Validation of Point-of-Care Ultrasound to Measure Perioperative Edema in Infants With Congenital Heart Disease

Purpose: Fluid overload is a common post-operative issue in children following cardiac surgery and is associated with increased morbidity and mortality. There is currently no gold standard for evaluating fluid status. We sought to validate the use of point-of-care ultrasound to measure skin edema in infants and assess the intra- and inter-user variability.Methods: Prospective cohort study of neonates (≤30 d/o) and infants (31 d/o to 12 m/o) undergoing cardiac surgery and neonatal controls. Skin ultrasound was performed on four body sites at baseline and daily post-operatively through post-operative day (POD) 3. Subcutaneous tissue depth was manually measured. Intra- and inter-user variability was assessed using intraclass correlation coefficient (ICC).Results: Fifty control and 22 surgical subjects underwent skin ultrasound. There was no difference between baseline surgical and control neonates. Subcutaneous tissue increased in neonates starting POD 1 with minimal improvement by POD 3. In infants, this pattern was less pronounced with near resolution by POD 3. Intra-user variability was excellent (ICC 0.95). Inter-user variability was very good (ICC 0.82).Conclusion: Point-of-care skin ultrasound is a reproducible and reliable method to measure subcutaneous tissue in infants with and without congenital heart disease. Acute increases in subcutaneous tissue suggests development of skin edema, consistent with extravascular fluid overload. There is evidence of skin edema starting POD 1 in all subjects with no substantial improvement by POD 3 in neonates. Point-of-care ultrasound could be an objective way to measure extravascular fluid overload in infants. Further research is needed to determine how extravascular fluid overload correlates to clinical outcomes.

Interstitial Washdown and Vascular Albumin Refill During Fluid Infusion: Novel Kinetic Analysis From Three Clinical Trials

Background and Aims. Increased capillary filtration may paradoxically accelerate vascular refill of both fluid and albumin from the interstitial space, which are claimed to be edema-preventing. We characterized “interstitial washdown” by kinetic analyses of the hemodilution induced by intravenous infusion of crystalloid fluid during 3 distinctphysiological states.Methods. The dilution of blood hemoglobin and plasma albumin was compared by population volume kinetic analysis during and after intravenous infusion Ringer´s solution over 30 min in 24 conscious volunteers and 30 anesthetized patients. Data were also retrieved from 31 patients with ketoacidosis from hyperglycemia who received 1 L of0.9% saline. Greater plasma dilution of hemoglobin as compared to albumin indicated recruitment of albumin.Results. “Interstitial washdown” increased plasma albumin concentration by 0.6 g/L in volunteers, by 1.0 g/L during anesthesia, and by 0.3 g/L in ketoacidosis patients. The albumin concentration in extravascular fluid returning to the plasma was approximately 29, 29, and 22 g/L during the respective infusions, but decreased to an average of 50% to 75% lower during the subsequent 2-3 h. Pronounced washdown was associated with increased capillary filtration (high k12) and, in conscious subjects, with fluid retention due to restricted urine flow. During anesthesia, the main effect was an increase the nonexchangeable fluid volume (“third-spacing”).Conclusions. Fluid infusion induces interstitial washdown by accelerated lymphatic flow and an increase in plasma albumin. The mechanism becomes exhausted after 2-3 hours. Albumin refill helps retain infused volume within the vascular compartment.

P1085EFFECT OF INTRAVASCULAR FLUID REMOVAL ON THE RATE OF CHANGE OF THE INFERIOR VENA CAVA DIAMETER, EARLY DIASTOLIC MITRAL VALUE INFLOW AND NUMBER OF LUNG ECHO B-LINES IN HEMODIALYSIS PATIENTS

Background and Aims In hemodialysis therapy, intravascular fluid is removed first. As intravascular water is removed, the circulating serum protein concentrations increase, resulting in a marked increase in the driving force which pulls water from the extravascular space into the blood vessels, by a process called plasma refilling. We examined the effect of total fluid removal and intravascular fluid removal as estimated by the change of the hematocrit value during dialysis on the rate of change of the inferior vena cava (IVC) diameter, early diastolic mitral valve inflow (E wave), and lung echo B-lines. Method We enrolled 59 patients under maintenance hemodialysis for this study. Lung ultrasound was performed at the first session of the week. Bilateral scanning of the anterior and lateral chest walls was performed with the patient in a supine position. The chest wall was divided into 8 areas (2 anterior and 2 lateral areas per side), and 1 scan was obtained for each area. The total number of B-lines was estimated. Echocardiographic measurements were obtained at the same time and the IVC dimensions and E wave were estimated. We performed each ultrasound examinations at two time-points (just after the start and just before the end of the hemodialysis therapy). We then investigated the rate of change ((post-pre)/post) of the IVC diameter, E wave, and number of B-lines. A peripheral blood sample was obtained before and after the hemodialysis session and the hematocrit was measured. We estimated the intravascular fluid volume as pre body weight /13, and estimated intravascular fluid removal as (post hematocrit – pre hematocrit)/post hematocrit x estimated intravascular fluid. We also defined estimated extravascular fluid removal as total fluid removal – estimated intravascular fluid removal. We investigated the relationship between the total, intravascular and extravascular fluid removals and the rate of change of the IVC diameter, E wave, and number of B-lines. Results The rate of change of the IVC diameter was negatively related to the estimated intravascular fluid volume (r=-0.285, P=0.033), but not to the estimated extravascular fluid or total fluid removal. The rate of change of the E wave was negatively related to the estimated intravascular fluid volume (r=-0.422, P=0.001), and the estimated extravascular fluid (r=-0.369, P=0.006) and total fluid removal (r=-0.419, P=0.002). Among these, the rate of change of the E wave was most closely related to the estimated intravascular fluid volume. The rate of change of the number of B-lines was not associated with the estimated intravascular fluid volume, but was negatively correlated with the estimated extravascular fluid (r=-0.368, P=0.005) and total fluid removal (r=-0.353, P=0.008). The estimated extravascular fluid removal was the most closely related to the rate of change of the number of B-lines. Conclusion The rates of changes of the IVC diameter and E wave were strongly associated with the estimated intravascular fluid removal, whereas the rate of change of the number of B-lines was correlated with estimated extravascular fluid removal. The E wave represents the flow to the left ventricle, which occurs after left ventricular diastole, reflecting the preload status. The IVC dimensions are strongly associated with the right atrial pressure and blood volume and therefore reflect the intravascular volume. Therefore, both the E wave and the IVC diameter may represent the intravascular fluid volume. On the other hand, the number of B-lines has been reported to be correlated with the amount of extravascular lung water. Our results were consistent with these reports.

Angiographic features of drug-induced bilateral angle closure and transient myopia with Ciliochoroidal effusion

Background To report five cases of acute drug-induced angle closure and transient myopia with ciliochoroidal effusion and to analyze angiographic findings of these cases. Methods This study is an observational case series. Five patients with acute drug-induced angle closure and transient myopia with ciliochoroidal effusion were examined by fluorescein angiography, indocyanine green angiography (ICGA) and ultrasound biomicroscopy (UBM). Results Five patients presented with bilateral visual loss and ocular pain after intake of topiramate, methazolamide, phendimetrazine tartrate or mefenamic acid. All patients showed elevated intraocular pressure (IOP) with shallow anterior chamber and myopic shift from − 0.5 to − 17.0 diopters (D). UBM showed ciliochoroidal effusions with diffuse thickening of the ciliary body in all cases. Rapid normalization of IOP and decrease of myopic shift occurred in all patients after discontinuing the suspected drugs. We classified the ICGA findings into 2 major signs (hypofluorescent dark spots, hyperfluorescent pinpoints) and 3 minor signs (diffuse choroidal hyperfluorescence, early hyperfluorescence of choroidal stromal vessel, and leakage and dilated retinal vessels). Conclusions The pathogenesis of acute drug-induced angle closure and transient myopia with ciliochoroidal effusion may be idiosyncratic reaction of uveal tissue to systemic drugs. Accumulation of extravascular fluid in the ciliochoroidal layer had a major role in the pathogenesis. ICGA could be a useful method to examine the pathophysiology of this condition by imaging of the choroidal layer.

Angiographic Features of Drug-Induced Bilateral Angle Closure and Transient Myopia with Ciliochoroidal Effusion

Background: To report five cases of acute drug-induced bilateral angle closure and transient myopia with ciliochoroidal effusion, and to suggest a pathogenesis for this condition based upon angiography. Methods: This study is an observational case series. Five patients with acute drug-induced angle closure with ciliochoroidal effusion were examined by ultrasound biomicroscopy, fluorescein angiography, and indocyanine green angiography (ICGA). Results: Five patients presented with bilateral visual impairment and ocular pain after treatment with mefenamic acid, phendimetrazine tartrate, topiramate, or methazolamide. All patients presented a shallow anterior chamber and elevated intraocular pressure in both eyes. They showed a myopic shift from -0.5 to -17.0 diopters. Ultrasound biomicroscopy revealed annular ciliochoroidal effusions with diffuse thickening of the ciliary body in all cases. Rapid clinical improvement occurred in all patients after discontinuing the suspected drugs. ICGA findings were classified into two major signs (hypofluorescent dark spots and hyperfluorescent pinpoints) and three minor signs (early choroidal stromal vessel hyperfluorescence and leakage, diffuse hyperfluorescence of the choroid, and tortuous and dilated retinal vessels). Conclusions: The basic mechanism of pathogenesis involved an idiosyncratic reaction in uveal tissue to systemic drugs. Angiography showed that accumulation of extravascular fluid in the ciliochoroidal layer had a major role in pathogenesis. Angiography could therefore be a useful method to examine the pathophysiology of this condition by imaging of the choroidal layer.

Escharotomies

Following a significant thermal or electrical injury, tissues beneath the skin swell through fluid loss into the interstitial space. The increase in extravascular fluid together with the inelastic nature of the overlying burned skin compound to increase pressure within the affected limb. This increase in pressure can compromise the vascular supply distally in an affected limb or increase ventilatory pressures in those with circumferential burns of the chest and abdomen. This chapter will give guidance on when and how to perform escharotomies; however, the final decision is usually based on experience and clinical judgment. Figures illustrate detail markings and techniques for escharotomies and fasciotomies of the upper limb, lower limb, chest and abdomen.

Ultrasound lung comets in extravascular fluid diagnostics

The review is devoted to the analysis of ultrasound lung comets (ULCs) that may be observed during ultrasound lung examination in cardiac patients in the case of accumulation of extravascular fluid in the lungs. Recent data on the mechanisms of these artefacts, examination and outcome evaluation methods are discussed. Differential diagnostics problems in patients with cardiac and pulmonary genesis of ULCs are also covered.