AKI kidney emergency case Lecture (1).pptx

AKI LECTURE

1. Acute Kidney injury in children Dr.Israel amanuael ( MD, lecturer ) 1 04/12/2024

2. Out line Definition of AKI Epidemiology Pathophysiology and Etiology Clinical manifestation Investigations Treatment approach Prognosis 2 AKI

3. Definition AKI is a sudden deterioration of renal function due to different causes resulting in inability of the kidneys to maintain fluid and electrolyte homeostasis. AKI results in the disturbance of renal physiological functions including: Impairment of nitrogenous waste product excretion Loss of water and electrolyte regulation Loss of acid-base regulation 3 AKI

4. Definition: cont… A classification system proposed to standardize the definition of AKI is pRIFLE criteria. which is acronym for p ediatric R = Risk for renal dysfunction , I = Injury to the kidney, F = failure of kidney function, L = loss of kidney function , and E = end stage renal disease It was developed to characterize the pattern of AKI in critically ill children 4 AKI

5. Pediatric modified Rifle (PRIFLE) criteria 5 AKI

6. RIFLE 6 AKI

7. KDIGO : AKI definition AKI 7 Increase in SCr by >= 0.3 mg/dl (>=26.5 mmol /l) within 48 hours; or Increase in SCr to >=1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or Urine volume < 0.5 ml/kg/h for 6 hours.

8. Acute Kidney Injury Network(AKIN) Categorizes severity by rise in serum creatinine: stage 1 >150% stage II >200% stage III >300%. 8 AKI

9. Epidemiology Generally the prevalence of AKI is increasing both in developed and developing countries. AKI occurs in 2-3% of children admitted to pediatric tertiary care centers ̴ 8% of infants in neonatal intensive care units. 9 AKI

10. Classification Clinical Prerenal Intrinsic renal Postrenal Epidemiologic Community acquired Hospital acquired Urine output Oliguric AKI (UOP<1 mL /kg/h in infants, < 0.5 mL /kg/h in children, or Anuria Nonoliguric AKI 10 AKI

11. Pathogenesis Three phases in the development of AKI Initiation phase : ischemia or a toxin sets in motion a sequence of events which produce an injury to tubular epithelial cells Maintenance phase : GFR remains relatively low for several days Recovery phase : characterized by gradual and progressive restoration of GFR and tubular function 11 AKI

12. Pathogenesis Three major factors that may account for the development of AKI: Renal hemodynamics Nephronal factors Metabolic/cellular factors 12 AKI

13. Renal hemodynamics Tubular injury Decreased cortical BF Altered reabsorption of solute & water Release of vasoactive compounds Increased cortical VR Diminished GF dynamics Decreased GFR AKI 13 AKI

14. 14 Nephronal factors in ARF Proximal tubule injury Epithelial cell necrosis Loss of tubule integrity Impacted cellular debris Back leak of solute/fluid Tubule obstruction Diminished GFR Diminished tubule flow AKI AKI

15. Cellular and metabolic factors Oxygen free radical production contributing to an ischemic insult Calcium accumulation in tissues who have undergone necrosis contributing to renal cell injury Depletion of tissue adenine nucleotide levels which is a source of energy 15 AKI

16. Disruption and recovery of renal tubule architecture in acute ischemia 16 AKI

17. Etiology AKI has been conventionally classified into 3 categories: pre renal, intrinsic renal, and post renal Can be related to the renal anatomy most affected by the disorder as follows: Vascular Glomeruli Renal tubule Urinary tract Any process that interferes with any of these structures and/or functions can cause renal disease. 17 AKI

18. Etiology 1. Pre renal AKI - also called pre renal azotemia, characterized by diminished effective circulating arterial volume, which leads to inadequate renal perfusion and a decreased GFR. Evidence of kidney damage is absent. Common causes of pre renal AKI include dehydration , sepsis , hemorrhage , severe hypoalbuminemia, and cardiac failure. If the underlying cause of the renal hypo perfusion is reversed promptly, renal function returns to normal. If hypo perfusion is sustained, intrinsic renal parenchyma damage can develop. 18 AKI

19. Etiology pre renal 19 AKI

20. Etiology 2. Intrinsic renal AKI - includes a variety of disorders characterized by; Renal parenchyma damage, including sustained hypo perfusion and ischemia Many forms of Glomerulonephritis Hypoxic injury and nephrotoxic insults are the most common causes of intrinsic AKI , and are more common with an underlying co morbid condition Vasodilation /vasoconstriction: sepsis, hepatorenal syndrome 20 AKI

21. Etiology 3. Post renal AKI – characterized by obstruction of the urinary tract. In neonates and infants, congenital conditions: Posterior urethral valves and Bilateral ureteropelvic junction obstruction, account for the majority of cases of AKI. Relief of the obstruction usually results in recovery of renal function most of the causes 21 AKI

22. Etiology: Prerenal Dehydration, Shock Hemorrhage Sepsis Hypoalbuminemia Cardiac failure Burn 22 AKI

23. Etiology: Intrinsic renal Glomerulonephritis Postinfectious / poststreptococcal Lupus erythematosus Henoch-Schönlein purpura Membranoproliferative Anti– glomerular basement membrane Hemolytic-uremic syndrome Acute tubular necrosis Cortical necrosis Renal vein thrombosis Rhabdomyolysis Acute interstitial nephritis Tumor infiltration Tumor lysis syndrome 23 AKI

24. Etiology: Post Renal Posterior urethral valves Ureteropelvic junction obstruction Ureterovesicular junction obstruction Ureterocele Tumor Urolithiasis Hemorrhagic cystitis Neurogenic bladder 24 AKI

25. Clinical evaluation History Risk factors History of fluid or blood loss Nephrotoxic drug intake Recent sore throat or skin rash Preceding bloody diarrhea Recent Circumcision or trauma Dietary history Family history of renal disease 25 AKI

26. Symptoms of AKI Reddish urine, decreased urine out put, body swelling( peri orbital to generalized)---- Glomerulonephritis Eagerness to drink, sunken eye balls , change in mentation with history of fluid loss suspect dehydration. Cloudy or frothy urine – shows WBC and high protein in urine respectively History of urgency, frequency, dysurea – suspect UTI History of fever, fast breathing – may be due to sepsis History of preceding bloody stool, symptoms of anemia, - suspect HUS History of skin rash, female sex – autoimmune causes 26 AKI

27. Physical examination An initial rapid assessment must be thorough, with careful attention to: Airway, breathing and circulation should be assessed to determine how ill the child is. Volume status - Tachycardia, dry mucous membranes, and poor peripheral perfusion suggest an inadequate circulating volume and the possibility of pre renal AKI. The level of consciousness 27 AKI

28. Cont . . . Any obvious dysmorphic features should be recorded. Pain can be a manifestation of renal disease and is often confused with back pain and other causes of abdominal pain in childhood. A record of the mood and demeanor of the child together with the family interaction is informative. 28 AKI

29. Cont . . . V/S – tachycardia/ bradycardia , tachypnea / bradypnea , or hypotention – sepsis, dehydration/shock. Hypertension, rales , and a cardiac gallop suggest volume overload and the possibility of intrinsic AKI from glomerulonephritis or ATN. Palpable flank masses may be seen with renal vein thrombosis , tumors , cystic disease , or urinary tract obstruction. 29 AKI

30. Cont . . . Peripheral edema or Anasarca can be sign of hypoalbuminemia Skin findings, such as purpura, malar rash, or petechiae , and/or joint pain favor a diagnosis of systemic vasculitis , such as systemic lupus erythematosus or Henoch Schönlein purpura 30 AKI

31. Investigations 1. CBC Delusional or hemolytic anemia Thrombocytopenia Leukocytosis or leukopenia 2.Urinalysis Urinary indices may be useful in differentiating pre renal AKI from intrinsic AKI . 31 AKI

32. Comparison of Laboratory Findings in AKI 32 AKI

33. Cont… Urinalysis 1 . Deep stick Specific gravitiy PH Ketone Nitrite Leukocyte esterase Protienuria 2 . Microscopy: Pyuria Casts: RBC cast- GN WBC cast- inflamation Granular cast- ATN 33 AKI

34. Cont . . . Serum C3 level - may be depressed (post infectious glomerulonephritis, SLE, or membranoproliferative glomerulonephritis ) Antibodies - may be detected in the serum to; streptococcal (post streptococcal glomerulonephritis), Anti nuclear (SLE), Anti Glomerular basement membrane ( Goodpasture disease) antigens. 34 AKI

35. Cont . . . Chest radiography - may reveal cardiomegaly, pulmonary congestion (fluid overload), or pleural effusions. Renal ultrasonography - should be performed in all children with AKI of unclear etiology. 35 AKI

36. Cont… Serum creatinine - is used to measure kidney function, it is an insensitive and delayed measure of decreased kidney function following AKI. BUN – is affected by diet, state of hydration of the child, gastrointestinal bleeding, catabolic medications like steroid. 36 AKI

37. Renal biopsy Indications Isolated glomerular hematuria Isolated nonnephrotic proteinurea Nephrotic syndrome Unexplained acute renal failure Acute nephritic syndrome 37 AKI

38. Complications of acute kidney injury 38 AKI

39. Treatment Medical treatments Urinary catheter – acute urinary retention due to obstruction Fluid replacement – if hypovolemia is detected , give 20ml/kg of iv NS to run over 30min. If no response bolus can be repeated. If there is blood loss or sever hypoalbuminemia colloids might be preferred. If no urine after 2hours:-- Diuretics - intrinsic renal injury with fluid over load, furosemide (2-4mg/kg) and mannitol (0.5g/kg) iv stat. 39 AKI

40. Cont. . . Vasopressors – dopamine vs norepinephrine Dopamine The use of dopamine for AKI has been controversial, but recent studies don’t recommend its use. Fluid restriction – insensible loss(400ml/m²/day + urine out put for the day) plus fluid loss 40 AKI

41. Cont . . . Electrolyte imbalance; Hyperkalemia - >6meq/L can be treated with Po Kayexalate (1gm/kg), decrease K+ by 1meq/L. If serum K+ >6.5 - 7meq/L or any ECG abnormality- give IV treatment. Options are: Calcium gluconate 1ml/kg over 5-10 min. Sodium bicarbonate 1-2 meq /kg over 10-15min. Regular insulin(0.1iu/kg) with 1ml/kg of dextrose over 1hour. Beta adrenergic agonist ECG:--Peaked T waves  Widened QRS  ST depression Ventricular Arrhythmia Arrest 41 AKI

42. Cont . . . Hyponatremia – usually mild so use fluid restriction. If <120meq/L or patient develops neurologic manifestations treat with iv 3% saline. Hypernatremia - Sodium intake should be restricted to 2–3 mEq /kg/day, together with fluid restriction Hypocalcemia – reduced phosphate diet, phosphate binding drugs, calcium is given if only patient develops tetany . 42 AKI

43. Cont. . . Metabolic acidosis – usually mild due to retention of H+, phosphate, sulphate . Treat with sodium bicarbonate if PH is <7.15 or bicarbonate is <8meq/L target is to make PH >7.2 and bicarbonate >12meq/L GI Prophylaxis – prevent GI bleeding due to uremic platelet dysfunction, give IV H2 blockers like rantidine Hypertention –Diuretics, salt and fluid restriction, calcium channel blockers and beta blockers 43 AKI

44. Cont . . . Anemia - mostly mild with Hg of 9-10mg/dl but transfuse with fresh blood if Hg <7mg/dl Neurologic manifestations – treat the underlying cause, use benzodiazepines for seizure control. Nutrition; Restrict Na+, k+ and phosphate diet. Maximize calories Restrict protein moderately Keep RBS 110 - 149 mg/dl 44 AKI

45. Dialysis Indications for dialysis in AKI: Anuria / oliguria Volume overload with evidence of hypertension and/or pulmonary edema refractory to diuretic therapy Persistent hyperkalemia Severe metabolic acidosis unresponsive to medical management Uremia (encephalopathy, pericarditis , neuropathy) Blood urea nitrogen >100-150 mg/ dL (or lower if rapidly rising) Calcium : phosphorus imbalance, with hypocalcemic tetany that cannot be controlled by other measures 45 AKI

46. Dialysis: Types 1. Intermittent hemodialysis : Useful in stable hemodynamic state fluid and electrolyte removal in 3-4 hours 3-7 times a week 2. Peritoneal dialysis: most commonly employed in neonates and infants with AKI 3. Continuous renal replacement therapy (CRRT) 46 AKI

47. 47 AKI

48. Prognosis **Depends on Underlying Condition** Renal Function Likely to Return: Prerenal causes, HUS, ATN, Acute interstitial nephritis, or tumor lysis syndrome Renal Recovery Unlikely: Rapidly progressive glomerulonephritis , bilateral renal vein thrombosis, or bilateral cortical necrosis 48 AKI

49. THANK YOU 49 AKI