APPROACH TO AKI IN CHILDREN ACUTE KIDNEY INJURY It is defined as abrupt loss of kidney function leading to rapid decline in GFR , accumulation of waste products BUN and creatinine and dysregulation of extracellular volume and electrolyte homeostasis. AKI can ranges from small increase in creatinine to complete anuric renal failure . INCIDENCE 2-5 % of all hospitalization. >25% in critically ill children . CLASSIFICATION OF AKI CAUSES CLINICAL MANIFESTATION DIAGNOSTIC TEST HISTORY AND PHYSICAL EXAMINATION IDENTIFICATION OF PRECIPTATING CAUSE COMPLICATION MANAGEMENT MANAGEMENT There is no definitive therapy for AKI, supportive care is mainstay of management regardless of aetiology. Goal of treatment is : Minimize degree of insult. Reduce extrarenal complication. Restoration of AKI. Optimize the systemic and renal hemodynamic(fluid resuscitation or use of vasopressor). Avoid the nephrotoxic drugs (e.g aminoglycoside, NSAIDs, ACE inhibitor, ARB blocker, acyclovir) or adjust the dose . Catheterize the patient in case of obstruction like PUV, UPJ obstruction POST-RENAL AKI Prompt relieve of urinary tract obstruction. Relief of obstruction is usually followed by an appropriate diuresis and may require continue administration of iv fluids and electrolyte. RENAL REPLACEMENT THERAPY The purpose of RRT is to prevent morbidity. It may be necessary for days or upto 12 weeks. Mostly require dialysis support for 1-3 weeks. Indication Of RRT : A= ACIDOSIS, ANURIA E= ELECTROLYTE DISTURBANCE (hypokalemia) I= INTOXICATION O= OVERLOAD(hypertension, pulmonary edema) U= UREMIA PROGNOSIS Pre-renal and post-renal have better prognosis. In case of post-infectious glomerulonephritis is 1% In case of multi organ failure >50%. Kidney may recover even after dialysis . 10% cases requiring dialysis develop CKD. CARRY HOME MESSAGE Diagnose early- biomarkers have great potential. Look for aetiology. Prevent rather than treat. No role of low dose dopamine prevention and treatment . Initiate RRT when indicated.

1. APPROACH TO AKI IN
CHILDREN
DR Raheel Ahmed
FCPS(Paediatrics)
Children Hospital, Chandka Medical College, Larkana

2. ACUTE KIDNEY INJURY
• It is defined as abrupt loss of kidney function leading to rapid decline
in GFR , accumulation of waste products BUN and creatinine and
dysregulation of extracellular volume and electrolyte homeostasis.
• AKI can ranges from small increase in creatinine to complete anuric
renal failure .

4. INCIDENCE
• 2-5 % of all hospitalization.
• >25% in critically ill children .

5. CLASSIFICATION OF AKI
1. KDIGO
2. AKIN
3. RIFLE

6. KDIGO

7. RIFLE

8. AKIN

9. CAUSES

10. CLINICAL MANIFESTATION
• PERIPHERAL EDEMA
• WEIGHT GAIN
• NAUSEA ,VOMITING , DIARRHEA, ANOREXIA
• MENTAL STATUS CHANGE
• FATIGUE
• SHORTNESS OF BREATH
• PRURITIS

11. DIAGNOSTIC TEST
• HISTORY AND PHYSICAL EXAMINATION
• IDENTIFICATION OF PRECIPTATING CAUSE
• CBC
• SERUM CREATININE AND BUN LEVEL
• SERUM ELECTROLYTE
• RENAL US
• RENAL SCAN (DMSA, DTPA, MAG3)
• CT & MRI
• URINARY ELECTROLYTE
• URINARY SPOT CREATININE RATIO
• ABGS
• URINE DR &CS

12. URINALYSIS, URINE CHEMISTRY AND
OSMOLALITY

13. IMPORTANT BIOMARKER
Cystatin c
• Superior to serum creatinine, surrogate marker of early and subtle
change of kidney function.
• It allows detection of AKI 24-48hrs earlier than serum creatinine.
Neutrophil gelatinase associated lipocalin (NGAL)
• Detected in plasma and urine within 2 hrs of cardiopulmonary bypass.
Interleukin -18
Kidney injury molecule-1
• Marker of severity of AKI.

14. COMPLICATION

16. MANAGEMENT
• There is no definitive therapy for AKI, supportive care is mainstay of
management regardless of aetiology.
• Goal of treatment is :
1. Minimize degree of insult.
2. Reduce extrarenal complication.
3. Restoration of AKI.

17. 1. Optimize the systemic and renal hemodynamic(fluid resuscitation
or use of vasopressor).
2. Avoid the nephrotoxic drugs (e.g aminoglycoside, NSAIDs, ACE
inhibitor, ARB blocker, acyclovir) or adjust the dose .
3. Catheterize the patient in case of obstruction like PUV, UPJ
obstruction

18. FLUIDS
• KIDGO suggest using isotonic crystalloids rather than colloid.
• Colloids are used in blood loss or hypoproteinemia.
• 20ml/kg over 30mins ns bolus (patient must void within 2 hr)
• Hypotension caused by sepsis may require vasopressors.
• Diuretic therapy (furosemide 2-4mg/kg iv single dose or bumetanide
0.1mg/kg).
• If no response to diuretic than fluid restriction is necessary i-e
400ml/m2/24hr + amount of fluid equal to renal and GI losses.

19. METABOLIC ACIDOSIS
• It is common in AKI.
• Treatment is required only in sever acidosis (ph <7.15 hco3 <8mEq/l)
• Treated partially by iv route and remaining by orally.
• Iv Nahco3 1-2 mEq/kg over 5-10mins( to raise ph 7.20 and hc03 to
12mEq/l).
• Remaining correction by oral administration.

20. HYPONATREMIA
• It is most commonly a dilutional disturbance that can be corrected by
fluid restrictions rather than Na administration.
• Hypertonic saline (3%) is used in case of symptomatic hyponatremia
(seizures, lethargy) or serum level of <120mEq/l.
• Acute correction of hyponatremia is done by using formula:
mEq Na required=0.6*body wt in kg*(125-serum Na)

21. HYPERKALEMIA
• Restrict dietary intake +parenteral.
• Keyxlate 1gm/kg lower 1meq/L, (dose may repeated every 2 hr).
• Iv ca gluconate 100mg/kg/dose iv slowly.
• Glucose solution of 50% (1ml/kg/hr) +insulin (0.1units/kg)
• Dialysis if medical management fails.

22. HYPERPHOSPHATEMIA AND
HYPOCALCEMIA
• Usually controlled by dietary restriction.
• Orally phosphate binders eg sevelamer (Renagel)or ca carbonate
(Tums tablets or titralac suspensions ) or ca acetate (phoslo), they
reduce GI absorption.
• Hypocalcemia Usually does not require treatment bcoz they are
normalise by lowering phosphate.

23. NUTRITION
• Adequate protein intake(0.6-2mg/kg/day) depending on degree of
catabolism.
• Pottasium restriction.
• Phosphate restriction.
• Sodium restriction.

24. HYPERTENSION
• Salt and water restriction.
• Diuretic therapy.
• Isradipine(0.05-0.15mg/kg/dose) for rapid reduction of bp.
• Long acting ca-channel blocker( amlodipine 0.1-0.6 mg/kg/24hr) or B-
blocker (labetolol 4-40mg/kg /24hr) for maintaing the control of bp.
• In case of hypertensive emergency or urgency
• Nicardipine infusion ( 0.5-5mcg/kg/min)
• Labetolol infusion (0.25-3mg/kg/hr)
• Esmolol infusion (150-300mcg/kg/min)
• Sodium nitropursside infusion(0.5-10mcg/kg/min)

25. • ANEMIA
• BLEEDING

26. POST-RENAL AKI
• Prompt relieve of urinary tract obstruction.
• Relief of obstruction is usually followed by an appropriate diuresis
and may require continue administration of iv fluids and electrolyte.

27. RENAL REPLACEMENT THERAPY
• The purpose of RRT is to prevent morbidity.
• It may be necessary for days or upto 12 weeks.
• Mostly require dialysis support for 1-3 weeks.
• Indication Of RRT :
A= ACIDOSIS, ANURIA
E= ELECTROLYTE DISTURBANCE (hypokalemia)
I= INTOXICATION
O= OVERLOAD(hypertension, pulmonary edema)
U= UREMIA
contin.............

28. INTERMITTENT HEAMODIALYSIS:
• Relatively stable hemodynamic patient, highly efficient process
accomplish both fluid and electrolyte removal in 3-4 hr session
through large central venous catheter or pump driven extracorporeal
circuit.
• 3-7 times /week based on patient status.
PERITONEAL DIALYSIS:
• Most commonly employed in neonate and infant.
• Hyperosmlar dialysate is used for 45-60min.
• Cycles are repeated for 8-24hr/day

29. CONTINUOUS RENAL REPLACEMENT THERAPY:
• It is useful for hemodynamically unstable patient, with sepsis or multi
organ failure or icu settings.
• Extracorporeal therapy that is used 24/day.

31. PROGNOSIS
• Pre-renal and post-renal have better prognosis.
• In case of post-infectious glomerulonephritis is 1%
• In case of multi organ failure >50%.
• Kidney may recover even after dialysis .
• 10% cases requiring dialysis develop CKD.

32. CARRY HOME MESSAGE
• Diagnose early- biomarkers have great potential.
• Look for aetiology.
• Prevent rather than treat.
• No role of low dose dopamine prevention and treatment .
• Initiate RRT when indicated.