Spontaneous Urinary Bladder Research Articles

Intra-Abdominal Hemorrhage Due to Spontaneous Urinary Bladder Diverticulum Rupture in a Female: An Autopsy Case Report and Brief Review of the Literature

Urinary bladder diverticula are formed by the herniation of the mucosa into the muscle layer of the bladder wall, often ending with a narrow neck that communicates with the bladder lumen. They may be congenital or acquired, and they most often affect males. Urinary bladder diverticula discovery during autopsy incidence described in the literature is approximately 5–10%. Various causative factors have been described, including urinary tract obstruction (e.g., benign prostate hyperplasia) and neurogenic and iatrogenic causes. The most described site of occurrence is adjacent to the ureteral orifice. Their clinical presentation does not often facilitate diagnosis, as most are small and asymptomatic. Complications of urinary bladder diverticulosis include infections, lithiasis, neoplasia, pressure on adjacent tissues, obstruction, and rupture. Indeed, urinary bladder diverticula may lead to spontaneous bladder rupture in extremely rare cases. This paper presents the case of an 87-year-old female suffering from atrial fibrillation and under anticoagulant therapy who was pronounced dead in a hospital and was subsequently referred to our department for medico-legal examination. Upon macroscopic examination of the body, intra-abdominal hemorrhage was observed in the vicinity of the urinary bladder, extraperitoneally. A meticulous examination excluded the possibility of injury as the cause of this finding, and tissue samples were collected for histopathological examination. A ruptured urinary diverticulum was discovered and confirmed histopathologically. Death was attributed to intra-abdominal hemorrhage after rupture of urinary bladder diverticulum. A forensic pathologist should be aware of this diagnosis, as although extremely rare, such pathology may lead to death, especially when the patient is under anticoagulant therapy.

Spontaneous Rupture of the Urinary Bladder: A Case Report

Spontaneous rupture of the bladder (SRUB) is a rare occurrence globally (<1%). The most common cause of bladder rupture is trauma (96%). We present a case of a 34-year-old man with a history of heavy alcohol consumption and significant smoking history. He presented with diffuse abdominal pain and urinary retention. On blood tests, he was found to have increased creatinine. A urinary catheter was inserted and there was improvement in his kidney function. However, on removal of the catheter, his creatinine function would elevate. This occurred two times before further investigations were performed. CT cystography was performed and there was a significant amount of free intraperitoneal fluid found in the pelvis. After retrograde filling of the bladder with contrast material, a tear in the dome of the bladder was discovered. The patient underwent a surgical repair of the tear and there were no complications during surgery. In summation, spontaneous urinary bladder rupture is a rare emergency which can cause acute abdomen, oliguria, peritoneal effusion and abnormal renal function. In patients with heavy alcohol consumption and especially without an associated trauma history, physicians should consider SRUB. CT scan can help in diagnosis. Diagnostic laparoscopy or explorative laparotomy should not be delayed.

Spontaneous urinary bladder regeneration after subtotal cystectomy increases YAP/WWTR1 signaling and downstream BDNF expression: Implications for smooth muscle injury responses.

Rodents have the capacity for spontaneous bladder regeneration and bladder smooth muscle cell (BSMC) migration following a subtotal cystectomy (STC). YAP/WWTR1 and BDNF (Brain-derived neurotrophic factor) play crucial roles in development and regeneration. During partial bladder outlet obstruction (PBO), excessive YAP/WWTR1 signaling and BDNF expression increases BSMC hypertrophy and dysfunction. YAP/WWTR1 and expression of BDNF and CYR61 were examined in models of regeneration and wound repair. Live cell microscopy was utilized in an ex vivo model of STC to visualize cell movement and division. In Sprague-Dawley female rats, STC was performed by resection of the bladder dome sparing the trigone, followed by closure of the bladder. Smooth muscle migration and downstream effects on signaling and expression were also examined after scratch wound of BSMC with inhibitors of YAP and BDNF signaling. Sham, PBO and incision (cystotomy) were comparators for the STC model. Scratch wound in vitro increased SMC migration and expression of BDNF, CTGF and CYR61 in a YAP/WWTR1-dependent manner. Inhibition of YAP/WWTR1 and BDNF signaling reduced scratch-induced migration. BDNF and CYR61 expression was elevated during STC and PBO. STC induces discrete genes associated with endogenous de novo cell regeneration downstream of YAP/WWTR1 activation.

Pathological studies on spontaneous urinary bladder lesions in Indian buffaloes

The present investigation describes the spontaneous pathological lesions in urinary bladders (n = 177) of slaughtered buffaloes collected from Northern India. Gross examination revealed congestion, haemorrhages, oedematous changes and thickening of mucosa. Microscopically, epithelial abnormalities, inflammatory and neoplastic conditions were noticed. Epithelial abnormalities included epithelial hyperplasia, von Brunn’s nests, cystitis cystica and cystitis glandularis. Inflammatory conditions such as congestion, haemorrhages and cystitis were noticed. Cystitis was classified as lymphocytic, plasmo-lymphocytic, follicular and interstitial types. However, only single case of haemangiosarcoma was observed. Polymerase chain reaction revealed the presence of DNA of only BPV-1 in one sample out of 21, while one sample showed the presence of DNA of both BPV-1 and BPV-2. On immunohistochemistry, Ki-67 expression was observed only in haemangiosarcoma and one case of plasmo-lymphocytic cystitis with immunostaining restricted to nuclei. COX-2 immunostaining was observed in one case each of flat hyperplasia, von Brunn’s nest, haemangiosarcoma and two cases of plasmo-lymphocytic cystitis. Among epithelial abnormalities, COX-2 immunostaining was restricted to epithelial component of the lesions, and it was diffused cytoplasmic type with occasional perinuclear staining particularly in the cytoplasmic membrane. However, in haemangiosarcoma the COX-2 immunoreactivity was noticed in epithelial as well as connective tissue stroma. In conclusion, it may be stated that urinary bladders of slaughtered buffaloes showed a number of epithelial abnormalities, inflammatory conditions and occasionally neoplasms. Further studies to explore the infectious as well as non-infectious etiologies should be undertaken.

The mast cell stimulator compound 48/80 causes urothelium-dependent increases in murine urinary bladder contractility.

Mast cells and degranulation of preformed inflammatory mediators contribute to lower urinary tract symptoms. This study investigated pathways by which the mast cell stimulator compound 48/80 alters urinary bladder smooth muscle contractility via mast cell activation. We hypothesized that 1) mast cell degranulation causes spontaneous urinary bladder smooth muscle contractions and 2) these contractions are caused by urothelium-derived PGE2. Urothelium-intact and -denuded urinary bladder strips were collected from mast cell-sufficient (C57Bl/6) and mast cell-deficient (B6.Cg-Kitw-sh) mice to determine if compound 48/80 altered urinary bladder smooth muscle (UBSM) contractility. Electrical field stimulation was used to assess the effects of compound 48/80 on nerve-evoked contractions. Antagonists/inhibitors were used to identify prostanoid signaling pathways activated or if direct activation of nerves was involved. Compound 48/80 caused slow-developing contractions, increased phasic activity, and augmented nerve-evoked responses in both mast cell-sufficient and -deficient mice. Nerve blockade had no effect on these responses; however, they were eliminated by removing the urothelium. Blockade of P2 purinoreceptors, cyclooxygenases, or G protein signaling abolished compound 48/80 responses. However, only combined blockade of PGE2 (EP1), PGF2α (FP), and thromboxane A2 (TP) receptors inhibited compound 48/80-induced responses. Thus, the effects of compound 48/80 are urothelium dependent but independent of mast cells. Furthermore, these effects are mediated by druggable inflammatory pathways that may be used to manage inflammatory nonneurogenic bladder hyperactivity. Finally, these data strongly suggest that great care must be taken when using compound 48/80 to determine mast cell-dependent responses in the urinary bladder.NEW & NOTEWORTHY Urothelial cells are first responders to noxious contents of the urine. Our study demonstrates that the urothelium is not only a barrier but also a modulator of urinary bladder smooth muscle phasic activity and contractility independent of immune cell recruitment in response to an inflammatory insult.

Spontaneous urinary bladder perforation presenting as bowel obstruction in a child: a case report

BackgroundSpontaneous perforation of the urinary bladder is a rare disease entity. Due to its rarity, it is often hard to diagnose.Case presentationWe present a case of a 2-year-old patient who presented with bowel obstruction and renal failure after scheduled correctional vertebroplasty due to congenital kyphosis. During exploratory laparotomy, two perforations were found at the dome of the urinary bladder, and an idiopathic spontaneous perforation of the urinary bladder was diagnosed. Primary double repair of the perforations was done, and no primary or secondary cause of the perforation was found.ConclusionThe constellation of an acute abdomen and abnormal kidney function tests should increase the index of suspicion towards urinary bladder perforation. Due to its rarity, exploratory laparotomy is the gold standard method of diagnosis and treatment.

A Case of Spontaneous Urinary Bladder Rupture

A Case of Spontaneous Urinary Bladder Rupture

Spontaneous rupture of the bladder: Report of two cases

To report two cases of spontaneous urinary bladder rupture following binge-drinking. Two male patients with history of alcohol abuse and no history of trauma, presented with progressive abdominal distension and features of peritonitis. In both cases. exploratory laparotomy revealed intraperitoneal rupture of the bladder. Primary repair was performed which was followed by an uneventful recovery. Spontaneous rupture of the bladder is a rare occurrence and when encountered, it presents a diagnostic challenge. A diagnosis of spontaneous perforation of the bladder should be considered in alcoholic patients presenting with an acute abdomen in a relatively stable condition and blood biochemistry showing a disproportionately elevated urea and creatinine.

Acute abdomen caused by spontaneous perforation of the urinary bladder in childhood: Report of one case

Spontaneous urinary bladder rupture in children is a very rare clinical occurrence that can be life threatening if left untreated. Patients usually present with symptoms of peritonitis and the correct diagnosis is usually made at surgery. Here, we present a case of spontaneous bladder perforation that was operated with a diagnosis of acute abdomen. No etiological factor for bladder perforation was found, and after the operation, the patient experienced no further problems.

Spontaneous, idiopathic urinary bladder perforation – case report

Spontaneous, idiopathic urinary bladder rupture is a very rare disease entity, which may face the problem of proper preoperative diagnosis. In many cases the medical history, physical examination, and additional tests raise false suspicion of gastrointestinal perforation. The study presented a case of a female patient with spontaneous urinary bladder perforation, paying particular attention to the diagnostic difficulties associated with the above-mentioned pathology. The aim of the study was to analyse the presence of symptoms and imaging and laboratory results observed in case of spontaneous urinary bladder rupture, as well as differentiate the above-mentioned pathology with gastrointestinal perforation. Whenever diagnosing a patient with acute peritonitis symptoms, in whom the predominating symptoms include sudden abdominal pain, peritoneal cavity fluid presence, hematuria, oliguria, and coexisting increased urea, creatinine, and potassium levels, one should consider the possibility of urinary bladder rupture.

Spontaneous Urinary Bladder Rupture Due to a Hypnotics Overdose

We reported on a hypnotic overdose young female who was taken to the emergency department because of abdominal pain, acute kidney injury, and an unexplained massive ascites. The final diagnosis was spontaneous urinary bladder rupture due to hypnotic-induced semi-coma. Hypontics overdose greatly influenced the patient’s ability to urinate and contributed to prolonged urinary retention, which resulted in the rupture of urinary bladder. However, the history and physical examinations of these intoxicated patients are usually questionable. As a result, we proposed a triad of clinical manifestations – abdominal pain, acute kidney injury and a massive ascites. The presence of these clinical findings together should prompt physicians to consider spontaneous urinary bladder rupture.

腹腔内遊離ガスを伴った膀胱自然破裂の1例

症例は78歳，男性．突然の右下腹部痛を主訴に前医を受診．消化管穿孔が疑われ当センターへ紹介となった．腹部造影CT検査にて腹腔内遊離ガスと腹水の貯留を認めた．また膀胱前壁に接しガスを伴う液体貯留を認めた．消化管穿孔を否定しきれず同日試験開腹術を行った．術中，消化管には異常を認めなかった．術後3日目に逆行性膀胱造影を行い膀胱穿孔と診断した．尿道留置カテーテルによって尿のドレナージは良好であることから保存的治療を行い軽快した．膀胱自然破裂はまれな疾患であり，臨床症状も様々であることから術前正診率が低く，他の急性腹症との鑑別が問題となる．本症例と文献的考察から膀胱周囲の液体貯留やガス像といった腹膜外の所見は本疾患を疑うべき所見である可能性が示唆された．

An unusual cause of death: spontaneous urinary bladder perforation

Spontaneous urinary bladder perforation is a rare and life-threatening condition similar to traumatic and iatrogenic perforation. The connection with the underlying bladder damage due to previous radiotherapy, inflammation, malignancy, obstruction, or other causes can be found in almost all cases. The symptoms are often nonspecific, and misdiagnosis is common. Here, we present a case of spontaneous urinary bladder perforation due to bladder necrosis in a diabetic woman. She presented to the emergency department with abdominal pain. Exploratory laparotomy was performed by surgeons and revealed necrosis of the anterior and lateral walls of the urinary bladder. Microscopic examination revealed necrotic changes throughout the bladder wall. Ghost-like cellular outlines were compatible with coagulative necrosis. Clusters of bacteria were also present in some necrobiotic tissues. Malignant cells were not present. It appears probable that the infection was due to local interference with the blood supply (arterial, capillary, or venous) combined with the systemic metabolic upset that led to the bladder condition. In our case, we observed partial necrosis of the bladder rather than distortion of the entire blood supply to the bladder as consequences of the microvascular effects of diabetes. Urinary bladder perforation must be considered in the differential diagnosis of patients presenting with free fluid in the abdomen/peritonitis, decreased urine output, and hematuria, and in whom increased levels of urea/creatinine are detected in serum and/ or peritoneal fluid aspirate.

Opioid toxicity as a cause of spontaneous urinary bladder rupture

Substance abuse, predominantly alcohol, is a recognized etiology of spontaneous bladder rupture. This is the first documented case of spontaneous urinary bladder rupture due to opioid toxicity in an adult.

Neonatal urinary ascites secondary to urinary bladder rupture

We describe the clinical presentation, radiology and clinical management of four neonates with spontaneous urinary bladder rupture and secondary urinary ascites seen in 1984 and two recent cases seen in 2007. All neonates had normal genitourinary systems on antenatal serial ultrasound scans. The management of these cases ranged from conservative management (n=3) to surgical repair of bladder (n=1). We present a review of the current literature covering management strategies and the possible role of ischemia in the pathogenesis of neonatal bladder rupture which continues to be a clinically challenging entity to diagnose and manage.

Spontaneous Perforation of Urinary Bladder Secondary to Candida Cystitis: Acute Abdomen of Urologic Origin

Spontaneous urinary bladder perforation is a rare event; presentation as an acute abdomen is rarer still. Fungal cystitis has seldom, and Candida albicans cystitis has never, to our knowledge, been reported as a cause of perforation. Case report and literature review. A 70-year-old woman with diabetes mellitus presented with an acute abdomen and urinary symptoms. A diagnosis of an intraperitoneal bladder perforation was made during emergency operation; culture of the peritoneal fluid and urine yielded Candida albicans. The initial high blood urea nitrogen and serum creatinine concentrations mimicked acute renal failure but were caused by urine absorption across the peritoneum. The patient was treated successfully with emergency laparotomy, a three-week course of fluconazole, and a five-day course of bladder irrigation with amphotericin B. Spontaneous urinary bladder perforation secondary to Candida cystitis should be considered as a possible cause of acute abdomen, especially when the biochemical profile suggests urine absorption and yeast is reported in the urinalysis of an immunocompromised patient.

Spontaneous Urinary Bladder Tumors in DA/Han Rats: A Feasible Model of Human Bladder Cancer

In a life-span study of virgin DA/Han inbred rats, 53.9% of the males and 14.4% of the females developed spontaneous urinary bladder tumors. A peak incidence was noted between the ages of 25 and 30 months. With the exception of 1 leiomyosarcoma, all neoplasms were of epithelial origin. After the papilloma, the majority of tumors were classified as transitional cell carcinoma of the papillary, solid, or mixed type. Less frequent were unclassified microcarcinoma, squamous cell, adenoid, and undifferentiated carcinomas. A sexual difference was found for almost every tumor type. Of the rats bearing tumors, 3.5% of the males and 64.4% of the females also were affected with urinary bladder stones. Squamous cell and glandular metaplasias of the tumors commonly were observed, and invasive growth into the bladder wall occurred frequently in less-differentiated tumors. Metastases were rare. The DA/Han rat strain is discussed as a suitable animal model for human urinary bladder cancer.

The effects of nicotine on spontaneous contractions of cat urinary bladder in situ.

Nicotine and dimethyl-phenylpiperazinium (DMPP) increased intravesicular pressure and then transiently depressed the spontaneous activity of the urinary bladder in chloralose anaesthetized cats. Adrenaline (5-10 micrograms kg-1), noradrenaline (5-20 micrograms kg-1) and isoprenaline (40-50 micrograms kg-1) which depressed spontaneous urinary bladder activity, were antagonized by the beta-receptor blocking agent propranolol (1 mg kg-1). Phenylephrine (10-30 micrograms kg-1) was ineffective on the urinary bladder though it increased the systemic blood pressure. This latter effect was blocked by the alpha-receptor blocking agent phentolamine (2 mg kg-1). Acetylcholine (2-8 micrograms kg-1) caused a marked fall in systemic blood pressure, which was potentiated by physostigmine, but failed to produce any response on the intravesicular pressure even after physostigmine (50-100 micrograms kg-1) treatment. ATP (2 mg kg-1) produced an increase in intravesicular pressure accompanied by a fall in systemic blood pressure. The increased intravesicular pressure was antagonized by quinidine (20 mg kg-1); however, the fall in blood pressure remained unaltered. The increased intravesicular pressure induced by nicotine (20-40 micrograms kg-1) or DMPP (50-100 micrograms kg-1) was not affected by phentolamine (2 mg kg-1), propranolol (1 mg kg-1) or guanethidine (15-20 mg kg-1). Physostigmine (50-100 micrograms kg-1), hemicholinium 3 (2 mg kg-1) or atropine (1 mg kg-1) were also unable to affect the response to nicotine. Hexamethonium (1 mg kg-1), reduced the amplitude of spontaneous bladder contractions and quinidine (20 mg kg-1) abolished the effect of nicotine. 7 Bilateral sectioning of the cervical sympathetic or hypogastric nerves did not alter the effect of nicotine or DMPP. Higher spinal cord transection (Cl-C2) blocked the spontaneous, as well as the nicotine- and DMPP-induced, contractions of the bladder. 8 It is concluded that the increase in intravesicular pressure induced by nicotine is atropineresistant and is not mediated either through adrenergic or cholinergic mechanisms. It is probable that a purinergic mechanism is involved, via the activation of P2-receptors present in the urinary bladder.

Opioid receptor subtypes involved in the central inhibition of urinary bladder motility

Intracerebroventricular morphine consistently inhibited spontaneous urinary bladder contractions recorded from the anesthetized rat. This effect was reversed by naloxone and appeared to be exerted within the forebrain. Neither dynorphin-(1–13) nor U-50, 488 (κ-agonists) affected bladder motility. Ethylketocyclazocine inhibited contractions only at higher doses, possibly due to μ-receptor interactions. Bladder activity was consistently inhibited by the μ-agonists morphiceptin and [D-Ala 2, MePhe 4, Gly-(ol) 5]enkephalin (DAGO) and by [D-Ala 2, D-Leu 5]enkephalin (DADLE, δ-agonist). DAGO was the most potent compound tested. These observations support the involvement of μ- and possibly δ-receptors in the centrally mediated inhibition of urinary bladder motility by opioids.

Morphine and the centrally-mediated inhibition of urinary bladder motility in the rat

Systemic administration of morphine consistently inhibited spontaneous urinary bladder contractions in the ketamine-anesthetized rat. In addition, i.c.v. morphine and levorphanol but not dextrophan inhibited bladder function by a naloxone-sensitive mechanism. Naloxone alone increased the frequency of bladder contractions and intravesicular pressure. Systemic loperamide did not affect bladder function while N,N-diallylnormorphinium only reversed bladder inhibition by morphine when administered i.c.v. These observations suggest that morphine inhibits bladder activity by a central mechanism and that endogenous opioids are involved in the central control of bladder function.