Fluids and Electrolytes

Pediatric GU Review

UCSD Pediatric UrologyGeorge 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