Reflex anuria post-prophylactic bilateral ureteric catheterisation: a rare postoperative complication

Abstract

We highlight the case of a woman who had elective gynaecological surgery with bilateral prophylactic ureteric catheterisation, indicated for the excision of a mucinous cystadenoma arising from the right ovary. Surgery was successful with no intraoperative complications. Anuria and subsequent acute kidney injury developed within 12 hours of surgery. A CT of the kidneys, ureters and bladder revealed mild bilateral hydronephrosis and perinephric stranding surrounding the left kidney with no discernible injury to the lower urinary tract. Further investigation did not reveal a clear cause for her anuric state. Management involved aggressive renal support, rigid cystoscopy and bilateral ureteric stenting. Diuresis and a prompt improvement in renal function ensued with no further complications. She was discharged a week after her initial operation, with a 6-week review for stent removal. We believe this to be a rare instance of reflex anuria due to ureteric spasm and encourage consideration of ureteric stenting as part of subsequent management.

Background

Anuria and acute renal failure are common postoperative complications cited to occur in around 1% of surgical patients.¹ Reflex anuria is a rare cause of postoperative anuria. It has a rapid onset leading to a sudden deterioration in kidney function. Reflex anuria was described by Hull in 1980 as ‘cessation of urine output from both kidneys in response to irritation or trauma to one kidney or its ureter, or severely painful stimuli to the other organs’.² Reference to reflex anuria is scant in medical literature such that it is often not included within the differential diagnosis for postoperative anuria. There are various pathophysiological mechanisms proposed in case reports describing reflex anuria, however, there is little consensus on which mechanisms are truly viable. As such, reflex anuria remains a diagnosis of exclusion. By discussing this case, we hope to add to the current literature and provide further insight into the presentation, mechanism and management of reflex anuria.

Case presentation

An 80-year-old woman, with a past medical history of chronic hypertension and a transient ischaemic attack in early 2016, presented to the rapid access clinic with marked right iliac fossa pain and nausea. Past surgical history involved a total abdominal hysterectomy with conservation of ovaries 30 years prior: a curative treatment for disabling menorrhagia. She was para 2, both children born via spontaneous vaginal deliveries. On both bimanual and speculum examination, there were no abnormalities detected. Ultrasound scans (transvaginal and transabdominal) revealed a unilocular cyst on the right ovary. The ovarian cyst measured 75 mm by 64 mm and had two central echogenic areas within diffuse low-level echoes with no associated colour flow (figure 1). There was no free fluid adjacent to the cyst. An MRI scan, requested in view of the complex nature of the cyst, a raised carbohydrate antigen-125 level of 54 (Normal Range (NR) <37) and an alpha-fetoprotein of 9 (NR<7), deemed the cyst benign. Both kidneys were deemed unremarkable on review of the preoperative computed topography and magnetic resonance scans (figures 2 and 3). Subsequent histological investigation confirmed a benign mucinous cystadenoma.

Figure 1.

Transvaginal ultrasound scan of unilocular right ovarian (RO) cyst with internal echoes. Within the second image, a hyperechoic structure can be seen within the cyst.

Figure 2.

Preoperative coronal MRI scan showing no evidence of hydronephrosis.

Figure 3.

Preoperative coronal CT scans showing no evidence of hydronephrosis or perinephric stranding.

The patient was consented for an elective laparoscopic bilateral salpingo-oophorectomy to include cystoscopy and prophylactic bilateral ureteric catheterisation. Bilateral prophylactic ureteric stents were placed to prevent possible intraoperative ureteric injury in view of her previous history of total abdominal hysterectomy. Preoperative assessment showed good renal function, with a creatinine of 55 μmol/L (NR 45–84 mmol/L) and a urea of 5.1 mmol/L (NR 2.5–7.8 mmol/L). The operation was successful; there were no complications or significant blood loss.

Within 12 hours of surgery, the patient became anuric, passing just 15 mL of urine over the next 12 hours. Blood tests revealed deranged kidney function with a rise of creatinine to a peak of 286 mmol/L (NR 45–84 mmol/L), rise in urea to 12 mmol/L (NR 2.5–7.8 mmol/L) and an estimated glomerular filtration rate of just 14 mL/min. These values were consistent with acute kidney injury stage 3. Sodium and potassium levels remained within normal range throughout. On clinical examination, the patient was haemodynamically stable and showed no signs consistent with renal compromise.

Investigations

A CT of the kidneys, ureters and bladder (CT-KUB) demonstrated mild bilateral hydronephrosis of the renal calyces, slightly more advanced on the left side (figure 4). There was perinephric stranding seen in the left paracolic gutter (figure 5). When compared with preoperative imaging (figure 3), these findings are not seen. On postoperative CT-KUB, both ureters were normal in shape and calibre with no evidence of injury, highlighted by the absence of contrast leaking into the peritoneal cavity. There was no oedema of the ureteral orifices leading into the bladder when visualised during cystoscopy. Urine microscopy, culture and sensitivity were negative for white blood cells and organisms. On urinalysis, she was positive for blood (1+) however this appeared to be longstanding as this was noted on previous urine dipstick results. No epithelial cells, yeasts or crystals were seen on microscopy. Urine culture showed no bacterial growth. Wound drain fluid analysis was insignificant and showed no evidence of urine leakage into the abdomen. Serum creatine kinase was within normal range (77 units/L, NR 25–200). Complement C3 and complement C4 were slightly low: 0.76 (NR 0.79–1.52) and 0.15 (NR 0.16–0.38), respectively. There was no evidence of sepsis or bacteraemia as blood cultures were negative throughout her admission and the patient remained apyrexial. The patient was only exposed to piperacillin–tazobactam during her admission.

Figure 4.

Postoperative coronal and axial CT scan showing mild bilateral hydronephrosis (arrowed).

Figure 5.

Postoperative sagittal CT scan showing perinephric stranding around the left kidney (arrowed).

Differential diagnosis

Acute kidney injury can occur due to prerenal, intrinsic and postrenal causes.

Acute kidney injury according to the Kidney Disease Improving Global Outcomes (KDIGO) guidelines can be defined as³:

• ‘An increase in serum creatinine by ≥0.3 mg/dL within 48 hours or’.³

• ‘An increase in serum creatinine by ≥1.5 times baseline which is known or presumed to have occurred within the prior 7 days or’.³

• ‘Urine volume <0.5 mL/kg/h for 6 hours or’.³

Prerenal aetiology revolve around various causes of hypoperfusion, such as reduced intravascular volume, reduced arterial pressure and medications like angiotensin-converting enzyme inhibitors and nonsteroidal anti-inflammatory drugs. Our patient was haemodynamically stable throughout surgery and the immediate postoperative period and she was not exposed to any medication which could induce an ischaemic state.

Intrinsic renal causes depend on damage to the renal architecture (glomeruli, tubules or interstitium). Acute tubular necrosis, the most common, has multiple aetiology dependent on ischaemic or nephrotoxic factors. Acute interstitial necrosis is often associated with infection or adverse reactions to medication. Urinalysis and further biochemical investigations gave no indication to suggest an intrinsic reason behind the anuria.

Postrenal causes of acute renal failure are often associated with an obstructive uropathy or damage to the lower urinary tract. When investigated, the CT-KUB, cystoscopy and retrograde ureteropyelogram all showed no implicit injury or obstruction beyond the level of the renal calyces thus making this diagnosis unlikely. As a result, this patient was diagnosed with reflex anuria, a diagnosis of exclusion.

Treatment

Further management in intensive care involved intravenous fluid administration to encourage diuresis with regular assessment of fluid balance. Cystoscopy and retrograde ureteropyelogram were normal with no abnormalities detected. Bilateral stents were inserted day two postoperative, with subsequent prompt diuresis and normalisation of kidney function.

Outcome and follow-up

Renal function improved considerably with encouraging diuresis and concomitant reduction in urea and creatinine levels. From a preoperative creatinine level of 63 mmol/L to a peak 286 mmol/L recorded on the second day following surgery and just prior to ureteric stent insertion, creatinine levels steadily declined once the stents were inserted and were recorded as 55 mmol/L on the day of discharge. Her renal function had returned to baseline. The patient was discharged 7 days after her initial operation with no complications as a result of her anuric state. Prevention of postoperative sepsis with a 5-day course of intravenous piperacillin–tazobactam continued in the community with a 5-day course of amoxicillin with clavulanic acid on discharge. Both stents were removed simultaneously under general anaesthetic 6 weeks after discharge.

Discussion

Our patient’s presentation was consistent with the reflex anuria classification described by Hull in 1980.² Hou et al inferred from Hull’s description that reflex anuria could develop through six mechanisms.⁴ Their classification is dependent on two factors: the site where the stimulus may have originated and the proposed anuric mechanism (either spasm of intrarenal arterioles or spasm of ureters).⁴ Due to the scarcity of published reports, it is difficult to identify which mechanism/s may actually occur.

We believe our patient demonstrates reflex anuria due to ureteral spasm. There are similar case reports in literature describing reflex anuria due to a postrenal cause. Gholyaf et al described a patient who underwent hysterectomy for endometrial cancer with subsequent postoperative anuria, believed to be a case of ureteral spasm.⁵ Adediran and Dhakarwal documented a similar case of postoperative oliguria investigated by renal ultrasound, showing mild hydronephrosis and no implicit signs of ureteric injury.⁶ Reflex anuria and proposed ureteral spasm is not a solely gynaecological surgery complication. Reflex anuria due to ureteric spasm has been discussed in colorectal and cardiac surgery cases.^{7 8}

Many case reports imply fluid management and renal support as essential components in the treatment of reflex anuria.^5–8 Some have gone further to advocate therapeutic ureteric stenting to prompt diuresis, as done for our patient.^{8 9} It is unclear whether stenting should be an integral part of management or considered on a case-to-case basis. Another aspect to consider is the duration of therapeutic stenting and the method of removal. Favourable outcomes have been described by different authors who have utilised varying periods of ureteric stenting in their management of reflex anuria. Singh et al documented two cases where ureteric stents were removed 14 days after the onset or anuria⁷ yet in comparison, similar to the case we have presented, Jeegavan et al adopted an approach where stents were retained for more than 4 weeks.⁸ Stepwise removal of ureteric stents compared with simultaneous removal has also been explored in literature.^{7 9}

Elucidating the exact mechanism/s of reflex anuria remains difficult due to the rarity of the condition and the lack of clinical awareness. As a result, determining optimum therapy also proves difficult. Fluid management and renal support with or without therapeutic stenting seems to recur in literature as a possible treatment, ideally to keep the patient stable until adequate diuresis returns. The diagnosis and management protocol will vary on a patient specific basis but we hope that our case adds to the existing literature and raises clinical awareness about this rare clinical state.

Learning points.

• Reflex anuria is a rare cause of postsurgical anuria and acute kidney injury.

• Reflex anuria is often a diagnosis of exclusion.

• Other aetiology must be considered and investigated for prior to a diagnosis of reflex anuria.

• Management of reflex anuria may include bilateral ureteric stenting, renal support and fluid resuscitation.