Fluids, Electrolytes and Acid

Base Corrections

Noran Hazem
Assistant lecturer of pediatrics and
pediatric ICU
Normal physiological fluid distribution

What is TBW
 Basic Metabolic Panel

Na +
Cl- BUN Ca++
Glu Mg++
K+ CO3-- Cr Phos--

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 Intravenous Fluids : Goals
•Volume expansion
•Rehydration
•Replacement of (excessive/ abn.) losses
•Maintenance

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 Volume expansion
• Type of fluid : isotonic saline

• When ringer is preferred : situations with acidosis (not in

lactic acidosis).

• For colloids , albumin is indicated in septic shock with

capillary leak and hypoalbuminemic patients

• Blood products are used for their own indications not as

volume expander

• Pleases asses fluid responsiveness

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 Maintenance therapy ( fluid balance)

IN OUT
 Obligatories  Insensible

 Enteral  Urine

(food, fluid)  (sweat, stool)

 IV therapy  Abnormal
 uF

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 Usual prescription
IN OUT
• Obligatories  Insensible
• Enteral  Urine
(food,
fluid)  (sweat, stool)
• IV therapy  Abnormal
 uF

Maintainence in case of normal urine output =

1500 ml/m2
In
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abnormal urine output (oliguric or polyuric)?
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 Deficit
 Amount depends on degree of dehydration
• Mild 30-50 mL/Kg
• Moderate 60-80 mL/Kg
• Severe 90-120 mL/Kg

 Type
• Na 75-90 mmol/L
• K 20-40 mmol/L
• Glucose 5%
Different combination if electrolyte imbalance

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 Plasma Osmolality and sodium
balance
• Plasma Osmolality (mOsm / kg H2O)= 2*Na + glucose / 18 +
BUN /2.

• The normal range is between 280 and 295 mOsm/kg H2O

• Plama Osmolality is regulated by ADH secretion

• When correcting sodium disturbance , you have to consider both

volume staus and osmolality

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 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Causes of Hyponatremia

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 Management hyponatremia
Depends on the severity and duration of hyponatremia , volume and symptoms of
patient
– As a rule rapid correction is dangerous leads to pontine myelinosis
– Don’t rise Na to more than 10meq from baseline in 24 hours.
– In symptomatic patients rise 5 meq in 2 hours
– Amount of Na needed = Total body water ×desired Na − actual Na
– Ex : 10 kg infant na 115 ( 10*0.6*8) = 48 meq, nacl 3% is
513meq, 48 meq is 93 ml hypertonic, over 24 hours or over 3
hours if symptomatic
– First line management of SIAD is fluid restriction ( actually free
water restriction)

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 Hypernatremia (Na+)
 Losses : renal (e.g. ATN or mannitol), GIT or
cutaneous
 Diabetes insipidus
 iatrogenic

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 Hypernatremia Treatment

– Rate of correction for Na+ 0.5 mEq/L/hr, maxium 10-12 in

24 hours
– Calculate water deficit
» Water deficit in liters = 0.6 x wt (kg) x [(current
Na+/140) – 1]
» Type of fluid is glucose 5% saline 1:1 and mointor
– Rate of correction for calculated water deficit
» 50% first 12-24 hrs
» Remaining next 24 hrs
– Monitor every 4 hours and adjust according rate or
concentration according to the rate of drop

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 Basic Metabolic Panel

Na +
Cl- BUN Ca++
Glu Mg++
K+ CO3-- Cr Phos--

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 Potassium (K+)
• Normal range: 3.5-5
• Largely contained intra-cellular  SK does not reflect total
body K
• Important roles: contractility of muscle cells, electrical
responsiveness
• Principal regulator: kidneys

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 Potassium (K+)
• Daily requirement 1-2 mEq/100 ml maintance fluids
• Complete absorption in the upper GI tract
• Glucocorticoid effect
• Kidneys regulate balance
– 10-15% filtered is excreted
• Acidosis
– Low pH  shifts K+ out of cells (into serum)
– Hi pH  shifts K+ into cells
– 0.3-1.3 mEq/L K+ change / 0.1 unit change in pH in the opposite
direction

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 Hypokalemia
Causes
» DKA
» Diuretics: thiazide, loop diuretics
» Drugs: amphotericin B, Cisplastin
» Hypomagnesemia
» Alkalosis
» Hyperaldosteronism
» Licorice ingestion
» Gitelman & Bartter syndrome
» GIT losses
» Burns
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 Potassium (K+)
Presentation
– Usually asymptomatic
– Skeletal muscle: weakness & cramps; respiratory failure
– Flaccid paralysis & hyporeflexia
– Smooth muscle: constipation, urinary retention
– ECG changes

Management
Add to fluids , knowing maximum peripheral conc. 40
Mild hypokalemia with no excess losses increase k conc. In fluids
Severe cases do correction over minimum 2 hours : 0.6 * BW* deficit( target-
serum K)= in meq
Rise only 0.5 meq/l per hour
Target k is 3 in patients who are chronic tolerating , and 4 in those prone to
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arrthymia like cardiac patients
 Potassium (K+)

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 Hyperkalemia
– Potential lethal arrhythmias that needs urgent management
– Causes
» Difficult blood draw  hemolysis  false reading
» Iatrogenic: IV or oral
» Blood transfusions
» Renal failure
» Adrenal insufficiency or CAH
» ACE inhibitors
» Potassium sparing diureticsAcidemia
» Rhadomyolysis; Tumor lysis syndrome; Tissue necrosis
» Succinylcholine
» Malignant hyperthermia

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 Hyperkalemia
Clinical presentation
– EKG changes
» ~6: peak T waves
» ~7: increased PR interval
» ~8-9: absent P wave with widening QRS complex
» Ventricular fibrillation
» Asystole

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 Hyperkalemia
Treatment
Stop intake immediately, then :
» Calcium gluconate 100mg/kg IV
» Bicarb: 1-2 mEq/kg IV
» Salbutamol (β2 selective agonist) nebulizer
» Insulin & glucose
• Insulin 0.1 u/kg IV + D10W 5ml/kg (0.5gm/kg)
» Dialysis
» Agents that increase K removal like kayexalate ( not in
acute situations)

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 Basic Metabolic Panel

Na +
Cl- BUN Ca++
Glu Mg++
K+ CO3-- Cr Phos--

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 Calcium
• Normal range: 8.8-10.1 with half bound to albumin
• Majority is stored in bone
• Hypoalbuminemia  falsely decreased calcium
– Cac = Cam + [0.8 x (Albn – Alb m)]

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 Calcium
• Hypercalcemia: Causes
– Excess parathyroid hormone
– Excess vitamin D
– Malignancy
– Renal failure
– High bone turn over
» Prolonged immobilization
» Hyperthyroidism
» Thiazide use, vitamin A toxicity
» Paget’s disease
» Multiple myeloma

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 Calcium
• Hypercalcemia Treatments
– Fluid & diuretics
» Forced diuresis
» Loop diuretic
– Oral supplement: biphosphate or calcitonine
– Glucocorticoids
– Dialysis

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 Calcium
• Hypocalcemia Cause
– Hungry bone syndrome
– Decreased PTH
– Ineffective PTH: CRF, absent or ineffective vitamin D,
pseudohypoparathyroidism
– Deficient in PTH: acute hyperphos: TLS, ARF, Rhabdo
– Blood transfusions

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 Calcium
• Hypocalcemia: Treatments
– Supplements
» IV: gluconate or chloride with EKG change
» 200-500 mg/kg/day IV by divided q6hr as intermittent infusions
» Calcium chloride
» Oral calcium with vitamin D

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 Basic Metabolic Panel

Na +
Cl- BUN Ca++
Glu Mg++
K+ CO3-- Cr Phos--

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 Magnesium
• Normal range: 1.5-2.3
• 60% stored in bone
• 1% in extracellular space
• Necessary cofactor for many enzymes
• Renal excretion is primary regulation

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 Magnesium
• Hypermagnesemia: Causes
– Hemolysis
– Renal insuficiency
– DKA, adrenal insufficiency, hyperparathyroidism, lithium intoxication

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 Magnesium
• Hypermagnesemia: Treatments
– Calcium infusion
– Diuretics
– Dialysis

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 Magnesium
• Hypomagnesemia Causes
– malnutrition + diarrhea; Thiamine deficiency
– GI causes: Crohn’s, UC, Whipple’s disease, celiac sprue
– Renal loss: Bartter’s syndrome, postobstructive diuresis, ATN,
kidney transplant
– DKA
– Drugs
» Loop and thiazide diuretics
» Abx: aminoglycoside, ampho B, pentamidine, gent, tobra
» PPI
» Others: digitalis, adrenergic, cisplastin, ciclosporine

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 Magnesium
• Hypomagnesemia: Treatments
– Oral or IV supplement
– Correct on going loss

• IV/IM: 25-50 mg/kg q4-6hr for 3-4 doses

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 Basic Metabolic Panel

Na +
Cl- BUN Ca++
Glu Mg++
K+ CO3-- Cr Phos--

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 Phosphorus
• Normal range: 2.3 - 4.8
• Most store in bone or intracellular space
• <1% in plasma
• Intracellular major anion, most in ATP
• Concentration varies with age, higher during early childhood
• Necessary for cellular energy metabolism

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 Phosphorus
• Hyperphosphatemia
– Causes
» Hypoparathyroidism
» Chronic renal failure
» Osteomalacia
– Presentations
» Ectopic calcification
» Renal osteodystrophy
– Treatments
» Dietary restriction
» Phosphate binder

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 Phosphorus
• Hypophosphatemia Causes
– Re-feeding syndrome
– Respiratory alkalosis
– Alcohol abuse
– Malabsorption

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 Phosphorus
• Hypophosphatemia
– Treatments
» Glycophos 1ml (1mmol) per kg must be diluted and given over 4
hours at least

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Acid-base disorders
Acid-base status
• pH 7.38-7.42
• pCO2 35-45
• HCO3/ BE 22-26 (infants 20-24)/ -2 +2
Handerson-Hasselbach’s
equation
Hydrogen ion = pH H (nmol/L)
24 x CO2 / HCO3 6.9 120
7.0 100
7.1 80
7.2 60
7.3 50
7.4 40
7.5 30
7.6 25
7.7 20
Handerson-Hasselbach’s
equation
Hydrogen ion = pH H (nmol/L)
24 x CO2 / HCO3 6.9 120
7.0 100
ACIDOSIS 7.1 80
*Increased CO2 7.2 60
(RESP) 7.3 50
*Decreased HCO3 7.4 40
(MET) 7.5 30
7.6 25
7.7 20
Handerson-Hasselbach’s
equation
Hydrogen ion = pH H (nmol/L)
24 x CO2 / HCO3 6.9 120
7.0 100
ACIDOSIS 7.1 80
*Increased CO2 (RESP) 7.2 60
*Decreased HCO3
7.3 50
(MET)
-Loss of base (++ Cl)
7.4 40
-Buffering fixed acid 7.5 30
(an gap) 7.6 25
7.7 20
Respiratory acidosis
• CO2 retention
• Low pH
• Kidney compensates by ++ bicarbonate
– EARLY (acute)
pH drop 0.008/ mmHg CO2, (near) normal
bicarbonate
– LATER (chronic, compensated)
pH drop 0.003/ mmHg CO2, INCREASED bicarbonate
Respiratory acidosis
• CO2 retention = HYPOVENTILATION
• TREAT THE CAUSE
Metabolic acidosis
• Low bicarbonate
• Compensatory HYPERVENTILATION  LOW
CO2 (CO2 = HCO3 x 1.5 + 8)
• Normal ventilation is inappropriate (=mixed
acidosis)
Metabolic acidosis
• Tissue hypoxia
(hypoxemia, severely increased work
of breathing, low cardiac output,
decompensated anemia, etc)
• Loss of base-rich fluid eg diarrhea
• Ketoacidosis
• Renal failure, RTA
• In-born errors
Metabolic acidosis
• Treat the cause
• Bicarbonate
– Mild cases will correct with treating cause
– Correct tissue hypoxia and ensure adequate
ventilation
– Effect on intracellular and CSF pH
– Effect on O2 dissociation curve
– Effect of hypertonic Na in bicarbonate
– Effect on Ca and K
Metabolic acidosis
• Treat the cause
• Bicarbonate
B.W. x deficit /3 mEq
Alkalosis
• Respiratory = hyperventilation
• Metabolic = increased bicarbonate
– Acid loss eg vomiting
– Excessive alkali intake
– Hypokalemia (cause & effect)
– Tubular eg Bartter
– Diuretics
 Pros: trusted publisher
2018
very comprehensive

Cons: not pediatric specific

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