Renal colic

Notes

Introduction

Renal colic classically refers to acute severe loin pain that occurs secondary to a urinary stone.

Urinary stones, also termed urolithiasis, refer to stone formation anywhere within the urinary tract. They may be asymptomatic or cause acute loin-to-groin pain due to acute ureteric obstruction.

Urinary stones are extremely common with men affected up to three times more than women. The peak incidence of symptomatic urinary stones is between 40-60 years in males and late 20’s in females.

Renal colic statistics

Aetiology

The most common cause of renal colic is obstruction to urinary flow within the ureter that occurs secondary to urinary stones.

Stones may develop from the supersaturation of urine and/or deposition of stone material within the renal interstitium.

Approximately 80% of urinary stones are composed of calcium. The most common being calcium oxalate, but calcium phosphate is also seen. Other types of stones include struvite (2-15%), uric acid (10%) and cystine (1-2%).

Calcium oxalate

Calcium oxalate is the most common type of stone that is thought to develop from the precipitation of calcium crystals within the interstitium. Accumulation of these crystals leads to the formation of ‘Randall's plaques’, which are subepithelial calcification of renal papillae. They are thought to act as a nidus for stone formation. 

The development of calcium oxalate stones is associated with a number of factors. These include high concentrations of oxalate in the urine, loss of natural stone inhibitors (e.g. citrate, magnesium) and high urinary pH.

Struvite 

Struvite stones are composed of magnesium ammonium phosphate. They may grow rapidly and can lead to the development of staghorn calculi, which fill the entire intrarenal collecting system and cause renal dysfunction.

Struvite stones are associated with urease-producing microorganisms including Proteus and Klebsiella. These microorganisms are able to convert urea into ammonia which reacts with water increasing the pH of the urine. Collectively, the increased ammonia and alkaline urine promote stone formation. 

Uric acid

The development of uric acid stones is strongly associated with a low urinary pH and a high urinary concentration of uric acid. The proportion of uric acid stones is higher in hot, dry climates because of the tendency to produce more acidic and low volume urine.

Circumstances that increase the levels of uric acid predispose patients to the formation of uric acid stones. Classically, uric acid stones are seen in patients with gout who have hyperuricaemia and, therefore, hyperuricosuria. However, the likelihood of stone formation is still strongly related to urinary pH.

Cystine

Cystine is a homodimer of the amino acid cysteine. The development of cystine stones is usually secondary to the genetic disorder cystinuria, in which there is impairment in the normal renal handling of cystine. 

This leads to failed reabsorption of cystine and precipitation within the renal tubules. Patients with cystinuria typically present with stones at a younger age. 

Risk factors

A number of risk factors have been associated with stone formation.

Modifiable

Modifiable risk-factors are those that patients can change to help reduce the risk of calculi forming. Understanding these helps to form advice that can be given following the occurrence of a stone.

Certain medications may also be related to the development of renal calculi. These include protease inhibitors and diuretics - whether these can or cannot be adjusted depends on numerous factors.

Modifiable risk factors

Non-modifiable risk factors

There are a number of factors that cannot be modified. Those with a family history of renal calculi, white ethnicity or male gender are at increased risk.

Non-modifiable risk factors

Pathophysiology

Urinary stones classically obstruct at three major sites: pelvi-ureteric junction (PUJ), mid-ureter where they cross the iliac vessels and vesico-ureteric junction (VUJ).

Locations of impaction of renal calculi

The obstruction to flow within the ureter leads to the release of prostaglandins. Prostaglandins cause vasodilatation of surrounding vessels and stimulate ureteric smooth muscle spasm.

Blood vessel vasodilatation promotes a natural diuresis, which further places pressure on the kidney and can lead to distention of the renal capsule. Distention of this capsule causes the intense pain of renal colic, which is further exacerbated by ureteric smooth muscle spasm.

Renal colic occurs in paroxysms of 20-60 minutes and can be extremely intense requiring parenteral analgesics. Renal colic pain usually settles quickly following relief of the obstruction (e.g. by a stent) or passage of the stone.

Clinical features

The classical presentation of renal colic is loin-to-groin pain.

The pain may occur in a colicky manner with waves a severe pain which settle before further episodes. Vomiting is common and normally occurs in association with the pain.

Some patients may present with signs of infection - fever, tachycardia, malaise, confusion - and at times become frankly septic. An infected-obstructed urinary system is a urological emergency requiring urgent drainage.

Symptoms

  • Loin-to-groin pain
  • N&V
  • Haematuria
  • Dysuria
  • Urgency

Signs

  • Flank tenderness
  • Haematuria (typically microscopic)
  • Fever
  • Rigors

It is important to monitor observations (e.g HR, BP, RR, Temp) and look for signs of infection as this could represent the development of urosepsis, which may require urgent urological management.

Clinical features of renal colic

NOTE: It is always important to consider differentials such as an abdominal aorta aneurysm.

Diagnosis

The imaging of choice in the diagnosis of acute renal colic in non-pregnant adults is a non-contrast computed tomography (CT) scan.

CT KUB

A CT KUB (kidneys-ureters-bladder) is a non-contrast scan that can be used to help identify both stones and urinary tract obstruction. They have a sensitivity in the high 90’s and have the benefit of being readily available and easily interpreted in a short space of time.

Importantly, non-contrast CT does not expose the patient to IV contrast, which can be nephrotoxic. It is the first-line investigation in adult, non-pregnant, patients.

Ultrasonography

Ultrasonography can be reserved for patients where there is a risk of using ionising radiation. It is useful for the identification of hydronephrosis, and may be used to look for stones and other gross abnormalities. It is the first-line investigation in:

  • Pregnant women
  • Children and young adults (i.e. people under 16 years)

Ultrasound is best suited for picking up large, proximal stones (e.g. > 5mm at the PUJ). It is difficult to visualise small, distal stones.

X-ray

Most urinary stones are composed of calcium, which makes them radio-opaque to plain radiograph. X-rays are inexpensive and quick ways of assessing stone size, composition, location and overall burden.

Although X-ray KUB’s have largely been superseded by non-contrast CT, they may play a role in follow-up of radio-opaque stones or to check stent placement.

A small number of stones (e.g. uric acid, indinavir-induced, cystine) are radiolucent and cannot be detected on X-ray.

NOTE: Interestingly, indinavir-induced renal calculi are not visualised on non-contrast CT and require the use of contrast-enhanced CT (i.e. CT urogram).

Investigations

Investigations are important for the basic workup of renal colic, diagnosis, assessment of complications and preparation for any surgical intervention.

Bedside

  • Observations
  • ECG
  • Urinalysis
  • Urine MC&S

Bloods

  • FBC
  • U&Es
  • CRP
  • LFTs
  • Amylase
  • Bone profile
  • Uric acid

Imaging

As above

Stone work-up

A metabolic stone workup can be completed in patients with significant stone disease. This involves:

  • Stone analysis
  • Serum calcium

Other tests may include uric acid levels and parathyroid hormone. Urinary collections may be arranged to look at oxalate, calcium, uric acid and citrate levels.

Management

In the majority of patients, renal colic can be managed conservatively with the use of analgesia and hydration.

In general, the management of renal colic is dependent on the size and location of the stone. The larger (e.g. > 10mm) and more proximal (e.g. PUJ) the stone, the more likely intervention will be needed.

A stone that is < 4 mm in size will have an 80% chance of spontaneous passage whereas a stone > 8 mm in size only has a 20% chance of spontaneous passage.

In all patients, appropriate analgesia and hydration are important in the ongoing management. Urgent urological assessment should be considered in the following circumstances:

  • Urosepsis
  • Acute kidney injury / anuria
  • Solitary functioning kidney
  • Unresponsive pain

Analgesia & anti-emetics

NSAIDs are considered excellent for pain relief in renal colic as they help to reduce the ureteral spasm - particularly when given via the rectal route. They should be used with caution in patients with an AKI or with a history of gastritis or peptic ulcer disease.

Paracetamol may be given to aid or in place of NSAIDs whilst opioids are reserved for those whose pain is still uncontrolled.

Anti-emetics (e.g. ondansetron or cyclizine) can be used to help control nausea and vomiting.

Medical therapy

Medical expulsive therapy involves the use of medications, most commonly tamsulosin (an alpha-blockers) to help induce spontaneous passage of the stone.

This type of therapy can be considered in patients with small distal stones, controlled symptoms and no evidence of sepsis.

Patient's should receive follow-up in 'stone clinic' and be appropriately counselled on signs of potential complications.

NOTE: The SUSPEND did not reduce the proportion of patients requiring further treatment for stone clearance at four weeks. It remains however an area of debate with some clinicians continuing to prescribe tamsulosin, pointing to studies indicative of benefit for stones 5-10mm in size.

Surgical/radiological interventions

Definitive management of urinary stones depends on the size of the stone, site of obstruction and the clinical presentation. It is normally required for ongoing pain associated with stones unlikely to pass naturally.

Therapeutic options for the management of urolithiasis include:

  • Shockwave lithotripsy (SWL): non invasive procedure that uses shockwaves to break up stones. Normally indicated in those with stones less than 20mm in size.
  • Ureteroscopy (URS): urological procedure where energy devices (e.g. lasers) are used to break up the stones, normally indicated in stones 10-20mm in size or less than 10mm where SWL fails or is contraindicated.
  • Percutaneous nephrolithotomy (PCNL): nephroscope is passed into the collecting system and used to break up stones. Tends to be reserved for larger stones (> 20mm) or in smaller stones where other measures have failed.

Patients who have uncontrolled symptoms or develop complications (e.g. urosepsis, AKI) may require initial relief of obstruction before more definite interventions can take place. The two main options for relieving obstruction include radiologically-guided insertion of a nephrostomy tube into the renal pelvis under local anaesthetic or endoscopic insertion of a ureteric JJ stent under general anaesthetic.

Prevention

Measures may be taken to help prevent and reduce the risk of recurrence of renal calculi.

NICE CG 118 (2019 update) outline measures that can be used in the prevention of calculi. These are summarised below.

Address modifiable risk factors

There are a number of changes patients can make (where relevant and appropriate) that can help to reduce the chance of recurrence:

  • Avoiding excess salt
  • Good oral hydration (and adding lemon juice to drinking water)
  • Avoiding carbonated drinks
  • A balanced diet
  • Healthy weight loss

Potassium citrate

In addition to the above advice potassium citrate may be given to:

  • Adults: With recurrent stones that are > 50% calcium oxalate.
  • Children and young people: With recurrent stones that are > 50% calcium oxalate with either hypercalciuria or hypocitraturia.

Citrate acts to inhibitor of crystallisation of calcium salts - hypocitraturia has been shown to be a risk factor for the development of calcium oxalate.

Thiazides

In addition to the advice regarding modifiable risk factors, thiazide diuretics may be given to adults with:

  • Recurrence and
  • Stones that are > 50% calcium oxalate and
  • Hypercalciuria after
  • Restricting salt intake to 6g / day

Thiazides are relatively inexpensive and reduce urinary calcium, reducing the risk of calcium based stones.

Pulsenotes uses cookies. By continuing to browse and use this application, you are agreeing to our use of cookies. Find out more here.