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Urinary stones management
Moderator: Dr Rishi Agarwal (MS, MCh Urosurgery)
By: Dr. Shruti Devendra JR1, General Surgery, RMCH
Outline
 Clinical history
 Evaluation
 Medical management
 Surgical management
Clinical History
Clinical history is important
 Type of pain
 Setting in which the patient presented (emergency or OPD)
 First-time stone formers or recurrent
 Risk factors
Renal colic
Renal colic and non colicky renal pain are two types of pain originating from the
kidney. Renal colic is usually caused by the stretching of the collecting system or
ureter, whereas non colicky renal pain is caused by renal capsule distention
Renal colic does not always wax and wane but maybe relatively constant and
patient with renal calculi have pain primarily due to urinary obstruction
Renal calyx: non-obstructing stones cause pain only periodically, owing to
intermittent obstruction. The pain is deep, dull ache in the flank or back that can
vary in intensity from severe to mild. Pain may be exacerbated after consumption
of large amounts of fluids.
Renal pelvis: Stones >1cm in diameter commonly obstruct the ureteropelvic
junction, generally causing severe pain in the costovertebral angle, just lateral to
the erector spinae muscle and just below 12th rib. This pain may vary from dull to
excruciatingly sharp and is usually constant, boring, and difficult to ignore. It
often radiates to the flank and also anteriorly to the upper ipsilateral abdominal
quadrant. It may be confused with biliary colic or cholecystitis if on the right side
and with gastritis, acute pancreatitis, or peptic ulcer disease if on the left.
Ureteric colic
• A stone in the ureter can cause acute severe spasmodic pain
• Local mechanisms such as inflammation, edema, hyperperistalsis, and mucosal
irritation may contribute to the perception of pain in patients
• Small ureteral stones frequently present with severe pain, whereas large staghorn
configured calculi may present with a dull ache or flank discomfort.
• The pain frequently is abrupt in onset and severe, and may awaken a patient from
sleep. The severity of the pain is worsened by the unexpected nature of its onset.
Patients frequently move constantly into unusual positions in an attempt to relieve
the pain. This movement is in contrast to the lack of movement of someone with
peritoneal signs; such a patient lies in a stationary position
• Radiation of pain with various types of ureteral stone.
Upper left: Ureteropelvic stone Severe costovertebral
angle pain from capsular and pelvic distention; acute
renal and urethral pain from hyperperistalsis of smooth
muscle of calyces, pelvis, and ureter, with pain radiating
along the course of the ureter (and into the testicle, since
the nerve supply to the kidney and testis is the same). The
testis is hypersensitive. Upper right: Mid ureteral stone.
Same as described earlier but with more pain in the lower
abdominal quadrant. Left: Low ureteral stone. Same as
described earlier, with pain radiating into bladder, vulva,
or scrotum. The scrotal wall is hyperesthetic. Testicular
sensitivity is absent. When the stone approaches the
bladder, urgency and frequency with burning on urination
develop as a result of inflammation of the bladder wall
around the ureteral orifice.
Normal anatomical narrowing's
(1–5) of the ureter
The ureter descends from the
renal pelvis through the
retroperitoneum on the psoas
muscle, and enters the pelvis in
front of the common iliac vessels,
anterior to the sacroiliac joint.
The ureter then courses
downwards and backwards to the
level of the ischial spine before
turning forwards and medially to
enter the posterior wall of the
bladder.
History
• Underlying predisposing conditions
• Medications (calcium, vitamin C, vitamin D, acetazolamide, steroids)
• Dietary excesses, inadequate fluid intake, excessive fluid loss
Patient
OPD
Low dose
NCCT
USG + X ray
KUB
ER
Pain management
Low dose NCCT is the
investigation of choice
A 28 year old female came to the emergency department with a severe
colicky pain in the right iliac fossa radiating to the groin. Patient is restless,
not able to sit still and her BP is 130/90 mmHg, PR 98/min, RR 26/min,
patient is afebrile. There is no history of fever, burning micturition, or
increased frequency. No similar episode in the past. Her menstrual cycle is
regular and normal. LMP 2 week ago. What is the investigation of choice for
this patient?
1) NCCT scan abdomen
2) USG whole abdomen
3) Urine pregnancy test
4) X ray KUB
5) MRI abdomen
6) USG and X ray KUB
• Urine pregnancy test came negative. Now what is the investigation of
choice?
• CT scan facility not available at the moment. Preferred investigation?
• Investigation for follow up?
American College of Radiology
ACR Appropriateness Criteria
• NCCT is the most accurate technique for evaluating flank pain.
• Low-dose NCCT should be performed when evaluating for renal or ureteral
stones.
• If there is uncertainty about whether a calcific density represents a ureteral
stone or a phlebolith, intravenous contrast material can be administered and
excretory-phase images obtained for definitive diagnosis.
• In pregnant patients with flank pain, US is the best initial study.
• Abdominal radiography combined with US may be able to diagnose most
clinically significant stones and should be considered, especially in young
patients and those with known stone disease.
• MR could be considered to evaluate for hydronephrosis though is less
accurate for the direct visualization of renal and ureteral stones.
Computed Tomography
• The study with the highest (>95%) sensitivity and specificity for
urolithiasis. Virtually all stones are radiopaque on CT, and stone size
can be measured accurately in cross-section, aiding in predicting
outcome. Stone location, accurately depicted by NCCT, has also been
associated with spontaneous stone passage rates, with the more
proximal stones having a higher need for intervention
• The effective radiation dose from a single abdominal radiograph is
approximately 0.8 mSv as compared to 10–12 mSv for conventional
NCCT of the abdomen and pelvis and 3–4 mSv for low-dose NCCT of
the abdomen and pelvis
Ultrasound
• US can be a useful tool in the evaluation of patients with suspected
renal colic and does not expose the patient to ionizing radiation
• In the setting of acute flank pain and with meticulous technique, US
has been shown to be 61%–90% sensitive for the detection of stones.
Using color Doppler imaging to assess for the twinkle artifact may
improve the ability to detect stones. The twinkle artifact is visible as
an intense multicolored signal behind a stone with the use of color
Doppler technique
• US has been found to be up to 100% sensitive and 90% specific for
the diagnosis of ureteral obstruction in patients presenting with acute
flank pain
• US findings of obstructive uropathy include hydronephrosis,
ureterectasis, and perinephric fluid. However, within the first 2 hours
of presentation, these findings are less sensitive because, for example,
hydronephrosis may not have had time to develop
• Outcomes were similar but radiation exposure was lower when
individuals with suspected nephrolithiasis who presented to the
emergency department were evaluated initially with US as compared
to CT in a recent randomized study. There were no statistically
significant differences in return emergency department visits,
hospitalizations, or high-risk diagnoses with complications for
individuals whose initial imaging workup began with US as compared
to individuals whose initial imaging workup began with CT
Intravenous Urography
• The IVU is the previous standard study for ureterolithiasis. It provides
information regarding site and degree of obstruction, stone size, and effect
of obstruction on renal excretion.
• IVU has a number of relative contraindications, including renal
insufficiency, dehydration, past reaction to iodinated contrast agents, and
pregnancy
• It may take several hours for excretion to occur in the presence of acute
obstruction, in which case IVU is more time-consuming than the alternative
techniques
Nuclear scintigraphy
Nuclear scintigraphic imaging of stones has recently been appreciated.
Bisphosphonate markers can identify even small calculi that are difficult
to appreciate on a conventional KUB film. Differential radioactive
uptake dependent on stone composition appreciated during in vitro
studies cannot be appreciated on in vivo studies. Nuclear scintigraphy
cannot delineate upper-tract anatomy in sufficient detail to help direct a
therapeutic plan.
A: Scout abdominal
radiograph
demonstrating large left
staghorn renal calculus.
B: Nuclear scintigraphic
evaluation of renal
calculi. Posterior view
demonstrating uptake on
large left staghorn
calculus after furosemide
(Lasix) diuresis. Note
right kidney with uptake
in lower pole.
First-time and recurrent stone formers
• Although it is recommended to thoroughly investigate first time stone
formers but it is a shared decision made by the physician and patient. The
cost involved is also very high and so the trial of conservative management
maybe preferred depending upon the availability of resources and feasibility
• Patients at higher risk for repeat episodes are those with a family
history of stones and those with intestinal disease (particularly when
causing chronic diarrheal states), pathologic skeletal fractures,
osteoporosis, urinary tract infection (UTI), or gout. In these patients, an
extensive evaluation is recommended. In addition, obese patients with
stones, particularly obese women, have significantly elevated risk for
recurrence and should be given consideration for metabolic evaluation
Indications for a Metabolic Stone Evaluation
• Recurrent stone formers
• Strong family history of stones
• Intestinal disease (particularly chronic diarrhea)
• Pathologic skeletal fractures
• Osteoporosis
• History of urinary tract infection with calculi
• Personal history of gout
• Infirm health (unable to tolerate repeat stone episodes)
• Solitary kidney
• Anatomic abnormalities
• Renal insufficiency
• Stones composed of cystine, uric acid, struvite
Stone evaluation
Multichannel blood screen
• Basic metabolic panel (sodium, potassium,
chloride, carbon dioxide, blood urea nitrogen,
creatinine)
• Calcium
• Intact parathyroid hormone
• Uric acid
Urine
• Urinalysis
• pH > 7.5: infection lithiasis
• pH < 5.5: uric acid lithiasis
• Sediment for crystalluria
Urine culture
• Urea-splitting organisms: suggestive of
infection lithiasis
• Qualitative cystine
Stone analysis
Conservative medical management
• Fluid recommendations
• Dietary recommendations
Fluid recommendation
• One mainstay of conservative management is the forced increase in fluid intake to
achieve a daily urine output of at least 2 litres
• Increased urine output may have two effects. First, the mechanical diuresis that
ensues may prevent urinary stagnation and the formation of symptomatic calculi.
It is more likely that the creation of dilute urine alters the supersaturation of stone
components.
• Although the 24-hour urine calcium, magnesium, and citrate levels increased
directly with drinking hard water, no significant change was found in urinary
oxalate, uric acid, pH, or volume. Most importantly, the number of total lifetime
stone episodes was similar between patients residing in areas with soft public
water and hard public water.
• A number of studies suggest that carbonated water offers increased protection
against recurrent stone formation as compared to still water. Soda flavored with
phosphoric acid may increase stone risk, whereas those with citric acid may
decrease risk.
• Lemonade and orange juice have long been used as an adjunct to water to provide
increased urinary volume as well as increased urinary citrate excretion
• Overall, most evidence suggests that it is not the type of fluid ingested that is
important for stone prevention but rather the absolute amount of fluid volume
taken in per day. We therefore encourage all of our stone formers to drink at least
3000 mL/day to maintain a urine output greater than 2500 mL/day.
• Ureteral calculi 4–5 mm in size have a 40–50% chance of spontaneous
passage. In contrast, calculi >6 mm have a >15% chance of
spontaneous passage.
• This does not mean that a 1-cm stone will not pass or that a 1- to 2-
mm stone will always pass uneventfully. The vast majority of stones
that pass do so within a 6-week period after the onset of symptoms
• Ureteral calculi discovered in the distal ureter at the time of
presentation have a 50% chance of spontaneous passage, in contrast to
a 25% and 10% chance in the mid and proximal ureter, respectively
Dietary recommendations
• Epidemiologic studies from a number of countries have shown that the
incidence of renal stones is higher in populations in which there is an
increased animal protein intake. For example, in the northern and western
regions of India, animal protein intake is approximately 100% greater than
in the southern and eastern regions and the rate of kidney stones is four
times greater.
• Protein intake increases urinary calcium, oxalate, and uric acid excretion
and the mathematically calculated probability of stone formation even in
normal subjects. Indeed, according to , ingestion of protein is second only to
ingestion of vitamin D in enhancing intestinal absorption of calcium
• More recently, the Dietary Approaches to Stop Hypertension (DASH) style
diet has been evaluated for its effect on kidney stone formation. The DASH
diet is rich in fruit and vegetables, moderate in low-fat dairy products, and
low in animal protein. In a prospective population-based study, higher
DASH scores were associated with a lower risk for kidney stone formation
• Sodium restriction has been widely recommended as an important element
of dietary prevention of recurrent nephrolithiasis. When combined with
animal protein restriction and moderate calcium ingestion, a reduced-
sodium diet will decrease stone episodes by roughly 50%.
Other recommendations
• Weight loss: increased BMI, larger waist size, and weight gain
correlated with an increased risk for stone episodes. This increased
stone risk was still more pronounced for women than men
• Metabolic syndrome is associated with lower urinary pH. Obese
patients have a higher propensity for uric acid calculi.
• Dietary calcium restriction actually increases stone recurrence risk.
Calcium supplementation is likely safest when taken with meals.
Calcium citrate appears to be a more stone-friendly calcium
supplement because of the additional inhibitory action of citrate.
• Vitamin D repletion is likely safe for stone formers; however, 24-hour
urine calcium should be monitored during vitamin D therapy.
• general advice on a restricted-oxalate intake might be given to patients
with recurrent nephrolithiasis
• large amounts of vitamin C may demonstrate increases in 24-hour
oxalate excretion and therefore calcium oxalate supersaturation. It
seems reasonable to avoid heavy dosing of vitamin C. Limiting one’s
intake to a maximum daily dose of less than 2 g.
• After 3 to 4 months on conservative management, patients should be
re-evaluated using either standard laboratory assays or an automated
urinalysis package. If the patient’s metabolic or environmental
abnormalities have been corrected, the conservative therapy can be
continued and the patient followed every 6 to 12 months with repeat
24-hour urine testing as indicated
Medical therapy
• One potential criticism of the “selective” metabolic management of
nephrolithiasis is that the collection of multiple urine and serum
studies can be too time-consuming to be feasible outside of an
academic medical centre with its dedicated research staff. Although a
commitment to follow-up can be tedious, it should be no worse for
patients with kidney stones than it is for those followed for urologic
cancer or voiding dysfunction.
Absorptive Hypercalciuria
Normal calcium intake averages approximately 900–1000 mg/day.
Approximately one-third is absorbed by the small bowel. and of that
portion, approximately 150–200 mg is obligatorily excreted In the urine.
Absorptive hypercalciuria is secondary to increased calcium absorption
from the small bowel, predominantly from the jejunum.
This results in an increased load of calcium filtered from the
glomerulus. The result is suppression of parathyroid hormone, leading
to decreased tubular reabsorption of calcium, culminating in
hypercalciuria 4 mg/ kg)
Absorptive
Hypercalciuria
Type I
Type I absorptive
hypercalciuria is independent
of diet and represents 15% of
all calcareous calculi. There is
an elevated urinary calcium
level >150–200 mg/24 hour)
even during a calcium-
restricted diet
Type II
Absorptive hypercalciuria
is dietary dependent.
There is no specific
medical therapy. Calcium
excretion returns to
normal on a calcium-
restricted diet
Type III
Absorptive hypercalciuria is
secondary to a phosphate renal
leak and accounts for 5% of all
urinary calculi. Decreased serum
phosphate leads to an increase in
1,25-dihydroxyvitamin D
synthesis. The physiologic
cascade culminates in an
increased absorption of
phosphate, and calcium, from
the small bowel and an increased
renal excretion of calcium
• Type I: Thiazides directly stimulate calcium resorption in the distal nephron
while promoting excretion of sodium.
• The retained calcium may be accreted in bone at least during the first few
years of therapy. Bone density, determined in the distal third of the radius
by photon absorptiometry, increases significantly during thiazide treatment
• Dietary moderation of calcium and oxalate, combined with thiazide and
potassium citrate, satisfactorily controlled hypercalciuria, while preventing
the complication of osteopenia commonly associated with absorptive
hypercalciuria.
• Hydrochlorothiazide 25 mg PO bid
• Sodium cellulose phosphate, given orally, is a nonabsorbable ion
exchange resin that binds calcium and inhibits calcium absorption. Is
given with the meals.
• Unfortunately, despite early enthusiasm, the use of sodium cellulose
phosphate has largely fallen out of favor and this medication is no
longer available in the United States.
• Type II: Moderate calcium intake (400 to 600 mg/day) and high fluid
intake
• Type III: Orthophosphate (neutral or alkaline salt of sodium and/or
potassium, 0.5 g phosphorus three or four times per day) has been
shown to inhibit 1,25-(OH)2D synthesis
• Best taken as 250 mg three to four times daily. Taken after meals and
before bedtime. Orthophosphates do not alter intestinal calcium
absorption.
Resorptive hypercalciuric nephrolithiasis
• A subset (<10%) of patients with clinically obvious primary
hyperparathyroidism present with nephrolithiasis. This group represents less
than 5% of all patients with urinary stones and are more commonly seen in
women.
• Parathyroid hormone results in a cascade of events starting with an increase
in urinary phosphorus and a decrease in plasma phosphorus, followed by an
increase in plasma calcium and a decrease in urinary calcium. Its action on
the kidney and on the bone is independent of each other. Ultimately, renal
damage is secondary to the hypercalcemia. It limits the concentrating ability
of the kidney and impairs the kidney’s ability to acidify urine
• Surgical removal of the offending parathyroid adenoma is the most
effective way of treating this disease. However, up to 25% of these
patients will develop new urinary stones after successful surgery, most
commonly seen in men. Attempts at long-term medical management
are challenging.
Renal-induced hypercalciuric nephrolithiasis
• Hypercalciuria of renal origin is due to an intrinsic renal tubular defect in
calcium excretion. This creates a physiologically vicious cycle. Excessive
urinary calcium excretion results in a relative decrease in serum calcium,
which leads to a secondarily increased parathyroid hormone level that
mobilizes calcium from the bone and increases calcium absorption from the
gut. This step completes the pathologic cycle by delivering increased levels
of calcium back to the kidney, whereby the renal tubules excrete large
amounts of calcium
• These patients have an elevated fasting urinary calcium level, normal serum
calcium level, and a secondarily elevated parathyroid hormone level.
• Renal hypercalciuria is effectively treated with hydrochlorothiazides. They
decrease the circulating blood volume and subsequently stimulate proximal
tubular absorption of calcium as well as other constituents. They also
increase reabsorption at the distal tubule. Both mechanisms correct the
secondary hyperparathyroid state.
• To help differentiate primary hyperparathyroidism from secondary
hyperparathyroidism in patients with urinary stone disease, one can
prescribe a hydrochlorothiazide challenge (50 mg twice a day for 7–10
days). Patients with secondary hyperparathyroidism will have a return to
normal serum parathyroid levels, while those with primary
hyperparathyroidism will continue to have elevated serum values.
Hyperuricosuric calcium nephrolithiasis
• Hyperuricosuric calcium nephrolithiasis is due to either an excessive
dietary intake of purines or an increase in endogenous uric acid
production. In both situations, there is an increase in urinary
monosodium urates. Monosodium urates absorb and adsorb urinary
stone inhibitors and facilitate heterogeneous nucleation.
• Patients have elevated urinary uric acid levels (>600 mg/ 24 hour in
women and >750 mg/24 hour in men) and consistently have a urinary
pH >5.5. The urinary pH helps to differentiate hyperuricosuric calcium
from hyperuricosuric uric acid stone formation
• Allopurinol (300 mg/day) may be used to block the ability of xanthine
oxidase to convert xanthine to uric acid. The resultant decrease in
serum uric acid will ultimately lead to a decrease in urinary uric acid
as well.
• Allopurinol’s use in hyperuricosuria associated with dietary purine
overindulgence also may be reasonable if patients are unable or
unwilling to comply with dietary purine restriction
Hyperoxaluric calcium nephrolithiasis
• Hyperoxaluric calcium nephrolithiasis is secondary to increased urinary
oxalate levels (>40 mg/24 hour). It is frequently found in patients with
inflammatory bowel disease or other chronic diarrheal states that result in
severe dehydration.
• Fat restriction is necessary and Oral administration of over-the-counter
calcium preparations (0.25 to 1 g four times per day) or magnesium has
been recommended for the control of calcium nephrolithiasis of ileal disease
• Cholestyramine may be used to bind acidic components in the gut lumen,
including oxalate. Intestinal bypass may need to be reversed.
Primary hyperoxaluria
• Primary hyperoxaluria is a rare hereditary disease. It is associated with
calcium oxalate renal calculi, nephrocalcinosis, and other distant
deposits of oxalate, culminating in progressive renal failure and
eventual death
• Oxalate crystal deposits develop rapidly in transplanted kidneys.
Combined liver and renal transplantation has cured this previously
fatal rare disease
• Large doses of pyridoxine reduce urinary oxalate excretion in 20–50%
of patients. Neutral orthophosphates may be used to halt the growth of
existing calculi.
Renal tubular acidosis type I
• Sodium or potassium bicarbonate or citrate is given, resulting in an
increased renal citrate excretion.
• Potassium citrate (20 mEq PO Bid/Tid) therapy is able to correct the
metabolic acidosis and hypokalemia found in patients with distal RTA
In addition, this medication is capable of restoring normal urinary
citrate
Stones associated with infection
• After surgical removal, antimicrobial prophylaxis should be
maintained for 3–12 months. Urinary acidification with ammonium
chloride may be used in conjunction. Dissolution of stones with
hemiacridrin or Suby G and M solutions is an option.
• Stone composition: struvite stones need to be completely removed
because of associated infection. Patient should be counselled that
multiple sessions maybe needed for the removal of the stone.
Uric acid stones
• Treatment is centered on maintaining a urine volume >2 L/day and a
urinary pH >6.0. Reducing dietary purines or the administration of
allopurinol also helps reduce uric acid excretion. Alkalinization,
however, is the mainstay of therapy (with oral sodium bicarbonate,
potassium bicarbonate, potassium citrate, or intravenous 1/6 normal
sodium lactate) and may dissolve calculi
• Patients present with a urinary pH consistently <5.5, in contrast to
patients with hyperuricosuric calcium nephrolithiasis, who have a
urinary pH >5.5.
Cystinuria
• Potassium citrate is preferred to sodium bicarbonate for this condition. The
aim is to increase the urinary pH to 7.5–7.8
• D-penicillamine (250 mg PO OD) may be used which reacts with cysteine
to form a soluble salt that reduces, through competition, the formation of
cystine. It is a potentially toxic drug and should only be used if hydration
and alkalinisation fail. Adverse effects include rashes, fever,
agranulocytosis, arthralgia and lymphadenopathy.
• 6-mercaptopropionyl glycine (MPG) (100mg PO Bid) is an alternative and
has fewer side effects. Captopril (25mg PO Tid) may be used to lower
urinary cystine levels in homozygous cystinuric patients.
Urosepsis implies clinically evident
severe infection of the urinary tract
with features consistent with systemic
inflammatory response syndrome. It
may be associated with multi-organ
dysfunction, hypoperfusion, or,
hypotension
Extracorporeal Shock Wave Lithotripsy
• It was during the investigation of pitting on supersonic aircraft that
Dornier, a German aircraft corporation, rediscovered that shock waves
originating from passing debris in the atmosphere can crack something
that is hard.
• The first clinical application with successful fragmentation of renal
calculi was in 1980. The HM-1 (Human Model-1) lithotriptor
underwent modifications in 1982 leading to the HM-2 and, finally, to
the widespread application of the HM-3 in 1983 (Figure 17–16). Since
then, thousands of lithotriptors have been put into use around the
world, with millions of patients successfully treated.
Shock wave physics—In contrast to the familiar ultrasonic wave with
sinusoidal characteristics and longitudinal mechanical properties,
acoustic shock waves are not harmonic and have nonlinear pressure
characteristics. There is a steep rise in pressure amplitude that results in
compressive forces. There are two basic types of shock wave sources,
supersonic and finite amplitude emitters
Supersonic shock
wave emission from a
spark gap electrode.
B: Reflecting the
shock wave from
focus 1 to focus 2
allows for stone
fragmentation
Piezoceramic
finite amplitude
emitter. Ceramic
components are
placed on the
concave surface
of a
sphere and each
component is
directed to an
identified focus
Incoming
shock
waves result
in
fragmentati
on from
erosion and
shattering
• Patients with small renal pelvic stones (<1.5 cm) have approximately a 90%
stone-free rate in comparison with those with similar stones in a middle
calyx (approximately 75%) or lower calyx (approximately 50%).
• Stones can be localised for treatment using either fluoroscopy or USS
• Different methods of generating shockwaves include spark gap,
electromagnetic, piezoelectric and microexpulsive. Shockwaves generated
using the spark-gap method need to be coordinated with the patient’s
electrocardiogram (ECG) to prevent cardiac arrhythmias.
• This is the common form of treatment these days for renal calculi and
stones up to approximately 1.5 cm in size are suitable for this form of
treatment. More than one treatment session may be needed to fully
treat the stone, especially if it is sizeable.
• Prophylactic antibiotics are used to prevent infection as stones are
often colonised by bacteria. Cystine stones are relatively resistant to
ESWL due to their hardness.
• In addition to infection, ESWL may result in haematuria, parenchymal
haemorrhage and even perirenal haematoma. A collection of stone
fragments in a ureter after ESWL for a significant renal stone is given
the German name of steinstrasse (‘street of stones’)
• Contraindications to ESWL are obese patients, pregnant patients, large
aortic aneurysm and patients taking oral anticoagulants.
Right lower pole calculi and
steinstrasse in the distal
right ureter (arrow).
Ureteroscopic Stone Extraction
• Ureteroscopic stone extraction is highly efficacious for lower ureteral
calculi. The use of small-caliber ureteroscopes and the advent of
balloon dilation or ureteral access sheaths have increased stone-free
rates dramatically.
• Calculi that measure <6–8 mm are frequently removed intact. Nitinol
baskets are less traumatic than older round or flat-wired stone baskets.
Excessive force with any instrument in the ureter may result in ureteral
injury
Dormia stone-catching
basket in use. (a) Basket
introduced past stone. (b)
Opened. (c) Enclosing
stone, ready for
withdrawal.
Ureteroscopy. X-ray
showing a ureteroscope and
guidewire in the ureter.
• A variety of lithotrites can be placed through an ureteroscope,
including electrohydraulic, solid and hollow-core ultrasonic probes, a
variety of laser systems, and pneumatic systems such as the Swiss
lithoclast
• Stones can also be fragmented using mechanical disintegration using
the lithoclast. The most significant complications relate to injury to the
ureteric mucosa or wall and include ureteric perforation and
extravasation, avulsion of the ureter and ureteric stricture.
PERCUTANEOUS NEPHROLITHOTOMY
(PCNL)
• Percutaneous removal of renal and proximal ureteral calculi is the
treatment of choice for large (>2.5 cm) calculi; those resistant to SWL;
select lower pole calyceal stones with a narrow, long infundibulum
and an acute infundibulopelvic angle
• Needle puncture is directed by fluoroscopy, ultrasound, or both, and is
routinely placed from the posterior axillary line into a posterior
inferior calyx. Superior caliceal puncture may be required, and in such
situations, care should be taken to avoid injury to the pleura, lungs,
spleen, and liver.
• Tract dilation is performed by sequential plastic dilators (Amplatz
system), telescoping metal dilators (Alken), or balloon dilation.
• Residual calculi can be retrieved with the aid of flexible endoscopes,
additional percutaneous puncture access, follow-up irrigations, SWL,
or additional percutaneous sessions.
• Patients should be informed that complex calculi frequently require
numerous procedures.
Sequential plastic dilators
(Amplatz system)
Telescoping metal dilators
(Alken)
balloon dilation
PCNL is indicated for:
1. An obstruction: anatomic abnormalities such as PUJ obstruction,
calyceal diverticula or ureteric obstruction might prevent the passage
of stone fragments after ESWL.
2. Obese patients in whom ESWL is contraindicated.
3. Lower calyceal stones: these are less likely to pass after ESWL.
4. Stone composition: struvite stones need to be completely removed
because of associated infection. As previously mentioned, some
stones with a very hard composition are difficult to fragment using
ESWL, including calcium oxalate monohydrate and cystine stones.
Complications relating to PCNL include:
1. Injury to the spleen, pleura and colon.
2. Haemorrhage from usually the renal parenchyma but also from major
renal vessels. If the latter occurs, the treatment of choice is embolisation
but, if this doesn’t work, nephrectomy very occasionally has to be
considered.
3. Sepsis.
4. Extravasation due to rupture of the collecting system.
5. Retained stone fragments.
6. Open surgery to the kidney is sometimes more complicated after PCNL.
Percutaneous renal stone removal. (a)
The stone is in the right renal pelvis.
(b) Placement of a cannula under
radiological control into the renal
pelvis and through it a balloon catheter
to stop fragments migrating into the
upper ureter. (c) The stone is disrupted
by contact lithotripsy and the
fragments have been successfully
removed by irrigation. (d) A
nephrostogram confirms that the renal
pelvis is intact.
OPEN STONE SURGERY
• Open stone surgery other than total nephrectomy is incredibly
infrequently undertaken. Partial nephrectomy is appropriate with a
large stone burden in a renal pole with marked parenchymal thinning.
• Long-standing ureteral calculi—those inaccessible with endoscopy
and those resistant to SWL—can be extracted with an
ureterolithotomy.
Thank You!

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Urinary stones managment

  • 1. Urinary stones management Moderator: Dr Rishi Agarwal (MS, MCh Urosurgery) By: Dr. Shruti Devendra JR1, General Surgery, RMCH
  • 2. Outline  Clinical history  Evaluation  Medical management  Surgical management
  • 3. Clinical History Clinical history is important  Type of pain  Setting in which the patient presented (emergency or OPD)  First-time stone formers or recurrent  Risk factors
  • 4. Renal colic Renal colic and non colicky renal pain are two types of pain originating from the kidney. Renal colic is usually caused by the stretching of the collecting system or ureter, whereas non colicky renal pain is caused by renal capsule distention Renal colic does not always wax and wane but maybe relatively constant and patient with renal calculi have pain primarily due to urinary obstruction
  • 5. Renal calyx: non-obstructing stones cause pain only periodically, owing to intermittent obstruction. The pain is deep, dull ache in the flank or back that can vary in intensity from severe to mild. Pain may be exacerbated after consumption of large amounts of fluids. Renal pelvis: Stones >1cm in diameter commonly obstruct the ureteropelvic junction, generally causing severe pain in the costovertebral angle, just lateral to the erector spinae muscle and just below 12th rib. This pain may vary from dull to excruciatingly sharp and is usually constant, boring, and difficult to ignore. It often radiates to the flank and also anteriorly to the upper ipsilateral abdominal quadrant. It may be confused with biliary colic or cholecystitis if on the right side and with gastritis, acute pancreatitis, or peptic ulcer disease if on the left.
  • 6. Ureteric colic • A stone in the ureter can cause acute severe spasmodic pain • Local mechanisms such as inflammation, edema, hyperperistalsis, and mucosal irritation may contribute to the perception of pain in patients • Small ureteral stones frequently present with severe pain, whereas large staghorn configured calculi may present with a dull ache or flank discomfort. • The pain frequently is abrupt in onset and severe, and may awaken a patient from sleep. The severity of the pain is worsened by the unexpected nature of its onset. Patients frequently move constantly into unusual positions in an attempt to relieve the pain. This movement is in contrast to the lack of movement of someone with peritoneal signs; such a patient lies in a stationary position
  • 7.
  • 8. • Radiation of pain with various types of ureteral stone. Upper left: Ureteropelvic stone Severe costovertebral angle pain from capsular and pelvic distention; acute renal and urethral pain from hyperperistalsis of smooth muscle of calyces, pelvis, and ureter, with pain radiating along the course of the ureter (and into the testicle, since the nerve supply to the kidney and testis is the same). The testis is hypersensitive. Upper right: Mid ureteral stone. Same as described earlier but with more pain in the lower abdominal quadrant. Left: Low ureteral stone. Same as described earlier, with pain radiating into bladder, vulva, or scrotum. The scrotal wall is hyperesthetic. Testicular sensitivity is absent. When the stone approaches the bladder, urgency and frequency with burning on urination develop as a result of inflammation of the bladder wall around the ureteral orifice.
  • 10. The ureter descends from the renal pelvis through the retroperitoneum on the psoas muscle, and enters the pelvis in front of the common iliac vessels, anterior to the sacroiliac joint. The ureter then courses downwards and backwards to the level of the ischial spine before turning forwards and medially to enter the posterior wall of the bladder.
  • 11. History • Underlying predisposing conditions • Medications (calcium, vitamin C, vitamin D, acetazolamide, steroids) • Dietary excesses, inadequate fluid intake, excessive fluid loss
  • 12. Patient OPD Low dose NCCT USG + X ray KUB ER Pain management Low dose NCCT is the investigation of choice
  • 13. A 28 year old female came to the emergency department with a severe colicky pain in the right iliac fossa radiating to the groin. Patient is restless, not able to sit still and her BP is 130/90 mmHg, PR 98/min, RR 26/min, patient is afebrile. There is no history of fever, burning micturition, or increased frequency. No similar episode in the past. Her menstrual cycle is regular and normal. LMP 2 week ago. What is the investigation of choice for this patient? 1) NCCT scan abdomen 2) USG whole abdomen 3) Urine pregnancy test 4) X ray KUB 5) MRI abdomen 6) USG and X ray KUB
  • 14. • Urine pregnancy test came negative. Now what is the investigation of choice? • CT scan facility not available at the moment. Preferred investigation? • Investigation for follow up?
  • 15. American College of Radiology ACR Appropriateness Criteria • NCCT is the most accurate technique for evaluating flank pain. • Low-dose NCCT should be performed when evaluating for renal or ureteral stones. • If there is uncertainty about whether a calcific density represents a ureteral stone or a phlebolith, intravenous contrast material can be administered and excretory-phase images obtained for definitive diagnosis. • In pregnant patients with flank pain, US is the best initial study. • Abdominal radiography combined with US may be able to diagnose most clinically significant stones and should be considered, especially in young patients and those with known stone disease. • MR could be considered to evaluate for hydronephrosis though is less accurate for the direct visualization of renal and ureteral stones.
  • 16. Computed Tomography • The study with the highest (>95%) sensitivity and specificity for urolithiasis. Virtually all stones are radiopaque on CT, and stone size can be measured accurately in cross-section, aiding in predicting outcome. Stone location, accurately depicted by NCCT, has also been associated with spontaneous stone passage rates, with the more proximal stones having a higher need for intervention • The effective radiation dose from a single abdominal radiograph is approximately 0.8 mSv as compared to 10–12 mSv for conventional NCCT of the abdomen and pelvis and 3–4 mSv for low-dose NCCT of the abdomen and pelvis
  • 17.
  • 18. Ultrasound • US can be a useful tool in the evaluation of patients with suspected renal colic and does not expose the patient to ionizing radiation • In the setting of acute flank pain and with meticulous technique, US has been shown to be 61%–90% sensitive for the detection of stones. Using color Doppler imaging to assess for the twinkle artifact may improve the ability to detect stones. The twinkle artifact is visible as an intense multicolored signal behind a stone with the use of color Doppler technique
  • 19.
  • 20. • US has been found to be up to 100% sensitive and 90% specific for the diagnosis of ureteral obstruction in patients presenting with acute flank pain • US findings of obstructive uropathy include hydronephrosis, ureterectasis, and perinephric fluid. However, within the first 2 hours of presentation, these findings are less sensitive because, for example, hydronephrosis may not have had time to develop
  • 21. • Outcomes were similar but radiation exposure was lower when individuals with suspected nephrolithiasis who presented to the emergency department were evaluated initially with US as compared to CT in a recent randomized study. There were no statistically significant differences in return emergency department visits, hospitalizations, or high-risk diagnoses with complications for individuals whose initial imaging workup began with US as compared to individuals whose initial imaging workup began with CT
  • 22. Intravenous Urography • The IVU is the previous standard study for ureterolithiasis. It provides information regarding site and degree of obstruction, stone size, and effect of obstruction on renal excretion. • IVU has a number of relative contraindications, including renal insufficiency, dehydration, past reaction to iodinated contrast agents, and pregnancy • It may take several hours for excretion to occur in the presence of acute obstruction, in which case IVU is more time-consuming than the alternative techniques
  • 23.
  • 24. Nuclear scintigraphy Nuclear scintigraphic imaging of stones has recently been appreciated. Bisphosphonate markers can identify even small calculi that are difficult to appreciate on a conventional KUB film. Differential radioactive uptake dependent on stone composition appreciated during in vitro studies cannot be appreciated on in vivo studies. Nuclear scintigraphy cannot delineate upper-tract anatomy in sufficient detail to help direct a therapeutic plan.
  • 25. A: Scout abdominal radiograph demonstrating large left staghorn renal calculus. B: Nuclear scintigraphic evaluation of renal calculi. Posterior view demonstrating uptake on large left staghorn calculus after furosemide (Lasix) diuresis. Note right kidney with uptake in lower pole.
  • 26. First-time and recurrent stone formers • Although it is recommended to thoroughly investigate first time stone formers but it is a shared decision made by the physician and patient. The cost involved is also very high and so the trial of conservative management maybe preferred depending upon the availability of resources and feasibility • Patients at higher risk for repeat episodes are those with a family history of stones and those with intestinal disease (particularly when causing chronic diarrheal states), pathologic skeletal fractures, osteoporosis, urinary tract infection (UTI), or gout. In these patients, an extensive evaluation is recommended. In addition, obese patients with stones, particularly obese women, have significantly elevated risk for recurrence and should be given consideration for metabolic evaluation
  • 27. Indications for a Metabolic Stone Evaluation • Recurrent stone formers • Strong family history of stones • Intestinal disease (particularly chronic diarrhea) • Pathologic skeletal fractures • Osteoporosis • History of urinary tract infection with calculi • Personal history of gout • Infirm health (unable to tolerate repeat stone episodes) • Solitary kidney • Anatomic abnormalities • Renal insufficiency • Stones composed of cystine, uric acid, struvite
  • 28. Stone evaluation Multichannel blood screen • Basic metabolic panel (sodium, potassium, chloride, carbon dioxide, blood urea nitrogen, creatinine) • Calcium • Intact parathyroid hormone • Uric acid Urine • Urinalysis • pH > 7.5: infection lithiasis • pH < 5.5: uric acid lithiasis • Sediment for crystalluria Urine culture • Urea-splitting organisms: suggestive of infection lithiasis • Qualitative cystine Stone analysis
  • 29.
  • 30. Conservative medical management • Fluid recommendations • Dietary recommendations
  • 31. Fluid recommendation • One mainstay of conservative management is the forced increase in fluid intake to achieve a daily urine output of at least 2 litres • Increased urine output may have two effects. First, the mechanical diuresis that ensues may prevent urinary stagnation and the formation of symptomatic calculi. It is more likely that the creation of dilute urine alters the supersaturation of stone components. • Although the 24-hour urine calcium, magnesium, and citrate levels increased directly with drinking hard water, no significant change was found in urinary oxalate, uric acid, pH, or volume. Most importantly, the number of total lifetime stone episodes was similar between patients residing in areas with soft public water and hard public water.
  • 32. • A number of studies suggest that carbonated water offers increased protection against recurrent stone formation as compared to still water. Soda flavored with phosphoric acid may increase stone risk, whereas those with citric acid may decrease risk. • Lemonade and orange juice have long been used as an adjunct to water to provide increased urinary volume as well as increased urinary citrate excretion • Overall, most evidence suggests that it is not the type of fluid ingested that is important for stone prevention but rather the absolute amount of fluid volume taken in per day. We therefore encourage all of our stone formers to drink at least 3000 mL/day to maintain a urine output greater than 2500 mL/day.
  • 33. • Ureteral calculi 4–5 mm in size have a 40–50% chance of spontaneous passage. In contrast, calculi >6 mm have a >15% chance of spontaneous passage. • This does not mean that a 1-cm stone will not pass or that a 1- to 2- mm stone will always pass uneventfully. The vast majority of stones that pass do so within a 6-week period after the onset of symptoms • Ureteral calculi discovered in the distal ureter at the time of presentation have a 50% chance of spontaneous passage, in contrast to a 25% and 10% chance in the mid and proximal ureter, respectively
  • 34. Dietary recommendations • Epidemiologic studies from a number of countries have shown that the incidence of renal stones is higher in populations in which there is an increased animal protein intake. For example, in the northern and western regions of India, animal protein intake is approximately 100% greater than in the southern and eastern regions and the rate of kidney stones is four times greater. • Protein intake increases urinary calcium, oxalate, and uric acid excretion and the mathematically calculated probability of stone formation even in normal subjects. Indeed, according to , ingestion of protein is second only to ingestion of vitamin D in enhancing intestinal absorption of calcium
  • 35. • More recently, the Dietary Approaches to Stop Hypertension (DASH) style diet has been evaluated for its effect on kidney stone formation. The DASH diet is rich in fruit and vegetables, moderate in low-fat dairy products, and low in animal protein. In a prospective population-based study, higher DASH scores were associated with a lower risk for kidney stone formation • Sodium restriction has been widely recommended as an important element of dietary prevention of recurrent nephrolithiasis. When combined with animal protein restriction and moderate calcium ingestion, a reduced- sodium diet will decrease stone episodes by roughly 50%.
  • 36. Other recommendations • Weight loss: increased BMI, larger waist size, and weight gain correlated with an increased risk for stone episodes. This increased stone risk was still more pronounced for women than men • Metabolic syndrome is associated with lower urinary pH. Obese patients have a higher propensity for uric acid calculi.
  • 37. • Dietary calcium restriction actually increases stone recurrence risk. Calcium supplementation is likely safest when taken with meals. Calcium citrate appears to be a more stone-friendly calcium supplement because of the additional inhibitory action of citrate. • Vitamin D repletion is likely safe for stone formers; however, 24-hour urine calcium should be monitored during vitamin D therapy.
  • 38. • general advice on a restricted-oxalate intake might be given to patients with recurrent nephrolithiasis • large amounts of vitamin C may demonstrate increases in 24-hour oxalate excretion and therefore calcium oxalate supersaturation. It seems reasonable to avoid heavy dosing of vitamin C. Limiting one’s intake to a maximum daily dose of less than 2 g.
  • 39. • After 3 to 4 months on conservative management, patients should be re-evaluated using either standard laboratory assays or an automated urinalysis package. If the patient’s metabolic or environmental abnormalities have been corrected, the conservative therapy can be continued and the patient followed every 6 to 12 months with repeat 24-hour urine testing as indicated
  • 40. Medical therapy • One potential criticism of the “selective” metabolic management of nephrolithiasis is that the collection of multiple urine and serum studies can be too time-consuming to be feasible outside of an academic medical centre with its dedicated research staff. Although a commitment to follow-up can be tedious, it should be no worse for patients with kidney stones than it is for those followed for urologic cancer or voiding dysfunction.
  • 41.
  • 42.
  • 43. Absorptive Hypercalciuria Normal calcium intake averages approximately 900–1000 mg/day. Approximately one-third is absorbed by the small bowel. and of that portion, approximately 150–200 mg is obligatorily excreted In the urine. Absorptive hypercalciuria is secondary to increased calcium absorption from the small bowel, predominantly from the jejunum. This results in an increased load of calcium filtered from the glomerulus. The result is suppression of parathyroid hormone, leading to decreased tubular reabsorption of calcium, culminating in hypercalciuria 4 mg/ kg)
  • 44. Absorptive Hypercalciuria Type I Type I absorptive hypercalciuria is independent of diet and represents 15% of all calcareous calculi. There is an elevated urinary calcium level >150–200 mg/24 hour) even during a calcium- restricted diet Type II Absorptive hypercalciuria is dietary dependent. There is no specific medical therapy. Calcium excretion returns to normal on a calcium- restricted diet Type III Absorptive hypercalciuria is secondary to a phosphate renal leak and accounts for 5% of all urinary calculi. Decreased serum phosphate leads to an increase in 1,25-dihydroxyvitamin D synthesis. The physiologic cascade culminates in an increased absorption of phosphate, and calcium, from the small bowel and an increased renal excretion of calcium
  • 45. • Type I: Thiazides directly stimulate calcium resorption in the distal nephron while promoting excretion of sodium. • The retained calcium may be accreted in bone at least during the first few years of therapy. Bone density, determined in the distal third of the radius by photon absorptiometry, increases significantly during thiazide treatment • Dietary moderation of calcium and oxalate, combined with thiazide and potassium citrate, satisfactorily controlled hypercalciuria, while preventing the complication of osteopenia commonly associated with absorptive hypercalciuria. • Hydrochlorothiazide 25 mg PO bid
  • 46. • Sodium cellulose phosphate, given orally, is a nonabsorbable ion exchange resin that binds calcium and inhibits calcium absorption. Is given with the meals. • Unfortunately, despite early enthusiasm, the use of sodium cellulose phosphate has largely fallen out of favor and this medication is no longer available in the United States.
  • 47. • Type II: Moderate calcium intake (400 to 600 mg/day) and high fluid intake
  • 48. • Type III: Orthophosphate (neutral or alkaline salt of sodium and/or potassium, 0.5 g phosphorus three or four times per day) has been shown to inhibit 1,25-(OH)2D synthesis • Best taken as 250 mg three to four times daily. Taken after meals and before bedtime. Orthophosphates do not alter intestinal calcium absorption.
  • 49. Resorptive hypercalciuric nephrolithiasis • A subset (<10%) of patients with clinically obvious primary hyperparathyroidism present with nephrolithiasis. This group represents less than 5% of all patients with urinary stones and are more commonly seen in women. • Parathyroid hormone results in a cascade of events starting with an increase in urinary phosphorus and a decrease in plasma phosphorus, followed by an increase in plasma calcium and a decrease in urinary calcium. Its action on the kidney and on the bone is independent of each other. Ultimately, renal damage is secondary to the hypercalcemia. It limits the concentrating ability of the kidney and impairs the kidney’s ability to acidify urine
  • 50. • Surgical removal of the offending parathyroid adenoma is the most effective way of treating this disease. However, up to 25% of these patients will develop new urinary stones after successful surgery, most commonly seen in men. Attempts at long-term medical management are challenging.
  • 51. Renal-induced hypercalciuric nephrolithiasis • Hypercalciuria of renal origin is due to an intrinsic renal tubular defect in calcium excretion. This creates a physiologically vicious cycle. Excessive urinary calcium excretion results in a relative decrease in serum calcium, which leads to a secondarily increased parathyroid hormone level that mobilizes calcium from the bone and increases calcium absorption from the gut. This step completes the pathologic cycle by delivering increased levels of calcium back to the kidney, whereby the renal tubules excrete large amounts of calcium • These patients have an elevated fasting urinary calcium level, normal serum calcium level, and a secondarily elevated parathyroid hormone level.
  • 52. • Renal hypercalciuria is effectively treated with hydrochlorothiazides. They decrease the circulating blood volume and subsequently stimulate proximal tubular absorption of calcium as well as other constituents. They also increase reabsorption at the distal tubule. Both mechanisms correct the secondary hyperparathyroid state. • To help differentiate primary hyperparathyroidism from secondary hyperparathyroidism in patients with urinary stone disease, one can prescribe a hydrochlorothiazide challenge (50 mg twice a day for 7–10 days). Patients with secondary hyperparathyroidism will have a return to normal serum parathyroid levels, while those with primary hyperparathyroidism will continue to have elevated serum values.
  • 53. Hyperuricosuric calcium nephrolithiasis • Hyperuricosuric calcium nephrolithiasis is due to either an excessive dietary intake of purines or an increase in endogenous uric acid production. In both situations, there is an increase in urinary monosodium urates. Monosodium urates absorb and adsorb urinary stone inhibitors and facilitate heterogeneous nucleation. • Patients have elevated urinary uric acid levels (>600 mg/ 24 hour in women and >750 mg/24 hour in men) and consistently have a urinary pH >5.5. The urinary pH helps to differentiate hyperuricosuric calcium from hyperuricosuric uric acid stone formation
  • 54. • Allopurinol (300 mg/day) may be used to block the ability of xanthine oxidase to convert xanthine to uric acid. The resultant decrease in serum uric acid will ultimately lead to a decrease in urinary uric acid as well. • Allopurinol’s use in hyperuricosuria associated with dietary purine overindulgence also may be reasonable if patients are unable or unwilling to comply with dietary purine restriction
  • 55. Hyperoxaluric calcium nephrolithiasis • Hyperoxaluric calcium nephrolithiasis is secondary to increased urinary oxalate levels (>40 mg/24 hour). It is frequently found in patients with inflammatory bowel disease or other chronic diarrheal states that result in severe dehydration. • Fat restriction is necessary and Oral administration of over-the-counter calcium preparations (0.25 to 1 g four times per day) or magnesium has been recommended for the control of calcium nephrolithiasis of ileal disease • Cholestyramine may be used to bind acidic components in the gut lumen, including oxalate. Intestinal bypass may need to be reversed.
  • 56. Primary hyperoxaluria • Primary hyperoxaluria is a rare hereditary disease. It is associated with calcium oxalate renal calculi, nephrocalcinosis, and other distant deposits of oxalate, culminating in progressive renal failure and eventual death • Oxalate crystal deposits develop rapidly in transplanted kidneys. Combined liver and renal transplantation has cured this previously fatal rare disease • Large doses of pyridoxine reduce urinary oxalate excretion in 20–50% of patients. Neutral orthophosphates may be used to halt the growth of existing calculi.
  • 57. Renal tubular acidosis type I • Sodium or potassium bicarbonate or citrate is given, resulting in an increased renal citrate excretion. • Potassium citrate (20 mEq PO Bid/Tid) therapy is able to correct the metabolic acidosis and hypokalemia found in patients with distal RTA In addition, this medication is capable of restoring normal urinary citrate
  • 58. Stones associated with infection • After surgical removal, antimicrobial prophylaxis should be maintained for 3–12 months. Urinary acidification with ammonium chloride may be used in conjunction. Dissolution of stones with hemiacridrin or Suby G and M solutions is an option. • Stone composition: struvite stones need to be completely removed because of associated infection. Patient should be counselled that multiple sessions maybe needed for the removal of the stone.
  • 59. Uric acid stones • Treatment is centered on maintaining a urine volume >2 L/day and a urinary pH >6.0. Reducing dietary purines or the administration of allopurinol also helps reduce uric acid excretion. Alkalinization, however, is the mainstay of therapy (with oral sodium bicarbonate, potassium bicarbonate, potassium citrate, or intravenous 1/6 normal sodium lactate) and may dissolve calculi • Patients present with a urinary pH consistently <5.5, in contrast to patients with hyperuricosuric calcium nephrolithiasis, who have a urinary pH >5.5.
  • 60. Cystinuria • Potassium citrate is preferred to sodium bicarbonate for this condition. The aim is to increase the urinary pH to 7.5–7.8 • D-penicillamine (250 mg PO OD) may be used which reacts with cysteine to form a soluble salt that reduces, through competition, the formation of cystine. It is a potentially toxic drug and should only be used if hydration and alkalinisation fail. Adverse effects include rashes, fever, agranulocytosis, arthralgia and lymphadenopathy. • 6-mercaptopropionyl glycine (MPG) (100mg PO Bid) is an alternative and has fewer side effects. Captopril (25mg PO Tid) may be used to lower urinary cystine levels in homozygous cystinuric patients.
  • 61. Urosepsis implies clinically evident severe infection of the urinary tract with features consistent with systemic inflammatory response syndrome. It may be associated with multi-organ dysfunction, hypoperfusion, or, hypotension
  • 62. Extracorporeal Shock Wave Lithotripsy • It was during the investigation of pitting on supersonic aircraft that Dornier, a German aircraft corporation, rediscovered that shock waves originating from passing debris in the atmosphere can crack something that is hard. • The first clinical application with successful fragmentation of renal calculi was in 1980. The HM-1 (Human Model-1) lithotriptor underwent modifications in 1982 leading to the HM-2 and, finally, to the widespread application of the HM-3 in 1983 (Figure 17–16). Since then, thousands of lithotriptors have been put into use around the world, with millions of patients successfully treated.
  • 63. Shock wave physics—In contrast to the familiar ultrasonic wave with sinusoidal characteristics and longitudinal mechanical properties, acoustic shock waves are not harmonic and have nonlinear pressure characteristics. There is a steep rise in pressure amplitude that results in compressive forces. There are two basic types of shock wave sources, supersonic and finite amplitude emitters
  • 64.
  • 65.
  • 66. Supersonic shock wave emission from a spark gap electrode. B: Reflecting the shock wave from focus 1 to focus 2 allows for stone fragmentation
  • 67. Piezoceramic finite amplitude emitter. Ceramic components are placed on the concave surface of a sphere and each component is directed to an identified focus
  • 69. • Patients with small renal pelvic stones (<1.5 cm) have approximately a 90% stone-free rate in comparison with those with similar stones in a middle calyx (approximately 75%) or lower calyx (approximately 50%). • Stones can be localised for treatment using either fluoroscopy or USS • Different methods of generating shockwaves include spark gap, electromagnetic, piezoelectric and microexpulsive. Shockwaves generated using the spark-gap method need to be coordinated with the patient’s electrocardiogram (ECG) to prevent cardiac arrhythmias.
  • 70. • This is the common form of treatment these days for renal calculi and stones up to approximately 1.5 cm in size are suitable for this form of treatment. More than one treatment session may be needed to fully treat the stone, especially if it is sizeable. • Prophylactic antibiotics are used to prevent infection as stones are often colonised by bacteria. Cystine stones are relatively resistant to ESWL due to their hardness.
  • 71. • In addition to infection, ESWL may result in haematuria, parenchymal haemorrhage and even perirenal haematoma. A collection of stone fragments in a ureter after ESWL for a significant renal stone is given the German name of steinstrasse (‘street of stones’) • Contraindications to ESWL are obese patients, pregnant patients, large aortic aneurysm and patients taking oral anticoagulants.
  • 72. Right lower pole calculi and steinstrasse in the distal right ureter (arrow).
  • 73. Ureteroscopic Stone Extraction • Ureteroscopic stone extraction is highly efficacious for lower ureteral calculi. The use of small-caliber ureteroscopes and the advent of balloon dilation or ureteral access sheaths have increased stone-free rates dramatically. • Calculi that measure <6–8 mm are frequently removed intact. Nitinol baskets are less traumatic than older round or flat-wired stone baskets. Excessive force with any instrument in the ureter may result in ureteral injury
  • 74. Dormia stone-catching basket in use. (a) Basket introduced past stone. (b) Opened. (c) Enclosing stone, ready for withdrawal.
  • 75. Ureteroscopy. X-ray showing a ureteroscope and guidewire in the ureter.
  • 76. • A variety of lithotrites can be placed through an ureteroscope, including electrohydraulic, solid and hollow-core ultrasonic probes, a variety of laser systems, and pneumatic systems such as the Swiss lithoclast • Stones can also be fragmented using mechanical disintegration using the lithoclast. The most significant complications relate to injury to the ureteric mucosa or wall and include ureteric perforation and extravasation, avulsion of the ureter and ureteric stricture.
  • 77. PERCUTANEOUS NEPHROLITHOTOMY (PCNL) • Percutaneous removal of renal and proximal ureteral calculi is the treatment of choice for large (>2.5 cm) calculi; those resistant to SWL; select lower pole calyceal stones with a narrow, long infundibulum and an acute infundibulopelvic angle • Needle puncture is directed by fluoroscopy, ultrasound, or both, and is routinely placed from the posterior axillary line into a posterior inferior calyx. Superior caliceal puncture may be required, and in such situations, care should be taken to avoid injury to the pleura, lungs, spleen, and liver.
  • 78.
  • 79. • Tract dilation is performed by sequential plastic dilators (Amplatz system), telescoping metal dilators (Alken), or balloon dilation. • Residual calculi can be retrieved with the aid of flexible endoscopes, additional percutaneous puncture access, follow-up irrigations, SWL, or additional percutaneous sessions. • Patients should be informed that complex calculi frequently require numerous procedures.
  • 80. Sequential plastic dilators (Amplatz system) Telescoping metal dilators (Alken) balloon dilation
  • 81. PCNL is indicated for: 1. An obstruction: anatomic abnormalities such as PUJ obstruction, calyceal diverticula or ureteric obstruction might prevent the passage of stone fragments after ESWL. 2. Obese patients in whom ESWL is contraindicated. 3. Lower calyceal stones: these are less likely to pass after ESWL. 4. Stone composition: struvite stones need to be completely removed because of associated infection. As previously mentioned, some stones with a very hard composition are difficult to fragment using ESWL, including calcium oxalate monohydrate and cystine stones.
  • 82. Complications relating to PCNL include: 1. Injury to the spleen, pleura and colon. 2. Haemorrhage from usually the renal parenchyma but also from major renal vessels. If the latter occurs, the treatment of choice is embolisation but, if this doesn’t work, nephrectomy very occasionally has to be considered. 3. Sepsis. 4. Extravasation due to rupture of the collecting system. 5. Retained stone fragments. 6. Open surgery to the kidney is sometimes more complicated after PCNL.
  • 83. Percutaneous renal stone removal. (a) The stone is in the right renal pelvis. (b) Placement of a cannula under radiological control into the renal pelvis and through it a balloon catheter to stop fragments migrating into the upper ureter. (c) The stone is disrupted by contact lithotripsy and the fragments have been successfully removed by irrigation. (d) A nephrostogram confirms that the renal pelvis is intact.
  • 84. OPEN STONE SURGERY • Open stone surgery other than total nephrectomy is incredibly infrequently undertaken. Partial nephrectomy is appropriate with a large stone burden in a renal pole with marked parenchymal thinning. • Long-standing ureteral calculi—those inaccessible with endoscopy and those resistant to SWL—can be extracted with an ureterolithotomy.