Malani K*, Samant PY**, Thakur H***.
(* Junior Resident, ** Academic Professor, *** Assistant Professor. Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M Hospital, Mumbai, India.)
Bladder and uterine injury during instrumental delivery is a known complication but isolated intraperitoneal bladder rupture following instrumentation is rare. Etiology cannot be established if historical sequence is unclear and bladder injury may be blamed on the instrumentation which in all probability was without complications. We present a case of isolated spontaneous postpartum bladder rupture without uterine rupture because of its rarity.
Assisted vaginal delivery is application of art of obstetrics in stressful conditions. The application outcome depends more on judgment, training and experience of obstetrician. The rate of operative vaginal delivery broadly varies worldwide and is commonly about 10-12 % of all deliveries.[1,2] Though forceps application is associated with genital tract as well as bladder trauma, isolated injury to bladder after instrumental delivery is rare. The sequence of events requires close scrutiny before bladder rupture is attributed to instrumentation. Spontaneous puerperal bladder rupture may occur if bladder emptying does not occur due to painful episiotomy and spasm; or unanticipated pressure necrosis due to prolonged pressure of compression by fetal head against symphysis pubis.
A 31 year old para 1 living 1 delivered a child of 2.6 kg via outlet forceps for fetal indication at a tertiary care center. She was discharged uneventfully after 3 days. On the 7th postpartum day, she had multiple low grade fever spikes along with complaints of abdominal distension, pain, constipation, burning micturition and incomplete urinary evacuation. She followed up in the previous center and was referred to our hospital in view of deranged renal function tests, requiring super specialty management. On admission, she had stable vital parameters. Bowel sounds were sluggish, there was suprapubic tenderness, and it was dull on percussion. The fundus of the uterus could not be felt well on account of distension and tenderness. Vaginal examination revealed closed internal os, healthy lochia and a healing episiotomy wound. She was kept nil by mouth, started on intravenous fluids, and empirical antibiotics. Urethral catheter (PUC) was inserted and 1.5 liters of clear urine was drained. In her serological and biochemical investigations, her renal function tests were deranged with serum creatinine levels of 3.8 mg%, blood urea nitrogen levels of 65.3 mg%, and blood urea level of 139 mg%. Tests for malaria, leptospirosis and dengue were negative. Hemoglobin (Hb) was 8.9 gm% and WBC Count was 14,600/cmm, C reactive protein was 158 mg/L. She was assessed by a nephrologist. Intake output charting, urine routine, microscopy, urine culture and antibiotic sensitivity and ultrasonography (USG) for kidney, ureters, and bladder were advised. The urologist advised continuous bladder drainage, full bladder and post void USG, non-contrast CT ( NCCT) with intravesical contrast (CT cystogram). USG was suggestive of mild bilateral hydronephrosis with mild jejunal dilatation. NCCT scan (with intravesical contrast, no intravenous contrast used due to deranged renal function tests) was suggestive of mild ascites with multiple pockets of collection with diffuse omental and mesenteric fat stranding. Postpartum bulky uterus and normal adnexae were noted. Final diagnosis was paralytic ileus with cystitis and acute kidney injury. Urine culture grew Klebsiella pneumoniae sensitive to Piperacillin tazobactum (Piptaz) / Amikacin/ and Imipenem. She was started on injection Piptaz (4.5 mg), Injection Metronidazole (100 c.c.), and was gradually shifted to oral fluids after assessing her bowel sounds. She recovered clinically, passed flatus and stools. The renal function gradually improved. Foley’s catheter was removed after 4 days. Catheter drained adequate clear urine on each of these 4 days. She was able to pass urine with no urinary complaints. She was discharged at a creatinine level of 0.7 mg%. She was referred from a private hospital to our center again on day 20 postpartum, with recurrence of fever spike, pain in abdomen, inability to pass urine and pyuria. Contrast enhanced CT scan done in private hospital showed loculated peripheral enhancing fluid collection continuous with bladder suggestive of intraperitoneal bladder rupture.
She was received in surgical emergency unit with catheter in situ, she was afebrile with stable vital parameters. There was abdominal distension (bowel sounds were present) with suprapubic tenderness. Involuting uterus with closed os was noted. Episiotomy wound had gaped superficially. She was kept nil by mouth, started on intravenous fluids. In her biochemical reports the Hb was 9.5gm%, WBC was 8900/ cmm, serum creatinine was 0.5 mg%, Blood urea nitrogen was 5.2 mg%. Serum electrolytes were within normal limits. USG was suggestive of 83 cc of thick septated collection in the right paracolic gutter extending into inter bowel space suggestive of bladder rupture. CECT showed hypo dense collection of 5 x 2.4 cm with enhancing walls and a track extending from pouch of Douglas to sub hepatic region, clumped bowel loops in left iliac fossa with collection around them. Distended bladder showed a breach of 1.9 cm in left anterio-superior border with spillage in left iliac fossa. Exploratory laparotomy with bladder repair was advised by urologist. Intraoperatively, an abscess cavity formed by small bowel, sigmoid colon, uterus and bladder fundus with approximately 30 c.c. of pus was evident. Cavity was opened, with sharp dissection. Uterus was found intact. A 2 x 1 cm accidental bowel serosal tear during dissection was identified and sutured. Rest of small bowel and sigmoid colon were normal. A 4 x 5 cm of rupture site with irregular inflamed margins was seen on the bladder dome. Its edges were freshened. Bilateral ureteric orifices were cannulated and brought out via 20 Fr urethral catheter. Bladder fundus was sutured with polyglactin 2-0 in two layers after placing 16 Fr. suprapubic catheter. Methylene blue test was done to rule out leak. Abdominal drain was kept in pelvis before closure to facilitate drainage of any pelvic collection. Episiotomy wound needed only dressing. She recovered uneventfully and was discharged with catheters in situ. At follow up, her ureteric and suprapubic catheters were removed after normal cystogram. This was followed by per urethral catheter removal after the 21st post operative day. Episiotomy wound healed by secondary intention.
An isolated intraperitoneal bladder rupture following vaginal delivery is rare.[3,4] The term “spontaneous rupture of urinary bladder- SRUB” was coined by Sisk and Wear. In obstetric patients, bladder rupture is often accompanied by uterine rupture. In obstetrics, isolated bladder rupture is observed in very few cases. Sustained pressure from fetal head against bladder during forceful uterine contractions can lead to pressure necrosis of the weakest part that is bladder dome and bladder rupture. Other factors include large baby weight, prolonged duration of the second stage, history of previous pelvic surgery, bladder diverticula and neuropathic bladder. Bladder rupture is likely during labor if it is not emptied before instrumentation. If the rupture occurs in spite of regular drainage; it is likely to have occurred postpartum. Unnoticed urinary retention or incomplete evacuation during puerperium due to pain of perineal repair causing retention may lead to subsequent bladder rupture. Bladder rupture in our case is most likely to have occurred postpartum since the patient gave history of being catheterized before forceps application and had no urinary complaints at discharge. We feel that our patient had a neuropathic bladder which must have overdistended again on discharge and ruptured spontaneously at some point at home. Already her urine had infection (Klebseilla had grown) and on Day 20 pyuria was also seen suggestive of infection. Patients usually present with anuria/ oliguria/ haematuria and abdominal pain. Urinary ascites is not seen as frequently because there is rapid absorption of urine from peritoneal cavity.
The choice of imaging is CT cystogram. Inadequate filling with dye, obstruction by omentum, clot or surrounding organ could temporarily block small bladder rent leading to false negative CECT. High index of suspicion and prompt intervention are required if a patient presents post-delivery with acute urinary retention and ascites.
Presence of acute renal failure, bowel ileus and new onset ascites in a postpartum patient with uneventful immediate postpartum course should always raise a suspicion of bladder rupture and prompt the treating physician to confirm the diagnosis. One should be cautious before incriminating the instrumentation for the same.
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Malani K, Samant PY, Thakur H. Postpartum Urinary Bladder Rupture. JPGO 2019. Vol 6 No. 5. Available from: https://www.jpgo.org/2019/05/postpartum-urinary-bladder-rupture.html