![SLED
Sustained Low Efficiency Daily Dialysis
Hybrid haemodialysis[CRRT and IHD]
Is continuous low-efficiency haemodialysis using low
blood and dialysis flow rates-100-300mls/min
Timing 6- 12 hrs/day
Ideal for ICU patient improves survival](https://image.slidesharecdn.com/acutekidneyinjury-1-250808184706-3992fabd/85/Management-of-Acute-Kidney-Injury-at-LAUTECH-71-320.jpg)
![Continuous Peritoneal Dialysis
One fifth small solute clearance and buffer
absorption rates
Equal ultrafiltration rates
Higher rate of protein loss
“Sodium sieving”
Hypernatremia due to differential
water/sodium clearance [Aquaporins].](https://image.slidesharecdn.com/acutekidneyinjury-1-250808184706-3992fabd/85/Management-of-Acute-Kidney-Injury-at-LAUTECH-76-320.jpg)
Management of Acute Kidney Injury at LAUTECH
- 1. MANAGEMENT OF ACUTE KIDNEY INJURY BY DR. B. A. GBADEGESIN DEPARTMENT OF MEDICINE LAUTECH TEACHING HOSPITAL OGBOMOSO OYO STATE
- 2. DEFINITION ARF also known as Acute Kidney Injury is defined as a sudden deterioration in renal function which is usually, but not invariably reversible over a period of hours to days, characterized by accumulation of nitrogenous waste and disturbance of fluid and electrolyte homeostasis, with or without a reduction in urinary output.
- 3. RIFLE Classification of ARF into 5 categories (published in 2004 by the Acute Dialysis Quality Initiative (ADQI) group – based on changes from the patient's baseline either in serum creatinine level or glomerular filtration rate (GFR), urine output (UO), or both.
- 4. Risk (R) - Increase in serum creatinine level X 1.5 or decrease in GFR by 25%, or UO <0.5 mL/kg/h for 6 hours Injury (I) - Increase in serum creatinine level X 2.0 or decrease in GFR by 50%, or UO <0.5 mL/kg/h for 12 hours Failure (F) - Increase in serum creatinine level X 3.0, decrease in GFR by 75%, UO <0.3 mL/kg/h for 24 hours, or anuria for 12 hours
- 5. Loss (L) - Persistent ARF, complete loss of kidney function >4 wk End-stage kidney disease (E) - Loss of kidney function >3 months
- 7. Work Group Recommendations Diagnostic Criteria for AKI: Proposal An abrupt (within 48 hours) reduction in kidney function currently defined as an: 1.Absolute increase in serum creatinine of either >0.3mg/dl (>25 micromole/L) or a percentage increase of 50% OR 1.A reduction in urine output (documented oliguria of < 0.5ml/kg/hr for > 6 hour)*
- 8. MODIFICATION PROPOSED BY AKIN AMSTERDAM, 2006 Increased creatinine x 1.5 OR >0.3mg/dl UO < 0.5ml/kg/h x 6 hr Increased creatinine x 2 UO < 0.5ml/kg/h x 12 hr Increased creatinine x 3 or creatinine ≥4 mg/dl (acute rise of ≥0.5mg/dl) UO < 0.3ml/kg/h x 24 hr or Anuria x 12 hrs RRT Started High Sensitivity High Specificity R(I) I(II) F(III)
- 9. EPIDEMIOLOGY ARF affects approximately 1% of patients on admission to the hospital ( community aquired) 2% to 5% of patients develop ARF during hospital stay 4% to 15% develop ARF after cardiopulmonary bypass surgery. Prevalence in OAUTHC found to be 2% amongst hospitalized patients. (okunola et al)
- 10. EPIDEMIOLOGY In critically ill, 23-35%of ICU admissions Study by Okunola; 19.6% With RIFLE criteria 2/3 of ICU admission. common causes are severe sepsis and septic shock. high mortality in ARF assoc with sepsis (~70%)
- 11. mortality The mortality rate estimates, vary from 25- 90% depending on the cause The in-hospital mortality rate is 40-50%, and 70-80% in intensive care settings and correlates directly to the severity of the patients other disease processes. The mortality rate among patients presenting to the ED with prerenal ARF may be as low as 7%.
- 12. CLASSIFICATION 1. Volume of urine: - Oliguric - Non-Oliguric - Anuric 2. Etiology - Pre-renal 60-70% - intrinsic renal 25-40% - Post-renal 5-10% 3. Place of occurrence - ICU based - Hospital based - Community based
- 16. Peculiar aetiological factors in our Peculiar aetiological factors in our environment environment Nephrotoxins Nephrotoxins Native herbs Native herbs Drugs Drugs Cholera Cholera Sepsis Sepsis CuSo4 (green water) CuSo4 (green water)
- 17. Hypovolaemia Hypovolaemia Renal Perf Renal Perf Tubular damage Tubular damage GFR GFR Structural Proteins Structural Proteins Proteinuria Proteinuria Lipid Lipid peroxidation peroxidation Renal Renal Microvascular Microvascular Injury Injury Acute Acute Kidney Injury Kidney Injury / Failure / Failure Pathways Leading to AKI Pathways Leading to AKI Renal Renal Growth factor and Growth factor and cytokine activation cytokine activation ransdifferentiation of ransdifferentiation of enal Cells to fibroblast enal Cells to fibroblast phenotype phenotype Inflammation Inflammation Influx of Infl cells Influx of Infl cells Uraemia Uraemia Oedema Oedema Acidosis Acidosis Others eg Anaemia, Others eg Anaemia, Ca X PO bal Ca X PO bal Nephrotoxins Nephrotoxins Obstructive Obstructive Uropathy Uropathy
- 18. Investigations URINE Urine output: Approx 50-60% of all causes of ARF are nonoliguric. Anuria (<100 mL/d) - Urinary tract obstruction, renal artery obstruction, rapidly progressive glomerulonephritis, bilateral diffuse renal cortical necrosis Oliguria (100-400 mL/d) - Prerenal failure, hepatorenal syndrome Nonoliguria (>400 mL/d) - Acute interstitial nephritis, acute glomerulonephritis, partial obstructive nephropathy, nephrotoxic and ischemic ATN, radiocontrast-induced ARF, and rhabdomyolysis
- 19. Urinalysis Most important test in the initial evaluation of ARF . Reddish brown or cola-colored urine is present in patients with AGN or in the presence of myoglobin or hemoglobin. Dipstick assay findings may show the presence of significant proteinuria such as occurs in intrinsic renal diseases, including glomerulonephritis, acute interstitial nephritis, tubular necrosis, and vascular diseases.
- 20. Microscopy Normal urinary sediment without hemoglobin, protein, cells, or casts generally consistent with prerenal and postrenal failure, HUS/thrombotic thrombocytopenic purpura (TTP), preglomerular vasculitis, or atheroembolism Findings of granular muddy-brown casts are suggestive of tubular necrosis.
- 21. Granular casts - ATN, glomerulonephritis, interstitial nephritis The presence of tubular cells or tubular cell casts also supports the diagnosis of acute tubular necrosis (ATN). RBC casts - Glomerulonephritis, malignant HTN WBC casts - Acute interstitial nephritis, pyelonephritis Eosinophiluria – (wright or Hansel stain)Acute allergic interstitial nephritis, atheroembolism
- 22. Crystalluria - Acyclovir, sulfonamides, methotrexate, ethylene glycol toxicity, radiocontrast agents The presence of uric acid crystals may represent ATN associated with uric acid nephropathy, while calcium oxalate crystals may be present in ARF due to ethylene glycol poisoning.
- 23. Non-dysmorphic RBCs in urine (black arrows) and Dysmorphic RBCs (white arrow)
- 24. Dysmorphic RBCs in urine
- 25. Red Blood cell casts
- 32. Urine chemical indices To help with the differentiation of prerenal azotemia, analysis of urine may provide important clues. If possible, collect urine prior to any administration of diuretics. Urine indices that suggest prerenal ARF include the following: Urine specific gravity >1.018 Urine osmolality (mOsm/kg H2O) >500 Urine sodium (mEq/L) <15-20 Plasma BUN/creatinine ratio >20 Urine/plasma creatinine ratio >40
- 33. Urine indices that suggest ATN include the following: Urine specific gravity <1.012 Urine osmolality (mOsm/kg H2O) <500 Urine sodium (mEq/L) >40 Plasma BUN/creatinine ratio <10-15 Urine/plasma creatinine ratio <20
- 34. FeNa: useful in the presence of oliguria to diff. between Pre and Intrinsic ARF FeNa = (urine Na/plasma Na)/(urine creatinine/plasma creatinine) FeNa <1 % = prerenal ARF FeNa >1% = ATN Advantages of FeNa compared to other indices Physiologic measure of sodium reabsorption FeNa increased before oliguric phase is established and predictive of incipient ARF
- 35. Exceptions (intrinsic renal failure with FeNa <1%) Urinary tract obstruction Acute glomerulonephritis Hepatorenal syndrome Radiologic contrast–induced ATN Myoglobinuric and hemoglobinuric ARF Renal allograft rejection Drug-related alterations in renal hemodynamics (eg, captopril, NSAIDs)
- 36. In the presence of liver disease, FeNa can be < 1% in the presence of ATN. On the other hand, because administration of diuretics may cause the FeNa to be > 1%, these findings cannot be used as the sole indicators in ARF. In patients who are receiving diuretics, a fractional excretion of urea (FeUrea) can be obtained because urea transport is not affected by diuretics. The formula for calculating the FeUrea is as follows: FeUrea = (Uurea/Purea) / (UCr/PCr) X 100
- 38. Pre- renal Pre- renal azotemia azotemia Intrinsic Acute Renal Failure Intrinsic Acute Renal Failure Post renal Post renal azotemia azotemia ATN (oliguric ATN (oliguric or polyuric) or polyuric) AGN AGN AIN AIN aetiology aetiology Renal Renal hypoperfus hypoperfus ion ion Ischemia Ischemia Nephrotoxins Nephrotoxins Post strept Post strept Collagen Collagen vascular dz vascular dz Allergic rxn Allergic rxn Drug rxn Drug rxn Obstruction Obstruction BUN:Cr BUN:Cr >20:1 >20:1 <20:1 <20:1 >20:1 >20:1 <20:1 <20:1 >20:1 >20:1 Urine Na Urine Na <20 <20 >20 >20 <20 <20 Variable Variable Variable Variable FeNa FeNa <1 <1 >1 >1 <1 <1 <1;>1 <1;>1 Variable Variable Urine Urine osmolality osmolality mOsm/L mOsm/L >500 >500 250 – 300 250 – 300 Variable Variable Variable Variable <400 <400 Urine Urine microscop microscop y y Hyaline Hyaline casts casts Granular casts Granular casts Renal Tubular Renal Tubular casts casts Dysmorphic Dysmorphic RBC RBC RBC casts RBC casts WBC, WBC WBC, WBC casts ± casts ± eosinophils eosinophils N or RBCs, N or RBCs, WBCs, or WBCs, or crystals crystals Differences btw the various types of ARF
- 39. BLOOD INVESTIGATIONS Blood urea nitrogen and serum creatinine Although increased levels of serum urea and creatinine are the hallmarks of renal failure, the rates of BUN and creatinine increases are also very important. Serum urea test findings showing an increase that is disproportionately larger than that of creatinine suggest prerenal ischemia.
- 40. The ratio of serum urea to creatinine also is an important finding because the ratio is > 20:1 in pre- renal ARF, and < 20:1 in intrinsic ARF. Other conditions causing a serum urea-to-creatinine ratio of greater than 20:1 are increased enteral or parenteral protein load, corticosteroid therapy, and a hypercatabolic state
- 41. Serum electrolytes: may show : hyperkalaemia, metabolic acidosis, hypocalcaemia, hyperphosphataemia Complete blood cell count and peripheral smear Leucocytosis may be seen in cases of septicaemia Anaemia may be evident Peripheral smear results may show schistocytes in conditions such as HUS or TTP
- 42. Rouleaux formation suggests multiple myeloma, and the workup should be directed toward protein electrophoresis of serum and urine. The presence of schistocytes, myoglobin or hemoglobin, increased serum uric acid level, and other related findings may help further define the etiology of ARF. Findings from serology tests for ANA indicate intrinsic renal disease due to vasculitis.
- 43. IMAGING Renal ultrasonography is useful for evaluating existing renal disease and obstruction of the urinary collecting system. This test is also useful for detecting intrinsic renal disease, which enhances renal echogenicity; however, this finding is nonspecific. Ultrasonography also aids in performing a renal biopsy.
- 44. Doppler scans Doppler scans are useful for detecting the presence and nature of renal blood flow. Useful in the diagnosis of thromboembolic or renovascular disease. Nuclear scans Radionuclide imaging with a technetium Tc 99m diethylenetriamine pentaacetic acid (DTPA), 99m Tc-DTPA iodine I 131 – hippuran scan can be used to assess renal blood flow and tubular functions.
- 45. Aortorenal angiography can be very helpful in the diagnosis of renal vascular diseases, including renal artery stenosis, renal atheroembolic disease, atherosclerosis with aortorenal occlusion, and in certain cases of necrotizing vasculitis (eg, polyarteritis nodosa).
- 46. Renal biopsy A renal biopsy can be very useful in the diagnosis of intrarenal causes of ARF. In as many as 40% of cases, renal biopsy results reveal an unexpected diagnosis. A renal biopsy is especially useful in rapidly progressive glomerulonephritis due to crescentic glomerulonephritis when clinical differentiation between acute glomerulonephritis and interstitial nephritis becomes difficult. Acute cellular rejection in a renal transplant can be definitively diagnosed only by performing a renal biopsy.
- 48. Other diagnostic Markers of Acute Renal Other diagnostic Markers of Acute Renal Injury Injury Increase in Serum creatinine Increase in Serum creatinine N-acetly N-acetly β β-D glucosamine NAG, (increase) -D glucosamine NAG, (increase) β β2 2 microglobulin (> 500ng/min) microglobulin (> 500ng/min) Increase low mol.protein Increase low mol.protein Very LMW protein Very LMW protein Retinol binding protein Retinol binding protein Albumin- microalbuminuria Albumin- microalbuminuria
- 49. Management The aim of mgt of AKI is to keep the pt alive until spontaneous recovery of renal function occurs, prevent complications and prevent further insults. Pt should be managed by a nephrologist General measures Good nursing Strict I/o Daily weighing Regular oral toileting Physiotherapy
- 50. Lines of treatment in established ARF Continued treatment of the initiating cause of ARF The use of drugs that may alter the course of ARF. Adequate nutrition Renal replacement therapy Management of specific problems
- 51. Management of AKI Treat precipitating event / condition Conservative Management RRT
- 52. AKI Management AKI Management Conservative Conservative RRT RRT Fluid Balance Fluid Balance Electrolytes Electrolytes Acute Intermittent • Intermittent PD Intermittent PD • Intermittent HD Intermittent HD • Intermittent HF Intermittent HF • SLED SLED • EDD EDD • SCUF SCUF • CAVH CAVH • CVVH CVVH • CAVHD CAVHD • CVVHD CVVHD • CAVHDF CAVHDF • CVVHDF CVVHDF Continuous Diet Diet Treat Primary Condition Treat Primary Condition • APD APD • AHD AHD • CAPD CAPD • CCPD CCPD
- 53. Fluid Management Limit fluid intake to insensible loss (500-1200mls/day) Replace volume of urine / other documented losses in the previous 24 hours Avoid Potassium containing fluids Diuretics may be useful in pre-renal ARF
- 54. Maintenance of fluid homeostasis In pre-renal ARF Rapid replacement of lost volume in cases of hypovolaemia or haemorrhage is essential in preventing development of ATN Use of isotonic saline intravenously restores circulatory volume In cases of CCF, use of diuretics (frusemide) is important to reduce LV pressure and encourage renal perfusion In cases where fluid challenge is done, it is advocated that the CVP or the pulmonary capillary wedge pressure be monitored to prevent circulatory overload
- 55. In intrinsic ARF Fluid management depends on the phase of ARF In the oliguric phase (iniation phase) fluid intake is restricted to previous day’s urinary output + insensible loss (1500ml). This is to prevent overloading the patient with fluid, hence preventing development of life threatening pulmonary edema
- 56. In the diuretic phase, renal perfusion improves but tubular cells have not fully recovered their functional capacity. There is thus gross diuresis amounting to litres/day Prompt replacement of fluid ml for ml is important in this phase. Failure to do this results in mortality from volume depletion and shock Continued fluid homeostasis monitoring is continued in the recovery phase.
- 58. Emergency Measures - Manage hyperkalemia Immediate: (a) Protect myocardium 10ml of 10% calcium glucomate (can be repeated) Do ECG (b) Drive K+ into cells Insulin 10units + 50ml of 50% glucose (c) Salbutamol 0.5mg in 100ml of 50% Glucose near 15min. (d) Later: Deplete body K+ with polystyrene sulphonate resin 15g p.o x tds with laxatives OR 30g rectally ff by enema. (f) Haemodialysis or peritoneal dialysis
- 61. - Manage pulmonary oedema - Treat infection - Fluid and electrolyte balance - Diet decrease Na, low or normal protein (40/704). High colorie diet (CH20 100g/day) - Correct acidosis if +Hco3- is <15mmol/L - Hyperphosphotamic – Rx with CaCo3 or other po42+ binders. - Renal replacement therapy
- 62. Acidosis Corrected using IV 8.4% Sodium bicarbonate Amount required is calculated thus: requirement = HCO3 – deficit x 0.3 x weight Hypocalcaemia Calcium lactate may be used to correct hypocalcaemia It also prevents absorption of phosphate from the GIT Dose 150 – 300 mg t.d.s
- 63. Nutrition in ARF ARF is a catabolic state: Hormonal disturbances (including glucocorticoid excess and insulin resistance) Metabolic acidosis The release of proteinases into the circulation Changes in the metabolism of branched-chain amino acids Loss of different nutritional ingredients in dialysis or haemofiltration
- 64. Diet and Calorie High calorie low protein in acute phase High calorie normal protein in recovery phase Parenteral hyperalimentation may become necessary in prolonged cases
- 65. Newer Treatment modalities Modulating Vasoconstriction Calcium channel antagonists eg Transplant, CyA exposure, Radiocontrast Nephropathy Dopamine – Not effective from studies ANP may initiate diuresis in oliguric patients Endothelin blockade Nitric oxide modulation N acetyl cysteine use
- 66. Newer Treatment modalities Limiting Inflammation Inhibition of chemokine production eg α-MSH Anti Adhesion strategies Anti ICAM Anti Integrins PPAR ligands eg etomoxir Biocompatible membranes Cytokine absorbing membranes
- 67. Renal Replacement Therapy For ARF CRRT HD PD
- 68. Haemodialysis Removes solutes by diffusion across a concentration gradient Movement of water carrying solutes across the dialysis membrane is NOT necessary for solute transport Have 3 types: Low Efficiency, High Efficiency and High Flux
- 69. Haemofiltration Removes small solutes and middle molecules by convection with High Flux dialyzers Can remove large amounts of fluid No dialysate is used only sterile replacement fluid infused after haemofiltration occurs CAVH / CVVH or Intermittent HF (expensive)
- 70. Haemodiafiltration 2 types CAVHDF and CVVHDF Removes solutes by convection with High Flux dialyzers like CAVH and CVVH Used in ICU as a CRRT therapy Dialysate flows continuously in dialysate compartment to increase solute removal by diffusion. Convection is major route of solute removal
- 71. SLED Sustained Low Efficiency Daily Dialysis Hybrid haemodialysis[CRRT and IHD] Is continuous low-efficiency haemodialysis using low blood and dialysis flow rates-100-300mls/min Timing 6- 12 hrs/day Ideal for ICU patient improves survival
- 72. Advantages of SLED Haemodynamic stability Requires less anticoagulation Cheaper than the CRRT treatments Requires less manpower than CRRT Offers CRRT on a haemodialysis machine Ideal for ARF improves survival
- 73. RRT STARTING CRITERIA Anuria – Oliguria (diuresis 200ml in 12 h) Severe metabolic acidosis (pH < 7.10) Hyperazotemia (BUN ≥ 80 mg/100 ml) Hyperkalemia (K ≥ 6.5 mEq/L) Clinica signs of uremic toxicity Severe Dysnatremia (Na+ 15 0 ≥ 160 mEq/L) Hyperthermia Anasarcha or severe fluid overload Multiple Organ Failure including renal dysfunction SIRS, Sepsis or Septic shock with renal dysfunction ADQI
- 74. DIALYTIC THERAPY IHD VS CRRT
- 75. PD PD offers safe, effective, low cost and biocompatible dialysis system for ARF patient.
- 76. Continuous Peritoneal Dialysis One fifth small solute clearance and buffer absorption rates Equal ultrafiltration rates Higher rate of protein loss “Sodium sieving” Hypernatremia due to differential water/sodium clearance [Aquaporins].
- 77. Advantages Haemodynamical stability Slow correction of metabolic imbalances Easy access placement Systemic anticoagulation not required
- 78. Summary Data do not support the superiority of any particular mode of RRT in patients with AKI. Selection of modality should therefore be based upon local expertise and availability of staff and equipment. However, in selected patients other factors may prevail. E.g in patients with acute brain injury or fulminant hepatic failure, CCRT may be associated with better preservation of cerebral perfusion.
- 79. Poor prognostic factors age > 70 advanced malignancy Liano score > 85% Multi-organ failure > 3 Mortality > 83% with 4 or more failed organs Prognosis
- 80. Other poor prognostic factors include the following: Co morbidities Multi-organ failure (> 3 organ failure is associated with 100% mortality) Anuria Hypotension Vasopressor support Number of transfusions Failure to institute RTT when needed