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Persistent UTI

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Persistent UTI

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  1. Recurrent / Persistent UTI andManagement of Kidney Stones Julian Mander RPH Urology

  2. Persistent UTI Persistent UTI implicates an underlying infective focus, not cleared until the underlying problem is dealt with. Always the same organism on MSU. MSUs remain positive after treatment and between clinical episodes. Classically Proteus and infection staghorn stones, classically older females. Infection not cleared unless stone cleared. In males, commonly persisting prostatic infection, typically not cleared with cephalexin or amoxycillin – use trimethoprim or norfloxacin (or ciprofloxacin) in men.

  3. Recurrent UTI Recurrent UTI means reinfection, typically with varying or different organisms. Definition: Three or more MSU documented UTIs within 12 months. 3% of women, uncommon in men. Urine cleared of bacteria in between clinical episodes c/f persistent UTI not cleared.

  4. Recurrent UTI 1/3 of women with recurrent UTI in adult life had their initial UTI during childhood. UTIs tend to occur in clusters in those with recurrent UTI. Predisposing factors are unclear – sexual intercourse in women estrogen deficiency in post menopausal women altering vaginal flora Role of residual urine poorly studied, assumed that PVR > 100 ml associated with recurrent UTI (?180 ml), but PVR proportional to starting volume and bladders always overfilled for U/S.

  5. Pathophysiology Recurrent UTI Bacteriuria is common in women, but established UTI/cystitis relatively uncommon – why do some women get recurrent UTI whilst most don’t ? All bacteria invading the urinary tract activate an inflammatory response in terms of neutrophil infiltration, important to clear the bacteria. Extent to which different organisms activate the inflammatory response varies markedly, and the relationship of this activation to different disease states is complex. Deficiency in activation of inflammatory response in some people predisposes them to infection. Bacterial attachment to mucosa is important, bacteria – host interaction here is important and poorly understood.

  6. Secretor Status Mendelian dominant inherited characteristic of secretion of water soluble form of antigen immunodominant sugars - Blood group A: N acetyl-D-galactosamine B: D-galactosamine Non secretors linked with relative deficiency of certain immunoglobulin classes. Non secretors have more infections, including UTI’s. Suggestion that non-secretors have less efficient immune systems

  7. ABO Blood Group Status Blood group B have 50% greater chance of UTI than non-B group. Blood group AB also have a higher incidence of UTI. Absence of anti-B isohaemaglutinin renders individual more susceptible to UTI. Large number of bacteria cross react with anti ABO blood group isohaemaglutinins. These cross reacting antigens vary in their immunogenicity. “B-like” immunogen is particularly antigenic and may increase the naturally occurring isohaemaglutinins, inhibiting bacterial attachment and colonization and increasing susceptibility to compliment.

  8. Humoral Response Superficial infection results in the formation and release of secretory IgA. UTI causes a selective and up to four fold increase in IgA secretion. Some adults with UTI appear to have a defect in the maturation of sIgA. Superficial vs Intracellular infection – recent work on intracellular infection and the detection of IBCs – intracellular bacterial communities – relevant to clearance of infection and persistent UTIs. Moving from superficial to intracellular infection is poorly understood, but humoral and subsequent inflammatory response and neutrophil recruitment is thought to be important.

  9. Investigation MSUs critical for correct management Ultrasound kidneys and bladder residual (n.b. without bladder overdistension, which will give artificially elevated PVR – good U.K. study showing PVR proportional to pre void volume) Cystoscopy usually unnecessary if PVR is OK and patient not had frank haematuria.

  10. MSU tests Critical in the management of recurrent / persistent UTIs. Irritative LUTS not always UTI! - Interstistial cystitis, lower ureteric stone, bladder cancer esp CIS. Urinalysis dipstick tests – OK for screening / diagnosis in non complicated UTI 90% specificity 90% sensitivity. ►Females - if more than one presentation with cystitis within 12 month time frame – DO MSUs.◄ ►Males – any presentation with cystitis symptoms – DO MSUs◄

  11. Treatment Persistent UTIs Remove the source of persisting infection: Staghorn stones – require complete clearance and follow up. Clear prostatic infection in men. Remove foreign bodies – JJ stents, catheters

  12. Treatment Recurrent UTIs Behavioural modification Cranberry juice Probiotics – “Good bacteria” Antibiotic treatment Antibiotic prophylaxis Bacterial vaccines

  13. Behavioural Modification Avoiding sex works for some women, but strains relationships. Anal sex probably predisposes men to UTI, but is generally not discussed, and there are no scientific papers discussing this. General hygiene advice is a waste of time, and makes women feel they have poor hygiene.

  14. Cranberry Juice Antibacterial action due to aromatization of quinic to benzoic acid in the gut. Benzoic acid converted to hippuric acid in the liver, excreted in urine. Hippuric acid (Hiprex!) converted to formalin in the bladder in the presence of acidic urine (Hence Hiprex + NH4Cl or ascorbic acid). Requires high residual volumes. (Kass 1959) Also said to release organic molecules into urine which block bacterial adherence (pro-anthocyanidins which prevent docking of bacteria on A-type linkage of flavanols). (Analogous to secretion blood gp Antigns) Some evidence for effectiveness in simple recurrent UTI in women (300ml/day)

  15. Probiotics “Good Bacteria” (By definition, a probiotic is any substance containing live organisms that, when ingested, have a beneficial effect on the host by altering the body's intestinal microflora) No evidence that they reduce incidence of UTIs Lactobacillus preparation and antibiotic associated diarrhea with Rx UTI 17% absolute risk reduction in diarrhea associated with antibiotic administration, and significant reduction in risk of Clostridium difficile infection, in patients given lactobacillus drink – suggested as routine admin to hospital patients > 50 that are receiving antibiotics Use of probiotic Lactobacillus preparation Hickson et al BMJ 2007; 335 (7610): 80

  16. Antibiotic Resistance Most commonly associated with multiple courses of full dose antibiotics for recurrent UTIs. Do not use antibiotics in patient with an indwelling catheter unless they are septicaemic. Do not use antibiotics in patients with infection stones, unless septicaemic. Do not use antibiotics in pateints with JJ stent unless MSU positive. In patient with recurrent UTIs, MSU documentation is vital for assessment of antibiotic sensitivities and resistance.

  17. Antibiotic Treatment Amoxycillin simply doesn’t work – always recurs (Kincaid Smith) – seems OK with clavulinic acid though. Urosepsis T > 38 = hospital and I/V antibiotics + renal U/S exclude infected obstructed. Gentamicin + Amoxycillin (Enterococcus) monitor levels or Timentin Males – all males with UTI have prostatitis (just (don’t) do PSA!!) – prostatic persistence allegedly due to inactivity Abs in acidic pH prostatic fluid. Trimethoprim or fluoroquinolones (Norfloxacin) best – requires 2 weeks Rx, 4 weeks if recurs. Most commonly older men with Rx Cephalexin failure seen. Pyelonephritis best at least 2 weeks antibiotics.

  18. Antibiotic Treatment New work on intracellular infection as cause of complicated UTI. Diagnosis of IBCs on urine cytology or biopsy with EM. Most effective intracellular Abs are fluoroquinolones. May explain observed increased efficacy for these drugs – but should be reserved for complicated UTI.

  19. Antibiotic Prophylaxis Treatment for recurrent UTIs 95% success Use after clearance of UTI with full dose Ab, U/S clear. Prescribe antibiotic pending sensitivities. Not for catheter (IDC) related infection, or persisting UTI. Nitrofurantoin most commonly 50 mg before bed (no alteration gut/vaginal flora) Cephalexin 250 mg Augmentin Duo Trimethoprim (150 mg) linked to early multi resistance Authority prescription for “complicated UTI” on 1800 888333 6 months generally ? 12 months for elderly. Permanent on 6 month rotation for early recurrence or repeated problems. Post intercourse tablet can work.

  20. Bacterial Vaccines Phase II trial published April 07 in a group of women with 3 or more UTIs in 12 months Vaginal pessaries containing “Urovac” vaccine contains heat killed bacteria from 10 human uropathogenic bacteria: 6 strains E coli 1 strain each of Proteus, Morganella, Klebsiella, Enterococcus Vaccine with or without boosters. 3 pessaries at weekly intervals with boosters 1 pessary monthly for 3 months. 72% infection free over 6months in treatment group with boosters vs 30% infection free in placebo group, but placebo group only 3 subjects. Vaginal Mucosal Vaccine for Recurrent UTI in Women Hopkins et al J Urol 2007; 177:1349

  21. Management of Kidney Stones Julian Mander

  22. Spontaneous Stone Passage • Most stones will pass spontaneously and don’t require surgical intervention. • 80% of 5 mm stones will pass spontaneously. • 50% of 8 mm stones will pass spontaneously. • Stones in the lower ureter at presentation more likely to pass than stones in the upper ureter. • Typically episodic pain will be experienced while stone is passing. • Adequate pain relief is important for expectant management – NSAIDs. • Irritative LUTS with stone in lower 1/3 ureter ≠ UTI.

  23. Dissolution of Uric Acid Stones pKa Uric acid = 5.75 Urine pH 7 80% urate ionized Urine pH > 7.5, increase Ca deposition on stone -> insoluble Rx Sodibic 840 mg qid or Ural sachets one qid Repeat imaging 6 +/- 12 weeks Not dissolved -> surgery Prevention increase urine output > 2 li / 24 hours allopurinol 300 mg or 100 mg daily ? decrease protein intake 90 gm / 24 hours ? Run urine pH 7

  24. Indications for Surgical Intervention 1.Infected obstructed kidney = surgical emergency 2. Pain uncontrolled despite PR NSAIDS 3. Stone clearly too large to pass > 8mm 4. Significant CRF creatinine >200 5. Solitary kidney – risk obstructive uropathy

  25. Surgical Intervention – JJ Stents GA + Cystoscopy – low morbidity Initially described late 1970’s, not in common usage until 1980’s Initially no longer than 6 or 12 weeks because of encrustation Now new polymers 6 months, silastic stents 12 months Risks - septicaemia following insertion infected obstructed - ureteric perforation - misplacement if not done with contrast and II - stent pain 15% unable to tolerate Rx as renal colic NSAIDs - loin pain with voiding - cystitis symptoms - do MSU not dipstick which is always +ve - delays stone passage, but enables future instrumentation

  26. JJ Stents

  27. Surgical Intervention – Rigid Ureteroscopy Scopes Perez – Castro early 1980’s 12 F Uromat water pressure devices mid 1980’s 7.5 – 8.5 scopes 1990s Fragmentation EHL probes and U/S probes 1980’s Pneumatic lithoclast probes 1990’s Risks: - ureteric perforation - ureteric stricture Use: still best option for lower 1/3 ureteric stones

  28. Rigid Ureteroscope

  29. Surgical Intervention – Flexible Ureteroscopy and Laser Flexible ureteroscopes 1990’s 7.5 F late ’90s poor durability – 6 week lifespan @ $15,000 Holmium YAG laser 1990’s, prostates initially $120,000 machine 200 micron fibers $800 - $2000 Risks - ureteric strictures - urosepsis and death still with infection staghorns Failures – narrow UOs - dilators - narrow ureters – pre stent - lower pole access

  30. Flexible Ureteroscopy

  31. Flexible UreteroscopyViews

  32. Surgical Intervention - ESWL First treatment Stuttgart 1980 Dornier HM3 1983 RPH SeimensLithostar 1991 RPH Dornier 2001 GA or LA Opaque stones only (U/S guidance available) 3000 shocks – treatment about one hour Pre stenting – stones > 2 cm - infection stones Risks – pain passing stone fragments ?late hypertension - obstruction (steinstrasse) +/- infection - renal haemorrhage and kidney loss (beware coagulopathies) Success rates – pelvicalyceal 80% stone free rates

  33. Surgical Intervention – PercutaneousNephrolithotomy 1970’s Whickham, London – Seldinger technique for renal puncture 1982 – 83 Pat Bary RPH pioneered in WA Upper vs Lower pole punctures – upper pole later + supra 11th rib Access failures Anatomical failures – parallel punctures, coagulum extraction Single stage 30F Amplatz dilatation eventually Fragmentation development – EHL, U/S, pneumatic Lithoclast Risks – bleeding 7% transfusion rate RPH (Kaye tamponade balloon) - 1/200 kidney lost with each puncture & dilatation - nephrectomy for bleeding occasionally - deaths from urosepsis with infection staghorns - bowel, sleen and liver injuries

  34. PCN

  35. Open Surgery Uretero/Pyelo/Nephrolithotomy Occasionally pyeloplasty for PUJ obstruction, with pyelolithotomy Pyelonephrolithotomy for staghorn stones – lost art - splitting kidney on Brodel’s line - Renacidin irrigation - Coagulum pyelolithotomy - renal Xray plate - Gil – Vernet’s plane in pyelolithotomy - clamp and cool kidney Risks – loss renal function - sepsis - loss kidney

  36. Staghorn Stones Generally elderly, unfit and infected Mortality from urosepis High recurrence rate 15 – 30% Sepsis not cleared unless stone cleared Commonest cause of persisting Proteus infection Surgery - now the most common indication for PCN - “sandwich” with ESWL - ? role of flexi ureteroscopy and laser - ? ESWL de novo – some reports

  37. Staghorn Stones

  38. Pregnancy – Special Case Concern is preterm labour – with or without intervention Greater concern the earlier the pregnancy Xray exposure concerns at all stages, greater in first trimester NSAIDs unable to use because of ductus closure risks Traditional management: U/S diagnosis hydronephrosis +/- stone manage with U/S alone if small and pain manageable – rare intervention required – do V. Limited IVP - control +5min + 30min ureteroscopicvs open - issues with stents AVOID Latest: U/S diagnosis followed by immediate flexi ureteroscopy + laser No Xray usage at all Waterson et al Urology 60:383-7 2002

  39. “Metabolic Workup” Recurent stone former = 2 or more stones Biochemical stone analysis important IVP for medullary sponge kidney in Ca Ox stones Serum calcium, albumin, uric acid repeated MSU ?UTI ?pH (Type 1 distal RTA fasting urine always pH > 5.3) 24 hour urine Calcium Oxalate Uric acid +/- Cystine PTH assay in Calcium stone patients Renal Acid load test for RTA “persisting fasting alkaline urine in presence of hypercalciuria and CaPO4 stones

  40. Medical Management – Cystine Stones Inherited defect renal tubular reabsorption 4 amino acids COLA Autosomal recessive, but some heterozygous have problem pKacystine higher than uric acid - increase solubility only at pH > 7.2 - double solubility at pH 7.8 Dissolution - > 2 li urine / 24 hours – best 3 – 4 li !! - pH > 7.8 Kcitrate thought best, but can use NaHCO3 - often not successful Thiol group donors – D Penicillamine 1.5 gm / day - form cystine-S-penicillamine soluble molecule ? ACE inhibitor - captopril

  41. Medical Management – Infection Stones MgNH4PO4 = struvite with proteinaceous matrix Urea splitting bacteria, produce urease enzymes, splitting urea to ammonium, increase urine pH and may provide initial glycocalyxproteinaceous compound. Urine pH > 7.2 required Proteus commonly, also some Pseudomonas, Klebsiella, E coli Persisting Proteus UTI is hallmark (esp diabetic Aboriginals – E coli) Surgery to clear stone, followed by one month full dose bacteriocidal antibiotic, followed by 12 month surveillance with monthly MSUs ? Hemiacidrin irrigation following surgery ? Oral urease inhibitors

  42. Medical Management – Calcium Stones 47gm calcium filtered daily, UOP 200 mg Ca/day = > 99% reabsorbed Tubular transport max exceeded -> hypercalciuria Ksp need only exceed 15 – 30 minutes to nucleate stone Concept of heterogenous nucleation Hypercalciuria Vs Hyperoxaluria - Ionic activity ? Oxalate 10 x more important in CaOx stone formation

  43. Medical Management - Hypercalciuria Hypercalciuria Absorptive 1. Type 1 hypercalciuric on low Ca diet 2. Type 2 hypercalciuric on normal Ca diet 3. Type 3 hypercalciuric + hyperphosphatemic + low renal tubular reabsorption of phosphorous Excretive 4. Renal leak hypercalciuria 5. Hyperparathyroidism 6. Hypercalciuria in response to CHO ingestion + sarcoidosis, multiple myeloma, hyperthyroidism, leukemia, lymphoma, milk – alkali syndrome, Vit D intoxication, immobilization syndrome, renal tubular acidosis

  44. Medical Management – Hypercalciuria Treatment – Theoretical Hyperabsorbers – methylcellulose - oral oxalate! Hyperexcretors - diuresis > 2 li / day - thiazides decrease calcium excretion ? just work through volume – polyuria - all hyperabsorber treatments

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