Analysis of correlations of inferior vena cava diameter in patients with acute cerebrovascular accident
Abstract
Background. Considerable attention is paid to the correction of ischemia and neuronal hypoxia within the set of therapeutic interventions, as this approach has demonstrated proven efficacy. The use of adequate and rational infusion therapy in patients with acute cerebrovascular accident (ACVA) enables the maintenance of optimal cerebral perfusion pressure, reduction of intracranial pressure, and correction of fluid and electrolyte balance. The purpose was to evaluate the correlations between inferior vena cava (IVC) diameter, clinical and laboratory parameters, and infusion therapy volume in patients with ischemic ACVA in order to optimize volemic support. Materials and methods. A retrospective multicenter study was conducted. Data from 30 patients with ACVA aged 69.6 ± 13.4 years were analyzed. All of them were treated in the intensive care unit and maintained spontaneous breathing without tracheal intubation. Ultrasound examination of IVC was performed in all patients. Exclusion criteria were cardiac tamponade, isolated right ventricular failure, elevated intra-abdominal pressure, mechanical ventilation, and obesity. IVC diameter was measured at end-expiration, 0.5–3.0 cm proximal to the junction with the right atrium, using a subcostal approach. Results. The results obtained demonstrated that IVC diameter was significantly associated with a number of clinical and laboratory parameters characterizing volemic status of patients with ACVA. An inverse relationship was found between IVC diameter and hemoglobin and hematocrit levels, indicating that smaller IVC diameter was associated with hemoconcentration. These findings confirm that IVC may be considered not only an ultrasonographic marker of preload, but also an integrated indicator of intravascular volume reflecting the biological manifestations of fluid deficiency. The ROC analysis additionally supported this hypothesis: IVC diameter demonstrated moderate ability to detect hemoconcentration (AUC = 0.76). This finding suggests the potential utility of IVC assessment as a noninvasive tool for evaluating volemic status in clinical practice. At the same time, the absence of a diagnostic value of IVC diameter in terms of fluid balance (AUC = 0.19) highlights the fundamental difference between biological and integral indicators. Fluid balance is influenced by multiple factors, including infusion therapy volume, diuresis, and physician-related clinical decisions, which limits its use as an independent marker of volemia. The observed association between IVC diameter and body temperature may reflect the role of systemic inflammatory response in the formation of volemic status. Increased body temperature likely contributes to greater fluid loss, indirectly resulting in reduced IVC diameter. However, this mechanism requires further investigation and should currently be regarded as hypothetical. A direct correlation between IVC diameter and daily diuresis suggests a possible association with renal perfusion, whereby greater intravascular volume is associated with higher urine output. The obtained findings also emphasize an important clinical implication: IVC diameter reflects the current volemic status but does not allow assessment of responsiveness to infusion therapy. Dynamic assessment methods are required for this purpose. Conclusions. To optimize volemic support in patients with ischemic stroke, IVC diameter should be evaluated as part of a multimodal approach that includes laboratory parameters (hemoglobin, hematocrit), clinical indicators (body temperature, diuresis), and, whenever possible, dynamic tests or invasive monitoring.