IMPROVING  OUTCOME  IN PERITONEAL DIALYSIS<br />DR.M.B.M GHALIB<br />MBBS,ABIM,MD,MRCP (UK)	<br />CONSULTANT NEPHROLOGIST<...
Improving Outcome in PD Patients<br /><ul><li>Introduction.
Staff selection.
Staff training.
PD center facilities.
Patients selection.
Patient training.
Catheter insertion techniques.
New connectology techniques.
Peritonitis.
Conclusion. 	</li></li></ul><li>INTRODUCTION<br />
Incidence of ESRD in EDTA/ERA Registryfrom 1991-2001<br />
Incidence of RRT 1997-2002by country code EDTA/ERA<br />
Percent distribution per age category of incident Flemish ESRD patients<br />
Age distribution of prevalent ESRD patients in relation with population<br />Flemish population<br />
Classification of Renal Function<br />“Chronic Kidney Disease” (CKD)<br />Kidney Function<br />GFR (mL/min/1.73m2)≈ CrCl (...
ESRD – The Tip of the Iceberg<br />1988-1994<br />1999-2000<br />Prevalence<br />n=400,000<br />Stage 5 – Kidney Failure (...
Percentage of subjects with de novo CKD (eGFR< 60 ml/min) after a mean of 4.2 years of follow-up in the PREVEND study<br /...
Prevalence of eGFR < 60 ml/min in selected European studies<br />Percentage<br />
Distribution of CKD stages in Belgian population at screening<br />
Prevalence of CKD (eGFR < 60 ml/min/1.73 m²)<br />%<br />Van Biesen et al, NDT,2006<br />
Mortality in different stages of CKD, based on MDRD (10 year FU)<br />Percentage<br />New cases<br />
Age-standardized rates of death from any cause (A) or cardiovascular events (B)<br />Go et al New Engl J Med 2004, 351:129...
Kaplan-Meier of survival from CVD according to proteinuria-the Framingham cohort<br />Arnlov et al, Circulation 112: 969-9...
I have found a weapon of mass destruction...<br />Diabetic Nephropathy<br />
Clinical relevance<br />A patient on PD is exposed to<br /><ul><li>3000-7000 litres of fluid
50-175 kilo pure glucose</li></ul>roughly<br /><ul><li>fructose 			      3 kg
acetaldehyde			  100 ml
formaldehyde		      6 ml
3-DG			           100 g
3,4-DGE			    10 g</li></li></ul><li>Long-term PD: Structural Changes<br />AT START PD                         AFTER 25 MO...
Longitudinal changes in Solute Transport<br />Solute transport<br />Ultrafiltration<br />Davies S, ASN 2002<br />
AGEs<br />Glucose<br />Matrix protein<br />amino groups<br />Amadori<br />products<br />Extravasated<br />lipoproteins<br ...
AGE - RAGE Interaction<br />AGE<br />RAGE<br />TGF<br />IL-1<br />VEGF<br />PDGF<br />Procoagulant factors<br />Adhesion ...
AGE Accumulation in the Peritoneal Membrane<br />Honda et al, NDT, 14, 1541-1549, 1999<br />
Bioincompatibility of current PD fluids<br />Unphysiological composition:<br />acidic pH <br />[high lactate concentration...
What  is the clinical importance of  GDPs?<br />Inflow pain during initial peritoneal contact<br />Inhibition of growth, v...
Peritoneal dialysis solutions (glucose-based) <br />with reduced GDP content<br /><ul><li>Gambrosol Trio, Gambro
Lactate-buffered (40 mM),  pH~ 6.4
Balance, Fresenius
Lactate-buffered (35 mM),  pH~7.4
Bicavera, Fresenius
Bicarbonate-buffered (34 or 38 mM), pH~7.4
Physioneal, Baxter
Bicarbonate/lactate-buffered (15/25 mM), pH~7.4</li></li></ul><li>Mixed Solution<br />Solution A<br />Solution B<br />Lact...
Biocompatibility of new peritoneal dialysis solutions.What is the clinical evidence?<br />Less infusion pain<br />Better p...
Frequency of peak infusion painseverity using the verbal rating scale.<br />Bicarbonate/lactate<br />Bicarbonate<br />Lact...
Plasma fluorescence during the low GDP and conventional PD fluid periods.<br />Zeier et al Kidney Int 63: 298-305, 2003<br />
CA 125 in spent dialysate after<br />long-term treatment with PD-Bio<br />(23)   (22)    (7)<br />100<br />1 month<br />6 ...
Peritonitis incidence in patients prescribed PhysionealEuropean PD Solutions Registry<br />Van Bree et al, JASN,2002; 13:4...
Euro Balance Trial: Effluent CA125<br />Patient group I, n = 24<br />Patient group II, n = 23<br />U/ml<br />U/ml<br />p <...
Euro Balance Trial: Serum Imidazolone<br />100,00<br />80,00<br />ns<br />p<0.01<br />60,00<br />68,22<br />Imidazolone (n...
The Korean outcome study-patient survival<br />Lee HY, PDI 25:248-255, 2005<br />
The Korean outcome study-peritonitis incidence<br />Lee HY, PDI 25:248-255, 2005<br />
Benefits of Residual Renal Function<br />Provides endocrine functions<br /><ul><li> Erythropoietin production
 Ca++, phosphorus and vitamin D homeostasis</li></ul>Contributes to total solute clearance  (1 ml/min CrCl = 10 liter CrCl...
PERITONITIS<br />One of the major problems of PD<br />Decreasing incidence: most centers less than 1episode/24 ptms.<br />...
Peritoneal defense mechanisms (1)<br />Cellular defense :<br />Peritoneal PMN in PD-patients are in a “chronically elicite...
GDP : Effects on Host Defense<br />3000<br />2000<br />1000<br />0<br />IL-1 (pg/mL)<br />1.5% glucose<br />4.0% glucose<...
Phagocytosis and TNF- release in monocytes are dependent on intracellular pH<br />5<br />50<br />4<br />40<br />3<br />30...
Effect of pH on respiratory burst activation of PMN<br />Chemiluminescence response<br />175<br />150<br />125<br />pH 7.3...
Peritoneal defense mechanisms (2)<br />Cellular defense :<br />Peritoneal PMN in PD-patients are in a “chronically elicite...
Peritoneal defense mechanisms (1)<br />Humoral factors:<br />Fast influx of immunoglobins and complement factors, probably...
Impact of peritonitis (1)<br />On survival:<br />Direct cause of death in 1-6% of PD patients<br />Peritonitis rate itself...
Impact of peritonitis (2)<br />On technique failure :<br /><ul><li>50% of transfers to HD related to peritonitis (Van Bies...
High mortality up to 1 year in period following technique failure due to peritonitis. </li></li></ul><li>Impact of periton...
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Improving Outcome in PD Patients

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Improving Outcome in PD Patients

  1. 1. IMPROVING OUTCOME IN PERITONEAL DIALYSIS<br />DR.M.B.M GHALIB<br />MBBS,ABIM,MD,MRCP (UK) <br />CONSULTANT NEPHROLOGIST<br />ASSOCIATE PROFESSOR OF MEDICINE<br />NATIONAL RIBAT UNIVERSITY<br />إنا كفيناك المستهزئين<br />
  2. 2. Improving Outcome in PD Patients<br /><ul><li>Introduction.
  3. 3. Staff selection.
  4. 4. Staff training.
  5. 5. PD center facilities.
  6. 6. Patients selection.
  7. 7. Patient training.
  8. 8. Catheter insertion techniques.
  9. 9. New connectology techniques.
  10. 10. Peritonitis.
  11. 11. Conclusion. </li></li></ul><li>INTRODUCTION<br />
  12. 12. Incidence of ESRD in EDTA/ERA Registryfrom 1991-2001<br />
  13. 13. Incidence of RRT 1997-2002by country code EDTA/ERA<br />
  14. 14. Percent distribution per age category of incident Flemish ESRD patients<br />
  15. 15. Age distribution of prevalent ESRD patients in relation with population<br />Flemish population<br />
  16. 16.
  17. 17. Classification of Renal Function<br />“Chronic Kidney Disease” (CKD)<br />Kidney Function<br />GFR (mL/min/1.73m2)≈ CrCl (mL/min)<br />Stage IV<br />Stage I<br />Stage II<br />Stage III<br />Stage V<br />Severe  Kidney Function<br />Mild  Kidney Function<br />CKD Risk Factors/Damage with Preserved GFR<br />Kidney Failure ESRD<br />Moderate  Kidney Function<br />130 120 110 100 90 80 70 60 50 40 30 20 15 10 0 <br />Chronic Kidney Disease<br />ESRD, end stage renal disease<br />National Kidney Foundation. Am J Kid Dis. 2004;43(Suppl 1):S16-S41.<br />
  18. 18. ESRD – The Tip of the Iceberg<br />1988-1994<br />1999-2000<br />Prevalence<br />n=400,000<br />Stage 5 – Kidney Failure (GFR <15)<br />Stage 4 – GFR 15–29<br />n=300,000<br />0.1%<br />0.2%<br />n=7,400,000<br />3.7%<br />4.2%<br />Stage 3 – GFR 30–59<br />Stage 2 – Kidney damage<br />& GFR 60–89<br />n=5,700,000<br />2.8%<br />2.2%<br />Stage 1 – Kidney damage<br />& GFR >90<br />n=5,600,000<br />2.8%<br />2.2%<br />Total: 19 M adults with CKD <br /> 8 M adults with GFR<60<br />Coresh et al.<br />Am J Kidney Dis, 41:1-12, 2003<br />
  19. 19. Percentage of subjects with de novo CKD (eGFR< 60 ml/min) after a mean of 4.2 years of follow-up in the PREVEND study<br /><ul><li>In the baseline screening of </li></ul>the albuminuria-enriched cohort<br />312 out of the 8592 (3.6% ) had <br />a GFR < 60 ml/min/1.73m² <br /><ul><li>In a FU study, eGFR was evaluated </li></ul>after a mean of 4.2 years in subjects<br /> with previously normal renal function <br />but albuminuria. Out of the 6022 <br /> subjects 253 (4.2%) developed an<br /> eGFR of < 60 ml/min/1.73 m²<br />Verhave et al Kidney Int 66 (suppl 92) : S18-S21, 2004<br />
  20. 20. Prevalence of eGFR < 60 ml/min in selected European studies<br />Percentage<br />
  21. 21. Distribution of CKD stages in Belgian population at screening<br />
  22. 22. Prevalence of CKD (eGFR < 60 ml/min/1.73 m²)<br />%<br />Van Biesen et al, NDT,2006<br />
  23. 23. Mortality in different stages of CKD, based on MDRD (10 year FU)<br />Percentage<br />New cases<br />
  24. 24. Age-standardized rates of death from any cause (A) or cardiovascular events (B)<br />Go et al New Engl J Med 2004, 351:1296-1305.<br />
  25. 25. Kaplan-Meier of survival from CVD according to proteinuria-the Framingham cohort<br />Arnlov et al, Circulation 112: 969-975,2005<br />
  26. 26. I have found a weapon of mass destruction...<br />Diabetic Nephropathy<br />
  27. 27. Clinical relevance<br />A patient on PD is exposed to<br /><ul><li>3000-7000 litres of fluid
  28. 28. 50-175 kilo pure glucose</li></ul>roughly<br /><ul><li>fructose 3 kg
  29. 29. acetaldehyde 100 ml
  30. 30. formaldehyde 6 ml
  31. 31. 3-DG 100 g
  32. 32. 3,4-DGE 10 g</li></li></ul><li>Long-term PD: Structural Changes<br />AT START PD AFTER 25 MONTHS PD<br />Mateijsen et al, PDI, 19, 517-525, 1999<br />
  33. 33.
  34. 34. Longitudinal changes in Solute Transport<br />Solute transport<br />Ultrafiltration<br />Davies S, ASN 2002<br />
  35. 35. AGEs<br />Glucose<br />Matrix protein<br />amino groups<br />Amadori<br />products<br />Extravasated<br />lipoproteins<br />AGEs<br />Covalent AGE<br />crosslinks<br />Brownlee et al, NEJM, 318, 1315-1321, 1998<br />
  36. 36. AGE - RAGE Interaction<br />AGE<br />RAGE<br />TGF<br />IL-1<br />VEGF<br />PDGF<br />Procoagulant factors<br />Adhesion molecules<br />
  37. 37. AGE Accumulation in the Peritoneal Membrane<br />Honda et al, NDT, 14, 1541-1549, 1999<br />
  38. 38. Bioincompatibility of current PD fluids<br />Unphysiological composition:<br />acidic pH <br />[high lactate concentration]<br />high glucose concentration<br />hyperosmolality<br />Heat sterilisation of glucose gives rise to glucose degradation products which may increase AGE formation<br />Acute toxicity<br />Chronic toxicity<br />
  39. 39. What is the clinical importance of GDPs?<br />Inflow pain during initial peritoneal contact<br />Inhibition of growth, viability and function of different peritoneal cell types including mesothelial cells<br />GDP’s are a major catalyst of AGE formation<br />Peritoneal AGE formation (associated with loss of ultrafiltration) over time<br />Wieslander et al, Adv Perit Dial 1996, 12: 57- 60 <br />
  40. 40. Peritoneal dialysis solutions (glucose-based) <br />with reduced GDP content<br /><ul><li>Gambrosol Trio, Gambro
  41. 41. Lactate-buffered (40 mM), pH~ 6.4
  42. 42. Balance, Fresenius
  43. 43. Lactate-buffered (35 mM), pH~7.4
  44. 44. Bicavera, Fresenius
  45. 45. Bicarbonate-buffered (34 or 38 mM), pH~7.4
  46. 46. Physioneal, Baxter
  47. 47. Bicarbonate/lactate-buffered (15/25 mM), pH~7.4</li></li></ul><li>Mixed Solution<br />Solution A<br />Solution B<br />Lactate<br />Electrolytes<br />Glucose<br />pH 6.8-7.4<br />Lactate<br />Electrolytes<br />Glucose<br />pH<br />8.0-8.6<br />pH<br />2.6-3.1<br />PDF with Reduced GDP Content<br />CAPD Balance, Fresenius Medical Care<br />
  48. 48. Biocompatibility of new peritoneal dialysis solutions.What is the clinical evidence?<br />Less infusion pain<br />Better preservation of mesothelial cell mass<br />Less peritoneal neovascularisation<br />Preservation or restoration of peritoneal ultrafiltration<br />Reduced intraperitoneal AGE/ALE formation<br />Less beta-2 microglobulin amyloidosis?<br />Reduced incidence of peritonitis?<br />
  49. 49. Frequency of peak infusion painseverity using the verbal rating scale.<br />Bicarbonate/lactate<br />Bicarbonate<br />Lactate<br />Very severe pain<br />Severe pain<br />Moderate pain<br />Mild pain<br />No pain<br />0 2 4 6 8 10 12 14 16 18 20 22 <br />Frequency<br />Mactier et al, KI, 53, 1061-1067, 1998.<br />
  50. 50. Plasma fluorescence during the low GDP and conventional PD fluid periods.<br />Zeier et al Kidney Int 63: 298-305, 2003<br />
  51. 51. CA 125 in spent dialysate after<br />long-term treatment with PD-Bio<br />(23) (22) (7)<br />100<br />1 month<br />6 months<br />75<br />12 months<br />U/ml<br />50<br />(27)<br /> (9)<br />(16)<br />25<br />0<br />Conventional glucose<br />PD-Bio<br />
  52. 52. Peritonitis incidence in patients prescribed PhysionealEuropean PD Solutions Registry<br />Van Bree et al, JASN,2002; 13:43A abstract ASN 2002<br />
  53. 53. Euro Balance Trial: Effluent CA125<br />Patient group I, n = 24<br />Patient group II, n = 23<br />U/ml<br />U/ml<br />p < 0.01<br />p < 0.01<br />p < 0.01<br />0 <br />3 <br />6 <br />0 <br />3 <br />6<br />Month<br />Month <br />mean ± SD<br />conventional PDF<br />CA125 measured with electrochemi-luminescence immuno assay (ECLIA)<br />CAPD balance<br />
  54. 54. Euro Balance Trial: Serum Imidazolone<br />100,00<br />80,00<br />ns<br />p<0.01<br />60,00<br />68,22<br />Imidazolone (ng/ml)<br />mean ± SD<br />58,18<br />40,00<br />n = 11<br />43,99<br />20,00<br />0,00<br />Baseline <br />3 months conventional PDF<br />3 months CAPD balance<br />Imidazolone measured with ELISA<br />
  55. 55. The Korean outcome study-patient survival<br />Lee HY, PDI 25:248-255, 2005<br />
  56. 56. The Korean outcome study-peritonitis incidence<br />Lee HY, PDI 25:248-255, 2005<br />
  57. 57. Benefits of Residual Renal Function<br />Provides endocrine functions<br /><ul><li> Erythropoietin production
  58. 58. Ca++, phosphorus and vitamin D homeostasis</li></ul>Contributes to total solute clearance (1 ml/min CrCl = 10 liter CrCl/week)<br />Improves 2-microglobulin and middle molecule clearance<br />Reduces Mortality<br />Improves QOL<br />Facilitates volume control<br />Allows for more liberal diet and fluid intake<br />Increases nutritional status<br />
  59. 59. PERITONITIS<br />One of the major problems of PD<br />Decreasing incidence: most centers less than 1episode/24 ptms.<br />Most common cause of technique failure (up to 50%)<br />23% of hospital admissions in PD patients are related to infection.<br />Mortality risk: presence of peritonitis related to later mortality (Piraino et al, JASN, 9, 1958-1964, 1998)<br />
  60. 60. Peritoneal defense mechanisms (1)<br />Cellular defense :<br />Peritoneal PMN in PD-patients are in a “chronically elicited” state, with a decreased response upon stimulation, possibly due to low pH, glucose, GDP’s, osmolarity and the presence of uremic toxins in the dialysate<br />Topley et al, oa Kidney Int, 34, 404-411, 1988<br />Jörres et al, Perit Dial Int, 13, suppl 2, S291-S294<br />Vanholder et al, Kidney Int, 50, 643-652, 1996<br />
  61. 61. GDP : Effects on Host Defense<br />3000<br />2000<br />1000<br />0<br />IL-1 (pg/mL)<br />1.5% glucose<br />4.0% glucose<br />*<br />culture<br />medium<br />heat-<br />sterilized<br />PDF<br />filter-<br />sterilized<br />PDF<br />filter-<br />sterilized<br />PDF<br />heat-<br />sterilized<br />PDF<br />Wieslander et al, PDI, 15, S52-59, 1995.<br />
  62. 62. Phagocytosis and TNF- release in monocytes are dependent on intracellular pH<br />5<br />50<br />4<br />40<br />3<br />30<br />2<br />20<br />10<br />1<br />0<br />0<br />TNF- (ng/ml/106 cells)<br />% Phagocytosis<br />*<br />*<br />*<br />*<br />con<br />6.0<br />6.3<br />6.5<br />7.1<br />con<br />6.0<br />6.3<br />6.5<br />7.1<br />Intracellular pH<br />Intracellular pH<br />* p < 0.05 vs. control <br />Douvdevani et al, J Am Soc Nephrol 1995, 6: 207-213<br />
  63. 63. Effect of pH on respiratory burst activation of PMN<br />Chemiluminescence response<br />175<br />150<br />125<br />pH 7.3<br />*<br />100<br />CL response (%)<br />*<br />75<br />50<br />25<br />*<br />*<br />pH 5.2<br />0<br />0<br />10<br />20<br />30<br />40<br />Lactate concentration (mM)<br />Liberek, Topley, Jörres et al, Nephron 1993; 65: 260-265<br />
  64. 64. Peritoneal defense mechanisms (2)<br />Cellular defense :<br />Peritoneal PMN in PD-patients are in a “chronically elicited” state, with a decreased response upon stimulation, possibly due to pH, glucose, osmolarity and the presence of uremic toxins in the dialysate<br />Interaction of bacteria and PMN initiates release of chemotactic factors, interaction of the peritoneal macrophage with the mesothelial cell and the subsequent release of pro-and anti-inflammatory cytokines.<br />Topley et al, oa Kidney Int, 34, 404-411, 1988<br />Jörres et al, Perit Dial Int, 13, suppl 2, S291-S294<br />Vanholder et al, Kidney Int, 50, 643-652, 1996<br />
  65. 65. Peritoneal defense mechanisms (1)<br />Humoral factors:<br />Fast influx of immunoglobins and complement factors, probably induced by increased levels of PGE2 and PGI2(vasodilators)<br />Secretion of cytokines by mesothelial cells: IL6, IL8, IL1-alfa and IL1-beta<br />Expression and release of ICAM -1 and VCAM-1 by mesothelial cells<br />Secretion of IL-1 and TNF-alfa by PMN resulting in a fast upregulation of inflammatory response<br />
  66. 66. Impact of peritonitis (1)<br />On survival:<br />Direct cause of death in 1-6% of PD patients<br />Peritonitis rate itself is an independent risk factor for death, especially in whites, non-diabetics, and patients >60 years old (Fried, Piraino;: JASN 7, 2176-2182, 1996)<br />peritonitis indirectly related to 15.8% of deaths; Gram- peritonitis indirectly related to 8.8% <br />use of Y-set made no difference for death risk<br />for every 0.5/year increase in peritonitis rate, death risk increased 10-11%<br />
  67. 67. Impact of peritonitis (2)<br />On technique failure :<br /><ul><li>50% of transfers to HD related to peritonitis (Van Biesen et al, Advances in Peritoneal Dialysis, 14, 90-94, 1998)</li></ul> 36% of transfers to HD related to peritonitis (Maiorca et al, Perit Dial Int, 16, 276-287, 1996)<br /> 78% of transfers to HD related to peritonitis (Woodrow et al, Perit Dial Int, 17, 360-364, 1997)<br /><ul><li>Use of Y-system did not influence technique survival, despite better peritonitis rate
  68. 68. High mortality up to 1 year in period following technique failure due to peritonitis. </li></li></ul><li>Impact of peritonitis<br />Causes of hospitalization<br />Fried et al, AJKD, 33, 927-933, 1997<br />
  69. 69. Infection routes (1)<br />Intra (trans) luminal infection=<br />Infection occurs through the endoluminal site of the catheter<br />Mostly (not always) related to manipulation: touch contamination <br />Mostly organisms from the skin: Gram+; Staph <br />Periluminal infection=<br />Infection occurs through the space between catheter and skin.<br />Most frequently related to exit site infection or tunnel infection<br />
  70. 70. Infection routes (2)<br />Impact of double-bag Y-set (flush before fill)<br />Woodrow et al (Perit Dial Int, 17, 360-364, 1997)<br />
  71. 71. Peritonitis incidence in a single centre<br />Episodes/pt year<br />Kim et al, Seoul, unpublished data<br />
  72. 72. Infection routes (3)<br />Impact of APD vs CAPD:<br />a lower peritonitis incidence in APD was reported by several groups:<br />French multicenter study: CAPD 1/24 ptm vs APD 1/29.2ptm (p<0.01) (Perit Dial Int, 19, S32, 1999)<br />Locatelli et al: CAPD 1/8.3ptm vs APD 1/18.9ptm (Perit Dial Int, 19, S33, 1999)<br /> Perez-Fontan et al CAPD 1/16ptm vs APD 1/35ptm (Perit Dial Int, 19, S35, 1999)<br />Italian study group: CAPD 1/27ptm vs APD 1/22 ptm (Perit Dial Int, 19, S38, 1999)<br />
  73. 73. Consensus is what elderly statesmen agree upon in public, <br />but never believe in private.<br /> Aba Eban<br />
  74. 74. Treatment (1)<br />Antibiotics: no consensus on<br />empiric antibiotic treatment of choice<br />route of administration (oral, intravenously, intraperitoneally)<br />duration of therapy<br />Peritoneal lavage:<br />premise: wash out bacteria<br />however: also wash out of PMN and defense mechanisms<br />Heparin:<br />inhibits fibrin formation<br />potential reduction of number of adhesions, and potential protective effect on peritoneal membrane<br />
  75. 75. Empiric Treatment<br />Consider the following:<br />epidemiology of organisms causing peritonitis<br />clinical efficacy<br />pharmacokinetics/dynamics of antibiotics<br />safety of antibiotics<br />convenience<br />cost<br />
  76. 76. Staph Aureus Prophylaxis<br />Staph A. leading cause of exit-site and tunnel infections<br />Staph A. carriage on exit-site is associated with more infection than nasal carriage<br />Screening for carriage: use swab humified with saline<br />
  77. 77. Staphylococcus peritonitisRelation with carriers<br />% cultures same organism as in dialysate<br />Amato et al, AJKD, 37, 43-48, 2001<br />
  78. 78. Nasal Prophylaxis(Mupirocin study group)<br />Nasal swabs: 2 out of 3 positive = carrier<br />1144 patients screened; 23.3% carriers<br />nasal ointment, 5 days every month: mupirocin vs placebo<br />nasal carriage after treatment: 10% in mupirocin vs 48% in placebo group<br />no direct evidence for resistance; however: Perez-Fontan et al: increase of mupirocine resistance over a two year application period (AJKD 1993)<br />
  79. 79. Nasal Prophylaxis(Mupirocin study group)<br />P = 0,17<br />P < 0,01<br />P = NS<br />Infections per 100 patient years<br />JASN, 7, 2403-2408, 1996<br />
  80. 80. Exit-site prophylaxis<br />N=188<br />Staph A peritonitis rate/100 pty<br />P=0,05<br />Bernardini et al, AJKD, 27, 695-700, 1996<br />Thodis, PDI, 18, 261-270, 1998<br />
  81. 81. 24-48 hours<br />Gram Positive<br />Organism on <br />culture*<br />Other Gram<br />Positive Organisms<br />S.aureus<br />Enterococci<br />Discontinue<br />Aminoglycoside<br />Continue Cephalosporin<br />STOP Cephalosporin<br />Add Ampicillin-125 mg/L<br />Continue Aminoglycoside<br />Discontinue<br />Aminoglycoside<br />Continue Cephalosporin<br />Add Rifampin 600 mg/d PO<br />If no improvement<br />Re-culture and evaluate**<br />96 hours<br />Peritonitis with Exit<br />or Tunnel Infection <br />Consider Removal of catheter<br />Evaluate for Occult<br /> Tunnel Infection<br />Duration<br />of Therapy<br />21 days<br />14 days<br />14 days<br />
  82. 82. Gram Negative Organisms on culture*<br />24-48 hours<br />Pseudomonas/<br />Xanthomonas<br />Multiple Organisms<br />and/or Anaerobes<br />Single Gram Negative<br />(Non-Xanthomonas)<br />Continue Continous<br />Aminoglycoside Therapy, <br />Discontinue Cephalosporin<br />Add agent with Activity Against<br />this Pseudomonas/Xanthomonas<br />Adjust Antibiotics<br />to Sensitivity Patterns<br />Discontinue<br />Aminoglycoside<br />Continue Cephalosporin<br />If Clinical Improvement : Continue Above therapy<br />If No Clinical Improvement : Repeat Cell Count; Cultures and Gram Stain;<br /> If Culture Positive Remove Catheter<br />If No Clinical Improvement and Exit Site Infection Present - Remove Catheter <br />96 hours<br />21 days<br />14 days<br />14 days<br />Duration<br />of Therapy<br /> Agents with Anti-Pseudomonas or Anti-Xanthomonas Activity<br /> AgentDosage<br /> 1. Ceftazidime 125 mg/L IP<br /> 2. Piperacillin 4 gm every 12 hours IV (adults)<br /> 150 mg/kg every 12 hours (children)<br /> 3. Ciprofloxacin 500 mg BID PO (avoid in children)<br /> 4. Aztreonam LOAD : 1000 mg/L MAINT : 250 mg/L IP<br /> 5. Imipenem LOAD : 500 mg/L MAINT : 200 mg/L IP<br /> 6. Sulfamethoxazole/Trimethoprim LOAD : 1600/320 PO Q 1-2d<br /> 7. Aminoglycosides Increase dose to 6-8 mg/L IP in each exchange**<br />
  83. 83. 24-48 hours<br />*<br />Yeast on Gram<br />Stain or Culture<br />*<br />Flucytosine** Load : 2000 mg PO<br /> Maint : 1000 mg/d PO<br /> and<br />Fluconazole** 200 mg PO/IP daily <br />4 - 7 days<br />If No Clinical Improvement<br />Repeat Cell Count, Gram<br />Stain, Culture and Consider<br />Catheter Removal.<br />If Clinical Improvement : <br />Therapy Duration<br />4-6 Weeks<br />
  84. 84. Cloudy Fluid and/or Abdominal Pain<br />and/or Unexplained Fever<br />Cell count/<br />differential Gram Stain Culture<br />Initiate Empiric*<br />Therapy<br />Cefazolin or Cephalothin<br />and Aminoglycoside<br />0 hours<br />Culture<br />Negative<br />Gram Positive<br />Organism<br />on Culture<br />Yeast on<br />Gram Stain or <br />Culture<br />Gram Negative<br />Organism on<br />Culture<br />24 hours<br />* Empiric Therapy<br />Agent Continuous Dose Intermittent Dose<br /> (in 1 exchange/day)<br /> Residual urine output (mL/day)<br />Anuria (<500) Non-anuria (>500)<br />cefazolin or 500 mg/L load then 500 mg/L increase dose<br /> cephalothin 125 mg/L in each exchange (or 15 mg/kg) by 25%<br />gentamycin 8 mg/L load, then 4 mg/L 0.6 mg/kg 1.5 mg/kg initial loading dose<br />metilmicin in each exchange body weight See footnote for maintenance<br />tobramyxin dose recommendations<br />amikacin 25 mg/L load, then 12 mg/L 2 mg/kg 5 mg/kg initial loading dose.<br /> in each exchange body weight See footnote for maintenance<br /> dose recommendations <br />
  85. 85. Indications for catheter removal<br />Simultaneous exit-site/ tunnel infection (role for ultrasound)<br />Fungal peritonitis<br />Persisting or relapsing peritonitis, especially Staph A., Pseudomonas, Acinetobacter, or other water-borne bacteria<br />
  86. 86. CONCLUSION <br />Better facilities & training(patients & staff).<br />Prevention, prophylaxis & treatment of peritonitis.<br />Biocompatible PD fluids.<br />APD for high transporters.<br />Preservation of residual renal function.<br />Treat co-morbidities.<br />Audit.<br />Research.<br />
  87. 87. THANK YOU<br />

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