logging in or signing up ACUTE RENAL FAILURE IN NEONATES hanumesh Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 2553 Category: Entertainment License: All Rights Reserved Like it (6) Dislike it (0) Added: February 18, 2009 This Presentation is Public Favorites: 3 Presentation Description No description available. Comments Posting comment... By: arunasliubsys (1 month(s) ago) Great presentation! Would you be so kind sending it to my E-mail: arunasliubsys@gmail.com Saving..... Post Reply Close Saving..... Edit Comment Close By: ganeshjetti (4 month(s) ago) ITS GOOD CAN I DOWNLOAD DIS Saving..... Post Reply Close Saving..... Edit Comment Close By: drpavan007 (5 month(s) ago) you have done a nice presentation. i am doing fellowship in neonatalogy. i have to do presentation on acute renal failure. can i borrow some of your slides. thanks in advance.drpavan007@gmail.com Saving..... Post Reply Close Saving..... Edit Comment Close By: blaise (6 month(s) ago) It is really a great presentation. Would yoyu please send me a copy of it into my box email? joy.blaise@gmail.com Thank you Saving..... Post Reply Close Saving..... Edit Comment Close By: abdelhafiz (10 month(s) ago) thank u very much, excellent presentation... i would be very grateful if u send this presentation to my email: a.h.mamoun420@hotmail.com Saving..... Post Reply Close Saving..... Edit Comment Close loading.... See all Premium member Presentation Transcript GOOD AFTERNOON : GOOD AFTERNOON Slide 2: ACUTE RENAL FAILURE IN NEONATES DR.HANUMESH K M CLINICAL FELLOW DEPARTMENT OF PEDIATRICS DIVISION OF NEONATOLOGY BVU MEDICAL COLLEGE, PUNE OVERVIEW : INTRODUCTION RENAL FUNCTION IN A TERM NEONATE RENAL FUNCTION IN A PRE-TERM NEONATE ACUTE RENAL FAILURE OVERVIEW INTRODUCTION : INTRODUCTION INTRODUCTION : INTRODUCTION Develops from Metanephros Normal growth & development of ureteric bud is essential Nephrogenesis proceeds centrifugally Nephrogenesis is complete by 36 wks Urine production begins at 8-10 wks One million nephrons per kidney NORMAL COLLECTING DUCT : NORMAL COLLECTING DUCT Principal cell: -absorbs salt (sodium) through epithelial Na channels (ENaC) -secretes potassium into the urine -absorbs water from the urine Intercalated cell: -secretes acid or base into the urine RENAL FUNCTION IN A TERM NEONATE : RENAL FUNCTION IN A TERM NEONATE GLOMERULAR FILTRATION RATE RENAL BLOOD FLOW & FILTRATION FRACTION PROXIMAL TUBULAR FUNCTION DISTAL TUBULAR FUNCTION WHY RENAL FUNCTION IS LOW IN NEONATES ? RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE : RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE Is low in neonates At birth: 2.5-5 ml / min (20-40 ml /min/1.73m2) At 1 month : 50 ml /min/1.73m2 At 3 months : 60 ml /min/1.73m2 At 6 months : 80 ml /min/1.73m2 At 12 months : 100 ml /min/1.73m2 At 2 years : 120 ml /min/1.73m2 RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE : RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE Most widely used proxy for GFR measurement is Plasma Creatinine concentration (Pcr) Plasma Creatinine concentration (Pcr): -At birth:70-90 micromoles/l(1mg/dl) -By 1 week: 15-40 micromoles/l(0.17-0.45mg/dl) -at low levels routine methods of estimations are unreliable RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE : RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE GFR (ml /min/1.73m2) = k x height / Pcr - k for pre-terms: 30 - k for terms : 40 - k for infants : 50 PLASMA CREATININE CLEARANCE ( Pcr) : PLASMA CREATININE CLEARANCE ( Pcr) NORMAL RANGES OF Pcr RELATION b/n Pcr & GA RENAL FUNCTION IN A TERM NEONATE contdRenal blood flow & filtration fraction : RENAL FUNCTION IN A TERM NEONATE contdRenal blood flow & filtration fraction Filtration fraction is similar to that of adults(0.2) RBF is regulated by vascular tone of afferent & efferent glomerular arterioles Drugs that can cause constriction / dilatation of these vessels can lead to ARF Renal Blood Flow : Renal Blood Flow F = ?P/R Slide 17: Raff Reff RAP PGC Renal blood flow & filtration fraction RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Amino acid reabsorption: -For adults & Children: >98%(except histidine) - For term & young infants: mild aminoaciduria (glycine, imino acids, dibasic amino acids, & taurine) -d/t immaturity of proximal tubular AA transporters -No significant adverse effects if intake is adequate RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Glucose reabsorption: -Equal or exceeds that in adults when factored by GFR - Trivial degree of glycosuria in term is of no significance -Marked glycouria should be investigated ( hyperglycemia, inherited tubulopathies) -mean urinary glucose excretion is slightly higher than that of older children & adults (15mg/dl Vs 6mg/dl) RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Phosphate reabsorption: -renal tubular phosphate threshold is higher than in adults - reflecting the need for phosphate retention for skeletal growth -urinary phosphate excretion is normally low, because kidney is programmed to retain,not to excrete, phosphate & other minerals RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Bicarbonate reabsorption: -completely reabsorbed provided plasma HCO3 is below the threshold - infact renal HCO3 threshold determines the plasma HCO3 -Normal plasma HCO3 in healthy term neonates is 20-23 mmol/l, about 3mmol/l lower than adults RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary concentrating & diluting ability, and urine flow rate Urinary acidifying capacity Sodium excretion RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary concentrating ability: -adult kidney :can achieve osmolality of >1000 (1200-1400) mOsmol/kg water -neonate kidney: 500-700 mOsmol/kg water -reaches adult value by 1 year -because of anabolism, infants have a less need to produce highly concentrated urine in order to conserve water RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Diluting ability: -matches that of adults (minimum urine osmolality < 50mOsmo/kg water ) Urine flow rate ( V ) is determined by: -water intake -solute excretion rate -ability to concentrate & dilute the urine RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Solute content of breastfed infant: 20mOsmol/kg/day, but most of it is retained & incorporated in new tissue Actual load requiring excretion is:5-10mOsmol/kg /day Urine flow rate of ~0.5ml/kg/hr is needed to avoid solute retention (Uremia) Sick babies are catabolic & generate more solute for excretion Urine out-put in normal demand breast fed infant:3ml/kg/hr RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary acidifying capacity: -neonates can lower urinary pH to values similar to those of adults -capacity to excrete an acid load depends on presence of urinary buffers( mainly inorganic phosphate & ammonium) -Maximal net acid excretion(NAE) in term neonates is comparable to that of adults if factored by GFR RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Sodium excretion: -Healthy term neonates are able to produce virtually Na+ free urine -Fractional excretion of sodium ( FE Na % ) =(UNa x Pcr / PNa x Ucr) x 100 RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Why is renal function is so low in the neonates: -low solute excretion rate of growing baby places a proportionately low demand on the kidney -if GFR is similar to that of adults, large increase in filtered sodium would have to be reabsorbed by tubules. This is an energy-intensive process & this will increase the energy expenditure by 3% RENAL FUNCTION IN A PRE-TERM NEONATE : RENAL FUNCTION IN A PRE-TERM NEONATE GLOMERULAR FILTRATION RATE RENAL BLOOD FLOW & FILTRATION FRACTION PROXIMAL TUBULAR FUNCTION DISTAL TUBULAR FUNCTION WHY SODIUM REABSORPTION IS INEFFICIENT IN PRE-TERM NEONATES ? RENAL FUNCTION IN A PRE-TERM NEONATE contdGLOMERULAR FILTRATION RATE : RENAL FUNCTION IN A PRE-TERM NEONATE contdGLOMERULAR FILTRATION RATE During first week GFR is 0.5-1.0ml/min in 28-32 wk babies Rises in linear fashion from 32 wks to achieve 3-5 ml/min at 40 wks Sick pre-term babies have low GFR if they are hypoxic, hypotensive or mechanically ventilated Both pre-term & term babies follow similar patterns of postnatal development of GFR RENAL FUNCTION IN A PRE-TERM NEONATE contdRENAL BLOOD FLOW & FILTRATION FRACTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdRENAL BLOOD FLOW & FILTRATION FRACTION There is progressive increase in RBF with development, in parallel increase in GFR Primarily d/t fall in vascular resistance rather than rise in perfusion pressure Juxtamedullary nephrons are preferentially perfused during early development RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Amino acid reabsorption: -AA excretion is generally higher than term babies -occasionally severe generalized aminoaciduria cab be seen -aminoaciduria may persist for > 4wks -the degree & persistence of aminoaciduria is not influenced by dietary intake -fractional excretion of Taurine is particularly high RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Glucose reabsorption: -Mean Urinary glucose excretion:65mg/dl -d/t low renal tubular glucose threshold -even moderate hyperglycemia can lead to substantial glycosuria & osmotic diuresis RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Phosphate reabsorption: -threshold is still higher than term babies, indicates importance of renal phosphate retention for normal growth & development -this threshold falls with increase in postnatal age -increase the dietary phosphate intake if baby is passing phosphate free urine -phosphaturia in the presence of low/normal plasma phosphate is abnormal & should be investigated RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Bicarbonate reabsorption: -the bicarbonate threshold is lower in pre-terms - An infant who has a low pH & bicarbonate(by adult standards),but who is thriving & not producing maximally acidic urine, should be regarded as having physiological hypobasaemia of prematurity rather than pathological acidosis -The syndrome of late metabolic acidosis is due to imbalance b/n the non-volatile acid production rate & the capacity of the distal tubule to excrete the hydrogen ion load RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary concentrating & diluting ability, and urine flow rate: -limited capacity to concentrate(Maxm:500 mOsmol/kg water) -also osmotic threshold for release of ADH is higher (290+/- 4) -do not begin to concentrate their urine until significantly dehydrated -at any degree of dehydration, they produce less concentrated urine than term babies & are vulnerable to hypernatraemia and hyperosmolality -diluting ability ,by contrast is well developed in even in very pre-terms (upto 50-60 mOsmoll/kg water) -Urine flow rate:2-3ml/kg/hr(range:1-10ml/kg/hr) RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary acidifying capacity: -even very pre-term babies can lower urine pH to a level that would be adequate to prevent acidosis ( urine pH<5.5 ) -however defence against systemic acidosis also depends on GFR & adequate supply of buffers: Phosphate is little available & ammonia is also less synthesized d/t low tubular mass -so the main non-volatile acid needing urinary excretion is sulphuric acid d/f protein metabolism. If infant is well fed & growing ,anabolism limits the sulphuric acid production -if the infant is sick & catabolic, or fed protein much in excess of dietary need, metabolic acidosis can easily develop RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION Sodium excretion: -neonates born at or after 32-34 wks can produce virtually sodium free urine(FE Na:<<1%) -if born before this period, they lose sodium in the urine -prone for negative sodium balance -extreme pre-terms can have FE Na > 5%, commonly leads to hyponatraemia by second or third week of life -salt supplementation ,begun after first 3-6 days of life, improves early weight gain without apparent adverse effects RENAL FUNCTION IN A PRE-TERM NEONATE contdWHY SODIUM REABSORPTION IS INEFFICIENT IN PRE-TERMS? : RENAL FUNCTION IN A PRE-TERM NEONATE contdWHY SODIUM REABSORPTION IS INEFFICIENT IN PRE-TERMS? -Proximal tubule accounts for a smaller fraction of total sodium reabsorption in newborns than adults(65%), and this fraction is even less in the premature than term babies -this leads to increase in sodium concentration at distal tubule -in extreme pre-terms, distal tubule is incapable of reabsorption of sodium d/t immaturity & impaired response to circulating aldosterone: resulting natriuresis,negative salt balance & hyponatraemia FE Na & GFR in pre-term : FE Na & GFR in pre-term TRANSITION FROM FOETAL TO NEONATAL KIDNEY : TRANSITION FROM FOETAL TO NEONATAL KIDNEY Fetal diuresis is sustainable & after birth,diuresis is markedly attenuated First 2-3 days: negative salt & water balance: necessary to prevent circulatory overload Although very pre-term can develop hyponatraemia secondary to urinary sodium loss after first few days, it is not appropriate to attempt to prevent this by giving additional sodium or fluid in the first few days Both GFR & FE Na are much higher in the fetus than in the prematurely born infant at the same absolute GA ACUTE RENAL FAILURE IN NEONATES : ACUTE RENAL FAILURE IN NEONATES INCIDENCE IN NEONATES CLINICAL FEATURES BIOCHEMICAL FEATURES CLASSIFICATION & CAUSES ACUTE TUBULAR NECROSIS DIAGNOSIS MANAGEMENT ACUTE RENAL FAILURE IN NEONATESINCIDENCE IN NEONATES : ACUTE RENAL FAILURE IN NEONATESINCIDENCE IN NEONATES Syndrome that results from an abrupt ,potentially reversible, reduction in GFR Volume and composition of ECF is adversely affected No consensus as to what absolute or proportional change in GFR is necessary for the diagnosis A persistent rise in Pcr>1.5mg.dl(130mmols/l),corresponding to a fall in GFR to < 50% was suggested by Chevalier et al ACUTE RENAL FAILURE IN NEONATESINCIDENCE IN NEONATES : ACUTE RENAL FAILURE IN NEONATESINCIDENCE IN NEONATES The apparent incidence depends on the definition used Incidence:3-8% of NICU admissions Incidence of ARF severe enough to need dialysis:1% of NICU admissions Incidence among all live births:0.1% In poor & developing countries, incidence may be much higher ACUTE RENAL FAILURE IN NEONATESCLINICAL FEATURES : ACUTE RENAL FAILURE IN NEONATESCLINICAL FEATURES History suggestive of predisposing factors Oliguria (V:<1ml/kg/hr) :not necessary to the diagnosis Nonoliguric ARF may be more common (lower spectrum) Oedema:commonest clinical sign (not in non-oliguric ARF ) Polyuria, natriuresis, salt depletion & dehydration Commonly detected by typical biochemical abnormalities while investigating sick infant ACUTE RENAL FAILURE IN NEONATESBIOCHEMICAL FEATURES : ACUTE RENAL FAILURE IN NEONATESBIOCHEMICAL FEATURES By the time ARF is suspected, hyponatraemia is present in most cases ACUTE RENAL FAILURE IN NEONATESCLASSIFICATION & CAUSES : ACUTE RENAL FAILURE IN NEONATESCLASSIFICATION & CAUSES Renal function depends on: -Perfusion -Functional integrity of the kidney -Patency of urinary passages ACUTE RENAL FAILURE IN NEONATESCLASSIFICATION & CAUSES : ACUTE RENAL FAILURE IN NEONATESCLASSIFICATION & CAUSES ACUTE RENAL FAILURE IN NEONATESCAUSES : ACUTE RENAL FAILURE IN NEONATESCAUSES ANTENATL VASCULAR DAMAGE: 1.Maternal treatment: NSAIDS, ACE inhibitors 2.Twin to twin transfusion 3.Co-twin death 4.IUGR & Severe oligohydramnios ACUTE RENAL FAILURE IN NEONATESCAUSES : ACUTE RENAL FAILURE IN NEONATESCAUSES PRIMARY RENAL & UROLOGICAL DISEASES: 1.Congenital B/L obstructive uropathies ( PUV ) 2.Polycystic kidney 3.Renal dysplasia / hypoplasia 4.Multicystic dysplasia 5.Renal tubular dysgenesis 6.Idiopathic diffuse mesangial sclerosis 7.Glomerular immaturity 8.Finnish-type congenital nephrotic syndrome ACUTE RENAL FAILURE IN NEONATESCAUSES : ACUTE RENAL FAILURE IN NEONATESCAUSES ACQUIRED POSTNATAL RENAL DISEASES: Shock, Dehydration,Perinatal hemorrhage NEC with a third space loss Heart failure, Cardiopulmonary bypass, ECMO DIC, Vascular thrombosis (artery, vein) Perinatal asphyxia, HUS Isoimmune haemolytic diseases with massive haemoglobinuria Myoglobinuria, haemoglobinuria, uric acid nephropathy Infection:pyelonephritis, toxoplasmosis,fungal, syphilis Closure of congenital abdominal wall defects Nephrotoxic drugs:NSAIDs,ACE inhibitors,contast,amphotericin B, aminoglycosides, Vancomycin ACUTE RENAL FAILURE IN NEONATESCAUSES : ACUTE RENAL FAILURE IN NEONATESCAUSES 1.Intrinsic ARF due to acquired renal disease is virtually unknown in neonates 2.For practical purposes, intrinsic renal failure in neonates is synonymous with ACUTE TUBULAR NECROSIS (ATN ), with renal vein thrombosis a rare complication 3.Congenital Chronic (i.e irreversible ) commonly mimics ARF in its presentation 4.Pre-renal failure can progress to ATN if the predisposing factors persist to the point where hypoxic ischaemic injury to kidney develops FACTORS PREDISPOSING TO ATN : FACTORS PREDISPOSING TO ATN Hypoxia, sepsis & exposure to Nephrotoxic drugs, separately or in combination, cause most episodes of ARF in neonates Failure to recognize ATN can lead to marked biochemical abnormalities Both Myoglobinuria ,Myoglobinuria & increased urinary excretion of RBP are highly predictive of ATN Hyperuricemia has also been suggested as a marker of severity of tissue injury Slide 54: A microscopic picture of renal biopsy specimen showing renal medulla, which is composed mainly of renal tubules. Patchy or diffuse denudation of the renal tubular cells is observed, suggesting acute tubular necrosis (ATN) as the cause of acute renal failure (ARF). ACUTE TUBULAR NECROSIS (ATN) Slide 55: ACUTE TUBULAR NECROSIS (ATN) Acute tubular necrosis (ATN). Flattening of the renal tubule cells due to tubular dilation Slide 56: ACUTE TUBULAR NECROSIS (ATN) Acute tubular necrosis. Intratubular cast formation DIAGNOSIS OF ARF : DIAGNOSIS OF ARF Evidence of reduced GFR is essential for diagnosis, whether or not oliguria is present. Pcr is widely used as a rough marker for GFR and a value >1.5mg/dl(130mmol/l) persisting for >24hours is a reasonable criterion Plasma urea concentration is influenced by many factors, although high levels indicate that the baby’s excretory needs are not being met and may be one factor pointing to the need for dialysis Ultrasonography Radionuclide imaging studies are of little value in distinguishing b/n causes of ARF in neonates DIAGNOSIS OF ARFUrinary indices in the diagnosis of ARF: : DIAGNOSIS OF ARFUrinary indices in the diagnosis of ARF: DIAGNOSIS OF ARFUrinary indices in the diagnosis of ARF: : DIAGNOSIS OF ARFUrinary indices in the diagnosis of ARF: The most discriminating test is for differentiating pre-renal ARF & ATN is FE Na Renal failure index (RFI) is used as an alternative to EF Na RFI= U Na x Pcr / Ucr Very pre-term babies(<32wks) have high urinary sodium concentrations and excretion rates even in health. In this sub group, suitable cut off for diagnosis of ATN are an RFI of > 8 & FE Na >6% DIAGNOSIS OF ARF : DIAGNOSIS OF ARF The diagnosis of pre-renal ARF is confirmed by improvement in urine flow and renal function in response to fluid replacement Provided there is no circulatory overload, a fluid challenge of isotonic saline 10 ml/kg should be given iv over one hour Failure to respond confirms ATN as the diagnosis NATURAL COURSE OF ARF : NATURAL COURSE OF ARF MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE FLUID BALANCE: -Meticulous attention -correction of hypovolumia -monitor the total input and output -regular weighing -Maintenance fluid: IWL(180-310 ml/m2/day) + output - URINE OUT-PUT MONITORING : URINE OUT-PUT MONITORING MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE NUTRITION: -is essential to promote anabolism & prevent catabolism HYPERPHOSPHATAEMIA: -oral calcium carbonate -aluminum hydroxide should not be used -additional calcium should not be given until the plasma phosphate has been reduced to normal MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE HYPERKALAEMIA: -severe hyperkalaemia is a medical emergency -hypocalcaemia & hypomagnesaemia potentiate toxic effect of hyperkalaemia -maintain normocalcemia MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE HYPERKALAEMIA: -severe hyperkalaemia is a medical emergency -hypocalcaemia & hypomagnesaemia potentiate toxic effect of hyperkalaemia -maintain normocalcemia EKG Manifestations of Hyperkalemia : EKG Manifestations of Hyperkalemia Earliest to appear MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE SEVERE HYPERKALAEMIA: -intravenous /nebulised salbutamol (4mcg/kg over 5 mins) -IV glucose & Insulin infusion( 12 units of soluble insulin in 100 ml 25% glucose: 5ml /kg over 30 mins -IV sodium bicarbonate -Oral/rectal cation exchange resins (calcium polystyrene sulphate) ADEQUATE SODIUM INTAKE: CORRECTION OF ACIDOSIS MANAGEMENT OF ACUTE RENAL FAILURE MANAGEMENT BY DIALYSIS : MANAGEMENT OF ACUTE RENAL FAILURE MANAGEMENT BY DIALYSIS PERITONEAL DIALYSIS HEMODIALYSIS CONTINUOUS HEMOFILTRATION Continuous Arteriovenous Hemofiltration (CAVH ) Continuous Venovenous Hemofiltration (CVVH) Continuous Arteriovenous Hemodiafiltration (CAVHD) DIALYSISINDICATIONS : DIALYSISINDICATIONS VOLUME OVERLOAD HYPERKALAEMIA SEVERE METABOLIC ACIDOSIS HYPERPHOSPHATAEMIA/HYPOPCALCEMIA TO MAKE SPACE FOR FLUID & DRUG ADMINISTRATION FAILURE OF CONSERVATIVE MANAGEMENT : PERITONEALDIALYSIS Slide 72: COMPOSITION OF PD FLUID PD CATHETERS : PD CATHETERS Two double-cuff Tenckhoff peritoneal catheters: standard (A), curled (B). PERITONEAL DIALYSISCOMPLICATIONS : PERITONEAL DIALYSISCOMPLICATIONS PERITONITIS CATHETER EXIT SITE INFECTION CATHETER BLOCKAGE HYPERGLYCEMIA HAEMOFILTRATION & HAEMODIALYSIS : HAEMOFILTRATION & HAEMODIALYSIS REFERENCES : REFERENCES ROBERTON’S TEXTBOOK OF NEONATOLOGY, 4TH EDITION,929-940 ROBERTON’S TEXTBOOK OF NEONATOLOGY, 4TH EDITION,335-347 Pediatr Nephrol (2000) 14:1037-1044 Slide 77: THANK YOU You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
ACUTE RENAL FAILURE IN NEONATES hanumesh Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 2553 Category: Entertainment License: All Rights Reserved Like it (6) Dislike it (0) Added: February 18, 2009 This Presentation is Public Favorites: 3 Presentation Description No description available. Comments Posting comment... By: arunasliubsys (1 month(s) ago) Great presentation! Would you be so kind sending it to my E-mail: arunasliubsys@gmail.com Saving..... Post Reply Close Saving..... Edit Comment Close By: ganeshjetti (4 month(s) ago) ITS GOOD CAN I DOWNLOAD DIS Saving..... Post Reply Close Saving..... Edit Comment Close By: drpavan007 (5 month(s) ago) you have done a nice presentation. i am doing fellowship in neonatalogy. i have to do presentation on acute renal failure. can i borrow some of your slides. thanks in advance.drpavan007@gmail.com Saving..... Post Reply Close Saving..... Edit Comment Close By: blaise (6 month(s) ago) It is really a great presentation. Would yoyu please send me a copy of it into my box email? joy.blaise@gmail.com Thank you Saving..... Post Reply Close Saving..... Edit Comment Close By: abdelhafiz (10 month(s) ago) thank u very much, excellent presentation... i would be very grateful if u send this presentation to my email: a.h.mamoun420@hotmail.com Saving..... Post Reply Close Saving..... Edit Comment Close loading.... See all Premium member Presentation Transcript GOOD AFTERNOON : GOOD AFTERNOON Slide 2: ACUTE RENAL FAILURE IN NEONATES DR.HANUMESH K M CLINICAL FELLOW DEPARTMENT OF PEDIATRICS DIVISION OF NEONATOLOGY BVU MEDICAL COLLEGE, PUNE OVERVIEW : INTRODUCTION RENAL FUNCTION IN A TERM NEONATE RENAL FUNCTION IN A PRE-TERM NEONATE ACUTE RENAL FAILURE OVERVIEW INTRODUCTION : INTRODUCTION INTRODUCTION : INTRODUCTION Develops from Metanephros Normal growth & development of ureteric bud is essential Nephrogenesis proceeds centrifugally Nephrogenesis is complete by 36 wks Urine production begins at 8-10 wks One million nephrons per kidney NORMAL COLLECTING DUCT : NORMAL COLLECTING DUCT Principal cell: -absorbs salt (sodium) through epithelial Na channels (ENaC) -secretes potassium into the urine -absorbs water from the urine Intercalated cell: -secretes acid or base into the urine RENAL FUNCTION IN A TERM NEONATE : RENAL FUNCTION IN A TERM NEONATE GLOMERULAR FILTRATION RATE RENAL BLOOD FLOW & FILTRATION FRACTION PROXIMAL TUBULAR FUNCTION DISTAL TUBULAR FUNCTION WHY RENAL FUNCTION IS LOW IN NEONATES ? RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE : RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE Is low in neonates At birth: 2.5-5 ml / min (20-40 ml /min/1.73m2) At 1 month : 50 ml /min/1.73m2 At 3 months : 60 ml /min/1.73m2 At 6 months : 80 ml /min/1.73m2 At 12 months : 100 ml /min/1.73m2 At 2 years : 120 ml /min/1.73m2 RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE : RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE Most widely used proxy for GFR measurement is Plasma Creatinine concentration (Pcr) Plasma Creatinine concentration (Pcr): -At birth:70-90 micromoles/l(1mg/dl) -By 1 week: 15-40 micromoles/l(0.17-0.45mg/dl) -at low levels routine methods of estimations are unreliable RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE : RENAL FUNCTION IN A TERM NEONATE contdGLOMERULAR FILTRATION RATE GFR (ml /min/1.73m2) = k x height / Pcr - k for pre-terms: 30 - k for terms : 40 - k for infants : 50 PLASMA CREATININE CLEARANCE ( Pcr) : PLASMA CREATININE CLEARANCE ( Pcr) NORMAL RANGES OF Pcr RELATION b/n Pcr & GA RENAL FUNCTION IN A TERM NEONATE contdRenal blood flow & filtration fraction : RENAL FUNCTION IN A TERM NEONATE contdRenal blood flow & filtration fraction Filtration fraction is similar to that of adults(0.2) RBF is regulated by vascular tone of afferent & efferent glomerular arterioles Drugs that can cause constriction / dilatation of these vessels can lead to ARF Renal Blood Flow : Renal Blood Flow F = ?P/R Slide 17: Raff Reff RAP PGC Renal blood flow & filtration fraction RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Amino acid reabsorption: -For adults & Children: >98%(except histidine) - For term & young infants: mild aminoaciduria (glycine, imino acids, dibasic amino acids, & taurine) -d/t immaturity of proximal tubular AA transporters -No significant adverse effects if intake is adequate RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Glucose reabsorption: -Equal or exceeds that in adults when factored by GFR - Trivial degree of glycosuria in term is of no significance -Marked glycouria should be investigated ( hyperglycemia, inherited tubulopathies) -mean urinary glucose excretion is slightly higher than that of older children & adults (15mg/dl Vs 6mg/dl) RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Phosphate reabsorption: -renal tubular phosphate threshold is higher than in adults - reflecting the need for phosphate retention for skeletal growth -urinary phosphate excretion is normally low, because kidney is programmed to retain,not to excrete, phosphate & other minerals RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Bicarbonate reabsorption: -completely reabsorbed provided plasma HCO3 is below the threshold - infact renal HCO3 threshold determines the plasma HCO3 -Normal plasma HCO3 in healthy term neonates is 20-23 mmol/l, about 3mmol/l lower than adults RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary concentrating & diluting ability, and urine flow rate Urinary acidifying capacity Sodium excretion RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary concentrating ability: -adult kidney :can achieve osmolality of >1000 (1200-1400) mOsmol/kg water -neonate kidney: 500-700 mOsmol/kg water -reaches adult value by 1 year -because of anabolism, infants have a less need to produce highly concentrated urine in order to conserve water RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Diluting ability: -matches that of adults (minimum urine osmolality < 50mOsmo/kg water ) Urine flow rate ( V ) is determined by: -water intake -solute excretion rate -ability to concentrate & dilute the urine RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Solute content of breastfed infant: 20mOsmol/kg/day, but most of it is retained & incorporated in new tissue Actual load requiring excretion is:5-10mOsmol/kg /day Urine flow rate of ~0.5ml/kg/hr is needed to avoid solute retention (Uremia) Sick babies are catabolic & generate more solute for excretion Urine out-put in normal demand breast fed infant:3ml/kg/hr RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary acidifying capacity: -neonates can lower urinary pH to values similar to those of adults -capacity to excrete an acid load depends on presence of urinary buffers( mainly inorganic phosphate & ammonium) -Maximal net acid excretion(NAE) in term neonates is comparable to that of adults if factored by GFR RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Sodium excretion: -Healthy term neonates are able to produce virtually Na+ free urine -Fractional excretion of sodium ( FE Na % ) =(UNa x Pcr / PNa x Ucr) x 100 RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A TERM NEONATE contdDISTAL TUBULAR FUNCTION Why is renal function is so low in the neonates: -low solute excretion rate of growing baby places a proportionately low demand on the kidney -if GFR is similar to that of adults, large increase in filtered sodium would have to be reabsorbed by tubules. This is an energy-intensive process & this will increase the energy expenditure by 3% RENAL FUNCTION IN A PRE-TERM NEONATE : RENAL FUNCTION IN A PRE-TERM NEONATE GLOMERULAR FILTRATION RATE RENAL BLOOD FLOW & FILTRATION FRACTION PROXIMAL TUBULAR FUNCTION DISTAL TUBULAR FUNCTION WHY SODIUM REABSORPTION IS INEFFICIENT IN PRE-TERM NEONATES ? RENAL FUNCTION IN A PRE-TERM NEONATE contdGLOMERULAR FILTRATION RATE : RENAL FUNCTION IN A PRE-TERM NEONATE contdGLOMERULAR FILTRATION RATE During first week GFR is 0.5-1.0ml/min in 28-32 wk babies Rises in linear fashion from 32 wks to achieve 3-5 ml/min at 40 wks Sick pre-term babies have low GFR if they are hypoxic, hypotensive or mechanically ventilated Both pre-term & term babies follow similar patterns of postnatal development of GFR RENAL FUNCTION IN A PRE-TERM NEONATE contdRENAL BLOOD FLOW & FILTRATION FRACTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdRENAL BLOOD FLOW & FILTRATION FRACTION There is progressive increase in RBF with development, in parallel increase in GFR Primarily d/t fall in vascular resistance rather than rise in perfusion pressure Juxtamedullary nephrons are preferentially perfused during early development RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Amino acid reabsorption: -AA excretion is generally higher than term babies -occasionally severe generalized aminoaciduria cab be seen -aminoaciduria may persist for > 4wks -the degree & persistence of aminoaciduria is not influenced by dietary intake -fractional excretion of Taurine is particularly high RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Glucose reabsorption: -Mean Urinary glucose excretion:65mg/dl -d/t low renal tubular glucose threshold -even moderate hyperglycemia can lead to substantial glycosuria & osmotic diuresis RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Phosphate reabsorption: -threshold is still higher than term babies, indicates importance of renal phosphate retention for normal growth & development -this threshold falls with increase in postnatal age -increase the dietary phosphate intake if baby is passing phosphate free urine -phosphaturia in the presence of low/normal plasma phosphate is abnormal & should be investigated RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdPROXIMAL TUBULAR FUNCTION Bicarbonate reabsorption: -the bicarbonate threshold is lower in pre-terms - An infant who has a low pH & bicarbonate(by adult standards),but who is thriving & not producing maximally acidic urine, should be regarded as having physiological hypobasaemia of prematurity rather than pathological acidosis -The syndrome of late metabolic acidosis is due to imbalance b/n the non-volatile acid production rate & the capacity of the distal tubule to excrete the hydrogen ion load RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary concentrating & diluting ability, and urine flow rate: -limited capacity to concentrate(Maxm:500 mOsmol/kg water) -also osmotic threshold for release of ADH is higher (290+/- 4) -do not begin to concentrate their urine until significantly dehydrated -at any degree of dehydration, they produce less concentrated urine than term babies & are vulnerable to hypernatraemia and hyperosmolality -diluting ability ,by contrast is well developed in even in very pre-terms (upto 50-60 mOsmoll/kg water) -Urine flow rate:2-3ml/kg/hr(range:1-10ml/kg/hr) RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION Urinary acidifying capacity: -even very pre-term babies can lower urine pH to a level that would be adequate to prevent acidosis ( urine pH<5.5 ) -however defence against systemic acidosis also depends on GFR & adequate supply of buffers: Phosphate is little available & ammonia is also less synthesized d/t low tubular mass -so the main non-volatile acid needing urinary excretion is sulphuric acid d/f protein metabolism. If infant is well fed & growing ,anabolism limits the sulphuric acid production -if the infant is sick & catabolic, or fed protein much in excess of dietary need, metabolic acidosis can easily develop RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION : RENAL FUNCTION IN A PRE-TERM NEONATE contdDISTAL TUBULAR FUNCTION Sodium excretion: -neonates born at or after 32-34 wks can produce virtually sodium free urine(FE Na:<<1%) -if born before this period, they lose sodium in the urine -prone for negative sodium balance -extreme pre-terms can have FE Na > 5%, commonly leads to hyponatraemia by second or third week of life -salt supplementation ,begun after first 3-6 days of life, improves early weight gain without apparent adverse effects RENAL FUNCTION IN A PRE-TERM NEONATE contdWHY SODIUM REABSORPTION IS INEFFICIENT IN PRE-TERMS? : RENAL FUNCTION IN A PRE-TERM NEONATE contdWHY SODIUM REABSORPTION IS INEFFICIENT IN PRE-TERMS? -Proximal tubule accounts for a smaller fraction of total sodium reabsorption in newborns than adults(65%), and this fraction is even less in the premature than term babies -this leads to increase in sodium concentration at distal tubule -in extreme pre-terms, distal tubule is incapable of reabsorption of sodium d/t immaturity & impaired response to circulating aldosterone: resulting natriuresis,negative salt balance & hyponatraemia FE Na & GFR in pre-term : FE Na & GFR in pre-term TRANSITION FROM FOETAL TO NEONATAL KIDNEY : TRANSITION FROM FOETAL TO NEONATAL KIDNEY Fetal diuresis is sustainable & after birth,diuresis is markedly attenuated First 2-3 days: negative salt & water balance: necessary to prevent circulatory overload Although very pre-term can develop hyponatraemia secondary to urinary sodium loss after first few days, it is not appropriate to attempt to prevent this by giving additional sodium or fluid in the first few days Both GFR & FE Na are much higher in the fetus than in the prematurely born infant at the same absolute GA ACUTE RENAL FAILURE IN NEONATES : ACUTE RENAL FAILURE IN NEONATES INCIDENCE IN NEONATES CLINICAL FEATURES BIOCHEMICAL FEATURES CLASSIFICATION & CAUSES ACUTE TUBULAR NECROSIS DIAGNOSIS MANAGEMENT ACUTE RENAL FAILURE IN NEONATESINCIDENCE IN NEONATES : ACUTE RENAL FAILURE IN NEONATESINCIDENCE IN NEONATES Syndrome that results from an abrupt ,potentially reversible, reduction in GFR Volume and composition of ECF is adversely affected No consensus as to what absolute or proportional change in GFR is necessary for the diagnosis A persistent rise in Pcr>1.5mg.dl(130mmols/l),corresponding to a fall in GFR to < 50% was suggested by Chevalier et al ACUTE RENAL FAILURE IN NEONATESINCIDENCE IN NEONATES : ACUTE RENAL FAILURE IN NEONATESINCIDENCE IN NEONATES The apparent incidence depends on the definition used Incidence:3-8% of NICU admissions Incidence of ARF severe enough to need dialysis:1% of NICU admissions Incidence among all live births:0.1% In poor & developing countries, incidence may be much higher ACUTE RENAL FAILURE IN NEONATESCLINICAL FEATURES : ACUTE RENAL FAILURE IN NEONATESCLINICAL FEATURES History suggestive of predisposing factors Oliguria (V:<1ml/kg/hr) :not necessary to the diagnosis Nonoliguric ARF may be more common (lower spectrum) Oedema:commonest clinical sign (not in non-oliguric ARF ) Polyuria, natriuresis, salt depletion & dehydration Commonly detected by typical biochemical abnormalities while investigating sick infant ACUTE RENAL FAILURE IN NEONATESBIOCHEMICAL FEATURES : ACUTE RENAL FAILURE IN NEONATESBIOCHEMICAL FEATURES By the time ARF is suspected, hyponatraemia is present in most cases ACUTE RENAL FAILURE IN NEONATESCLASSIFICATION & CAUSES : ACUTE RENAL FAILURE IN NEONATESCLASSIFICATION & CAUSES Renal function depends on: -Perfusion -Functional integrity of the kidney -Patency of urinary passages ACUTE RENAL FAILURE IN NEONATESCLASSIFICATION & CAUSES : ACUTE RENAL FAILURE IN NEONATESCLASSIFICATION & CAUSES ACUTE RENAL FAILURE IN NEONATESCAUSES : ACUTE RENAL FAILURE IN NEONATESCAUSES ANTENATL VASCULAR DAMAGE: 1.Maternal treatment: NSAIDS, ACE inhibitors 2.Twin to twin transfusion 3.Co-twin death 4.IUGR & Severe oligohydramnios ACUTE RENAL FAILURE IN NEONATESCAUSES : ACUTE RENAL FAILURE IN NEONATESCAUSES PRIMARY RENAL & UROLOGICAL DISEASES: 1.Congenital B/L obstructive uropathies ( PUV ) 2.Polycystic kidney 3.Renal dysplasia / hypoplasia 4.Multicystic dysplasia 5.Renal tubular dysgenesis 6.Idiopathic diffuse mesangial sclerosis 7.Glomerular immaturity 8.Finnish-type congenital nephrotic syndrome ACUTE RENAL FAILURE IN NEONATESCAUSES : ACUTE RENAL FAILURE IN NEONATESCAUSES ACQUIRED POSTNATAL RENAL DISEASES: Shock, Dehydration,Perinatal hemorrhage NEC with a third space loss Heart failure, Cardiopulmonary bypass, ECMO DIC, Vascular thrombosis (artery, vein) Perinatal asphyxia, HUS Isoimmune haemolytic diseases with massive haemoglobinuria Myoglobinuria, haemoglobinuria, uric acid nephropathy Infection:pyelonephritis, toxoplasmosis,fungal, syphilis Closure of congenital abdominal wall defects Nephrotoxic drugs:NSAIDs,ACE inhibitors,contast,amphotericin B, aminoglycosides, Vancomycin ACUTE RENAL FAILURE IN NEONATESCAUSES : ACUTE RENAL FAILURE IN NEONATESCAUSES 1.Intrinsic ARF due to acquired renal disease is virtually unknown in neonates 2.For practical purposes, intrinsic renal failure in neonates is synonymous with ACUTE TUBULAR NECROSIS (ATN ), with renal vein thrombosis a rare complication 3.Congenital Chronic (i.e irreversible ) commonly mimics ARF in its presentation 4.Pre-renal failure can progress to ATN if the predisposing factors persist to the point where hypoxic ischaemic injury to kidney develops FACTORS PREDISPOSING TO ATN : FACTORS PREDISPOSING TO ATN Hypoxia, sepsis & exposure to Nephrotoxic drugs, separately or in combination, cause most episodes of ARF in neonates Failure to recognize ATN can lead to marked biochemical abnormalities Both Myoglobinuria ,Myoglobinuria & increased urinary excretion of RBP are highly predictive of ATN Hyperuricemia has also been suggested as a marker of severity of tissue injury Slide 54: A microscopic picture of renal biopsy specimen showing renal medulla, which is composed mainly of renal tubules. Patchy or diffuse denudation of the renal tubular cells is observed, suggesting acute tubular necrosis (ATN) as the cause of acute renal failure (ARF). ACUTE TUBULAR NECROSIS (ATN) Slide 55: ACUTE TUBULAR NECROSIS (ATN) Acute tubular necrosis (ATN). Flattening of the renal tubule cells due to tubular dilation Slide 56: ACUTE TUBULAR NECROSIS (ATN) Acute tubular necrosis. Intratubular cast formation DIAGNOSIS OF ARF : DIAGNOSIS OF ARF Evidence of reduced GFR is essential for diagnosis, whether or not oliguria is present. Pcr is widely used as a rough marker for GFR and a value >1.5mg/dl(130mmol/l) persisting for >24hours is a reasonable criterion Plasma urea concentration is influenced by many factors, although high levels indicate that the baby’s excretory needs are not being met and may be one factor pointing to the need for dialysis Ultrasonography Radionuclide imaging studies are of little value in distinguishing b/n causes of ARF in neonates DIAGNOSIS OF ARFUrinary indices in the diagnosis of ARF: : DIAGNOSIS OF ARFUrinary indices in the diagnosis of ARF: DIAGNOSIS OF ARFUrinary indices in the diagnosis of ARF: : DIAGNOSIS OF ARFUrinary indices in the diagnosis of ARF: The most discriminating test is for differentiating pre-renal ARF & ATN is FE Na Renal failure index (RFI) is used as an alternative to EF Na RFI= U Na x Pcr / Ucr Very pre-term babies(<32wks) have high urinary sodium concentrations and excretion rates even in health. In this sub group, suitable cut off for diagnosis of ATN are an RFI of > 8 & FE Na >6% DIAGNOSIS OF ARF : DIAGNOSIS OF ARF The diagnosis of pre-renal ARF is confirmed by improvement in urine flow and renal function in response to fluid replacement Provided there is no circulatory overload, a fluid challenge of isotonic saline 10 ml/kg should be given iv over one hour Failure to respond confirms ATN as the diagnosis NATURAL COURSE OF ARF : NATURAL COURSE OF ARF MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE FLUID BALANCE: -Meticulous attention -correction of hypovolumia -monitor the total input and output -regular weighing -Maintenance fluid: IWL(180-310 ml/m2/day) + output - URINE OUT-PUT MONITORING : URINE OUT-PUT MONITORING MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE NUTRITION: -is essential to promote anabolism & prevent catabolism HYPERPHOSPHATAEMIA: -oral calcium carbonate -aluminum hydroxide should not be used -additional calcium should not be given until the plasma phosphate has been reduced to normal MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE HYPERKALAEMIA: -severe hyperkalaemia is a medical emergency -hypocalcaemia & hypomagnesaemia potentiate toxic effect of hyperkalaemia -maintain normocalcemia MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE HYPERKALAEMIA: -severe hyperkalaemia is a medical emergency -hypocalcaemia & hypomagnesaemia potentiate toxic effect of hyperkalaemia -maintain normocalcemia EKG Manifestations of Hyperkalemia : EKG Manifestations of Hyperkalemia Earliest to appear MANAGEMENT OF ACUTE RENAL FAILURE : MANAGEMENT OF ACUTE RENAL FAILURE SEVERE HYPERKALAEMIA: -intravenous /nebulised salbutamol (4mcg/kg over 5 mins) -IV glucose & Insulin infusion( 12 units of soluble insulin in 100 ml 25% glucose: 5ml /kg over 30 mins -IV sodium bicarbonate -Oral/rectal cation exchange resins (calcium polystyrene sulphate) ADEQUATE SODIUM INTAKE: CORRECTION OF ACIDOSIS MANAGEMENT OF ACUTE RENAL FAILURE MANAGEMENT BY DIALYSIS : MANAGEMENT OF ACUTE RENAL FAILURE MANAGEMENT BY DIALYSIS PERITONEAL DIALYSIS HEMODIALYSIS CONTINUOUS HEMOFILTRATION Continuous Arteriovenous Hemofiltration (CAVH ) Continuous Venovenous Hemofiltration (CVVH) Continuous Arteriovenous Hemodiafiltration (CAVHD) DIALYSISINDICATIONS : DIALYSISINDICATIONS VOLUME OVERLOAD HYPERKALAEMIA SEVERE METABOLIC ACIDOSIS HYPERPHOSPHATAEMIA/HYPOPCALCEMIA TO MAKE SPACE FOR FLUID & DRUG ADMINISTRATION FAILURE OF CONSERVATIVE MANAGEMENT : PERITONEALDIALYSIS Slide 72: COMPOSITION OF PD FLUID PD CATHETERS : PD CATHETERS Two double-cuff Tenckhoff peritoneal catheters: standard (A), curled (B). PERITONEAL DIALYSISCOMPLICATIONS : PERITONEAL DIALYSISCOMPLICATIONS PERITONITIS CATHETER EXIT SITE INFECTION CATHETER BLOCKAGE HYPERGLYCEMIA HAEMOFILTRATION & HAEMODIALYSIS : HAEMOFILTRATION & HAEMODIALYSIS REFERENCES : REFERENCES ROBERTON’S TEXTBOOK OF NEONATOLOGY, 4TH EDITION,929-940 ROBERTON’S TEXTBOOK OF NEONATOLOGY, 4TH EDITION,335-347 Pediatr Nephrol (2000) 14:1037-1044 Slide 77: THANK YOU