Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (627 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Bleeding Times; Time, Bleeding; Times, Bleeding; Template Bleeding Time; Bleeding Time, Template; Bleeding Times, Template; Template Bleeding Times; Times, Template Bleeding.
Where it fits in the MeSH classification
- Broader topics
- Platelet Function Tests; Blood Physiological Phenomena
- See also
- Platelet Activation
Research landscape
PubMed indexes 2,788 records tagged with the MeSH heading “Bleeding Time” (counts retrieved 2026-10-31). 55 of them (2.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,784 records.
Reviews account for 189 records (6.8%) and meta-analyses for 4. Randomized controlled trials number 245 (8.8%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,784 |
| 2000-2009 | 622 |
| 2010-2019 | 327 |
| 2020 onward | 55 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 189 | 6.8% |
| Meta-analyses | 4 | 0.1% |
| Randomized controlled trials | 245 | 8.8% |
Method: PubMed query "Bleeding Time"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| A microengineered vascularized bleeding model that integrates the principal components of hemostasis | 2018 | Research article Design not recorded in structured metadata | 82 | cc by PMID 29410404 · DOI · PMC5802762 |
| Pathophysiological classification of chronic rhinosinusitis | 2005 | Research article Design not recorded in structured metadata | 22 | cc by PMID 16364180 · DOI · PMC1343550 |
| Association of the bleeding time test with aspects of traumatic brain injury in patients with alcohol use disorder | 2020 | Research article Design not recorded in structured metadata | 4 | cc by PMID 32424564 · DOI · PMC7232602 |
A microengineered vascularized bleeding model that integrates the principal components of hemostasis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Hemostasis encompasses an ensemble of interactions among platelets, coagulation factors, blood cells, endothelium, and hemodynamic forces, but current assays assess only isolated aspects of this complex process.
- Closing excerpt
- These results establish the versatility and clinical utility of our microfluidic bleeding model.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
Hemostasis encompasses an ensemble of interactions among platelets, coagulation factors, blood cells, endothelium, and hemodynamic forces, but current assays assess only isolated aspects of this complex process. Accordingly, here we develop a comprehensive in vitro mechanical injury bleeding model comprising an "endothelialized" microfluidic system coupled with a microengineered pneumatic valve that induces a vascular "injury". With perfusion of whole blood, hemostatic plug formation is visualized and "in vitro bleeding time" is measured. We investigate the interaction of different components of hemostasis, gaining insight into several unresolved hematologic issues. Specifically, we visualize and quantitatively demonstrate: the effect of anti-platelet agent on clot contraction and hemostatic plug formation, that von Willebrand factor is essential for hemostasis at high shear, that hemophilia A blood confers unstable hemostatic plug formation and altered fibrin architecture, and the importance of endothelial phosphatidylserine in hemostasis. These results establish the versatility and clinical utility of our microfluidic bleeding model.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29410404 · DOI · PMC5802762
Pathophysiological classification of chronic rhinosinusitis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundRecent consensus statements demonstrate the breadth of the chronic rhinosinusitis (CRS) differential diagnosis.
- Closing excerpt
- We predict that future clinical studies and treatment decisions will be more logical when these interactive disease mechanisms are used to stratify CRS patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (182 words)
BackgroundRecent consensus statements demonstrate the breadth of the chronic rhinosinusitis (CRS) differential diagnosis. However, the classification and mechanisms of different CRS phenotypes remains problematic.MethodStatistical patterns of subjective and objective findings were assessed by retrospective chart review.ResultsCRS patients were readily divided into those with (50/99) and without (49/99) polyposis. Aspirin sensitivity was limited to 17/50 polyp subjects. They had peripheral blood eosinophilia and small airways obstruction. Allergy skin tests were positive in 71% of the remaining polyp subjects. IgE wasConclusionCRS subjects were retrospectively classified in to 4 categories using the algorithm of (1) polyp vs. nonpolyp disease, (2) aspirin sensitivity in polyposis, and (3) sinus mucosal thickening vs. nasal osteomeatal disease (CT scan extent of disease) for nonpolypoid subjects. We propose that the pathogenic mechanisms responsible for polyposis, aspirin sensitivity, humoral immunodeficiency, glandular hypertrophy, eosinophilia and atopy are primary mechanisms underlying these CRS phenotypes. The influence of microbial disease and other factors remain to be examined in this framework. We predict that future clinical studies and treatment decisions will be more logical when these interactive disease mechanisms are used to stratify CRS patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 16364180 · DOI · PMC1343550
Association of the bleeding time test with aspects of traumatic brain injury in patients with alcohol use disorder [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Background-aimTraumatic brain injury (TBI) and alcohol use disorder (AUD) can occur concomitantly and be associated with coagulopathy that influences TBI outcome.
- Closing excerpt
- Therefore, the bleeding time test should only be used in combination with the patient's bleeding history and careful assessment of other hematologic parameters.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (294 words)
Background-aimTraumatic brain injury (TBI) and alcohol use disorder (AUD) can occur concomitantly and be associated with coagulopathy that influences TBI outcome. The use of bleeding time tests in TBI management is controversial. We hypothesized that in TBI patients with AUD, a prolonged bleeding time is associated with more severe injury and poor outcome.Material and methodsModerate and severe TBI patients with evidence of AUD were examined with bleeding time according to IVY bleeding time on admission during neurointensive care. Baseline clinical and radiological characteristics were recorded. A standardized IVY bleeding time test was determined by staff trained in the procedure. Bleeding time test results were divided into normal (≤ 600 s), prolonged (> 600 s), and markedly prolonged (≥ 900 s). Normal platelet count (PLT) was defined as > 150,000/μL. This cohort was compared with another group of TBI patients without evidence of AUD.ResultsFifty-two patients with TBI and AUD were identified, and 121 TBI patients without any history of AUD were used as controls. PLT was low in 44.2% and bleeding time was prolonged in 69.2% of patients. Bleeding time values negatively correlated with PLT (p 0.05). Subjects with TBI and no evidence for AUD had lower bleeding time values and higher platelet count compared with those with TBI and history of AUD (p ConclusionsAlthough differences in the bleeding time values between TBI cohorts exist and prolonged values may be seen even in patients with normal platelet count, the bleeding test is a marker of primary hemostasis and platelet function with low specificity. However, it may provide an additional assessment in the interpretation of the overall status of TBI patients with AUD. Therefore, the bleeding time test should only be used in combination with the patient's bleeding history and careful assessment of other hematologic parameters.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32424564 · DOI · PMC7232602
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article A critical reappraisal of the bleeding time [4]
- Research article How to interpret and pursue an abnormal prothrombin time, activated partial thromboplastin time, and bleeding time in adults [5]
- Research article The bleeding time does not predict surgical bleeding [6]
- Research article Mouse models of hemostasis [7]
- Research article Prolonged bleeding time [8]
- Research article Bleeding time. A guide to its diagnostic and clinical utility [9]
References
- Sakurai Y, Hardy ET, Ahn B, Tran R, Fay ME, Ciciliano JC, et al.. A microengineered vascularized bleeding model that integrates the principal components of hemostasis. . 2018. PMID 29410404 · DOI · PMC5802762
- Baraniuk JN, Maibach H. Pathophysiological classification of chronic rhinosinusitis. . 2005. PMID 16364180 · DOI · PMC1343550
- Tsitsopoulos PP, Marklund N, Rostami E, Enblad P, Hillered L. Association of the bleeding time test with aspects of traumatic brain injury in patients with alcohol use disorder. . 2020. PMID 32424564 · DOI · PMC7232602
- Rodgers RP, Levin J. A critical reappraisal of the bleeding time. Semin Thromb Hemost. 1990. PMID 2406907 · DOI
- Kamal AH, Tefferi A, Pruthi RK. How to interpret and pursue an abnormal prothrombin time, activated partial thromboplastin time, and bleeding time in adults. Mayo Clin Proc. 2007. PMID 17605969 · DOI
- Lind SE. The bleeding time does not predict surgical bleeding. Blood. 1991. PMID 2043759 · DOI
- Mohammed BM, Monroe DM, Gailani D. Mouse models of hemostasis. Platelets. 2020. PMID 31992118 · DOI · PMC7244364
- Lind SE. Prolonged bleeding time. Am J Med. 1984. PMID 6431815 · DOI
- Burns ER, Lawrence C. Bleeding time. A guide to its diagnostic and clinical utility. Arch Pathol Lab Med. 1989. PMID 2535679
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.