泌尿系统结石URINARY

泌尿系统结石URINARY 泌尿系統結石URINARY STONES 教學目標 最終目標(Terminal objectives) 針對一位泌尿道結石病患,醫學系六年級學生能收集必需的臨床資訊,執行適當的檢查,做出正確的診斷及列出治療的。 執行目標(Enabling objectives) 1. 能說出常見泌尿系統結石的分類 2. 能清楚描述出結石流行病學 3. 看到及描述Renal coli病人痛時的情形 4. 能針對患者的臨床資訊安排適當的檢查項目 5. 能列出結石病患的臨床處置及治療方法 6. 能實際參與體外震波碎石治療術的施行 貳:參考資料 th, Urinary stone disease (Chapter 17), in: Smith’s General Urology, 15 edition, 2000, Lange Medical Books/ McGraw-Hill. , Charles YC Pak, Martine I Resnick: Medical therapy and new approaches to management of Urolithiasis, Urol. Clinics North America, 2000, (27): 243-53 , Studies & papers of Prof. Lee, Y. H. 簡介: URINARY STONES Theories of stone formation Nucleation theory Stone matrix theory Inhibitor of crystallization theory More than one factor in causing stone diseases. Epidemiology Intrinsic factor Heredity Family history First degree relative 30% versus 15% in a p’t with stone. Family history: increase in multiple and early recurrences Spouse: increased incidence of stone. Age and sex 1 Male: female = >3:1 30-50 adults Extrinsic factor Socioeconomic factors: Industrialized countries are more common, soft water no change. Diet: Risk factors: Animal protein, fat, sugar, high Na, Fluid intake: Low urine volume 1. Low urine volume: < 1000 ml/day 2. Inadequate urine volume: < 2000 ml/day 3. Minimal fluid ingestion 4. Chronic diarrheal state Occupation: Risk factor: Physicians and white-collar worker, high temperature Climate: Risk factor: Hot climate: esp. uric acid stone Sunshine (?) Medications: Additional risk factors Metabolic state Environmental factor Dietary excesses Protein & fat excess Anatomic abnormalities Possible stone promoters: Ions: Ca, Oxalate, Phosphate, Uric acid, Na, Possible stone inhibitor: Citrate, Mg, Sulfate, Glycosaminoglacans, Pyrophosphate, Uropontin Stone formation site theory Mass precipitation or intranephroinic stone theory: distal tubules or collecting duct Fixed particle theory: occur on tips of renal papilla as submucosal plaques Stone forms in obstructed lymphatics 尿路結石之病因學 concentrated urine Excessive excretion of low soluble substance in urine Urine stasis & urinary tract infection Less in inhibition substance for stone formation in the urine SYMPTOMS AND SIGNS 2 Symptoms related to stones at specific sites Caliceal stones asymptomatic gross hematuria flank pain recurrent infection Renal pelvic stones asymptomatic intermittent flank pain infection with fever Proximal ureteral stones sharp flank pain nausea, vomiting Distal ureteral stones intermittent sharp pain radiating to scrotum in man and labia in women Associated nonrenal symptoms Autonomic nervous system relationship nausea, vomiting, abdominal distention from reflex ileus. PHYSICAL EXAMINATION P't toss about and unable to find comfort in any position Diaphoresis, tachycardia, tachypnea, palpation or knocking Tenderness over flank LAB. FINDING Microscopic or gross hematuria Pyuria Bacteriuria Presence of crystals in urine RADIOGRAPHIC FINDINGS At least 90% stone are radiopaque. Stone of Ca. phosphate-- most radiopaque Radiolucent---composed solely of uric acid or matrix IVU R-P Sonography CT Stone size < 4 mm: most pass spontaneously , 4-6 mm: 50% pass spontaneously Treatment for ureteral colic and promotion of spontaneous passage of stone 1. Initial analgesia 2. Extended spasmoanalgesia (promotion of spontaneous passage) 3. Adjuvant therapy 1. Anti-edema therapy 2. Increased diuresis 3 3. Physical exercise Compared between treatment of colic by acupuncture and analgesics Acupuncture was better CALCIUM STONES As Ca phosphate or Ca oxalate or mixed of both Ca oxalate is solely or major component of 80% of stones as monohydrate, dihydrate or both Ca phosphate as more common apatite Ca[PO][OH]10462 less common brushite CaHPO-2HO42 Epidemiology Highest in 30-50 years of age In men is 3 times more than in women: testosterone effect , Liver enzyme and testosterone and oxalate Probable cause dehydration sedentary life style food(rich in Ca, p, oxalate) amount of water Solitary defect: Hypercalciuria: 12%, Hyperuricosuria: 8%, Hyperoxaluria: 5%, Hypocitraturia 17%, No identifiable metabolic defect: 1/3 Diagnosis evaluation Screen studies CBC, U/A, U/C, electolytes Complete metabolic evaluation Radiological evidence of new stone formation or stone growth or documented passage of gravel within 1 year Criteria of hypercalciuria Urine excretion of Ca > 300 mg/d (male), Ca> 250mg/d (female) or 4 mg/kg/d HYPERCALCIURIA Ca absorbed from G-I tract , most in duodenum and upper jejunum Active absorption by a Vit-D dependent Ca-binding protein Some by passive diffusion Absorptive hypercalciuria 3 types: Type 1: Independent of diet. >150-200mg/24h; 4mg/kg Cellulose phosphate resin bind Ca in the gut to lower urine Ca Taken with meal: contraindicated in postmenopausal women and children Hydrochlorothiazides to reduce renal excretion of Ca. 3-5 year Type II: 4 Diet dependent Calcium restriction to 400-600 mg/d. < 200 ml /day milk 少吃甲殼類食物 or sea foods 以毒攻毒 Type III: 2nd to phosphate renal leak to increase Vit. D to increase Ca absorption and renal excretion Orthophospate (Neutra-Phos) Medical treatment Diet Na (100 meq/d) restriction Rich in natural fiber to bind diet Ca to be an insoluble and un-absorbable complex Avoid colas, fruit juices, tea, spinach Hydration Maintain urine output of 2L/d Cellulose phosphate An ion exchange resin Exchange Na for Ca in G-I tract Take with meal 5 g 2-3 times /d Orthophosphates By decreasing urine excretion of Ca and increasing urine excretion of pyrophosphate and citrate (2 potent inhibitors of Ca stone formation in urine) 3-6g/d Renal hypercalciuria kidney fail to conserve Ca Stimulate parathyroid hormone secretion, increase Vit-D3 , increase Ca absorption from G-I or bone High fasting Urine Ca, 2-nd elevated PTH. Hydrochlorothiazide challenge test: 50 mg b.i.d for 10 day. 2-nd: return to normal PTH Medical treatment Thiazides Decrease renal excretion of Ca Effect begin 2-3 days after start, to max. in 6 days. Hydrochlorothiazide 50 mg bid /d Resorptive hypercalciuria In p't of hyperparathyroidism About 4-6% of Ca stone p't More in female than in male Excess secretion of parathyroid hormone induce bone destruction and increase G-I Ca absorption Hypercalcemia Other cause Cushing disease, hyperthyroidism, multiple myeloma, metastatic 5 ca, prolonged immobilization. Treatment Surgical resection of the abnormal parathyroid tissue NORMOCALCIURIA Maintain optimal weight Drink 10 glasses of water Moderate intake of Ca. Thiazide Citrate intake Decrease oxalate intake Other metabolic disorders associated with Ca stones Sarcoidosis Due to increased sensitivity of the intestinal epithelium to vit-D3 Treatment Corticosteroids Renal tubular acidosis Persistent metabolic acidosis Three types reported only type I associated with stone formation Type I renal tubular acidosis AD 70% female 70% of p't form Ca stones decreased urine citrate level moderate hypercalciuria urine PH always > 6.0 Stone formation is due to hypercalciuria and low urine citrate Stone frequently of pure Ca phosphate Incomplete type can make urine PH to 5.4 but not lower. HYPEROXALURIA Ca STONE Oxalic acid --end product of metabolism Extreme insolubility of the Ca salt of oxalate Minimal affected by change in the PH of urine Rich in green leafy vegetables, cranberries, plums, tea , cocoa, almonds, carbonated beverages, and coffee. Oxalate poorly absorbed from G-I tract , only 2.3 to 12 % absorbed. Endogenous oxalate From 2 major sources: ascorbic acid and glyoxalic acid Criteria: 40 mg/24h urine oxalate Primary hyperoxaluria AR Recurrent Ca oxalate stones in children Result in nephrocalcinosis and death from renal failure before 40. Two types type I: Glyoxalate carboligase deficiency type II: D-Glycerate dehydrogenase deficiency Treatment large dose of pyridoxine (100-400 mg/d) bid 6 maintain large urine volume restriction of food rich in oxalate Ingestion and inhalation hyperoxaluria Ethylene glycol: ingredient of antifreeze solutions Ascorbic acid: chronic intake if >5 g/d Enteric hyperoxaluria Occurs in inflammatory diseases of the G-I tract or small-bowel bypass surgery or intestinal mal-absorption syndromes, or chronic diarrhea ( usual Ca + oxalate as non-absorbable salt, but with this syndrome the unabsorbed fatty acid bind with intra-luminal Ca , thus oxalate increase.) Treatment Low oxalate diet, increase fluid intake (urine 3-4 L/d), low fat diet, oral Ca, or other cations, e.g. Mg supplements, ( bind oxalate), or reversal of the intestinal bypass. K-citrate (20 meq tid/d) HYPOCITRATURIA Ca STONE A possible contributing factor in 19-63% of all p'ts with stone Citrate act as an inhibitor for stone formation by Complexing urine Ca to decrease saturation of Ca-P, Ca-oxalate act by inhibiting crystal nucleation formation, decrease monosodium urate < 320 mg/24h treatment K-citrate (20 –30meq b.i.d or tid/d) or 6-8 glasses of lemonade CYSTINE STONES AR;, chromosome 2p.16, and 19q13.1 Impaired reabsorption of dibasic amino acid (cystine, lysine, ornithine, arginine) from renal tubule and G-I tract 1-4% of stones (Taiwan, < 0.5%) Low solubility of cystine in urine but higher in more alkaline urine Normal daily cystine excretion : < 100 mg/d Diagnosis Urine is acidic, contain hexagonal cystine crystals X-ray show ground-glass appearance. Stone analysis Urine sodium cyanide nitroprusside test Medical treatment 3 principles Decrease the total cystine conc. in urine Increase the solubility of cystine in urine Decrease urinary excretion of cystine Hydration Maintain urine output of about 2 ml/min (3L/d water intake) Alkalization of urine: > PH 7.5 7 To PH 7.5 the solubility to more than 800mg/L Na-bicarbonate 15-20 g/d Na-K-citrate 60-80 meq/d Direct irrigation of stone via R-P with alkaline sol. Cystine -binding drugs Penicillamine: D-penicillamine can bind with cystine to form a cystine-S-penicillamine complex 50 times more soluble than cystine. 1-2 g/d Alpha-mercaptopropionylglycine:like penicillamine Methionine restriction Methionine is the dietary precursor of cystine INFECTION STONE (STRUVITE STONES) Occur 2 times in female than male 15-20% of all stones Composed of magnesium ammonium phosphate [MAP] (MgNHPO-6HO ) and carbonate apatite ( Ca[PO4]-CO )4421963 Infection with urea-splitting bacteria, the bacteria can alkaline the urine above PH > 7 , increase bicarbonate and ammonium ions conc. Stone precipitate at pH>7.19 Common urea-splitting bacteria Proteus, Pseudomonas, Klebsiella and staphylococcus, Providencia, Mycoplasma. Frequently become staghorn type Treatment Surgical removal is the choice Medical is only adjunctive. Chemical dissolution Hemiacidrin, Suby G solution Urease inhibitors Acetohydroxamic acid and hydroxyurea Follow-up and prognosis Treat all possible infection and long-term prophylactic Rx Stone recurrence rate :30% within 6 years ( Regular medical prophylaxis: 7.8% Irregular medical prophylaxis: 30% No medical prophylaxis: 46.1% Lee) URIC ACID STONES Only human and Dalmatian dogs to develop Uric acid: end product of purine 2 types of uric acid in urine: Insoluble uric acid and 20 times more soluble urate salt. Radiolucent stone Classification 4 categories of uric acid stone disease Idiopathic uric acid lithiasis 8 Stone with hyperuricemia Metabolic abnormality: gout Myeloproliferative disorder: lymphoma Receive chemotherapy with increased cell destruction, or rapid weight loss. Stone with chronic dehydration Chronic diarrhea, ileostomy p't Stone with hyperuricosuria without hyperuricemia Thiazide or salicylate can cause hyperuricosuria Treatment( most medically ) Hydration: at least 2L/d Alkalization of urine: pH> 6.0 Oral: Na-bicarbonate 650-1000 mg every 6-8 hrs, or K-bicarbonate or K-citrate to maintain a urine PH 6.5-7.0 Ureteral irrigation Na-bicarbonate solution irrigation stone via R-P IV alkalization lactate 1 mol/L Diet Low purine food, limit protein intake to 90 g/d Allopurinol 200-600 mg/d Prophylactic measures Maintain urine > 2L/d Restrict protein intake TREATMENT OF URINARY STONES Treatment of urinary stone ( renal and ureteral stones ) Conservative treatment Complication of conservative treatment 1. Infections 2. Urinary obstruction Surgery Indication for surgery 1. intractable urinary tract infection 2. Progressive renal damage 3. Urinary obstruction 4. Persistent pain Methodology of treatment of urinary stones SWL Endourological manipulation Advantage: Decreased morbidity Shorter hospital day and convalescence period Lack of abdominal or flank incision PCNL Ureteroscopy Success rate for stone retrieval 9 Upper 1/3: 22-60% Middle 1/3: 36-83% Lower 1/3: 84-99% Laparoscopy Anatrophic surgical management Chemolysis Control by medicines and foods Treatment of renal stone PCNL ESWL Stone size and treatment < 2 cm: SWL 2-3.5 cm: D-J stenting & SWL > 3.5 cm: PCNL & SWL TREATMENT OF URETERAL STONES Expectant therapy 90% < 4 mm stone pass spontaneously URS-SM Surgical Stone recurrence 50-70% within 5 years BLADDER STONES Primary is rare, believed related to low protein and P diet or dehydration Secondary is due to urinary stasis (outlet obstruction e.g. BPH, neurogenic bladder), or chronic UTI. Treatment Transurethral irrigation EHL Open vesicolithotomy URETHRAL STONES Primary rare Secondary Urethral diverticulum, stricture, foreign body in urethra, etc. Treatment Surgical repair of underlying disease EHL 10