ACUTE ureteric colic is one of the most severe and distressing pains experienced in clinical medicine.

Each year thousands of people present to general practitioners and hospital emergency departments in distress with urinary stone disease. Modern diagnostic and therapeutic technologies, combined with astute clinical judgment, can minimise the pain and inconvenience of urinary stone disease. In certain cases, a conservative management of urinary stone disease or stone dissolution is indicated where the stone composition is such that dissolution is possible.

Prevention of stone reformation is a significant principle of management. In this regard, patient motivation is key.

EPIDEMIOLOGY AND AETIOLOGY

Australians have one of the highest incidences of calcium oxalate stone formation in the western world.

This high incidence is attributed to a lifestyle that involves minimal water consumption and a constant state of relative dehydration secondary to a warm climate, exposure to low-humidity air-conditioning, and the consumption of caffeine and alcoholic beverages. The incidence is higher in men, with a peak incidence occurring in professional men in their fourth and fifth decades.

Ninety-five per cent of stones seen in common clinical practice are calcium oxalate, which is radio-opaque and generally visible on plain x-rays. Uric acid stones, cystine stones and struvite, or infection, stones are less common, though need to be distinguished from calcium oxalate stones as the treatment and prevention strategies differ.

The process of stone crystallisation is the subject of much research. There appears to be a balance between promoters and inhibitors of crystallisation.

Recent work suggests that citrate is a significant inhibitor of the process of nucleation, which is at the centre of crystallisation and subsequent stone formation.

The end result of purine metabolism within the body is uric acid. Five per cent of urinary
stones have a uric acid composition. These stones tend to form in acid urine. Uric acid stones do not contain calcium and are therefore not radio-opaque and not visible on plain x-ray. Because they are non-calcium containing, they may be dissolved in an alkaline urine.

Women in particular are prone to struvite stones, which form in infected urine. Urea-splitting
bacteria such as Klebsiella and Proteus cause the urine to become alkaline with the subsequent precipitation of calcium, magnesium and phosphate stones.

Struvite formation within the kidney may form an internal cast of the kidney. Such stones are known as staghorn calculi as they branch into the major and minor calyces of the kidney. They are particularly destructive of renal tissue.

Congenital cystinuria is a genetically determined inborn error of metabolism whereby large amounts of cystine are excreted in the urine. Cystine stones contain sulphur and, as such, are poorly seen on plain radiography. As with uric acid calculi, cystine stones are more likely to form in acid urine, and therefore the alkalinisation of urine is an important management
strategy.

Calcium oxalate stones may occur secondary to hyperpara-thyroidism, which causes hypercalcaemia due to the increased mobilisation of calcium from bones.

Hyperparathyroidism is diagnosed by the concurrent finding of an elevated serum calcium in conjunction with a raised para-thyroid hormone (PTH) level. Other causes of hypercalcaemia include malignant states and sarcoidosis.

Excess dietary sodium has been implicated in the genesis of calcium oxalate stones. It is postulated that increased urinary sodium concentration may increase urinary calcium levels while concurrently decreasing the inhibitory effect of urinary citrate, which acts as an inhibitor
of crystallisation.

Patients suffering with inflammatory bowel disease are known to suffer with a citrate deficit. This is possibly a contributory factor to the increased incidence of calcium oxalate and oxalate stone disease in patients with inflammatory bowel disease.

Recurrent urinary tract infections or anatomical abnormalities of the urinary tract, especially those that cause poor drainage, will always pre-dispose to stone formation and re-formation.

For example, there is an increased incidence of urinary stone formation in congenital pelviureteric junction obstruction, in ureteric stricture disease and an increased formation of bladder stones in men with prostatic hypertrophy and high residual volumes of urine in the bladder.

Differential diagnosis of flank pain should always be borne in mind during an acute presentation of abdominal pain.

Occasionally, an acute vascular event such as a dissecting aortic or ileac aneurysm in the elderly may masquerade as ureteric colic. Other conditions in the differential diagnosis
include gall stone colic, early appendicitis and, occasionally, tubal disease.

In the diagnosis of urinary tract stones, the spiral CT scan is now the investigation of choice for the patient presenting with acute renal colic typical of urinary stone disease.

The spiral CT scan has the advantage of being quick and is able to detect both radiolucent and radio-opaque stones. It is particularly useful at identifying ureteric stones.

Extra-renal and extra-ureteric abnormalities may also be diagnosed with the spiral CT scan.

Spiral CT scanning does not involve the use of IV contrast medium. The spiral CT scan will identify, but not distinguish, between calcium oxalate and uric acid stones.

A plain x-ray is therefore necessary to determine whether a urinary stone is radio-opaque or radiolucent. This is relevant if the stone is to be treated by x-ray guided
extracorporeal shock wave lithotripsy therapy.

Urinary tract ultrasono-graphy is useful for monitoring the progress of stone dissolution
therapies as applied to the management of cystine and uric acid stones. It is also a good screening test for ureteric obstruction.

First-time stone-formers do not generally require extensive investigation. For radio-opaque calcium oxalate stones, screening with serum calcium to exclude hypercalcaemic states is mandatory.

If hypercalcaemia is present, hyperparathyroidism must be excluded by measuring the PTH level.

Uric acid stone-formers must have their uric acid levels monitored.

Recurrent stone-formers should be referred for more intensive metabolic investigation,
including the analysis of 24-hour urinary specimens, in an attempt to identify and treat a specific metabolic abnormality.

URETERIC STENTS

Ureteric – or ‘JJ’ – stents are critical to the modern practice of endourology.

JJ stents are inserted under a general anaesthetic using a cystoscope.

Stents are inserted for the acute relief of pain, obstruction and infection.

JJ stents may be inserted electively prior to rigid or flexible ureteroscopy. The pre-stenting of the ureter causes ureteric dilatation and facilitates easier, safer instrumentation for the definitive removal of ureteric stones.

RIGID URETEROSCOPES

Rigid ureteroscopes use fibre-optic technology. A digital camera is attached to the lens. Ureteroscopy gives excellent access and visualisation of the ureter.

With JJ pre-stenting, rigid ureteroscopy can access up to the proximal ureteric third. Stone fragmentation can occur via the rigid ureteroscope using technologies such as the ballistic in situ lithoclast lithotriptor or the holmium YAG laser.

After stone fragmentation occurs, stone retrieval baskets can be passed via the rigid ureteroscope to extract stone fragments.

FLEXIBLE URETEROSCOPY

Urinary stones in the proximal ureter or within the kidneys can now be accessed using miniaturised fibre-optic flexible ureteroscopes.

Stenting with a JJ stent for at least one week is advisable prior to flexible ureteroscopy of the ureter and kidney.

Under a general anaesthe-tic, a guide wire and an access sheath are passed into the ureter.
This facilitates the passage of the flexible ureteroscope to the proximal ureter and kidney.
Laser fibres and stone retrieval baskets can be used to remove upper urinary tract stones. Flexible urethroscopy is also useful for the diagnosis of transitional cell cancers of the upper urinary tract.

The introduction of extracor-poreal shockwave lithotripsy (ESWL) revolutionised the management of urinary stone disease
in the mid-1980s.

These machines focus shock-waves through an acoustic lens onto the stone. The shockwave
may be generated with spark gap, piezoelectric or electromagnetic technology. The electro-
magnetic lithotripters are most commonly used.

The shockwave is generated with electromagnetic lithotripsy by the acute deflection of alloy
under the influence of opposing magnetic fields. Once generated, the shockwave is focused
using the physical properties of a biconcave acoustic lens.

The stone is identified using either radiological or ultrasonic imaging. The technology can be
applied under either sedation and local anaesthetic creams or general anaesthesia.

Lithotripsy therapy is usually performed as a day-only procedure.

Provided there is no infundibular pelviureteric junction or ureteric obstruction, most radio-
opaque stones less than 2 cm in maximum diameter are suitable for shockwave therapy. About
25% of such stones require more than one treatment.

The aim of shockwave lithotripsy is to reduce fragments to a size that will pass easily
without pain. Ureteric pain and obstruction may occur following shockwave lithotripsy and
may require endourological interventions such as JJ stenting, with or without the use of
rigid or flexible ureteroscopy, and in situ lithotripsy using the lithoclast ballistic lithotriptor or
in situ laser fibre technology.

Stone fragmentation and stone fragment clearance can take up to six weeks following
successful treatment. Following shockwave lithotripsy, patients may experience
modest bruising and pain in the flank, and blood in the urine for a short time.

PERCUTANEOUS NEPHROLITHOTOMY

Percutaneous access to the kidney is achieved using x-ray guidance and guide-wire technology.

A tract is dilated through the skin into the kidney under general anaesthesia, and through this tract a nephroscope coupled with a three-chip digital camera is inserted into the renal pelvis to directly visualise the stone.

Once the stone has been visualised, in situ lithotripsy can occur using the ballistic lithoclast master or laser technology. Stone fragments are removed using stone retrieval baskets and forceps.

Percutaneous nephrolithotomy is particularly useful where the urinary stone is greater than 2 cm in diameter and is therefore unsuitable for lithotripsy. Large staghorn calculi may also be treated successfully with the percutaneous technique.

OPEN STONE SURGERY

‘Cutting for the stone’ is an ancient art first performed by the Egyptians 5000 years ago. Using the technology of ‘the new stone age’, cutting for the stone occurs now in less than 1% of cases. Large chronically impacted ureteric stones may require open stone surgery, as may complex staghorn stones of the renal pelvis.

The appropriate management of urinary stone disease requires careful clinical judgment and the availability and expert knowledge of the modern endourological techniques described above.

Certain stones do not require active intervention, while other cases require appropriate application of endourological procedures.

The small stone in the lower pole calyx of either kidney is a common incidental finding.
Small lower-pole calyceal stones do not respond well to extracorporeal shockwave lithotripsy.
They do not need intervention unless they move into the ureter and fail to pass spontaneously. In certain occupations, such as the aviation industry, even small asymptomatic stones may warrant an attempt at resolution using either ESWL or flex-
ible ureteroscopy with direct visualisation and extraction.

The most common clinical presentation of urinary stone disease is the small, less than
5 mm stone obstructing the ureter. The vesicoureteric junction is the narrowest part of the
urinary tract and it is here that most small stones lodge.

Stones less than 5 mm in diameter in an otherwise normal urinary tract have in excess of a 95% chance of spontaneously passing. Initially, a trial of passage is indicated. The best pain relief during this period is non-steroidal anti-inflammatory medication delivered in suppository form.

Provided the pain is adequately controlled, a progress spiral CT scan should be per-
formed two to three weeks after the initial episode to document that the stone has passed and that the kidney is once again unobstructed.

The absolute indication for intervention is the presence of obstruction with urinary tract
infection. An obstructed infected ureter causes pyonephrosis, which can rapidly lead to the
septicaemic state. Any patient with an obstructed urinary tract experiencing fevers, rigors or
hypotension should be treated as a medical and surgical emergency.

In the acute setting, the obstruction is best relieved by radiological percutaneous nephrostomy drainage of the kidney. Once the septic episode has settled, the stone can be
managed by an endourological procedure.

The excessive application of endourological technology is to be avoided. For example, for a
complex staghorn calculus of the kidney or an impacted large ureteric stone, it is often better
to proceed initially to a definitive single open stone operation rather than multiple endouro-
logical procedures involving multiple hospital admissions and instrumentations. The appropri-
ate choice of stone management is as important as the expert application of each individual
procedure.

Dissolution therapy for uric acid and cystine stones should be considered. This involves the
consumption of 3-4 L of water per day in concert with urinary alkalinisation using bicarbo-
nate.

There is no credible evidence to support the use of so-called complementary and alternative
therapies.

Normal urinary drainage from the kidney, ureter and bladder is critical to the prevention of urinary stone disease. The elimination of infection is mandatory.

The single most useful advice that can be given to stoneformers of all types is that the patient must drink a minimum of 2-3 L of water per day.

 The colour of the voided urine should be clear like water: “If it’s white, it’s right!” High urine outputs prevent saturated urine from developing, which in turn inhibits the process of nucleation, with subsequent crystallisation around the protein matrix of the stone.

Modifying behaviour in stone-forming patients is particularly difficult, with many patients forsaking their increased water consumption once the memory of the acute renal colic has passed.

 It is important to stress that there is no evidence that complementary and alternative substances can dissolve calcium oxalate stones, and that water is by far the best ‘natural’ intervention they can choose.

Recurrent calcium oxalate stone-formers may benefit from the administration of thiazide diuretics, as these decrease urinary calcium levels. Potassium citrate supplements or even lemon juice may in certain calcium oxalate stone-formers increase urinary citrate levels, thereby decreasing calcium oxalate crystallisation.

For uric acid stone-formers, serum uric acid levels must be normalised by diet and by allopurinol therapy if necessary. Purine-containing food stuffs such as beer, red wine and red meat should be minimised.

Uric acid stone formers should drink 3 L of water per day and attempt to alkalinise their urine using sodium bicarbonate in solution.

Patients with congenital cystinuria should be concurrently managed by a nephro-
logist and urologist. Consuming 4-5 L of water per day is mandatory along with urinary alkalinisation. Penicillamine may need to be administered under the supervision of a nephrologist.

CONCLUSION

Urinary tract stone disease is very common in Western society. Clinical management should focus on prevention of stone reformation, relief of pain and the expeditious use of minimally invasive stone technology.

REFERENCE

Tolley DA, Segura JW. Urinary Stones,
first edition, Health Press Limited, Abingdon UK 2002