Urinary Stones
Urinary stones are solid crystalline deposits formed within the urinary tract from supersaturated urine, most commonly composed of calcium oxalate, that can cause obstruction, pain, and renal damage.
Urinary Stones (Urolithiasis)
Urolithiasis ("uro" = urine, "lith" = stone, "iasis" = condition) refers to the formation of calculi (stones) anywhere within the urinary tract — kidneys (nephrolithiasis), ureters (ureterolithiasis), bladder (vesical calculi), or rarely the urethra. These stones form when dissolved minerals in the urine supersaturate and crystallise, aggregate, and grow into macroscopic concretions that can obstruct urinary flow, cause intense pain, and predispose to infection.
The classic clinical presentation is renal colic (colicky loin-to-groin pain) with haematuria. This is one of the most common urological emergencies you'll encounter. [1][2]
- Lifetime prevalence is substantial: up to 16% in males and 8% in females will have ≥1 symptomatic stone episode by age 70 [1][3]
- Male predominance (M:F historically ~3:1, now narrowing to approximately 4:3 in recent series) [1][3]
- Peak incidence between 30–50 years of age [3]; other sources cite the 40–60 age bracket [1]
- Recurrence is the rule, not the exception: risk of recurrence after the first stone is ~15% at 1 year, 35–40% at 5 years, and 50% at 10 years [3]
- Overall population prevalence approximately 10% [2]
- Geographic variation: more common in hot, arid climates (the "stone belt" phenomenon — higher rates in Middle East, Southeast Asia, southern United States) due to dehydration and concentrated urine
- In Hong Kong, the prevalence follows regional Asian trends with calcium oxalate stones being the most common. Hong Kong's subtropical climate with hot, humid summers predisposes to dehydration. There is also a relatively high dietary sodium and animal protein intake in the local diet, both of which are modifiable risk factors
Recurrence Rate — High Yield
Stones are a recurrent disease. After a first episode, quote "50% at 10 years" for exams. This justifies metabolic workup and secondary prevention in every patient.
Anatomy of the Urinary Tract Relevant to Stone Disease
Understanding the anatomy is essential because it tells you where stones get stuck and why they cause pain.
The Kidney
- The functional unit is the nephron, which filters plasma → produces urine
- Urine drains from collecting ducts → renal papillae → minor calyces → major calyces → renal pelvis
- Stones typically form at the renal papillae — this is where Randall's plaques (see Pathophysiology) begin
The Ureter
- A 25–30 cm muscular tube (smooth muscle, peristaltic) connecting the renal pelvis to the bladder
- Course on KUB: exits the renal pelvis at L1/L2, runs along the tips of the transverse processes, in front of the sacroiliac joint (SIJ), laterally down the pelvic wall towards the ischial spine, then curves anteromedially into the bladder [2][3]
- Divided into three segments for clinical purposes:
- Upper third (above the pelvic brim)
- Middle third (at the SIJ level)
- Lower third (below the pelvic brim to the bladder)
Three Anatomical Points of Ureteric Narrowing [1][2][3]
These are the three classic sites where stones lodge, because the ureter naturally narrows here:
| Site | Anatomy | Why Stones Get Stuck |
|---|---|---|
| Pelvi-ureteric junction (PUJ) | Where the renal pelvis funnels into the ureter | Transition from a wide pelvis to a narrow tube |
| Pelvic brim | Where the ureter crosses the common iliac artery bifurcation | External compression by the vessel narrows the lumen |
| Vesico-ureteric junction (VUJ) | Where the ureter pierces the bladder wall obliquely | Narrowest point of the ureter (~1–3 mm); the oblique intramural course provides a valve mechanism but also a bottleneck |
Why does this matter? When a stone lodges at one of these points, it causes ureteric obstruction → upstream dilation (hydroureter, hydronephrosis) → increased intraluminal pressure → pain. The VUJ is the narrowest and is the most common site of impaction.
The Bladder
- A distensible smooth-muscle organ (detrusor muscle) that stores urine
- Bladder stones are more common in males (due to BPH causing urinary stasis) and in settings of chronic indwelling catheters, neurogenic bladder, or bladder diverticula
Pain Referral Patterns (Dermatome Basis)
- The ureter is innervated by sympathetic fibres from T10–L2
- Stone pain is visceral pain (poorly localised, colicky, often associated with autonomic symptoms like nausea and vomiting)
- Upper ureteric stones → pain referred to the flank/loin (T10–T12)
- Mid-ureteric stones → pain radiates to the lower abdomen/groin (L1)
- Lower ureteric/VUJ stones → pain referred to the groin, scrotum/labia (L1–L2), and can cause irritative bladder symptoms (frequency, urgency, dysuria) because the intramural portion of the ureter irritates the bladder trigone
Etiology and Risk Factors
Stones form when the balance between factors promoting crystallisation and factors inhibiting it tips in favour of crystal formation. Think of it as a "chemistry of urine" problem:
- Promoters of stone formation: supersaturation (high concentration of stone-forming solutes), low urine volume, low pH (for uric acid/cystine), high pH (for calcium phosphate/struvite), presence of a nidus (Randall's plaque)
- Inhibitors of stone formation: citrate, magnesium, pyrophosphate, glycosaminoglycans, Tamm-Horsfall protein, nephrocalcin
Specific Risk Factors
| Factor | Stone Type Favoured | Mechanism |
|---|---|---|
| High calcium (hypercalciuria) | Calcium oxalate/phosphate | More Ca²⁺ in urine → supersaturation |
| High oxalate (hyperoxaluria) | Calcium oxalate | Oxalate binds Ca²⁺ to form insoluble crystals |
| High uric acid (hyperuricosuria) | Uric acid (also CaOx — uric acid crystals act as a nidus) | Supersaturation + heterogeneous nucleation |
| High cystine (cystinuria) | Cystine | Cystine is poorly soluble, especially at acidic pH |
| High pH (alkaline urine) | Calcium phosphate, struvite | Phosphate dissociates more at alkaline pH → binds Ca²⁺ |
| Low pH (acidic urine) | Uric acid, cystine | Uric acid is poorly soluble at pH < 5.5; cystine at pH < 7 |
| Low volume | All types | Concentrates all solutes → supersaturation |
| Low citrate (hypocitraturia) | Calcium stones | Citrate chelates Ca²⁺ in urine, keeping it soluble; also inhibits crystal aggregation |
Hypocitraturia is usually caused by metabolic acidotic states (e.g. RTA) which enhance renal tubular reabsorption of citrate [1]. This is a critical concept: in metabolic acidosis, the proximal tubule avidly reabsorbs citrate (to use it as a metabolic buffer), leaving less in the urine to inhibit stone formation.
| Dietary Factor | Effect | Mechanism |
|---|---|---|
| Low fluid intake (dehydration) | ↑ All stone risk | Concentrated urine → supersaturation |
| High oxalate intake | ↑ CaOx stones | More oxalate absorbed → excreted in urine. Examples: tea, cocoa, spinach, mustard greens, beets [3] |
| High protein (animal) intake | ↑ Uric acid + CaOx stones | High protein intake leads to hyperuricosuria [1]; also generates acid load (purines, sulphur-containing amino acids) → ↓ urine pH → ↑ uric acid precipitation; also ↑ urinary calcium excretion |
| High sodium intake | ↑ Calcium stones | Na and Ca compete for renal reabsorption in the proximal tubule — ↑ Na intake → ↑ Na excretion → drags Ca²⁺ with it → hypercalciuria [2] |
| Low calcium diet | Paradoxically ↑ CaOx stones | Low calcium diet is paradoxically predisposing to urinary stone formation since dietary Ca binds oxalate in the GIT to prevent its absorption into blood and subsequently excretion in urine [1][2]. This is a classic exam point! |
| High dietary calcium | Protective | Same mechanism — binds oxalate in gut [3] |
| Calcium supplements | ↑ risk (paradox) | Dietary Ca intake is protective but Ca supplement is associated with ↑ risk [3] — because supplements are usually taken separate from meals, so they can't bind dietary oxalate in the intestine |
| High sucrose/fructose | ↑ Risk | ↑ Urinary calcium excretion |
| High vitamin C | ↑ CaOx stones | Vitamin C is metabolised to oxalate |
| Low potassium intake | ↑ Risk | ↓ Urinary citrate excretion |
The Calcium Paradox — Must Know
Students often think "more calcium in diet = more calcium stones." The opposite is true. Dietary calcium REDUCES stone risk by binding oxalate in the gut. It is calcium SUPPLEMENTS (taken away from meals) that increase risk. This is frequently tested.
Conditions favouring calcium stones:
- Primary hyperparathyroidism: the most important medical cause — ↑ PTH → ↑ bone resorption → hypercalcaemia → hypercalciuria [1][4]
- Sarcoidosis: granulomatous disease → macrophages express 1α-hydroxylase → ↑ 1,25-(OH)₂-D₃ → ↑ intestinal Ca absorption → hypercalciuria [1][4]
- Idiopathic hypercalciuria: the commonest metabolic abnormality found in calcium stone formers (~50%)
- Inflammatory bowel disease / Crohn's disease: bile acid malabsorption → fatty acids bind Ca instead of oxalate → ↑ free oxalate absorption → hyperoxaluria [3]
- Renal tubular acidosis (RTA) Type 1 (Distal): cannot excrete H⁺ → chronic metabolic acidosis → ↑ bone Ca mobilisation + ↓ urinary citrate (citrate reabsorbed in acidotic states) + alkaline urine (cannot acidify) → calcium phosphate stones [1][3]
- Medullary sponge kidney: dilated collecting ducts → urinary stasis → stone formation [3]
Conditions favouring uric acid stones:
- Gout (hyperuricaemia and hyperuricosuria) [1]
- Lymphoproliferative / Myeloproliferative disease: high cell turnover → ↑ purine metabolism → ↑ uric acid production [1]
- Diabetes mellitus / Metabolic syndrome: insulin resistance → defective renal ammoniagenesis → ↓ urinary pH → uric acid precipitation [3]
Conditions favouring struvite stones:
- Recurrent upper UTI with urease-producing organisms (see below) [3]
Conditions favouring cystine stones:
- Cystinuria: autosomal recessive defect in renal tubular reabsorption of dibasic amino acids (cystine, ornithine, lysine, arginine — mnemonic: COLA) [2]
- Horseshoe kidney: altered drainage → urinary stasis → stone formation
- Medullary sponge kidney: ectatic collecting ducts with stasis
- Other congenital anomalies: duplex collecting system, calyceal diverticulum, UPJ obstruction
- Gastric bypass surgery / Bowel resection: Dietary Ca²⁺ is bound by unabsorbed dietary fats by saponification after bypass, which prevents it from binding to dietary oxalate, thereby making oxalate more available for intestinal absorption and increasing oxalate excretion [1]
- This is essentially the same mechanism as Crohn's/IBD — fat malabsorption → calcium binds free fatty acids → oxalate has no calcium to bind → oxalate is absorbed freely → hyperoxaluria
- Family history of urolithiasis confers ~2× risk [3]
- Genetic factors in idiopathic hypercalciuria, cystinuria, primary hyperoxaluria, and certain renal tubular defects
- Prior history of urinary stones is one of the strongest risk factors [1]
- Medications: antacids, salicylates, antivirals (acyclovir, indinavir — form radiolucent crystals), topiramate (carbonic anhydrase inhibitor → ↑ urine pH), vitamin D supplements [3]
- Occupation: outdoor workers with heavy sweating / insufficient fluid intake [5]
- Obesity and diabetes mellitus: insulin resistance → acidic urine → uric acid stones [3]
Pathophysiology
Step-by-Step: How Do Stones Form?
Think of stone formation as a 3-step process:
- When the concentration of stone-forming ions (e.g., calcium and oxalate) exceeds the solubility product in urine, the solution becomes supersaturated
- This is the necessary precondition for crystal formation
- Factors that promote supersaturation: low urine volume, high solute excretion, unfavourable urine pH
- Homogeneous nucleation: crystals form de novo in a pure supersaturated solution (requires very high supersaturation — rare)
- Heterogeneous nucleation (more common): crystals form on a pre-existing surface (a "nidus")
- Randall's plaque: calcium crystal deposits in the interstitial space of the renal papilla that serve as a nidus for stone formation [2]. This is a key concept — calcium phosphate (apatite) deposits form in the basement membrane of the thin loops of Henle, extend into the papillary interstitium, and eventually erode through the urothelium to become exposed to urine. Once exposed, calcium oxalate crystals can nucleate on this surface
- Crystals that form must be retained in the urinary tract (otherwise they are simply flushed out)
- Inflammation around the crystal and Randall's plaque contribute to retention [2]
- Small crystals aggregate into larger ones, grow, and eventually become macroscopic stones
- The balance between promoters (supersaturation, inflammatory matrix, low urine volume) and inhibitors (citrate, magnesium, pyrophosphate, Tamm-Horsfall protein, nephrocalcin) determines whether a crystal becomes a clinically significant stone
Once a stone forms and moves into the ureter:
- Obstruction → ↑ intraluminal pressure → distension of the renal pelvis and ureter → pain (renal colic)
- The pain is visceral, mediated by stretch receptors in the renal capsule and ureteral wall
- Peristalsis of the ureter trying to push the stone past the obstruction causes the colicky nature (waxing and waning)
- Mucosal irritation → the stone's rough surface (especially calcium oxalate with its sharp "mulberry" projections) scratches the urothelium → haematuria
- Obstruction + stasis → urine pooling above the stone → breeding ground for bacteria → urinary tract infection → can progress to pyelonephritis and urosepsis
- Prolonged obstruction → progressive hydronephrosis → renal parenchymal thinning → obstructive nephropathy → potential AKI (if bilateral or in a solitary kidney) [2][3]
Classification of Urinary Stones
There are 5 main types of urinary stones [1]:
| Type | Frequency | Urine pH | Etiology/Risk Factors | Radio-opacity on KUB | Appearance | Key Features |
|---|---|---|---|---|---|---|
| Calcium oxalate | 70–80% | Variable | Hypercalciuria, hyperoxaluria, hypocitraturia, ↓ fluid intake, FHx, medullary sponge kidney | Radio-opaque | Irregular "mulberry" stones with sharp projections | Symptomatic early even at small size due to sharp surfaces [3]; may be monohydrate (whewellite — hard) or dihydrate (weddellite — softer) |
| Calcium phosphate | ~15% (often mixed with CaOx) | Alkaline | Distal RTA (Type 1), hyperPTH, medullary sponge kidney | Radio-opaque | Smooth or chalky | Alkaline urine pH favours phosphate stones (not oxalate); brushite stones are hard and ESWL-resistant |
| Uric acid | 5–10% | Acidic (< 5.5) | Gout, myeloproliferative disease, tumour lysis, DM/metabolic syndrome, chronic diarrhoea, ↑ animal protein | Radiolucent (the classic radiolucent stone) | Hard, smooth, faceted, light brown | Only stone type amenable to dissolution by urine alkalinisation (target pH 6.5–7.0); acidic urine is the key driver |
| Struvite (MgNH₄PO₄) | 5–15% | Alkaline | Infection by urease-splitting organisms: Proteus vulgaris, Klebsiella, Staphylococcus aureus | Radio-opaque | Large, can form staghorn calculi (filling ≥ 2 calyces) | Urease splits urea → ammonia + CO₂ → alkaline urine → MgNH₄PO₄ crystallises; require antibiotics × 6 weeks and complete stone removal to eradicate infection [2] |
| Cystine | 1–2% | Acidic | Cystinuria (autosomal recessive) — defective tubular reabsorption of dibasic amino acids (COLA) | Mildly radio-opaque (faint) | Hexagonal crystals on microscopy, waxy yellow-green | Treatment: increase fluid intake, urine alkalinisation (target pH > 7.0), chelating agents (e.g., penicillamine, tiopronin) [2] |
Rare types: indinavir-induced (radiolucent), xanthine/pyruvate stones [2]
Hardness scale: struvite < uric acid < calcium phosphate < calcium oxalate < cystine [2]
Radio-opacity — High Yield
Radio-opaque (visible on KUB): Calcium oxalate, Calcium phosphate, Struvite (most radio-opaque to least). Mildly radio-opaque: Cystine, Struvite. Radiolucent (invisible on KUB): Uric acid, Xanthine, Indinavir. Remember: "All calcium-containing stones are radio-opaque." For the exam, if they show you a stone on KUB, it's almost certainly calcium.
- Renal stones (nephrolithiasis): calyceal, pelvic, or staghorn
- Ureteric stones: upper, mid, or lower third
- Bladder stones (vesical calculi): more common with bladder outlet obstruction (BPH)
- Urethral stones: rare, usually migrated from above
- A stone that occupies ≥ 2 calyces [2]
- Most commonly struvite (infection stones) but can be any composition
- Fills the renal pelvis and branches into the calyces — looks like a "stag's horn"
- Often asymptomatic until complicated by infection or renal failure
- Requires active treatment (usually PCNL) regardless of symptoms because of progressive renal damage
Clinical Features
| Symptom | Pathophysiological Basis |
|---|---|
| Renal colic (colicky pain from loin to groin) [2] | Stone moves into ureter → obstruction → ↑ intraluminal pressure → ureteric peristalsis against the obstruction → stretch of the ureteric wall and renal capsule → visceral pain via T10–L2 afferents. The "colicky" nature (waves of severe pain with brief respites) reflects rhythmic ureteric peristalsis trying to propel the stone distally |
| Flank/loin pain (constant) | If the stone is in the renal pelvis or upper ureter, the distension is more steady → dull, constant ache in the costovertebral angle |
| Pain radiation to groin/scrotum/labia | As the stone moves distally, the referred pain follows the dermatomal distribution — lower ureteric stones refer to L1–L2 dermatomes (groin, genitalia) |
| Nausea and vomiting [2] | Visceral pain from ureteric obstruction triggers the vomiting centre via vagal afferents (the kidneys and GI tract share autonomic innervation — coeliac and superior mesenteric ganglia). This is why stone pain is so commonly confused with GI pathology |
| Haematuria (gross or microscopic) [2] | Stone's rough surface (especially CaOx with its "mulberry" shape and sharp projections) traumatises the urothelium → bleeding. Also, mucosal inflammation contributes. May be gross (visible) or microscopic (dipstick/microscopy only) |
| Irritative LUTS (frequency, urgency, nocturia, dysuria) — "FUN" [2] | Lower ureteric/VUJ stones irritate the bladder trigone and detrusor → mimics cystitis symptoms. These are sometimes the only symptoms of a distal ureteric stone! |
| Sudden cessation of pain | If the stone passes into the bladder, the obstruction is relieved → immediate pain relief. Patients may then pass the stone during voiding |
| Stranguria | Painful urination with bladder spasms — from a stone at the VUJ or in the bladder |
| Anuria/oliguria | Bilateral ureteric obstruction (rare) or obstruction in a solitary functioning kidney → post-renal AKI |
Classic Presentation
A 40-year-old male presenting with sudden-onset severe colicky loin pain radiating to the groin, with nausea/vomiting and haematuria on dipstick. "Rolling around in agony" — unlike peritonitis where patients lie perfectly still, renal colic patients cannot find a comfortable position. This restlessness is a key clinical clue.
Pain Patterns by Stone Location
| Stone Location | Pain Pattern | Associated Symptoms |
|---|---|---|
| Renal pelvis | Deep flank/costovertebral angle pain, may be dull or absent if non-obstructing | Haematuria |
| Upper ureter (PUJ) | Severe loin pain, may radiate to flank | N/V, haematuria |
| Mid ureter (pelvic brim) | Pain radiates to lower abdomen, may mimic appendicitis (R) or diverticulitis (L) | N/V |
| Lower ureter / VUJ | Pain radiates to groin, scrotum/labia | Irritative symptoms (FUN), dysuria |
| Bladder | Suprapubic pain, intermittent urinary stream (stone rolls over bladder neck) | Irritative symptoms, terminal haematuria |
| Sign | Pathophysiological Basis |
|---|---|
| Loin/renal angle tenderness [2] | Distension of the renal capsule and surrounding tissues from hydronephrosis → tenderness at the costovertebral angle (Murphy's kidney punch may be positive — but this is more classically for pyelonephritis) |
| Symptoms out of proportion to signs [3] | This is a hallmark of ureteric colic — the patient is in severe distress (writhing, unable to keep still), but the abdominal examination is often remarkably unremarkable. Why? Because the pain is visceral (from ureteric/renal capsule distension), not somatic (no peritoneal involvement). There is usually no peritoneal signs (guarding, rebound) [3] |
| May have tenderness at renal angle [3] | Mild to moderate — from distension of the renal pelvis |
| Restlessness / inability to lie still | Unlike peritonitis (where movement worsens pain → patient lies still), renal colic patients are restless because visceral pain is not worsened by movement and the patient instinctively tries different positions to relieve the distension |
| RARELY associated with ballotable kidneys | Due to hydronephrosis / pyonephrosis [3] — massive distension of the kidney. This is very late/severe |
| Fever and rigors | NOT from the stone itself — indicates superimposed infection (pyelonephritis/urosepsis). This is a surgical emergency requiring urgent decompression |
| Haematuria on urinalysis | Haematuria (gross or microscopic) [3] — present in ~85% of acute stone episodes. Absence does not rule out stones (complete obstruction may prevent urine flow) |
| Pyuria | Can be present without infection due to irritation of urothelium [3] by the stone. However, if accompanied by bacteriuria and fever, infection must be treated urgently |
| Ileus (absent bowel sounds, abdominal distension) | Sympathetic overstimulation from severe renal colic can cause reflex ileus |
Red Flags — Infected Obstructed Urinary Tract
If a patient with ureteric colic develops fever, rigors, hypotension, or confusion, think obstructed pyelonephritis/urosepsis. This is a urological emergency requiring:
- IV antibiotics
- Urgent decompression (JJ stent or percutaneous nephrostomy) Stone treatment is deferred until the infection is controlled. Do NOT attempt ESWL or definitive stone surgery in the septic patient.
Bladder stones (more relevant from GC 180 on BPH) present differently from ureteric stones:
- Suprapubic pain worsened at the end of micturition (stone falls onto trigone → irritation)
- Irritative symptoms: frequency, urgency, nocturia [5]
- Terminal haematuria (stone irritates bladder base at end of voiding when bladder contracts)
- Sudden interruption of urinary stream — pathognomonic: the stone rolls over the internal urethral meatus during voiding, blocking flow; relieved by changing position
- Usually secondary to bladder outlet obstruction (BPH, urethral stricture) or neurogenic bladder → chronic urinary stasis → crystal precipitation
High Yield Summary
Definition: Urolithiasis = stone formation anywhere in the urinary tract, most commonly calcium oxalate.
Epidemiology: M > F (~4:3), peak 30–50y, lifetime prevalence up to 16% (M). Recurrence: 50% at 10 years.
Three sites of ureteric narrowing: PUJ, pelvic brim (iliac artery crossing), VUJ (narrowest).
Five stone types: Calcium oxalate (70–80%), Calcium phosphate (15%), Uric acid (5–10%, radiolucent, dissolves with alkalinisation), Struvite (infection-related, urease-splitting organisms, staghorn), Cystine (1%, AR cystinuria, hexagonal crystals).
Key pathophysiology: Supersaturation → nucleation (Randall's plaque) → growth/aggregation → obstruction → pain, haematuria, infection.
The Calcium Paradox: Dietary calcium is PROTECTIVE (binds oxalate in gut). Calcium supplements (taken away from meals) INCREASE risk.
Classic presentation: Colicky loin-to-groin pain + haematuria + N/V. Symptoms out of proportion to signs. Patient cannot lie still.
Red flag: Fever + obstructed stone = urological emergency → urgent decompression (JJ stent or PCN) + IV antibiotics.
Urine pH matters: Acidic → uric acid, cystine. Alkaline → calcium phosphate, struvite.
Radio-opacity: Calcium = opaque, Uric acid = lucent, Cystine = faintly opaque.
Active Recall - Urinary Stones (Definition, Epidemiology, Anatomy, Etiology, Pathophysiology, Classification, Clinical Features)
[1] Senior notes: felixlai.md (Urological Diseases — Urinary Stones) [2] Senior notes: maxim.md (Section 2.3: Urinary stones — Urolithiasis) [3] Senior notes: Ryan Ho Urogenital.pdf (Section 7.2: Urolithiasis, pp. 137–143) [4] Senior notes: Ryan Ho Endocrine.pdf (Sections 2.2.1–2.2.2: Hypercalcemia, Primary Hyperparathyroidism, pp. 40–43) [5] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.5.1: Haematuria, pp. 340–344)
Differential Diagnosis of Urinary Stones
When a patient walks in with the "classic" presentation — acute loin pain, haematuria, nausea/vomiting — your brain immediately jumps to ureteric colic. And most of the time, you'll be right. But the differential diagnosis of urinary stones is really the differential diagnosis of its presenting symptoms: acute flank/loin pain, haematuria, and lower urinary tract symptoms. Several serious and time-critical conditions can mimic ureteric colic, and missing them can be catastrophic.
The approach is best organised by the system of origin — urological, abdominal/GI, vascular, and gynaecological — because different organ systems can produce overlapping pain patterns due to shared visceral innervation (T10–L2 dermatomes overlap between the ureter, appendix, ovary, colon, and retroperitoneal structures) [1][3].
Systematic Differential Diagnosis
| Condition | Key Distinguishing Features | Why It Mimics Urolithiasis |
|---|---|---|
| Pyelonephritis | Frequently presents with fever, flank pain and pyuria. Fever is uncommon in patients with renal stones unless it is complicated [1]. High spiking fever, rigors, Murphy's kidney punch positive, systemic toxicity | Loin pain + haematuria + pyuria overlap. However, pyelonephritis has prominent systemic upset (fever, rigors, tachycardia) that uncomplicated stones do NOT cause. Pyuria can occur with stones (from urothelial irritation) but fever should not [1] |
| Renal cell carcinoma (RCC) | Bleeding within the kidney can produce blood clots which lodge temporarily in the ureter leading to renal colic [1]. Classic triad: painless haematuria, flank pain, palpable mass (rare — only ~10%). Constitutional symptoms (weight loss, anorexia). Paraneoplastic features: polycythaemia, hypercalcaemia, HTN [3] | "Clot colic" — haemorrhage from a renal tumour produces blood clots that enter the ureter and obstruct it, mimicking ureteric colic exactly. Key difference: glomerular bleeding does NOT lead to clot formation or symptoms of renal colic [1] — so if you see clots + colic, think urological source (tumour, not GN) |
| CA bladder | Painless gross haematuria (classic), irritative LUTS (frequency, urgency, nocturia), constitutional symptoms [3]. Risk factors: smoking, occupational exposure (dye/rubber workers), aristolochic acid in TCM [5] | Lower ureteric/bladder stones also cause irritative LUTS + haematuria. Key distinguisher: bladder cancer is usually painless, whereas VUJ stones cause pain. Painless gross haematuria in > 35 y/o = malignancy until proven otherwise [5] |
| UTI / Cystitis | Dysuria, frequency, urgency, suprapubic pain, cloudy/foul-smelling urine. No fever or systemic upset in simple cystitis [8] | Overlapping irritative LUTS. Key: cystitis has no flank colic, and urinalysis shows significant bacteriuria + nitrites (not just haematuria/pyuria). Sterile pyuria DDx includes: TB, bladder cancer (CIS), urinary tract stones, schistosomiasis, partially treated UTI, interstitial cystitis, ketamine cystitis [6] |
| Renal TB | Sterile pyuria (classic), chronic/recurrent "UTI" not responding to standard antibiotics, needs early morning urine (EMU) for TB [6]. Calcification of kidney (autonephrectomy). History of pulmonary TB or endemic exposure (important in Hong Kong) | Chronic loin pain + haematuria + pyuria can overlap with stone disease. TB can also cause calcification that mimics stones on imaging |
| Polycystic kidney disease | Bilateral flank masses, family history (autosomal dominant), insidious HTN, progressive CKD [3] | Cyst haemorrhage or cyst infection can cause acute flank pain ± haematuria, mimicking stones. Also, patients with ADPKD have an increased incidence of nephrolithiasis (~20%) |
| Renal papillary necrosis | Seen in diabetes, sickle cell disease, NSAID abuse, analgesic nephropathy. Sloughed papillae pass down the ureter → colic + haematuria. "Ring shadow" on IVU | Sloughed papilla literally acts like a stone — obstructs the ureter and causes identical symptoms. NCCT may show the papilla as a soft-tissue density, not a dense calcification |
| Renal infarction | Sudden severe loin pain, haematuria, raised LDH. Risk factors: AF (embolus), aortic surgery, hypercoagulable states [3] | Acute loin pain + haematuria. Key: no stone on CT; wedge-shaped non-enhancing area on contrast CT. LDH is markedly elevated |
Clot Colic vs Stone Colic
If a patient has ureteric colic with visible blood clots in the urine, consider a bleeding source above the stone — RCC, urothelial carcinoma, or AV malformation. True stone colic usually produces haematuria without formed clots (the urine is "smoky" or pink, not clotted). Clots forming in the ureter and passing as "worm-like" casts strongly suggest upper tract pathology beyond just a stone.
This is the most dangerous overlap zone because several of these conditions are surgical emergencies:
| Condition | Key Distinguishing Features | Why It Mimics Urolithiasis |
|---|---|---|
| Acute appendicitis | Periumbilical pain migrating to RIF (McBurney's point), anorexia, low-grade fever, guarding/rebound tenderness, Rovsing's sign positive. May have mild pyuria (from adjacent ureteric inflammation) | Right-sided ureteric colic can mimic appendicitis and vice versa. Key: appendicitis has peritoneal signs (guarding, rebound) — ureteric colic typically does NOT have peritoneal signs [3]. Also, appendicitis causes the patient to lie still; renal colic makes the patient restless |
| Acute diverticulitis | Left-sided lower abdominal pain (sigmoid), fever, localised guarding, change in bowel habit. CT shows bowel wall thickening + fat stranding [9] | Left-sided ureteric stone can mimic sigmoid diverticulitis. Key: diverticulitis has bowel-related features (altered bowel habit, localised peritonism) and CT findings centred on the colon, not the ureter |
| Intestinal obstruction | Colicky central abdominal pain, vomiting (bilious if distal), absolute constipation, distension, tinkling/absent bowel sounds. AXR shows dilated loops with air-fluid levels | Both can cause colicky abdominal pain + vomiting. Key: bowel obstruction pain is central/periumbilical, not flank-to-groin; there is abdominal distension and abnormal bowel sounds. No haematuria |
| Abdominal aortic aneurysm (AAA) — ruptured or symptomatic | Sudden severe back/flank/abdominal pain, haemodynamic instability (hypotension, tachycardia), pulsatile abdominal mass. Risk factors: elderly male, smoker, HTN, known AAA | This is the most dangerous mimic. Ruptured AAA can present with sudden flank pain radiating to the groin — identical to ureteric colic. The patient may even have microscopic haematuria (from renal hypoperfusion). Key: haemodynamic instability is NOT a feature of uncomplicated stones. Always check BP and pulse in "renal colic." An elderly male with first presentation of "renal colic" and hypotension = ruptured AAA until proven otherwise |
| Acute cholecystitis / Biliary colic | RUQ pain radiating to right shoulder/scapula (phrenic nerve), Murphy's sign positive, association with fatty meals | Right renal colic can overlap anatomically with biliary pain. Key: biliary colic is usually RUQ/epigastric (not flank), associated with meals, and Murphy's sign is positive. USG differentiates easily |
| Acute pancreatitis | Epigastric pain radiating to the back, relieved by leaning forward, raised amylase/lipase, alcohol/gallstone history | Back pain component overlaps. Key: pancreatitis pain is central/epigastric, not unilateral; markedly elevated amylase/lipase clinches the diagnosis |
| Mesenteric ischaemia | Severe, poorly localised abdominal pain out of proportion to findings (like stones!), AF or vascular disease, raised lactate, metabolic acidosis | "Pain out of proportion to signs" is shared with renal colic. Key: mesenteric ischaemia patients are typically older with vascular risk factors, and develop peritoneal signs later. CT angiography is diagnostic |
The AAA Trap
An elderly male presenting with "first episode of renal colic" who is haemodynamically unstable: think ruptured AAA before ureteric stone. Sending this patient for NCCT looking for stones while they are exsanguinating is a fatal error. Always assess haemodynamic stability first.
| Condition | Key Distinguishing Features | Why It Mimics Urolithiasis |
|---|---|---|
| Ectopic pregnancy | Missed period / positive β-hCG, unilateral lower abdominal/pelvic pain, PV bleeding, adnexal tenderness/mass on bimanual examination. Haemodynamic instability if ruptured. Underlying cause of pain can be clarified by obtaining a renal or pelvic USG [1] | Lower ureteric colic can present as unilateral lower abdominal/groin pain in a young woman — exactly where an ectopic pregnancy presents. Key: always do a pregnancy test (β-hCG) in any woman of reproductive age with acute lower abdominal pain before imaging with CT (radiation risk!) |
| Ovarian torsion | Sudden severe unilateral lower abdominal/pelvic pain, nausea/vomiting, adnexal mass/tenderness, Doppler USG shows absent ovarian blood flow | Sudden unilateral pain + N/V can perfectly mimic distal ureteric colic. Key: no haematuria; pelvic USG shows enlarged ovary with absent blood flow |
| Ruptured ovarian cyst | Sudden onset lower abdominal pain (often mid-cycle), may have mild peritoneal irritation from fluid. Free fluid on USG | Similar acute onset. Key: timing with menstrual cycle, no haematuria, pelvic free fluid on imaging |
| Dysmenorrhoea | Rarely presents with flank pain that begins just before or concurrent with the onset of menstruation [1]. Crampy suprapubic pain, cyclical pattern | Usually easy to distinguish by its cyclical nature and timing with menses |
| Pelvic inflammatory disease (PID) | Bilateral lower abdominal pain, fever, cervical motion tenderness ("chandelier sign"), vaginal discharge | Bilateral lower abdominal pain is not typical for stones (which are unilateral). Vaginal discharge and sexual history provide clues |
| Condition | Key Distinguishing Features | Why It Mimics Urolithiasis |
|---|---|---|
| Musculoskeletal back pain | Paravertebral tenderness, worsened by specific movements/positions, no haematuria, no colicky pattern | Dull chronic flank ache from a non-obstructing renal stone can overlap. Key: no haematuria, normal NCCT |
| Herpes zoster (shingles) | Dermatomal vesicular rash (T10–L2), burning/lancinating pain preceding rash by days | Pre-rash phase can perfectly mimic flank pain. Key: wait for rash; no haematuria; no stone on imaging |
| Testicular torsion | Acute onset scrotal pain, nausea, absent cremasteric reflex, high-riding testis | Lower ureteric stones can cause referred pain to the scrotum/testis. Key: in torsion, the testis itself is abnormal on examination; in ureteric colic, the testis is normal but pain is referred there |
Differential Diagnosis of Specific Stone Presentations
Sterile pyuria (pyuria without bacteriuria on standard culture) is an important clinical scenario. The lecture slides specifically list this differential:
- Tuberculosis — always send early morning urine (EMU) for TB culture/PCR [6]
- Bladder cancer (carcinoma-in-situ) — can shed inflammatory cells without bacteria
- Urinary tract stones — mechanical irritation of urothelium causes pyuria without infection
- Schistosomiasis — important in patients from endemic areas (not common in HK but relevant for travellers)
- Partially treated UTI — prior antibiotics have suppressed but not cleared the organism
- Other inflammatory bladder conditions — interstitial cystitis, ketamine cystitis [6]
When you see a radio-opacity on KUB and wonder "is that a stone?", consider:
- Calcified mesenteric lymph node — usually central, round, with a lucent centre ("eggshell")
- Gallstone — usually radiolucent, but 10–15% are radio-opaque; located in RUQ, not along the ureteric course
- Faecolith / Appendicolith — in the RIF, may mimic a distal right ureteric stone
- Phlebolith — venous calcification in the pelvis; round with a central lucency, very common; the most frequent mimic of a distal ureteric stone on KUB
- Ossified tip of 12th rib — can mimic an upper ureteric/PUJ stone
- Nephrocalcinosis — diffuse medullary calcification (e.g., in RTA, hyperPTH), not a discrete stone
- Calcified adrenal gland — TB, old haemorrhage, Addison's disease [3]
Tip: If in doubt, compare the opacity's position with the known ureteric course (along transverse process tips → SIJ → ischial spine → VUJ). If the opacity lies outside this line, it's less likely to be a ureteric stone. NCCT resolves most ambiguity.
Recurrent UTI with urease-producing organisms → may indicate underlying urolithiasis [6] (struvite stones from Proteus/Klebsiella). Conversely, if you diagnose stones, always check for concurrent infection.
Recurrent bacterial persistence, especially with urease-producing organisms [6] should prompt stone workup.
"Recurrent" UTI with gross haematuria or persistent microscopic haematuria → formal urologist referral required to rule out malignancy (requires cystoscopic assessment) [6].
Recurrent UTI with pyuria but no growth → needs early morning urine (EMU) for TB; needs to rule out stone formation; is this ketamine cystitis? [6]
The key decision points are: (1) Haemodynamic stability (rule out AAA, ruptured ectopic), (2) Pregnancy status (avoid CT, think ectopic), (3) Fever (infected system is a surgical emergency), (4) Urinalysis (haematuria points towards urological cause; its absence widens the DDx).
High Yield Summary
Three most dangerous mimics of renal colic to never miss:
- Ruptured AAA — elderly, hypotensive, pulsatile mass
- Ruptured ectopic pregnancy — woman of reproductive age, positive β-hCG
- Obstructed infected system — fever + stone = emergency decompression
Key distinguishing features of ureteric colic vs peritoneal pathology:
- Stones: symptoms OUT OF PROPORTION to signs, no peritoneal signs, patient RESTLESS
- Peritoneal causes (appendicitis, diverticulitis): peritoneal signs present (guarding, rebound), patient lies STILL
Sterile pyuria DDx (lecture slide): TB, bladder CIS, stones, schistosomiasis, partially treated UTI, interstitial cystitis, ketamine cystitis.
Phleboliths are the most common mimic of distal ureteric stones on KUB.
Clot colic: haematuria with formed clots passing down the ureter → think RCC or urothelial tumour, not just simple stone.
Red flags for malignancy: painless gross haematuria in > 35 y/o, constitutional symptoms, smoking history, occupational exposure.
Active Recall - Differential Diagnosis of Urinary Stones
References
[1] Senior notes: felixlai.md (Urological Diseases — Urinary Stones, DDx section) [3] Senior notes: Ryan Ho Urogenital.pdf (Section 7.2: Urolithiasis, pp. 137–139; DDx of renal stone on KUB p. 139) [5] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.5.1: Haematuria, pp. 340–344) [6] Lecture slides: GC 210. Urinary tract infection.pdf (Sterile pyuria DDx p. 32; Red flags p. 69; Xanthogranulomatous pyelonephritis p. 125) [7] Senior notes: Ryan Ho Critical Care.pdf (AKI — Post-renal causes, p. 25) [8] Senior notes: Ryan Ho Urogenital.pdf (Section 6.2.2: Acute Cystitis DDx, p. 125) [9] Senior notes: felixlai.md (Acute Diverticulitis)
Diagnostic Criteria, Algorithm, and Investigations for Urinary Stones
Unlike many medical conditions (e.g., rheumatic fever with Jones criteria, or SLE with ACR/EULAR criteria), urolithiasis does not have a formal set of "diagnostic criteria" with scoring systems. Instead, the diagnosis is established by a combination of:
- Clinical presentation (history and physical examination)
- Confirmation by diagnostic imaging (the definitive step)
- Supportive laboratory findings
In practice, the diagnosis of an acute ureteric stone is made when all three components converge:
| Component | What Establishes Diagnosis | Explanation |
|---|---|---|
| History | Acute colicky loin-to-groin pain + haematuria ± N/V ± irritative LUTS | The clinical picture is highly suggestive but not pathognomonic — many conditions can mimic it (see DDx section) |
| Physical Examination | Symptoms out of proportion to signs, renal angle tenderness, no peritoneal signs, restlessness [3] | Helps narrow the differential and exclude surgical abdomen |
| Diagnostic Imaging | Direct visualisation of the stone on imaging (NCCT is the gold standard) [1][2][3] | This is the definitive diagnostic step. A stone must be SEEN on imaging to confirm the diagnosis. Clinical suspicion alone is insufficient for treatment planning |
| Urinalysis | Haematuria (gross or microscopic), ± pyuria, ± crystals | Supportive but not diagnostic — haematuria is absent in ~15% of confirmed stones (if completely obstructed, no urine flows past the stone to carry RBCs). Pyuria can be reactive |
| Blood Tests | CBC, RFT, Ca²⁺, PO₄³⁻, urate | For assessing complications (infection, renal impairment) and underlying causes — not diagnostic of the stone itself |
Diagnosis = Imaging
The bottom line: you cannot diagnose a urinary stone without imaging. A patient with classic renal colic but no stone on NCCT does NOT have a confirmed stone — you must rethink the differential.
The clinical approach to urolithiasis involves four sequential steps [3]:
- Establish the diagnosis based on history, physical examination, and diagnostic imaging (most important)
- Acute treatment: conservative vs ESWL vs PCNL vs URS ± JJ stent
- Establish the type of stone based on:
- Stone composition analysis if stone is collected
- Metabolic evaluation to evaluate underlying metabolic predisposing factors
- Secondary prevention based on underlying predisposing factors
This section focuses on Steps 1 and 3 (diagnosis and metabolic evaluation). Steps 2 and 4 will be covered in the Management section.
Investigation Modalities — Detailed Breakdown
The investigations for urolithiasis serve three purposes:
- Confirm the stone and plan treatment (imaging)
- Assess for complications (infection, obstruction, renal impairment)
- Identify the underlying cause/stone type (metabolic workup)
A. Imaging Investigations
This is the imaging modality of choice (1st line) in patients with urinary stones [1].
Why NCCT and not contrast CT?
- Stones are dense mineral concretions — they show up brilliantly on non-contrast CT as bright white (hyperdense) foci against the soft-tissue background
- Adding IV contrast would opacify the renal collecting system with dense contrast material, potentially obscuring small stones within the bright contrast column
- NCCT also avoids the risks of contrast (nephrotoxicity, allergic reactions) — particularly important in the acute setting where renal function may already be compromised by obstruction
What NCCT tells you [1][2][3]:
| Parameter | Clinical Significance |
|---|---|
| Size of stone | Determines treatment: < 5 mm likely to pass spontaneously; > 10 mm likely needs intervention |
| Location of stone | Upper, mid, or lower ureter; renal pelvis; calyceal — determines choice of procedure |
| Stone density (Hounsfield Units, HU) | > 1000 HU is considered hard [2] (likely calcium oxalate monohydrate or brushite) → ESWL may be less effective; < 1000 HU predicts success of ESWL [5]. Calcium stones: densest. Struvite stones: less dense. Urate stones: least dense [3] |
| Signs of obstruction | Ureteral dilatation, collecting system dilatation (hydronephrosis), perinephric stranding [1][3] — perinephric stranding occurs because obstructed urine leaks into the retroperitoneal fat surrounding the kidney, causing oedema visible as haziness/"streaking" around the kidney |
| Bilateral calcification at corticomedullary junction | Suggests medullary sponge kidney [1] |
| Large calculus in renal pelvis | Suggests struvite stone [1] |
| Number of stones | Affects treatment strategy (single vs multiple) |
Performance: Sensitivity 97%, Specificity 95% [3] — far superior to any other modality. May be less reliable for small stones < 2 mm [3].
Even if KUB is negative, it has to be followed up with NCCT as KUB misses 10% of stones [1].
Indinavir-induced stones are soft tissue density on CT → cannot be seen on CT → often missed [3]. This is the exception to the rule that NCCT catches everything.
NCCT — First and Foremost
In the exam, if asked "What is the single best investigation for suspected ureteric colic?" → Low-dose non-contrast CT abdomen and pelvis. It confirms the stone, shows its size/location/density, demonstrates obstruction, and excludes alternative diagnoses — all without contrast.
Role: Usually for screening only [3] and as a baseline for future follow-up [1][3].
Why still do KUB if NCCT is better?
- KUB is cheap, quick, and low-radiation
- If a stone is confirmed on NCCT and is radio-opaque, a KUB is taken as a baseline — future follow-up of stone size/passage can be done with KUB alone instead of repeating NCCT every time (reducing radiation exposure) [1]
- Do not perform NCCT every time for follow-up [1]
What KUB shows:
- ~90% of stones are radio-opaque [3][5] — calcium-containing stones (CaOx, CaPO₄) are the most visible, struvite is moderately visible, cystine is faintly visible
- Radiolucent stones (invisible on KUB): urate, xanthine, indinavir [3]
- Mildly radio-opaque: cystine, struvite [3]
- Only detects 29–59% of stones seen on NCCT — misses small stones (< 5 mm) and those overlying bony structures
- Unable to detect urinary tract obstruction [1] (cannot see hydronephrosis)
- Cannot detect radiolucent stones
- Stones can be confused with: calcified mesenteric lymph nodes, gallstones, faecolith/appendicolith, phleboliths, ossified tip of 12th rib, nephrocalcinosis, calcified adrenal gland [3]
How to read stones on KUB — trace the ureteric course [1][3][5]:
- Travels along the medial aspect of the psoas muscle and lies anterior and slightly medial to the tip of the L2–L5 transverse processes [1]
- Enters the pelvis anterior to the SI joint at the bifurcation of the common iliac vessels [1]
- Courses anteriorly down the lateral pelvic sidewall
- Turns forward and medially at the level of the ischial spine and enters the posterolateral wall of the bladder [1]
Role: Acceptable initial screening test, particularly for patients who should avoid radiation including pregnant women and women of childbearing age [1]. Also preferred in pregnancy or children [3].
What USG can detect:
- Hydronephrosis (dilated pelvicalyceal system — indirect sign of obstruction)
- Renal stones (echogenic foci with posterior acoustic shadowing)
- Bladder stones (if large enough)
- Cortical thinning due to chronic obstruction [5]
- Prostate size measurement (relevant for bladder stones associated with BPH)
What USG cannot do well:
- Difficulty in defining ureteric lesions — only the proximal (PUJ region) and distal (VUJ region) ends of the ureter are visualised; the mid-ureter is obscured by overlying bowel gas [5]
- Limited sensitivity — 57% only [3]
- Does not see ureteric stones but demonstrates obstruction [3]
- Cannot determine stone density or composition
Use USG as the first-line test in pregnancy and paediatrics, and as a bedside screening tool. If positive for hydronephrosis in a non-pregnant adult, proceed to NCCT for definitive characterisation.
What it is: A multi-phase contrast-enhanced CT scan specifically designed for urinary tract evaluation. CTU has largely replaced IVU [5].
Phases [5]:
- Pre-contrast phase: for gross anatomy — detects stones (same as NCCT)
- Corticomedullary (arterial) phase: for renal perfusion and vasculature
- Nephrographic (venous) phase: for assessment of renal parenchyma (detecting renal tumours)
- Excretory (delayed/pyelographic) phase: for visualisation of the lower urinary tract (detecting urothelial tumours)
When to use in stone disease [1][3]:
- Evaluating the pelvicalyceal system for complex anatomy or recurrent stones
- Complex stones or urinary system anatomy [3]
- Not for routine acute loin pain evaluation [3] — NCCT is sufficient
- Reflects renal function while evaluating for gross anatomical abnormalities [1]
Disadvantages: ↑↑ radiation, contrast allergy/nephropathy [5]
What it is: A specialised CT technique that acquires images at two different X-ray energy levels simultaneously. Different stone compositions attenuate X-rays differently at different energies, allowing differentiation of stone composition [2] in vivo without needing to retrieve the stone.
Clinical utility: Distinguishing uric acid stones (which can be dissolved medically) from calcium stones (which cannot) — this changes management.
What it is: IV non-ionic contrast injected → excreted by kidneys → opacifies and visualises urinary system on serial plain films.
IVU has been largely replaced by CTU [5][10], but understanding it is still relevant for exams.
Preparation [10]:
- Laxatives → ↓ faecal matter (↑ contrast visualisation)
- Fasting ≥ 4h
- Hydration → ↑ distension of urinary collecting system
- Preliminary KUB → may already give diagnosis
- Compression band → distend pelvicalyceal system for evaluation
Procedure timing [10]:
- 0 min → kidneys highlighted (nephrogram)
- 5 min → calyces and renal pelvis
- 10 min → ureter and urinary bladder
Stone findings on IVU [5]:
- Filling defect, proximal dilatation, ↓ distal passage of contrast
- Hydroureter and hydronephrosis
Contraindications [10]:
- Pregnancy (radiation)
- Previous history of serious reactions to contrast media
- Diabetes with renal insufficiency (risk of acute renal failure)
What it is: Injection of radioisotope technetium Tc-99m MAG3 (mercaptoacetyltriglycine) to assess renal excretory function. Provides both anatomical and functional information.
When to use in stone disease [1]:
- Indicated in patients presenting with complications due to prolonged obstruction and requiring measurement of renal function
- Differentiates between obstructive and non-obstructive hydronephrosis — by adding a "diuretic stimulus" (furosemide) and watching whether the tracer washes out (non-obstructive) or is retained (obstructive)
- Identifies difference in function between two kidneys — differential renal function
Critical for surgical planning [1]:
- Kidney with < 15% of total renal function (normal 50% each side) is non-functional and not worth salvaging
- Proceed to PCNL for preserved functional kidney function whereas nephrectomy may be indicated for non-functional kidney
A MAG3 renogram is not for diagnosing a stone — it's for deciding what to do about a kidney that's been damaged by a stone.
What it is: Injection of contrast via a catheter placed in the ureteric orifice during cystoscopy → outlines the ureter and pelvicalyceal system retrogradely.
When to use: When excretion of contrast cannot be used to outline the urological tract (e.g., poor renal function) [5]. Can intervene at the same time (e.g., insertion of JJ stent) [3].
Invasive: Requires cystoscopy under anaesthesia.
| Modality | Sensitivity | Key Advantage | Key Limitation | When to Use |
|---|---|---|---|---|
| NCCT | 97% | Gold standard; size, location, density, obstruction; no contrast needed | Radiation; misses indinavir stones; < 2 mm stones | First-line for all suspected ureteric colic [1][3] |
| KUB | 29–59% | Cheap, quick, baseline for F/U | Misses radiolucent + small stones; no obstruction assessment | Baseline for follow-up after NCCT confirms stone [1][3] |
| USG | 57% | No radiation; bedside; detects hydronephrosis | Cannot see ureteric stones; limited sensitivity | Pregnancy, paediatrics, screening [3] |
| CTU | ~97% | Full anatomical assessment; detects tumours and anomalies | High radiation + contrast risks | Complex anatomy, recurrent stones, haematuria workup |
| DECT | Similar to NCCT | Can differentiate stone composition in vivo | Availability, slightly higher radiation | When stone composition affects management [2] |
| IVU | ~70% | Functional information; economic | Largely obsolete; contrast risks; misses small lesions | Rarely used now [5][10] |
| MAG3 renogram | N/A | Differential renal function | Does not diagnose stones | Prolonged obstruction; surgical planning [1] |
| MRU | Variable | No radiation, no contrast | Misses small stones, expensive, inferior resolution | Pregnancy, children, contrast allergy [5] |
B. Laboratory Investigations
This should be done in every patient with suspected urolithiasis. It serves multiple roles:
| Test | What to Look For | Clinical Significance |
|---|---|---|
| Dipstick | Blood (haem), WBCs, nitrites, pH | Haematuria supports stone diagnosis; nitrites + WBCs suggest UTI; pH is important — overly alkaline urine (> 7.5) suggests infection by urease-producing organism, especially in the presence of stones [6] |
| Microscopy | RBCs, WBCs, crystals, organisms | Haematuria (gross or microscopic) present in ~85% [3]; pyuria can be present without infection due to irritation of urothelium [3]; crystal morphology may suggest stone type (hexagonal = cystine, coffin-lid = struvite, envelope = CaOx dihydrate, rhomboid = uric acid) |
| Urine pH | Acidic vs alkaline | Acidic (pH < 5.5): uric acid, cystine stones. Alkaline (pH > 7.5): struvite, calcium phosphate stones [6] |
| Culture and sensitivity (C/ST) | Organisms, antibiotic sensitivity | Must rule out UTI before any definitive treatment [2]; identifies urease-producing organisms (Proteus, Klebsiella) suggesting struvite stones |
Always Culture Before Operating
MSU C/ST to rule out UTI before any definitive treatment [2]. Operating on an infected stone without antibiotics can seed bacteria into the bloodstream → urosepsis. A positive culture mandates antibiotics before/during the procedure.
| Test | Rationale | Key Findings |
|---|---|---|
| CBC with differentials | Detect infection (leukocytosis); anaemia if chronic; baseline before surgery | Mild leukocytosis may be present even without infection (stress response). Marked leukocytosis with left shift suggests pyelonephritis/urosepsis [1] |
| Clotting profile | Preoperative baseline to look for underlying bleeding diathesis [1] — needed before ESWL, PCNL, or URS | Must be checked before any interventional procedure |
| RFT (Renal Function Tests) | Detect obstructive nephropathy; baseline Cr/eGFR | Rarely impaired in unilateral obstruction [3] — because the contralateral kidney compensates. May be impaired if bilateral staghorn calculi or solitary kidney [3] |
| Serum calcium and phosphate | Screen for primary hyperparathyroidism (the most important metabolic cause) [3][4]; also sarcoidosis, malignancy | ↑ Ca²⁺ + ↓/normal PO₄³⁻ + ↑ PTH = primary hyperPTH. Check albumin-corrected calcium to avoid factitious hypercalcaemia [4] |
| Serum uric acid (urate) | Screen for hyperuricaemia — gout, myeloproliferative disease, high purine diet | ↑ Urate supports uric acid stone diagnosis; also a risk factor for calcium stones (uric acid crystals act as a nidus) |
| PTH | If calcium is elevated — distinguish PTH-dependent from PTH-independent hypercalcaemia [4] | ↑ or inappropriately normal PTH with ↑ Ca = primary hyperPTH |
| Serum bicarbonate | Screen for distal RTA (Type 1) — chronic metabolic acidosis → ↓ citrate → calcium phosphate stones [3] | Low bicarbonate with hyperchloraemic metabolic acidosis + alkaline urine pH (inability to acidify) = distal RTA |
| CRP | Acute-phase reactant for infection/inflammation | Elevated in pyelonephritis/urosepsis |
When a stone is retrieved (after spontaneous passage, or during surgical procedure), it should always be sent for composition analysis:
- Methods: Infrared spectroscopy (IRS) or X-ray diffraction (XRD) [3]
- Obtain stone by stone retrieval procedure or by patient when they pass stones [3]
Clinical relevance of stone composition [3]:
- Calcium oxalate monohydrate / brushite are hard stones and may not be fragmented as easily with ESWL
- Uric acid stone indicates acidic urine and alkalinisation of urine may be helpful
- May suggest underlying conditions — e.g., Type 1 RTA / hyperPTH in calcium phosphate stones; upper UTI in struvite stones
Always instruct patients to strain their urine through a sieve/filter after an episode of renal colic. If they catch a stone, it must be sent to the laboratory. This small step can change the entire management plan.
This is done after the acute episode is managed, particularly in:
- First-time stone formers with risk factors
- All recurrent stone formers
- Children/young adults with stones
- Patients with specific stone types (cystine, uric acid, struvite)
| Investigation | What It Assesses | Key Findings |
|---|---|---|
| Serum calcium | Primary hyperparathyroidism (most important medical cause) [3] | ↑ Ca → check PTH → if ↑/inappropriately normal → primary hyperPTH |
| Serum bicarbonate | Distal RTA [3] | ↓ HCO₃⁻ + normal anion gap metabolic acidosis + alkaline urine → Type 1 RTA |
| Urine pH | Guides stone type prediction | ↑ pH in phosphate and struvite stones; ↓ pH in uric acid stones [3] |
| Urine crystals | Morphological clue to stone type | Oxalate, phosphate, uric acid, cystine (hexagonal — pathognomonic) |
| 24-hour urine collection | Comprehensive metabolic profile | Calcium, uric acid, citrate, oxalate, sodium, potassium, creatinine excretion, volume, pH, specific gravity [3]. This is the cornerstone of secondary prevention — identifies which metabolic abnormality to target |
24-Hour Urine — Key Abnormalities and Their Implications:
| Abnormality | Target Value | Implication |
|---|---|---|
| Hypercalciuria | > 7.5 mmol/day (M) or > 6.25 mmol/day (F) | Idiopathic (most common), hyperPTH, sarcoidosis, RTA |
| Hyperoxaluria | > 0.5 mmol/day | Dietary (common), enteric (IBD, bariatric surgery), primary (rare genetic) |
| Hyperuricosuria | > 4.8 mmol/day (M) or > 4.5 mmol/day (F) | High purine diet, gout, myeloproliferative disease |
| Hypocitraturia | < 1.7 mmol/day | Metabolic acidosis (RTA, chronic diarrhoea), high animal protein diet, idiopathic |
| Low urine volume | < 2 L/day | Inadequate fluid intake — the most modifiable risk factor |
| High urine sodium | > 200 mmol/day | High dietary sodium → competes with Ca for tubular reabsorption → hypercalciuria |
| Cystinuria | > 1.3 mmol/day | Autosomal recessive cystinuria — COLA amino acids |
C. Special Situations
Cystoscopy should be done in ALL patients with gross non-glomerular haematuria, even if a stone is found on KUB [5]. Why? Because the presence of stones does not rule out concomitant malignancy [5]. A bladder transitional cell carcinoma can coexist with a ureteric stone, and cystoscopy is the only way to directly visualise the bladder mucosa for tumours as small as 1 mm [5].
CTU + cystoscopy is mandatory for the complete haematuria workup [5]. The standard urological workup for haematuria = cystoscopy + upper tract imaging.
If renal function is compromised (suspect bilateral obstruction or solitary kidney):
- USG first to detect hydronephrosis → if bilateral → urgent decompression
- Radioisotope scintigraphy (MAG3) for differential renal function → guides surgical planning [1]
| Category | Investigation | Purpose |
|---|---|---|
| Imaging (acute) | Low-dose NCCT abdomen + pelvis | Confirm stone; size, location, density, obstruction |
| Imaging (baseline) | KUB (if stone radio-opaque) | Baseline for future follow-up without repeating CT |
| Imaging (special) | USG (if pregnant/child/screening) | Detect hydronephrosis; limited stone detection |
| Urine | Dipstick + microscopy | Haematuria, pyuria, pH |
| Urine | MSU C/ST | Rule out UTI before definitive treatment |
| Blood | CBC, CRP | Infection, baseline |
| Blood | Clotting profile | Pre-procedural |
| Blood | RFT | Renal function; bilateral obstruction |
| Blood | Serum calcium, phosphate | Hyperparathyroidism screening |
| Blood | Serum urate | Hyperuricaemia screening |
| Stone | Composition analysis (IR spectroscopy / XRD) | Determines stone type → guides prevention |
| Follow-up | 24-hour urine collection | Metabolic evaluation for secondary prevention |
| Special | MAG3 renogram | Differential renal function if prolonged obstruction |
| Special | DECT | In vivo stone composition differentiation |
High Yield Summary
Gold standard imaging: Low-dose NCCT abdomen + pelvis (Sensitivity 97%, Specificity 95%). No contrast needed — stones are inherently hyperdense.
KUB role: NOT for diagnosis — for follow-up baseline. 90% of stones are radio-opaque. Radiolucent stones (uric acid, xanthine, indinavir) are invisible on KUB.
USG role: First-line in pregnancy/children. Limited sensitivity (57%). Good for hydronephrosis, poor for ureteric stones.
Urine pH is diagnostic gold: pH > 7.5 with stones → think struvite (urease-producing infection). pH < 5.5 → think uric acid.
Always send MSU C/ST before any intervention — operating on infected stones without antibiotics → urosepsis.
Always send the stone for composition analysis (IR spectroscopy or XRD) — it determines secondary prevention strategy.
MAG3 renogram for differential renal function: kidney < 15% function → not worth salvaging → consider nephrectomy.
24-hour urine is the cornerstone of metabolic evaluation: calcium, oxalate, urate, citrate, sodium, volume, pH.
Screen for primary hyperPTH (serum Ca + PTH) in every calcium stone former — it is the most important treatable medical cause.
Active Recall - Diagnosis and Investigations for Urinary Stones
References
[1] Senior notes: felixlai.md (Urological Diseases — Urinary Stones, Diagnosis section) [2] Senior notes: maxim.md (Section 2.3: Urinary stones — Investigations) [3] Senior notes: Ryan Ho Urogenital.pdf (Section 7.2: Urolithiasis, pp. 137–143; DDx on KUB p. 139; Imaging workup p. 139–140) [4] Senior notes: Ryan Ho Endocrine.pdf (Primary Hyperparathyroidism standard Ix, pp. 42–43) [5] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.5.1: Haematuria investigations, pp. 343–345; Ryan Ho Urogenital.pdf pp. 134–135) [6] Lecture slides: GC 210. Urinary tract infection.pdf (Urinary pH and struvite p. 30; Role of imaging in UTI p. 25) [10] Senior notes: Ryan Ho Diagnostic Radiology.pdf (IVU, p. 17)
Management of Urinary Stones
Management of urolithiasis is structured around three phases, each with distinct goals [2][3]:
- Acute management: relieve pain, treat/exclude sepsis, decompress if needed
- Definitive stone removal: conservative observation vs active intervention
- Secondary prevention: prevent recurrence based on stone type and metabolic risk factors
The choice of treatment for any individual patient depends on a triad of factors [3]:
| Stone Factor | Patient Factor | Surgeon Factor |
|---|---|---|
| Size, Number, Composition, Site, Unilaterality/bilaterality | Function and anatomy of renal unit, Calyceal anatomy, Obstruction, Renal anomalies, Fitness for anaesthesia, Body habitus (ESWL not suitable for obese), Underlying bleeding tendency, Susceptibility for radiation | Surgeon expertise, Availability of technology |
Definitive treatment should be initiated ONLY when an acute episode of urosepsis (if present) has resolved [1]. Never operate on a hot, infected, obstructed system — decompress first, treat infection, then plan definitive surgery.
Phase 1: Acute Management
The immediate priorities when a patient presents with acute ureteric colic are:
A. Pain Control
Pain control is the first priority — renal colic is one of the most painful conditions patients experience.
- Examples: Indomethacin, Ketorolac, Diclofenac [1]
- Why NSAIDs first? Two reasons:
- Anti-inflammatory: reduces ureteric wall oedema around the impacted stone → reduces obstruction
- NSAIDs have the possible advantage of decreasing ureteral smooth muscle tone, thereby directly treating the mechanism (ureteral spasm) by which pain is thought to occur [1]. Prostaglandins (PGE₂) normally promote ureteric smooth muscle contraction; by inhibiting cyclooxygenase (COX), NSAIDs reduce prostaglandin synthesis → relax the ureter → less spasm → less pain
- They also reduce afferent nerve sensitisation at the kidney (less prostaglandin-mediated signal amplification)
- Require RFT to check for deranged renal function [1] before prescribing — NSAIDs reduce renal blood flow (by inhibiting prostaglandin-mediated afferent arteriolar vasodilation), which can worsen renal function in an already obstructed kidney
- Contraindicated in: renal impairment, peptic ulcer disease, significant cardiovascular disease, pregnancy
- Indicated for pain control in patients with acute renal colic who have deranged RFT [1] (i.e., when NSAIDs are contraindicated)
- Examples: Morphine, Pethidine, Tramadol, Hydromorphine, Pentazocine [1][3]
- Opioids are pure analgesics — they do NOT address ureteric spasm (unlike NSAIDs)
- Side effects: nausea/vomiting (already present from colic), sedation, respiratory depression, constipation
NSAIDs vs Opioids
NSAIDs are preferred over opioids for renal colic because they address the underlying ureteric spasm (not just pain perception) and cause fewer side effects (no sedation, no nausea worsening). Reserve opioids for NSAID failures or contraindications (impaired RFT).
- α-blockers can help reduce recurrent colic [3] — tamsulosin relaxes ureteric smooth muscle, reducing spasm even in the acute phase
- IV fluids for hydration if dehydrated/vomiting (but aggressive "flushing" with large-volume IV fluids does NOT help pass stones faster and may worsen pain by increasing hydrostatic pressure above the obstruction)
- Antiemetics (ondansetron, metoclopramide) as needed
This is the critical safety step. An infected obstructed urinary tract is a urological emergency:
- If there is fever, rigors, haemodynamic instability, or raised inflammatory markers with evidence of obstruction: treat as urosepsis
- Antibiotics if complicated by infection [3]
- Broad-spectrum empirical antibiotics targeting Gram-negatives (e.g., IV ceftriaxone, or piperacillin-tazobactam if Pseudomonas coverage needed)
Indications for urgent decompression [1][3]:
The 7 Ss of indications for urgent intervention are:
| 7S mnemonic | Clinical indication | Explanation |
|---|---|---|
| Sepsis / Urosepsis | Obstructed infected system | Bacteria cannot be cleared without drainage → septic shock |
| Single kidney | Solitary kidney obstruction | No contralateral kidney to compensate → rapid AKI |
| Stones on both sides | Bilateral obstruction | Both kidneys obstructed → anuria → AKI |
| Serum creatinine rising | Deteriorating renal function (AKI) | Progressive ↑ creatinine indicates ongoing renal damage from obstruction |
| Severe pain | Uncontrolled pain | Intractable pain despite maximal analgesia |
| Stone stuck / too large | Stone unlikely to pass | > 10 mm, impacted, or persistent after 4–6 weeks |
| Suppuration | Pyonephrosis | Infected hydronephrosis (pus under pressure) — NOT just pyelonephritis [1] |
Two methods of urgent decompression [3]:
| Method | Percutaneous Nephrostomy (PCN) | JJ Ureteric Stent |
|---|---|---|
| Approach | Needle puncture through skin into dilated pelvicalyceal system under USG guidance [11] | Retrograde insertion via cystoscopy under fluoroscopy |
| Speed | Quicker — preferred in septic shock [3] | Takes longer (requires cystoscopy + OT) |
| Comfort | Less comfortable (external drainage bag) | More comfortable (internal, no external bag) [3] |
| C/I | Bleeding tendency, distorted surface anatomy, obesity [3] | BPH (cannot pass scope), incompliant bladder, stone impaction [3] |
| Complications [11] | Minor (10%): bleeding, infection, pain. Serious (4–5%): haemorrhage, sepsis, pneumothorax, peritonitis | Stent migration, encrustation, irritative LUTS, haematuria |
| Key advantage | Can be done at bedside by IR; no GA needed | No external bag; patient can mobilise |
Monitor for post-obstructive diuresis after decompression [2]: once the obstruction is relieved, the kidney may produce large volumes of dilute urine (polyuria) due to accumulated osmotic load and temporary impairment of tubular concentrating ability → risk of dehydration and electrolyte disturbance (hyponatraemia, hypokalaemia). Monitor I/O and replace fluids/electrolytes accordingly.
Phase 2: Definitive Stone Removal
A. Conservative Management (Expectant / Medical) [1][2][3]
Not every stone needs active removal. The decision depends on stone size and location:
| Ureteric Stone Size | Chance of Spontaneous Passage | Management |
|---|---|---|
| ≤ 4 mm | 95% pass spontaneously [3] | Conservative with MET |
| 4–10 mm | Progressive ↓ chance, especially for proximal stones [3] | MET + follow-up at 4 weeks |
| ≥ 10 mm | Unlikely to pass spontaneously; stone removal definitely indicated [3] | Active intervention |
| > 10 mm diameter unlikely to pass [1] | — | — |
| Measure | Details | Rationale |
|---|---|---|
| Adequate hydration | 2–3 L/day (until urine is light in colour) [2] | Dilutes urine → reduces supersaturation → prevents new stone formation; promotes urine flow to flush stone fragments |
| Strain urine | Patient instructed to strain urine for several days and bring in any stones that pass for analysis [1][2] | Enables clinician to better plan preventive therapy [1] — stone composition determines secondary prevention |
| Dietary modification [1][2] | NORMAL calcium diet (not low-calcium!); ↓ protein (red meat, organs); ↓ oxalate (peanuts, spinach, beetroot, strawberries); ↓ salt (sodium); ↑ dietary fibre (fruits, wheat, corn) [1] | See Etiology section — the calcium paradox; high sodium competes with Ca for renal reabsorption; high protein → acid load → ↑ uric acid |
| Approach | Target Stone Type | Agent | Mechanism |
|---|---|---|---|
| Alkalinisation of urine | Uric acid or cystine stones [1] | Potassium citrate or sodium bicarbonate (baking soda) [1][2] | Uric acid is poorly soluble below pH 5.5; raising urine pH to 6.5–7.0 ionises uric acid → much more soluble → dissolves. Cystine solubility also increases above pH 7.0 |
| Acidification of urine | Struvite stones [1] | Ammonium chloride (rarely used in practice) | Struvite forms in alkaline urine; acidification reduces supersaturation. However, clinical utility is limited — complete surgical removal is usually required for struvite |
Uric acid stones are the ONLY common stone type that can be completely dissolved medically. This is a major management distinction — if DECT or stone analysis confirms pure uric acid composition, a trial of oral alkalinisation can render surgery unnecessary.
- Indicated for patients with stones of 5–10 mm [1], best for distal ureteric stones [2][3]
- α-blockers (tamsulosin 0.4 mg QD × 4 weeks, off-label use) [2][3]
- Why α-blockers work: The distal ureter (especially the intramural portion at the VUJ) has a high density of α₁-adrenoreceptors [3]. Tamsulosin ("tam" from its selective α₁A/α₁D blockade) relaxes the ureteric smooth muscle → widens the lumen → reduces peristaltic frequency and intraureteric pressure → facilitates stone passage
- Efficacy: α-blockers 1.45× more likely to pass ureteric stones, more useful for those 5–10 mm in size [3]
- Spontaneous passage of stone may take up to 3–4 weeks [1]
- CCBs (e.g., nifedipine) also increase passage rate [1] but are less commonly used than tamsulosin
- Follow-up at 4 weeks with KUB/NCCT [2] — if stone has not passed, proceed to active intervention
MET — Must Know
Medical expulsive therapy = tamsulosin for distal ureteric stones 5–10 mm. It works by relaxing α₁-receptors in the distal ureter. Follow up at 4 weeks. If the stone hasn't passed, escalate to surgical options. Not useful for renal or proximal ureteric stones (few α₁-receptors there).
B. Surgical / Interventional Treatment
The EAU Guidelines and senior notes provide a clear framework [1][2][3]:
| Location | Size | Treatment of Choice |
|---|---|---|
| Renal | Asymptomatic | Conservative; chemolysis (alkalinisation) for urate stones [3] |
| < 10 mm | ESWL or RIRS > PCNL [3] | |
| 10–20 mm (non-lower pole) | ESWL or RIRS or PCNL [3] | |
| 10–20 mm (lower pole) | RIRS or PCNL > ESWL if unfavourable factors for ESWL (steep infundibular angle, long calyx, long skin-to-stone distance, narrow infundibulum, shockwave-resistant stones) [3] | |
| > 20 mm | PCNL > RIRS or ESWL [3] | |
| Upper ureter | < 5 mm | Conservative / MET |
| 5–10 mm | ESWL [1]; or URS | |
| > 10 mm | URS or ESWL (+ JJ stent) [1][2] | |
| Mid / Lower ureter | < 5 mm | Conservative / MET |
| > 5 mm | URS (preferred) [1][2] | |
| Bladder | < 30 mm | Cystolitholapaxy [1] |
| > 30 mm | Open cystolithotomy [1]; also treat underlying outflow obstruction (e.g., BPH) [2] |
Name breakdown: "extra" = outside, "corporeal" = body, "litho" = stone, "tripsy" = crushing. So: crushing stones from outside the body using shock waves.
- US/XR-guided shock waves aimed at stones → crystalline stones disintegrate under the impact of shock waves [3]
- Patient lies on a table; a lithotripter generates shock waves that are focused on the stone (located by fluoroscopy or ultrasound)
- The shock waves travel through water/gel and soft tissue (which have similar acoustic impedance) without causing damage, but at the stone surface (acoustic impedance mismatch), the energy is deposited → fragmentation
- Setting: optimal 1–1.5 Hz, can ↑ energy gradually (↓ renal injury) [3]
- Best for renal and upper ureteric stones that are visible under imaging [3]
- Not so good for lower system due to difficulty in access + bowel gas obscuration especially at middle ureter [3]
- Stones with density < 1000 HU on CT predict success [2][3]
- Absolute: pregnancy, active UTI or urosepsis, uncontrolled bleeding diathesis [1]
- Relative: distal obstruction (e.g., strictures) [3] — fragments cannot pass if there is a downstream blockage
Limitations / When ESWL Fails [1][3]:
- Subject to skin-to-stone distance → poorer efficacy in obese patients [1]
- NOT ideal for large or hard calculi: cystine, calcium oxalate monohydrate, brushite stones [1] (predicted on CT as > 1000 HU) [3]
- NOT ideal for stones in unfavourable locations: lower pole of kidney, mid-to-distal ureter, within calyceal diverticulum [1]
- Lower pole stones: gravity causes stone fragments to be retained inside the lower pole [3]
- Calyceal diverticulum: narrow infundibulum traps stone fragments [3]
- NOT ideal in complex renal anatomy (horseshoe kidneys) [1]
Pros and Cons [3]:
- Pros: minimally invasive, does not need anaesthesia, can be repeated
- Cons: indirect, subject to stone-skin distance, may not work for hard stones, limitations by renal anatomy
Complications [1]:
- Incomplete fragmentation
- Urosepsis
- Perinephric or subcapsular haematoma — shock waves can cause parenchymal bleeding
- Ureteric obstruction by stone fragments (Steinstrasse — "stone street") — a column of stone fragments stacks up in the ureter after ESWL, causing obstruction. "Steinstrasse" is German: "Stein" = stone, "Strasse" = street [1]
Name breakdown: "per" = through, "cutaneous" = skin, "nephro" = kidney, "litho" = stone, "tomy" = cutting. Accessing the kidney through the skin to directly remove stones.
- Flexible cystoscopy for ureteral cannulation → inject contrast + distend pelvicalyceal system [3]
- Needle puncture at prone position just below the rib to gain entry into the pelvicalyceal system [3]
- Tract dilatation using Alken's dilator system or balloon dilator [1]
- Nephroscope passed into kidney via the percutaneous tract [3]
- Stone retrieval in whole (if small) or in fragments after laser/USG/electrohydraulic lithotripsy (if large) [3]
- Lower pole approach preferred to avoid supracostal puncture
- Posterior calyx to take advantage of the bloodless plane (Brödel's line — the watershed zone between anterior and posterior segmental renal artery branches, which has the least vasculature)
- Transpapillary directed towards renal pelvis to avoid puncturing the infundibulum [1][3]
- Posterolateral access to kidney (least vascular) to spare blood vessels because all renal arteries are end arteries [3]
- Supracostal puncture to upper pole possible, but 7% associated with thoracic complications requiring chest drain (cf 0.5% from subcostal puncture) [1][3]
Pre-operative preparation [1][3]:
- Antibiotics on induction MUST be given in PCNL — stone is usually infectious [1]
- Should cover Pseudomonas: piperacillin, ticarcillin, aminoglycoside, 3rd generation cephalosporin [1]
- Routine bloods, T&S, MSU (should treat all positive cultures before OT) [3]
- Large calculi > 2 cm in diameter [1]
- Hard stones (cystine, calcium oxalate monohydrate) [1]
- Stones in unfavourable locations for ESWL (lower pole, calyceal diverticulum) [1]
- Anatomical abnormalities (horseshoe kidney, PUJ obstruction) [1]
- Staghorn calculi
- ± Placement of nephrostomy tube for drainage (the pelvicalyceal system will be swollen/injured post-PCNL; the normal PUJ/ureteric route will likely be inflamed and obstructed) [1]; also provides tamponade effect on the tract and leaves access for second-look PCNL [1][3]
- ± Ureteral stent if anticipate incomplete stone retrieval
- Access failure (5%)
- Incomplete fragmentation
- Urosepsis (fever 10%, sepsis 1%)
- Bleeding requiring transfusion (7%) or embolisation (1%) [3]
- Hydrothorax (if supracostal puncture traverses the lower pleura → irrigating fluid enters pleural space) [1]
- Bowel perforation (< 1% colon, but 5% population have retrorenal colon) [3]
- Mortality < 0.5% [1][3]
Name breakdown: "uretero" = ureter, "reno" = kidney, "scopy" = looking. Passing a scope up the ureter.
- Ureteroscope introduced transurethrally across the bladder into the ureter [3]
- Small stones can be extracted by baskets or grasping forceps [1]
- Large stones are fragmented prior to removal with [1]:
- Laser (Holmium:YAG) — most commonly used
- Ultrasonic lithotripsy
- Ballistic/pneumatic (Lithoclast)
- Electrohydraulic lithotripsy (EHL)
Types:
- Rigid/semi-rigid URS: for middle and lower ureteric stones [1] — the treatment of choice for this location
- Flexible URS (= Retrograde Intrarenal Surgery, RIRS): deflection capabilities allow access to the entire upper urinary tract including the intrarenal collecting system [1]
- Mid and distal ureteric stones (rigid URS preferred)
- Upper ureteric and renal stones (flexible URS/RIRS)
- Especially useful for larger stones (earlier stone-free status compared to ESWL) and obese patients [3]
- Independent of body habitus and can be used in patients with bleeding diathesis [1][3]
Contraindications [3]:
- C/I to GA, untreated UTI (otherwise none — not limited by bleeding diathesis) [3]
Pros and Cons [3]:
- Pros: minimally invasive, direct fragmentation of stone, body habitus-independent, can be used in those with bleeding diathesis
- Cons: requires anaesthesia and radiation, technology-driven
- Limitation: calyceal anatomy (not all calyceal curvatures allow URS entry) [3]
Adjuncts: JJ stent placement post-URS may be considered for those with ↑ risk of complications [3]
- Intra-op (3.6%): mucosal injury (1.5%), ureteral perforation (1.7%), significant bleeding (0.1%), ureteral avulsion (0.1%) [3]
- Early (6.0%): fever/urosepsis (1.1%), persistent haematuria (2.0%), renal colic (2.2%) [3]
- Late (0.2%): ureteral stricture (0.1%), persistent VUR (0.1%) [3]
- Urosepsis: endoscopic irrigation can force bacteria into renal parenchyma and result in sepsis if performed in the setting of infection [1]
URS vs ESWL: URS has better stone-free rate and less need for re-treatment. ESWL has less procedure-related complications but may not be possible for large/complex stones [3].
| Procedure | Size | Method |
|---|---|---|
| Cystolitholapaxy | < 30 mm [1] | Transurethral endoscopic fragmentation (laser, pneumatic, or electrohydraulic) + aspiration/extraction via cystoscope |
| Open cystolithotomy | > 30 mm [1] | Open surgical removal through a suprapubic incision into the bladder |
- Always treat the underlying cause of bladder stones (e.g., BPH → TURP, neurogenic bladder → intermittent catheterisation) [2]
| Feature | ESWL | PCNL | URS/RIRS |
|---|---|---|---|
| Invasiveness | Least | Most | Moderate |
| Anaesthesia | Not required | GA required | GA required |
| Best for | Renal + upper ureteric stones < 2 cm, density < 1000 HU | Renal stones > 2 cm, staghorn, hard stones, lower pole | Mid/lower ureteric stones; also renal via RIRS |
| Body habitus | Not suitable for obese | Can be limited by body habitus | Body habitus-independent |
| Bleeding diathesis | Contraindicated | Contraindicated | NOT limited |
| Stone-free rate | Lower (may need multiple sessions) | Highest for large stones | Higher than ESWL for ureteric stones |
| Key complication | Steinstrasse | Bleeding, hydrothorax | Ureteric stricture/avulsion |
Phase 3: Secondary Prevention
Prevention of recurrence is essential given the 50% recurrence rate at 10 years.
| Measure | Target | Rationale |
|---|---|---|
| ↑ Fluid intake to 2–3 L/day | Urine output > 2 L/day; urine should be light in colour [2] | Dilutes all solutes → reduces supersaturation |
| Normal calcium diet | Dietary calcium binds oxalate in gut | Paradox: low dietary calcium ↑ oxalate absorption → ↑ CaOx stones |
| ↓ Salt < 2 g/day [2] | ↓ Sodium excretion → ↓ calcium excretion | Na and Ca compete for tubular reabsorption |
| ↓ Animal protein [2] | ↓ Acid load, ↓ uric acid, ↓ urinary calcium | High protein → ↑ purine metabolism → ↑ uric acid; also → acid load → ↑ Ca mobilisation from bone |
| ↓ Oxalate-rich foods | Spinach, chocolate, tea, beets, nuts | Direct ↓ urinary oxalate |
| ↑ Citrus fruit [2] | ↑ Urinary citrate | Citrate chelates calcium in urine → inhibits crystal formation |
| Stone Type | Specific Prevention |
|---|---|
| Calcium oxalate | Treat underlying cause (hyperPTH → parathyroidectomy; RTA → alkali therapy); thiazide diuretics (↓ urinary Ca); potassium citrate (↑ urinary citrate) |
| Calcium phosphate | Treat RTA; avoid excessive alkalinisation (CaPO₄ precipitates at high pH) |
| Uric acid | Urine alkalinisation: potassium citrate / sodium bicarbonate [1][2] (target pH 6.5–7.0); allopurinol/febuxostat if hyperuricaemia [12] |
| Struvite | Antibiotics × 6 weeks [2]; complete surgical stone removal is essential (fragments harbour bacteria → recurrence); treat and prevent UTI |
| Cystine | ↑ Fluid intake (target > 3 L/day); urine alkalinisation (target pH > 7.0); chelating agents (e.g., penicillamine, tiopronin) [2] — these bind cystine to form more soluble complexes |
Struvite Stones — Complete Removal is Mandatory
Unlike other stone types where residual fragments may be tolerated, struvite stones MUST be completely removed. Any fragment left behind harbours bacteria → recurrence. This is why struvite staghorn calculi are treated aggressively with PCNL (sometimes requiring multiple sessions) followed by prolonged antibiotics.
If metabolic workup reveals primary hyperparathyroidism (↑ Ca + ↑/inappropriately normal PTH + normal RFT), this is the most important treatable medical cause of calcium stones [3]. Management:
- Surgical treatment (parathyroidectomy) indications (JCEM 2014): age < 50 or any one of [4]:
- Clearly symptomatic or documented complications
- Serum Ca > 0.25 mmol/L above ULN (i.e., 2.85 mmol/L)
- Nephrolithiasis or nephrocalcinosis by XR/US/CT
- CrCl < 60 mL/min
- 24h urine Ca > 400 mg/day + ↑ stone risk
- DXA T-score < -2.5
- Conservative management if surgery contraindicated: calcimimetics (cinacalcet) + regular monitoring (serum Ca annually, DXA every 1–2 years, renal imaging if stone suspected) [4]
High Yield Summary
Acute management triad: (1) Pain — NSAIDs first line (reduce spasm + inflammation); opioids if NSAIDs C/I. (2) Infection — IV antibiotics if septic. (3) Decompression — PCN (faster, for septic shock) or JJ stent (more comfortable) if sepsis/AKI/intractable pain.
Spontaneous passage rates: ≤ 4 mm = 95%; 5–10 mm = variable; ≥ 10 mm = unlikely → needs intervention.
MET: Tamsulosin 0.4 mg QD × 4 weeks for distal ureteric stones 5–10 mm. Works via α₁-receptor blockade in distal ureter. Follow up with KUB/NCCT at 4 weeks.
ESWL: Best for renal + upper ureteric stones < 2 cm; not for hard stones (> 1000 HU), obese, lower pole, bleeding diathesis. No GA needed. Complications: Steinstrasse, haematoma.
PCNL: Best for renal stones > 2 cm, staghorn, hard stones, lower pole. Requires GA. Access via posterior calyx at lower pole (bloodless plane). Antibiotics on induction mandatory. Complications: bleeding (7%), hydrothorax (supracostal), mortality < 0.5%.
URS/RIRS: Best for mid/lower ureteric stones (rigid URS) and renal stones when ESWL fails (flexible RIRS). Body habitus-independent. CAN be used in bleeding diathesis.
Prevention: ↑ fluids, normal Ca diet, ↓ Na/protein/oxalate, ↑ citrus. Uric acid: alkalinise urine. Struvite: complete removal + antibiotics × 6 weeks. Cystine: alkalinise + chelating agents.
Never operate on a septic, obstructed system — decompress first, treat infection, then plan definitive surgery.
Active Recall - Management of Urinary Stones
References
[1] Senior notes: felixlai.md (Urological Diseases — Urinary Stones, Treatment section) [2] Senior notes: maxim.md (Section 2.3: Urinary stones — Management) [3] Senior notes: Ryan Ho Urogenital.pdf (Section 7.2: Urolithiasis management, pp. 140–143) [4] Senior notes: Ryan Ho Endocrine.pdf (Primary Hyperparathyroidism surgical indications, pp. 43) [11] Senior notes: Ryan Ho Diagnostic Radiology.pdf (Percutaneous Nephrostomy, p. 83) [12] Senior notes: Ryan Ho Rheumatology.pdf (Gout — urate-lowering therapy, pp. 39–40)
Complications of Urinary Stones
Urinary stones can be thought of as causing harm through three fundamental mechanisms: obstruction, infection, and direct tissue injury. Every complication listed below stems from one — or a combination — of these three mechanisms. Understanding this triad from first principles lets you predict, recognise, and manage complications logically.
1. Infection: Pyelonephritis, Pyonephrosis, and Urosepsis [1][2]
The chain of events:
- A stone lodges in the ureter → obstruction → urine pools above the stone → stasis
- Stagnant urine is an excellent culture medium → bacteria (from ascending UTI or haematogenous seeding) multiply unchecked
- Bacteria ascend from the stagnant urine into the renal parenchyma → pyelonephritis (infection of the kidney)
- If the collecting system fills with pus under pressure → pyonephrosis ("pyo" = pus, "nephros" = kidney) — this is essentially an empyema of the renal pelvis
- Bacteria and endotoxins enter the bloodstream through the infected, inflamed, and congested renal parenchyma → urosepsis → can rapidly progress to septic shock and multi-organ failure if not decompressed
This is the single most dangerous acute complication of urinary stones. An obstructed infected system is a closed-space infection under pressure — analogous to an undrained abscess. Antibiotics alone cannot sterilise a system where pus has no way out.
- Pyelonephritis: high spiking fever, rigors, loin pain, renal angle tenderness (Murphy's kidney punch positive), nausea/vomiting, tachycardia, leukocytosis with left shift
- Pyonephrosis: similar to pyelonephritis but more toxic-appearing; may have palpable ballotable kidney due to massive distension with pus; requires urgent decompression [1] — this is the indication for PCN or JJ stent, NOT just pyelonephritis [1]
- Urosepsis: features of sepsis (fever/hypothermia, tachycardia, tachypnoea, hypotension, altered mental status, raised lactate) in the setting of urinary tract infection. Can evolve to septic shock with cardiovascular collapse
- IV antibiotics — broad-spectrum (e.g., piperacillin-tazobactam, or ceftriaxone + metronidazole; cover Pseudomonas if healthcare-associated) guided by local sensitivities
- Urgent decompression by PCN (preferred in septic shock — quicker, bedside) or JJ stent [3]
- Definitive stone removal is deferred until sepsis has completely resolved [1]
- Resuscitation: IV fluids, inotropes if needed, ICU admission for multi-organ support
Pyonephrosis vs Pyelonephritis — Key Distinction
Pyonephrosis (pus under pressure in an obstructed collecting system) requires urgent drainage. Pyelonephritis alone (without obstruction) does NOT require drainage — antibiotics suffice. [1] The critical difference is whether there is obstruction. Always check for hydronephrosis on USG/NCCT in febrile patients with stones. Pyonephrosis = pus + obstruction = surgical emergency.
This is a rare but important chronic complication, particularly relevant in Hong Kong exam material:
- A chronic destructive granulomatous process that typically occurs with long-standing obstruction (often by a staghorn calculus) + chronic infection
- Characterised by lipid-laden macrophages (xanthoma cells) — "xantho" = yellow (from lipid content), "granulomatous" = granuloma formation [6]
- CT shows classic "bear's paw" appearance — an enlarged non-functioning kidney with dilated calyces containing stones, surrounded by inflammatory tissue replacing normal parenchyma [6]
- The kidney is essentially destroyed and non-functional
- Treatment: nephrectomy — the kidney cannot be salvaged [6]
2. Obstruction: Hydroureter, Hydronephrosis, and Obstructive Nephropathy [1][2]
- Stone lodges at a point of ureteric narrowing (PUJ, pelvic brim, VUJ) → partial or complete obstruction
- Urine produced by the kidney cannot pass → back-pressure builds up
- The ureter dilates upstream → hydroureter
- The renal pelvis and calyces dilate → hydronephrosis [2]
- If obstruction persists, the rising intraluminal pressure is transmitted to the renal parenchyma → compresses the renal tubules and microvasculature → ischaemia + direct pressure-induced tubular damage → obstructive nephropathy
- Scarring around the stone or post-obstructive effects can maintain hydronephrosis even after the stone passes [2]
| Feature | Acute Obstruction | Chronic Obstruction |
|---|---|---|
| Duration | Hours to days | Weeks to months |
| Reversibility | Fully reversible if relieved promptly | May be irreversible if prolonged |
| Renal damage | Minimal if decompressed early | Cortical thinning, parenchymal atrophy, tubulointerstitial fibrosis |
| Clinical picture | Severe pain, acute hydronephrosis | May be painless (slowly progressive dilation), chronic hydronephrosis, progressive renal impairment |
- May be asymptomatic (especially if chronic and unilateral — the contralateral kidney compensates)
- Dull aching flank pain (from capsular distension)
- Rarely ballotable kidneys [3] (only in massive hydronephrosis/pyonephrosis)
- On imaging: dilated pelvicalyceal system on USG; perinephric stranding and dilated system on NCCT
- Identify and relieve obstruction (PCN or JJ stent for urgent cases; definitive stone removal for the cause)
- Monitor renal function (serial RFT)
- Radioisotope scintigraphy (MAG3/DTPA) for differential renal function if prolonged obstruction → kidney with < 15% of total renal function is non-functional and not worth salvaging → consider nephrectomy [1]
3. Acute Kidney Injury (AKI) [1][2][7]
AKI from urolithiasis is a post-renal (obstructive) cause [7]:
- Urinary stones are listed as a cause of post-renal AKI due to obstructive uropathy [7]
- For a stone to cause clinically significant AKI, obstruction must be bilateral, or the stone must obstruct a solitary functioning kidney (e.g., the other kidney was previously removed or is congenitally absent/non-functional). Why? Because a single functioning kidney can maintain adequate GFR — unilateral obstruction alone rarely causes AKI
- Exception: bilateral staghorn calculi → bilateral obstruction → may present with chronic renal failure [3]
- However, prolonged post-renal disease will progress to become tubulointerstitial fibrosis, i.e., intrinsic renal disease [7] — so early decompression is critical
- Oliguria (< 0.5 mL/kg/h): important early sign
- ↑ Creatinine, hyperkalaemia ± hyponatraemia
- Fluid overload: oedema, hypertension
- Anuria: complete bilateral obstruction
- Ensure and manage ABC
- Consider and reverse post-renal disease: palpable bladder, blocked catheter, hydronephrosis on imaging
- Urgent decompression (PCN or JJ stent)
- Management of life-threatening complications:
- Hyperkalaemia (K > 6 → ECG monitoring; IV calcium gluconate for membrane stabilisation, insulin-dextrose, salbutamol nebuliser, polystyrene sulphonate; dialysis if refractory)
- Fluid overload (IV furosemide; dialysis if refractory)
- Metabolic acidosis (IV bicarbonate; dialysis if refractory)
- Haemodialysis if indications met (AEIOU: Acidosis, Electrolytes, Intoxication, Overload, Uraemia) [8]
Post-Renal AKI is Reversible — If Caught Early
Recognising post-renal AKI is particularly important because it is often rapidly reversible compared to intrinsic renal disease [7]. A simple USG showing bilateral hydronephrosis + rising creatinine should trigger urgent decompression — the reward is restoration of renal function that would otherwise be permanently lost.
4. Post-Obstructive Diuresis [2][5]
This is a complication that occurs after the obstruction is relieved — an important concept to understand and anticipate.
- During prolonged obstruction, the kidney accumulates solute and water that it could not excrete
- Additionally, the high back-pressure damages the tubular concentrating mechanism (medullary washout, impaired aquaporin expression, decreased sodium reabsorption in the loop of Henle)
- When obstruction is relieved, two things happen simultaneously:
- Physiological diuresis: the kidney excretes the accumulated backlog of urea, sodium, and water — this is appropriate and self-limiting
- Pathological diuresis: damaged tubules cannot concentrate urine properly → massive, persistent, dilute urine output → risk of dehydration, hypovolaemia, and electrolyte disturbances
- Post-obstructive diuresis: > 200 mL/h urine × ≥ 2 hours, or > 3 L urine in 24 hours [5]
- Hyponatraemia, hypokalaemia, hypovolaemia [5]
- Dehydration, hypotension
- Can be life-threatening if not recognised and replaced
- Close monitoring of intake/output (chart urine output every 2 hours) [5]
- Fluid and electrolyte status monitoring with appropriate replacement and resuscitation [5]
- Prefer oral hydration; aim to replace half of urine output in the past hour [5]
- Do NOT over-replace — excessive IV fluids can perpetuate the diuresis. Match roughly 50–75% of urine output
- Usually resolves within 24–48 hours as tubular function recovers
5. Haematuria [2][3]
- The stone's rough surface (particularly calcium oxalate with its irregular "mulberry" shape and sharp projections [3]) directly traumatises the urothelium → bleeding
- Can be gross (visible red urine) or microscopic (detected on dipstick/microscopy)
- Haematuria is the single most discriminating predictor of kidney stone in unilateral flank pain (apart from passage of stones) [3]
- Present in ~95% of symptomatic ureteric stone episodes [3]
- Usually self-limiting once the stone passes or is removed
- Persistent or significant haematuria after stone treatment may indicate:
- Mucosal injury from instrumentation (URS, PCNL)
- Residual stone fragments
- Coexisting pathology (e.g., bladder cancer — always consider in patients > 35 with gross haematuria)
- Haemorrhage ex-vacuo (transient haematuria): occurs after sudden emptying of a greatly distended bladder → bladder mucosal disruption with sudden emptying [5] — usually self-limiting, rarely significant
Pathophysiology
- Prolonged obstruction → tubulointerstitial fibrosis [7] → irreversible renal parenchymal damage → CKD
- Particularly relevant in:
- Bilateral staghorn calculi: chronic bilateral obstruction → progressive loss of renal function
- Nephrocalcinosis: chronic deposition of calcium in the renal parenchyma (e.g., in hyperparathyroidism, distal RTA) → may result in CKD if chronic [4]
- Recurrent stones with repeated episodes of obstruction and infection → cumulative scarring
- Primary hyperparathyroidism renal complications include: renal stone, nephrocalcinosis, tubular dysfunction, CKD [4]
7. Ureteric Stricture [1][3]
- Chronic impaction of a stone against the ureteric wall → persistent inflammation → fibrosis → cicatricial narrowing (stricture) of the ureteric lumen
- Also an iatrogenic complication of stone treatment: ureteric stricture is a late complication of URS (0.1%) [3]; can also occur after prolonged JJ stent placement or ESWL with steinstrasse
- Once a stricture forms, it becomes a new point of obstruction → predisposes to recurrent hydronephrosis and stone formation in a vicious cycle
- Balloon dilatation (endoscopic)
- Endoureterotomy (incision of the stricture)
- Ureteric reimplantation (for distal strictures)
- Boari flap or ileal ureter interposition (for long strictures)
8. Complications of Stone Treatment Procedures
These are iatrogenic complications that are important to know for exam purposes:
| Complication | Mechanism |
|---|---|
| Incomplete fragmentation | Stone too hard (> 1000 HU) or too large for effective shock wave energy delivery |
| Steinstrasse ("stone street") | Multiple stone fragments stack in the ureter post-ESWL → ureteric obstruction. "Stein" = stone, "Strasse" = street (German) |
| Perinephric or subcapsular haematoma | Shock waves damage renal parenchymal microvasculature → bleeding into the perirenal space or under the renal capsule |
| Urosepsis | Fragmentation of an infected stone releases bacteria into the bloodstream |
| Complication | Mechanism |
|---|---|
| Access failure (5%) | Cannot establish percutaneous tract into the collecting system |
| Bleeding requiring transfusion (7%) | Puncture through vascularised parenchyma; all renal arteries are end-arteries → no collateral compensation |
| Hydrothorax (15% if supracostal) | If the supracostal puncture tract traverses the lower pleura → irrigating fluid enters the pleural space [1] |
| Bowel perforation (< 1%) | 5% of the population have a retrorenal colon → at risk during posterior access [3] |
| Urosepsis (fever 10%, sepsis 1%) | Flushing bacteria into the bloodstream during manipulation of infected stones [2] |
| Mortality (< 0.5%) | Cumulative risk from the above |
| Complication | Mechanism |
|---|---|
| Ureteral perforation (1.7%) | Scope or laser energy perforates the thin ureteric wall |
| Ureteral avulsion (0.1%) | Excessive traction during stone basket extraction tears the ureter off — catastrophic |
| Urosepsis (1.1%) | Endoscopic irrigation can force bacteria into renal parenchyma → bacteraemia [1] |
| Ureteric stricture (0.1%) | Late fibrosis from mucosal injury/thermal damage |
| Persistent VUR (0.1%) | Damage to the VUJ anti-reflux mechanism during instrumentation |
9. Recurrence [3]
- Urolithiasis is fundamentally a chronic, recurrent disease driven by underlying metabolic, dietary, and genetic predispositions that persist after the acute episode is treated
- Unless the modifiable risk factors are addressed, the same conditions that formed the first stone will form the next
- Risk of recurrence after 1st stone: ~15% at 1 year, 35–40% at 5 years, 50% at 10 years
- This is precisely why metabolic evaluation and secondary prevention are essential — not optional
- See Management section (Phase 3: Secondary Prevention) for detailed stone-type-specific measures
| Complication | Mechanism | Key Clinical Feature | Urgency |
|---|---|---|---|
| Urosepsis | Obstruction + infection → bacteria enter bloodstream | Fever, rigors, hypotension, tachycardia | Emergency — urgent decompression |
| Pyelonephritis | Ascending infection from stagnant urine | High fever, loin pain, renal angle tenderness | Urgent — antibiotics ± decompression |
| Pyonephrosis | Pus under pressure in obstructed collecting system | Toxic patient, ballotable kidney | Emergency — urgent drainage |
| XGP | Chronic obstruction + infection → granulomatous destruction | Non-functioning kidney, "bear's paw" on CT | Elective — nephrectomy |
| Hydronephrosis | Back-pressure from obstruction | May be painless if chronic; cortical thinning on imaging | Semi-urgent — decompress to preserve function |
| AKI | Bilateral obstruction or solitary kidney obstruction | Oliguria/anuria, rising Cr, hyperkalaemia | Emergency — urgent decompression |
| CKD | Prolonged/recurrent obstruction → tubulointerstitial fibrosis | Progressive ↓ GFR, small kidneys | Chronic — prevent further damage |
| Post-obstructive diuresis | Damaged tubular concentrating mechanism after relief | Massive urine output, electrolyte derangement | Monitor closely after decompression |
| Ureteric stricture | Chronic inflammation/fibrosis from impacted stone or instrumentation | Recurrent obstruction, hydronephrosis | Elective — endoscopic or surgical repair |
| Haematuria | Mucosal trauma by stone surface | Pink/red urine, positive dipstick | Usually self-limiting |
| Steinstrasse | Stone fragments pile up in ureter post-ESWL | Recurrent colic after ESWL | May need URS if symptomatic |
| Recurrence | Persistent underlying metabolic risk factors | Another stone episode | Long-term — metabolic evaluation + prevention |
High Yield Summary
Three fundamental mechanisms of stone complications: Obstruction, Infection, Direct Tissue Injury.
Most dangerous complication: Urosepsis from an obstructed infected system → septic shock → multi-organ failure. Requires urgent decompression (PCN or JJ stent) + IV antibiotics. Never attempt definitive stone surgery until sepsis resolved.
Pyonephrosis ≠ Pyelonephritis: Pyonephrosis = pus under pressure in an obstructed system → requires drainage. Pyelonephritis without obstruction → antibiotics alone.
AKI from stones is post-renal: Requires bilateral obstruction or solitary kidney. Reversible if decompressed early. Prolonged obstruction → tubulointerstitial fibrosis → CKD (irreversible).
Post-obstructive diuresis: > 200 mL/h × 2h or > 3 L/day after relief of obstruction. Risk of dehydration and electrolyte disturbance. Monitor I/O closely; replace ~50% of urine output.
XGP: Chronic destruction by staghorn stone + infection → lipid-laden macrophages → "bear's paw" on CT → nephrectomy.
Recurrence: 50% at 10 years. Metabolic evaluation (24h urine) and secondary prevention are mandatory.
Treatment complications to know: ESWL → Steinstrasse, haematoma; PCNL → bleeding (7%), hydrothorax (supracostal), bowel perforation; URS → perforation, avulsion, stricture.
Active Recall - Complications of Urinary Stones
References
[1] Senior notes: felixlai.md (Urological Diseases — Urinary Stones, Complications and Treatment sections) [2] Senior notes: maxim.md (Section 2.3: Urinary stones — Complications, Management) [3] Senior notes: Ryan Ho Urogenital.pdf (Section 7.2: Urolithiasis, pp. 137–143) [4] Senior notes: Ryan Ho Endocrine.pdf (Primary Hyperparathyroidism — renal complications, p. 42) [5] Senior notes: Ryan Ho Fundamentals.pdf (Post-obstructive diuresis, p. 353; Haemorrhage ex-vacuo, p. 353) [6] Lecture slides: GC 210. Urinary tract infection.pdf (Xanthogranulomatous pyelonephritis — bear's paw, lipid-laden macrophages, p. 125) [7] Senior notes: Ryan Ho Critical Care.pdf (AKI — post-renal causes including urinary stones, pp. 25–26) [8] Senior notes: Ryan Ho Critical Care.pdf (Management of AKI — life-threatening complications and haemodialysis indications, p. 26)
High Yield Summary
Definition: Urolithiasis = stone formation anywhere in the urinary tract, most commonly calcium oxalate.
Epidemiology: M > F (~4:3), peak 30–50y, lifetime prevalence up to 16% (M). Recurrence: 50% at 10 years.
Three sites of ureteric narrowing: PUJ, pelvic brim (iliac artery crossing), VUJ (narrowest).
Five stone types: Calcium oxalate (70–80%), Calcium phosphate (15%), Uric acid (5–10%, radiolucent, dissolves with alkalinisation), Struvite (infection-related, urease-splitting organisms, staghorn), Cystine (1%, AR cystinuria, hexagonal crystals).
Key pathophysiology: Supersaturation → nucleation (Randall's plaque) → growth/aggregation → obstruction → pain, haematuria, infection.
The Calcium Paradox: Dietary calcium is PROTECTIVE (binds oxalate in gut). Calcium supplements (taken away from meals) INCREASE risk.
Classic presentation: Colicky loin-to-groin pain + haematuria + N/V. Symptoms out of proportion to signs. Patient cannot lie still.
Red flag: Fever + obstructed stone = urological emergency → urgent decompression (JJ stent or PCN) + IV antibiotics.
Urine pH matters: Acidic → uric acid, cystine. Alkaline → calcium phosphate, struvite.
Radio-opacity: Calcium = opaque, Uric acid = lucent, Cystine = faintly opaque.
High Yield Summary
Three most dangerous mimics of renal colic to never miss:
- Ruptured AAA — elderly, hypotensive, pulsatile mass
- Ruptured ectopic pregnancy — woman of reproductive age, positive β-hCG
- Obstructed infected system — fever + stone = emergency decompression
Key distinguishing features of ureteric colic vs peritoneal pathology:
- Stones: symptoms OUT OF PROPORTION to signs, no peritoneal signs, patient RESTLESS
- Peritoneal causes (appendicitis, diverticulitis): peritoneal signs present (guarding, rebound), patient lies STILL
Sterile pyuria DDx (lecture slide): TB, bladder CIS, stones, schistosomiasis, partially treated UTI, interstitial cystitis, ketamine cystitis.
Phleboliths are the most common mimic of distal ureteric stones on KUB.
Clot colic: haematuria with formed clots passing down the ureter → think RCC or urothelial tumour, not just simple stone.
Red flags for malignancy: painless gross haematuria in > 35 y/o, constitutional symptoms, smoking history, occupational exposure.
High Yield Summary
Gold standard imaging: Low-dose NCCT abdomen + pelvis (Sensitivity 97%, Specificity 95%). No contrast needed — stones are inherently hyperdense.
KUB role: NOT for diagnosis — for follow-up baseline. 90% of stones are radio-opaque. Radiolucent stones (uric acid, xanthine, indinavir) are invisible on KUB.
USG role: First-line in pregnancy/children. Limited sensitivity (57%). Good for hydronephrosis, poor for ureteric stones.
Urine pH is diagnostic gold: pH > 7.5 with stones → think struvite (urease-producing infection). pH < 5.5 → think uric acid.
Always send MSU C/ST before any intervention — operating on infected stones without antibiotics → urosepsis.
Always send the stone for composition analysis (IR spectroscopy or XRD) — it determines secondary prevention strategy.
MAG3 renogram for differential renal function: kidney < 15% function → not worth salvaging → consider nephrectomy.
24-hour urine is the cornerstone of metabolic evaluation: calcium, oxalate, urate, citrate, sodium, volume, pH.
Screen for primary hyperPTH (serum Ca + PTH) in every calcium stone former — it is the most important treatable medical cause.
High Yield Summary
Acute management triad: (1) Pain — NSAIDs first line (reduce spasm + inflammation); opioids if NSAIDs C/I. (2) Infection — IV antibiotics if septic. (3) Decompression — PCN (faster, for septic shock) or JJ stent (more comfortable) if sepsis/AKI/intractable pain.
Spontaneous passage rates: ≤ 4 mm = 95%; 5–10 mm = variable; ≥ 10 mm = unlikely → needs intervention.
MET: Tamsulosin 0.4 mg QD × 4 weeks for distal ureteric stones 5–10 mm. Works via α₁-receptor blockade in distal ureter. Follow up with KUB/NCCT at 4 weeks.
ESWL: Best for renal + upper ureteric stones < 2 cm; not for hard stones (> 1000 HU), obese, lower pole, bleeding diathesis. No GA needed. Complications: Steinstrasse, haematoma.
PCNL: Best for renal stones > 2 cm, staghorn, hard stones, lower pole. Requires GA. Access via posterior calyx at lower pole (bloodless plane). Antibiotics on induction mandatory. Complications: bleeding (7%), hydrothorax (supracostal), mortality < 0.5%.
URS/RIRS: Best for mid/lower ureteric stones (rigid URS) and renal stones when ESWL fails (flexible RIRS). Body habitus-independent. CAN be used in bleeding diathesis.
Prevention: ↑ fluids, normal Ca diet, ↓ Na/protein/oxalate, ↑ citrus. Uric acid: alkalinise urine. Struvite: complete removal + antibiotics × 6 weeks. Cystine: alkalinise + chelating agents.
Never operate on a septic, obstructed system — decompress first, treat infection, then plan definitive surgery.
High Yield Summary
Three fundamental mechanisms of stone complications: Obstruction, Infection, Direct Tissue Injury.
Most dangerous complication: Urosepsis from an obstructed infected system → septic shock → multi-organ failure. Requires urgent decompression (PCN or JJ stent) + IV antibiotics. Never attempt definitive stone surgery until sepsis resolved.
Pyonephrosis ≠ Pyelonephritis: Pyonephrosis = pus under pressure in an obstructed system → requires drainage. Pyelonephritis without obstruction → antibiotics alone.
AKI from stones is post-renal: Requires bilateral obstruction or solitary kidney. Reversible if decompressed early. Prolonged obstruction → tubulointerstitial fibrosis → CKD (irreversible).
Post-obstructive diuresis: > 200 mL/h × 2h or > 3 L/day after relief of obstruction. Risk of dehydration and electrolyte disturbance. Monitor I/O closely; replace ~50% of urine output.
XGP: Chronic destruction by staghorn stone + infection → lipid-laden macrophages → "bear's paw" on CT → nephrectomy.
Recurrence: 50% at 10 years. Metabolic evaluation (24h urine) and secondary prevention are mandatory.
Treatment complications to know: ESWL → Steinstrasse, haematoma; PCNL → bleeding (7%), hydrothorax (supracostal), bowel perforation; URS → perforation, avulsion, stricture.
Testicular Cancer
Testicular cancer is a malignant neoplasm arising from germ cells or, less commonly, stromal cells of the testis, most frequently presenting as a painless scrotal mass in young men aged 15–35 years.
Urinary Tract Infection
A urinary tract infection is an infection of the urinary system, most commonly caused by bacteria ascending through the urethra to the bladder or kidneys, presenting with dysuria, frequency, and urgency.