OBJECTIVE: Lower urinary tract obstruction (LUTO) with massive bladder distension impacts on a variety of developing organ systems with consequent morbidity and mortality. The impact of LUTO on the fetal cardiovascular system has not previously been investigated. We hypothesize that a giant, distended bladder within the pelvis may cause vascular compression with observable consequences. METHODS: Fetal echocardiography was performed in 42 fetuses with LUTO and compared with 35 normal controls matched for gestational age. Parameters investigated included cardiothoracic ratio, presence or absence of ventricular hypertrophy and pericardial effusion. Doppler echocardiographic examination of mitral and tricuspid valve inflow and the ductus venosus was performed. To assess arterial vascular impedance, pulsatility indices (PIs) were calculated for segments of the descending aorta and right and left iliac arteries (RIA and LIA). RESULTS: In the LUTO group an increased cardiothoracic ratio was seen in nine (21%), ventricular hypertrophy in 12 (29%) and small pericardial effusion in 15 (36%). Filling characteristics of the right ventricle in the LUTO group demonstrated greater dependency upon atrial contraction, and ductus venosus flow demonstrated higher downstream impedance to filling, than in controls, suggesting altered compliance. The LUTO group also had lower distal descending aorta PI (1.53 ± 0.38 vs. 1.76 ± 0.44, P = 0.04), lower RIA-PI (1.31 ± 0.29 vs. 1.76 ± 0.44, P < 0.001) and lower LIA-PI (1.41 ± 0.44 vs. 1.73 ± 0.31, P < 0.01) than controls, suggesting vascular compression and increased impedance to flow. CONCLUSIONS: LUTO with giant urinary bladder compresses the iliac arteries, which may lead to increased afterload. Further study is warranted to examine the impact of fetal treatment such as bladder drainage on these cardiovascular parameters.
OBJECTIVE: Lower urinary tract obstruction (LUTO) with massive bladder distension impacts on a variety of developing organ systems with consequent morbidity and mortality. The impact of LUTO on the fetal cardiovascular system has not previously been investigated. We hypothesize that a giant, distended bladder within the pelvis may cause vascular compression with observable consequences. METHODS: Fetal echocardiography was performed in 42 fetuses with LUTO and compared with 35 normal controls matched for gestational age. Parameters investigated included cardiothoracic ratio, presence or absence of ventricular hypertrophy and pericardial effusion. Doppler echocardiographic examination of mitral and tricuspid valve inflow and the ductus venosus was performed. To assess arterial vascular impedance, pulsatility indices (PIs) were calculated for segments of the descending aorta and right and left iliac arteries (RIA and LIA). RESULTS: In the LUTO group an increased cardiothoracic ratio was seen in nine (21%), ventricular hypertrophy in 12 (29%) and small pericardial effusion in 15 (36%). Filling characteristics of the right ventricle in the LUTO group demonstrated greater dependency upon atrial contraction, and ductus venosus flow demonstrated higher downstream impedance to filling, than in controls, suggesting altered compliance. The LUTO group also had lower distal descending aorta PI (1.53 ± 0.38 vs. 1.76 ± 0.44, P = 0.04), lower RIA-PI (1.31 ± 0.29 vs. 1.76 ± 0.44, P < 0.001) and lower LIA-PI (1.41 ± 0.44 vs. 1.73 ± 0.31, P < 0.01) than controls, suggesting vascular compression and increased impedance to flow. CONCLUSIONS: LUTO with giant urinary bladder compresses the iliac arteries, which may lead to increased afterload. Further study is warranted to examine the impact of fetal treatment such as bladder drainage on these cardiovascular parameters.