Acute kidney injury - Pediatrics Flashcards
Etiology of AKI
Prerenal:
Severe volume depletion leads to ↓↓ renal blood flow. Nephrons remain structurally intact.
* Volume depletion
o GIT losses (vomiting, diarrheal)
o Renal losses (diuretics, polyuria)
o Cutaneous losses (burns)
o Hemorrhage
* ↓↓ effective circulating volume
o Congestive heart failure
o Liver disease
o Nephrotic syndrome
o Shock
Renal (intrinsic):
Structural/functional damage to glomerulus/tubules.
* Vascular
o Renal artery or vain obstruction
o HUS
o Vasculitis
* Glomerular: Acute GN
* Tubular: Acute tubular necrosis
* Interstitial
o Acute interstitial nephritis
o Infection
o Systemic disease (sarcoid, lupus, lymphoma, leukemia)
Post renal causes:
Obstruction to urine outflow → renal damage
* Urinary tract obstruction
o Posterior urethral valves
o Renal stones
o Tumors
o Strictures
o Obstructed Foley catheter
Clinical picture of AKI
❖ Manifestations of the cause
❖ Oliguric phase:
* Early: - oliguria or anuria, oedema, hypertension, deep and rapid respiration (acidotic breathing)
* Advanced: Plus, the early manifestation there are:
o Uremic encephalopathy (confusion, convulsion, coma)
o Arrythmias due to hyperkalaemia.
o Convulsions due to hyponatremia.
o Heart failure due to hypervolemia and hypertension.
o Stress ulcer 2ry to severe metabolic acidosis.
❖ Polyuric phase: it may occur indicating early recovery → tubular cells can’t retain fluid & electrolytes → polyuria & electrolyte loss.
Diagnosis of AKI
❖ Differential diagnosis: depends on classification and clinical picture of the cause.
❖ Laboratory findings
* Diagnosis of renal failure
- Urine volume: oliguria (urine output < 1 ml/kg/hr or < 400 ml/m2/day).
Anuria (urine output < 30 ml/m2/day)
- Renal function tests: increased serum creatinine, blood urea.
- Acid/base disturbance: metabolic acidosis (↓↓ pH, ↓↓PaC02, ↓↓HC03).
* Diagnosis of the cause:
* Abdominal and pelvis ultrasound to exclude postrenal causes.
* Other investigations to differentiate between different types and specific ones to detect the cause in the following table: (No table in the book idk)
Treatment of AKI
❖ Hospitalisation: with monitoring blood pressure, urine output, serum electrolyte & Ph
❖ Correct post-renal causes: remove obstruction (by catheterization ± surgical)
❖ Correct pre-renal causes to improve renal blood flow:
* Fluid loss → saline 20 ml/kg over 1 hr.
* Blood loss → fresh blood transfusion or plasma transfusion
❖ Treatment of intrinsic renal failure
Diet: - Restriction of salt, fruits, and proteins.
Fluid’s intake = insensible loss + ongoing losses
Diuretics:
o Value: Reduce volume overload & enhance potassium excretion
o Use: Furosemide 2-4 m/kg/dose intravenous
Metabolic acidosis:
By giving Na bicarbonate 1-2 mg /kg slow IV
Electrolyte disturbance:
* Hyperkalaemia (potassium level > 6 meq/L): -
1. Enhance GIT excretion by kayexalate (oral or enema).
2. Shift potassium intracellular by:
o Regular insulin; 0.1 u/kg with glucose 20 % solution, 1 ml /kg over 1 hour
o Salbutamol nebulizer
o Sodium bicarbonate 1-2 meq/kg over 10 minutes IV.
3. Stabilize cardiac membranes by calcium gluconate 10% (1 ml/kg) slow I.V
4. Remove potassium by dialysis.
* Hyponatremia (Na <130 meq/L): Usually dilutional; respond to fluid restriction.
* Hypocalcaemia and hyperphosphatemia: (tetany is rare as acidosis increases ionized ca). Reduce dietary phosphate & give phosphate binders (calcium carbonate oral)
Treatment of complications of AKI
- Anaemia → Fresh packed RBCs transfusion.
- Hypertension → See glomerulonephritis.
- Infections → Use non-nephrotoxic antibiotics
- Dialysis: either hemodialysis or peritoneal dialysis indicated in :
Clinical - Uremic encephalopathy
- Anuria not responding to diuretics.
- Volume overload with heart failure
- Interactable GIT bleeding
Laboratory - Hyperkalemia > 7 meq/L uncontrolled by medical treatment
- Interactable metabolic acidosis.
- Symptomatic hypocalcemia with severe ↓↓PO4
- Blood urea nitrogen > 100 mg/dl.
