Renal colic and nephrolithiasis

Renal colic is the severe pain produced when a calculus lodges in and acutely obstructs the ureter, generating proximal urinary stasis, ureteric spasm and a rise in capsular pressure. The Fellowship candidate must hold two quite different patients in mind at once: the otherwise well, afebrile patient with an uncomplicated ureteric stone who needs analgesia and safe discharge with a stone filter and urology follow-up, and the septic patient with an infected obstructed system (pyonephrosis) who needs urgent surgical decompression within hours. Confusing the two — discharging the febrile obstructed patient as "simple colic" — is the classic Fellowship pitfall and a cause of renal loss and death. The emergency task is to make the diagnosis, exclude the lethal mimics (the abdominal aortic aneurysm, the testicular torsion, the ectopic pregnancy), provide analgesia with a non-steroidal agent before reaching for an opioid, identify the infected or solitary-kidney patient who cannot go home, and arrange safe disposition.[1][3]

Definition and classification

Nephrolithiasis (urolithiasis) is stone formation anywhere in the urinary tract. Renal colic is the clinical syndrome of acute ureteric obstruction by a stone — the term "colic" denoting the wave-like, building-and-fading character of the pain, not the lesser meaning of intestinal cramp. Stones are classified by composition: calcium oxalate is by far the commonest (about 70 to 80 per cent), followed by calcium phosphate, uric acid (radiolucent, in gout and acidic concentrated urine), struvite (magnesium-ammonium-phosphate, the infection stone formed by urease-splitting organisms such as Proteus, forming large staghorn calculi), and cysteine (the inherited tubular transport defect). Stones are also classified by location — renal, or ureteric at the proximal ureter, mid-ureter, or the vesicoureteric junction (VUJ), the narrowest point and the commonest site of impaction. [1]

Epidemiology and risk

The lifetime risk of a stone is roughly 10 to 15 per cent in Western populations, with men affected roughly twice as often as women, and the peak incidence between the ages of 20 and 50. Australia sits in the stone belt — the hot, arid climate drives chronic dehydration and concentrates urine, so prevalence is among the highest in the world, matched by the Middle East and the southern United States. After a first stone, recurrence is roughly 50 per cent at 10 years, so every first stone-former deserves an outpatient metabolic workup (serum calcium, urate, and a 24-hour urine where indicated). [1]

Pathophysiology

Stone formation begins when urine becomes supersaturated with a stone-forming salt — calcium oxalate, uric acid, cysteine. Dehydration, low urinary volume, and dietary or metabolic excess drive supersaturation; crystals nucleate, aggregate, and grow into a stone within the renal collecting system. Most stones lie silently in the kidney until they migrate into the ureter, where they lodge at one of the three natural narrowings — the pelviureteric junction, the pelvic brim where the ureter crosses the iliac vessels, and the vesicoureteric junction (narrowest, commonest site of impaction). [1]

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The pain localisation follows the embryological origin of the ureter: visceral afferents from T11 to L2 produce flank and loin pain when the stone is in the proximal ureter; as it descends past the pelvic brim the pain radiates via the genitofemoral nerve (L1–L2) to the groin, testis or labia; and a stone lodged at the vesicoureteric junction produces urethral, perineal or testicular pain with urinary urgency, frequency and strangury — the latter easily mistaken for cystitis or torsion. [1]

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Clinical presentation

The classic presentation is unmistakable: sudden-onset, severe, colicky flank pain that builds to a peak over minutes, lasts hours, radiates from loin to groin as the stone descends, and is accompanied by nausea and vomiting. The patient is characteristically unable to find a comfortable position and writhes around the bed — the single most useful behavioural clue at the bedside, and the opposite of the patient with peritonitis who lies perfectly still. [1]

Haematuria — microscopic in roughly 85 to 90 per cent and occasionally macroscopic — supports the diagnosis, but its absence does not exclude a stone. A stone at the vesicoureteric junction produces a misleading constellation of lower urinary tract symptoms — urgency, frequency, dysuria and strangury — easily mistaken for cystitis or, in the male, for prostatitis. Fever, rigors, hypotension or a frankly septic appearance are not features of uncomplicated colic and signal an infected obstructed system that requires a fundamentally different, urgent pathway. [1]

Differential diagnosis

Loin pain radiating to the groin overlaps with several lethal and several benign mimics, and the first task is to exclude the abdominal aortic aneurysm, the testicular torsion, and the ectopic pregnancy before attributing the picture to a stone. Crucially, the presence of a stone on imaging does not exclude a concomitant lethal mimic — an older patient may have a small incidental renal calculus and a leaking aneurysm at the same time. [1]

Other considerations include renal papillary necrosis (in sickle cell trait, analgesic abuse, diabetes — sloughed papilla obstructs the ureter), renal infarction (atrial fibrillation, severe flank pain with haematuria and a raised lactate dehydrogenase), retroperitoneal fibrosis, and ureteric transitional cell carcinoma with clot colic. A pregnancy test is mandatory in every woman of reproductive age — a right-sided ectopic and a right-sided ureteric stone present identically. [1]

Bedside assessment

Begin with airway, breathing and circulation — the septic patient with pyonephrosis may be in established septic shock within the first hour. Attach monitoring, establish intravenous access, and give analgesia early: pain control is both humane and diagnostic, because the patient who settles on an NSAID has the classic analgesic response of ureteric colic. A focused history establishes the onset, character, radiation and duration of the pain, associated urinary symptoms, prior stone history, fever or rigors, and the vascular and reproductive risk factors (age, hypertension, smoking for AAA; last menstrual period for pregnancy). [1]

Examination looks for loin tenderness (mild, in keeping with capsular distension), assesses the abdomen for peritonism (which is NOT colic and demands another diagnosis), and crucially palpates the abdominal aorta in every older patient. Examine the genitalia in every male — a high-riding, tender, transverse testis with an absent cremasteric reflex is torsion until proven otherwise, and the six-hour window to detorsion cannot be missed while attributing the pain to a stone. An explicit screen for organ dysfunction — temperature, blood pressure, respiratory rate, oxygen saturation, conscious level, urine output and a venous lactate — separates the well patient who can be discharged from the septic patient who needs urgent decompression. [1]

Investigations

Send blood for urea and electrolytes with creatinine (baseline renal function — obstruction causes a post-renal acute kidney injury), full blood count, C-reactive protein, and a venous lactate (the septic marker in the infected obstructed system). Check a β-hCG in every woman of reproductive age, regardless of contraception history. Urinalysis is central: blood (haematuria) supports a stone, while leucocytes and nitrites suggest infection and, in the obstructed kidney, transform the case into a urological emergency. Send a urine culture in any febrile or septic patient. A coagulation screen is worthwhile if intervention (stent, nephrostomy, surgery) is anticipated. [1]

Ultrasound is the first-line imaging in pregnancy, in children, and in the recurrent known stone-former where radiation should be minimised. It demonstrates hydronephrosis and renal stones (with the characteristic "twinkling artefact" on colour Doppler), but it visualises the ureter poorly and misses many ureteric stones; in pregnancy it is the screening test, with magnetic resonance urography as the second line when the diagnosis remains unclear. A plain KUB radiograph captures only radiopaque stones (about 80 per cent of calcium-containing stones; uric acid and cysteine stones are radiolucent) and is reserved for follow-up of a known radiopaque stone, not for the initial diagnosis. [1]

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The ED first 60 minutes

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Immediate management and resuscitation

The priority is analgesia, and the analgesic ladder has a non-steroidal agent on the bottom rung. Give diclofenac 75 mg intramuscularly (or 100 mg rectally) as the first-line agent — it blocks the prostaglandin-mediated ureteric spasm and reduces the renal capsular pressure that drives the pain. The Holdgate systematic review established that NSAIDs achieve equivalent or superior analgesia to opioids in acute renal colic, with fewer rescue doses and fewer adverse effects, and a recent randomised trial confirmed the superiority of intramuscular diclofenac over intravenous tramadol.[1][4] Reserve morphine 5 mg intravenously, titrated, for refractory or severe pain, or use fentanyl 50 to 100 micrograms intravenously when the intramuscular route is contraindicated or rapid titration is required. Add an antiemetic — metoclopramide 10 mg intravenously or ondansetron 4 mg intravenously — for the nausea and vomiting that accompany the visceral afferent stimulation.

Give intravenous fluids only to correct dehydration from vomiting or to maintain euvolaemia in the septic patient — routine aggressive hydration does not improve stone passage and may worsen the pain by further distending the renal capsule. If the patient is febrile or shows any sign of infection in an obstructed system, give broad-spectrum antibiotics immediately (ceftriaxone 2 g intravenously plus gentamicin, or piperacillin-tazobactam 4.5 g intravenously) after taking blood and urine cultures, and activate the urgent urology pathway — antibiotics alone will not cure an obstructed infected kidney. [1]

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Definitive management and disposition

The disposition splits cleanly along the line of infection, obstruction and pain control. [1]

The uncomplicated ureteric stone — discharge pathway

A patient with a stone of 10 mm or less, no fever, no evidence of infection, controlled pain, normal renal function, and single-kidney function preserved is managed as an outpatient. Provide: [1]

• Discharge analgesia: diclofenac 50 mg orally three times daily (with a proton-pump inhibitor) or naproxen 500 mg orally twice daily, with paracetamol and oral morphine for breakthrough pain.
• Medical expulsive therapy (MET): tamsulosin 0.4 mg nocte for 4 to 6 weeks for a distal ureteric stone between 5 and 10 mm. α-blockers relax the smooth muscle at the vesicoureteric junction and modestly increase the spontaneous passage rate and shorten the time to passage. MET is not indicated for proximal stones, stones under 5 mm (which pass anyway), or stones over 10 mm (which will not pass).[2]
• A stone filter (urine strainer) to catch the passed stone for analysis.
• Return precautions in writing: new fever or rigors, uncontrolled pain, intractable vomiting, or a marked reduction in urine output.
• Urology or general-practitioner follow-up in 2 to 4 weeks with repeat imaging to confirm passage.

The urological emergency — the infected obstructed system

The infected obstructed kidney (pyonephrosis) is the single most dangerous renal-colic scenario and a Fellowship favourite. The diagnosis is made when a patient with an obstructing stone has fever, rigors, leucocytosis, raised lactate, hypotension or any systemic sign of sepsis. Management is not antibiotics alone — the raised intraluminal pressure prevents antibiotic penetration of the urine and renal parenchyma, and the patient develops bacteraemia and septic shock. The definitive treatment is urgent surgical decompression of the obstructed upper tract within hours, by: [1]

• Percutaneous nephrostomy (the radiologically-placed drain, preferred in the haemodynamically unstable or septic patient), or
• Retrograde ureteric stent (placed cystoscopically in theatre). [1]

Decompression is combined with broad-spectrum intravenous antibiotics (ceftriaxone 2 g plus gentamicin, or piperacillin-tazobactam 4.5 g), fluid resuscitation titrated to mean arterial pressure and lactate, and admission to a monitored bed — high-dependency or intensive care for the patient with septic shock. The stone itself is dealt with electively once the sepsis has resolved. The same urgency applies to anuria in a patient with a solitary kidney, a renal transplant, or bilateral obstructing stones — these are emergencies because bilateral (or single-functioning-kidney) obstruction produces acute kidney injury rapidly and threatens renal loss. [1]

Definitive stone removal — extracorporeal shock-wave lithotripsy, ureteroscopy with laser lithotripsy, or percutaneous nephrolithotomy — is decided later by urology and depends on stone size, site and composition. Emergency indications for non-elective urology referral (within hours) are: infected obstructed system, anuria in a solitary or transplanted kidney or bilateral obstruction, intractable pain despite analgesia, and a rising creatinine with obstruction. Urgent (within days) referral applies to large stones over 10 mm, persistent obstruction, and failure of medical expulsive therapy. [1]

Special populations

Pregnancy: symptomatic stones are the commonest non-obstetric cause of admission in pregnancy. Ultrasound is the first-line imaging test; MR urography is second-line when the diagnosis remains unclear, and low-dose CT KUB is reserved for the refractory diagnostic dilemma in the third trimester. Avoid NSAIDs after 28 weeks (premature ductus arteriosus closure, oligohydramnios) — use paracetamol and opioid analgesia. Ureteric stenting or percutaneous nephrostomy is the definitive temporising measure when obstruction or infection complicates pregnancy. Children are imaged with ultrasound first, reserving CT for the equivocal case. The elderly patient with apparent colic has an abdominal aortic aneurysm excluded first — palpate the aorta, and image before attributing the pain to a stone. The patient with a solitary kidney or transplant is admitted with a lower threshold, because loss of the single functioning kidney is catastrophic. The anticoagulated patient bleeds more readily from the trauma of stone passage and from any intervention — coordinate anticoagulation reversal with urology. [1]

Complications and pitfalls

Complications of an obstructing stone include post-renal acute kidney injury (especially in the solitary or bilaterally obstructed kidney), pyonephrosis with progression to urosepsis and septic shock, permanent renal parenchymal loss from prolonged obstruction, and the long-term consequences of recurrent stones (chronic kidney disease, the infected staghorn calculus destroying the kidney). The common pitfalls invert good care. Discharging the febrile obstructed patient as simple colic misses pyonephrosis and may cost a kidney or a life. Missing the abdominal aortic aneurysm in the older patient with flank pain — the patient may have both an incidental stone and a leaking aneurysm. Failing to examine the genitalia in the male misses testicular torsion, which presents identically and has a six-hour window to detorsion. Relying on the absence of haematuria to exclude a stone — up to 15 per cent of confirmed stones have no blood on dipstick. Over-hydrating the well patient does not aid stone passage and may worsen the pain. Giving an NSAID to the dehydrated, septic or solitary-kidney patient worsens the acute kidney injury. Delaying drainage in pyonephrosis while awaiting cultures or a urology review in the morning kills patients — organ dysfunction mandates decompression within hours. [1]

Prognosis and disposition

The spontaneous passage rate depends on size: stones under 5 mm pass in roughly 80 per cent of cases, stones of 5 to 10 mm in about 50 per cent (improved modestly by tamsulosin for distal stones), and stones over 10 mm in under 20 per cent. The uncomplicated patient is discharged with analgesia, a stone filter and return precautions, and passes the stone at home in most cases. The infected obstructed patient is admitted for urgent decompression and intravenous antibiotics and, in septic shock, to intensive care — mortality in urosepsis from pyonephrosis is determined by the timeliness of source control, not the choice of antibiotic. A patient with a single functioning kidney, bilateral obstruction, anuria, intractable pain or a rising creatinine is admitted for urgent urological decompression. [1]

Evidence and regional guidelines

The contemporary evidence base for emergency management rests on three pillars. The Holdgate systematic review (BMJ 2004) established that NSAIDs achieve equivalent or superior analgesia to opioids in acute renal colic, with fewer rescue doses and side effects — the basis for the NSAID-first ladder used worldwide.[1] A recent Australasian randomised trial (2025) reaffirmed the superiority of intramuscular diclofenac over intravenous tramadol.[4] The evidence for medical expulsive therapy with α-blockers is more contested: a 2017 systematic review of tamsulosin, nifedipine and placebo showed a modest benefit of α-blockers, with the effect concentrated in distal ureteric stones over 5 mm — the basis for offering tamsulosin 0.4 mg nocte to that subgroup.[2] The European Association of Urology (EAU) urolithiasis guideline and the American Urological Association (AUA) ureteral calculi guideline provide the definitive stone-management pathway, while the Australasian College for Emergency Medicine endorses the NSAID-first analgesic strategy and CT KUB as the first-line imaging test. Across all guidelines, the three fixed points are: give an NSAID before an opioid; image with non-contrast CT KUB; and decompress the infected obstructed system within hours.

Key trials

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Exam pearls

• The patient who writhes has colic; the patient who lies still has peritonitis — behavioural observation is the first bedside clue.
• NSAID before opioid: diclofenac 75 mg intramuscularly is first-line; morphine 5 mg intravenously is reserved for refractory pain.
• CT KUB (non-contrast) is the gold standard — 95 to 98 per cent sensitive and the only first-line test that also identifies the lethal mimics.
• Ultrasound in pregnancy, children and recurrent stone-formers; a plain KUB is for follow-up only.
• Examine the testes in every male with apparent colic — torsion presents identically and has a six-hour window.
• β-hCG in every woman of reproductive age — ectopic pregnancy is the lethal mimic.
• Palpate the aorta in every older patient — a ruptured abdominal aortic aneurysm is the lethal mimic and may coexist with an incidental stone.
• The infected obstructed kidney is decompressed, not just given antibiotics — ureteric stent or percutaneous nephrostomy within hours.
• MET is tamsulosin 0.4 mg nocte for 4 to 6 weeks, for distal ureteric stones of 5 to 10 mm — not for proximal, very small or large stones.
• Absence of haematuria does not exclude a stone — up to 15 per cent of confirmed stones have no blood on dipstick.
• Stone composition — know the four: calcium oxalate is the commonest (70 to 80 per cent); uric acid is radiolucent and dissolves with alkalinisation; struvite is the infection stone forming staghorns; cystine is hereditary.
• The uric-acid stone is the one you can dissolve — alkalinise the urine with potassium citrate to a pH above 6.5; it is radiolucent on KUB but visible on CT (200 to 400 HU).
• A staghorn calculus is struvite until proven otherwise — urease-splitting organisms (Proteus) in a woman with recurrent UTIs; refer for clearance, not antibiotics.
• The three narrowings of the ureter — pelviureteric junction, pelvic brim (iliac vessels), and the vesicoureteric junction (narrowest, commonest impaction site).
• A VUJ stone with sterile pyuria is the trap — leucocytes without nitrites from the irritated bladder; image the VUJ on CT before labelling it cystitis.
• Forced fluids do NOT flush a stone — they raise the capsular pressure and worsen the pain; hydrate only the dehydrated or the septic.
• Tamsulosin is controversial, not standard — SUSPEND and STE showed no overall benefit; offer it only for a distal stone over 5 mm and never let it delay urology.
• The first stone earns a metabolic workup — serum calcium (hyperparathyroidism), urate, and a 24-hour urine; recurrence is 50 per cent at 10 years. [1]

Red flags

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References

1. [1]Holdgate A, Pollock T. Systematic review of the relative efficacy of non-steroidal anti-inflammatory drugs and opioids in the treatment of acute renal colic BMJ, 2004.PMID 15178585
2. [2]Gottlieb M, Long B, Koyfman A. Comparison of Tamsulosin, Nifedipine, and Placebo for Ureteric Colic CJEM, 2017.PMID 26584627
3. [3]Ali A, Niaz S, Waris S, et al. Non-Contrast Enhanced Multi-Slice Ct-Kub In Renal Colic: Spectrum Of Abnormalities Detected On Ct Kub And Assessment Of Referral Patterns J Ayub Med Coll Abbottabad, 2019.PMID 31535518
4. [4]Yaowalaorng J, Rakkarn S, Phakdee B, et al. Superior efficacy of intramuscular diclofenac compared to intravenous tramadol for acute renal colic in northern Thai patients: A randomised double-blind, sham-controlled trial Emerg Med Australas, 2025.PMID 39763427
5. [5]Smith-Bindman R, Aubin C, Bailitz J, et al. Ultrasonography versus computed tomography for suspected nephrolithiasis N Engl J Med, 2014.PMID 25229916
6. [6]Pickard R, Starr K, MacLennan G, et al. Use of drug therapy in the management of symptomatic ureteric stones in hospitalised adults: a multicentre, placebo-controlled, randomised controlled trial and cost-effectiveness analysis of a calcium channel blocker (nifedipine) and an alpha-blocker (tamsulosin) (the SUSPEND trial) Health Technol Assess, 2015.PMID 26244520
7. [7]Meltzer AC, Burrows PK, Wolfson AB, et al. Effect of Tamsulosin on Passage of Symptomatic Ureteral Stones: A Randomized Clinical Trial JAMA Intern Med, 2018.PMID 29913020