Biosensor-Based Point-of-Care Devices: Metabolites and Pulse Oximetry

Author(s):  
Inga M. Hwang ◽  
Xuwen A. Lou ◽  
Adam A. Toubian ◽  
Daniel T. Kamei
Keyword(s):  
Author(s):  
Herbert G. Masigati ◽  
Grant W. Potter ◽  
Masahiro J. Morikawa ◽  
Rashid S. Mfaume

Background: Rural hospitals in sub-Saharan Africa suffer from numerous disparities in resources and practices, and subsequently patient care is affected.Methods: In order to assess current practices and opportunities for improvement in pulse oximetry use and patient-care handoffs, a cross-sectional survey was administered to clinicians at a referral level hospital serving a large rural area in Shinyanga, Tanzania.Results: Respondents (n=46) included nurses (50%), medical doctors (48%), and clinical officers (2%). A response rate of 92% was achieved, and 81% of clinicians acknowledged routine difficulties in the use of current devices when obtaining pulse oximetry. Although 83% of respondents reported using a written handoff at shift change, information reporting was inconsistent and rarely included specific management guidance.Conclusions: Further research is needed to elucidate handoff practices in developing settings, but there is a large opportunity for novel point-of-care devices and tools to improve both pulse oximetry use and patient care handoffs in rural Africa.


2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Koichiro Shinozaki ◽  
Lee S. Jacobson ◽  
Kota Saeki ◽  
Hideaki Hirahara ◽  
Naoki Kobayashi ◽  
...  

Abstract Background Traditional capillary refill time (CRT) is a manual measurement that is commonly used by clinicians to identify deterioration in peripheral perfusion status. Our study compared a novel method of measuring peripheral perfusion using an investigational device with standardized visual CRT and tested the clinical usefulness of this investigational device, using an existing pulse oximetry sensor, in an emergency department (ED) setting. Material and methods An ED attending physician quantitatively measured CRT using a chronometer (standardized visual CRT). The pulse oximetry sensor was attached to the same hand. Values obtained using the device are referred to as blood refill time (BRT). These techniques were compared in its numbers with the Bland-Altman plot and the predictability of patients’ admissions. Results Thirty ED patients were recruited. Mean CRT of ED patients was 1.9 ± 0.8 s, and there was a strong correlation with BRT (r = 0.723, p < 0.001). The Bland-Altman plot showed a proportional bias pattern. The ED physician identified 3 patients with abnormal CRT (> 3 s). Area under the receiver operator characteristic curve (AUC) of BRT to predict whether or not CRT was greater than 3 s was 0.82 (95% CI, 0.58–1.00). Intra-rater reliability of BRT was 0.88 (95% CI, 0.79–0.94) and that of CRT was 0.92 (0.85–0.96). Twelve patients were admitted to the hospital. AUC to predict patients’ admissions was 0.67 (95% CI, 0.46–0.87) by BRT and 0.76 (0.58–0.94) by CRT. Conclusions BRT by a pulse oximetry sensor was an objective measurement as useful as the standardized CRT measured by the trained examiner with a chronometer at the bedside.


VASA ◽  
2011 ◽  
Vol 40 (6) ◽  
pp. 429-438 ◽  
Author(s):  
Berent ◽  
Sinzinger

Based upon various platelet function tests and the fact that patients experience vascular events despite taking acetylsalicylic acid (ASA or aspirin), it has been suggested that patients may become resistant to the action of this pharmacological compound. However, the term “aspirin resistance” was created almost two decades ago but is still not defined. Platelet function tests are not standardized, providing conflicting information and cut-off values are arbitrarily set. Intertest comparison reveals low agreement. Even point of care tests have been introduced before appropriate validation. Inflammation may activate platelets, co-medication(s) may interfere significantly with aspirin action on platelets. Platelet function and Cox-inhibition are only some of the effects of aspirin on haemostatic regulation. One single test is not reliable to identify an altered response. Therefore, it may be more appropriate to speak about “treatment failure” to aspirin therapy than using the term “aspirin resistance”. There is no evidence based justification from either the laboratory or the clinical point of view for platelet function testing in patients taking aspirin as well as from an economic standpoint. Until evidence based data from controlled studies will be available the term “aspirin resistance” should not be further used. A more robust monitoring of factors resulting in cardiovascular events such as inflammation is recommended.


2018 ◽  
Vol 23 (11) ◽  
pp. 38-41
Author(s):  
Sebastian Krolop ◽  
Florian Benthin ◽  
Constanze Knahl

Cloud-Computing gewinnt auch in Kliniken zunehmend an Bedeutung. Über das Internet bereitgestellte Lösungen verändern nicht nur Verwaltung und Logistik – im klinischen Bereich geht es zum Beispiel um die Nutzung elektronischer Patientenakten am Point-of-Care.


2003 ◽  
Vol 23 (04) ◽  
pp. 181-185 ◽  
Author(s):  
H. Patscheke
Keyword(s):  

ZusammenfassungUnabhängig von ihrem Wirkungsmechanismus greifen Antikoagulanzien stets unmittelbar in die Bildung und Wirkung von Thrombin und damit die Endstrecke der Gerinnung ein. Von den Aggregationshemmern hemmen nur die GPIIb/IIIa-Antagonisten die gemeinsame Endstrecke der Plättchenaggregation, indem sie die Bildung von Fibrinogen/von-Willebrand-Faktor-vermittelten Plättchen-Plättchen-Brücken hemmen.Azetylsalizylsäure (ASS), NSARs, Clopidogrel oder Ticlopidin begrenzen die Plättchenaktivierung dagegen, indem sie die Bildung bzw. Wirkung der sekundären Plättchenagonisten Thromboxan A2 bzw. ADP ausschalten, aber z. B. die durch Thrombin direkt induzierbare Plättchenaggregation nicht. Deshalb rufen ASS, Clopidogrel oder Ticlopidin allein kein wesentliches Blutungsrisiko hevor, wenn nicht weitere, die Hämostase beeinträchtigende Faktoren (z.B. ausgeprägte Thrombozytopenie, Antikoagulation) vorliegen. Deshalb entfällt für diese Hemmstoffe auch die Notwendigkeit der Therapiekontrolle. Beim therapeutischen Einsatz von ASS als Aggregationshemmer ist vielmehr die Dosierung darauf abzustellen, eine vollständige Blockade (mind. 90%) der Thromboxanbiosynthese in den Plättchen zu erreichen, um überhaupt einen therapeutischen bzw. prophylaktischen Effekt zu erzielen.Von den GPIIb/IIIa-Antagonisten sind nur die parenteral eingesetzten (Abciximab, Eptifibatid, Tirofiban) zugelassen. Orale GPIIb/IIIa-Antagonisten zeigten bisher in klinischen Studien ein erhöhtes Blutungsrisiko bei nicht ausreichendem therapeutischen Nutzen. Die meisten GPIIb/IIIa-Antagonisten verursachen eine leichte Thrombozytopenie, als deren Auslöser die Inhibitor-Rezeptor-Wechselwirkung bzw. immunologische Mechanismen diskutiert werden. Für das spezifische Monitoring dieser potenten Aggregationshemmer ist ein »Point-of-Care«-Testsystem verfügbar. Für die Einschätzung des Blutungsrisikos müssen jedoch stets alle, die Hämostase beeinflussende Faktoren berücksichtigt werden. Das gilt insbesondere, wenn neben GPIIb/IIIa-Antagonisten Heparin u.a. Wirkstoffe eingesetzt werden.


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