S10C97 - Urologic Stone Disease Flashcards
Epidemiology of stones
MEN
- first episode usually b/w 20-50yo
- rarely have 1st episode >60yo
WOMEN
-bimodal: 35yo and 55yo
PEDS: usually from metabolic d/o, urologic anomaly, infx or immobilization
Types of stones
- calcium oxalate
- calcium phosphate
- struvite: magnesium ammonium phosphate – most common cause of staghorn calculi
- urate stones - from elevated uric acid, assoc with gout, radiolucent
- cystine stones - caused by autosomal recessive d/o
- other: indinavir, triamterene, xanthene, silicate
- calcium excretion is increased by hperparathyroidism, renal hypercalciuria, immobilization
- oxalate excretion is increased by IBD , small bowel resection, jejunoileal bypass
- struvites are caused by bacterial infxn that split urea (proteus, klebsiella, staph, providencia, corynebacerium) and b/c Abx don’t penetrate stones surgery is required for staghorns otherwise sepsis can occur
Renal colic pain
- caused by ureter spasm
- also caused by hydronephrosis and pressure against gerota fascia leading to flank pain
How long does it take for irreversible renal damage to occur if complete obstruction by stone?
- 3w
- during acute obstruciton often there is no rise in creatinine b/c the other kidney functions at 185% of baseline
Sites of obstruction:
- obstructed stones have lower rates of spontaneous passage
- ureteropelvic jxn
- pelvic brim (where ureter crosses over pelvis and iliac vessels)
- ureterovesical jxn
- ureterovesical junction
Passage of stones:
- 98% of 7mm will pass w/in 4w
- stone size on plain xr are magnified up to 20% and stones on CT are 88% of actual stone size
Risk Factors for Kidney Stones
- bowel dz: decreases urine volume and causes acidic urine
- excess meat intake
- excess dietary oxalte
- excess dietary sodium
- family history
- insulin resistance: ammonia mishandling, alters pH of urine
- gout: increases uric acid in urine
- dehydration, low urine volume
- obesity: promotes hypercalciuria
- primary hyperparathyroidism
- prolonged immobilization: bone turn over creates hypercalciuria
- renal tubular acidosis (Type 1): alkaline urine promotes calcium phosphate
Clinical presentation of nephrolithiasis:
- acute onset
- crampy intermittent pain
- originates in flank, radiates to groin
- n/v
- tachy, HTN, diaphoresis
- hematuria in 85%, gross hematuria in 30%
3 important pieces of info on hx:
- ask about risk factors for stones
- ask about risk factors for poor outcome (solitary kidney, DM, HTN, pre-existing kidney dz, transplant, hx of stents/extractions, symptoms of sepsis)
- risk factors for mimickers of stones (AAA, renal artery infarction)
**renal artery infarction won’t be detected on CT-kub b/c too early to see swelling and can’t see blood flow
Diagnosis of nephrolithiasis:
-clinical suspicion, hematuria and confirmation with diagnostic imaging
-labs: evaluate for infection, kidney dysfunction, pregnancy
u/a, Cr/GFR/BUN, beta-hCG
- 15% of pts with nephrolithiasis have no hematuria
- 24% of pts with flank pain and hematuria have no radiographic evidence of ureterolithiasis
Imaging in nephrolithiasis
- purpose: identifies stone and location, r/o other dx, identifies complications, assists with management
- all pts presenting for first time with renal colic should be imaged, rpt imaging depends on hx of complications, alternate diagnoses, cumulative radiation
- non-contrast CT: 97% sens, 99% specif
- IV urogram 64-90% sens, 94-100% specif (evaluates renal fxn however it requires a contrast load)
- U/S: 63-85% sens, 79-100% specif (good for pregnancy, misses stones 22% of hydronephrosis will be d/t abn anatomy, full bladder, renal cyst)
- AXR: 29-58% sens, 69-74% specif (poor sens/spec)
-low-dose CT: as good as non-contrast CT in stones >3mm and BMI
Renal colic: DDx
*** dissected or ruptured AAA
Vascular: Ao dissection, AAA, renal artery embolism, renal vein thrombosis, mesenteric ischemia
Renal: pyelonephritis, papillary necrosis, RCC, renal infarct, renal hemorrhage
Ureter: blood clot, stricture, tumor
Bladder: tumor, variocse vein, cystitis
GI: biliary colic, pancreastitis, perforated PUD, appendicitis, inguinal hernia, diverticulitis, cancer, obstruction
Gyne: ectopic, PID, abscess, ovarian cyst, ovarian torsion, endometriosis
Other: drug-seeking, shingles, retroperitoneal hematoma/abscess/tumor
Nephrolithiasis: treatment
-pain: NSAIDs
NSAIDs act on ureter by inhibiting prostaglandin synthesis, IV provides more rapid relief –> toradol 30mg IV
narcotics aren’t good for addressing cause of pain but are good analgesics
-n/v: maxeran is only anti-nauseant that has been studied, also provides pain relief equivalent to a narcotic
(maxeran = dopamine antagonist)
-abx if infected: gentamicin/tobramycin 3mg/kg/d divided Q8h
OR ticarcillin-clavulanic acid 3.1g q6h
OR ciprofloxacin 400mg q12h
if no obstruction/fever/systemic illness then can be treated as o/pt (levofloxacin 500mg OD x10-14d)
Abx should cover gm- rods
-medical expulsion therapy
alpha-blockers increase rate of expulsion, decrease time to expulsion (by 2-6d), decrease pain, NNT 3.3
better for stones in distal 1/3 of ureter
fllomax 0.4mg PO OD x4w
terazosin 5-10mg OD is as effective
- IV hydration makes no difference in pain control or stone passage compared to minimal IV hydration, give fluids to correct fluid deficits from vomiting or decr intake
- consider steroids
Nephrolithiasis: pts requiring admission
Absolute Indications for Admission
- frail elderly/severe comorbidities
- solitary kidney with complete obstruction
- ureterolithiasis with hydronephrosis and fever
- urosepsis
- intractable n/v
- AKI
- hypercalcemic crisis
close f/u if:
- renal insufficiency
- severe undelrying dz
- IV urogram with extravasation or complete obstruction
- multiple ED visits
- stone >6mm
- sloughed renal papillae
- assoc UTI w/o sepsis
- pts with >5mm proximal stones (less success at spontaneous passage)
-everyone should f/u with a urologist in 7d if not sooner
Average time for stone passage:
-7-20d for stones 5-6mm
