Acute Kidney Injury

Gezahegn D.(pediatrian)

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 Definition
• Acute kidney injury (AKI) has been traditionally defined as
– an abrupt loss of kidney function leading to a rapid decline in the
glomerular filtration rate (GFR)
– accumulation of waste products such as blood urea nitrogen (BUN) and
creatinine, and
– dysregulation of extracellular volume and electrolyte homeostasis.
• AKI embodies a continuum of renal dysfunction that ranges from a small in
serum creatinine to complete anuric renal failure

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 Definition co..
• AKI is defined as
– Increase in serum creatinine by ≥ 0.3 mg/dL from baseline within
48 hr or

– Increase in serum creatinine to ≥ 1.5 times baseline within the

prior 7 days or

– Urine volume ≤ 0.5 mL/kg/hr for 6 hr

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 Epidemiology
• Etiology of AKI varies widely according to age, geographic region,
and clinical setting
• The incidence of AKI varies from
– 2–5% of all hospitalizations
– > 25% in critically ill infants and children
• AKI complicates up to 24% of neonatal intensive care unit
admissions
• Present in more than 60% of neonates with severe asphyxia

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 Classification
• AKI can be divided into pathophysiologic categories based on the
anatomical location of the initial injury

– Prerenal AKI due to inadequate renal perfusion

– Intrinsic AKI due to intrarenal pathology
– Postrenal AKI due to obstruction to the flow of urine

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Common causes of prerenal azotemia

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Pathophysiology

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Common causes of intrinsic acute renal failure

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Pathophysiology of intrinsic AKI

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• The typical pathologic feature of ATN is tubular cell necrosis,
although significant histologic changes are not consistently seen in
patients with clinical ATN.
• The mechanisms of injury in ATN can include
– alterations in intrarenal hemodynamics
– tubular obstruction
– passive backleak of the glomerular filtrate across injured tubular cells
into the peritubular capillaries

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Common causes of postrenal AKI

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 Patient Evaluation

History
The evaluation is directed towards
– identifying the underlying cause
– distinguishing between prerenal and intrinsic AKI
– discriminating between AKI and chronic renal failure (CKD)
• A carefully taken history is critical in defining the cause of AKI
– Vomiting/diarrhea
– Urine color change
– Urine amount change
– Bleeding/trauma
– Nephrotoxic drug exposure
– Critically ill
– Skin rash, pharyngitis
– joint pain/swelling
– Failure to gain weight
– Prenatal u/s report

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 Physical examination

• General appearance: irritable, puffy face,comatous

• Vital signs: Tachycardia, hypertension/hypotension, breathing rate and
pattern, fever/hypothermia
• Careful attention to volume status
– Dry mucous membranes, and poor peripheral perfusion
suggest an inadequate circulating volume
– Peripheral edema, rales, and a cardiac gallop
• The presence of a rash and arthritis.
• Palpable flank masses may be seen with
– renal vein thrombosis
– tumors, cystic disease, or
– urinary tract obstruction.

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 Laboratory studies
• Urinalysis
• RFT
• CBC
• Electrolytes
• Urine chemistries
• Serum complement level
• Abdominal U/S
• CXR
• Renal biopsy rarely indicated

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• The sensitivity and specificity of urine sodium of < 20 mEq/L
in differentiating prerenal azotemia from acute tubular
necrosis are 90% and 82%, respectively.

• The sensitivity and specificity of fractional excretion of sodium

of < 1% in differentiating prerenal azotemia from acute tubular
necrosis are 96% and 95%, respectively.
• The fractional excretion of sodium may be < 1% in acute
tubular necrosis secondary to radiocontrast material or
rhabdomyolysis

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 Management principle
• Fluid management
• Electrolyte management
• Nutritional support
• Adjustment of drug dosing
• Specific pharmacologic therapies
• Renal replacement therapy

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 MONITORING

• Serum potassium should be checked more frequently in patients

who have
– elevated serum potassium on presentation
– who are oliguric
– hemodynamically unstable
• The serum calcium should be measured more frequently (twice
daily) in patients who require calcium or bicarbonate.
• In stable pt monitor daily
– Weights
– Fluid intake and
– Total serum calcium
– Phosphate and
– Albumin

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 Prognosis
• The mortality rate is variable and depends entirely on the nature of the
underlying disease process rather than on the renal failure itself.
• Children with AKI caused by a postinfectious glomerulonephritis have a very
low mortality rate (<1%)
• AKI related to multiorgan failure have a very high mortality rate (>50%).
• The prognosis for recovery of renal function depends on the disorder that
precipitated AKI.
• Recovery of renal function is likely after AKI resulting from prerenal causes,
ATN, acute interstitial nephritis, or tumor lysis syndrome.

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• Complete recovery of renal function is unusual when AKI results
from
– Most types of rapidly progressive glomerulonephritis
– bilateral renal vein thrombosis
– bilateral cortical necrosis
• Medical management may be necessary for a prolonged period to
treat the sequelae of AKI, including
– chronic renal insufficiency
– Hypertension
– renal tubular acidosis, and
– urinary concentrating defect.

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 Dialysis
• Indications for dialysis in AKI
– Anuria/oliguria
– Volume overload with evidence of hypertension and/or pulmonary edema
refractory to diuretic therapy
– Persistent hyperkalemia
– Severe metabolic acidosis unresponsive to medical management
– Uremia (encephalopathy, pericarditis, neuropathy)
– Calcium:phosphorus imbalance, with hypocalcemic tetany that cannot be
controlled by other measures
– inability to provide adequate nutritional intake because of the need for
severe fluid restriction

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 Fluid and electrolyte management
• Total body water (TBW) as a percentage of body weight varies with
age
• The fetus has very high TBW, which gradually decreases to
approximately 75% of birth weight for a term infant.
• Premature infants have higher TBW than term infants.
• During the 1st yr of life, TBW decreases to approximately 60% of
body weight and remains at this level until puberty.

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 Fluid Compartments

• TBW is divided intracellular fluid (ICF) and extracellular fluid (ECF) .

• In the fetus and newborn, the ECF volume is larger than the ICF
volume .
• The normal postnatal diuresis causes an immediate decrease in the
ECF volume.
• This is followed by continued expansion of the ICF volume, which
results from cellular growth.
• By 1 yr of age, the ratio of ICF volume to ECF volume approaches
adult levels.

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Electrolyte Composition ICF ad ECF

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• Serum concentrations of electrolytes—[Na+ ], [K+ ], and [Cl- ]—do
not always reflect total body content.
• Intracellular [K+ ] is much higher than the serum concentration.
• A shift of K+ from the intracellular space (ICS) can maintain a
normal or even an elevated serum [K+ ] despite massive losses of
K+ from the ICS.
• This effect is seen in diabetic ketoacidosis, in which significant K+
depletion is masked by transmembrane shift of K+ from the ICF to
the ECF.
• Therefore, for K+ and phosphorus, electrolytes with a high
intracellular concentration, serum level may not reflect total body
content.

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 Fluid management
• Maintenance
• Deficit
• Replacement

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 Maintenance fluid
• Maintenance fluids are composed of a solution of water,
glucose, sodium (Na+ ), and potassium (K+ ).
• This solution has the advantages of simplicity, long shelf
life, low cost, and compatibility with peripheral IV administration.
• Such a solution accomplishes the major objectives of
maintenance fluids.
• Patients lose water, Na+ , and K+ in their urine and stool; water
is also lost from the skin and lungs.
• Maintenance fluids replace these losses, thereby avoiding the
development of dehydration and Na+ or K+ deficiency.

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• The glucose in maintenance fluids provides approximately 20% of
the normal caloric needs of the patient, prevents the development of
starvation ketoacidosis, and diminishes the protein degradation that
would occur if the patient received
no calories
• A patient receiving maintenance IV fluids is receiving inadequate
calories and will lose 0.5–1% of weight each day.

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 Maintenance Water

• Water is a crucial component of maintenance fluid therapy because

of the obligatory daily water losses.
• These losses are both measurable (urine, stool) and not
measurable (insensible losses from the skin and lungs).
• Failure to replace these losses leads to a child who is thirsty,
uncomfortable, and ultimately dehydrated.

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Maintenance Fluid Requirements neonates

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 Fluid Deficit

• Dehydration
– Causes: GI losses, renal losses, poor intake
– Classification: some DHN, severe DHN
– Treatment: iv fluid for neonates
• Hypovolemic shock
– Causes: similar to DHN,bleeding
– Treatment: 20ml/kg NS as fast as possible

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 Replacement fluid
• Diarrhea
• Vomiting
• Drainages(NG tube, colostomy losses)

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 Common electrolyte disorders

• Hypernatremia
• Hyponatremia
• Hypokalemia
• Hyperkalemia
• hypocalcaemia

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 Hyperkalemia
• Common and potentially life-threatening complication of AKI
• Prevalent in
– oliguric patients
– active cellular break-down, such as rhabdomyolysis and tumor lysis
syndrome
• Few symptoms or signs tend to occur
– only with very high serum potassium levels
– are related to impaired neuromuscular transmission
– cardiac conduction abnormalities
• Malaise
• nausea and
• muscle weakness

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• Rapid development of hyperkalemia (serum potassium level > 6
mEq/L) can lead to cardiac arrest, and death
• The earliest electrocardiographic change seen in patients with
developing hyperkalemia is the appearance of
– peaked T waves, followed by widening of the QRS intervals
– ST segment depression
– ventricular arrhythmias, and
– cardiac arrest

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 Treatment Principle
• Restrict exogenous source
• Cardiac stabilization
• Shift potassium to intracellular
– Regular insulin and dextrose
– Sodium bicarbonate
– Salbutamol
• Remove from body
– Loop diuretics
– Resin cation exchanger
– Dialysis

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 Hypokalemia
• Causes - NGT or Ileostomy drainage, Gastroenteritis, NEC, Diuretics,
ATN
• Manifestations
– Arrhythmia, paralytic Ileus, abdominal distension, feeding intolerance,
obtundation or altered level of consciousness
– ECG changes: prolonged QT interval, ST interval & T-wave depression, U wave
• Treatment
– Reduce Gastrointestinal and renal loses
– Mild (serum level 3–3.5 mmol/L): No intervention needed
– Significant hypokalaemia (serum level <3 mmol/L)
– When significant, treat by slow potassium replacement, either IV or PO (1
mEq/kg KCl → ↑serum K+ by 1 mEq/L), with dose adjustment based on serum
K+ level.
– Oral therapy: 0.5-1 mEq/kg/day divided and given with feedings
– IV therapy: KCl (1 mEq/kg) over a minimum of 1 hr.

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 Hypernatremia
1. With ECF deficit 2. With Excess ECF volume
– Increased Insensible water – Excessive Administration of
lose Isotonic or hypertonic solution
– Inadequate feeding – Administration of Sodium
– Extensive skin lesion containing medication like
– ADH deficiency NaHCo3.
– Acute Gastroenteritis – Feeding with high solute
formula

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 Hypernatremia co..

• Clinical manifestations
– irritable, restless, weak,
– lethargic, high-pitched cry
– hyperpnoea
– In severe cases brain shrinkage leading to cerebral hemorrhage,
– seizures, paralysis, and encephalopathy.

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 Treatments
• Threat DHN or shock with 10-20 ml/kg of bolus Normal saline,
repeat the same dose until thermodynamically stable till 60 ml/kg
followed by rehydration phase
• Rehydrate= (free water deficit+ maintenance)
• Fluid deficit in/24 hours = 4 x wt(kg)x 12 or
0.7 x Wt (kg) [1- 145/ current Na)
• 5% D/W is the recommended fluid .
• Based on the calculated fluid deficit over 48-72hrs.

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 References
• Nelson Textbook of Pediatrics,21st edition
• National NICU guideline, 2021
• Clinical Pediatric Nephrology, 2nd edition
• Uptodate2023

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THANK YOU

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