Sepsis-associated thrombocytopenia

Larkin, Caroline M.; Santos-Martínez, María José; Ryan, Thomas; Radomski, Marek W.

doi:10.1016/j.thromres.2016.02.022

Cited by 60 publications

(51 citation statements)

References 67 publications

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“…Observational studies have demonstrated an association between sepsis-induced coagulopathy and miRNA expression [85, 86]. Compared with severe sepsis patients with normal platelet counts, the expression of miR-130a in peripheral blood monocytic cells was significantly lower in septic patients with thrombocytopenia [86].…”

Section: Discussionmentioning

confidence: 99%

The involvement of regulatory non-coding RNAs in sepsis: a systematic review

Chan

Wong

et al. 2016

Crit Care

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BackgroundSepsis coincides with altered gene expression in different tissues. Accumulating evidence has suggested that microRNAs, long non-coding RNAs, and circular RNAs are important molecules involved in the crosstalk with various pathways pertinent to innate immunity, mitochondrial functions, and apoptosis.MethodsWe searched articles indexed in PubMed (MEDLINE), EMBASE and Europe PubMed Central databases using the Medical Subject Heading (MeSH) or Title/Abstract words (“microRNA”, “long non-coding RNA”, “circular RNA”, “sepsis” and/or “septic shock”) from inception to Sep 2016. Studies investigating the role of host-derived microRNA, long non-coding RNA, and circular RNA in the pathogenesis of and as biomarkers or therapeutics in sepsis were included. Data were extracted in terms of the role of non-coding RNAs in pathogenesis, and their applicability for use as biomarkers or therapeutics in sepsis. Two independent researchers assessed the quality of studies using a modified guideline from the Systematic Review Center for Laboratory animal Experimentation (SYRCLE), a tool based on the Cochrane Collaboration Risk of Bias tool.ResultsObservational studies revealed dysregulation of non-coding RNAs in septic patients. Experimental studies confirmed their crosstalk with JNK/NF-κB and other cellular pathways pertinent to innate immunity, mitochondrial function, and apoptosis. Of the included studies, the SYRCLE scores ranged from 3 to 7 (average score of 4.55). This suggests a moderate risk of bias. Of the 10 articles investigating non-coding RNAs as biomarkers, none of them included a validation cohort. Selective reporting of sensitivity, specificity, and receiver operating curve was common.ConclusionsAlthough non-coding RNAs appear to be good candidates as biomarkers and therapeutics for sepsis, their differential expression across tissues complicated the process. Further investigation on organ-specific delivery of these regulatory molecules may be useful.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1555-3) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

The involvement of regulatory non-coding RNAs in sepsis: a systematic review

Chan

Wong

et al. 2016

Crit Care

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“…Multiple mechanisms cause thrombocytopenia during sepsis. Decreased bone marrow production, hemophagocytosis, platelet consumption in microvascular beds, sequestration, and hemodilution may all contribute to varying degrees [64]. Septic patients are at high risk for DIC which can further lower platelet counts.…”

Section: Step 5: Evaluation For Sepsismentioning

confidence: 99%

Thrombocytopenia in the Intensive Care Unit

Walter

2020

Evidence-Based Critical Care

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A 68-year-old male is admitted to the medical ICU with acute hypoxemic respiratory failure from community acquired pneumonia. He was recently hospitalized for acute cholecystitis during which he received prophylactic subcutaneous heparin. He is placed on invasive mechanical ventilation and given ceftriaxone and azithromycin. A lower extremity duplex ultrasound is performed for unilateral leg swelling which demonstrates an acute right femoral deep vein thrombosis. He is subsequently started on an infusion of unfractionated heparin. The following morning, his platelet count is noted to have dropped from 250 × 10 9 cells/L to 110 × 10 9 cells/L.

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“…12 Enhanced platelet consumption results from ongoing thrombin generation and increased adhesion of platelets to endothelial cells. 17,28 In critically ill septic patients, thrombocytopenia is associated with a dysregulated host response, 29,30 and it indicates poor prognosis in patients with septic shock. Therapy of sepsis 32 requires source control, antibiotic therapy, and supportive measures.…”

Section: Commentmentioning

confidence: 99%

“…33,78 In many ICU patients, thrombocytopenia is associated with acquired mild to moderate platelet function defects, [79][80][81] which are caused or aggravated by medications such as antibiotics and 82,83 analgesics, platelet activation on extracorporeal circuits, 84 or cleavage of platelet receptors by released enzymes in cases of sepsis. 28 Therefore, in thrombocytopenic patients, bleeding symptoms are much more relevant than the platelet count when deciding whether platelets should be transfused. In patients with immune-mediated thrombocytopenia (eg, ITP and DITP), however, platelet transfusions should be restricted to patients with serious or life-threatening bleeding.…”

Section: Platelet Transfusions In Icu Patientsmentioning

confidence: 99%

How I evaluate and treat thrombocytopenia in the intensive care unit patient

Greinacher

Selleng

2016

Blood

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Multiple causes (pseudothrombocytopenia, hemodilution, increased consumption, decreased production, increased sequestration, and immune-mediated destruction of platelets) alone or in combination make thrombocytopenia very common in intensive care unit (ICU) patients. Persisting thrombocytopenia in critically ill patients is associated with, but not causative of, increased mortality. Identification of the underlying cause is key for management decisions in individual patients. While platelet transfusion might be indicated in patients with impaired platelet production or increased platelet destruction, it could be deleterious in patients with increased intravascular platelet activation. Sepsis and trauma are the most common causes of thrombocytopenia in the ICU. In these patients, treatment of the underlying disease will also increase platelet counts. Heparin-induced thrombocytopenia requires alternative anticoagulation at a therapeutic dose and immune thrombocytopenia immunomodulatory treatment. Thrombocytopenia with symptomatic bleeding at or above World Health Organization grade 2 or planned invasive procedures are established indications for platelet transfusions, while the evidence for a benefit of prophylactic platelet transfusions is weak and controversial. If the platelet count does not increase after transfusion of 2 fresh ABO blood group–identical platelet concentrates (therapeutic units), ongoing platelet consumption and high-titer anti-HLA class I antibodies should be considered. The latter requires transfusion of HLA-compatible platelet concentrates.

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Sepsis-associated thrombocytopenia

Cited by 60 publications

References 67 publications

The involvement of regulatory non-coding RNAs in sepsis: a systematic review

The involvement of regulatory non-coding RNAs in sepsis: a systematic review

Thrombocytopenia in the Intensive Care Unit

How I evaluate and treat thrombocytopenia in the intensive care unit patient

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