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.

Exam domain	One-glance essentials
Definition / diagnosis	Urolithiasis is calculi anywhere in the urinary tract, formed by urinary supersaturation, crystallisation, aggregation and growth. ^[1] Most stones are calcium oxalate; ureteric stones commonly cause renal colic and haematuria. ^[1]
Epidemiology / risks	Low fluid intake, high sodium, animal protein or oxalate, obesity and prior stones increase risk. ^[1] Normal dietary calcium is protective by binding gut oxalate; calcium supplements taken away from meals may increase risk. ^[1] Consider hyperparathyroidism, distal RTA, bowel disease, gout and cystinuria. ^[1]
Core mechanism	Supersaturation causes nucleation, crystal growth, aggregation and retention. ^[1] Randall plaque is a papillary calcium deposit that acts as a nidus. ^[1] Obstruction causes upstream pressure and hydronephrosis; mucosal trauma causes haematuria, while stasis promotes infection. ^[1]
Clinical picture	Classic renal colic is severe colicky loin-to-groin pain with haematuria, nausea or vomiting. ^[1] Patients are typically restless, with pain out of proportion to examination and no peritoneal signs. ^[1] Fever, rigors, toxicity, AKI, anuria or a solitary kidney indicate complicated disease. ^[1]
Investigations	Low-dose NCCT abdomen/pelvis is the definitive acute test: localises stones, measures size and shows obstruction. ^[1] Urinalysis, urine culture, CBC, renal function, calcium, phosphate and urate assess infection, renal injury and cause. ^[1] Use ultrasound first in pregnancy or children; KUB is mainly a baseline for radio-opaque stones and follow-up. ^[1] Send passed or retrieved stones for composition analysis; use 24-hour urine for recurrent or high-risk stone formers. ^[1]
Management	Give NSAIDs first-line if renal function permits; use opioids when NSAIDs are contraindicated, plus antiemetics. ^[1] Fever or sepsis with obstruction requires IV antibiotics and urgent JJ stent or PCN; defer definitive stone surgery until sepsis resolves. ^[1] Stones ≤ 4 mm often pass; distal 5–10 mm stones may receive medical expulsive therapy with follow-up. ^[1] ESWL, URS/RIRS or PCNL is selected by site, size, density, anatomy and renal function; stones ≥ 10 mm are unlikely to pass. ^[1]
Complications	Obstructed infected system causes pyonephrosis and urosepsis: drainage, not antibiotics alone, is essential. ^[1] Bilateral obstruction or obstruction of a solitary kidney can cause post-renal AKI; prolonged obstruction may cause CKD. ^[1] After decompression, post-obstructive diuresis is > 200 mL/h for 2 hours or > 3 L/day; monitor and replace fluids carefully. ^[1] Chronic staghorn stone and infection may cause XGP with a bear-paw kidney, usually requiring nephrectomy. ^[1]
Prevention / follow-up	Maintain high fluid intake, normal dietary calcium, and reduce sodium, excessive animal protein and high-oxalate foods. ^[1] Perform metabolic evaluation and tailor prevention to stone composition; address hyperparathyroidism or other causes. ^[1] Alkalinise urine for uric acid or cystine stones; struvite stones require infection control and complete removal where possible. ^[1] Confirm clearance with appropriate follow-up imaging, using KUB when the stone is radio-opaque to limit CT exposure. ^[1]
Exam traps	Fever plus obstruction is an emergency; never perform definitive stone treatment on a septic obstructed system. ^[1] A negative KUB does not exclude stones: uric acid, xanthine and indinavir stones may be radiolucent; phleboliths can mimic distal stones. ^[1] Haematuria may be absent in complete obstruction; painless gross haematuria, especially over 35, needs malignancy assessment. ^[1] In acute loin pain, exclude ruptured AAA and ectopic pregnancy; check haemodynamics and beta-hCG where appropriate. ^[1]

References

^[1] Senior notes: felixlai.md (Urological Diseases — Urinary Stones)

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]

Limitations ^[1]^[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.

Role: Alternative when CT and IVU are contraindicated — pregnancy, contrast allergy, children, renal impairment ^[5].

Limitations: Less able to detect smaller urothelial lesions and non-obstructing stones ^[1]. Image inferior to CT scan (because the kidney is a moving organ) ^[5]. Expensive ^[5].

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:
1. Anti-inflammatory: reduces ureteric wall oedema around the impacted stone → reduces obstruction
2. 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
3. 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

Persistent pain / Symptomatic
Unresolved with conservative treatment
Too large to pass spontaneously (≥ 10 mm)
Failure to pass after 4–6 weeks ^[1]
Complications: haematuria, UTI, obstructive uropathy (obstructed solitary kidney / bilateral obstruction), AKI ^[1]

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.

How it works ^[1]^[3]:

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]

Indications ^[1]^[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]

Contraindications ^[1]^[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.

How it works ^[1]^[3]:

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]

Puncture technique ^[1]^[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]

Indications ^[1]^[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

Contraindications ^[1]^[3]:

Uncontrolled bleeding diathesis ^[1]^[3]
Patient unfit for GA ^[1]^[3]

Adjuncts ^[1]^[3]:

± 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

Complications ^[1]^[3]:

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.

How it works ^[1]^[3]:

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]

Indications ^[1]^[3]:

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]

Complications ^[1]^[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]

Types: pyelolithotomy (from pelvis), ureterolithotomy (from ureter) ^[3]
Indications: if failed all above means ^[3] — truly a last resort
Problems: ↑ morbidity, ↑ blood loss, significant damage to renal function compared to endourological techniques ^[3]
Rarely done in modern practice ^[1]

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:
1. Physiological diuresis: the kidney excretes the accumulated backlog of urea, sodium, and water — this is appropriate and self-limiting
2. 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)