Abstract
Infections cause varying degrees of haemostatic dysfunction which can be detected by clot waveform analysis (CWA), a global haemostatic marker. CWA has been shown to predict poor outcomes in severe infections with disseminated intravascular coagulopathy. The effect of less severe bacterial and viral infections on CWA has not been established. We hypothesized that different infections influence CWA distinctively. Patients admitted with bacterial infections, dengue and upper respiratory tract viral infections were recruited if they had an activated partial thromboplastin time (aPTT) measured on admission. APTT-based CWA was performed on Sysmex CS2100i automated analyser using Dade Actin FSL reagent. CWA parameters [(maximum velocity (min1), maximum acceleration (min2) and maximum deceleration (max2)] were compared against control patients. Infected patients (n = 101) had longer aPTT than controls (n = 112) (34.37 ± 7.72 s vs 27.80 ± 1.59 s, p < 0.001), with the mean (± SD) aPTT longest in dengue infection (n = 36) (37.99 ± 7.93 s), followed by bacterial infection (n = 52) (33.96 ± 7.33 s) and respiratory viral infection (n = 13) (29.98 ± 3.92 s). Compared to controls (min1; min2; max2) (5.53 ± 1.16%/s; 0.89 ± 0.19%/s2; 0.74 ± 0.16%/s2), bacterial infection has higher CWA results (6.92 ± 1.60%/s; 1.04 ± 0.28%/s2; 0.82 ± 0.24%/s2, all p < 0.05); dengue infection has significantly lower CWA values (3.93 ± 1.32%/s; 0.57 ± 0.17%/s2; 0.43 ± 0.14%/s2, all p < 0.001) whilst respiratory virus infection has similar results (6.19 ± 1.32%/s; 0.95 ± 0.21%/s2; 0.73 ± 0.18%/s2, all p > 0.05). CWA parameters demonstrated positive correlation with C-reactive protein levels (min1: r = 0.54, min2: r = 0.44, max2: r = 0.34; all p < 0.01). Different infections affect CWA distinctively. CWA could provide information on the haemostatic milieu triggered by infection and further studies are needed to better define its application in this area.
Highlights
Infections, with or without sepsis can cause varying degrees of haemostatic dysfunction ranging from subclinical coagulopathy to disseminated intravascular coagulation (DIC) through several mechanisms
Our study has reaffirmed the notion that infections can cause significant changes to haemostatic mechanisms even in the absence of DIC and these alterations could be detected by Clot waveform analysis (CWA)
Previous studies on CWA have mainly focused on the biphasic waveform which is observed in patients with sepsis and is a marker of early DIC18,19
Summary
Infections, with or without sepsis can cause varying degrees of haemostatic dysfunction ranging from subclinical coagulopathy to disseminated intravascular coagulation (DIC) through several mechanisms. CWA is touted to be a global haemostatic assay, reflecting the overall effects of all the haemostatic factors[9] It provides additional information on the coagulation processes while measuring the PT and aPTT and can be conveniently obtained using special software in coagulation analyzers. The biphasic waveform detected in CWA has been studied extensively in the setting of DIC arising from different causes including infection. This biphasic waveform is caused by the formation of calcium-dependent precipitates of very low-density lipoprotein and C-reactive protein (CRP) upon recalcification of plasma in vitro[10]. The relationship between CWA and existing biological markers in infections (CRP and procalcitonin) was explored
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