Educational disclaimer. This article is a historical surgical case report accompanied by an updated discussion. It is intended for clinician education and is not medical advice. Management of pediatric urolithiasis should follow current clinical practice guidelines and individualized assessment by the treating pediatric urology and nephrology teams.
Bladder Stone in a Child
Introduction
A case of a 20-month-old boy with an endemic-pattern bladder stone prompted a historical and pathophysiologic review of bladder calculus disease. The history of “cutting for stone,” the principal hypotheses of stone formation, and the contemporary management of children with bladder calculi are outlined. Modern recommendations are anchored to the EAU Guidelines on Paediatric Urology and the EAU Guidelines on Urolithiasis — 2025 update, with a comprehensive 2026 synthesis available in Paediatric Urolithiasis: Medical & Surgical Management.
Historical case report
This one-year eight-month old boy had a 5-month history of straining and crying on passing urine and a 1-day history of passing blood in the urine. On physical examination he appeared well nourished, afebrile and normotensive. He had a distended bladder but his kidneys were not palpable. His genitalia and other systems were normal. Results of investigations were:
| Test | Result | Unit | Test | Result | Unit | |
|---|---|---|---|---|---|---|
| Hb | 11.4 | gm/dL | PCV | 35 | L/L | |
| WBC | 6.5×10^9 | /L | Plts | 255×10^9 | /L | |
| Na | 135 | mmol/L | K | 3.6 | mmol/L | |
| Cl | 108 | mmol/L | HCO3 | 20 | mmol/L | |
| BUN | 5.9 | mmol/L | Creat | 62 | µmol/L | |
| Calcium | 2.2 | mmol/L | Phosphate | 1.6 | mmol/L | |
| Uric acid | 0.24 | mmol/L | Proteins | 67 | g/L | |
| Albumin | 40 | g/L | Globulin | 27 | g/L | |
| Alk phos | 86 | IU/L |
Sickle test was negative. Urinalysis confirmed microscopic hematuria; urine culture grew E. coli and Klebsiella pneumoniae. Abdominal radiographs showed an oval opacity in the pelvis (Fig 1). The intravenous urogram (IVU) showed a filling defect within the bladder. The kidneys and ureters appeared normal with prompt bilateral excretion of contrast. Voiding cystourethrogram was normal. Twenty-four-hour urine and stone analyses were not available.
Modern equivalent: First-line imaging in pediatric stone workup is renal–bladder ultrasound, with low-dose non-contrast CT reserved for cases where ultrasound is inconclusive or detailed anatomy is needed for surgical planning; IVU is no longer used. Stone-composition analysis (Fourier Transform Infrared {FT-IR} spectroscopy or X-ray diffraction) and a 24-hour urine metabolic profile (calcium, oxalate, citrate, uric acid, cystine, creatinine, sodium, volume, pH) are standard of care after a first pediatric stone (EAU Paediatric Urology; Paediatric urolithiasis review 2026, PMC13010805; Pediatric metabolic evaluation 2025, PMC12219921).
A diagnosis of bladder calculus associated with urinary tract infection but no underlying anomaly was made. Gentamicin was started preoperatively. At open cystolithotomy a 3-cm oval bladder calculus was removed. No bladder or bladder-neck abnormality was detected. A retropubic drain was placed and bladder drainage achieved with a Foley urethral catheter. Oral nalidixic acid was added postoperatively for a gentamicin-resistant Klebsiella. The drain and catheter were removed on postoperative days 2 and 4. The patient was discharged on day 7. At four-week follow-up he was asymptomatic with no vesical pathology.
Modern equivalent: A 3-cm bladder stone in a toddler today would typically be managed endoscopically — by transurethral cystolitholapaxy for accessible stones, or by percutaneous cystolithotripsy (PCCL) for larger or hard stones in small children, where a 2025 randomized trial showed PCCL achieved higher stone-free rates with shorter operative time than transurethral cystolitholapaxy (Sharifiaghdas et al., Urology 2025). Open cystolithotomy is reserved for selected complex cases (very large or multiple stones, concurrent bladder reconstruction, severe outlet obstruction, or limited access to endourologic instrumentation) (Endourology vs open cystolithotomy systematic review, PMC11406119). Nalidixic acid is no longer recommended in pediatric UTI; current practice is culture-directed antibiotic therapy informed by local antibiograms (AAP UTI clinical practice guideline).
Discussion
1. History of “cutting for stone”
The oldest bladder stone ever discovered came from a 16-year-old’s grave at El Amrah in upper Egypt, dated to about 4800 BC. Among the Egyptians and Indians, “cutting for stone” was performed many centuries before Christ. The first well-recognized operation for bladder stone was perineal lithotomy, popularized by Ammonius of Alexandria in the third century BC and unchanged until Joannis de Romanis of Cremona devised a better perineal operation about 1520 AD. Frère Jacques introduced lateral lithotomy in the seventeenth century and reportedly removed 4,500 bladder stones during his career. Cheselden was a lateral lithotomist who two centuries ago operated on 213 patients with a mortality of 9.3%. Franco (1556) employed suprapubic lithotomy, later placed on a scientific basis by John Douglas. Crushing calculi by open operation was known to Ammonius (~230 BC); Sanctorius (1626) devised a crude crushing instrument; Civiale (1824) made the operation reasonably safe; and Bigelow (1878) introduced litholapaxy, in which the calculus is crushed and the fragments evacuated through a metal tube. The visualizing lithotrite followed, and later the electronic lithoclast.
Contemporary endourologic instrumentation includes pneumatic (Lithoclast), ultrasonic, electrohydraulic, and laser (holmium:YAG, thulium fibre laser) intracorporeal lithotripsy delivered through transurethral or percutaneous access (Paediatric urolithiasis review 2026, PMC13010805).
2. Epidemiology and aetiology
Primary (endemic) bladder stones remain rare in Europe and North America and prevalent in parts of South Asia, North Africa, sub-Saharan Africa, and the Middle East, where they typically occur in boys under 10 years, with a male predominance of approximately 8–12:1. Endemic bladder stones are strongly associated with low socioeconomic status, breastfeeding-to-cereal weaning transitions (low-phosphate, high-cereal diets), recurrent diarrhoea, and chronic dehydration (Endemic Bladder Stone Disease in Children, Urology Journal 2024; Global burden of urolithiasis — GBD 2025).
Urolithiasis has a multifactorial aetiology with genetic, dietary, environmental, and infectious contributions. Stone-formers commonly show increased urinary oxalate, calcium, ammonia, and urate, decreased urinary citrate, pyrophosphate, sulphate, and magnesium, and frequent oxalate crystalluria. The key physicochemical factors are urine volume (concentration), concentrations of specific crystalloids (calcium, oxalate, uric acid), urinary colloids, pH, infection, and damage to the urothelium (Paediatric urolithiasis review 2026, PMC13010805).
3. Crystallization and stone-formation theories
Crystalluria and free particles: The solubility product and formation product define a metastable zone in which nucleation determines whether crystals form. The nucleus may be the same chemical (homogeneous nucleation) or a different crystal (heterogenous nucleation/epitaxy), or other particles/surfaces. Within the metastable range, nucleation followed by rapid aggregation (driven by Van der Waals forces) can lead to retention and stone formation. Episodic dehydration, lithogenic diet, and changes in pH act as trigger factors.
Calcium oxalate: Calcium oxalate remains the dominant constituent in many stone populations. Urate favors its crystallization; oxalate (rather than phosphate) is the key determinant of calcium crystallization at normal urinary pH. Post-prandial alkaline tides favor calcium-phosphate nuclei on which calcium oxalate can crystallize. Factors affecting oxalate excretion include diet, pyridoxine deficiency, steatorrhoea, intestinal surgery, and primary genetic hyperoxaluria.
Matrix theory: Renal and bladder epithelium produce a matrix of mucoproteins and mucopolysaccharides (Tamm–Horsfall protein/uromodulin, albumin, globulins, uromucoid, matrix substance A) that participate in stone initiation, mineralization, and aggregation. Most calculi show concentric inorganic-and-organic deposits. Modern work integrates the matrix framework with microbiome–lithogenesis interactions, especially for struvite and infection stones (Bacteria and urinary stones — review 2024, Frontiers in Medicine).
Inhibitor theory: Urinary colloids — high-molecular-weight glycosaminoglycans and mucoproteins — adsorb cations, inhibit nucleation, aggregation, and growth, and explain the metastable zone in normal urine. Smaller-molecular-weight inhibitors include citrate, pyrophosphate, and magnesium. Decreased urinary fibrinolytic activity has been documented in some stone-formers, but fibrinolytics have not entered clinical guidelines; modern guideline-supported preventive therapies are fluid liberalization, potassium citrate, thiazides (for hypercalciuria), allopurinol (for selected uric-acid stones), and dietary modification (EAU Urolithiasis 2025).
4. Infection and stone disease
In children with infection-associated stones, E. coli and Proteus species are common. Modern series also report Klebsiella, Pseudomonas, Providencia, Morganella, Staphylococcus saprophyticus, and other urease-positive organisms. Urease activity generates ammonia, alkalinizes the urine, and drives deposition of struvite (magnesium ammonium phosphate) and apatite (basic calcium phosphate). Alkaline urine also reduces the protective effect of urothelial-surface macromolecules, favouring both nucleation and retention. Emerging evidence implicates the urinary microbiome in stone susceptibility and recurrence (Frontiers in Medicine 2024 review).
5. Stone composition
In children with endemic bladder stones, calcium oxalate and ammonium acid urate are the dominant constituents; struvite appears with infection. Calcium phosphate, uric acid, and cystine stones are seen in the broader pediatric urolithiasis population, particularly when an underlying metabolic disorder is present (Endemic Bladder Stone 2024; PMC13010805).
6. Clinical presentation
A boy with a bladder stone characteristically pulls on his penis, while a girl may press on her perineum during micturition. The classic constellation is interruption of the urinary stream, dysuria, frequency, suprapubic pain, and intermittent hematuria. Typical renal colic is not a major presenting symptom. The differential includes UTI, foreign body, and anatomic outflow problems. Important predispositions in older children and adolescents include bladder augmentation/reconstruction, Mitrofanoff and other continent catheterizable channels, neuropathic bladder, exstrophy-epispadias complex, bladder-neck procedures for incontinence, and bladder diverticula (PMC13010805).
7. Workup
- Imaging: First-line renal-bladder ultrasound; low-dose non-contrast CT when ultrasound is inconclusive or surgical planning requires it. Voiding cystourethrogram in selected cases for bladder/urethral anatomy (EAU Paediatric Urology).
- Stone composition: FT-IR or X-ray diffraction on the retrieved stone — standard of care after a first pediatric stone.
- Metabolic workup (24-hour urine): Calcium, oxalate, citrate, uric acid, cystine, creatinine, sodium, magnesium, volume, and pH; serum chemistries including calcium, phosphate, magnesium, bicarbonate, uric acid, parathyroid hormone, and 25-OH vitamin D (PMC12219921 (2025); PMC13010805).
- Genetic testing for primary hyperoxaluria, cystinuria, distal renal tubular acidosis, Dent disease, and other monogenic stone disorders when indicated by metabolic profile or family history.
8. Surgical management
A tiered, minimally-invasive-first algorithm is the current standard, with open cystolithotomy reserved for selected complex cases or resource-limited settings:
| Approach | Indications | Notes |
|---|---|---|
| Transurethral cystolitholapaxy (TUCL) | Smaller, accessible stones; cooperative anatomy | Pneumatic (Lithoclast), ultrasonic, or laser (Ho:YAG, thulium fibre) intracorporeal lithotripsy |
| Percutaneous cystolithotripsy (PCCL) | Larger or hard stones, small children with limited urethral working channel, multiple stones | 2025 RCT shows higher stone-free rate and shorter OR time vs TUCL in selected pediatric patients (Sharifiaghdas 2025) |
| Shock-wave lithotripsy (SWL) | Selected cases, generally less effective for bladder stones than for renal stones | Limited role for bladder stones |
| Open cystolithotomy | Very large/multiple stones, concurrent bladder reconstruction, severe outlet obstruction, limited endourologic resources | Remains “simple, safe, and satisfactory” and allows concurrent correction of bladder-neck obstruction or diverticulum |
Concurrent correction of any predisposing anomaly (bladder-neck obstruction, diverticulum, posterior urethral valves, exstrophy/epispadias-related issues) should be planned at the same operation when feasible (EAU Paediatric Urology; PMC11406119; PMC13010805).
9. Medical management of underlying metabolic conditions
- General measures: Age-appropriate fluid liberalization to maintain dilute urine; balanced diet; treat UTIs promptly with culture-directed antibiotics.
- Hypercalciuria: Maintain normal age-appropriate calcium intake (calcium restriction is no longer recommended), sodium restriction, and fluid liberalization; use thiazide diuretics and potassium citrate for refractory hypercalciuria.
- Hyperoxaluria: Distinguish primary hyperoxaluria (PH1, PH2, PH3) from secondary/dietary. Lumasiran (RNA-interference therapy targeting hepatic glycolate oxidase; FDA-approved 2020) is the major net-new therapy for PH1; pyridoxine remains useful for selected pyridoxine-responsive PH1 mutations. Dietary oxalate restriction and calcium with meals for secondary/enteric hyperoxaluria (FDA lumasiran label; PMC13010805).
- Distal renal tubular acidosis: Urinary alkalinization with potassium citrate preferred over bicarbonate alone.
- Uric-acid stones: Allopurinol for hyperuricosuria, with urinary alkalinization (potassium citrate) and hydration.
- Cystinuria: Hyperhydration; urinary alkalinization with potassium citrate to pH 7.0–7.5; dietary sodium and protein restriction; tiopronin (α-mercaptopropionylglycine) is preferred over D-penicillamine because of fewer adverse events (EAU Urolithiasis 2025; Cystinuria stone in a child, 2025).
- Struvite/infection stones: Complete surgical clearance plus culture-directed antibiotics.
- Reconstructed/neurogenic bladders: Optimize catheterization technique, mucus management for augmented bladders (regular bladder irrigation), and prevent retention.
10. Recurrence and follow-up
Recurrence of endemic bladder stones in otherwise normal children is low (often quoted <1%). In metabolic stone formers and in reconstructed or neurogenic bladders, recurrence is substantially higher and lifelong surveillance is appropriate, with periodic ultrasound, metabolic re-evaluation, and adjustment of medical therapy (PMC13010805; PMC12219921 (2025)).
Conclusion
Endemic pediatric bladder stones persist in regions where nutritional and socioeconomic risk factors remain, and continue to decline where those factors improve. For an individual child with a bladder stone, modern best practice combines ultrasound-first imaging, stone-composition and 24-hour urine metabolic evaluation, endourologic surgery (transurethral cystolitholapaxy or percutaneous cystolithotripsy) as first-line, with open cystolithotomy reserved for selected complex or resource-limited situations, and guideline-directed medical therapy of any underlying metabolic, infective, or anatomic disorder, with risk-stratified long-term follow-up.
References
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