Physiologically, an acute mechanical obstruction causes an immediate stagnation of urine flow, triggering a significant, retrograde increase in hydrostatic pressure within the renal pelvis and calyces. According to Laplace’s Law, when the expanding intraluminal pressure outpaces the structural tensile strength of the delicate calyceal fornices, a macro-perforation occurs at the reflection point of the minor calyces. This rupture acts as a temporary, endogenous decompressing “safety valve” that drops intrapelvic pressure and can paradoxically mitigate acute renal colic.

However, when the obstructed urinary column is colonized by pathogenic bacteria, this protective mechanism is lost. The extravasation of infected urine into the highly vascularized retroperitoneal spaces significantly escalates morbidity, predisposing the patient to urosepsis, perirenal abscess formation, retroperitoneal fibrosis, and irreversible ischemic nephron loss. Management strategies vary from strict conservative observation in small, sterile leaks to aggressive intervention in complex scenarios. This case report highlights the critical role of timely endourological decompression and culture-targeted antimicrobial stewardship in managing an infected SRF secondary to obstructive urolithiasis.

A 43-year-old female with no prior history of urolithiasis or renal anomalies presented to the emergency department at Desouk General Hospital with an acute, unremitting left-sided flank pain of 24 hours’ duration. The pain was accompanied by high-grade fever, chills, nausea, and general malaise.

On physical examination, the patient was febrile (temperature: 38.8˚C), tachycardic (heart rate: 108 bpm), and normotensive (blood pressure: 115/75 mmHg). Extreme tenderness was elicited upon deep palpation of the left lumbar region and at the left costovertebral angle. There were no signs of generalized peritonitis, and no palpable abdominal masses or distended bladder were noted. Based on the temperature of 38.8˚C, heart rate of 108 bpm, and profound leukocytosis, the patient met the clinical criteria for Systemic Inflammatory Response Syndrome (SIRS) secondary to an acute urological infection.

Initial laboratory evaluations revealed a profound inflammatory response and a decline in renal function:

White Blood Cell (WBC) Count: 17.6 × 10³/μL (normal range: 4.0 - 11.0 × 10³/μL) with an absolute neutrophilic shift.C-Reactive Protein (CRP): 27.9 mg/L (normal: <5.0 mg/L).Serum Creatinine: 1.32 mg/dL. While the patient’s prior baseline creatinine was unknown, this elevated presentation value indicated a presumed Stage 1 Acute Kidney Injury (AKI) secondary to acute upper urinary tract obstruction.Urinalysis: Gross microscopic hematuria (>50 RBCs/HPF) and pyuria (>30 WBCs/HPF); positive for nitrites and leukocyte esterase.

An urgent transabdominal urological ultrasound was performed, revealing a left-sided obstructive pathology, severe distention of the extra-renal pelvis, and an irregular, hypoechoic fluid collection within the left perinephric space measuring approximately 4.5 × 3.2 cm.

To definitively characterize the collection and delineate the anatomy of the upper urinary tract, contrast-enhanced computed tomography (CECT) urography was performed. The corticomedullary and nephrographic phases confirmed moderate left hydroureteronephrosis secondary to an obstructing proximal ureteral calculus measuring 6 mm. Crucially, the delayed excretory phase (obtained 10 to 15 minutes post-injection) demonstrated a clear tear in the superior calyceal anatomy with active, high-attenuation contrast medium pooling outside the renal parenchyma into the perirenal space, confirming an acute urinoma secondary to spontaneous fornix rupture (Figure 1).

Figure 1. Axial and Coronal views of CECT Urography showing contrast extravasation from the left upper pole calyceal fornix into the retroperitoneum, establishing a localized urinoma.

Empiric broad-spectrum antibiotic therapy was initiated with third-generation cephalosporins (Ceftriaxone 2 g IV q24h). Concurrently, peripheral blood cultures were drawn, which subsequently showed no growth after 5 days. Clean-catch urine culture and sensitivity testing isolated Escherichia coli (>10⁵ CFU/mL) displaying an extended-spectrum beta-lactamase (ESBL) phenotype, characterized by absolute resistance to Ceftriaxone but marked susceptibility to Ertapenem and Levofloxacin.

Given the volatile combination of an obstructed, infected upper tract, active urine extravasation, severe SIRS criteria, and an escalating AKI, immediate endourological intervention was pursued. Under spinal anesthesia, the patient was placed in the lithotomy position. Rigid cystoscopy was performed, and a retrograde ureteropyelogram was deliberately avoided at the start of the procedure to prevent forcing infected urine further into the retroperitoneum under high pressure.

Under fluoroscopic guidance, a 0.035-inch hydrophilic guidewire was successfully negotiated past the obstructing ureteral stone. A 6 French, 26 cm polyurethane Double-J (DJ) stent was retrogradely deployed across the site of rupture to bridge the defect and bypass the obstruction. Cloudy urine was drained from the bladder and sampled for secondary intraoperative culture. This secondary intraoperative specimen subsequently confirmed the presence of the identical ESBL-producing E. coli strain found in the initial clean-catch sample.

Postoperatively, the patient was transferred to the inpatient ward, and antimicrobial therapy was narrowed to intravenous Ertapenem (1 g once daily) based on the sensitivity profile. The clinical response was prompt:

Within 24 hours: The patient became completely afebrile, and narcotic requirements for flank pain ceased entirely.Within 72 hours: Overall inflammatory markers and metabolic parameters stabilized drastically (WBC: 8.4 × 10³/μL), and renal parameters normalized completely, with serum creatinine stabilizing at its true baseline of 0.8 mg/dL.A chronological summary of the patient’s entire clinical timeline and lab transitions is detailed in Table 1.

Table 1. Clinical and laboratory timeline of the patient’s management course.

The patient was discharged on day 5 post-intervention with a 10-day course of oral Levofloxacin (500 mg once daily). Although the strain exhibited an ESBL phenotype, the in-vitro sensitivity profile explicitly confirmed complete susceptibility to fluoroquinolones, making oral Levofloxacin an ideal, highly bioavailable choice for oral step-down stewardship.

The DJ stent was kept in place for 6 weeks to ensure complete structural remodeling and sealing of the disrupted calyx. At the 6-week mark, the patient returned for elective stent removal. Following cystoscopic retrieval of the DJ stent, an on-table retrograde pyelogram (RPG) was performed. The RPG demonstrated a completely intact left pelvicalyceal system with normal calyces, unobstructed down-flow of contrast into the bladder, and an absolute absence of contrast extravasation or infundibular stricture formation (Figure 2). Fluoroscopic inspection and follow-up imaging at this time confirmed that the original 6 mm obstructing ureteral calculus had passed spontaneously, likely displaced or fractured during initial guidewire negotiation and subsequent internal stenting, leaving the patient entirely stone-free.

Figure 2. Retrograde Pyelogram (RPG) obtained after 6 weeks of stenting, demonstrating a normal pelvicalyceal architecture with complete resolution of the fornix leak and stone-free status.

At her 3-month outpatient follow-up, the patient remained completely asymptomatic, with sterile urine cultures and preserved renal function.

However, the clinical paradigm changes completely when there is an active infection, a large urinoma, persistent pain, or worsening renal function. In this case, the patient presented with all four high-risk indicators: severe urosepsis meeting full SIRS criteria, acute kidney injury, a sizable perirenal urinoma, and an ESBL-producing E. coli infection. Waiting for spontaneous stone passage or relying solely on antibiotics in an obstructed, infected system carries an unacceptably high risk of septic shock and perirenal abscess formation.

Immediate urinary diversion is the standard of care for infected systems to decompress the upper collecting system. Decompression can be achieved via either retrograde Double-J stenting or percutaneous nephrostomy (PCN) tube placement. In our patient, retrograde DJ stenting was chosen because it effectively bridges the site of the caliceal tear, redirects urine flow internally, and eliminates the elevated back-pressure that drives retroperitoneal extravasation. This internal diversion allows the torn fornix to heal cleanly through secondary intention over several weeks.

This case also underscores the diagnostic superiority of CECT urography with delayed-phase imaging [5]. While initial ultrasound is an excellent, radiation-free tool to detect hydronephrosis and large fluid collections, it lacks the spatial resolution to accurately locate the perforation site or differentiate a sterile urinoma from an acute hematoma or abscess [5]. Delayed excretory imaging (typically 10 - 15 minutes post-contrast) is crucial, as it shows high-density contrast media actively mixing with the pooling urine in the retroperitonium, providing a clear map of the anatomical leak.

Finally, performing a retrograde pyelogram at the time of stent removal is highly recommended. It serves as an objective, dynamic verification tool to confirm that the caliceal tear has healed completely and that no late-stage ischemic complications, such as infundibular or ureteral strictures, have developed.