Our results show that delayed enhancement of ascites can be seen up to 3 days after initial administration of IV contrast material. The magnitude of delayed enhancement is greater when the prior IV contrast administration is more recent and when the serum creatinine level is higher. The likelihood of observing delayed enhancement drops by 83% for each additional day beyond the time of the initial IV contrast material administration. Furthermore, the likelihood of finding delayed contrast enhancement of ascites is greater with the finding of loculated ascites. Nonrecognition of the phenomenon of benign delayed enhancement of ascites resulted in misdiagnosis of abdominal catastrophe in 13% of the cases in our series.
Delayed enhancement of ascites was misdiagnosed as hemoperitoneum and bowel perforation in two patients. Furthermore, none of the radiology reports mentioned delayed enhancement as a possible explanation for the increased attenuation of ascites. In some cases, high-attenuation ascites caused by hemoperitoneum may be easily distinguished from delayed contrast enhancement. With delayed contrast enhancement of ascites, the abdominal fluid is homogeneously high attenuation (). A new intraperitoneal hemorrhage may be similar in attenuation to the surrounding abdominal fluid, but within hours, the intraperitoneal blood will clot, showing focal areas of increased attenuation compared with the surrounding abdominal fluid. Another imaging finding in fresh intraperitoneal hemorrhage is the hematocrit effect with erythrocytes layering dependently in the abdomen or pelvis [9
In prior reports, investigators have shown the phenomenon of delayed enhancement with increases in attenuation of 7 to 80 HU for time intervals of 10 minutes to 7.5 hours [5
]. Ours is the first systematic study to address delayed enhancement of ascites beyond 7.5 hours and to evaluate for predictors of this benign process. For CT scans obtained less than 1 day apart, our study found that 63% of patients showed delayed enhancement of the ascites. This finding is consistent with that of a previous study that showed delayed enhancement of ascites in 54% of patients with a 10-minute to 1.7-hour time delay between IV contrast material injection and follow-up CT [5
]. The same prior study found that the size of ascites was inversely proportional to the degree of enhancement [5
]. We did not find this correlation, possibly related to the longer time interval between the examinations in our study compared with this prior study. Another difference is that we found serum creatinine level to be a predictor of both a higher magnitude and a greater likelihood of delayed enhancement of ascites, whereas the prior study did not find this result [5
]. This difference in results can be explained simply on the basis of method: The prior study used a binary, and hence less sensitive, measure of renal failure versus normal renal function, whereas our study addressed serum creatinine level as a continuous variable.
The mechanism of delayed enhancement of ascites remains unknown, but our findings support prior speculation that it may be related to increased vascular–peritoneal permeability due to abdominal disease or injury [5
]. Our finding that delayed enhancement is more common in patients with peritoneal carcinomatosis or loculated ascites supports this claim because both processes are associated with increased vascular permeability. Additionally, loculation of fluid may prolong the dwell time of contrast material by restricting diffusion of contrast material out of this contained fluid. However, most of the patients with delayed enhancement of ascites did not have peritoneal disease, and we found that a strong predictor for delayed enhancement of ascites was poor renal function. Poor renal excretion of IV contrast material results in a prolonged dwell time of radiodense material in the body. In particular, water-soluble iodinated contrast materials are all of small molecular size, less than 2 kDa, and are known to readily diffuse through the pores of vasculature into the extravascular extracellular space [6
]—including into third-space fluid collections such as ascites. Given the direct correlation between the magnitude of delayed enhancement and serum creatinine level, another possible cause is retained contrast material in the body due to decreased renal excretion. Another new finding in our study is the occurrence of delayed contrast enhancement in loculated ascites, suggesting that the inflammatory process leading to loculation also increases the permeability of the blood–peritoneum barrier.
Our study has a number of limitations. First, it is a retrospective study. Patients had various times between studies and had only 2–3 CT examinations performed within a 7-day period. Although our study addressed delayed enhancement of the ascites beyond 7.5 hours, a previous study has shown that it may be present as early as 10 minutes [5
]. An ideal study design would be to image patients multiple times at set time intervals to fully understand the time to peak and the time to return to baseline for the attenuation of ascites. However, a study of this design would be unethical given the risks of unnecessary radiation exposure. A benefit of our study design is that patients who underwent repeated CT examinations for clinical reasons were evaluated, so our study group probably resembles the type of patient in whom delayed enhancement of ascites is likely to be seen.
A second limitation is that we did not investigate whether IV contrast material administered for the follow-up examination may potentially cause an increased attenuation of the ascites so as to mimic delayed enhancement. However, all the CT scans were obtained within 80 seconds of administration of IV contrast material; therefore, significant enhancement of ascites at that time on the follow-up scans is unlikely.
A third limitation is that renal function was not optimally assessed because serum creatinine level is a rough estimate of overall renal capacity. In this analysis, we judged estimated glomerular filtration rates (GFR) as a suboptimal alternative because the most accepted estimated GFR calculations are known to be inaccurate for patients with normal or only mildly impaired renal function [11
], which comprise most of the patients in our study.
A fourth limitation is that the researchers were not blinded to the time interval between studies or the use of IV contrast material, but we believe that the objective measurement of CT attenuation is unlikely to be subject to bias.
Last, our study did not contain a control group of patients with documented hemoperitoneum or extravasation of contrast material from the bowel or urinary tract. Future study will be needed to determine CT findings, such as a marbled appearance of fluid or fluid–debris levels, that may be useful for distinguishing true abdominal catastrophe from benign delayed enhancement of ascites.
In conclusion, our study showed that delayed contrast enhancement of ascites occurs commonly after recent prior IV contrast material administration and should not be mistaken for intraperitoneal catastrophe. The likelihood of finding delayed enhancement of ascites increases with a shorter time interval between the initial IV contrast-enhanced examination and subsequent CT examination and with higher serum creatinine levels.