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Ureteric stone / renal colic

Presentations of ureteric stone:

  • Renal colic
  • Haematuria
  • Vomiting
  • Sepsis
  • Non-specific pains
  • Reduced renal function
  • Incidental / asymptomatic

 

Indications for intervention:

  • Fever / infection
  • Solitary functioning kidney or bilateral ureteric stones
  • Stone size > 7 – 10 mm
  • Renal impairment
  • Uncontrolled pain
  • Failure to pass conservatively
  • Social or occupation reasons

 

A patient has a ureteric stone. What do you want to know?

 

Surgical treatment options:

  • Ureteroscopy offers better stone free rates cf. ESWL
  • URS has higher complication rates than ESWL
  • ESWL should not be offered for uric acid stones, cystine stones, obese patients, or other contra-indications

 

AUA guidelines:

  • Recommend URS over ESWL for (mid or distal) ureteric stones
  • No role for routine stenting in ESWL for ureteric stones
  • Pre-stenting for URS should not be performed routinely
  • Post URS stent can be omitted if:
    • No suspected injury
    • No ureteric stricture or anatomical impedance to fragment clearance
    • Normal contra-lateral kidney
    • No renal impairment
    • No plan for re-look procedure

 

 

Renal colic

Local pain – felt in or near the involved organ, hence kidney pain felt around T12-L1 and beneath 12th rib.

Referred pain – originates in an organ, but felt elsewhere – due to common nerve roots – i.e. testis innervated by sympathetics T11-T12 hence referred pain from renal colic.

 

Ureteric pain – typically stimulated by acute obstruction – combined cause of renal capsular distension (due to oedema) and renal pelvis and ureteric muscle spasm (and hyperperistalsis).

Nerve supply of testis and kidney are shared (T11-T12) hence referral to groin in upper stones.

Lower stones often cause vesical irritation.

 

Renal origin pain may be associated with GI symptoms (nausea/vomiting) due to reflex stimulation of coeliac ganglion (“shared splanchnic innervation”).

Smith’s – “renointestinal reflexes” – afferent stimuli from renal capsule or pelvis may cause reflex pylorospasm due to shared autonomic and sensory innervations.

 

Management of renal colic

NSAIDs have better analgesic efficacy than opioids.

Mechanism of NSAIDs:

  • Prostaglandins are synthesised from arachidonic acid by enzymatic reactions involving COX-1 and COX-2
  • NSAIDs inhibit COX-1 and COX-2 and inhibit prostaglandin production
  • Prostaglandins are typically involved in smooth muscle modulation, hence NSAIDs may reduce smooth muscle spasm and contraction (conflicting evidence)
  • The effect of NSAIDs in renal colic may actually be due to inhibition of PGE2-mediated vasodilation; causing afferent arteriole vasoconstriction and reducing renal blood flow and therefore reducing diuresis, oedema and ureteric stimulation
    • But hence may reduce GFR in patients especially CKD

 

Avoid hyperhydration but replace losses from dehydration and vomiting.