Icm renal 234

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  • -catheter in Int jug vein or in int femoral vein\n-can be in the body for 1 yr \n-do this when have no time to prepare patient\n-\n
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  • -subclavian vein can promote stenosis of subclavian vein and all the veins of the arm collapse\n-\n
  • -dialysis – wash machine\n-blood passes through cylinder- have diffusion and convection\n-need to put in dialysis on other side of machine – pure water \n
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  • -dialyzer w/ 1000s of microtubules inside \n-blood comes into each capillary of the dialyzer, the diaslysis is coming btwn the capilaries and exits the other side \n
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  • -blood and dialysis go in opp directions \n-can’t be in same direction b/c dialysis will be saturated - max diffusion \n
  • -waste products come from blood to dialysis \n-at other end substances from dialysis go to the blood \n
  • -depends on area of pore size \n-urea- small molecule \n-uremic – misnomer, symptoms not due to urea, uremia can be treatment for some patients eg. malaria \n-\n
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  • -used to have cellulose membranes\n-now use poly… membrane \n
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  • -give some heparin – so blood doesn’t coag as exit body to dialyzer \n-comes out of body – called arterial blood (even though from vein)\n-blood entering body called venous blood \n-if apply venous clamp – not complete block\n-P will build up in the dialyzer, as blood pump continues to go\n-P is important in chronic dialysis patients (or ppl in acute renal failure – everything stays in their body, can can easily have excess of water in body – pulm edema) \n-put venous clamp, to make more convection to remove excess water\n
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  • Icm renal 234

    1. 1. DIALYSISProcess where the solute composition of a solution A is altered by exposing solution A to a second solution(B) through a semi - permeable membraneSEMI-PERMEABLE MEMBRANE: sheet perforated by holes or pores
    2. 2. Mechanisms of solute transportDiffusion-random molecular motion concentration gradient molecular weight membrane resistanceUltrafiltration-water is pushed through membrane hydrostatic pressure osmotic pressure
    3. 3. Sand is swept away
    4. 4. Access for Dialysis
    5. 5. Access for Dialysis
    6. 6. Vascular Access-synthetic
    7. 7. Access for Dialysis
    8. 8. Access for Dialysis
    9. 9. PERMCATH
    10. 10. Vascular Access-catheter
    11. 11. Vascular Access-catheter
    12. 12. Portable hemodialysis Wearable hemodialysisHemodialysis machine machine apparatus
    13. 13. Dialyzer-hollow fiber
    14. 14. Dialyzer
    15. 15. DialyzersLow- efficiency-surface area:0.8-2.1 m²,small poresHigh- efficiency-bigger surface area, small or big poresHigh- flux-big pores (pass middle molecules)
    16. 16. Dialyzers
    17. 17. Dialyzer membrane
    18. 18. The Dialyzer Membrane
    19. 19. The Dialyzer Membrane
    20. 20. Dialyzer clearance
    21. 21. Dialyzer clearance
    22. 22. Dialysis Adequacy: Urea Kinetics
    23. 23. Dialysis Adequacy
    24. 24. Dialysis Adequacy Indices of urea removal Kt/V Reflects urea removalPopulation studies suggest Kt/V should be >1.2 URR Also reflects urea removal Current goal is URR>65%
    25. 25. KT/V and mortality
    26. 26. Kt/VK is the dialyzer blood urea clearance (Liters per hour)t is the dialysis session length [In a typical dialysis session:4 hs ] (hours) [Water content:~60% of dry body weight: If BW=70 kg then waterV is the volume of distribution content is ( 0.6 X 70) 42 L ] of urea ( Liters )
    27. 27. Dialysis Adequacy
    28. 28. Dialysis Adequacy
    29. 29. Dialysis Adequacy
    30. 30. Dialysis Adequacy
    31. 31. NO BREAK
    32. 32. Indications for Dialysis-acute GI: nausea ; vomiting (morning) ; poor appetite Symptoms: Mental status alteration; fatigued ; weakness Signs : asterixis ; pericardial friction rub ; fluid overload Lab : Hyperkalemia, Severe Metabolic Acidosis
    33. 33. Case 122 years old male, cocaine abuser, with a known obstructive uropathy presented to hospital with severe sepsis secondary to pneumonia.LAB: Hgb-9.6 g/dl ;WBC-25800 ;PLT-603000 Na-132meq/l; K-3.1meq/l; Cl-107; Glucose-90 ; BUN-130 mg/dl Creatinine-4.7 ; Osm-330 ; pH-6.95; pO2-109; pCO2- 10 ;HCO3-2; L.A.-0.6 ( Severe metabolic Acidosis with elevated Anion Gap )Chest X ray: Middle lobe+lingular pneumonia.U.S. Bilat. moderate hydronephrosisFollow-up: empiric Cephtriaxone and VancoBlood culture were positive for Staph. aureus and E.ColiAdmitted to ICU: despite IV Bicarbonate and 4 liters of crystalloids remained acidotic and oliguric therefore a regular standard dialysis was prescribed.2 ½ hours after starting dialysis became rapidly unresponsive and intubation was doneAt completion of HD and over the subsequent 4 hs the neurologic status deteriorated
    34. 34. Case 1 Computerized Tomography (CT) head showing diffuse cerebral edema with effacement of basal cisterns and generalized loss of gray-white differentiation LAB after dialysis: pH-7.36; HCO3-19 ; Na-132 ; K-2 ; BUN-37 (URR- 71%) AUTOPSY: Diffuse cerebral edema
    35. 35. Dialysis Disequilibrium SyndromeDialysis disequilibrium syndrome (DDS), a complication of haemodialysis, is characterized by neurological symptoms including headache, disorientation, nausea, seizures and coma. This syndrome is assumed to result from brain swelling occurring as a consequence of a rapid haemodialysis process.PATHOGENESIS:In uremic state there is a reduced expression of urea transporters and an increased expression of AQP in brain cells – consequentlyAcute urea removal occurs more slowly across BBB than from plasma generating a “reverse osmotic gradient” promoting water movement into brain.AVOID DDS initiating dialysis “gently”: less efficient dialyzer, reduce session length ,reduce blood flow rate , run blood and dialysate in the same direction ( less diffusion) , add osmols to dialysate
    36. 36. Dialysis Disequilibrium SyndromeDialysis disequilibrium syndrome (DDS), a complication of haemodialysis, is characterized by neurological symptoms including headache, disorientation, nausea, seizures and coma. This syndrome is assumed to result from brain swelling occurring as a consequence of a rapid haemodialysis process.PATHOGENESIS:In uremic state there is a reduced expression of urea transporters and an increased expression of AQP in brain cells – consequentlyAcute urea removal occurs more slowly across BBB than from plasma generating a “reverse osmotic gradient” promoting water movement into brain.AVOID DDS initiating dialysis “gently”: less efficient dialyzer, reduce session length ,reduce blood flow rate , run blood and dialysate in the same direction ( less diffusion) , add osmols to dialysate
    37. 37. ‫הגיע הזמן לנוח... אבל קודם לחדר‬ ‫…‬ ‫דיאליזה‬
    38. 38. Dialysis Adequacy
    39. 39. Dialysis Adequacy
    40. 40. Dialysis Adequacy
    41. 41. Dialysis Adequacy
    42. 42. Dialysis Adequacy
    43. 43. Dialysis Adequacy
    44. 44. Dialysis Adequacy
    45. 45. Dialysis Adequacy
    46. 46. Dialysis Adequacy
    47. 47. Access Recirculation
    48. 48. Peritoneal Dialysis
    49. 49. Peritoneal DialysisTenckhof catheter
    50. 50. Principles of peritoneal dialysis
    51. 51. Principles of peritoneal dialysis Continuous Ambulatory Peritoneal Dialysis-CAPD
    52. 52. Principles of peritoneal dialysis Continuous Cycling Peritoneal Dialysis or Automated Peritoneal Dialysis ( APD ) Cycler Nightly Intermittent Peritoneal Dialysis
    53. 53. Peritoneal Equilibration Test
    54. 54. PERITONEAL FIBROSIS : SIMPLE SCLEROSIS ANDSCLEROSING PERITONITIS Simple Sclerosis Sclerosing Peritonitis Frequency very common very rare poor biocompatibility of peritoneal dialysis unknown, only risk factors due to osmotic agents, peritoneal dialysis-dependent risk hyperosmolarity, low pH, factors: buffer duration of dialysis poor biocompatibility acetate buffer Etiology disinfectants catheter in-line bacterial filters particles of plastics plasticizers peritonitis peritoneal dialysis-independent risk factors: beta-blockers tumors genetic predisposition Reproducibility yes with dialysis no with dialysis in animal models no without dialysis yes without dialysis Clinical severe absent manifestations high mortality
    55. 55. Simple sclerosis Sclerosing Peritonitis of macrophagic origin Giant cellssclerotic tissue limited to visceral and Fibroblasts and mesoblasts occur throughout theparietal peritoneum sclerotic tissue, but are often more frequent in deeper layers. In sclerosing peritonitis unlike simplethe thickness of sclerotic tissue in sclerosis, the muscle layer is compressed. Thesimple sclerosis does not exceed thickness of the sclerotic tissue is not uniform in a given patient but normally reaches very high values40-50 µm between 1,000 and 4,000 µm
    56. 56. In sclerosing peritonitis, unlike simple sclerosis, a dramaticprogression of the sclerosis occurs. This is combined with aspectsnot found in simple sclerosis, such as inflammatory infiltrates,calcifications and typical vascular alterations.The peritoneal surface is reduced to a rough thickened membranesimilar to the sole of a shoe .In extreme cases of sclerosingencapsulating peritonitis, the sclerotic process completely fixesgroups of intestinal loops, almost completely preventing theirmovement.Often the sclerosis is not homogeneous, but one area of theabdomen may be more affected than others, forming a mass. Thissituation has been described with the term "abdominal cocoon“.The cocoon may be perfectly palpable, like a tumor; the sclerotictissue of the cocoon usually contains loops of the small intestineand sacs of ascites, and often calcifications.
    57. 57. Encapsulating sclerosing peritonitis

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