Arterial Stiffness During Negative Pressure Wound Therapy for Abdominal Wall Wounds

Postoperative Abdominal Wall Wound Complications, Surgical Wound Infection, Surgical Wound Dehiscence, Mesh-Associated Wound Complications

Negative Pressure Wound Therapy, Arterial Stiffness, Aortic Pulse Wave Velocity, Arteriograph, Abdominal Wall, Wound Healing, Wound Volumetry, Systemic Inflammation, C-Reactive Protein

WALLAS is a small observational study of 30 adults with complex wounds in the abdominal wall after surgery. All participants will receive negative pressure wound therapy (NPWT) because their treating team considers it appropriate. This treatment uses a sealed dressing connected to a suction device. The study will not decide which treatment participants receive or change their usual care. The main aim is to find out how the stiffness of the large arteries changes during treatment. Researchers will also examine whether larger reductions in wound size and inflammation are linked to larger reductions in artery stiffness. An upper-arm cuff device will estimate artery stiffness by measuring how quickly pressure waves travel along the aorta, the body's main artery. Measurements are planned before treatment starts, around day 5, and when the first course of NPWT ends. Blood pressure will be taken into account when interpreting the results. During planned dressing changes, researchers will record wound depth and, when safe and technically possible, measure the wound cavity using sterile saline. Photographs will document the wound. Results from routine blood tests will provide information about inflammation; no extra blood samples are required for research. Wound recovery and further treatment will be followed for about six months after NPWT starts. The study will also assess how practical and safe the measurement procedures are. Because there is no comparison group, it cannot determine whether NPWT itself causes any changes in artery stiffness.

This prospective, single-center observational pilot examines whether changes in local wound burden and systemic inflammatory activity are accompanied by changes in arterial stiffness during clinically indicated negative pressure wound therapy (NPWT). The biological hypothesis is that greater reductions in wound-cavity volume and inflammatory burden are associated with greater reductions in aortic pulse wave velocity (PWVao). Treatment decisions, including NPWT settings, dressing-change intervals, debridement, antimicrobial treatment and reconstruction, remain the responsibility of the clinical team. Day 0 is the recorded date and time of first NPWT activation. Baseline vascular assessment (T0) must be completed within the preceding 60 minutes and before foam placement. T1 targets day 5, with an acceptable window of days 3-7. The T2 vascular assessment is scheduled within 24 hours before or after clinician-documented cessation of the first NPWT episode and before planned definitive wound closure. Cessation may occur for any reason and is not assumed to indicate healing; the actual treatment duration and reason for cessation are recorded. Temporary interruptions do not end the episode, and a later restart is a subsequent episode. Clinical follow-up targets day 180 after first activation, with an acceptable window of days 150-210. Optional follow-up vascular measurements are analyzed separately. Core vascular assessments use the Arteriograph TL2 under standardized awake, supine conditions after at least 10 minutes of rest, before dressing removal, painful wound manipulation or procedural sedation. Necessary routine analgesia is permitted and documented. Each session averages the first three valid acquisitions for each outcome, with a maximum of five attempts. Technical validity is assessed separately for PWVao and native aortic augmentation index. Nonstandard or out-of-window measurements are documented and analyzed separately rather than substituted for core assessments. The principal quantitative wound measure is operationally defined saline-fill wound-cavity volume. During the corresponding clinical encounter, sterile 0.9% saline is instilled after clinically indicated cleansing or debridement and before foam placement or closure. The cumulative volume required to reach a predefined filling endpoint is recorded. Measurements are omitted when filling is unsafe or leakage, communication with a body cavity or fistula, trapped air or an unreliable endpoint prevents valid assessment. Debridement, mesh procedures and other interventions that alter wound geometry are recorded because volume change can reflect both healing and surgical alteration. Photographs provide supportive documentation; quantitative two-dimensional planimetry is not required. Routine C-reactive protein (CRP), albumin and available complete blood count results are paired with vascular measurements using the closest sample collection time within 24 hours before or after assessment; ties favor the earlier sample. No additional research blood sampling is required. Operation and source-control timing, hemodynamic treatments, renal status, temperature, infection status, pain and analgesia are recorded to support interpretation of concurrent recovery. The primary analysis uses a random-intercept mixed model with categorical visit and separate within-person and between-person mean arterial pressure components. The main estimate is the pressure-adjusted T2-minus-T0 PWVao difference, accompanied by unadjusted paired changes. A supportive model uses actual elapsed days. Two prespecified secondary regressions relate T2-minus-T0 PWVao change separately to percentage wound-volume reduction and signed CRP change, each adjusted for change in mean arterial pressure. Percentage volume reduction requires valid same-encounter vascular-volume pairs at both visits and a positive baseline volume. Effect estimates and 95% confidence intervals are emphasized. Technical feasibility, measurement safety and completeness of serial assessments are reported separately. Missing measurements and their reasons are documented, with complete T0-T2 paired summaries provided alongside the longitudinal analysis. The study characterizes temporal changes and associations during clinical recovery; it cannot isolate an NPWT-specific causal effect or directly establish a local vascular mechanism.

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