Detail presentation about Acute Kidney Injury in children

1. WELCOME TO
SEMINAR
Presented by
Dr. Bipin Karki
Dr. Amlendra Yadav
Dr. Chandra shekhar

2. CASE
Tuhin 7 yrs old male child from sylhet , admitted
with a complain of oliguria for 2 days associated
with respiratory distress for same duration. He had
h/o bee sting all over body surface 7 days back
when he was returning home from school. He was
afebrile , puffy face, restless , mild pale , dyspenic ,
edema present. Abdomen was soft, distended, non-tender,
no organomegaly , ascites present evidenced
by shifting dullness.

3. INVESTIGATION
 S creatinine: 8 mg/dl
 Blood urea: 400 mg/dl
 Urine R/E
Pus cell – (4-6)/ HPF
Epi. Cell – (2-4)/HPF
RBC – Nil
Protein – (++)

4. ACUTE KIDNEY
INJURY

5. DEFINITION
Rapid deteriotion of renal function resulting in
retention of nitrogenous wastes and inability of
kidney to regulate fluid and electrolyte
homeostasis.
In year 2004 the acute dialysis quality initiative
(ADQI) proposed RIFLE criteria for defining
AKI .
Later, Acute Kidney Injury Network (AKIN)
classified AKI based on the RIFLE system.

6. RIFLE CRITERIA
R = risk for renal dysfunction
I = injury to the kidney
F = failure of kidney function
L = loss of kidney function
E = end-stage renal disease

7. > 3 months

8. INCIDENCE
 The precise incidence of AKI in children is not well
known.
 Data from bangladesh is not available
 A data from india .
 4-6 % case of AKI seen in general ward and upto
40% in PICU .
 Affects childrens who have sepsis and multiorgan
failure.
 Children undergoing major cardiac surgery and organ
transplantation are at considerable risk for developing
AKI.

9. ETIOLOGY
 Pre renal
 Intrinsic or renal
 Post renal

10. PRE RENAL
 Acute gastroenteritis
 Blood loss
 Shock
 Fulminant hepatic failure
 Reye syndrome
 Congestive cardiac failure
 Nephrotic syndrome
 Hepatorenal syndrome

11. INTRINSIC RENAL
 Renal
Major vessel obstruction
- renal vein thrombosis , renal arterial obstruction, hemolytic uremic
syndrome , HSP , polyarteritis and other vasculitis
 Glomerular
Acute glomerulonephritis ( poststreptococcal , other infections ),
cresentic GN
Acute tubulointerstitial nephritis
Acute tubular necrosis
Prolongation of pre-renal insult , intravascular hemolysis , sepsis ,
nephrotoxixc agents , multiorgan failure , rhabdomyolysis , snakebite
, other envenomations , falciparum malaria , leptospirosis

12. POST RENAL
Posterior urethral valves
Ureteropelvic junction obstruction
Ureterovesicular junction obstruction
Ureterocele
Tumor
Urolithiasis
Hemorrhagic cystitis
Neurogenic bladder

14. PRE RENAL
 Also called prerenal azotemia, is
characterized by diminished effective
circulating arterial volume, which leads to
inadequate renal perfusion and a decreased
GFR .

15. Mechanisms of Sodium and Water
Conservation in Prerenal Azotemia
Renin
Angiotensin II
Aldosterone
Decreased Renal Perfusion
Renal Tubular Na
Reabsorption
Vasopressin
Renal Tubular H2O
Reabsorption
Urine Volume
Concentrated Urine
Urine Sodium

16. 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. RENAL CAUSES
 It includes a variety of disorders
characterized by renal parenchymal damage,
including sustained hypoperfusion , ischemia
and nephrotoxins.

18. OBSTRUCTION OF RENAL ARTERIES AND VEINS
 Bilateral renal arterial thrombosis may occur
after umbilical artery catheterization in
neonates.
 Renal vein thrombosis may be a complication of
infant of diabetic mother especially following
dehydration.
 In older children renal vein thrombosis may
occur with nephrotic syndrome with anasarca
and dehydration.
 Gross hematuria, enlargement of kidney and
azotemia are typical manifestation.

19. INVOLVEMENT OF RENAL MICROVASCULATURE
 Hemolytic uremic sundrome is a common
cause in children developing AKI .
 Following dysentry shigela-toxin enters the
circulation and lead to endothelial injury in
microvasculature .
 Localized coagulation and deposition of
platelet thrombi and fibrin in glomeruli
causing decrease in GFR.

20. ACUTE INTERSTITIAL NEPHRITIS
 Allergic: antibiotics (β-lactams, sulfonamides,
quinolones, rifampin), nonsteroidal anti-inflammatory
drugs, diuretics, other drugs
 Infection: pyelonephritis (if bilateral)
 Infiltration: lymphoma, leukemia, sarcoidosis
 Inflammatory, nonvascular: Sjögren’s syndrome,
tubulointerstitial nephritis with uveitis
 The patient may have fever , arthralgia , rash
and eosinophilia : urine often shows eosinophils
.

21. Etiology of AIN

22. ACUTE TUBULAR NECROSIS
 Occurs most often in critically ill infants and children
who have been exposed to nephrotoxic and/or
perfusion insults.
 Common causes of ATN include renal hypoperfusion
following volume contraction , severe renal
vasoconstriction , nephrotoxic agents , sepsis , shock
and hypotension.
 The mechanisms of injury in ATN can include
alterations in intrarenal hemodynamics, tubular
obstruction, and passive backleak of the glomerular
filtrate across injured tubular cells into the peritubular
capillaries.

24. CLINICAL PRESENTATION
Pre renal
There may be history of volume loss from
vomiting, diarrhea, or blood loss and may
present with dehydration , hypotension ,
tachycardia , pallor , and decreased urine
output .

25. RENAL
 Hematuria, edema, and hypertension indicates
a glomerular etiology for AKI.
 Dysentry, patechie and pallor- HUS
 Sudden passage of dark red urine, pallor and
jaundice- acute intravascular hemolysis
 Presence of rash, arthritis might suggest SLE or
HSP.
 History of prolong hypotension or with exposure
to nephrotoxic medication most likely have ATN.

26.  Allergic interstitial nephritis should be
suspected with fevers, rash, arthralgias, and
exposure to certain medications, including
NSAIDs and antibiotics.

27. POST RENAL
 History of interrupted urinary stream and
palpable bladder or kidney suggest
obstructive uropathy.
 Abdominal colic hematuria and dysuria
suggest urinary tract calculi.

28. DIAGNOSIS
Physical examination
Obtaining a thorough physical examination is extremely
important when collecting evidence about the etiology of
AKI. Clues may be found in any of the following
 Skin
 Eyes
 Ears
 Cardiovascular system
 Abdomen
 Pulmonary system

29. Skin :- Palpable purpura - Systemic vasculitis
Maculopapular rash - Allergic interstitial nephritis
Eye :- Evidence of uveitis may indicate interstitial nephritis
and necrotizing vasculitis. Ocular palsy may indicate
ethylene glycol poisoning or necrotizing vasculitis
Ear :- Hearing loss - Alport disease and aminoglycoside
toxicity
Mucosal or cartilaginous ulcerations - Wegener
granulomatosis
Pulmonary system :- Respiratory rate , pattern
On Auscultation of lungs basal crepts

30. CARDIOVASCULAR EXAMINATION
 Pulse rate and blood pressure recordings
 Close inspection of the jugulovenous pulse
 Careful examination of the heart and lungs
 Assessment for peripheral edema
Cardiovascular examination may reveal the
following:
 Murmurs - Endocarditis
 Pericardial friction rub - Uremic pericarditis
 Increased jugulovenous distention, rales, S3 -
Heart failure

31. Abdomen
 Abdominal or costovertebral angle tenderness -
Nephrolithiasis, papillary necrosis, renal artery
thrombosis, renal vein thrombosis
 distended bladder – Urinary obstruction
 The presence of tense ascites can indicate
elevated intra-abdominal pressure that can retard
renal venous return and result in AKI.

32. CONT…….
 Urine R/E
 CBC with PBF
 24 hour urinary protien
 Blood urea and S. creatinine level
 Serum electrolyte
 ASO titer
 C3 level
 Serum calcium
 Serum phosphate
 Serum uric acid
 ANA
 ABG

33. IMAGING
 Ultrasound of KUB - evaluates renal size,
able to detect masses, obstruction, stones
 Chest x-ray
 DTPA
 DMSA

34. RENAL BIOPSY
Indicated in
 Patient in whom the etiology is not identified.
 Unremitting AKI lasting longer then 2-3 wks
or in accessing the extent of renal damage
and out come.
 Suspected drug induced AKI in a patient
receiving therapy with a potentially
nephrotoxic drugs.

35. INDICES FOR DIFFERENTIATING PRE-RENAL FROM RENAL AKI
PRE-RENAL INTRINSIC
URINARY SODIUM (mEq/l) < 20 > 40
Urinary osmolality (mOsm/kg) > 500 < 300
Blood urea to creatinine ratio >20:1 < 20:1
Urine to plasma osmolality ratio >1.5 < 0.8 – 1.2
Fractional excretion of sodium < 1 > 1

36. MANAGEMENT
The basic principles of management include
 Treatment of life-threatening complications
 Maintenance of fluid and electrolyte balance
 Nutritional support.
 Specific management of underlying disorder

37. LIFE THREATENING COMPLICATIONS
 Hyperkalemia
 Fluid overload with heart failure
 Severe hypertension with encephalopathy
 Profound acidosis
 Severe anemia

38. MANAGEMENT OF COMPLICATION
Hperkalemia :
 Calcium gluconate 0.5-1 ml/kg over 5 to 10
minute
 Salbutamol nebulization
 Glucose 0.5-1 gm/kg with 0.1-0.2 unit/kg
insulin
 Sodium bicarbonate 1-2 ml/kg

39. Fluid overload :
 fluid restriction (insensible loss + POD)
Pulmonary Edema
 Oxygen
 Dopamine (5-10) mcg /kg /min infusion
 Frusemide (2-4)mg /kg

40.  Hypertension
 Nitroprusside 1-8 mcg/kg/min
 Frusemide 2-4 mg/kg
 Nifedipine 0.3-0.5 mg/kg

41.  Acidosis
Sodium bicarbonate
Anemia
Pack red cell 3-5 ml/kg

42. SUPPORTIVE CARE
 Fluids: amount given equals insensible loss
plus urine volume
 Nutrition: protein intake of 1 gm/kg
 Prevent infection and treat with appropriate
antibiotics.
 Avoid nephrotoxic drugs
 Measure Weight daily, Prevent weight gain
 Monitor urine output

43. DIALYSIS
Indication:
 Uremia: altered sensorium abnormal
behavior seizure
 Hyperkalemia: k+ > 6.5 meq/l, k+ 5.5-6.5
meq/l with ECG changes
 Hyponatremia: Na+ < 120 meq/l if
symptomtic
 Fluid overload: resistant to diuretics,
CCF,HTN
 Metabolic acidosis: PH< 7.2 despite
sodium bicarbonate therapy.

44. MANAGEMENT OF COMMON CONDITION
CAUSING AKI
 Prerenal AKI: administer crystalloids, stop
diuretics, NSAIDs, ACE inhibitors.
 ATN: supportive care, discontinue drugs or
toxin, treat cause of circulatory failure.
 Glomerulonephritis: supportive care If post-infectious,
antibiotic for endocarditis, shunt
infection, immunosuppressive medication.

45.  HUS: supportive care, plasma infusion, plasma
exchange
 Vasculitis: immunosuppressive medication, plasma
exchange
 Interstital nephritis: discontinue offending drugs,
consider steroid therapy.
 Renal artery , vein occlusion: anticoagulation,
thrombolysis or surgery.
 Intrarenal obstruction: discontinue offending drugs,
alkaline diuresis for rhabdomyolysis , haemoglobinuria
or urate crystal.
 Urinary tract obstruction: bladder cathaterization or
nephrostomy, surgical treatment of obstruction.

46. OUTCOME
 Mortality rates from 30-50% have been reported from
developing countries. But the results have markedly
improved at tertiary centers with proper experties 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 .

47. PREVENTION OF AKI
 Important measures includes prompt
rehydration therapy in acute diarrhea,
avoidance or judicious use of nephrotoxic
drugs.
 Maintenance of proper hydration for patients
undergoing diagnostic procedures with radio
contrast media.
 Force diuresis along with the use of
allopurinol is effective preventing AKI in
patient with TLS.