Acute kidney injury. Dr P Sigwadi Paediatric nephrology

Transcription

1 Acute kidney injury Dr P Sigwadi Paediatric nephrology

2 Introduction Is common in critically ill patients e.g. post cardiac surgery Occurs when renal function is diminished to a point where body fluid and electrolyte homeostasis can no longer be maintained Lack of standardized definition RIFLE Criteria used to define AKI

3 RIFLE Criteria for Acute Renal Dysfunction Risk Injury Failure Loss Increased creatinine x1.5 or GFR decrease > 25% Increased creatinine x2 or GFR decrease > 50% Increase creatinine x3 or GFR decrease ESKD GFR Criteria* Urine Output Criteria UO <.5ml/kg/h x 6 hr UO <.5ml/kg/h x 12 hr UO <.3ml/kg/h x 24 hr or Anuria x 12 hrs Persistent ARF** > 75% = complete loss of kidney function > 4 weeks End Stage Kidney Disease (> 3 months) High Sensitivity High Specificity

4 Acute Kidney Injury in Children In children: smaller in s-creatinine associated with significant risk of mortality S-Creatinine shows significant after 50% of GFR has been lost Modified pediatric RIFLE score was introduced

5 Paediatric Modified RIFLE (prifle) Creatinine clearance Urine output Risk eccl by 25 % <0.5 ml/kg/hr for 8 hrs Injury eccl by 50 % 0.5 ml/kg/hr for > 16hrs Failure eccl by 75 % <0.3 ml/kg/hr for 24 hr or anuria for 12 hr Loss Persistent failure > 4 weeks End stage End Stage Kidney Disease (> 3 months) Creatinine clearance (eccl) = 40 x height (cm) / s-creatinine (μmol/l)

6 Risk factors for AKI Age (neonates) Hypovolaemia Surgery Sepsis Pre-existing renal, hepatic or cardiac dysfunction Exposure to nephrotoxins

7 AKI Prerenal injury Intrinsic Post renal

8 Pathogenesis Pre-renal renal perfusion due to a decreased in the total circulating blood volume Vasoconstriction and desquamation of the tubular cell ( Forming casts) Intraluminal tubular obstruction and back leakage of glomerular filtrate

9 Pathogenesis Decreased intravascular volume leads in renal cortical blood flow GFR Neutrophils adhere to the ischaemic endothelium and promote inflammation

10 Causes of Pre renal failure Hypovolaemia Gastrointestinal losses e.g vomiting and diarrhoea Third space losses Excessive renal losses e.g renal tubular disorders

11 Causes of Pre renal failure Peripheral vasodilatation Sepsis Circulatory failure Cardiac failure, cardiac tamponade Drugs Diuretics

12 Prerenal injury If the underlying cause of renal hypo perfusion is reversed, renal function may return to normal If hypoperfusion persist, intrinsic renal parenchymal damage develop

13 Intrinsic renal injury Glomerular Acute Glomerulonephritis Arterial HUS, embolic, arteritis, Venous Renal venous thrombosis

14 Acute tubular necrosis Syndrome of acute renal failure in the absence of glomerular lesions Necrosis of tubular cells Causes: Infections Drugs e.g. NSAIDS, vancomycin, aminoglycosides Heavy metals, lead

15 Post-renal Due to obstruction of the urinary tract e.g. bilateral ureteric obstruction (schistosoma) Urethral obstruction e.g. posterior urethral valves Obstruction in a solitary kidney Neuropathic bladder

16 History Age: Infants Think of congenital abnormalities e.g PUV, PUJ/ VUJ obstruction Vomiting and diarrhoea Post surgical patient Antecedent skin and throat infection Exposure to chemicals or medications History of chronic renal disease

17 History History Polyuria and polydipsia Poor urinary stream Family history of renal diseases Long standing malaise Small or syndromic child

18 Pre renal Renal Post renal Diarrhea and vomiting Bloody diarrhea- HUS Previous UTI Cardiac disease Drugs Antenatally diagnosed anomalies Umbilical catheters Recent throat and skin infection Poor urine stream Birth asphyxia Birth asphyxia History of calculi Acute weight loss Prolonged convulsions Systemically unwell child Palpable bladder, spinal anomalies

19 Clinical manifestation Pallor Degree of dehydration Decreased urine output Edema Hypertension With warm peripheries think of volume overload With cold peripheries intravascular depletion Lethargy Flank masses may suggest cystic disease or obstruction, renal vein thrombosis, tumours

20 Volume responsive AKI Severe dehydration Sunken eyes Loss of skin turgor Dry mucous membranes Limp/ non-responsive

21 Clinical manifestation Late presentation Coma Pulmonary edema Uremic encephalopathy Heart failure Seizures

22 Investigations Urine dipstick Urine microscopy culture and sensitivity Microscopy Haematuria, proteinuria and red cell casts are suggestive of intrinsic ARF /glomerular disease White blood cell casts with low grade haematuria and proteinura are suggestive of tubulointerstitial disease Urine biochemistry fractional excretion of sodium (FeNa%)

23 Granular cast

24 Pre-renal Intrinsic U-Osmol (mosmol/l) > 320 Equal to serum osmol U-Na (mmol/l) < 30 > 30 Fe Urea % < 35 % > 50 % FeNa % * < 1 % (<2.5%in neonates) FeNa % = fractional excretion of Na (%) = U-Na/U-Creatinine x S-Creatinine/S-Na x 100 Remember S-Creatinine is measured in mol/l For the calculation the value should be by 1000) 3 %

25 Investigations Blood cultures if one suspects sepsis Full Blood Count + reticulocyte count haemoglobin- may be dilutional or due to haemolysis Thrombocytopaenia e.g. HUS, renal vein thrombosis, SLE

26 Investigations S- Urea and electrolytes Hyponatraemia-dilutional Acidosis (plasma bicarbonate) S-urea and creatinine S-uric acid and phosphate

27 Investigations Specific tests will be determined by the history and other findings on clinical examination C3, C4 ASO titres and anti-dnase B Auto-immune screen Acute on chronic renal failure PTH, long bone X-Ray for renal osteodystrophy (ROD) Suspected rhabdomyolysis CK Urine myoglobin

28 Investigation Chest X-ray if + cardiac signs Ultrasound of the kidneys Large echo bright kidneys-suggestive of an acute process To rule out obstruction, e g calculi Morphological abnormalities Vascular flow- Doppler ultrasound Renal biopsy with rapidly renal function

29 Management Attend to life threatening features first i.e.abc If dehydrated Fluid resuscitation- 20 ml/kg normal saline/ Ringers lactate rapidly Re assess the patient ( BP, weight,urine output, capillary refill time, level of consciousness) Repeat fluid bolus if necessary Continue rehydration

30 Management Fluid overloaded Challenge with IVI furosemide and assess urine output

31 Ongoing management Treat hypertension Manage electrolyte abnormalities Hyperkalaemia Hyper/hyponatraemia Hyperphosphataemia Hypocalcaemia

32 Absolute Indications for dialysis Fluid overload Pulmonary oedema Anuria > 24 hours Central nervous system signs e.g. convulsions or coma Bleeding diathesis Uraemic pericarditis

33 Relative indications for dialysis S-K / Na not responding to conservative treatment Persistent metabolic acidosis ph < 7.1 or S-HCO3 < 10 mmol / L Uncontrollable HT Severe S-phosphate / and S-Ca

34 Prognosis Depend on the underlying aetiology Children with AKI as a component of multisystem failure- Mortality rate Children who suffered substantial loss of nephrons as in Rapidly progressive glomerulonephritis (RPGN) are at risk for late development of CKD

35 References 1. Kliegman RM, Berhman RE, Jenson HB, Stanton BF. Nelson Textbook of paediatrics 18 th edition, Rees L, Webb NJA, Brogan AP. Paediatric nephrology, Avner ED, Harmon WE, Niaudet P, Yoshikawa N, Pediatric nephrology, Akcan-Arikan A et al. Modified RIFLE criteria in critically ill children with acute kidney injury Kidney Int 2007; 71: Andreoli SP. Acute kidney injury in children. Pediatr Nephrol 2009;24: Goldstein SL, Devarajan P. Acute kidney injury in childhood: should we be worried about progression to CKD? Pediatr Nephrol 2011;26: