Pedi gu review fluids and electrolytes

Fluids and Electrolytes Pediatric GU Review UCSD Pediatric Urology George Chiang MD Sara Marietti MD Outlined from The Kelalis-King-Belman Textbook of Clinical Pediatric Urology 2007 (not for reproduction, distribution, or sale without consent)

Renal Function
Kidneys function to excrete water, solutes and metabolic waste
Regulate salt and water excretion
99% of filtered water, sodium, chloride and bicarb is reabsorbed and returned to the plasma

Renal Function
Each nephron receives the ultrafiltrate of plasma, which passes through Bowman’s space and into the renal tubule
GFR=rate of ultrafiltrate formation
Term infant GFR is very low – 21ml/mn
Increases to 60ml/mn by 2 weeks
Adult level (120ml/mn) by 18-24 mo

Renal Function
Concentrating capacity of full-term and pre-term infant is diminished
Immature collecting tubules don’t respond to ADH
Infant can only increase urine osmolality to 600mOsm/kg vs 1200 in the adult
Newborn excretes dilute urine

Body Composition
Term newborn – total body water accounts for 70-75% of body weight
Decreases to 65% in infants/children
Decreases to 60% in adult male
Decreases to 55% in adult female

Body Composition
Body water is in constant state of osmotic equilibrium between intra/extracellular space
Fetus/newborn have more extracellular than intracellular fluid
With newborn diuresis and cellular growth, this changes

Body Composition
2/3 TBW intracellular, 1/3 TBW extra by age 1 year (adult composition)
Extracellular space made up of plasma, interstitial fluid, pleural, peritoneal, synovial

Body Composition
Intravascular volume of premature or critically ill infant – 100ml/kg
Nl newborn – 80-90ml/kg
1-6 y.o. – 75-80ml/kg
>6 y.o. – 65-70ml/kg

Body Composition
Plasma osmolality is maintained between 285-295 mOsm/kg
With extracellular loss (bleeding/dehydration), Increase ADH(from increased osmolality), Increase water

ADH
Bleeding/dehydration – osmoreceptors in hypothalamus sense increase-> release ADH-->bind to V2 receptors in collecting ducts->insertion of aquaporin 2 water channels->increase water permeabilty, concentrated urine
Osmoreceptors are very sensitive – respond to 1% change in osmolality
Other osmoreceptors stimulate thirst centers as well

Hypovolemia
MC – diarrhea
s/s – weight loss, tachycardia, low BP, dry mucous membranes, no tears, sunken fontanelle, decreased skin turgor
Mild dehydration (5% body weight loss) – if no clinical findings do not need blood work
Can usually attempt oral hydration

Hypovolemia
More severe (>5% body weight loss) – such as operative loss, goal is rapid extracellular fluid expansion to prevent shock and decreased renal perfusion
Bolus with NS or LR
Monitor weight, UOP and check frequent lytes

Sodium
Sodium is excreted in stool and sweat
Primarily excreted in kidneys and is main regulator of sodium balance
However, kids with CF have high sodium loss in their sweat

Sodium Abnormalities
Hyponatremia – hypervolemic, isovolemic, hypovolemic
Hypernatremia

Hyponatremia
Signs/Symptoms – nausea, anorexia, vomiting, muscle ache, headache, weakness, irritability, confusion, seizure, coma
Low sodium decreases the extracellular osmolality, thus water moves out of extracellular space and into the cells and causes cellular swelling, brain swelling can cause herniation

Correction
Need to correct the hyponatremia slowly to avoid CPM
CPM – when corrected too quickly, water will shift out of the brain too quickly and cause demyelination of the pons
No faster than 10-20 mEq/day

Hypervolemic Hyponatremia
CHF, liver disease, renal failure
Peripheral and pulmonary edema
Increase in TBW and Na, but more water
Decrease in blood volume secondary to third spacing or cardiac problem, so ADH increases water and aldosterone increases Na
If from renal failure, have expanded blood volume but kidneys fail to produce urine and get rid of the extra water

Hypervolemic Hyponatremia
Cardiac/liver – water/Na restriction, maybe diuretic
If renal failure – may need dialysis

Isovolemic Hyponatremia
SIADH – excess in water absorption
From CNS disorder, tumor, stress medications(narcotics, anesthesia), or extremely dilute feedings
Diagnosis of exclusion
ADH causes excess water and intravascular volume, thus kidneys lose Na to try to correct for this

SIADH
Urine osmolality > 100
Serum osmolality < 280
Serum Na < 135
Urine Na > 25

Treatment
If asymptomatic – water restriction
If symptomatic – 3% saline infusion, lasix infusion

Hypovolemic Hyponatremia
GI bug (diarrhea more than emesis), fasting, third space losses from burns, surgery, Na wasting nephropathy
Treat dehydration with isotonic saline (NS or LR)

Hypernatremia
Confusion, lethargy, weak, irritable, convulsions
Usually dehydrated with more water than Na loss
Improperly mixed formula, saltwater ingestion, hyperaldosteronism, nephrogenic/central DI, GI losses (ngt, emesis), post-obstructive diuresis

Hypernatremia
Because intravascular osmolality is high, water from cells moves out of the cell
In the brain, cells shrink and can cause decrease in brain volume and tearing of vessels ->intracranial bleeding (seizure/coma)

Hypernatremia by Cause
DI – only causes hypernatremia if pt does not have access to water or cannot drink it, newborn, neurologic impairment, emesis
Newborn – imbalance between loss and intake, usually lose water but may be increased if placed under the warmer, phototherapy for hyperbilirubineamia, or inadequate breast-feeding
Osmotic – mannitol or glucose (from diabetes) will cause pt to lose Na and water, but more water

Hypernatremia by Cause
Post-obstructive diuresis – increase in solutes causes loss of water, may have tubular damage may exacerbate water losses
Diarrhea – lose sodium and water, but more water, if child can drink they can replace the loss, at risk if also have emesis, anorexia or no access to water

Treatment
Most kids present dehydrated
Hydrate with NS bolus 10-20ml/kg
Frequent monitoring of Na level, do not want to correct too quickly (<12mEq/24 hr)
If correct too quickly and begin to have seizures, stop the hypotonic fluid and give 3% saline to increase Na and stop brain swelling

Potassium
Major intracellular cation
Low concentrations in extracellular fluid
Gradient between intracellular and extracellular allows muscle, cardiac and neuronal tissue to function

Hypokalemia
Arrhythmias, neuromuscular excitability, hyporeflexia, decreased peristalsis,
Usually due to GI (vomiting, ngt), gastroenteritis is MC cause in children
Treat with IV KCL if symptomatic (0.5-1 mEq/kg)

Hyperkalemia
Arrhythmias, muscle weakness, paralysis
Peaked T waves can turn to v.fib
Can be from hemolysis or drawing off a vein above K containing line, so re-chk
Causes – acidosis, rhabdo, tumor lysis, renal failure, CAH (21-hydroxylase deficiency), NSAID, diuretics

Treatment
K>6-6.5, chk EKG
If changes may need immediate cardiac stabilization with Calcium gluconate IV
Glucose with IV insulin drives K intracellularly
Bicarb drives K intracellularly
Exchange resins such as kayexalate po/pr will remove K from the body
If not in renal failure, a loop diuretic will also remove some K
HD

Hypocalcemia
Ca is mostly in bone matrix, only 0.1% is in ECF
Peri-op may be from low Mg, ARF, shock or rhabdo
S/S – Chvostek’s – facial nerve ->mouth twitch, Trousseau’s – finger twitch with BP cuff inflated
Only supplement if symptomatic

Hypomagnesemia
Dietary deficiency, chronic diuretic use
Can cause low Ca and make hypokalemia persist by causing renal K wasting
Should replace especially if have hypocalcemia and hypokalemia

Acid-Base Disturbance
Nl pH: 7.35-7.45
Need normal renal and pulmonary function to maintain this
If need to evaluate need AMA-renal and ABG

Metabolic Acidosis
Leads to: arrhythmia, hypotension and pulmonary edema
From addition of acid or removal of base from the plasma
Lungs compensate by increasing respiratory rate
Acids are buffered mostly by HCO3- but also other anions which make up the anion gap

Anion Gap
Na- (Cl + HCO3)
Normal range is 10-12 mEq/L

Non-Anion Gap Acidosis
Anion Gap within normal range
HCO3 is lost from kidneys/GI system, but Cl is absorbed to replace it
Hyperchloremic, non-anion gap, metabolic acidosis
Diarrhea can cause this
If acidosis mild-moderate (pH>7.2) – only require fluid and lyte replacement

Non-Anion Gap Acidosis
Once renal perfusion is restored, H+ can be excreted to correct the metabolic deficit
If severe (pH<7.2) – may also need IV bicarb
Chk K prior to bicarb because it can worsen hypokalemia

Anion Gap Acidosis
Lactic acidosis, diabetic ketoacidosis, poisons, renal failure
Lactic acidosis – sepsis, hypovolemia, treat according to the cause
Poison with salicylats or ethylene glycol – treat by removing the poison, gastric lavage, charcoal, occasionally HD

Metabolic Alkalosis
Symptoms – CNS changes, muscle irritability, cardiac arrhythmias, seizures
Lethargy and confusion from decrease in RR as body tries to hold onto C02
From losing acid or gaining base
Alkali ingestion, vomiting, ngt losses, hyperaldosteronism

Metabolic Alkalosis
If from vomiting – will need to give Cl, to allow renal excretion of bicarb, and K which is lost with vomiting
If due to hyperaldosteronism – spironolactone is an antagonist

Respiratory Acidosis
Increase in PCO2 from decreased RR
Airway obstruction, CNS depression, immaturity, neuromuscular problems
Treat by targeting the underlying problem

Respiratory Alkalosis
Decreaesed PCO2 from increased RR
Hyperventilation
Dizziness and confusion result from decreased cerebral blood flow
Treat the underlying problem

Maintenance Fluid
Weight based
100ml/kg/day for kg 1-10
50ml/kg/day for kg 11-20
20ml/kg/day for kg >21
Hourly rate is 4:2:1 rule
UOP should be kept 1-2ml/kg/hr

Nutrition
Hypoalbuminemia has been correlated with increased mobidity/mortality
Protein needs of neonates and infants >>children and adults
Infant maintenance:75-100 kcal/kg/day
Infant growth:100-120 kcal/kg/day
Measurement
Albumin (20 days)
Transferrin (8.8 days)
Prealbumin (2 days)
RBP (Retinol binding protein)-12 hrs excreted in urine

Enteral Alimentation
Preserve normal intestinal villus to prevent bacterial translocation
Commercial preparations 35-45 kcal/kg/day
Infusion rates start at 10 cc/hr to maximum 60 cc/hr
Minimal infusion of 20 cc/hr needed for gut preservation and immune stimulation
Malnutrition can exacerbate malabsorption and more aggressive approach may be warranted

Isotonic Parenteral
PPN
Solution is < 600 mOsm
Depends on mobilization of endogenous fat stores for fuel and provision of amino acids for protein needs
Minimizes catabolism but does not provide for anabolism

Hypertonic
Rebuild mass and achieve anabolism
Prolonged starvation
Term 4-5 days/pre-term 1-2 days
GI dysfunction, chronic malabsorption, diarrhea, bowel obstruction, EC fistulas
20-25% dextrose, 4.25% a.a.; essential fatty acids, glutamines (mucosal preservation)
Complications: Technical, Septic (2-3%), Metabolic
(HONK-->cerebral dehydration with coma/death)-->add insulin; elevation of LFTs from excess calories with increased insulin response and hepatic lipogenesis; electrolyte abnormalities

Pedi gu review fluids and electrolytes

by George Chiang

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