Acute Kidney Injury in Children

WELCOME TO SEMINARPresented by

Dr. Bipin Karki Dr. Amlendra Yadav Dr. Chandra shekhar

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.

INVESTIGATION

S creatinine: 8 mg/dl Blood urea: 400 mg/dl Urine R/E

Pus cell – (4-6)/ HPFEpi. Cell – (2-4)/HPFRBC – NilProtein – (++)

ACUTE KIDNEY INJURY

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.

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

> 3 months

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.

ETIOLOGY

Pre renal Intrinsic or renal Post renal

PRE RENAL

Acute gastroenteritis Blood loss Shock Fulminant hepatic failure Reye syndrome Congestive cardiac failure Nephrotic syndrome Hepatorenal syndrome

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

POST RENAL

Posterior urethral valves  Ureteropelvic junction obstruction  Ureterovesicular junction obstruction  Ureterocele  Tumor  Urolithiasis  Hemorrhagic cystitis  Neurogenic bladder

PRE RENAL

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

Renin

Angiotensin II

Aldosterone

Renal Tubular Na Reabsorption

Vasopressin

Renal Tubular H2O Reabsorption

Urine Volume

Concentrated Urine

Urine Sodium

Decreased Renal Perfusion

Mechanisms of Sodium and Water Conservation in Prerenal Azotemia

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.

RENAL CAUSES

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

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.

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.

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 .

Etiology of AIN

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.

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 .

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.

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

POST RENAL

History of interrupted urinary stream and palpable bladder or kidney suggest obstructive uropathy.

Abdominal colic hematuria and dysuria suggest urinary tract calculi.

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

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

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

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.

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

IMAGING

Ultrasound of KUB - evaluates renal size, able to detect masses, obstruction, stones

Chest x-ray DTPA DMSA

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.

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

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

LIFE THREATENING COMPLICATIONS

Hyperkalemia Fluid overload with heart failure Severe hypertension with

encephalopathy Profound acidosis Severe anemia

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

Fluid overload : fluid restriction (insensible loss + POD)

Pulmonary Edema Oxygen Dopamine (5-10) mcg /kg /min infusion Frusemide (2-4)mg /kg

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

Acidosis Sodium bicarbonate

Anemia Pack red cell 3-5 ml/kg

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

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.

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.

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.

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 .

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.

THANKYOU