfused component in COVID‐19‐infected patients with higher rates of use during vv‐ECMO. The use of fresh frozen plasma, cryoprecipitate and platelet transfusions was low in a period prior to the use of convalescent plasma.

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Dear Sir, Hyperhaemolysis is most frequently described in patients with sickle cell disease, although there are cases of this event occurring in patients with thalassaemia and myelofibrosis (Grainger et al., 2001;Treleaven & Win 2004). We report a case of hyperhaemolysis in a patient with Haemoglobin H (HbH) disease, and outline our institutions approach to the management of hyperhaemolysis.A 65-year-old lady with HbH disease and baseline haemoglobin (Hb) of 85 g L −1 , presented to hospital with breathlessness which was felt to be secondary to exacerbation of her asthma. Her Hb at the time of admission was 74 g L −1 , in view of her hypoxia she was transferred to the intensive care unit where she was treated with antibiotics and transfused 4 units of red cells. Iron studies pre-transfusion revealed a serum iron of 2·5 μmol L −1 (11-29 μmol L −1 ) and transferrin saturation of 8%. She made a good recovery and was discharged home, at this time her Hb was 115 g L −1 .She presented to hospital 12 days later with general lethargy, fever, right upper quadrant discomfort and dark urine. The Hb was 77 g L −1 , bilirubin 266 (0-21 μmol L −1 ), C-reactive protein CRP 125 (0-4 mg L −1 ). She was diagnosed with cholecystitis and commenced on antibiotics. In less than 24 hours her Hb had dropped to 51 g L −1 . At this stage haematology was contacted and the provisional working diagnosis was a delayed haemolytic transfusion reaction (DHTR).Lactate dehydrogenase (LDH) was >2000 IU L −1 (240-480 IU L −1 ), reticulocyte count 68 × 10 9 L −1 (10-100 × 10 9 ) and haptoglobin was <0·08 g/L (0.3-2.0 g/L). The direct antiglobulin test (DAT) was moderately positive against IgG 3+ and anti C3d 2+. Pre-transfusion red cell immunology detected the presence of a historical anti E, post-transfusion anti-Jkb and anti-Lua were detected by indirect antiglobulin test (IAT). The eluate revealed anti-Jkb and anti-Lua by IAT. On review of the pre-transfusion units, two of four packed red cell units were phenotyped and shown to be Jkb+ve and the remaining two were Lua+ve.The Hb continued to drop and was 44 g L −1 the following day. The patient became increasingly reticulocytopenic with a reticulocyte count of 13 × 10 9 L −1 and it was felt that the DHTR had triggered hyperhaemolysis with a drop in Hb below pre-transfusion baseline.

P hiladelphia (Ph)-negative myeloproliferative neoplasms (MPN) are acquired hematologic diseases with increased production of mature blood cells. They include polycythemia vera (PV), essential thrombocythemia (ET) and myelofibrosis (MF). The most frequent molecular abnormality found in Ph negative MPN is JAK2V617F, an activating mutation of JAK2 which is responsible for constitutive signaling of various cytokine receptors. Arterial and venous thromboses are the main complications of these diseases and are responsible for high rates of morbidity and mortality. Of note there is a disproportionate incidence of thrombosis at unusual sites including splanchnic vein thrombosis. 1 Splanchnic vein thromboses (SVT) involve one or more abdominal veins, the two most frequent are Portal Vein Thrombosis (PVT) and Budd Chiari Syndrome (BCS). Pathophysiology of thrombosis in MPN is complex and involves abnormalities in blood cells, plasma factors, and endothelial cells (ECs). Several groups, using different techniques, have shown JAK2V617F expression in endothelial cells (Supplemental Fig. 1, http://links.lww.com/HS/ A79). Using laser capture microdissection, JAK2V617F was demonstrated in ECs from hepatic venules in 2 of 3 patients with PV and BCS. 2 JAK2V617F endothelial cells were demonstrated in microdissected splenic capillaries and in ECs cultured from splenic vein in patients with myelofibrosis but without SVT. 3 Although these teams performed experiments to ensure that the DNA they obtained originated from ECs, it is difficult to completely rule out a possible contamination by blood cells. Analysis of endothelial progenitor cells, specifically endothelial colony forming cells (ECFCs), is an alternative way to look for JAK2V617F ECs. Indeed, ECFCs are reported to be the only "true" endothelial progenitor cells, as they are the only ones able to generate blood vessels in vivo: they display clonogenic potential, endothelial but not myeloid cell surface markers, and pronounced postnatal vascularisation ability in vivo. 4,5 ECFCs are a unique tool to investigate endothelial molecular dysfunction in disease, as they give access to endothelial cells from patients in a non-invasive way and a promising tool for vascular regenerative approaches and gene therapy. 6 Yoder et al studied 11 JAK2V617F MPN patients and reported 3 JAK2V617F ECFCs derived from only 1 of 11 patients. Of note, this patient presented with thrombosis and later developed PV. 4 In another study, the JAK2V617F mutation was not detected in any of 75 ECFCs obtained from 57 patients with JAK2V617F MPN but no thrombosis. 7 Teofili et al reported JAK2V617F ECFCs in 5 of 22 MPN patients, all with thrombotic complications including 1 with BCS and 1 with PVT. 8 Lastly, 4 of 5 JAK2V617F-positive patients with BCS but without overt MPN had JAK2V617F ECFCs cultured from the bone marrow. 9 Taken together, these results suggest that the presence of JAK2V617F ECFCs in patients is associated with thrombosis, even in the absence of overt MPN. Our groups have previously demonstr...