Hematological Issues in Liver Disease

Allison, Michael G.; Shanholtz, Carl; Sachdeva, Ashutosh

doi:10.1016/j.ccc.2016.03.004

Cited by 22 publications

(21 citation statements)

References 56 publications

(62 reference statements)

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“…Consistent with our findings, such studies found that INR improved over a short period of time in ICU and that bleeding was neither especially common nor clinically serious for the majority of patients . In this regard, the pathophysiology of hemostasis in ALF is complex with preserved clotting capability and even hypercoagulability, and apart from case reports, our study is only the second to systematically evaluate for thrombotic complications in patients with ALF.…”

Section: Discussionsupporting

confidence: 89%

Coagulation abnormalities, bleeding, thrombosis, and management of patients with acute liver failure in Australia and New Zealand

Warrillow

Fisher

Tibballs

et al. 2019

J of Gastro and Hepatol

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Background and Aim: To study the management of coagulation and hematological derangements among severe acute liver failure (ALF) patients in Australia and New Zealand liver transplant intensive care units (ICUs). Methods: Analysis of key baseline characteristics, etiology, coagulation and hematological tests, use of blood products, thrombotic complications, and clinical outcomes during the first ICU week. Results: We studied 62 ALF patients. The first day median peak international normalized ratio was 5.5 (inter-quartile range [IQR] 3.8-8.7), median longest activated partial thromboplastin time was 62 s (IQR 44-87), and median lowest fibrinogen was 1.1 (IQR 0.8-1.6) g/L. Fibrinogen was only measured in 85% of patients, which was less than other tests (P < 0.0001). Median initial lowest platelet count was 83 (IQR 41-122) × 10 9 /L. Overall, 58% of patients received fresh frozen plasma, 40% cryoprecipitate, 35% platelets, and 15% prothrombin complex concentrate. Patients with bleeding complications (19%) had more severe overall hypofibrinogenemia and thrombocytopenia. Thrombotic complications were less common (10% of patients), were not associated with consistent patterns of abnormal hemostasis, and were not immediately preceded by clotting factor administration and half occurred only after liver transplantation surgery. Conclusion: In ALF patients admitted to dedicated Australia and New Zealand ICUs, fibrinogen was measured less frequently than other coagulation parameters but, together with platelets, appeared more relevant to bleeding risk. Blood products and procoagulant factors were administered to most patients at variable levels of hemostatic derangement, and bleeding complications were more common than thrombotic complications. This epidemiologic information and practice variability provide baseline data for the design and powering of interventional studies.

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Section: Discussionsupporting

confidence: 89%

Coagulation abnormalities, bleeding, thrombosis, and management of patients with acute liver failure in Australia and New Zealand

Warrillow

Fisher

Tibballs

et al. 2019

J of Gastro and Hepatol

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“…However, if the FRC were part of each CBC, perhaps that extra phlebotomy, time, and cost for the FVIII level would not be needed. DIC is a microangiopathic condition where schistocytosis is common, while the coagulopathy of neonatal liver disease is not microangiopathic and the FRC remains normal [19]. 0D 6D 3D 9D 12D 15D 18D 21D 24D 27D 30D 33D 36D 39D 42D 45D 48D 51D 54D 57D 60D 63D 66D 69D 72D 75D 78D 81D 84D 87D 90D Day of life Extra-corporeal membrane oxygenation might generate schistocytes from RBC damage due to mechanical turbulence within the circuit [20].…”

Section: Discussionmentioning

confidence: 99%

Automated Quantification of Fragmented Red Blood Cells: Neonatal Reference Intervals and Clinical Disorders of Neonatal Intensive Care Unit Patients with High Values

et al. 2018

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Background: Schistocytes are circulating erythrocyte fragments. They can be identified microscopically from a blood smear; but automated systems evaluate more cells and avoid inconsistencies in microscopy. Studies using adult subjects indicate that automated quantification of schistocytes can be clinically useful. However, reference intervals for automated schistocyte counts of neonates have not been published, and the relevance of a high automated schistocyte count from neonates has not been reported. Objectives: Using retrospective automated neonatal complete blood count (CBC) data, we created reference intervals for fragmented red cells (FRCs) and sought to discover the clinical conditions of neonates with high FRCs (above the upper reference interval). Results: We created reference intervals based on 39,949 CBCs from 15,655 neonates 0–90 days old. The lower reference interval was 0 FRC/µL and the upper interval was 100,000/µL. The highest FRCs (96 CBCs from 44 neonates) were > 250,000/µL. These neonates clustered into the following groups: 37% had sepsis, 29% had disseminated intravascular coagulation (DIC), 17% had a genetic syndrome, 14% necrotizing enterocolitis (NEC), and 7% had iron deficiency (some had more than one diagnosis). Based on the reference intervals, we divided the 39,949 FRC values into 3 groups: (1) < 100,000/µL (“normal”), (2) 100,000–200,000/µL (“moderately elevated”), and (3) > 200,000/µL (“extremely elevated”). The odds that a microangiopathic condition (DIC, sepsis, NEC) or a microcytic disorder (iron deficiency) were present were significantly higher in the moderately elevated, and more so in the extremely elevated group. Conclusions: Our study suggests that a high FRC could prompt investigation into, or inform follow-up of, a neonatal microangiopathic or extremely microcytic disorder.

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“…4,5,7,10,12,15,16,57 Acute liver failure from any cause is associated with the decreased production of coagulation factors as well as a decrease in procoagulant proteins, leading to coagulopathy in coexistence with hypercoagulability. 58 A functional platelet defect may also occur in liver failure because of coexisting uremia and endothelial abnormalities and is related to the degree of liver dysfunction. 58 Decreased production of fibrinogen, reduced levels of antifibrinolytic pathway components, and upregulation of tissue plasminogen activator are observed, all of which promote hyperfibrinolysis and disseminated intravascular coagulation.…”

Section: Complicationsmentioning

confidence: 99%

“…58 A functional platelet defect may also occur in liver failure because of coexisting uremia and endothelial abnormalities and is related to the degree of liver dysfunction. 58 Decreased production of fibrinogen, reduced levels of antifibrinolytic pathway components, and upregulation of tissue plasminogen activator are observed, all of which promote hyperfibrinolysis and disseminated intravascular coagulation. 58 Some centers perform viscoelastic testing with thromboelastography or rotational thromboelastometry to guide prompt resuscitation and therapy.…”

Section: Complicationsmentioning

confidence: 99%