We examined the patient taking into account more than biochemical lab values and CT images (dubitative interpretation). We noticed that she had  diffuse abdominal tension and vague hypogastrium pain. Retrograde cystography (Figure 1) showed the flow of  contrast substance in the peritoneal space. To be noted that we made this investigation not due to the suspicion of uroperitoneum but because of our  previous experience, years ago, of a somewhat similar case: a 35 year old autistic man, sheared between two carriages of a circulating tram, without  pelvis fracture but with urinary  bladder rupture and consequent uroperitoneum.
We intervened surgically through an anterior abdominal incision and intraoperatively, an old an important vesical lesion was seen, on a bladder that  looked 'withered', well fixed on an intestinal loop, which explained the almost missing symptoms. Without bringing new information in  addition to the ones already reported in literature, we will note in the following, a few aspects on urinary peritonitis, with an intent of more  than attracting attention towards this type of pathology
Urine may get between intestinal loops by effraction through one of the urinary tract organs and the most frequently involved is the urinary  bladder, through the rupture of its peritoneal side. Theoretically, the uroperitoneum can appear also through renal or urethral trauma but, considering  their retroperitoneal location, causing agents must have a more complex and aggressive mechanism. (Figure 2)
As a consequence, urinary bladder ruptures can be spontaneous, traumatic or iatrogenic.Spontaneous ruptures presume in principle the existence of a  thin vesical wall, an immunosuppressant status or a lack in body proteins, such as consumption diseases. Quite a few at a first glance, these  pathological situations which lead to the spontaneous effraction of the bladder make us think that they are least probable to be juxtaposed in order to  make the optimal frame that causes urinary peritonitis. Nevertheless, it happens!
Most frequent vesical ruptures appear in situations like chronic alcohol intakes (drunk man's bladder) [ ], immunosuppression, cirrhosis, diabetes, tuberculosis, scarred or tumoral bladders, when there are large vesical diverticula or chronic vesical  obstacles with thin vesical wall. The question of a determining factor of vesical rupture was raised, in spite of the mentioned associated pathology.  Most of the times there is a traumatic mechanism involved, brought to light by a very detailed history but there are cases in which no trauma can be  traced.
Vesical ruptures are induced mainly by action of the injury agent directly on the inferior abdomen. This determines a great and sudden pressure on  the abdominal wall which spreads to the bladder, projects itself on the posterior wall of the pelvis and due to its resistance and comes back towards  the bladder (anterior), giving it a counter blow.
To this mechanism, a series of favourable conditions which may contribute to the extent of the lesions can be variably added.
The amount of urine present inside the bladder at the moment of injury plays an important part. If the bladder is empty, it can be torn only through  direct impact of the trauma agent on its walls because of its deep location in the pelvis and its protection by pelvic bones. Full bladder comes out of  that protection and becomes an intraperitoneal organ. Vesical wall grows thinner in proportion with the quantity of urine and the flexibility of its  muscular fibres decreases. Anatomical areas with least resistance are the superior and posterior walls.
Vesical pathologies which determine a decline in wall strength (inflammatory, tumoral, scaring processes) favour surprisingly serious lesions  following minor traumas.
Neurological lesions of vesical wall lower its ability of distension and also muscle tone and consequently allow an accumulation of a great amount  of urine. It is the case of neurogenic bladder patients. 
Last but not least, vesical ruptures can be accidentally produced during surgery of the pelvic area or during endoscopy procedures when, due to  vesical wall lesion, the washing endovesical fluid effuses in the peritoneal cavity and produces an iatrogenic uroperitoneum (the patient's  abdomen grows 'second by second').
The intimate substratum of urinary peritonitis symptoms is common to every peritonitis but noting that it depends greatly with the quantity and quality  of urine, if we're allowed to say it like this. When a sterile urine effuses, the symptoms are minimal, hidden and become clinically obvious when  this urine becomes infected. In the same way, the clinical suffering and the expressed symptoms can be seen when urine is infected per primam.
Many local defence mechanisms come to aid against infection and other immune as well. Mechanical ones belong to the structural anatomy and to  different characteristics of the peritoneum. Inside the immune mechanisms are cellular components, serum ones, unspecific immunity and the complement  system.
Confinement of infection is realised through direct absorption of bacteria in the lymphatic system, their fagocytosis and formation of  intraperitoneal abscesses. The systemic response to bacterial  aggression lies in the release of physiological messengers of inflammation: cytokines (TNF alpha, IL-1, IL-6, interferon, etc) and  cellular effectors (neutrophils, monocytes, macrophages, endothelial cells). These activated cellular effectors lead to the synthesis and secretion of  new cytokines and secondary inflammation mediators (prostaglandins, leucotriens, tromboxans, trombocyte activating factor etc).
Loss of local control is clinically identified with SIRS -systemic inflammatory response syndrome - which subsequently evolves toward  MODS -multiple organ dysfunction syndrome, which will not be detailed here. Most times, newly diagnosed uroperitoneum cases are comprised in the  above mentioned situations.
Finally, in serious and delayed treatment cases, multiple organ dysfunction becomes a sombre entity called CHAOS (Cardiovascular shock,  Homeostasis, Apoptosis, Organ dysfunction, immune Suppression), with minimal chances of survival [,  ].
Symptoms of vesical trauma and namely of urinary peritonitis are not specific.
In the case of a pathological bladder, a surprising discordance may appear between the low force of the injury agent and the emergence of vesical  lesions (a minor trauma may determine lesions of maximum gravity). Some other times, the tear of vesical wall is distanced from the moment of the  accident, representing the so-called 'two-stage vesical rupture' (a temporary obstruction of the lesion with omentum or intestinal loops  which determines tardy solution of continuity).
The presence of sterile urine in the peritoneal space can be tolerated for many days, with faded, inconclusive local symptoms. In this  situation, alteration in general wellbeing and imbalance of electrolytes are more obvious etc. Perforations and ruptures of urinary bladder usually begin  with a violent pain, located in the pelvis or the perineum and are relatively constantly accompanied by vesical and rectal tenesmes. If urine  emission continues to be spontaneous, it is accompanied by polakiuria, dysuria, haematuria, painful urine emission which is also weak, discontinuous and  with a sensation of incomplete evacuation. In principle, the  manifestations of uroperitoneum can be organised into the following symptoms and signs, one or two being present in common practice, thus making  diagnosis difficult:
actual signs of hypogastric lesions (excoriations, haematomas);
hypogastrium pain due to trauma;
increase of abdomen volume, a consequence of urine accumulation in the peritoneal cavity (ascites); intraperitoneal fluid can be perceived  by percussion, inspection and palpation of the abdomen;
muscle contraction situated at first in the pelvis takes over the entire superior abdomen;
abdominal pain irradiating to the shoulder, consecutive to urine accumulation under the diaphragm, with subsequent irritation of the  phrenic nerve (Kehr sign);
peritonitis signs in the first hours after vesical tear if urine is highly infected (purulent) or after a few days if urine is  initially sterile;
abdominal distension caused by paralytic ileus which installs slowly and aggravates itself continuously;
partial or complete ceasement or urine emission, with a slow, passive flow of urine in the peritoneum;
peritoneal irritation signs on rectal exam; The diagnosis is, as we mentioned before, pretty difficult because the uroperitoneum is a  hidden disease, with tardy manifestations most of the times. Diagnosis is based on traumatic history (pelvic fracture for example associates vesical tears  in 90% of cases), previous endoscopy manoeuvres and their juxtaposed pathology and presence of more than one of the above mentioned signs.
In a book, the only one about this subject published in Romania and also a beginning of trade cornerstone for experienced surgeons  - 'Surgical exploration of abdomen' by Dr. Dan Gerota (Medical Publishing House 1969, first edition, page 70, same publishing house  1987, second edition) - the unsurpassed surgeon and teacher pointed out: 'Other effusions (peritoneal effusion, authors note) are rarely encountered and more difficult to diagnose, especially urine, when mixed with blood  or in low quantity (the case of urether lesions). Even in the case of a vesical lesion, if empty during trauma, in the case of little continuity fluid,  with outlet or situated in an extraperitoneal area, we encounter the same difficulties.'
reno-vesical radiograph does not bring many information but can show pelvic bones fractures and eventually detect an area of  increased density in the hypogastrium or pelvis consecutive to the accumulation of urine or blood;
intravenous urography shows morphological and functional integrity of the superior urinary tract and vesical rupture will appear in late  stages or on the cystograms by contrast substance effusion in the peritoneal cavity;
retrograde cystography is possibly the most important diagnostic method of vesical rupture and consists in the instillation of a  certain quantity of contrast substance in the urinary bladder by means of an urethral-vesical catheter; many films can be obtained, in many views  that will show the effusion of contrast substance among intestines;
abdominal ultrasonography shows fluid accumulation in the peritoneal cavity, similar to ascites fluid;
abdominal and pelvic CT and MRI show the presence of fluid in the peritoneal cavity and if they are done with contrast substance, its  effusion can be observed when it reaches the urinary bladder (Figure 3)
Information offered by ultrasound and imaging explorations are doubtful and most often the interpretation offered by our specialist colleague is  charged with a high, subjective and lacking involvement dose (caused for example by 'the presence of air in between loops, numerous  artefacts' and so on). In the case that we presented their help was minimal at most.
Urethral cystoscopy is not recommended because the risk of aggravating the lesions is high (washing fluid will effuse in the peritoneum and become  an additional factor of infection). If the manoeuvre is done nonetheless, the actual lesion, where intestinal loops or parts of the epiploon enter, can  be seen inside the bladder.