Introduction

Renal colic is common, and generally regarded as one of the most painful surgical conditions. It can be life threatening when there is associated urinary sepsis. Exclude a ruptured abdominal aortic aneurysm (AAA) which can have a similar presentation.

Definition and classification

Renal colic most commonly results fromthe presence of a calculus in the upper urinary tract. Interference with normal cyclical peristalsis leads to the classic symptoms of intense colicky pain, stabbing in nature, often with nausea and vomiting.

Incidence (including predisposition according to sex and geography)

The incidence of stone disease is approximately 0.1 to 0.3%. Male to female ratio 3:1. Prevalence 2–3%. Peak incidence 20–40 years. More common in mountainous, desert and tropical areas.

Aetiology

The most common cause of renal colic is a ureteric stone. Other causes include blood clots (clot colic), and a sloughed renal papilla (associated with diabetes, sickle-cell disease). Partially obstructing ureteric transitional cell carcinomas can present with similar symptoms.

Pathogenesis (macro/microscopic pathology)

For stones to form, urine must be supersaturated with the salt that can then form crystals and ultimately the stone. Hypercalciuria (secondary to hypercalcaemia e.g. hyperparathyroidism, immobility), hyperoxaluria and hyperuricaemia may predispose to stone formation. Foreign bodies (e.g. ureteric stents) and certain proteins may form a framework for crystal deposition. The commonest types of stone are: calcium (oxalate, phosphate and mixed) 70%, infection stones (magnesium ammonium phosphate or struvite stones, associated with urease splitting organisms such as Proteus, leading to a high urinary pH and occasionally staghorn calculi) 15–20%, uric acid 5–10%, cystine 1–5% (autosomal recessive inheritance).