Acute Kidney Injury in Children: IAP Guidelines

BOX 1: Causes of AKI.

Prerenal

• Hypovolemia (dehydration, blood loss, and diabetic ketoacidosis)
• Third space losses (septicemia and nephrotic syndrome)
• Congestive heart failure
• Perinatal asphyxia
• Drugs (ACE inhibitors, NSAIDs, and diuretics)

Intrinsic

Acute tubular necrosis

• Prolonged prerenal insult (see above)
• Medications: Aminoglycoside, radiocontrast, and NSAIDs
• Exogenous toxins: Diethylene glycol and methanol
• Intravascular hemolysis and hemoglobinuria
• Snake bite
• Tumor lysis syndrome

Hemolytic uremic syndrome: Diarrhea associated (D+) and atypical (D-) forms Glomerulonephritis (GN)

• Postinfectious GN
• Systemic disorders: SLE, Henoch–Schönlein syndrome and microscopic polyangiitis
• Membranoproliferative GN

Interstitial nephritis (drug-induced and idiopathic) Bilateral renal vessel occlusion (arterial and venous)

Postrenal

• Posterior urethral valves and urethral stricture
• Bilateral pelviureteric junction obstruction
• Ureteral obstruction (stenosis, stone, and ureterocele)
• Neurogenic bladder

TABLE 2: Clinical features.

Clinical features

Likely diagnosis

Edema, hematuria, and hypertension

Acute glomerulonephritis

Dysentery, pallor, and jaundice

HUS

History of fluid loss with severe dehydration

ATN

Sudden passage of dark urine, pallor, and jaundice

Intravascular hemolysis

Interrupted urinary stream and palpable bladder

Obstructive uropathy

Abdominal colic, hematuria, and dysuria

Urinary tract calculi

Altered sensorium and seizures

Uremic encephalopathy

Acidotic breathing and pulmonary edema

Complications of AKI

BOX 2: Investigations in patients with AKI.

Blood

• Complete blood counts
• KFT
• Electrolytes (Na, K, and Ca)
• Venous blood gas (pH and bicarbonate)

Urine

• Urinalysis; culture (if symptoms of urinary infection)
• Sodium, osmolality, fractional excretion of sodium (if available to differentiate prerenal from intrinsic AKI)

Radiology

• Chest X-ray (for fluid overload and cardiomegaly)
• Ultrasonography (identify obstruction and dilatation)
• ECG for hyperkalemia

Investigations to determine cause

• Peripheral smear examination, platelet, and reticulocyte count; blood and LDH levels; and stool culture (suspected hemolytic uremic syndrome)
• Peripheral smear/RMAT—malaria
• Leptospiral serology/microscopic agglutination test (gold standard)—leptospirosis
• Blood culture—sepsis
• Blood ASO, complement (C3), antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA) (suspected acute and rapidly progressive GN)
• Doppler ultrasonography (suspected arterial or venous thrombosis)
• Renal biopsy in RPGN or nonresolving AKI
• Micturating cystourethrogram (suspected obstruction)

TABLE 3: Management of complications.

Complications

Management

Others

Fluid overload

• AKI regimen—insensible losses to be replaced by 5% Dextrose
• UO to be replaced by NS
• Modify according to Na level
• Replace other losses

þ Consider dialysis

þ 0.5–1% weight loss per day

Pulmonary edema

• O₂/IV furosemide (2–4 mg/kg)
• Respiratory support—HFNC/NIV/MV according to the patient condition
• Chest X-ray

þ Lung ultrasound—B line

þ IVC assessment and ejection fraction

þ Monitor by CVP line

þ Dialysis (for fluid removal)

Hypertension

• Symptomatic
• Labetalol infusion @ 0.25–1 mg/kg/h
• IV furosemide 2–4 mg/kg
• Asymptomatic—oral nifedipine/ amlodipine 0.3–0.5 mg/kg
• NTP—0.5–8 µg/kg/min (not to be given for >48 hours due to risk of toxicity)
• Maintenance with amlodipine/ hydralazine

Metabolic acidosis

IV or oral NaHCO₃

To monitor for fluid overload and hypernatremia

Hyperkalemia

• Stop all potassium in IVF and medications
• IV 10% Ca gluconate 1 mL/kg over 5–10 minutes if ECG changes
• Salbutamol (2.5–5 mg) nebulization. Can be repeated after 20 minutes
• Neutralizing glucose insulin drip— dextrose 0.5–1 g/kg and insulin 0.1–0.2 U/kg over 30 minutes. Can be repeated after 30 minutes
• NaHCO₃—1–2 mL/kg over 15–20 minutes if associated with metabolic acidosis
• Potassium binding resins—sodium polystyrene 1 g/kg (oral/NG/rectal)

maximum 30 g

• Monitor blood glucose for hypoglycemia

þ Continuous ECG monitoring

þ Repeat potassium level

Anemia

PCV transfusion at 5–10 mL/kg

Monitor for fluid overload

Hyper- phosphatemia

Phosphate binders such as calcium carbonate, and sevelamer hydrochloride (only if significant)

TABLE 4: Indications of kidney replacement therapy (KRT).

Indications

Features

Fluid overload

• Most common indication

þ Determines the outcome

þ >15% fluid overload resistant to diuretics

Metabolic acidosis

pH<7.2 despite bicarbonate therapy

Refractory hyperkalemia

K+ >6.0 or electrocardiogram (ECG) changes despite medical management

Hyponatremia/hypernatremia

Symptomatic

Uremia

Urea >160–200 mg/dL, encephalopathy

Create space for more fluid

Blood products, drugs, and nutrition

Removal of dialyzable toxins

Salicylate poisoning and phenobarbitone

TABLE 5: KRT modalities.

Modality

Potential setting in AKI

Advantages

Disadvantages

IHD

Hemodynamically stable

• Rapid removal of toxins
• Reduced exposure to anticoagulants

þ Lower cost than CRRT

• Hypotension with rapid fluid removal

þ Dialysis

disequilibrium

CRRT

Hemodynamically unstable

• Continuous removal of toxins

þ Hemodynamic stability

• Easy control of fluid balance

þ No risk of increased

ICP

• Slower clearance of toxins
• Need for prolonged anticoagulation

þ Patient

immobilization

• Increased cost

PD

• Hemodynamically unstable

þ Coagulopathy

þ Difficult access

• Under resourced region
• Technically simple

þ No anticoagulation

þ Hemodynamic stability

þ Lower cost

• No need for vascular access
• Poor clearance

þ Protein loss

þ Risk of peritonitis

• No control on rate of fluid removal

þ Hyperglycemia