10. fluids and electrolytes

Fluids and Electrolytes

Lea Marie Y. Angeles, M.D.

Composition of body fluidsTotal body water

Composition of body fluids

Fluid compartmentsTotal body water is

divided into:Intracellular fluid (ICF)Extracellular fluid

(ECF)

Composition of body fluids

Electrolyte composition

Composition of body fluids

OsmolalityThe ICF and ECF are in osmotic equilibriumNormal plasma osmolality: 285-295 mOsm/kgEffective osmolality (tonicity)

Determines the osmotic force that is mediating the shift of water between the ICF and ECF

Osmolal gapPresent when the measured osmolality exceeds the

calculated osmolality by >10 mOsm/kg

Regulation of Osmolality and VolumeRegulation of osmolality

↑ effective osmolality

↓

Hypothalamus

↓

Secretion of ADH

↓

V2 receptors in collecting duct cells of kidneys

↓

↑ cAMP

↓

↑permeability to water

↓

↑urine concentration, ↓water excretion

Regulation of osmolality and volume

Regulation of osmolality↑serum osmolality

↓

Hypothalamus

↓

Cerebral cortex

↓

Thirst stimulation

Regulation of osmolality and volume

Regulation of volumeNa balance

Main regulator of volume status

KidneyDetermines Na balanceRegulates Na balance by altering the percentage of

filtered Na that is resorbed along the nephron

Effective intravascular volumeMost important determinant of renal Na excretion

Regulation of osmolality and volume

Regulation of volumeNa resorption

Occurs throughout the nephron

Proximal tubule and loop of HenleSites where majority of filtered Na is resorbed

Distal tubule and collecting ductsMain sites for precise regulation of Na balance

Renin-angiotensin system

↓effective intravascular volume↓

Juxtaglomerular apparatus↓

Renin↓

Angiotensinogen↓

Angiotensin I ↓angiotensin converting enzyme

Angiotensin II

↑Na resorption ↑aldosterone↓

↑Na resorption↑K excretion

vasoconstriction ↓ ↑BP

Regulation of osmolality and volume

Regulation of volumeVolume expansion

↓

Atrial natriuretic peptide

↓

↑GFR

Inhibition of Na resorption (in collecting duct)

Sodium metabolism

SodiumDominant cation of ECFPrincipal determinant of extracellular osmolalityNecessary for maintenance of intravascular

volume

Sodium metabolism

IntakeDietPresence of glucose enhances Na absorption

due to the presence of a co-transport system

ExcretionOccurs in:

StoolSweatKidney

Hypernatremia

Na concentration >150 mEq/LEtiology

Excessive sodiumImproperly mixed formulaExcess sodium bicarbonateIngestion of sea water or NaClIntentional salt poisoning (child abuse or

Munchausen syndrome by proxy)Intravenous hypertonic salineHyperaldosteronism

Hypernatremia

EtiologyWater deficit

Nephrogenic diabetes insipidus• Acquired• X-linked• Autosomal recessive• Autosomal dominant

Central diabetes insipidus• Acquired• Autosomal recessive• Autosomal dominant• Wolfram syndrome

Hypernatremia

Etiology Water deficit

Increased insensible losses• Premature infants• Radiant warmers• Phototerapy

Inadequate intake• Ineffective breastfeeding• Child neglect or abuse• Adipsia

Hypernatremia Etiology

Water and sodium deficitsGastrointestinal losses

• Diarrhea• Emesis/nasogastric suction• Osmotic cathartics (lactulose)

Cutaneous losses• Burns• Excessive sweating

Renal losses• Osmotic diuretics (mannitol)• Diabetes mellitus• Chronic kidney disease (dysplasia and obstructive uropathy)• Polyuric phase of acute tubular necrosis

Postobstructive diuresis

Hypernatremia

Clinical manifestationsDehydrationIrritable, restless, weak, lethargicHigh-pitched cry, hyperpneaVery thirsty (if alert)May be febrileHyperglycemia, mild hypocalcemiaBrain hemorrhage

Hypernatremia

Clinical manifestationsSeizures and comaCentral pontine myelinosis, extrapontine

myelinosisThrombotic complications

StrokeDural sinus thrombosisPeripheral thrombosisRenal venous thrombosis

Hypernatremia

Treatment Goal

Decrease serum Na by 12 mEq/L every 24 hours, rate of 0.5 mEq/L/hr

Hypernatremia

Treatment In hypernatremic dehydration, 1st priority is

restoration of intravascular volume with isotonic fluid

Acute severe hypernatremia 20 to Na administration can be corrected rapidly

Peritoneal dialysisLoop diureticWith Na overload – hypernatremia is corrected

with Na-free IVF (D5W)

Hypernatremia

TreatmentHyperglycemia from hypernatremia is usually

not treated with insulin, rather, decrease the glucose concentration of IVF

Treat underlying cause

Hyponatremia

Serum Na level <135 mEq/LEtiology

PseudohyponatremiaHyperosmolality

HyperglycemiaMannitol

Hyponatremia

EtiologyHypovolemic hyponatremia

Extrarenal losses• Gastrointestinal (emesis, diarrhea)• Skin (sweating, burns)• Third space losses

Renal losses• Thiazide or loop diuretics• Osmotic diuresis• Postobstructive diuresis• Polyuric phase of acute tubular necrosis• Juvenile nephronophthisis

Hyponatremia

EtiologyHypovolemic hyponatremia

Renal losses• Autosomal recessive polycystic kidney disease• Tubulointerstitial nephritis• Obstructive uropathy• Cerebral salt wasting• Proximal (type II) renal tubular acidosis• Lack of aldosterone effect (high serum potassium)

Absent aldosterone Pseudohypoaldosteronism type Urinary tract obstruction and/or infection

Hyponatremia

EtiologyEuvolemic hyponatremia

Syndrome of inappropriate antidiuretic hormoneNephrogenic syndrome of inappropriate diuresisDesmopressin acetateGlucocorticoid deficiencyHypothyroidism

Hyponatremia

EtiologyEuvolemic hyponatremia

Water intoxication• Iatrogenic (excess hypotonic intravenous fluid)• Feeding infants excessive water products• Swimming lessons• Tap water enema• Child abuse• Psychogenic polydipsia• Diluted formula• Marathon running with excessive water intake • Beer protomania

Hyponatremia

EtiologyHypervolemic hyponatremia

Congestive heart failureCirrhosis Nephrotic syndromeRenal failureCapillary leak due to sepsisHypoalbuminemia due to gastrointestinal disease

(protein-losing enteropathy)

Hyponatremia

Clinical manifestationsHyponatremia →↑intracellular water →cellular

swellingBrain cell swelling → ↑ICPAcute severe hyponatremia → brainstem

herniation and apnea

Hyponatremia

Clinical manifestationsNeurologic symptoms:

AnorexiaNauseaEmesisMalaiseLethargyConfusionAgitationHeadacheSeizuresComaDecreased reflexes

Hyponatremia

Clinical manifestationsHypothermiaCheyne-Stokes respirationMuscle cramps, weaknessPatients with hyponatremic dehydration have

more manifestations of intravascular volume depletion than patients with equivalent water loss but with normal or increased serum Na concentration

Hyponatremia

TreatmentAvoid overly rapid correctionRapid correction may cause central pontine

myelinosisAvoid correcting serum Na by >12 mEq/L/day

(does not apply to acute hyponatremia)Severe symptoms (shock or sezures)

Give a bolus of hypertonic saline to produce a small rapid increase in serum Na and the effect on serum osmolality leads to a decrease in brain edema

Hyponatremia

TreatmentHypovolemic hyponatremia

1st step – restore intravascular volume with isotonic saline

Hypervolemic hyponatremiaCornerstone of therapy – water and Na restrictionNephrotic syndrome – albumin and diuresisCongestive heart failure – improve cardiac output

Hyponatremia

Treatment Isovolemic hyponatremia

Acute symptomatic hyponatremia 20 to water intoxication

• give hypertonic saline to reverse cerebral edemaChronic hyponatremia because of poor solute intake

• give appropriate formula, eliminate excess water intakeNon-physiologic stimuli for ADH production

• water restrictionHyponatremia of hypothyroidism or cortisol

deficiency• Specific hormone replacement

Hyponatremia

TreatmentIsovolemic hyponatremia

SIADH• Fluid restriction• Furosemide + hypertonic saline• Conivaptan

V2-receptot antagonist

Decreases permeability of collecting duct to water producing aquaresis

Approved for short-term therapy of euvolemic patients with hyponatremia (usually SIADH)

Potassium Metabolism

Intracellular K concentration: 150 mEq/LNa+K+-ATPase maintains high intracellular

K concentration by pumping Na out of the cell and K into the cell

Resulting chemical gradient is used to produce the resting membrane potential of cells

Potassium metabolism

PotassiumNecessary for electrical responsiveness of

nerve and muscle cells and for contractility of cardiac, skeletal, and smooth muscles

Intracellular concentration affects cellular enzymes

Necessary for maintaining cell volumeMajority of body K is in muscle

Potassium metabolism

Substances that increase K movement into cells Insulin↑pHβ-adrenergic agonists

Factors that increase extracellular [K]↓pHα-adrenergic agonistsExercise↑plasma osmolality

Potassium metabolism

Intake Recommended: 1-2 mEq/LMost absorption occurs in small intestinesColon – exchanges body K for luminal Na

ExcretionSweatColonUrine

Principal sites of K regulation: distal tubule and collecting duct

Potassium

Excretion Aldosterone – principal hormone regulating K

excretionFactors that increase urinary K excretion:

GlucocorticoidsADHHigh urinary flow rateHigh Na delivery to distal nephron Loop and thiazide diuretics

Potassium metabolism

ExcretionFactors that decrease K excretion

InsulinCatecholaminesUrinary ammonia

Hyperkalemia

EtiologySpurious laboratory value

HemolysisTissue ischemia during blood drawingThrombocytosisLeukocytosis

Increased intakeIntravenous or oralBlood transfusions

Hyperkalemia

EtiologyTranscellular shifts

AcidosisRhabdomyolysisTumor lysis syndromeTissue necrosisHemolysis/hematomas/gastrointestinal bleedingSuccinylcholineDigitalis intoxicationFluoride intoxication

Hyperkalemia

Etiology Transcellular shifts

β-adrenergic blockersExerciseHyperosmolalityInsulin deficiencyMalignant hyperthermiaHyperkalemic periodic paralysis

Hyperkalemia

EtiologyDecreased excretion

Renal failurePrimary adrenal disease

• Acquired Addison disease• 21-hydroxylase deficiency• 3β-hydroxysteroid dehydrogenase deficiency• Lipoid congenital adrenal hyperplasia• Adrenal hypoplasia congenita• Aldosterone synthase deficiency• Adrenoleukodystrophy

Hyperkalemia

Etiology Hyporeninemic hypoaldosteronism

Urinary tract obstructionSickle cell diseaseKidney transplantLupus nephritis

Renal tubular diseasePseudohypoaldosteronism type IPseudohypoaldosteronism type IIUrinary tract obstructionSickle cell diseaseKidney transplant

Hyperkalemia

Etiology Medications

Angiotensin-converting enzyme inhibitorsAngiotensin II blockersPotassium-sparing diureticsCalcineurin inhibitorsNonsteroidal anti-inflammatory drugsTrimethoprimHeparinDrug-induced potassium channel syndrome

Hyperkalemia

Clinical manifestationsMost important effects of hyperkalemia are due

to the role of potassium in membrane polarization

ECG changesPeaking of T wavesIncreased P – R intervalFlattening of P waveWidening of QRS complexVentricular fibrillation

Hyperkalemia

Clinical manifestationsAsystoleParesthesia, weakness, tingling

Hyperkalemia

Treatment 1st step: stop all sources of additional K (oral or

IV)If K level is >6-6.5mEq/L, obtain ECGGoals:

To stabilize the heart to prevent life-threatening arrythmias

To remove K from the body

Hyperkalemia

TreatmentIntravenous CaNaHCO3

Insulin – must be given with glucose to prevent hypoglycemia

Nebulized salbutamol

Hyperkalemia

TreatmentMeasures that remove K from the body

Loop diureticNa polysterene sulfonate (Kayexelate)Dialysis

• Hemodialysis• Peritoneal dialysis

Hypokalemia

EtiologySpurious

High white blood cell countTranscellular shifts

AlkalemiaInsulinβ-adrenergic agonistsDrugs/toxins (theophylline, barium, toluene, cesium

chloride)Hypokalemic periodic paralysisThyrotoxic periodic paralysis

Hypokalemia

EtiologyDecreased intake

Anorexia nervosa

Extrarenal lossesDiarrheaLaxative abuseSweatingSodium polystyrene sulfonate (Kayexelate) or clay

ingestion

Hypokalemia Etiology

Renal lossesWith metabolic acidosis

• Distal renal tubular acidosis• Proximal renal tubular acidosis• Ureterosigmoidostomy• Diabetic ketoacidosis

Without specific acid-base disturbance• Tubular toxins: amphotericin, cisplatin, aminoglycosides• Interstitial nephritis• Diuretic phase of acute tubular necrosis• Postobstructive diuresis• Hypomagnesemia• High urine anions (e.g. penicillin or penicillin derivatives)

Hypokalemia

EtiologyRenal losses

With metabolic alkalosis• Low urine chloride• Emesis/nasogastric suction• Chloride-losing diarrhea• Cystic fibrosis• Low-chloride formula• Posthypercapnia• Previous loop or thiazide diuretic use

Hypokalemia

EtiologyRenal losses

High urine chloride and normal blood pressure• Gitelman syndrome• Bartter syndrome• Autosomal dominant hypoparathyroidism• Loop and thiazide diuretics

Hypokalemia

Etiology Renal losses

High urine chloride and high blood pressure• Adrenal adenoma or hyperplasia• Glucocorticoid-remedial aldosteronism• Renovascular disease• Renin-secreting tumor• 17α-hydroxylase deficiency• 11β-hydroxylase deficiency• Cushing syndrome• 11β-hydroxysteroid dehydrogenase deficiency

Hypokalemia

EtiologyRenal losses

LicoriceLiddle syndrome

Hypokalemia

Clinical manifestationsAffects heart and skeletal musclesECG changes:

Flattened T waveDepressed ST segmentAppearance of a U wave

Hypokalemia makes the heart susceptible to digitalis-induced arrythmias such as SVT, ventricular tachycardia and heart block

Hypokalemia

Clinical manifestationsMuscle weakness, crampsParalysisSlowing of GI motilityImpairment of bladder function → urinary

retentionPolyuria and polydipsiaStimulation of renal ammonia production Kidney damagePoor linear growth

Hypokalemia

TreatmentIV potassium

Dose:0.5-1mEq/kg given x 1 hr, max dose in adults: 40 mEq

Oral potassium

Magnesium metabolism

4th most common cation and 3rd most common intracellular cation

50-60% of body Mg is in boneMost intracellular Mg is in muscle and liverNormal plasma concentration:

1.5-2.3 mg/dL or 1.2-1.9 mEq/L

Necessary cation for hundreds of enzymesImportant for membrane stabilization and nerve

conduction

Magnesium metabolism

Intake30-40% of dietary Mg is absorbedSmall intestine

Major site of Mg absorption

AbsorptionDecreases in the presence of substances that

complex with Mg (free fatty acids, fiber, phytate, phosphate, oxalate)

Decreases with increased intestinal motility and CaEnhanced by vitamin D, PTH

Magnesium metabolism

ExcretionRenal excretion

Principal regulator of Mg balanceNo defined hormonal regulatory system

Hypomagnesemia

Etiology Gastrointestinal disorders

DiarrheaNasogastric suction or emesisInflammatory bowel diseaseCeliac diseaseCystic fibrosisIntestinal lymphangiectasiaSmall bowel resection or bypassPancreatitisProtein calorie malnutritionHypomagnesemia with secondary hypocalcemia

Hypomagnesemia

Etiology Renal disorders

Medications: amphotericin, cisplatin, cyclosporin, loop diuretics, mannitol, pentamidine, aminoglycosides, loop diuretics

Diabetes Acute tubular necrosis (recovery phase)Postobstructive nephropathyChronic kidney diseases: interstitial nephritis,

glomerulonephritis, postrenal transplantHypercalcemiaIntravenous fluids

Hypomagnesemia

EtiologyRenal disorders

Primary aldosteronismGenetic diseases

• Gitelman syndrome• Bartter syndrome• Familial hypomagnesemianwith hypercalciuria and

nephrocalcinosis• Autosomal recessive renal magnesium wasting• Autosomal dominant renal magnesium wasting• Autosomal dominant hypoparathyroidism• Mitochondrial disorders

Hypomagnesemia

Etiology Miscellaneous causes

Poor intakeHungry bone syndromeInsulin administrationPancreatitisIntrauterine growth retardationInfants of diabetic mothersExchange transfusion

Hypomagnesemia

Clinical manifestationsUsually occurs only at Mg levels <0.7 mg/dLTetany, (+)Chvostek and Trosseau signs,

seizuresRicketsHypokalemia

Hypomagnesemia

Treatment Severe

Parenteral MgMgSO4 25-50 mg/kg (0.05-0.1 ml/kg of 50% solution;

2.5-5 mg/kg of elemental Mg); dose is repeated every 6 hours (every 8-12 hours in neonates) for 2-3 doses

Long-term therapyOral – dose is divided to decrease cathartic side

effectAlternatives: IM injection and nighttime nasogastric

infusion

Hypermagnesemia

Almost always secondary to excessive intake

Unusual except in neonates born to mothers receiving IV Mg for pre-eclampsia or eclampsia

Hypermagnesemia

EtiologyMg is present in high amounts in certain

laxatives, enemas, cathartics used to treat drug overdose and antacids

Neonates may receive high amounts transplacentally if maternal levels are elevated

Kidneys excrete excessive Mg but this is decreased in patients with chronic renal failure

Hypermagnesemia

Etiology Conditions predisposing to hypermagnesemia

Chronic renal failureFamilial hypocalciuric hypercalcemiaDiabetic ketoacidosisLithium ingestionMilk alkali syndromeTumor lysis syndrome

Hypermagnesemia

Clinical manifestationsSymptoms appear when plasma Mg level is

>4.5 mg/dLHypermagnesemia inhibits Ach release at

neuromuscular junction → hypotonia, hyporeflexia, weakness, paralysis

Nausea, vomiting, hypocalcemiaDirect CNS depression → lethargy, sleepiness,

poor suck

Hypermagnesemia

Clinical manifestationsHypotension, flushingECG changes

Prolonged P-R, QRS and Q-T intervals

Severe hypermagnesemia (>15 mg/dL) → complete heart block and cardiac arrest

Hypermagnesemia

TreatmentIV hydration and loop diureticsDialysisExchange transfusionIn acute emergencies:

100 mg/kg of IV Ca gluconate (transiently effective)

Phosphorus metabolism

Most phosphorus is in bone or is intracellular, w/ <1% in plasma

Phosphrous concentration varies with ageComponent of ATP and other trinucleotides,

critical for cellular energy metabolismNecessary for nucleic acid synthesisComponent of cell membranes and other

structuresEssential component of bone and is necessary

for skeletal mineralization

Phosphorus metabolism

IntakeReadily available in foodBest sources: milk and milk productsHigh concentration: meat and fishVegetables higher than fruits and grains65% of intake is absorbedAbsorption

Almost exclusively in small intestines via a paracellular diffuse process and a vitamin D regulated transcellular pathway

Phosphorus metabolism

ExcretionKidney – regulates phophorus balanceApproximately 85% of filtered load is resorbedPTH – decreases resorption of phosphate,

increasing urinary phosphate

Low plasma phosphorus↓

1α-hydroxylase (in kidney)↓

Converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol)↓

↑ intestinal absorption of phosphorusMaximal renal resorption of phosphorus

Phosphorus metabolism

Excretion Phosphatonin

Inhibits renal resorption of phosphorus → phosphaturia and hypophosphatemia

Inhibits synthesis of calcitriol by decreasing 1α-hydroxylase activity

Serum phosphorus during childhood

AGE

0-5 days1-3 years4-11 years12-15 years16-19 years

PHOSPHORUS

4.-8.2 mg/dL3.8-6.5 mg/dL3.7-5.6 mg/dL2.9-5.4 mg/dL2.7-4.7 mg/dL

Hypophosphatemia

EtiologyTranscellular shifts

Glucose infusionInsulinRefeedingTotal parenteral nutritionRespiratory alkalosisTumor growthBone marrow transplantationHungry bone syndrome

Hypophosphatemia

EtiologyDecreased intake

NutritionalPremature infantsLow phosphorus formulaAntacids and other phosphate binders

Hypophosphatemia

EtiologyRenal losses

HyperparathyroidismParathyroid hormone-related peptideX-linked hypophosphatemic ricketsTumor-induced osteomalaciaAutosomal dominant hypophosphatemic ricketsFanconi syndrome Dent diseaseHypophosphatemic rickets with hypercalciuria

Hypophosphatemia

Etiology Renal losses

Hypophosphatemia due to mutations in the sodium-phosphate cotransporter

Volume expansion and intravenous fluidsMetabolic acidosisDiureticsGlycosuriaGlucocorticoidsKidney transplantation

Hypophosphatemia

EtiologyMultifactorial

Vitamin D deficiencyVitamin D-dependent rickets type IVitamin D-dependent rickets type 2AlcoholismSepsisDialysis

Hypophosphatemia

Clinical manifestationsLong term phosphorus deficiency: ricketsSevere hypophosphatemia: <1-1.5 mg/dL, may

affect every organHemolysis and dysfunction of WBCImpaired release of oxygen to tissuesProximal muscle weakness and atrophyIn ICU – slow weaning from ventilator or acute

respiratory failure

Hypophosphatemia

Clinical manifestationsRhabdomyolysisCardiac dysfunctionNeurologic symptoms

TremorsParesthesiaAtaxiaSeizuresDeliriumComa

Hypophosphatemia

Treatment Mild hypophosphatemia

No treatment except if the situation suggests it’s a chronic depletion or if there are ongoing losses

Oral phosphorusIntravenous phosphorusIncrease dietary phosphorus

Hyperphosphatemia

EtiologyRenal insufficiency – most common causeCan occur because gastrointestinal absorption

of large dietary intake of phosphorus is unguarded

Develops when kidney function is <30% of normal

Hyperphosphatemia

EtiologyTranscellular shifts

Tumor lysis syndromeRhadomyolysisAcute hemolysisDiabetic ketoacidosis and lactic acidosis

Hyperphosphatemia

EtiologyIncrease intake

Enemas and laxativesCow’s milk in infantsTreatment of hypophosphatemiaVitamin D intoxication

Hyperphosphatemia

EtiologyDecreased excretion

Renal failureHypoparathyroidism or pseudohypoparathyroidismAcromegalyHyperthyroidismTumoral calcinosis with hyperphosphatemia

Clinical manifestations

Principal clinical consequences:HypocalcemiaSystemic calcification

HypocalcemiaDue to tissue deposition of Ca-P saltInhibition of 1,25-dihydroxyvitamin D productionDecreased bone resorption

Hyperphosphatemia

Clinical manifestationsSystemic calcification

Occurs because solubility of phosphorus and calcium in plasma is exceeded

Foreign body feeling in conjunctiva, erythema and injection

More ominous manifestation:• hypoxia from pulmonary calcification • renal failure from nephrocalcinosis

Hyperphosphatemia

TreatmentMild hyperphosphatemia in a patient with

reasonable renal function resolves spontaneouslyDietary phosphorus restrictionIntravenous fluids

Hyperphosphatemia

TreatmentMore significant hyperphosphatemia

Add oral phosphorus binder

Dialysis If unresponsive to conservative management or if

renal insufficiency is supervening

Fluid therapy

Degree of dehydrationMild (<5% in an infant; <3% in an older child or

adult)Normal or increased pulseDecreased urine outputThirstyNormal physical activity

Fluid therapyDegree of dehydration

Moderate (5-10% in an infant; 3-6% in an older child or adult)TachycardiaLittle or no urine outputIrritable/lethargicSunken eyes and fontanelDecreased tearsDry mucous membranesMild delay in elasticity (skin turgor)Delayed capillary refill (>1.5 sec)Cool and pale

Fluid therapyDegree of dehydration

Severe (>10% in an infant; >6% in an older child or adult)Rapid and weak or absent peripheral pulsesDecreased blood pressureNo urine outputVery sunken eyes and fontanelNo tearsParched mucous membranesDelayed elasticity (poor skin turgor)Very delayed capillary refill (>3 sec)Cold and mottledLimp depressed consciousness

Fluid therapyOral rehydration

Preferred mode of rehydration and replacement of ongoing losses

Risks associated with severe dehydration that may necessitate IV resuscitationAge <6 monthsPrematurityChronic illnessFever >38 0C if <3 months or 39 0C if 3-36 monthsBloody diarrheaPersistent emesis Poor urine outputSunken eyesDepressed level of consciousness

Fluid therapy

Limitations to ORTShockIleusIntussusceptionCarbohydrate intoleranceSevere emesisHigh stool output (>10ml/kg/hr)

Fluid therapy

Guidelines for oral rehydrationMild dehydration

50 ml/kg of ORS given within 4 hours Moderate dehydration

100 ml/kg of ORS over 4 hoursAdditional 10 ml/kg of ORS for each watery

stoolMaintenance

Volume of ORS ingested should equal volume of stool losses

Fluid therapyIntravenous therapy

Fluid management of dehydrationRestore intravascular volume

• Normal saline: 20 ml/kg over 20 min• Repeat as needed

Rapid volume repletion: 20 ml/kg normal saline or lactated ringer’s (max=1L) over 2 hours

Calculate 24-hour fluid needs: maintenance + deficit volume

Subtract isotonic fluid already administered from 24-hour fluid needs

Administer remaining volume over 24 hoursReplace ongoing losses as they occur

Fluid therapy

Phases of fluid therapyRehydration

Also called deficit therapyAimed at immediate correction o the abnormal

losses of fluids and electrolytes which are reflected in the body composition by an acute loss in body weight

Should be accomplished within 6 hours after initiation of treatment

Fluid therapy

Phases of fluid therapyMaintenance

Intended to stabilize internal milieu after it has been restored to normal during rehydration

Normal daily requirement of fluid and electrolytes which is engendered by metabolic activity or expenditure is provided and simultaneously, all ongoing and abnormal losses should be actively replaced