Case Presentation
An 85 year-old Caucasian man, affected by chronic renal failure, had been undergoing hemodialysis treatments three times a week for the previous three years. His fluid intake was controlled and he was unable to eat independently. Due to a severe episode of macrohematuria (International Normalized Ratio, I.N.R. 6.1), he was transferred to the local hospital where continuous bladder irrigation was promptly activated with a 3-way catheter. Irrigation fluid with 0.9% saline solution was injected from a height of about 150 cm without pressure. A urine bacteriologic culture test was immediately performed, whose results, obtained some days later, were negative. During the first three days of irrigation, the patient did not claim any problems and successfully underwent hemodialysis as usual. On the third day of his hospital stay, while still undergoing bladder irrigation, he suddenly experienced extreme shortness of breath, breathing difficulties, and a cough with frothy sputum. The nurse attending him immediately noted that there was no return of the fluid (5 liters) introduced through bladder irrigation. No manual evacuation of the bladder was performed during the treatment. A chest radiography revealed cardiomegaly, mild perihilar interstitial infiltrates and an increase of the pulmonary vasculature leading to pulmonary edema. An electrocardiography revealed nonspecific ST-T wave changes. Cardiac isoenzymes were within normal ranges; hemoglobin values were constantly >7 g/dL. A computed tomography (CT) of the abdomen was immediately performed and excluded the perforation of the bladder walls and an intraperitoneal fluid extravasation. The patient was treated urgently once again with hemodialysis. At the beginning of the dialysis, the patient had gained weight for 7.4 kg since the previous measurement (24 hours prior) without any clear explanation. Despite a significant weight loss (from 81 to 76 kg) following the dialysis, the patient died shortly after the final treatment.
The prosecutor opened an investigation, ordering that an autopsy was to be performed to clarify the exact mechanism of death. The autopsy was executed 24 hours after the patient's death. The results revealed that the brain and the lungs were heavily edematous: the brain weighed 1700 g, the left lung weighed 790 g while the right lung weighed 590 g. The heart was found increased in size (12 × 8.5 × 8 cm) and weight (660 g), coronary vessels and main branches showed slight stenoses. The kidneys were small and showed a finely granular external surface; in cross-section, a gross diminution of cortical thickness with loss of demarcation between cortex and medulla was evident; each kidney weighed 100 g. A small amount of soft blood clots was found in the bladder. Other organs were unremarkable. Samples of organs were taken for histological examination and sections were stained by Hematoxylin & Eosin. On bladder specimens an immunohistochemical study using mouse monoclonal anti-pan cytokeratin antibody AE1/AE3 was performed in order to investigate the urothelium cells. A microscopic examination of the bladder specimens revealed interstitial and mucosal swelling; loss of the umbrella cell layer (superficial urothelium) was evident while intermediate and basal urothelial cells were preserved. The bladder section expressed a very low positivity to AE1/AE3 antibody in comparison with a control case (bladder specimens in a 70 year-old man who had died of pulmonary embolism) which revealed a positive labeling with both AE/1 AE/3 antibodies. PAS and Alcian blue staining demonstrated a clear absence of the superficial layer of glycosaminoglycans (GAGs) in comparison with the control case (Figure 1). Altogether the abovementioned findings were suggestive of a diffuse disruption of the urothelium.
Figure 1.
Alcian Blue - PAS stained sections of (A) damaged bladder case (60 × magnification) and (B) control bladder (100× magnification). In A umbrella cells are completely denuded. AE1/AE3 immunoreaction confirms the superficial layer damage in C (60 x) if compared with the control case (D, 100x).
The histological examination of other organs was unremarkable except for a massive cerebral and pulmonary endoalveolar edema, myocardial colliquative myocitolysis and mild diffuse arteriolosclerosis.
In conclusion the death of the man was attributed to an acute severe pulmonary edema due to massive fluid absorption.
BMC Urol. 2014;14(91) © 2014 BioMed Central, Ltd.
