Renal Colic

Front 1

Definitions

Back 1

Urolithiasis (from Greek oûron, "urine" and lithos, "stone") is the condition where urinary stones are formed or located anywhere in the urinary system.[1] The term nephrolithiasis (or "renal calculus") refers to stones that are in the kidney, while ureterolithiasis refers to stones that are in the ureter

Front 2

Epidemiology

1:10 males & 1:20 females have stone episodes
50% recurrence

Back 2

Epidemiology
Annual incidence 0.2% (US); 0.13% (Aust)
Prevalence 7% males, 3% females
Risk of stone formation M : F = 3-4 : 1
(higher [Ucit] in women)
Peak age 20 - 40 yo
Recurrence rate 10% at 1 yr
(without Rx) 35% in 5 yrs
50% in 10 yrs
Significant impact on QoL

Front 3

Evolution of stone management in Australia: increasing rate of intervention

Back 3

greatest INC in endoscopy

Front 4

Why has treatment rate outstripped incidence of stone presentations?

Back 4

1. Increased rate of detection of asymptomatic stones: greater prevalence
better imaging
2. Lower intervention threshold: opportunistic treatment during intervention for symptomatic stones
3. Loss of efficiency with less invasive Rx

Front 5

Worldwide evidence

Back 5

Worldwide evidence
Increasing incidence and prevalence, more pronounced in industrialized countries
? Lifestyle & dietary factors
? Better medical access – detection
Renal stone formation & predominant stone composition are age & gender dependent
Correlation b/w body wt & Uca excretion
DM independent risk factor for stone development (Taylor & Curhan, AmJKid 2006)
Male preponderance for all stone types except struvite
Lower incidence struvite, uric acid incidence stable or same

Front 6

Dietary factors

Back 6

High protein and salt intake  risk of Ca stones
High purine diets lower UpH and cause hyperuricosuria
Vit B6 deficiency results in ^ formation and excretion of oxalate
Low dietary calcium increases oxalate absorption
Dehydration - excessive fluid loss, inadequate fluid intake
Drugs - Ca supplements, indinavir

Front 7

Dietary Calcium and Oxalate

Back 7

thus need to maintain normal dietary ca (because the oxlate normally binds the ca in the gut and to the faseces..)

Front 8

Geographical factors

Back 8

Higher incidence during summer months & in tropical countries – effect of global warming on US “stone belt” shifting north (est cost $1 bn US by 2050)
? Mechanism -  urinary concentration & acidity or  Vit D production and Ca absorption.

Front 9

Composition of renal stones

Back 9

Front 10

“Doctor, how / why did my stone form?”

Back 10

1. Structural / anatomical problems
2. Stone formation varies with stone type
a. Exceeding supersaturation: uric acid & cystine
b. Infection: triple phopshate (“struvite”) stones
c. Calcium stones: most common but least understood

Front 11

Structural / anatomical problems

Back 11

1. divitculum in the kidney
2. medullary sponge kidney

Front 12

Back 12

divticulium in kidney (thus stagnaented urine)

Front 13

Uric Acid Stones

Back 13

UA: end-product of purine metabolism of endogenous or exogenous sources.
Weak acid (pK 5.4 at physiologic pH)
At urine pH < 5.5 majority exists in its insoluble undissociated form, the major component of UA stone.
With more alkaline urine, more soluble Na urate crystals form (but favours Ca phosphate precipitation)
Round, smooth, yellow-orange; radiolucent
Risk factors: high [urate] - due to high urate excretion (hyperuricosuria) or low Uvol; or low UpH (eg. Idiopathic UA nephrolithiasis - acid urine due to low ammonium excretion, AD disorder, usually male)

Front 14

Cystine stones

Back 14

AR disorder due to mutation of SLC3A1 aa transporter gene on chr 2.
Causes impaired transtubular reabsorption of filtered dibasic aa’s (cystine, ornithine, lysine, arginine), resulting in their excessive urinary excretion
Cystine has low solubility - precipitates in hexagonal plates to form major constituent of cystine stones.

Front 15

Struvite stones
aka Triple Phosphate

Back 15

aka Triple phosphate, infected stone, matrix
Combination of magnesium ammonium phosphate and carbonic apatite
50% contain nidus of another stone composition
Form when urease producing organisms (Proteus, Haemophilus, Klebsiella etc) split urea into ammonia, bicarbonate and carbonate, producing alkaline microenvironment which favours crystallisation of ammonia
Risk factors: those which predispose to UTI ie congenital or acquired anatomic abnormalities, neurologic disorders, foreign bodies

Front 16

Aetiological factors for Calcium stones

Back 16

Ca oxalate develops in acidic urine (pH < 6)
Ca phosphate develops in alkaline urine (pH > 7.5)
Ca phosphate stones - risk factors: UTI, hyper PTH, RTA
Promoters of Ca oxalate stones include:
Hypercalciuria
Absorptive (intestinal)
Renal leak
Resorptive
Hypercalcaemic
Hypocitraturia
Hyperuricosuria
Hyperoxaluria

Front 17

Stone formation: latest evidence
Human stones arise by one of these pathways:

Back 17

Overgrowth of stones on plaque – idiopathic ca ox
Primary interstitial apatite crystal formation - Randall plaques (Lingeman, 2003)
Plugging of collecting duct, with growth on plugs or growth of expelled plugs in free solution –
Hyperoxaluria, RTA, cystinuria
Formation in free solution –
Crystal accumulation in lumen of tubules (cap) & erosion
Binding of ca ox & growth – mixed ca ox / phosphate stones
Calcification & atherosclerotic-type lesions in vasa recta

Front 18

Randall Plaques

Back 18

CaPh crystals and organic matrix initially deposited along BM of thin loop of Henle, and extend further into the interstitial space to the urothelium, constituting the so-called “Randall plaque”.
These CaPh crystals seem to be the origin for development of future CaOx stones, which form by attachment of further matrix molecules and urinary CaOx to the plaque.
Cause of idiopathic Ca Ox stone formation. Described by Randall 70 yrs ago on autopsy studies; more recently demonstrated in all idiopathic CaOx stone formers (vs zero in healthy controls; Evan, Lingeman et al, 2003) – demonstrated to connect stones to papilla on microscopic CT. Urothelium is lost at attachment site. No intratubular cystallization in tubules / CD’s in these patients.
Positive correlation between frequency of stone recurrences and total papillary surface area covered by plaques (Matlaga, 2006)
Currently unknown in this model – initial trigger for crystallization, driving forces, exact pathogenetic mechanisms, involved matrix molecules

Front 19

Clinical manifestations

Back 19

Asymptomatic - incidental discovery during unrelated Ix.
Pain - mild ache
Renal colic
occurs when stones produce obstruction
severe, sudden onset, intensifies over 15 - 30 min
Assoc nausea & vomiting
Can’t sit still or get comfortable (DDx to lower back pain)

Front 20

Sites of Obstruction

Back 20

Calyx / infundibulum (dull pain- due the low pressure)
PUJ
Pelvic brim, arching over iliac vessels
Posterior pelvis (females) under broad lig / pelvic vv
Above intramural ureter / VUJ - most common

Front 21

Assessment

Back 21

History: ? underlying cause for stones
Gout, FHx, IBD, hypercalcaemia
Examination: fever, sepsis, tenderness
MSU: pH - low: Urate, Ca ox
high: Ca phos
infection
Bloods: WCC often raised, >15 ? Infection
UEC, Ca, Urate

Front 22

Investigation

Back 22

1.Radiology
2.FBC UEC
3.Urinalysis / microscopy / culture
4.Delayed - stone analysis
serum Ca / UA / PTH
24 hr urine

Front 23

KUB

Back 23

In medicine, KUB refers to a diagnostic medical imaging technique of the abdomen[1] and stands for Kidneys, Ureters, and Bladder.

Quick, inexpensive and easily obtainable
Variable sensitivity - 60 - 90%
Useful adjunct to CT as a method of predicting stone composition – radiolucency = uric acid ? Dissolution Rx
Useful for follow up
KUB unless concerns about obstruction or stone lucency; then US or low dose NCCT
1-2% of cancers in US may be attributed to CT radiation

Front 24

Radiological investigation

Back 24

KUB
IVU
Renal U/S
Non-contrast helical CT

Front 25

Intravenous pyelogram (IVU)

Back 25

Variable quality
Functional study
Radiation dose less than CT
Good anatomical detail for planning appropriate treatment

Front 26

Renal Ultrasound


Back 26

Procedure of choice for pregnant females
Assess for other causes of acute pain
Not a functional study
Hydronephrosis  Obstruction

Front 27

Non-contrast helical CT Abd/Pelvis

Back 27

Fast, highly sensitive and specific > 99%
Strictly speaking is not a functional study, but can infer obstruction by indirect signs ie perinephric stranding, urinoma
Can use in patients with contrast allergy
Greater ability to detect alternative pathology
Good anatomical detail with coronal reconstruction
CT for prediction of stone composition
CT densitometry: stone > 1000 HU more likely to fail SWL
Stone size, position & skin-to-stone distance also assessable on NCCT and determine outcome

Front 28

Management

Back 28

1. Analgesia - oral, PR, parenteral
- NSAIDs, narcotics
2. ?? iv fluids - if dry (otherwise too much water can be painful)
3. Determine if renal unit is
- obstructed
- infected -> URGENT DRAINAGE
4. Other criteria for admission - ongoing pain, solitary kidney, renal impairment, pregnant
5. Rx: Conservative or Definitive if required -URS, SWL
6. Prevention – investigation of causes of urolithiasis, lifestyle modification, medication

Front 29

Treatment options

Back 29

Conservative:
Consider chances of spontaneous passage -
> 6 mm : 10%
4 - 6 mm : 50%
< 4 mm: 90%
Role of medical expulsive therapy - tamsulosin
Drainage:
Nephrostomy
Stent
Definitive
Ureteroscopy
SWL
PCNL
Laparoscopic or open surgery

Front 30

Spontaneous passage

Back 30

Front 31

Ureteroscopy

Back 31

Front 32

ENERGY SOURCES

Back 32

EHL
EKL, “lithoclast”
Laser

Front 33

Laser lithotripsy

Back 33

Ho:YAG – solid-state laser, 2100nm wavelength, pulsed
Photothermal & photodynamic capacity: thermal fragmentation most efficient
Pros: short tissue penetration due to water absorption(0.5 –1 mm), diverse applications incl stricture incision & tumour ablation, small fibers (0.2 – 0.6 mm)
Cons: long pulse width (= lower pulse energy), ureteric injury
Remains the best laser for stone disease in 2012

Front 34

SWL

Back 34

Requirements:
Shock wave generator
Coupling mechanism
Localisation
Image intensifier
US

Front 35

SWL – how does it work?

Back 35

Shock wave -> negative pressure bubble - acoustic cavitation; combined with positive (compression) wave causing shear / tensile stress.
Vascular response: transient but marked reduction in renal perfusion/GFR; structural changes due to rupture of small blood vessels with subsequent haemorrhage
Poor understanding until recently considering its broad utilisation
Recent evidence from US suggests increased incidence of DM & HT in patients treated with SWL.

Front 36

Back 36

Front 37

Percutaneous nephrolithotomy

Back 37

Principles:
Access
Removal
Drainage
Combined Rx

Front 38

Management of recurrent stone formers

Back 38

General
Fluids - how much ??
Lime / orange juice - boosts urinary K cit levels, increases bicarbonate release
Specific
Dietary advice - reduced protein, oxalate, NOT calcium
Hyperuricosuria - Allopurinol, urinary alkalinisation
Hypercalciuria - chlorthalidone

Front 39

AVOID…

Back 39

Front 40

Dietary Factors

Back 40

Fluids: 1996 RCT showed 5yr stone recurrence rate 12%(high uo) vs 27% (low vol uo)
Lemonade / OJ increase urinary citrate
Animal protein (meat, chicken, fish) increases urinary ca, UA and phosphate.
Salt increases ca & UA excretion. Restrict < 6g/day.
- do not restrict Ca
-

Front 41

Specific measures

Back 41

Dissolution therapy (uric acid stones)
hydration
pH manipulation – potassium citrate / sodibic
Allopurinol if hyperuricosuric
Hypercalciuria - Thiazides
Cystinuria – fluids, low protein, alkaline urine (Uro-cit-K); binders – thiola, penicillamine

Front 42

Renal Colic - Important DDs

Back 42

Abdominal aortic aneurysm
Retro-caecal appendicitis
Torsion of testis

Front 43

Dietary Advice for Stone Formers

Back 43

Increased fluid intake (2L urine/day)
Normal calcium intake
low oxalate intake (colas, tea, nuts, spinach/rhubarb)
Reduce salt intake

Front 44

Medical Treatment of Calcium Stone Formers

Back 44

Hypercalciuria
Exclude and treat hypercalcaemia (hyperparathyroidism, renal tubular acidosis, sarcoidosis)
Thiazide diuretics (HCT, Indapamide) enhance Ca reabsorption
Hypocitraturia
Lemon juice (120mls in 2L water)
Potassium citrate
Hyperoxaluria
Low oxalate diet, correct acidosis,oxalate binders
Hyperuricosuria
allopurinol

Front 45

Uric Acid Stones Tx

Back 45

Radiolucent
Causes
hyperuricaemia
gout
diuretics
high purine diet
Effective medical therapy (alkalinise urine to pH >6.5 and allopurinol) – the only stone that can be dissolved

Front 46

Staghorn Stones

Back 46

Infection stones (Urease producing Gm –ve , not E Coli)
Often no loin pain or presents with recurrent UTI
Risk of progressive renal damage / sepsis
Usually treated by Percutaneous nephrolithotomy +/-ESWL or retrograde pyeloscopy for any residual fragments