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Management of electrolytes and

acid base disorders in pediatric


acute kidney injury

Ahmedz Widiasta, dr, SpA(K), M.Kes


Pediatric nephrology working group
Indonesian Pediatric Society
Kidney function
• Filtration
• Reabsorbstion and secretion
• Excretion
• Gluconeogenesis
• Endocrine
• Proximal tubule
– Na+,Cl-,HCO3-, PO4-, Glucose, Amino acid, water
• Loop of Henle (lower part)
– Water move to medulla (diffusion)
– More concentrated tubular fluid
• Loop of Henle (upper part)
– Na and Cl to medulla (active transport)
– Less concentrated tubular fluid
• Distal tubule
– Na reabsorbtion
– Continue dilution of tubular fluid
• Collective duct (cortical part)
– Na reabsorbtion (change with K and H)
• Collective duct (medullar part)
– ADH  effective water reabsorbtion
(concentrating urine)
Acute kidney injury, is it reversible?

Kidney
Need:
1. Fluid balance
Acute kidney injury, is it reversible?
2. Restric nephrotoxic drug
3. Electrolyte correction
4. Nutrition
5. Anemia management
Kidney
6. Hypertension management
7. Acid base management
Impact of kidney injury

• Sodium
• Potassium
• Metabolic acidosis
• Metabolic alkalosis
• Water imbalance
Hyponatremia: Serum Na <130 mEq/L

Hypernatremia: Serum Na >150 mEq/L

Hypokalemia: Serum K <3.5 mEq/L

Hyperkalemia: Serum K >5.0 mEq/L


Hyponatremia
Detection:
• G I Tract:
• Mild:
– Anorexia
– Headache
– Vomit
– Apathy – Nausea
– Lethargy
• Moderate: • Musculosceletal:
– Agitation – Cramp
– Confuse – Decrease reflex
– Psychotic
• Severe:
– Sopor/coma
– Cheyne Stoke
– Death
Hyponatremia
Things we have to be aware before
hiponatremia treatment:

–Any symptoms?
–Acute or chronic?
–Risk factor of neurologic deficit?
Hyponatremia
Adjust the velocity of correction

Acute (hyponatremia onset < 1 hour):


Increase serum sodium 2 mmol/L/hours until
symptoms diasappear

Chronic (hyponatremia onset > 48 hours):


Increase serum sodium 10% from previous level
Monitoring neurologic sign, stop if sign disappear
Check for Urinary Cation (UNa+UK). The level must be lower than infus
sodium
Hyponatremia
Na deficit= (Na target – Na measured) x body
weight x 0.6

• 50% given in the first 8 hours, 50% in the


second 16 hours
• Na increase < 2mEq/L/hours to avoid
intracellular fluid leak
Hypokalemia
Reverse contractable causes
Discontinue diuretics
Correct magnesium deficiency

Symptomatic
Asymptomatic

Intravenous replacement up to
40 mEq/hour Metabolic Metabolic
Continue ECG monitoring acidosis alkalosis
Serial serum K monitoring

Normotensive Hypertensive
K citrate
K bicarbonate
KCL volume
K sparring
replacement
diuretic
Hypokalemia

K parenteral indication:
– Dysrhytmia
– Respiratory muscle paralyze
– Hypokalemia in hepatic encephalopathy
– K+ level very low < 2mEq/L
Hypokalemia

Oral/parenteral potassium until


3mEq/kgBW/24 hours
Hyperkalemia

Spurious Transcellular
shift
Impaired
renal
excretion
Hyperkalemia
Spurious: Transcellular shift:
• Hemolysis • Acidosis
• Ischemic blood draw • Non-anion gap
• Leucocytosis (WBC>50.000/mm3) • Respiratory
• Thrombocytosis • Hyperglycemia
(Platelete count > 1.000.000/mm3) • Hypertonicity
• Familial pseudohyperkalemia • β- adrenergic blockade
• Succinylcholine
• Digitalis intoxication
• Fluoride intoxication
• Hyperkalemic periodic paralysis
• Exercise
Hyperkalemia
Serum potassium

No ECG changes (-) ECG changes (+)

Institute therapy based on clinical


Rule out spurious
severity of hyperkalemia
hyperkalemia
Ca gluconate
Albuterol nebulizer 2.5 - 5 mg in 4 mL
normal saline onset 30 minutes
K change resin: oral (onset 2 hour) or
Redraw potassium enema (onset 60 minutes) 30-60g
without torniquet Hemodialysis
(once started removes 25-30 mEq/h)
Hyperkalemia
• Stop all potassium
• Bicarbonate sodium 2 mEq/KgBW during 5-10
minutes intravenously
• Glucose 0.5 g/kgBW with cristal insulin 0.3
unit/gram glucose or 0.1 unit/kgBW
intravenously/subcutan during 2 hours
• Ca gluconate 10% intravenously 0.5 mL/kgBW
during 2-10 minutes
• ECG monitoring during correction
Hyperkalemia
• K 5.5 – 7.0 mmol/L :
Kation exchange resin (kayeksalat) 1 g /kgBW
orally/rectal, 4x daily

• K> 7.0 mEq/L or hyperkalemia+abnormal ECG:


gluconas calcicus 10% 0.5 mL/kgBW within 10
– 15 minutes and bicarbonate natrium 7.5%
2.5 mEq/kgBW within 10 – 15 minutes
Hyperkalemia
Persistent:
Glucose 0.5 g/kgBW + insulin 0.1 unit/kgBW
i.v. within 30 minutes

Prepare
renal replacement therapy
Hyperkalemia treatment
• Stabilize myocardial membrane:
– Ca gluconas 10%
• Change extracellular to intracellular potassium
– Salbutamol
– Sodium bicarbonate
– Dextrose with insulin
• Release potassium outside the body
– Dialysis
– Resin
Hypernatremia
Treatment:
– Dextrose 5% and NaCL 0.2% during 48 hours
– Target sodium decrease 10 – 15 mEq/L/day
– Continue with maintenance
– Severe hypernatremia (Serum sodium >200
mEq/L)  peritoneal dialysis, start with peritoneal
dialysis solution 4.25% glucose, indwelling 1 hour
 until Na decrease  continue with peritoneal
dialysis solution 1.5%
Acid-bace imbalance
Metabolic acidosis
• Treatment:
• (Ki-Ku)xBWx0.6= mEq NaHCO3

Ki= target bicarbonate level (usually 15mEq/L)


Ku= bicarbonate level measured

• Correction during 1 hour


Metabolic alkalosis
Treatment:

Ammonium needed (mEq)= (Ki-Ku)xBWxfd

Ki= target bicarbonate level (usually 15mEq/L)


Ku= bicarbonate level measured
fd: distribution level in the body (0.2-0.3)
Clinical acid base problem solving
– pH 1st
– pCO2 step
– HCO3-
– Plasma anion gap
Na-Cl-HCO3= …… mEq/L

2nd
– Any laboratory error? step
[H+]= pCO2 x 24/HCO3-
Different result >10%laboratory error
3rd
• pH step
– pH > 7.44  alkalemia
– pH < 7.36  asidemia

– Metabolic or respiratoric 4th


– Alkalemia: step
• Respiratory alkalemia: pCO2 <38
• Metabolic alkalemia [HCO3-] >25
– Asidemia
• Respiratory acidemia: pCO2 > 44
• Metabolic acidemia: [HCO3-] < 25
5th
• Fifth step: step
– Count anion gap
– AG >10  probable metabolic acidemia
– AG>20  surely metabolic acidemia
• Sixth step 6th
Check for body compensation degree: step
– Metabolic acidemia:
Every lowering pCO2 = 1.3x lowering [HCO3-]
– Metabolic alkalemia
Every increase pCO2 = 0.6 x increase [HCO3-]
– Respiratory acidemia
• Acute
Every increase pCO2 10 mmHg= [HCO3-]increase 1 mEq/L
• Chronic
Every increase pCO2 10 mmHg = [HCO3-]increase 4mEq/L
– Respiratory alkalemia
• Acute
Every pCO2 lowering 10 mmHg = [HCO3-] decrease 2 mEq/L
• Chronic:
Every pCO2 lowering 10 mmHg=[HCO3-] decrease 5mEq/L
7th
step

Determine delta ratio (delta gap) = increase in anion gap / decrease in bicarbonate

Delta ratio Assessment guideline

< 0.4 Hyperchloraemic normal anion gap acidosis

0.4 – 0.8 Consider combined high AG and normal AG acidosis ratio often <1 in
acidosis associated kidney failure
1–2 Usual for uncomplicated high AG acidosis
Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1 due to ketone loss
>2 Suggests pre-existing elevated HCO3 level: consider a concurrent
metabolic alkalosis or a pre-existing compensated respiratory
• Common causes of metabolic acidosis with
increased anion gap:
– Methanol intoxication
– End stage renal disease
– Diabetic ketoacidosis
– Paraldehyde intoxication
– Iron overdose
– Alcoholic ketoacidosis
– Lactic acidosis
– Salicylate intoxication
• Common causes of metabolic acidosis with
normal anion gap:
– Mild to moderate kidney disease
– Acute diarrhea
– Type I Renal tubular acidosis
– Type II Renal tubular acidosis
Thank You

Source:

1. Konsensus gangguan ginjal akut. Unit Kerja Koordinasi Nefrologi


Anak, 2014.
2. Alatas H, Ambarsari CG. Buku Ajar Nefrologi Anak. IDAI, 2017
3. Ardanykusumah P. Buku Ajar Nefrologi Anak. IDAI, 2017

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