10. fluids and electrolytes
TRANSCRIPT
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Fluids and Electrolytes
Lea Marie Y. Angeles, M.D.
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Composition of body fluidsTotal body water
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Composition of body fluids
Fluid compartmentsTotal body water is
divided into:Intracellular fluid (ICF)Extracellular fluid
(ECF)
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Composition of body fluids
Electrolyte composition
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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
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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
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Regulation of osmolality and volume
Regulation of osmolality↑serum osmolality
↓
Hypothalamus
↓
Cerebral cortex
↓
Thirst stimulation
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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
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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
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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
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Regulation of osmolality and volume
Regulation of volumeVolume expansion
↓
Atrial natriuretic peptide
↓
↑GFR
Inhibition of Na resorption (in collecting duct)
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Sodium metabolism
SodiumDominant cation of ECFPrincipal determinant of extracellular osmolalityNecessary for maintenance of intravascular
volume
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Sodium metabolism
IntakeDietPresence of glucose enhances Na absorption
due to the presence of a co-transport system
ExcretionOccurs in:
StoolSweatKidney
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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
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Hypernatremia
EtiologyWater deficit
Nephrogenic diabetes insipidus• Acquired• X-linked• Autosomal recessive• Autosomal dominant
Central diabetes insipidus• Acquired• Autosomal recessive• Autosomal dominant• Wolfram syndrome
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Hypernatremia
Etiology Water deficit
Increased insensible losses• Premature infants• Radiant warmers• Phototerapy
Inadequate intake• Ineffective breastfeeding• Child neglect or abuse• Adipsia
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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
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Hypernatremia
Clinical manifestationsDehydrationIrritable, restless, weak, lethargicHigh-pitched cry, hyperpneaVery thirsty (if alert)May be febrileHyperglycemia, mild hypocalcemiaBrain hemorrhage
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Hypernatremia
Clinical manifestationsSeizures and comaCentral pontine myelinosis, extrapontine
myelinosisThrombotic complications
StrokeDural sinus thrombosisPeripheral thrombosisRenal venous thrombosis
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Hypernatremia
Treatment Goal
Decrease serum Na by 12 mEq/L every 24 hours, rate of 0.5 mEq/L/hr
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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)
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Hypernatremia
TreatmentHyperglycemia from hypernatremia is usually
not treated with insulin, rather, decrease the glucose concentration of IVF
Treat underlying cause
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Hyponatremia
Serum Na level <135 mEq/LEtiology
PseudohyponatremiaHyperosmolality
HyperglycemiaMannitol
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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
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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
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Hyponatremia
EtiologyEuvolemic hyponatremia
Syndrome of inappropriate antidiuretic hormoneNephrogenic syndrome of inappropriate diuresisDesmopressin acetateGlucocorticoid deficiencyHypothyroidism
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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
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Hyponatremia
EtiologyHypervolemic hyponatremia
Congestive heart failureCirrhosis Nephrotic syndromeRenal failureCapillary leak due to sepsisHypoalbuminemia due to gastrointestinal disease
(protein-losing enteropathy)
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Hyponatremia
Clinical manifestationsHyponatremia →↑intracellular water →cellular
swellingBrain cell swelling → ↑ICPAcute severe hyponatremia → brainstem
herniation and apnea
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Hyponatremia
Clinical manifestationsNeurologic symptoms:
AnorexiaNauseaEmesisMalaiseLethargyConfusionAgitationHeadacheSeizuresComaDecreased reflexes
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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
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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
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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
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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
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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)
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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
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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
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Potassium metabolism
Substances that increase K movement into cells Insulin↑pHβ-adrenergic agonists
Factors that increase extracellular [K]↓pHα-adrenergic agonistsExercise↑plasma osmolality
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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
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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
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Potassium metabolism
ExcretionFactors that decrease K excretion
InsulinCatecholaminesUrinary ammonia
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Hyperkalemia
EtiologySpurious laboratory value
HemolysisTissue ischemia during blood drawingThrombocytosisLeukocytosis
Increased intakeIntravenous or oralBlood transfusions
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Hyperkalemia
EtiologyTranscellular shifts
AcidosisRhabdomyolysisTumor lysis syndromeTissue necrosisHemolysis/hematomas/gastrointestinal bleedingSuccinylcholineDigitalis intoxicationFluoride intoxication
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Hyperkalemia
Etiology Transcellular shifts
β-adrenergic blockersExerciseHyperosmolalityInsulin deficiencyMalignant hyperthermiaHyperkalemic periodic paralysis
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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
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Hyperkalemia
Etiology Hyporeninemic hypoaldosteronism
Urinary tract obstructionSickle cell diseaseKidney transplantLupus nephritis
Renal tubular diseasePseudohypoaldosteronism type IPseudohypoaldosteronism type IIUrinary tract obstructionSickle cell diseaseKidney transplant
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Hyperkalemia
Etiology Medications
Angiotensin-converting enzyme inhibitorsAngiotensin II blockersPotassium-sparing diureticsCalcineurin inhibitorsNonsteroidal anti-inflammatory drugsTrimethoprimHeparinDrug-induced potassium channel syndrome
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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
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Hyperkalemia
Clinical manifestationsAsystoleParesthesia, weakness, tingling
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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
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Hyperkalemia
TreatmentIntravenous CaNaHCO3
Insulin – must be given with glucose to prevent hypoglycemia
Nebulized salbutamol
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Hyperkalemia
TreatmentMeasures that remove K from the body
Loop diureticNa polysterene sulfonate (Kayexelate)Dialysis
• Hemodialysis• Peritoneal dialysis
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Hypokalemia
EtiologySpurious
High white blood cell countTranscellular shifts
AlkalemiaInsulinβ-adrenergic agonistsDrugs/toxins (theophylline, barium, toluene, cesium
chloride)Hypokalemic periodic paralysisThyrotoxic periodic paralysis
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Hypokalemia
EtiologyDecreased intake
Anorexia nervosa
Extrarenal lossesDiarrheaLaxative abuseSweatingSodium polystyrene sulfonate (Kayexelate) or clay
ingestion
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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)
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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
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Hypokalemia
EtiologyRenal losses
High urine chloride and normal blood pressure• Gitelman syndrome• Bartter syndrome• Autosomal dominant hypoparathyroidism• Loop and thiazide diuretics
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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
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Hypokalemia
EtiologyRenal losses
LicoriceLiddle syndrome
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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
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Hypokalemia
Clinical manifestationsMuscle weakness, crampsParalysisSlowing of GI motilityImpairment of bladder function → urinary
retentionPolyuria and polydipsiaStimulation of renal ammonia production Kidney damagePoor linear growth
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Hypokalemia
TreatmentIV potassium
Dose:0.5-1mEq/kg given x 1 hr, max dose in adults: 40 mEq
Oral potassium
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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
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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
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Magnesium metabolism
ExcretionRenal excretion
Principal regulator of Mg balanceNo defined hormonal regulatory system
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Hypomagnesemia
Etiology Gastrointestinal disorders
DiarrheaNasogastric suction or emesisInflammatory bowel diseaseCeliac diseaseCystic fibrosisIntestinal lymphangiectasiaSmall bowel resection or bypassPancreatitisProtein calorie malnutritionHypomagnesemia with secondary hypocalcemia
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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
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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
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Hypomagnesemia
Etiology Miscellaneous causes
Poor intakeHungry bone syndromeInsulin administrationPancreatitisIntrauterine growth retardationInfants of diabetic mothersExchange transfusion
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Hypomagnesemia
Clinical manifestationsUsually occurs only at Mg levels <0.7 mg/dLTetany, (+)Chvostek and Trosseau signs,
seizuresRicketsHypokalemia
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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
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Hypermagnesemia
Almost always secondary to excessive intake
Unusual except in neonates born to mothers receiving IV Mg for pre-eclampsia or eclampsia
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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
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Hypermagnesemia
Etiology Conditions predisposing to hypermagnesemia
Chronic renal failureFamilial hypocalciuric hypercalcemiaDiabetic ketoacidosisLithium ingestionMilk alkali syndromeTumor lysis syndrome
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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
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Hypermagnesemia
Clinical manifestationsHypotension, flushingECG changes
Prolonged P-R, QRS and Q-T intervals
Severe hypermagnesemia (>15 mg/dL) → complete heart block and cardiac arrest
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Hypermagnesemia
TreatmentIV hydration and loop diureticsDialysisExchange transfusionIn acute emergencies:
100 mg/kg of IV Ca gluconate (transiently effective)
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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
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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
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Phosphorus metabolism
ExcretionKidney – regulates phophorus balanceApproximately 85% of filtered load is resorbedPTH – decreases resorption of phosphate,
increasing urinary phosphate
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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
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Phosphorus metabolism
Excretion Phosphatonin
Inhibits renal resorption of phosphorus → phosphaturia and hypophosphatemia
Inhibits synthesis of calcitriol by decreasing 1α-hydroxylase activity
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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
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Hypophosphatemia
EtiologyTranscellular shifts
Glucose infusionInsulinRefeedingTotal parenteral nutritionRespiratory alkalosisTumor growthBone marrow transplantationHungry bone syndrome
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Hypophosphatemia
EtiologyDecreased intake
NutritionalPremature infantsLow phosphorus formulaAntacids and other phosphate binders
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Hypophosphatemia
EtiologyRenal losses
HyperparathyroidismParathyroid hormone-related peptideX-linked hypophosphatemic ricketsTumor-induced osteomalaciaAutosomal dominant hypophosphatemic ricketsFanconi syndrome Dent diseaseHypophosphatemic rickets with hypercalciuria
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Hypophosphatemia
Etiology Renal losses
Hypophosphatemia due to mutations in the sodium-phosphate cotransporter
Volume expansion and intravenous fluidsMetabolic acidosisDiureticsGlycosuriaGlucocorticoidsKidney transplantation
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Hypophosphatemia
EtiologyMultifactorial
Vitamin D deficiencyVitamin D-dependent rickets type IVitamin D-dependent rickets type 2AlcoholismSepsisDialysis
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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
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Hypophosphatemia
Clinical manifestationsRhabdomyolysisCardiac dysfunctionNeurologic symptoms
TremorsParesthesiaAtaxiaSeizuresDeliriumComa
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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
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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
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Hyperphosphatemia
EtiologyTranscellular shifts
Tumor lysis syndromeRhadomyolysisAcute hemolysisDiabetic ketoacidosis and lactic acidosis
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Hyperphosphatemia
EtiologyIncrease intake
Enemas and laxativesCow’s milk in infantsTreatment of hypophosphatemiaVitamin D intoxication
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Hyperphosphatemia
EtiologyDecreased excretion
Renal failureHypoparathyroidism or pseudohypoparathyroidismAcromegalyHyperthyroidismTumoral calcinosis with hyperphosphatemia
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Clinical manifestations
Principal clinical consequences:HypocalcemiaSystemic calcification
HypocalcemiaDue to tissue deposition of Ca-P saltInhibition of 1,25-dihydroxyvitamin D productionDecreased bone resorption
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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
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Hyperphosphatemia
TreatmentMild hyperphosphatemia in a patient with
reasonable renal function resolves spontaneouslyDietary phosphorus restrictionIntravenous fluids
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Hyperphosphatemia
TreatmentMore significant hyperphosphatemia
Add oral phosphorus binder
Dialysis If unresponsive to conservative management or if
renal insufficiency is supervening
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Fluid therapy
Degree of dehydrationMild (<5% in an infant; <3% in an older child or
adult)Normal or increased pulseDecreased urine outputThirstyNormal physical activity
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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
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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
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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
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Fluid therapy
Limitations to ORTShockIleusIntussusceptionCarbohydrate intoleranceSevere emesisHigh stool output (>10ml/kg/hr)
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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
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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
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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
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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