19 Shoeb Bin Islam   Acute Renal Failure
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19 Shoeb Bin Islam Acute Renal Failure

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19 Shoeb Bin Islam   Acute Renal Failure 19 Shoeb Bin Islam Acute Renal Failure Presentation Transcript

  • Clinical Presentation SCU Dr. Shoeb Bin Islam Senior Clinical fellow Icddr,b
  • Case History Name : x Age : 18 years Sex : Female D/A : 20/04/09 D/D : 02/05/09 Admission problems : (Partial History at the beganing) 1) Diarrhoea - 1 days 2) Vomiting - 1days 3) Fever - 1days 4) Drowsy – 1 hour (Actually patient had no real attendant, we collected information from a person who did not give proper history and after than he left away )
  • ON EXAMINATION On Examination Patient was Drowsy followed by Unconciousness and febrile Pulse : 100 / min, regular, moderate volume R/R : 22 / min, no chest in drawing. Temperature : 39`C Blood Pressure : 100/65mmHg Pallor, cyanosis, jaundice, oedema - Nil Dehydration :Some DH
  • Nervous sytem Examination- patient unconcious Kernig`s Sign - Negative Pupil – normal in size and reacting to light After 10-12 hours patient developed repeated convulsion Urination- Urine Passed ?7-8 hour prior to admission (scanty) Other systems(CVS,RESPIRATORY,GIT) revealed nothing abnormalities •*Actually patient had no real attendant, we collected information from a person who did not give proper history and after than he left away .
  • PROBLEM LIST *ACUTE WATERY DIARRHOEA *SOME D/H *FEVER *UNCONCIOUSNESS (? MENINGITIES ) *?RENAL FAILURE( Uremic Encephalopathy) *SEPTECEMIA * LACK OF PROPER HISTORY
  • LABORATORY INVESTIGATIONS CBC:- Hemoglobin-10.9gm/dl Hct – 33.6%, TC- 12.97 / 10^u, Poly – 83.8%, Lymp – 12.7%, Band – 00%, Monocytes – 3.4%, Eosinophil – 00% Basophil- 0.1% ESR - 48 mm/1st hour R/S for Cholera:- Vibrio Cholera01 E1 Tor Ogawa CXR- Normal study Blood C/S No Growth USG and Urine R/M/E WBC cast and Epithelial cell-7-8 Protein-+
  • SERUM ELECTROLYTE REPORTS 21/04/09 24/04/09 25/04/09 01/05/09 S.Na+ 126.7mmol/l 128.6mmol/L 130.7mmol/L 141.2 S.K+ 2.4 mmol/L 2.73 mmol/L 2.45 mmol/L 3.02 S.Cl- 90.1mmol/l 93 mmol/L 95.8mmol/L 106 TCO2 16.8mmol/L 13.5mmol/L 14.8mmol/L 23.9 ANION 22.2mmol/L 24.83mmol/L 22.5 mmol/L 14.32 GAP OTHERS BUN- 138.94mg/dl BUN- 133.94mg/dl BUN- 60.76mg/dl UREA- 49.26 mmol/L UREA- 47.83mmol/L UREA- 21.7mmol/L URINARY ELECTROLYTE U.Sodium- 44.7mmol/L U.Potassium- 12.77mmol/L U.Cl- - 33mmol/L TCO2- 5mmol/L U.Creatinine (Random)- 7211 umol/L
  • SERUM CREATININE DATE SERUM SERUM 1000 CREATININE CREATININE 900 (UMOL/L) (mg/dl) 800 700 600 500 21/04/09 582.6 6.5 400 300 200 23/04/09 773.3 8.7 100 0 21/04/09 23/04/09 24/04/09 25/04/09 29/04/09 1/5/2009 24/04/09 882.3 9.9 25/04/09 915.6 10.3 *TOTAL DAYS - 11 DAYS 29/04/09 459.2 5.1 1 mg/dl = 88.4 umol/L 01/05/09 126.4 1.4
  • MANAGEMENT Tab.Azythromycin for Cholera Some D/H - I/V Acetate Septicemia – Inj. Ceftriaxone Convulsion - Inj. Diazepam + Inj. Phenoberbitone For Hypokalamia – Syp Kcl through NG Tube For Fluid over load - Inj Frusemide Changing position Frequently Proper Nursing care Maintain urine input &output chart and fluid Intake accordingly We had a plan to Refer the patient to Kidney hospital but we could not manage any attendant .
  • RENAL FAILURE DIAGNOSIS & MANAGEMENT OF AN UNCONCIOUS & UNATTENDENT PATIENT
  • Anatomy: The Renal System • Kidneys • Ureters – Enter at oblique angle – Peristalsis • Both prevent reflux • Bladder – Capacity 300–500 ml • Urethra – Excretion; outside of body. – In Males surrounded by prostate
  • How Do We Proceed? Reduce Urine output/Anuria /urine abnormality ?Renal failure ?Acute or Chronic Renal Failure If Acute renal Failure Prerenal Renal Postrenal ATN Develop or Not ATN cause by Ischemia ATN caused by Nephrotoxic Drugs Fig: Algorithm for diagnosis and causes of renal failure of a unconscious patient where proper history cannot elicited .
  • Classification system for AKI Classification system for AKI GFR Criteria Urine Output criteria Risk High Sensitivity Injury Failure High Specificity Loss EKSD
  • RIFLE criteria for diagnosis of AKI Increase in SCr Urine output Risk of renal injury 0.3 mg/dl increase < 0.5 ml/kg/hr for > 6 h Injury to the kidney 2 X baseline < 0.5 ml/kg/hr for >12h Failure of kidney 3 X baseline OR Anuria for >12 h function > 0.5 mg/dl increase if SCr >=4 mg/dl Loss of kidney Persistent renal failure function for > 4 weeks End-stage disease Persistent renal failure for > 3 months
  • DEFINATION Definition: Means an abrupt deterioration of renal function within hours, leading to retention of water, crystalloids and nitrogenous products. Rapid decline in the GFR over days to weeks- Cr increases by >0.5 mg/dL GFR <10mL/min, or <25% of normal Documented oliguria of <0.5 ml/kg/hr for 12 hrs Acute Renal Insufficiency- Deterioration over days-wks GFR 10-20 mL/min
  • Definition •Acute renal failure is • Chronic renal failure sudden loss of the is a gradual and ability of the kidneys to progressive loss of excrete the ability of the wastes, concentrate kidneys to excrete urine, and conserve wastes, concentrate electrolytes. ("Acute" urine, and conserve means sudden, "renal" electrolytes. refers to the kidneys.) – Kidney Damage for > 3 – Rapid decline in GFR months (Over Hours To Days) – Irreversible – Usually Reversible – 75-60% of function can be lost before its noticeable
  • Differentiating ARF vs. Chronic Renal Failure (CRF) 1) History 2) Oliguria = ARF; acute CRF decompensation 3) Renal ultrasound • Normal or large = acute • CRF – small (unless PKD, diabetes, amyloid) 4) ARF =Unstable azotemia (↑ or ↓ over days) 5) Anemia – unreliable for ARF vs. CRF 6) ↑PO4, ↑K+, metabolic acidosis, ↑uric acid –little diagnostic value 7) Urinalysis – no value unless normal suggesting pre-renal azotemia .
  • CLASSIFICATION OF RENAL FILURE Classification GFR (mls/min/1.73m2) Serum Creatinine (mol/L) Mild 20 to 50 150 to 300 Moderate 10 to 20 300 to 700 Severe < 10 > 700 Appendix 3 : BNF
  • Types of Acute Renal Failure Acute renal failure Prerenal Intrarenal Postrenal Factitious Vascular Glomerular Tubular Interstitial Ischemia Toxins Pigments JASN 1998;9(4):710-718
  • STAGES Onset – 1-3 days with ^ BUN and creatinine and possible decreased UOP Oliguric – UOP < 400/d, ^BUN,Crest, Phos, K, may last up to 14 d Diuretic – UOP ^ to as much as 4000 mL/d but no waste products, at end of this stage may begin to see improvement Recovery – things go back to normal or may remain insufficient and become chronic
  • Definitions Anuria: No UOP or urine output less than 50cc/24hr. Oliguria: UOP<400-500 mL/d Azotemia: Incr Cr, BUN • May be prerenal, renal, postrenal • Does not require any clinical findings Ureamia : Azotemia + Clinical Menifastation
  • Prerenal ARF • It occurs when renal blood flow is decreased before reaching the kidney, causing ischemia of nephrons. – ↓ Renal Perfusion = ↓ GFR leading to Oliguria – Most common type of ARF – Common Causes: • Hypotension (severe and abrupt) • Hypovolemia • Low Cardiac Output States – Treatment to correct cause, if not corrected it may lead to permanent renal damage. THE KIDNEYS ARE NORMAL
  • Prerenal Disease Prerenal Disease *True volume depletion *Advanced liver disease *Congestive heart failure *Renal arterial disease *Perinatal or Neonatal hemorrhage *Perinatal asphyxia and hyaline membrane disease *Gastroenteritis *Congenital and acquired heart diseases 26
  • Intrinsic Renal Failure Intrinsic Renal Failure I. Renovascular obstruction (bilateral, or unilateral in the setting of one kidney)- A. Renal artery obstruction: atherosclerotic plaque, thrombosis, embolism, dissection aneurysm, large vessel vasculitis . B. Renal vein obstruction: thrombosis or compression II. Diseases of the glomeruli or vasculature - A. Glomerulonephritis or vasculitis B. Other: thrombotic microangiopathy, malignant hypertension, collagen vascular diseases (SLE) III. Acute tubular necrosis - A. Ischemia: causes are the same as for prerenal ARF, but generally the insult is more severe and/or more prolonged B. Infection, with or without sepsis syndrome C. Toxins: 1. Exogenous: radiocontrast, calcineurin inhibitors, antibiotics (e.g., aminoglycosides), 2. Endogenous: rhabdomyolysis, hemolysis 27
  • IV. Interstitial nephritis – A. Allergic: antibiotics ( -lactams, sulfonamides, quinolones, rifampin), nonsteroidal anti- inflammatory drugs, diuretics, other drugs B. Infection: pyelonephritis (if bilateral) C. Infiltration: lymphoma, leukemia, sarcoidosis D. Inflammatory, nonvascular: Sjögren's syndrome, tubulointerstitial nephritis with uveitis V. Intratubular obstruction – A. Endogenous: myeloma proteins, uric acid (tumor lysis syndrome), systemic oxalalosis B. Exogenous: acyclovir, gancyclovir, methotrexate, indinavir
  • Prerenal Azotemia and Ischemic tubular necrosis Prerenal azotemia - Intact Tubular Function ATN - Renal Tubule Epithelium ( also Basement Membrane) Destruction. There are two major histiologic changes that take place in ATN: - (1) tubular necrosis with sloughing of the epithelial cells (2) occlusion of the tubular lumina by casts and by cellular debris. Prerenal Azotemia is the main factor that predisposes patients to ischemia- induced acute tubular necrosis (ATN) Most cases of ischemic ARF are reversible if the underlying cause is corrected.
  • In addition of the tubular obstruction, two other factors appear to contribute to the development of renal failure in ATN:- across the damaged tubular epithelia backleak of filtrate and a primary reduction in glomerular filtration. The decrease in glomerular filtration results both from arteriolar vasoconstriction and from mesangial contraction. The decline in renal function begins abruptly following a hypotensive episode, rhabdomyolysis, or the administration of a radiocontrast media. When aminoglycosides are the cause, the onset is more insidious, with the first rise in creatinine being at seven or more days.
  • AIN From Drugs Renal damage is NOT dose-dependent May take wks after initial exposure to drug • Up to 18 mos to get AIN from NSAIDS! But only 3-5 d to develop AIN after second exposure to drug • Fever (27%) • Serum Eosinophilia (23%) • Maculopapular rash (15%) • Bland sediment or WBCs, RBCs, non-nephrotic proteinuria • WBC Casts are pathognomonic! • Urine eosinophils on Wright’s or Hansel’s Stain – Also see urine eos in RPGN, renal atheroemboli...
  • Difference Between Ischemic and Nephrotoxic ATN Ischaemic ATN Nephrotoxic ATN (Due to Hypovolumia) Background History Diarrhoea,Vomitting,heart failure,Shock Drugs,Toxin Kidney Invilvement 3rd Segment of proximal tubule Mostly proximal convoluted (proximal tubule – Reabsorb 65% of tubule Sodium) and Assending Loop of henlee (Reabsorb 25% of Sodium) FeNa Usually >3% Usually >1% ( 2-3%) Clinical Triat Fever ,Rash ,Eosinophilia nit associated Mostly Present UNa Usually Greater >40 Comperatively low(>20) (Gradually Increasing from >20) Urinary Protein Absent/+ +/++ WBC Cast Absent pathognomic Eosinophiluria on Wrights Absent Mostly present or Hansels Strain Treatment Restore renal function Usually Fluid And Stop Offending drugs and sometimes Steroid
  • Reabsorb 25% of Sodium Reabsorb 65% of Sodium
  • How Do We Proceed Reduce Urine output/Anuria /urine abnormality ?Renal failure ?Acute or Chronic Renal Failure If Acute renal Failure Prerenal Renal Postrenal ATN Develop or Not ATN cause by Ischemia ATN caused by Nephrotoxic Drugs Fig: Algorithm for diagnosis and causes of renal failure of a unconscious patient where proper history cannot elicited .
  • MINIMUM STEPS FOR DIAGNOSIS History Taking General and Systemic Examination Laboratory investigation Serum Electrolyte Urine R/M/E USG OF ABDOMAN Serum Creatinine Urinary Electrolyte BUN Urinary Creatinine Urinary Urea Urea - Is the By-product of Protein metabolism Creatinine- Is the By-product of Muscle metabolism
  • Some Important Formula GFR = F (140 – age [yrs]) Ideal Body Wt (kg) Serum creatinine (mol/L) Where: F = 1.23 for males and 1.04 for females FeNa = (urine Na x plasma Cr) x100 (plasma Na x urine Cr) BUN: Cr = blood urea nitrogen:creatinine ratio Pre-renal=Creatinine cannot be reabsorbed, thus leading to a BUN/Cr ratio of > 20 UNa = urinary concentration of sodium;
  • Predicting GFR using serum and urine creatinine concentrations. Cockcroft and Gault Equation GFR = F (140 – age [yrs]) Ideal Body Wt (kg) Serum creatinine (mol/L) Where: F = 1.23 for males and 1.04 for females IBW = 50 kg + 2.23 kg for every 1” > 5 feet in height (male) IBW = 45.5 kg + 2.3 kg for every 1” > 5 feet in height (female)
  • Assessing the patient with acute renal failure – Laboratory analysis • Fractional excretion of sodium: (UrineNa+ x PlasmaCreatinine) FENa= ______________________ x 100 (PlasmaNa+ x UrineCreatinine) It is the Simple measurement of Tubular Excretory function – FENa < 1% → Prerenal – FENa > 2% → Epithelial tubular injury (acute tubular necrosis), obstructive uropathy – If patient receiving diuretics, can check FE of urea.
  • FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr) FeNa <1% 1. PRERENAL • Urine Na < 20. Functioning tubules reabsorb lots of filtered Na 2. ATN (unusual) • Postischemic dz: most of UOP comes from few normal nephrons, which handle Na appropriately • ATN + chronic prerenal dz (cirrhosis, CHF) 3. Glomerular or vascular injury • Despite glomerular or vascular injury, pt may still have well- preserved tubular function and be able to concentrate Na
  • More FeNa FeNa 1%-2% 1. Prerenal-sometimes (eg-Related with Sepsis) 2. ATN-sometimes 3. AIN-higher FeNa due to tubular damage FeNa >2%-3% 1. ATN Damaged tubules can't reabsorb Na.usually nephrotoxic ,Sepsis FeNa >3% Goes in Favour of Ischaemic ATN
  • Guide To The Differential Diagnosis of intrinsic ARF Eosinophiluria Present: Acute Interstitial nephritis likely Eosinophiluria Absent: Acute interstial nephritis possible Muddy Brown Granular Casts
  • Assessing patient with acute renal failure – Urinary Casts Red cell casts Glomerulonephritis Vasculitis White Cell casts Acute Interstitial nephritis Fatty casts Nephrotic syndrome, Minimal change disease Muddy Brown casts Acute tubular necrosis
  • RBC cast Hyaline cast Granular cast Granular cast Granular cast WBC cast Oval fat body WBC cast and Hyaline cast
  • Classification and differential diagnosis of acute renal failure Intrinsic Renal Disease Prerenal Azotemia Postrenal Azotemia Acute Tubular Acute Acute Necrosis Glomerulonephritis Interstitial (Oliguric or Polyuric) Nephritis Etiology Poor renal Obstruction of the Ischemia, Poststreptococcal; Allergic perfusion urinary tract nephrotoxins collagen-vascular reaction; drug disease reaction Serum BUN:Cr ratio > 20:1 > 20:1 < 20:1 > 20:1 < 20:1 Urinary indices UNa (mEq/L) < 20 Variable > 20 < 20 Variable FENa (%) <1 Variable >1 <1 < 1; > 1 Urine osmolality > 500 < 400 250–300 Variable Variable (mosm/kg) Urinary sediment Benign or Normal or red cells, Granular Dysmorphic red cells White cells, hyaline casts white cells, or crystals (muddy brown) and red cell casts white cell casts, renal tubular casts, with or casts without eosinophils BUN: Cr = blood urea nitrogen:creatinine ratio; UNa = urinary concentration of sodium; FENa = fractional excretion of sodium
  • ATN Prerenal Cr increases at increases 0.3-0.5 /day slower than 0.3 /day U Na, UNa>40 UNa<20 FeNa FeNa >2% FeNa<1% UA epi cells, Normal granular casts Response to Cr won’t Cr improves volume improve much with IVF BUN/Cr 10-15:1 >20:1 The FENa tends to be high in ischemic ATN but is often low in patients with sepsis-induced, pigment-induced, and some forms of nephrotoxic ATN (e.g., contrast-associated). Patients with acute interstitial nephritis may present with triad of fever, rash, and eosinophilia) UA (1 - 2+ protein, renal tubular epithelial cells, wbc’s - eosinophils, wbc casts)
  • Intervention by Inj.Frusemide and its outcome of an ARF ( Develop ATN) 1st 2nd 3rd 4th 5th 6th Total Duratio n Pt-1 6.9 9.45 6.09 2.7 2.0 1.4 6 Days Pt-2 4.6 3.4 6.0 4.8 3.3 2.3 (day 6) 7 days 1.3(day 7) Pt-3 6.5 8.7 9.9 10.3 5.1 1.4 11 Days -Day -3 day-4 Day-5 Day-9 day-11 Patient develop ATN Due to Prerenal cause Cholera patient-1 Cholera patient-2 Septicemia patient FeNa 4.24% 3% 1.13% GFR 7 ( Severe) 8 (Severe) 18.6 ( Moderate) BUN/Cr 13.92 5.06 20 Urinary Na 44.7 17.9 34.6 Renal Index 5.46 3.7 1.5 USG Noraml Normal Suggestive of bilateral parenchymal Diseases
  • Acute Renal Failure Urinary Indices ATN ATN PR PR ATN 500 40 40 1.0 1.0 350 20 20 ATN ATN PR PR PR UOsm (U/P)Cr UNa RFI FENa (mOsm/L) (mEq/L)
  • Pathoetiology Medication Clinical findings Treatment ACE, angiotensin-converting enzyme; ATN, acute tubular necrosis; CPK, creatinine phosphokinase; FENa, fractional excretion of sodium; LDH, lactate dehydrogenase; NSAIDs, nonsteroidal anti-inflammatory drugs; UOsm, urine osmolality. Diuretics, NSAIDs, ACE inhibitors, ciclosporin, Suspend or discontinue tacrolimus, radiocontrast Benign urine sediment, FENa medication, volume Prerenal injury media, interleukin-2, <1%, UOsm >500 replacement as clinically vasodilators (hydralazine, indicated calcium-channel blockers, minoxidil, diazoxide) Ciclosporin, tacrolimus, mitomycin C, conjugated Intrinsic renal injury (vascular estrogens, quinine, 5- Fever, microangiopathic, Discontinue medication, effects: thrombotic fluorouracil, ticlopidine, hemolytic anemia, supportive care, microangiopathy) clopidogrel, interferon, thrombocytopenia plasmapheresis if indicated valaciclovir, gemcitabine, bleomycin Fever, microangiopathic, Discontinue medication, Intrinsic renal injury (vascular Heparin, warfarin, hemolytic anemia, supportive care, effects: cholesterol emboli) streptokinase thrombocytopenia plasmapheresis if indicated Aminoglycosides, radiocontrast media, cisplatin, nedaplatin, methoxyflurane, outdated tetracycline, amphotericin B, cephaloridine, streptozocin, tacrolimus, carbamazepine, FENa >2%, UOsm <350, urinary Intrinsic renal injury (tubular Drug discontinuation, mithramycin, quinolones, sediment with granular casts, toxicity) supportive care foscarnet, pentamidine, tubular epithelial cells intravenous gammaglobulin, fosfamide, zoledronate, cidofovir, adefovir, tenofovir, mannitol, dextran, hydroxyethylstarch
  • Intrinsic renal injury Lovastatin, ethanol, codeine, Elevated CPK, ATN urine Drug discontinuation, (rhabdomyolysis) barbiturates, diazepam sediment supportive care Quinine, quinidine, Intrinsic renal injury sulfonamides, hydralazine, High LDH, decreased Drug discontinuation, (severe hemolysis) triamterene, nitrofurantoin, hemoglobin supportive care mephenytoin Penicillin, methicillin ampicillin, rifampin, sulfonamides, thiazides, cimetidine, phenytoin, allopurinol, Intrinsic renal injury Fever, rash, eosinophilia, cephalosporins, cytosine (immune-mediated urine sediment showing Discontinue medication, arabinoside, furosemide, interstitial pyuria, white cell casts, supportive care interferon, NSAIDs, inflammation) eosinophiluria ciprofloxacin, clarithromycin, telithromycin, rofecoxib, pantoprazole, omeprazole, atazanavir Gold, penicillamine, captopril, NSAIDs, lithium, mefenamate, Edema, moderate to severe Intrinsic renal injury Discontinue medication, fenoprofen, mercury, interferon- proteinuria, red blood cells, (glomerulopathy) supportive care , pamidronate, fenclofenac, red blood cell casts possible tolmetin, foscarnet Obstruction Aciclovir, methotrexate, Sediment can be benign Discontinue medication, (intratubular: crystalluria sulfanilamide, triamterene, with severe obstruction, supportive care and/or renal lithiasis) indinavir, foscarnet, ganciclovir ATN might be observed Discontinue medication, Methysergide, ergotamine, Obstruction (ureteral; Benign urine sediment, decompress ureteral dihydroergotamine, secondary to hydronephrosis on obstruction by intrarenal methyldopa, pindolol, retroperitoneal fibrosis) ultrasound stenting or percutaneous hydralazine, atenolol
  • Result Interpretations 24/04/09 24/04/09 S.Na + -128.6mmol/L GFR -6.5 ml/min(SEVERE RENAL FAILURE) S.K+ - 2.73 mmol/L FeNa -4% ( >2%) (ATN) S.Cl - 93 mmol/L FENa - 35% ( Pre Renal ) TCO2 - 13.5mmol/L Urinary Na+ - 44.7 mmol/L ( <20mmol/L ATN) Anion gap -24.83mmol/L Oliguria - Urine out put less than 500 cc BUN - 138.94mg/dl Urinary Creatinine = 8.17% (<20% ATN) UREA - 49.26 mmol/L Serum Creatinine Serum Creatinine – 882.3u mol/L BUN/Creatinine = 14.03 ( <20% Renal) URINARY ELECTROLYTE Urine R/M/E - No Eosinophilurea, WBC cast and U.Sodium - 44.7mmol/L Epithelial cell-7-8 Protein-+ U.Potassium - 12.77mmol/L BUN: Cr = blood urea nitrogen:creatinine ratio; UNa = urinary concentration of sodium; U.Cl- - 33mmol/L FENa = fractional excretion of sodium FeNa = (urine Na x plasmaCr) 100 TCO2 - 5mmol/L (plasma Na x urineCr) U.Creatinine (Random)-7211 umol/L
  • SO,PATIENT DEVELOPED- -SEVERE RENAL FAILURE - PRERENAL CAUSE AND - DEVELOPED ACUTE TUBULAR NECROSIS (ATN)
  • Etiology of ARF among Inpatients ATN (45%) Prerenal (21%) ARF on CKD (13%) Obstruction (10%) GN/vasc (4%) AIN (2%) Atheroemboli (1%) KI 50:811-818, 1996
  • Etiology of ARF among Outpatients P rerenal (70% ) Intrarenal (11% ) O bs truc tion(17% ) idiopathic (2% ) AJKD 17:191-198, 1991
  • Acute renal failure: Focused History • Nausea? Vomiting? Diarrhea? • Hx of heart disease, liver disease, previous renal disease, kidney stones, BPH? • Any recent illnesses? • Any edema, change in urination? • Any new medications? • Any recent radiology studies? • Rashes?
  • acute renal failure: common clinical features •azotemia • hypervolemia • electrolytes abnormalities:  K+  phosphate  Na+  calcium • metabolic acidosis • hypertension • oliguria - anuria
  • Assessing the patient with acute renal failure – Physical exam • Vital Signs: • Elevated BP: Concern for malignant hypertension • Low BP: Concern for hypotension/hypoperfusion (acute tubular necrosis) • Neuro: • Confusion: hypercalcemia, uremia, malignant hypertension, infection, malignancy • HEENT: • Dry mucus membranes: Concern for dehydration (pre-renal) • Abd: • Ascites: Concern for liver disease (hepatorenal syndrome), or nephrotic syndrome • Ext: • Edema: Concern for nephrotic syndrome • Skin: • Tight skin, sclerodactyly – Sclerodermal renal crisis • Malar rash - Lupus
  • Treatment of ARF • Eliminate the toxic insult • Hemodynamic support • Respiratory support • Fluid management • Electrolyte management • Medication dose adjustment • Dialysis
  • Acute Renal Failure: Fluid Therapy If patient is fluid overloaded • fluid restriction (insensible losses) • attempt furosemide 1-2 mg/kg • Renal replacement therapy (see later) If patient is dehydrated: • restore intravascular volume first • then treat as euvolemic (below) If patient is euvolemic: • restrict to insensible losses (30-35 ml/100kcal/24 hours) + other losses (urine, chest tubes, etc) or
  • Management of ARF - Volume status • Water balance – "Maintenance" is IRRELEVANT in ARF!!! – If euvolemic, give insensibles + losses + UOP – If volume overloaded, they don't need anything (except the minimum for meds and glucose) • concentrate all meds; limit oral intake – Need frequent weights and BP, accurate I/O – Insensibles = 30 cc/100 kcal or 400cc/M2/day – If has any UOP, Frusemide may help with fluid overload
  • HYPERKALAMIA • With ARF, K+ will increase and will be worsened by infection, hemolysis, acidosis • DON'T IGNORE A HIGH K+ just because the specimen is hemolyzed especially in a patient who could easily be hyperkalemic • How can you tell if it is “real”? -check EKG for peaked T waves, widened QRS • It’s real. What’s the first thing to do? - Restriction of dietary K+ intake - Eliminate K+ supplements and K+-sparing diuretics -Emergently stabilize membranes with calcium to prevent arrhythmia
  • Hyperkalemia • What’s next? – Shift K+ intracellularly with: • insulin + hypertonic dextrose: 1 unit of insulin/4 g glucose • bicarbonate infusion ((1-2 mEq/kg) • Inhaled –B2 agonist therapy to promote intracellular mobilization. – Check IV fluids to ensure no intake • What happens to ionized calcium level as you correct the acidosis? • Increases albumin binding so ionized calcium decreases • What’s the third step? – Remove from body with Lasix, dialysis
  • DIETARY MODIFICATION • total caloric intake– 35~ 50 kcal/kg/day to avoid catabolism Salt restriction– 2~4 g/day Potassium intake– 40 meq/day • Phosphorus intake– 800 mg/day • Uremia-nutrition – Restriction protein is not necessary in ARF, maintain caloric intake – Carbohydrate ≥ 100gm/day to minimize ketosis and protein catabolism • Drug – Review all medication, Stop magnesium-containing medication – Adjusted dosage for renal failure, Readjust with improvement of GFR
  • Management of Ischemic and Nephrotoxic Acute Renal Failurea Management Issue Therapy Reversal of Renal Insult Ischemic ATN Restore systemic hemodynamics and renal perfusion through volume resuscitation and use of vasopressors Nephrotoxic ATN Eliminate nephrotoxic agents Consider toxin-specific measures: e.g., forced alkaline diuresis for rhabdomyolysis, allopurinol/rasburicase for tumor lysis syndrome Prevention and Treatment of Complications Intravascular volume overload Salt and water restriction Diuretics Ultrafiltration Hyponatremia Restriction of enteral free water intake Avoidance of hypotonic intravenous solutions, including dextrose-containing solutions Hyperkalemia Restriction of dietary K+ intake Eliminate K+ supplements and K+-sparing diuretics Loop diuretics to promote K+ excretion Potassium binding ion-exchange resins (e.g., sodium polystyrene sulfonate or Kayexelate) Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote intracellular mobilization Inhaled –B2 agonist therapy to promote intracellular mobilization Calcium gluconate or calcium chloride (1 g) to stabilize the myocardium Dialysis
  • Metabolic acidosis Sodium bicarbonate (maintain serum bicarbonate >15 mmol/L or arterial pH >7.2) Administration of other bases, e.g., THAM Dialysis Hyperphosphatemia Restriction of dietary phosphate intake Phosphate binding agents (calcium carbonate, calcium acetate, sevelamer hydrochloride, aluminum hydroxide) Hypocalcemia Calcium carbonate or gluconate (if symptomatic) Hypermagnesemia Discontinue Mg++ containing antacids Hyperuricemia Treatment usually not necessary if <890 mol/L or <15mg/dL Allopurinol, forced alkaline diuresis, rasburicase Nutrition Protein and calorie intake to avoid net negative nitrogen balance Dialysis To prevent complications of acute renal failure Choice of agents Avoid other nephrotoxins: ACE inhibitors/ARBs, aminoglycosides, NSAIDs, radiocontrast unless absolutely necessary and no alternative Drug dosing Adjust doses and frequency of administration for degree of renal impairment
  • Acidosis • Maintain serum bicarbonate >15 mmol/L or arterial pH >7.2 • Acidosis makes the kids feel terrible • BUT... – watch sodium and fluid overload – watch lowering ionized calcium levels (by increasing binding of calcium to albumin)
  • INDICATION FOR DIALYSIS • Dialysis may not be necessary for all people, but is frequently lifesaving, particularly if serum potassium is dangerously high. • Common symptoms that require the use of dialysis include- Uremia - Obtundation, asterxis, seizures,decreased mental status,pericarditis increased potassium levels, Urine Output -total lack of urine production, Metabolic Acidosis – PH< 7.2mmol/L despite Sodium Bicarbonate Therapy Sodium Bicarbonate therapy not tolerate due to fluid over load
  • Indications for renal replacement therapy • Volume overload - - Resistance to Diuretics ,Specially pulmonary oedema – Pulmonary edema, CHF, refractory HTN – NOT for peripheral edema, esp. with cap. leak • Hyperkalemia - (S.Potassium >6.5mmol/L S.Potassium>5.5 mmol/L with ECG change) .waste products- uncontrolled accumulation of nitrogen waste products (serum creatinine > 10 mg/dl and BUN > 120 mg/dl). • Nutrition- Need to maximize nutrition • Sodium imbalance - Severe dysnatremias (sodium concentration greater than 155 meq/L or less than 120 meq/L) • Hyperthermia • Drug overdose-Overdose with a dialyzable drug/toxin
  • Mnemonic “AEIOU” • Acid-base Imbalances • Electrolyte Disturbances • Intoxication • Overload, Fluid • Uremic Symptoms
  • Modes of renal replacement therapy • Peritoneal dialysis - also gentle and don't need heparinization but slow and catheter may leak or not work. • Hemodialysis - very fast, but need big lines and systemic heparinization; causes hemodynamic instability and uremic dysequilibrium symptoms
  • Complications of acute renal failure Hyperkalemia. Acute pulmonary edema. Cardiac arrhythmia. Convulsions. Infections e.g. Pneumonia. Deep venous thrombosis and pulmonary embolism. Gastrointestinal bleeding.
  • ARF: Risk factors for mortality • Multi-organ failure • Bacterial Sepsis • Fungal sepsis • Hypotension/vasopressors • Ventilatory support • Initiation of dialysis late in hospital course • Oliguria/anuria: with oliguric ARF, mortality is > 50% compared to < 20% with non-oliguric ARF
  • Causes of death in acute renal failure • Infection e.g.pneumonia • Hyperkalemia. • Pulmonary edema. • Cardiac arrhythmia. • Deep venous thrombosis and pulmonary embolism. • Acute pericarditis. • Convulsions and coma.
  • Oliguria, renal failure. Dehydration: Obstruction •U.Na<20mmol/l. Renal failure •U.Osmol.>500 Chronic -U.catheter -Percutaneous nephrostomy. -Rehydrate. -Ureteric catheter. -Fluid and diuretic challenge -Correct Reversible Factors. -Mannitol -Dialysis. -AGN, RPGN and, Acute Acute tubular necrosis vasculitis •C3,ANCA,,ANA,Ad -CVP, fluid balance, electrolyte balance,acid sDNA… etc base balance, diet,dopamine infusion, high •Consider dose diuretic dose, monitoring, treatment of steroid,immunosuppr complications, and consideration of dialysis essive and plasma exchange. Management of acute renal failure
  • Best cure is to prevent • Have a high index of suspicion for reversible factors - volume depletion, decreasing cardiac function, sepsis, urinary tract obstruction • Be sure patient is well-hydrated when exposing patient to nephrotoxic drugs
  • Anticipate Problems • Avoid worsening the ARF – Adjust medicines for renal insufficiency – Avoid nephrotoxins if possible – Think about to avoid less potent drug prescribtion – Close observation of toxic effect of drugs. – Early detection of toxic effect of drug. – Avoid intravascular volume depletion (especially in third-spacing or edematous patients)
  • Nursing Interventions •Monitor I/O, including all body fluids • Monitor lab results • Watch hyperkalemia symptoms: malaise, anorexia, paresthesia, or muscle weakness, EKG changes • watch for hyperglycemia or hypoglycemia if receiving TPN or insulin infusions
  • • Maintain nutrition • Safety measures- Mouth care Daily weights • Assess for signs of heart failure • GCS • Skin integrity problems
  • Complications (ARF) • Increased risk of infections • Gastrointestinal loss of blood • Chronic renal failure • End-stage renal disease • Damage to the heart or nervous system • Hypertension
  • Patient / Family Education • Call your health care provider if decreased urine output or other symptoms indicate the possibility of acute renal failure. • Call your health care provider if nausea or vomiting persists for more than 2 weeks. • Call your health care provider if decreased urine output or other symptoms of chronic renal failure occur.
  • Thanks for your attention
  • PROBLEM-1 X- 80 years old male presented with Cough for 7, Fever for 6 days , diarrhoea and vomiting for 1 day. Patient was previously diagnosed as a case of COPD. On Examination Patient was drowsy, some D/H present,Pulse-101/min BP- 75/35 mmHg , SPO2 without O2-90% R/R-30/min RBS-6.8 mmol/L..Patient last pass urine 6 hour back (scanty). S.Electrolyte- S.Na - 133.2mmol/L S.K - 4.36 mmol/L S.Cl – 98.5 Tco2-19.9 mmol/L Anion Gap- 19.9mmol/L S.Creatinine-223.4 umol/L ( 2.5 mg/dl) BUN- 50.34mg/dl U.Creatinine- 5103 umol/L (57.7mg/dl) U.Specific Grvity – 1.003 U.Na – 34.6mmol/L Urine R/M/E – R.B.C- 1-2 Puss cell - 6-8 Epithelial Cell – 4-6 Cast - granular (1-2) USG of Whole Abdoman- Sugestive of bilateral paranchymal diseases.Kidney size is normal. Bilateral Pleural Effusion (mild?) Dilated portal vein But no spleenomegaly. QUESTIONS Q-1 In which stage patient is in RIFLE CRITERIA? Q-2 Is patient acute or chronic renal failure? Q-3 Is it Prerenal Renal or Post renal? Q-4 ATN developed or not? Q-5 What is the -daily raising of Creatinine? FeNa - ? U Na - ? Important findings related with diagnosis? Q-6 What is the final Diagnosis and Differential Diagnosis? Q-7 Treatment Option for the patient ? Q-8 Dialysis Needs or not?
  • PROBLEM-2 Y- 65years old male presented with diarrhoea and vomiting for 1 and half day.He Non Diabetic But Hypertensive. On Examination Patient was Alart but feeling restless his pulse-92/min ,BP-105/70mmHg Some D/H was present , RBS-6.1mmol/L..Patient last pass urine 5-6 hour back (scanty) 1st Day – S.Cretinine- 610umol/L (6.9mg/dl) S.Electrolyte- S.Na - 128.2mmol/L S.K - 3.6 mmol/L S.Cl – 90.5 Tco2-19 mmol/L Anion Gap- 22.4mmol/L S.Creatinine-836 umol/L ( 9.45 mg/dl) BUN- 50.34mg/dl U.Creatinine- 3940.1 umol/L U.Specific Grvity – 1.018 U.Na – 19.8mmol/L Urine R/M/E – R.B.C- 4-6 Puss cell - 15-20 Epithelial Cell – 4-6 Cast - granular (0-1) USG of Whole Abdoman-Normal Study QUESTIONS Q-1 In which stage patient is in RIFLE CRITERIA? Q-2 Is patient acute or chronic renal failure? Q-3 Is it Prerenal Renal or Post renal? Q-4 ATN developed or not? Q-5 What is the -daily raising of Creatinine? FeNa - ? U Na - ? Important findings related with diagnosis? Q-6 What is the final Diagnosis and Differential Diagnosis? Q-7 Treatment Option for the patient ? Q-8 Dialysis Needs or not?
  • PROBLEM-3 Z- 18 years old Female presented with diarrhoea and vomiting for 1and half day, Fever since morning , For Diarrhoea she took I/V Fluid and Some Medication from outside. On Examination Patient was drowsy follwed by unconciousness, some D/H present,Pulse-98/min BP- 95/60 mmHg , SPO2 without O2-90% R/R-30/min RBS-6.8 mmol/L..Patient last pass urine 5-6 hour back (scanty) Temp-39`C.No Pupil Dilated,No Neck rigidity, After 10-12 hour patient develop repeated convulsion. 1st S.creatinine – 582.6 umol/L ( 6.5 mg/dl) S.Electrolyte- S.Na - 132.6mmol/L S.K - 3.2 mmol/L S.Cl – 98.5 Tco2-14.9 mmol/L Anion Gap- 19.9mmol/L S.Creatinine-882.3 umol/L ( 9.9mg/dl) BUN- 138.94mg/dl U.Creatinine- 7481 umol/L , U.Na – 26.7mmol/L Urine R/M/E – R.B.C- 7-8 CBC – Hb%- 10 , TWBC -14700 Puss cell - 12-14 Nutrophil- 81.4% Poly-10% Epithelial Cell – 4-6 monocyte- 0.2% ,Eosinophil-7.4% Protien- ++ Cast - granular (2-4) Eosinophil-+ USG of Whole Abdoman- Normal Study. QUESTIONS Q-1 In which stage patient is in RIFLE CRITERIA? Q-2 Is patient acute or chronic renal failure? Q-3 Is it Prerenal Renal or Post renal? Q-4 ATN developed or not? Q-5 What is the -daily raising of Creatinine? FeNa - ? U Na - ? Important findings related with diagnosis? Q-6 What is the final Diagnosis and Differential Diagnosis? Q-7 Treatment Option for the patient ? Q-8 Dialysis Needs or not?