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	<title>internal jugular vein &#8211; Science</title>
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	<title>internal jugular vein &#8211; Science</title>
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		<title>Digital Twin Turns Vein Compression Into a Physics-Based Clot Detector</title>
		<link>https://scienmag.com/digital-twin-turns-vein-compression-into-a-physics-based-clot-detector/</link>
		
		<dc:creator><![CDATA[Katie Riggs]]></dc:creator>
		<pubDate>Thu, 01 Oct 2026 11:25:09 +0000</pubDate>
				<category><![CDATA[Medicine]]></category>
		<category><![CDATA[automated thrombosis diagnosis]]></category>
		<category><![CDATA[biomechanics]]></category>
		<category><![CDATA[biomechanics of vein compression]]></category>
		<category><![CDATA[biomedical engineering]]></category>
		<category><![CDATA[compression ultrasound]]></category>
		<category><![CDATA[computational biomechanics]]></category>
		<category><![CDATA[deep vein thrombosis]]></category>
		<category><![CDATA[digital twin]]></category>
		<category><![CDATA[Digital twin in vein compression]]></category>
		<category><![CDATA[European Space Agency biomedical research]]></category>
		<category><![CDATA[finite-element modelling]]></category>
		<category><![CDATA[force sensing]]></category>
		<category><![CDATA[force–area digital twin technology]]></category>
		<category><![CDATA[image-guided vascular diagnostics]]></category>
		<category><![CDATA[internal jugular vein]]></category>
		<category><![CDATA[medical simulation with digital twins]]></category>
		<category><![CDATA[non-invasive clot detection methods]]></category>
		<category><![CDATA[physics-based clot detection]]></category>
		<category><![CDATA[quantitative vein assessment]]></category>
		<category><![CDATA[Space medicine]]></category>
		<category><![CDATA[ultrasonography]]></category>
		<category><![CDATA[ultrasound imaging for deep vein thrombosis]]></category>
		<category><![CDATA[vein collapse analysis]]></category>
		<category><![CDATA[venous thrombosis]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=222338</guid>

					<description><![CDATA[Researchers have combined force-sensing ultrasound probes with a finite-element digital twin of the internal jugular vein to show that clot presence, stiffness and location leave distinct, quantifiable signatures in the vein's compression response.]]></description>
										<content:encoded><![CDATA[<p>For more than three decades, the diagnosis of deep vein thrombosis has rested on a deceptively simple question: does the vein collapse when the sonographer presses on it? Compression ultrasound, introduced in the late 1980s, remains the first-line test for a condition that affects an estimated ten million people each year and ranks as the third most common cardiovascular disease after heart attack and stroke. Yet the examination is fundamentally binary and subjective. The examiner applies an unmeasured, uncontrolled force with the ultrasound probe, watches the vein on the screen, and judges whether the lumen closes. A vein that fails to compress is labelled thrombosed; everything else is considered healthy. A new study published in Annals of Biomedical Engineering argues that this yes-or-no answer discards a wealth of mechanical information hiding in plain sight, and it proposes a way to capture it.</p>
<p>Researchers led by Janez Urevc of the University of Ljubljana, working with colleagues at the Medical University of Graz and supported by the European Space Agency, have built what they call a force–area digital twin of the internal jugular vein. The idea is to record, simultaneously and quantitatively, the force the probe exerts on the neck and the cross-sectional area of the vein visible in the B-mode ultrasound image. The resulting force–area curve is not merely a picture of collapse; it is a mechanical fingerprint of the vein–tissue system, one whose slope and shape change systematically depending on what is inside the vessel. By pairing real measurements with a physics-based computational model, the team has shown, in silico, that healthy veins, partially obstructed veins and fully occluded veins each leave distinct signatures in this curve.</p>
<p>The experimental half of the work relied on a custom-built force-sensing attachment mounted on a standard linear ultrasound transducer. Three load cells inside a rigid housing stream force data at roughly 100 hertz while the Philips CX50 system acquires images at 30 frames per second. Nine healthy adults underwent supine imaging of the internal jugular vein, with an experienced cardiovascular physician performing three slow compressions per recording, from minimal contact through full lumen closure and back. After rigorous quality control, which excluded six of seventeen recordings due to load-cell artefacts, alignment failures or unusable cycles, the team retained 34 compression cycles from eight subjects. Manual segmentation of the vein lumen in every frame, smoothed with a Savitzky–Golay filter, yielded the area trace that was paired with the force signal.</p>
<p>The measured response had a characteristic concave shape: at large vein areas the probe force stayed low, but as the vein approached collapse the force rose steeply. Fitting a straight line over the active compression regime, defined as forces above 0.2 newtons, gave a cohort reference slope of 0.148 plus or minus 0.113 newtons per square millimetre. That large spread, with a standard deviation equal to 76 percent of the mean, underscores how much inter-subject variability even healthy necks contain, and it foreshadows one of the study&#8217;s central challenges: how to compare a single representative computer model against a scattered population of real anatomies.</p>
<p>The digital twin itself is a finite-element model built in Abaqus, representing the principal load-bearing structures between the probe and the vertebral body: the internal jugular vein and carotid artery as thin pressurised shells, the sternocleidomastoid muscle and surrounding connective tissue as continuum blocks, and the probe as a rigid body pressing from above. Geometry came from cohort mean anatomical landmarks, including wall depths, vein diameter and the artery–vein centre distance, while the stress-free collapsed reference configuration was extrapolated from head-up tilt recordings in which progressively reducing venous pressure drives the vein toward collapse. Three unknown material parameters, the vein wall modulus and the effective stiffnesses of muscle and subvenous tissue, were identified by an inverse procedure that jointly matched the cohort mean closure force, indentation depth and anatomical landmarks, reproducing every target within roughly fifteen percent.</p>
<p>With the healthy model validated against experiment, the team turned to the question that motivates the whole framework: what does a thrombus do to the compression curve? Clots were modelled as isotropic linear-elastic bodies inserted into the already pressurised vein, ensuring that all simulated cases started from an identical pre-stressed baseline so that differences arose purely from the thrombus itself. Fully occlusive configurations spanned three lengths of two, four and eight centimetres and three stiffness levels of five, thirty and one hundred kilopascals, reflecting the reported mechanical range of venous thrombi. Partial, non-occlusive clots occupying about ten or fifty percent of the lumen were attached to either the lateral or the inferior wall, yielding seventeen thrombotic configurations in total.</p>
<p>The results were striking. Fully occlusive thrombi produced force–area slopes between roughly 2.5 and 14.7 times steeper than the healthy reference of 0.038 newtons per square millimetre, with thrombus stiffness, not length, acting as the dominant driver. Partial occlusions produced intermediate responses, with fifty percent obstructions approaching the fully thrombotic regime and ten percent obstructions shifting measurably toward greater mechanical resistance even though such veins would still appear compressible under conventional binary assessment. Crucially, the dimensionless version of the slope, which normalises both force and area and thereby removes the influence of anatomy and absolute scale, agreed closely between simulation and experiment: minus 0.81 for the model versus minus 0.86 plus or minus 0.33 for the cohort. That agreement indicates the digital twin captures the underlying shape of the compression response, even though the dimensional slope differed by a factor of about four, a gap the authors attribute to population variability, model simplifications and the intrinsically nonlinear experimental data.</p>
<p>The study also introduced a second, complementary indicator derived from the geometry of collapse. By computing the eigenvalues of the covariance matrix of the vein contour at each simulation step, the researchers defined an aspect ratio change that quantifies how strongly the lumen departs from its initial shape toward a flattened, slit-like geometry. Healthy veins produced large aspect ratio changes as they collapsed, while fully occlusive thrombi confined the response to a narrow low-deformation regime. Partial thrombi generated intermediate and asymmetric patterns, and, notably, the simulations distinguished between clots attached to the inferior wall and those on the lateral wall, information the slope alone could not provide. In one soft, small lateral configuration the slope stayed near the healthy value while the deformation trajectory remained clearly distinct, demonstrating exactly why the two indicators work best together: the slope measures how strongly the vein resists compression, the aspect ratio change measures how the lumen deforms as it yields.</p>
<p>The authors are careful to frame the work as a mechanistic proof of concept rather than a validated diagnostic tool. No patients with confirmed thrombosis were scanned, the reported indicator values are configuration-specific rather than diagnostic thresholds, and the thrombus model, while appropriate for quasi-static loading given published loss tangents of only 0.02 to 0.1, deliberately ignores viscoelasticity and nonlinear behaviour that emerges at strains near seventy percent. Intraluminal pressure was prescribed rather than measured, force and ultrasound streams were synchronised post hoc, and the cohort of nine subjects cannot establish population-level reference distributions. Clinical translation, the team writes, will require tissue-mimicking phantom studies followed by prospective trials in patients, ideally exploiting the natural within-subject control offered by unilateral jugular thrombosis.</p>
<p>Even so, the implications reach well beyond the laboratory. In space medicine, where microgravity distends the internal jugular vein, promotes blood stasis and has already produced one confirmed in-flight thrombosis in 2019, autonomous and objective diagnostics are essential because real-time teleguidance is unavailable on deep-space missions. A sensorised probe that reports continuous biomechanical indicators, potentially accelerated by reduced-order surrogates of the digital twin for near-real-time inference, could flag abnormal compression behaviour before complete occlusion develops. The framework is also not vein-specific: adapting it to the femoral or popliteal veins for standard deep vein thrombosis screening would require site-specific geometry and tissue representation but no change to the underlying method. By transforming a subjective visual judgement into a physics-informed biomechanical measurement, this work moves quantitative compression ultrasound from empirical observation toward a genuinely mechanistic biomarker, one in which learned image features can eventually be constrained by known biomechanics rather than treated as opaque outputs of a black box.</p>
<p><strong>Subject of Research:</strong> Quantitative compression ultrasound using a force–area digital twin to assess venous thrombosis biomechanics</p>
<p><strong>Article Title:</strong> Quantitative Compression Ultrasound via a Force–Area Digital Twin for Mechanistic Assessment of Venous Thrombosis</p>
<p><strong>Article References:</strong> Urevc, J., Kovšca, D., Maček, A., Halilovič, M., Goswami, N., &amp; Bergauer, A. (2026). Quantitative Compression Ultrasound via a Force–Area Digital Twin for Mechanistic Assessment of Venous Thrombosis. <em>Annals of Biomedical Engineering</em>. <a href="https://doi.org/10.1007/s10439-026-04362-9" rel="noopener noreferrer">https://doi.org/10.1007/s10439-026-04362-9</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.1007/s10439-026-04362-9" rel="noopener noreferrer">10.1007/s10439-026-04362-9</a></p>
<p><strong>Keywords:</strong> compression ultrasound, venous thrombosis, internal jugular vein, digital twin, finite-element modelling, biomechanics, deep vein thrombosis, force sensing, space medicine, computational biomechanics, ultrasonography, biomedical engineering</p>
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		<post-id xmlns="com-wordpress:feed-additions:1">222338</post-id>	</item>
		<item>
		<title>Massive Dialysis Study Reveals Why Catheters Fail Mid-Treatment</title>
		<link>https://scienmag.com/massive-dialysis-study-reveals-why-catheters-fail-mid-treatment/</link>
		
		<dc:creator><![CDATA[Jerry Hayes]]></dc:creator>
		<pubDate>Wed, 23 Sep 2026 23:49:30 +0000</pubDate>
				<category><![CDATA[Medicine]]></category>
		<category><![CDATA[anticoagulation]]></category>
		<category><![CDATA[antiplatelet therapy]]></category>
		<category><![CDATA[blood flow issues during dialysis]]></category>
		<category><![CDATA[catheter dysfunction]]></category>
		<category><![CDATA[catheter dysfunction risk factors]]></category>
		<category><![CDATA[central venous catheter]]></category>
		<category><![CDATA[central venous catheter analysis]]></category>
		<category><![CDATA[dialysis adequacy]]></category>
		<category><![CDATA[dialysis catheter failure]]></category>
		<category><![CDATA[dialysis device failure prevention]]></category>
		<category><![CDATA[dialysis session analysis]]></category>
		<category><![CDATA[dialysis treatment efficacy]]></category>
		<category><![CDATA[haemodialysis]]></category>
		<category><![CDATA[haemodialysis treatment complications]]></category>
		<category><![CDATA[internal jugular vein]]></category>
		<category><![CDATA[intradialytic complications]]></category>
		<category><![CDATA[Kt]]></category>
		<category><![CDATA[large-scale dialysis studies]]></category>
		<category><![CDATA[nephrology]]></category>
		<category><![CDATA[nursing]]></category>
		<category><![CDATA[retrospective study]]></category>
		<category><![CDATA[Spanish renal care research]]></category>
		<category><![CDATA[tunnelled catheter performance]]></category>
		<category><![CDATA[vascular access]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=211342</guid>

					<description><![CDATA[A session-level analysis of over 40,000 haemodialysis treatments in Spain identifies the clinical, anatomical, and technical factors linked to tunnelled catheter dysfunction and reduced dialysis efficacy.]]></description>
										<content:encoded><![CDATA[<p>For hundreds of thousands of people whose kidneys no longer work, haemodialysis is a lifeline that runs on a surprisingly fragile piece of plumbing: a tunnelled central venous catheter threaded into a large vein and used hundreds of times a year to shuttle blood through a dialysis machine. When that lifeline falters, the consequences cascade quickly. Blood flow drops, toxins linger in the body, dialysis sessions become less effective, and hospital visits multiply. Now one of the largest session-by-session analyses of this problem to date, drawing on more than 40,000 individual dialysis treatments across 15 Spanish centres, has mapped in unprecedented detail which clinical and technical factors travel alongside catheter dysfunction, offering clinicians a data-driven picture of when and why these devices fail.</p>
<p>The research, published in the open-access journal Nursing Open, took an unusual analytical approach: instead of studying patients as single units, the investigators examined every recorded haemodialysis session over a full year, from January to December 2021, in patients treated through tunnelled catheters within a national renal foundation network in Spain. The result was a dataset of 40,193 sessions from 743 patients, of which 987 sessions, or 2.5 percent, met the study&#8217;s operational definition of intradialytic catheter dysfunction. That definition was grounded in internationally recognised KDOQI thresholds: a machine-registered dysfunction flag appeared whenever blood flow fell below 300 millilitres per minute while arterial pre-pump pressure dropped below minus 250 millimetres of mercury, venous return pressure rose above plus 250 millimetres of mercury, or both, at the start of the session or at the 60-minute mark. Nursing staff then verified each flagged event in the electronic dialysis record system.</p>
<p>The cohort itself was clinically striking. The patients averaged 68.4 years of age and carried a heavy burden of chronic disease: 84.5 percent had arterial hypertension, 60.1 percent had cardiovascular disease, and nearly half lived with diabetes. Diabetic nephropathy was the leading cause of kidney failure, accounting for 34.3 percent of cases. Notably, women made up 63.7 percent of the cohort, a marked contrast with national registry data in which men typically account for roughly two-thirds of the haemodialysis population, a difference the authors attribute to the particular clinical profile of patients who end up dialysing through tunnelled catheters rather than through surgically created arteriovenous fistulas.</p>
<p>When the researchers compared dysfunctional sessions with smooth-running ones, the haemodynamic signatures diverged sharply, exactly as the outcome definition would predict. Sessions with dysfunction began with a mean blood flow of 257.9 millilitres per minute versus 350.7 in healthy sessions, and by the 60-minute mark the gap persisted, with flows of 256 versus 358.3. Arterial pressures plunged dramatically deeper into negative territory, averaging minus 215.2 millimetres of mercury across dysfunctional sessions compared with minus 172.2 in uneventful ones. Total blood volume processed fell from 75.6 litres to 56.2, and the final Kt, the routinely recorded marker of the dialysis dose actually delivered, dropped from 48.2 litres to 39.1. In plain terms, a failing catheter deprived patients of nearly a fifth of the intended cleansing capacity of each session.</p>
<p>Beyond the intradialytic pressure readings themselves, which the authors are careful to frame as manifestations of dysfunction rather than causes of it, the analysis identified baseline characteristics that clustered with failing sessions. Catheters placed in the left internal jugular vein showed a dysfunction rate of 5.1 percent, dramatically higher than the 0.7 percent observed with the right internal jugular vein, the most popular insertion site in the cohort. Femoral placement, though rare, performed poorly, with the right femoral vein showing dysfunction in 6.3 percent of sessions, consistent with earlier evidence that femoral and subclavian sites carry higher thrombotic and mechanical risks. Comorbidities also left fingerprints: diabetes, cardiopathy, peripheral arterial disease, prior stroke, and a history of malignancy were all significantly more frequent in dysfunctional sessions, as was systemic anticoagulant therapy, though the authors caution this may reflect the vascular risk profile of the patients rather than a drug effect.</p>
<p>Perhaps the most technically revealing part of the study was its stratification of dysfunction events into arterial and venous types. Of the 1,481 recorded events, 1,346 were arterial and 135 were venous, and the two behaved like distinct clinical entities. Arterial events featured severely negative pre-pump pressures, averaging minus 221.9 millimetres of mercury, signalling that the catheter was struggling to draw blood in, and were more common in older patients with hypertension, cerebrovascular disease, and prior SARS-CoV-2 infection. Venous events, by contrast, showed soaring return pressures averaging 220.4 millimetres of mercury, indicating obstruction on the outflow side, and occurred disproportionately in men, in patients with peripheral arterial disease, tumours, previous kidney transplants, and those on anticoagulants. Venous events also produced significantly lower final Kt values, suggesting the outflow type of failure may be particularly punishing for dialysis adequacy.</p>
<p>Two management variables, line reversal and 5 percent sodium heparin locking solution, appeared far more often in dysfunctional sessions, with line reversal documented in 3.5 percent of sessions without dysfunction versus an elevated share within dysfunctional ones, and 5 percent heparin locks showing a 4.3 percent dysfunction rate against 2 percent for the standard 1 percent heparin. But the researchers explicitly warn against reading these numbers causally. In routine practice, clinicians reverse catheter lines and escalate locking solutions precisely because a catheter is already underperforming, so the association plausibly reflects a rescue response rather than a culprit. This principle of reverse causality and confounding by indication permeates the entire analysis and is one of the paper&#8217;s most intellectually honest contributions to a field where such distinctions are often blurred.</p>
<p>The pharmacological findings followed the same cautious logic. Overall, systemic antiplatelet therapy showed no significant association with dysfunction when analysed as a single binary variable, yet drug-specific comparisons revealed significant heterogeneity, with acetylsalicylic acid regimens, clopidogrel, prasugrel, and dipyridamole each showing different dysfunction frequencies. Among anticoagulants, enoxaparin and especially tinzaparin were the agents most frequently associated with dysfunction events, while combined regimens such as enoxaparin with warfarin appeared far less often in failing sessions. The authors interpret these patterns as exploratory and hypothesis-generating, likely shaped by differences in patient indication and underlying vascular disease rather than by direct pharmacological effects on catheter patency, and they point to prior trials of agents like recombinant tissue plasminogen activator and taurolidine-based locks as avenues where randomised evidence has begun to clarify what observational data cannot.</p>
<p>Dialysis efficacy emerged as a second major storyline. Using sex-specific operational Kt thresholds, the researchers classified 24.7 percent of sessions as low efficacy, 20.8 percent as normal, and 52.6 percent as optimal. The sex split was dramatic: 41.4 percent of male patients&#8217; sessions fell into the low-Kt category, while 65.6 percent of women&#8217;s sessions reached the optimal range, a highly significant difference partly attributable to the fact that Kt depends on body size, and men on average process more blood volume through larger bodies. Because Kt was measured session-by-session through ionic dialysance rather than sampled sporadically, the study demonstrates how continuous, per-session adequacy monitoring can flag patients at risk of chronic under-dialysis, particularly catheter-dependent men, long before cumulative toxin buildup becomes clinically apparent.</p>
<p>The study&#8217;s limitations are considerable and openly acknowledged. The analysis was univariate and did not adjust for the fact that dozens of sessions belonged to the same patient, which may have inflated statistical significance. Being retrospective and built on routine electronic records, it could not capture insertion technique, operator experience, catheter tip design or position, or fibrin sheath formation, all recognised determinants of catheter survival, and all data came from a single institutional network, limiting generalisability. Still, the practical message is clear and actionable: continuous vigilance over blood flows, line pressures, and pressure trajectories during every dialysis session can catch failing catheters early, and the distinct arterial-versus-venous signatures described here give nurses and nephrologists a framework for interpreting what the machine alarms are actually telling them. The authors call for adjusted analytical studies, trials of locking strategies and anticoagulation protocols, and exploration of nursing-led interventions, all aimed at turning a descriptive atlas of catheter failure into genuine prediction and prevention.</p>
<p><strong>Subject of Research:</strong> Clinical and technical factors associated with tunnelled central venous catheter dysfunction in haemodialysis patients</p>
<p><strong>Article Title:</strong> Clinical and Technical Factors Associated With Tunnelled Central Venous Catheter Dysfunction in Haemodialysis: A Multicentre Session‐Level Retrospective Study</p>
<p><strong>Article References:</strong> Gimeno Hernán, V., Perez Ingidua, C., Rivas Paterna, A. B., Moreno, G., Vicente‐Galán, M. J., Orgaz‐Rivas, E., Meneses‐Monroy, A., &amp; Ortuño‐Soriano, I. (2026). Clinical and Technical Factors Associated With Tunnelled Central Venous Catheter Dysfunction in Haemodialysis: A Multicentre Session‐Level Retrospective Study. <em>Nursing Open, 13</em>(9), Article e70758. <a href="https://doi.org/10.1002/nop2.70758" rel="noopener noreferrer">https://doi.org/10.1002/nop2.70758</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.1002/nop2.70758" rel="noopener noreferrer">10.1002/nop2.70758</a></p>
<p><strong>Keywords:</strong> haemodialysis, central venous catheter, catheter dysfunction, dialysis adequacy, Kt, vascular access, anticoagulation, antiplatelet therapy, nephrology, internal jugular vein, retrospective study, nursing</p>
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