Urinary tract calculi Flashcards
intro to kidney stones
urolithiasis = stones in the lumen of the urinary tract (kidney, ureter, bladder)
nephrolithiasis = stones in the kidneys
peak incidence in
40-60 yo men
non-modifiable risk factors for renal stones
- age
- male gender
- ethnicity (white>black>asians)
- +ve family history
- anatomical anomalies in kidneys and urinary tract - eg. horseshoe kidney, ureteral stricture
- cystinuria (AR condition of reduced citrate in the urine)
- associated disease - gout, hyperPTHism
- metabolic disorders that increase excretion of solutes (chronic metabolic acidosis, hypercalcuria, hyperuricosuria)
- renal tubular acidosis
- medullary sponge kidney, polycystic kidney disease
modifiable risk factors for renal stones
- diet - excess Ca2+, oxalate, urate, Na+, so hypercalciuria, hyperparathyroidism, hypercalcaemia
- chronic dehydration - low urinary output increases urinary solutes, increases renal stones
- hot climates - risk of dehydration
- concentrated urine from dehydration - this chemical composition of urine favours stone crystallisation
- obesity - increased risk of uric/Ca2+ stones in obese people with low urine pH, hypercalciuria, uric acid stones
- hypertension
- drugs (Ca2+, vit D supplements)
- immobilisation
- beryllium or cadmium exposure
risk factors for recurrent stone formation
- +ve family history of stones
- previous stones
- early onset of stones
- type of stone - certain types are more likely to recur eg. Ca2+, uric acid, ammonium urate, infection (struvite)
aetiology (causes) of stone formation
when solute concentrations exceed saturation (exceed solubility in water) and crystallise
how do stones form
urine becomes supersaturated with minerals - leading to CRYSTAL FORMATION
crystals pass out in the urine OR stay in the kidney forming stones
types of stones
- calcium oxalate (MAIN)
- calcium phosphate
- uric acid
- struvite (infection stones)
- cystine
- drug-induced
stone formation is determined by
promoters (increase crystal formation and aggregation)
inhibitors (reduce stone formation, even if urine is plenty saturated with minerals)
promoters of stone formation
- calcium
- urate
- oxalate
- cystine
- low urine pH (uric acid)
- low urine flow (dehydration)
inhibitors of stone formation
- citrate (MAIN)
- magensium
- high urine flow
affects crystal formation and aggregation
to stop stones forming, gotta see me high CMH
calcium oxalate stones (MAIN)
associated with
- low urine volume
- hypercalciuria (high Ca2+) due to
*intestinal hyperabsorption of calcium
*reduced renal tubular Ca2+ absorption
*increased Ca2+ mobilisation from the bone (primary hyperPTHism) - hypocitraturia (low citrate)
*remember citrate is the main inhibitor so these stones are very likely to form - not inhibited - hyperuricosuria (increased uric acid)
*cause formation of uric acid stones
*these easily bind to calcium oxalate
*so promotes calcium oxalate crystallisation (as reduces its solubility) so more calcium stones form - hyperoxaluria (increased oxalate) due to
*hereditary, lots made in the liver
*increased diet intake from spinach, rhubarb, beetroot
*increased intestinal absorption w/ fat malabsorption
calcium phosphate stones are less common but they occur when pt has
- high urine pH (increases saturation of urine with Ca2+ and PO4-)
- renal tubular acidosis
certain drugs can promote calcium stones
- loop diuretics
- antacids
- steroids (glucocorticoids)
- theophylline
- acetazolamide
- vitamins C+D
which drugs prevent calcium stones from forming
- thiazides (increase distal tubular Ca2+ resorption, less excreted in the urine?)
uric acid stones caused by
- hyperuricosuria + hyperuricaemia (high uric acid because insoluble > soluble so crystal precipitates) = commonly seen in increased uric acid conditions:
*gout
*metabolic syndrome
*DM
*myeloproliferative/high cell turnover disorders (tumour lysis syndrome, myelodysplastic syndrome)
*purine overingestion (uric acid is a product of purine metabolism)
*diseases with extensive tissue breakdown eg. malignancy
*common in children with inborn errors of metabolism eg. rare hereditary enzyme deficiencies - low urinary pH (develop in acidic urine)
*ileostomy pts - loss of HCO3- and fluid results in acidic urine, causing precipitation of uric acid - low urine volume (dehydration, seen in hot climates)
certain drugs can promote uric acid stones
- thiazides
- salicylates
struvite (infection stones) caused by
- UTI’s with urease producing bacteria (from proteus, Klebsiella, pseudomonas)
so formed from any chronic infections
*bacterial infection hydrolyses urea to ammonium, which raises the urine pH
*this alkaline urine causes Mg, NH4, PO4- precipitate, forming a stone
- eventually struvite stones can form staghorn calculi which involve the renal pelvis and extend into calyceal spaces, forming kidney abscess, urosepsis and reduced kidney function
cystine stones (very rare, only in kids) caused by
- cystinuria causes cystine to leak through the kidneys into the urine
- due to an inherited AR disorder of a defective cystine (Aa) transporter
- so reduced absorption of cystine from PCT/SI
drug induced stones (very rare too) formed by
- crystallised compounds of drugs eg. amoxicillin/ampicillin are poorly soluble so crystallise in the urine
- unfavourable changes in urine composition eg. due to calcium/Vit D
- amoxicillin, loop diuretics increase calcium stones
- thiazides promote uric acid stones inhibit calcium stones
plain x-ray appearance of urinary stones
RADIOPAQUE (white/light) - main COP
*calcium oxalate
*calcium phosphate
RADIOLUCENT (black/dark) - DUA in the dark
*drug induced - penicillins, erythromycin, oestrogen
*uric acid
*ammonium urate
summary of stones
NON-INFECTION STONES
- calcium oxolate : hypercalciuria, hyperoxaluria, acidic urine,
- calcium phosphate : hypercalciuria, alkaline urine,
- uric acid : hyperuricuria, hyperuricaemia (high uric acid in blood and urine), acidic urine
INFECTION STONES
- struvite : alkalised urine from bacterial UTI - proteus, klebsiella
GENETIC STONES
- cystine : defective transporter
symptoms of urinary stones
most pt are ASYMPTOMATIC
but most common symptoms are:
- renal colic pain
- haematuria
what pain with urinary stones?
sudden, severe unilateral flank pain
intensifies with time
LOIN TO GROIN PAIN
radiates from the flank to the iliac fossa, testis or labia
why is renal colic pain described as loin to groin
radiates anteriorly along the abdomen,
inferiorly to the groin, testicles, labia majora,
as the stone moves towards UVJ
what causes the renal colic pain
when stones enter the kidney, renal pelvis, or ureter
and either obstructs it or causes dilation, stretch and spasm while it passes down the ureter
- obstructs urinary flow
because increased tension in the urinary tract stimulates PG release - VASODILATION - increases diuresis and pressure in the kidney when there’s obstruction
also SMC spasm due to PG acting on the ureter, causing oedema and hyperperistalsis
what makes the pain worse
fluids, diuretics, alcohol - increase peristaltic flow so worse pain if urinary tract is obstructed
exertion - mobile calculi move causing pain and haematuria
different sites of narrowing/obstruction from stones cause
different sites of pain
most likely the stone is in the ureteropelvic junction
so causes
classic flank pain
if stone is in the mid-ureter (at the crossing of the iliac artery)
causes
generalised lower abdo pain
if stone is in the distal ureter (at the ureterovesical junction)
causes
groin or referred testes/labia majora pain
associated symptoms with pain
- haematuria
- pallor
- sweating
- n+v due to ileus - reflex response to pain
- rigors, fever if UTI
- urinary retention
- urgency, frequency, dysuria with stones at the ureterovesical junction
- pt is restless - always moving in agony (but lie still when just peritoneal irritation)
differentials of renal colic pain
if there’s less specific groin pain poorly localised to the kidney
- acute pyelonephritis - fever, flank pain, costovertebral tenderness, but pain won’t spread to groin
- MSK pain (with mvt)
- gram -ve septicaemia
- appendicitis - RLQ tenderness at McBurney point
- cholecystitis - RUQ tenderness with Murphy sign (pain felt when dr touching inflamed gallbladder)
- dissection of an AAA - can lead to ruptured AAA esp if pt presents with renal colic for the first time over 60 yo
- colitis/diverticulitis - LLQ tenderness with GI symptoms
- testicular torsion - high riding testicle
- epididymo-orchitis - very tender testes
- ovarian torsion/ruptured cyst - adnexal tenderness
- ectopic preg
haematuria can be
either painless
or with loin/renal colic pain
macrohaematuria is a sign of
large calculi from the bladder
differentials of haematuria
- infection
- malignancy
- trauma
- glomerular disease
bladder stones occur where
stasis + infection come together
- bladder outflow obstruction (urethral stricture, neuropathic bladder, prostate obstruction)
- presence of a foreign body (catheters, non-absorbable sutures)
bladder calculi present w/
bacteriuria
frequency
dysuria
haematuria
severe perineal pain
taking a renal colic history
- symptoms + SQITARS
- previous episodes
- risk factors
physically examining a renal colic
- restless pt in agony, pt lies still with peritoneal pain
- COSTOVERTEBRAL ANGLE TENDERNESS
- pt is apyrexial (no fever) in uncomplicated renal colic, because pyrexia and fever suggests infection so body temp will be very high with pyelonephritis
- low blood pressure
- signs of UTO eg. voiding, intermittent stream, hesitancy
- full abdo exam to exclude differentials
- tenderness when palpating over the loin and reduced bowel sounds
biliary/intestinal colic vs renal colic
renal colic pain is CONSTANT with periods of relief or just a dull ache before it fully returns
whereas biliary colic is INTERMITTENT
also renal colic can move around from loin to groin - and so pt can point to area of most pain for where the stone is currently
complications of renal colic
complete blockage of urinary outflow from kidney
so reduced GFR
so irreversible renal damage
persisting obstruction can predispose to pyelonephritis and pyelonephrosis
if renal stones only cause symptoms after 4 weeks, may be sign of renal function deteriorating, sepsis and ureteric stricture
links between renal stones and CHD, stroke, RCC (renal cell carcinoma), UTUC (upper tract urothelial carcinoma)
rupture of a renal calyx, forming a urinoma
investigating renal stones - basic
urine dipstick
- RBC (haematuria)
- WBC, so leucocytes esterase
- nitrites (UTI)
- pH (<5 suggests uric acid stones, >7 suggests urea-splitting organisms eg. Proteus)
midstream sample of urine
- microscopy (crystals, pyuria suggests infection)
- culture
- sensitivities
bloods
- FBC / CRP (associated infection)
- urea + electrolytes / creatinine (renal function eGFR)
- calcium, phosphate, urate (underlying causes)
- clotting screen (PT/INR) if percutaneous intervention planned
- blood culture (if pyrexial and other signs of sepsis)
chemical analysis for passed stones
- adult pt catches stone through filter, gauze, strainer
investigating renal stones w/ imaging
CT-KUB (non-contrast)
- urgent imaging offered to all pt with suspected stones within 24 hrs
- should be done on all pt, within 14hrs of admission
- also do immediate CT if pt has fever, one kidney or when diagnosis is uncertain to help exclude other diagnoses eg. ruptured AAA
- best diagnosis test, but uses radiation so prefer US above (even tho CT is more widely available and more accurate)
- preferred imaging for adults and replaced IV pyelogram
ultrasonography
- kidney stones shown
- renal pelvis dilation shown
- ureteric stones missed
- offered to pregnant women, children, young adults
NICE guidelines on imaging children
if renal colic suspected in children but has -ve US, use a low dose CT scan
refer children with stones to paediatric dept
overall 1st line diagnostic imaging
adults : low dose non-contrast CT-KUB
children/preg : USS
when pt presents with renal/ureteric stones
- first do urgent diagnostic imaging to confirm diagnosis
- assess likelihood of stone passage
- offer pain relief
pharmacological management
renal colic is painful so ANALGESIA given
- 1st line : NSAIDs for pain relief = diclofenac (IM) but increases risk of CVS events
- if NSAIDs contraindicated/not working : paracetamol (IV)
paracetamol is safe and effective for mild pain, add codeine for more pain relief - if both NSAIDs and IV paracetamol contraindicated/not working : opioids (diamorphine or pethidine)
supportive therapy
- antiemetics
- rehydration therapy
- no antispasmodics
previously medical expulsive therapy was used
alpha-blockers eg. tamsulosin
would aid ureteric stone passage routinely as alpha-adrenergic receptors are present in the distal ureter and detrusor
so used for 5-10mm stones located distally
< 5mm stones that are asymptomatic, manage by
watchful waiting, to pass spontaneously - esp if hydration is maintained
most pass within 4 weeks of symptom onset
- pt shoudl drink lots of fluids
- void urine into a container through a gauze to catch any identifiable calculus
(can even watchful wait for stones that are > 5mm and pt agrees w/ risks and benefits)
watchful waiting can be done as either outpatient/inpatient if
outpatient if
- pt can drink large volumes to relieve pain
- if pain relief offered and fast track diagnostic imaging done
inpatient/immediate hospital admission if
- dehydrated (can’t take oral fluids due to n+v)
- signs of sepsis/shock
- pregnant
- no pain relief
- AKI/pre-existing CKD
- solitary/transplanted kidney
- unclear diagnosis
- can’t arrange imaging within 24hrs
- anuria
more intensive and urgent treatment (SURGERY) needed for
larger stones >2cm so unlikely to pass
pain can’t be tolerated
pt has ureteric obstruction
renal development abnormality (horseshoe kidney)
prev renal transplant
surgical emergency - when there is a ureteric obstruction + infection, the urinary system should be decompressed by
nephrostomy tube placement
insertion of ureteric catheters
ureteric stent placement
non emergency/within 48hrs of diagnosis or admission - treating large stones by
extra-corporeal shock wave lithotripsy (ESWL = 1st line)
percutaneous nephrolithotomy (PCNL)
ureteroscopy (URS)
open surgery (rare, only used if 3 above fail as prefer minimally invasive option)
shockwave lithotripsy (non-invasive, done in outpatients)
focuses shock waves on the stone
causing stone fragmentation
which can then pass spontaneously
CONTRAINDICATED in preg women!!
cons of shockwave lithotripsy
passage of shock waves can develop solid organ injury
fragmentation of larger stones can cause ureteric obstruction
procedure is uncomfortable and analgesia is needed during and afterwards
percutaneous nephrolithotomy
used for complex renal calculi (large stones > 2cm), staghorn calculi, cystine stones
nephroscope inserted into the collecting duct
stone is fragmented using intra-corporeal lithotripsy
stone fragments are extracted through the nephroscope
ureteroscopy (URS)
1st line for ureteral stones > 10mm??
ureteroscope passed retrograde through the ureter, travels up into the renal pelvis
lasers used to break up the stone
indicated for pregnant pt (where ESWL is contraindicated) + complex, larger stones
after the procedure, a stent is left in situ for 4 weeks
different management for pts:
stone < 5mm in all pt = watchful waiting
RETRIEVAL METHODS
stone < 2cm in most pt = ESWL
stone < 2cm in pregnant pt = URS
complex renal/staghorn calculi = PCNL
DECOMPRESSION/DRAINAGE (surgical emergency):
if ureteric obstruction + infection = NEPHROSTOMY tube insertion / ureteric stent insertion
metabolic testing
stone analysis to identify treatable conditions (esp for younger pts with recurrent stone formation)
- cystinuria : cystine stones
- gout : uric acid stones
measure serum Ca2+ (bloods) : high prevalence of primary hyperparathyroidism
preventing recurring stones
all pt should maintain a high fluid intake to ensure a daily urine volume of 2-2.5l
which reduces saturation of solute in the urine
and add lemon juice to water, avoid fizzy
risk factors for recurring stones
- previous stones
- family history
- non modifiable risks
- early onset stones (in childhood)
- stone type (calcium stones, uric acid, struvite stones have increased risk of recurrence)
preventing calcium stones recurring (MAIN)
- high fluid intake (2-3l/day)
- low salt diet (< 6g/day)
- low protein intake
- don’t restrict Ca2+ intake as low calcium diet doesn’t benefit over normocalcaemic diet and restricting calcium causes hyperabsorption of oxalate
if hypercalciuria stone formation persists,
THIAZIDE DIURETICS
- reduce urinary calcium excretion
- increase Ca2+ absorption in the PCT
- increase distal tubular Ca2+ resorption
preventing calcium oxalate stones recurring
- reduce oxalate intake (choc, rhubarb, nuts, spinach)
- potassium citrate - to alkalinise urine to a pH of 7
- cholestyramine/pyridoxine reduces urinary oxalate secretion
preventing uric acid stones recurring
- low urate rich foods (fish)
- long term allopurinol to maintain the serum urate and urinary uric acid excretion in the normal range
- next is long term oral sodium bicarbonate supplements to maintain an alkaline urine (as uric acid is more soluble at alkaline pH, but alkalinisation of the urine facilitates precipitation of calcium oxalate and phosphate)
preventing cystine stones recurring
- potassium citrate or bicarbonate to alkalinise urine to pH of 7
- long term chelating agent penicillamine so cystine is converted to a more soluble form
overall pharmacological of preventing recurrence of
calcium oxalate = potassium citrate
calcium oxalate and hypercalciuria forming stones, even after restricting Na+ intake = thiazide diuretics
uric acid stones = allopurinol
