Ppt

1. Acute Kidney Injury (AKI): Definition
Formerly referred to as acute renal failure (ARF).
Defined as an “sudden deterioration in kidney function results in
the inability to maintain fluid and electrolyte homeostasis”

2. Kidney function is dependent on
Adequacy of blood supply to the kidney
– Prerenal
Integrity of renal parenchyma
– Renal
Patency of urinary tract
– Post renal

3. Epidemiology

4.  The incidence of AKI varies in different regions of the
world.
 Estimates range from 20 cases per year per 1,00,000
population in neonates to as low as 2 cases per year per
1,00,000 population in older children
 The co-existence of AKI with critical illness occurs at a
rate of 10% and has 50% mortality in children requiring
dialysis.

5. ETIOLOGY

6. Pre renal
Intrinsic or renal
Post renal

7. Pre Renal AKI
 Also called prerenal azotemia, is characterized by diminished
effective circulating arterial volume, which leads to
inadequate renal perfusion and a decreased GFR .
 The kidneys are intrinsically normal, and prerenal failure is
reversible once the blood volume and hemodynamic conditions
are restored to normal.

8. Causes of PreRenal Azotemia
Decreased true intravascular volume
 Acute gastroenteritis, Burns, Hemorrhage, Sepsis
Decreased effective intravascular volume
 Burns, Nephrotic syndrome, Massive ascites, Anaphylaxis, Cardiac
failure, Shock
Medications
 NSAIDs ,ACE inhibitors, ARBs

9. Renal (Intrinsic)
CAUSES –
1. Obstruction of renal artery or veins –
Renal vein thrombosis, Renal arterial obstruction,
2. Involvement of renal microvasculature –
HUS, HSP, Poly-arteritis, Collagen vascular disease
3. Glomerular causes-
PSGN, Crescentic GN
4. Interstitial causes-
Acute tubulointerstitial nephritis
5. Tubular causes (ATN)
Prolongation of pre-renal insult, intravascular hemolysis, sepsis, nephrotoxic
agents, multiorgan failure, rhabdomyolysis, snakebite, falciparum malaria.

10. 1. OBSTRUCTION OF RENAL ARTERIES AND VEINS
 Bilateral renal arterial thrombosis may occur after umbilical
artery catheterisation in neonates
 Renal vein thrombosis may be a complication of IDM
especially following dehydration.
 In older children, renal vein thrombosis may occur with
nephrotic syndrome with anasarca and dehydration.
 Gross haematuria, enlargement of kidneys and azotemia
are typical manifestation.

11. 2. INVOLVEMENT OF RENAL MICROVASCULATURE
 HUS is a common cause of AKI in chidren.
 Causes thrombotic microangiopathy
 2 types- D+HUS and D-HUS
 Common causes of D+HUS – EHEC(in developed countries), Shigella dysentriae type I
(in India)
 Following dysentery shigella-toxin enters the circulation and leads to endothelial injury
in microvasculature .
 Localized coagulation and deposition of platelet thrombi and fibrin occurs in glomeruli
causing decrease in GFR.

12. 3. Glomerular disease
 PSGN,
 Post infectious GN,
 Cresentic GN,
 IgA nephropathy .

13. 4. ACUTE INTERSTITIAL NEPHRITIS
 Usually occurs due to hypersensitivity reaction to some drugs
(ampicillin, cephalosporins, sulfonamides, quinolones, NSAID’s,
phenytoin etc)
 The patient may have fever , arthralgia , rash and eosinophilia
: urine often shows eosinophils
 Renal biopsy should be done if it is strongly suspected.

14. 5. Acute Tubular Necrosis
 Characterized by renal tubular injury, may occur due to
ischaemia/hypoperfusion or due to injury froms drugs or
toxins.
 Ischaemic ATN is a continnum of physiologic responses that is
observed in prerenal azotemia.
 If the hypoperfusion is severe and prolonged, ATN can progress to renal
infarction and irreversible renal damage

15.  The course is subdivided into 4 phases :
 Initiation
 Extension
 Maintainance
 Recovery

16. (C) POST RENAL
 It includes a variety of disorders characterized by obstruction
of the urinary tract.
 In a patient with 2 functioning kidneys, obstruction must be
bilateral to result in AKI.
 Relief of the obstruction usually results in recovery of renal
function except in patients with associated renal dysplasia or
prolonged urinary tract obstruction.

17. Causes of post renal AKI
 Posterior urethral valves
 Ureteropelvic junction obstruction
 Ureterovesicular junction obstruction
 Ureterocele
 Tumor
 Urolithiasis
 Hemorrhagic cystitis
 Neurogenic bladder

18. CLINICAL EVALUATION

19.  Clinical features range from asymptomatic with mild
to moderate elevation in S.creatinine to anuric renal
failure
 Decrease or no urine output
 Fluid overload
 Hypertension
 Uraemia, dyselectrolytemia

20. Management

21. Management Goals
A. Maintenance of electrolyte and fluid balance.
B. Avoidance of life-threatening complications.
C. Adequate nutritional support.
D. Treatment of the underlying cause.

22. Management: FLUIDS
 If no evidence of volume overload or cardiac failure :
Fluid challenge of IV NS , 20 mL/kg over 30 min
 No void within 2-4 hr points to intrinsic or postrenal ARF
 Vigorous fluid resuscitation may be needed in sepsis
 Diuretics if no void with adequate circulation.
 In absence of urine output, strict fluid restriction.
 Renal dose of dopamine (2-3 g / kg / min)
μ

23. Hyperkalemia
1. Severe hyperkalemia (>7.0 mEq/L):
 Electrocardiographic changes or peripheral muscle weakness
 Can be life-threatening and requires immediate attention.
2. Acute management includes administration of:
 IV calcium to stabilize the cardiac membrane; and/or
glucose/insulin infusion,
 Sodium bicarbonate or Glucose-Insulin infusion (promotes
extracellular K shift into the cells)
 Kayexalate (an anion exchange resin): removes excess K from
the body.
 Renal replacement therapy: if medical management fails

24. Acidosis
1. In children with AKI:
 impaired acid excretion
 increased acid production (shock and sepsis)
2. Sodium bicarbonate should only be administered with life
threatening acidosis or hyperkalemia.
3. HCO3 > 12 mEq/L and/or arterial pH greater than 7.2 do
not require immediate intervention.

25. Hypertension
 Most often a result of hyper-reninemia or from expansion of
fluid volume.
 Most commonly seen with AGN and HUS
 Management :
 Salt and water restriction.
 Diuretic adminiistration
 Anti-Hypertensives

26. Hyponatremia
 Most commonly dilutional
 Management:
 Fluid restriction
 3% Hypertonic saline to symptomatic patients or sodium less than
120 mEq/L
 mEq sodium required = 0.6 X weight(kg) X ( 125-serum
sodium in mEq/L )

27. Hypocalcemia
 Primarily treated by lowering the serum phosphate levels.
 Phosphate binders can be administered.
 IV calcium should be avoided
 Aluminium-based binders should also be avoided.

28. Nutrition
 Sodium, potassium and phosphorous should be restricted.
 Protein intake should also be moderately decreased.
 Adequate calories are needed to promote recovery
 Renal replacement therapy if sufficient calories cannot be
achieved (patient with oliguria or anuria)
 Patients with inappropriate nutrition have poorer prognosis.

29. Indications for dialysis in ARF
 Severe fluid overload unresponsive to management
 Persistent hyperkalemia
 Severe met.acidosis unresponsive to management.
 Neurologic symptoms (altered mental status, seizures)
 BUN >100-150 mg/dL (or lower if rapidly rising)
 Ca:PO4 imbalance, with hypocalcemic tetany.
 Nutritional support in a child with oliguria or anuria.

30. 3 types of dialysis-
 a. intermittent haemodialysis (IHD)
 b. peritoneal dialysis(PD)
 c. CRRT.
a. Intermittent Haemodialysis:
 Preffered in patients with relatively stable hemodynamic
state.
 Highly efficient, 1 session completes in 3-4 hrs
 Can be done 3-7 times/week
 Complication : hypotension, bleeding, thrombosis.

31. b. Peritoneal Dialysis:
 Most commonly used in infants & neonates.
 For 1 session 1 cycle of 45-60 min needs to be repeated
→
for 2-4 times/day.
 The infused volume of the diasylate is 800-1100ml/m2
 No need for anticoagulation , so sed risk of bleeding ,
↓
may cause abdominal pain & peritonitis

32. c. CRRT:
 Continuous renal replacement therapy (CRRT) is associated with
reduced mortality.
 CRRT usually involves the removal and return of blood through
a single cannula placed in a large vein (venovenous therapy);
arteriovenous therapies are seldom used.
 CRRT causes less haemodynamic instability, because fluid
removal is slower and there is time for fluid to re-equilibrate
between body compartments.

33.  Indications - hemodynamic instability, sepsis, extensive
trauma, MODS.
 Continuous removal of solutes ,fluid & electrolytes
 3 types:
 CVVH - based on convection
 CVVHD - based on diffusion
 CVVHDF - based on convection and diffusion.

34. Outcomes
 Mortality rates from 30-50% have been reported from developing countries.
 But the results have markedly improved at tertiary centers with proper
expertise and modern facilities.
 Outcome depend upon underlying cause.
 Prognosis is favourable in ATN from volume depletion, intravascular hemolysis,
acute interstial nephritis and drugs or toxin related AKI especially when
complicating factor are absent .
 In cresentic GN, atypical HUS, and AKI associated with sepsis, multi organ
failure the prognosis is less satisfactory .

35. Take Home Message
 AKI is a common and serious problem
 All AKI are Not equal
 The diagnosis of AKI is often delayed.
 Earlier recognition and treatment of AKI sequelae may improve
outcome
 Novel biomarkers are providing tools for the early prediction of
AKI and outcomes, and for testing therapies

36. Thank you