1. The Diagnosis and Therapy for CommonThe Diagnosis and Therapy for Common
Fluid and Electrolyte ImbalancesFluid and Electrolyte Imbalances

3. Volume DepletionVolume Depletion

4. Volume DepletionVolume Depletion
 Loss of isotonic fluid from the extracellular fluidLoss of isotonic fluid from the extracellular fluid
at a rate exceeding net intake.at a rate exceeding net intake.
 Can occur through:Can occur through:
 gastrointestinal tract (vomiting, diarrhea, bleeding)gastrointestinal tract (vomiting, diarrhea, bleeding)
 skin (sweat, burns)skin (sweat, burns)
 lungs (bronchorrhea, pleural effusion, evaporation)lungs (bronchorrhea, pleural effusion, evaporation)
 urine (diuretics, osmotic diuresis, salt wastingurine (diuretics, osmotic diuresis, salt wasting
nephropathies, andnephropathies, and
hypoaldosteronism)hypoaldosteronism)
 acute sequestration in the body in a "third space" thatacute sequestration in the body in a "third space" that
is not in equilibrium with the extracellular fluid (GIis not in equilibrium with the extracellular fluid (GI

5. History and Symptoms of VolumeHistory and Symptoms of Volume
DepletionDepletion
HistoryHistory
vomiting, diarrhea, diuretic use, or polyuriavomiting, diarrhea, diuretic use, or polyuria
(may identify the source of fluid loss)(may identify the source of fluid loss)
SymptomsSymptoms
 lethargy, easy fatiguability, thirst, muscle cramps, andlethargy, easy fatiguability, thirst, muscle cramps, and
postural dizziness (volume depletion)postural dizziness (volume depletion)
 Generalized weakness, irritability, maybe twitching,Generalized weakness, irritability, maybe twitching,
seizures (if also severely hyponatremic)seizures (if also severely hyponatremic)
 muscle weakness, polyuria, polydipsia, confusionmuscle weakness, polyuria, polydipsia, confusion
(from concomitant electrolyte and acid-base disorders)(from concomitant electrolyte and acid-base disorders)

6. PEx findings in HypovolemiaPEx findings in Hypovolemia
 BP, HR, and JVDBP, HR, and JVD
 BP drops in upright positionBP drops in upright position
 ‘‘orthostatic hypotension’ – after two to five minutes of quietorthostatic hypotension’ – after two to five minutes of quiet
standing, one or more of the following is present:standing, one or more of the following is present:
 At least a 20 mmHg fall in systolic pressureAt least a 20 mmHg fall in systolic pressure
 At least a 10 mmHg fall in diastolic pressureAt least a 10 mmHg fall in diastolic pressure
 Symptoms of cerebral hypoperfusion (dizziness)Symptoms of cerebral hypoperfusion (dizziness)
 HR increase by more than 10-20 bpmHR increase by more than 10-20 bpm
 Decreased JVDDecreased JVD
 SkinSkin
 Increased pigmentation, decreased turgor, dry axillaIncreased pigmentation, decreased turgor, dry axilla
 Mucous membranesMucous membranes
 Tongue and oral mucosa dryTongue and oral mucosa dry

7. Laboratory StudiesLaboratory Studies
 UrineUrine
 urinalysis can be normalurinalysis can be normal
 sodium concentration < 25 meq/L and may be as low as 1sodium concentration < 25 meq/L and may be as low as 1
meq/Lmeq/L
 chloride concentration lowchloride concentration low
 osmolality >450 mosmol/kgosmolality >450 mosmol/kg
 specific gravity > 1.015specific gravity > 1.015
 oliguriaoliguria
 BloodBlood
 Elevated serum sodium = dehydrationElevated serum sodium = dehydration
 If [Na] WNL then pt not dehyrated but hypovolemicIf [Na] WNL then pt not dehyrated but hypovolemic
 Elevated BUN/plasma creatinine levelElevated BUN/plasma creatinine level
 HCT (relative polycythemia) and plasma albumin levelHCT (relative polycythemia) and plasma albumin level
increasesincreases

8. Replacement TherapyReplacement Therapy
 IVF BolusIVF Bolus
 5cc/kg over 20 minutes5cc/kg over 20 minutes
 Usually rounded to 500cc for adults and extended toUsually rounded to 500cc for adults and extended to
30 minutes30 minutes
 Normal Saline (isotonic) bestNormal Saline (isotonic) best
 Ringers lactate (has bicarb) if >4 liters will be givenRingers lactate (has bicarb) if >4 liters will be given
 This prevents development of metabolic acidosisThis prevents development of metabolic acidosis
 IV CathetersIV Catheters
 18 gauge best18 gauge best

9. Replacement Therapy PrecautionsReplacement Therapy Precautions
 Excess NS can cause pulmonary edema in someExcess NS can cause pulmonary edema in some
pts:pts:
 Elderly pts with hx of CHFElderly pts with hx of CHF
 Pts with known severe VHDPts with known severe VHD
 Renal failure ptsRenal failure pts
 In these pts use 3cc/kg over 30 minutes forIn these pts use 3cc/kg over 30 minutes for
boluses and listen to lungs often, measure SaO2boluses and listen to lungs often, measure SaO2
if possibleif possible

10. ……
 When have you given enough IVF?When have you given enough IVF?
 Recheck orthostatic pressuresRecheck orthostatic pressures
 If still orthostatic?If still orthostatic?
 Rebolus, repeat cycle until asymptomatic, makingRebolus, repeat cycle until asymptomatic, making
urine, mucous membranes moisturine, mucous membranes moist

11. Electrolyte abnormalities andElectrolyte abnormalities and
ECGECG

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Effects of ElectrolytesEffects of Electrolytes
 Potassium (K+)Potassium (K+)
 Prevents shortened action potentialPrevents shortened action potential
 Allows for organized fast heart ratesAllows for organized fast heart rates
 Protects from excitabilityProtects from excitability
 Slows heart in vagal responsesSlows heart in vagal responses
136

13. HypokalemiaHypokalemia

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HypokalemiaHypokalemia
 Serum level below 3.5Serum level below 3.5––5.0 mEq/L5.0 mEq/L
 Caused by vomiting, diarrhea, diuretics, gastricCaused by vomiting, diarrhea, diuretics, gastric
suctioningsuctioning
 HypomagnesemiaHypomagnesemia
 Muscle weakness, polyuriaMuscle weakness, polyuria

15. Hypokalemia: Signs andHypokalemia: Signs and
symptomssymptoms
 Generalized muscle weaknessGeneralized muscle weakness
 Paralytic ileusParalytic ileus
 Cardiac arrhythmiasCardiac arrhythmias
 Atrial tachycardiaAtrial tachycardia
 AV dissociationAV dissociation
 EKG changesEKG changes
 Flat/inverted T wavesFlat/inverted T waves
 ST segment depressionST segment depression
 U wavesU waves
 Ascending paralysis and impaired respiratory functionAscending paralysis and impaired respiratory function
(K<2)(K<2)

16. Hypokalemia: CausesHypokalemia: Causes
 Renal lossRenal loss
 Primary hyperaldosteronism, hypothermia, genetic syndromesPrimary hyperaldosteronism, hypothermia, genetic syndromes
(i.e. Liddle’s), type I and II RTA, drugs (I.e. amphotericin,(i.e. Liddle’s), type I and II RTA, drugs (I.e. amphotericin,
foscarnet)foscarnet)
 GI lossGI loss
 Vomiting, diarrhea ( enteric fistula, malabsorption, jejunoilealVomiting, diarrhea ( enteric fistula, malabsorption, jejunoileal
bypass)bypass)
 Transcellular shiftTranscellular shift
Alkalosis, beta agonists, caffeine, insulin, thryrotoxicosis,Alkalosis, beta agonists, caffeine, insulin, thryrotoxicosis,
hypokalemic periodic paralysishypokalemic periodic paralysis

17. Page, 12-Lead ECG for
Acute and Critical Care
Providers
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HypokalemiaHypokalemia
 ECG ChangesECG Changes
 ST segment depressionST segment depression
 T waves flatten or join U wavesT waves flatten or join U waves
 U waves get larger than TU waves get larger than T
 QT interval appears to lengthenQT interval appears to lengthen
 PR interval increasesPR interval increases

18. Hypokalemia:
Flat T with K~3
ST depression with prominent T
(actually U) and prolonged QT
when K<2.5-3

19. Page, 12-Lead ECG for Acute and
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HypokalemiaHypokalemia
 Potassium normalPotassium normal
 U waves overtake TU waves overtake T
137

20. Hypokalemia: treatmentHypokalemia: treatment
 Determine the causeDetermine the cause
 When to correct?When to correct?
 How much?How much?
 0.5-1 mEq/kg over 1 hour0.5-1 mEq/kg over 1 hour
 What to use?What to use?
 KCl po or IVKCl po or IV

21. Hypokalemia : treatmentHypokalemia : treatment
 Mild loss, K+ between 3.0 and 3.5 meq/LMild loss, K+ between 3.0 and 3.5 meq/L
 usually produces no symptomsusually produces no symptoms
 replace lost K+ and treat underlying disorder (such asreplace lost K+ and treat underlying disorder (such as
vomiting, diarrhea)vomiting, diarrhea)
 treatment is usually started with 10 to 20 meq oftreatment is usually started with 10 to 20 meq of
potassium chloridepotassium chloride given two to four times per day (20 to 80given two to four times per day (20 to 80
meq per day), depending on the severity of hypokalemia andmeq per day), depending on the severity of hypokalemia and
on whether hypokalemia developed acutely or is chronicon whether hypokalemia developed acutely or is chronic
 sequential monitoring of plasma K+ is essential to determinesequential monitoring of plasma K+ is essential to determine
continued requirements, with frequency of monitoringcontinued requirements, with frequency of monitoring
dependent on the severity of hypokalemiadependent on the severity of hypokalemia

22. HyperkalemiaHyperkalemia

23. HyperkalemiaHyperkalemia
 Definition: K>6 mEq/LDefinition: K>6 mEq/L
 SymptomsSymptoms
 EKG changes: peaked T waves, prolonged PR interval,EKG changes: peaked T waves, prolonged PR interval,
widened QRS, V-fibwidened QRS, V-fib
 Muscle weakness/paresthesiasMuscle weakness/paresthesias

24. Page, 12-Lead ECG for
Acute and Critical Care
Providers
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HyperkalemiaHyperkalemia
 Serum levels above normal rangeSerum levels above normal range
 Most common cause is renal failureMost common cause is renal failure
 Sinus node can quit at 7.5 mEq/LSinus node can quit at 7.5 mEq/L
 VF or asystole at 10VF or asystole at 10––12 mEq/L12 mEq/L

26. Hyperkalemia- CausesHyperkalemia- Causes
 Decreased ExcretionDecreased Excretion
 Renal failureRenal failure
 11°° adrenal disease - ↓aldosterone leads to ↑K+ by decreased excretionadrenal disease - ↓aldosterone leads to ↑K+ by decreased excretion
 Acquired Addison disease- metabolic acidosis, salt wasting and hyponatremia Acquired Addison disease- metabolic acidosis, salt wasting and hyponatremia
 21-hydroxylase deficiency 3β-hydroxysteroid dehydrogenase deficiency21-hydroxylase deficiency 3β-hydroxysteroid dehydrogenase deficiency
 Kidney damage- deficient Renin- Hyporeninemic hypoaldosteronism –Kidney damage- deficient Renin- Hyporeninemic hypoaldosteronism –
 Met acidosis/Na+ ok Met acidosis/Na+ ok
 Urinary tract obstruction Urinary tract obstruction
 Sickle cell disease Sickle cell disease
 Kidney transplant Kidney transplant
 Lupus nephritisLupus nephritis
 Renal tubular disease- Renal tubular disease-
 Pseudohypoaldosteronism type I- ↑Aldosterone- Met acidosis, Salt wasting (↓Na)Pseudohypoaldosteronism type I- ↑Aldosterone- Met acidosis, Salt wasting (↓Na)
 Acquired tubular dysfxn (Sickle cell, lupus)- impaired H+ and K+ excretionAcquired tubular dysfxn (Sickle cell, lupus)- impaired H+ and K+ excretion
 Medications Medications
 Angiotensin-converting enzyme inhibitors/ Angiotensin II blockers Angiotensin-converting enzyme inhibitors/ Angiotensin II blockers
 Potassium-sparing diuretics Potassium-sparing diuretics
 Nonsteroidal anti-inflammatory drugs Nonsteroidal anti-inflammatory drugs
 Trimethoprim Trimethoprim
 HeparinHeparin

27. Hyperkalemia: CausesHyperkalemia: Causes
 Impaired excretionImpaired excretion
 Renal failure, mineralocorticoid deficiency, drugs, type IV RTA,Renal failure, mineralocorticoid deficiency, drugs, type IV RTA,
 IatrogenicIatrogenic
 Transcellular shiftTranscellular shift
 Acidosis, beta blockers, digitalis overdose, somatostatinAcidosis, beta blockers, digitalis overdose, somatostatin
 OtherOther
 Tumor lysisTumor lysis
 rhabdomyolysisrhabdomyolysis

28. Hyperkalemia:
T wave in hyperkalemia is typically
tall and narrow,
but does not have to be tall
(may be just narrow and
peaked pulling ST segment).
Tall T means > 2 big boxes in
the precordial leads or >1
small box in limb leads,
or T wave taller than QRS.

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HyperkalemiaHyperkalemia –– ECGECG
 Tall T waves with aTall T waves with a
narrow basenarrow base
 QRS widensQRS widens
 Broad S waves in VBroad S waves in V
leadsleads
 Left axis deviationLeft axis deviation

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HyperkalemiaHyperkalemia –– ECGECG
 ST segment disappearsST segment disappears
 ““T wave grows, PT wave grows, P
wave goes”wave goes”
 Sine waves in severeSine waves in severe
casescases
138

32. Hyperkalemia: TreatmentHyperkalemia: Treatment
 Calcium gluconateCalcium gluconate
 100mg/kg IV peripheral or central100mg/kg IV peripheral or central
 Insulin/glucoseInsulin/glucose
 Insulin 0.1units/kg IVInsulin 0.1units/kg IV
 Glucose 2ml/kg D10 or D25Glucose 2ml/kg D10 or D25
 The most effective way to quickly lower K!!!The most effective way to quickly lower K!!!
 Sodium bicarbonateSodium bicarbonate
 1-2mEq/kg1-2mEq/kg
 HemodialysisHemodialysis
 KayexalateKayexalate
 1gram/kg po or PR1gram/kg po or PR

33. Ca, Mg, PhosCa, Mg, Phos

34. HypocalcemiaHypocalcemia
 Symptoms appear when iCa<0.7Symptoms appear when iCa<0.7
 Symptoms include:Symptoms include:
 Neuromuscular irritability (tetany)Neuromuscular irritability (tetany)
 Paresthesias of hands/feetParesthesias of hands/feet
 Circumoral numbnessCircumoral numbness
 Laryngospasm or bronchospasmLaryngospasm or bronchospasm
 Anxious/irritable/depressed/confusedAnxious/irritable/depressed/confused
 HypotensionHypotension
 RicketsRickets
 EKG changes include:EKG changes include:
 Prolonged QTProlonged QT
 Non-specific ST-Twave changesNon-specific ST-Twave changes

35. Hypocalcemia: Causes andHypocalcemia: Causes and
DiagnosisDiagnosis
 Determine the causeDetermine the cause
 PTH levelPTH level
 Vitamin D levels (25OHD3 and 1,25OHD3)Vitamin D levels (25OHD3 and 1,25OHD3)
 24 hour urine calcium24 hour urine calcium
 HypoparathyroidismHypoparathyroidism
 Irradiation, surgery, hypomagnesemia, DiGeorge, polyglandularIrradiation, surgery, hypomagnesemia, DiGeorge, polyglandular
autoimmune syndrome, storage disease, HIVautoimmune syndrome, storage disease, HIV
 Vitamin D deficiencyVitamin D deficiency
 Malnutrition, malabsorption, hepatobiliary disease, low sun exposureMalnutrition, malabsorption, hepatobiliary disease, low sun exposure

36. Hypocalcemia: CausesHypocalcemia: Causes
 Calcium chelation/precipitationCalcium chelation/precipitation
 Tumor lysis, rhabdomyolysis, citrate, foscarnetTumor lysis, rhabdomyolysis, citrate, foscarnet
 MultifactorialMultifactorial
 Sepsis, pancreatitis, burnsSepsis, pancreatitis, burns

37. Page, 12-Lead ECG for Acute and
Critical Care Providers
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CalciumCalcium
 Hypercalcemia: ShortHypercalcemia: Short
QT intervalQT interval
 Hypocalcemia:Hypocalcemia:
Prolonged QT intervalProlonged QT interval

38. Hypocalcemia:
Long QT that is due to a long ST segment, which is different from long
QT due to congenital long QT syndrome, drugs, or hypokalemia. T wave
is not wide, there is no T wave abnormality.

39. Hypercalcemia: short QTc <390 ms. No significant ST or T wave abnormality

40. Hypocalcemia: TreatmentHypocalcemia: Treatment
 Calcium gluconateCalcium gluconate
 25-100mg/kg IV25-100mg/kg IV
 Calcium chlorideCalcium chloride
 10-20 mg/kg IV10-20 mg/kg IV
 Must be given centrallyMust be given centrally
 Treat low MagnesiumTreat low Magnesium
 Treat underlying diseaseTreat underlying disease
 When should you avoid treating hypocalcemia?When should you avoid treating hypocalcemia?
 Tumor lysis syndrome (unless patient is symptomatic)Tumor lysis syndrome (unless patient is symptomatic)

41. Differential Diagnosis ofDifferential Diagnosis of
HypercalcemiaHypercalcemia
 HyperparathyroidismHyperparathyroidism
 >90% of ambulatory cases>90% of ambulatory cases
 Primary hyperparathyroidism is most often due to aPrimary hyperparathyroidism is most often due to a
parathyroid adenomaparathyroid adenoma
 CancerCancer
 solid tumors and leukemiassolid tumors and leukemias
 Local resorption of bone induced by metastases (mediated byLocal resorption of bone induced by metastases (mediated by
local release of cytokines such as tumor necrosis factor andlocal release of cytokines such as tumor necrosis factor and
interleukin-1) or the production of humoral osteoclastinterleukin-1) or the production of humoral osteoclast
activators, particularly PTH-related proteinactivators, particularly PTH-related protein
 HyperthyroidismHyperthyroidism
 15-20% of patients can develop mild hypercalcemia15-20% of patients can develop mild hypercalcemia

42. Evaluation of HypercalcemiaEvaluation of Hypercalcemia
 Correct diagnosis in 95% of cases by evaluating:Correct diagnosis in 95% of cases by evaluating:
 HistoryHistory
 PExPEx
 CXR (r/o malignancy or sarcoidosis) andCXR (r/o malignancy or sarcoidosis) and
 Lab data: PTH (serum intact), PTHRP related peptide, serumLab data: PTH (serum intact), PTHRP related peptide, serum
protein electrophoresis (r/o multiple myeloma), creatinineprotein electrophoresis (r/o multiple myeloma), creatinine
 Primary hyperparathyroidism is often associated withPrimary hyperparathyroidism is often associated with
borderline or mild hypercalcemia with the serumborderline or mild hypercalcemia with the serum
calcium concentration often being below 11 mg/dLcalcium concentration often being below 11 mg/dL
(2.75 mmol/L)(2.75 mmol/L)

43. Treatment Goals in HypercalcemiaTreatment Goals in Hypercalcemia
 Lowering serum Ca++ levelLowering serum Ca++ level
 Saline administration to produce volume expansionSaline administration to produce volume expansion
and increase urinary Ca++ excretion (oraland increase urinary Ca++ excretion (oral
hydration + high salt diet)hydration + high salt diet)
 Concurrent tx with biphosphonates) +/- calcitoninConcurrent tx with biphosphonates) +/- calcitonin
(decrease bone resorption)(decrease bone resorption)
 Oral phosphate 250-500 mg QID (decreaseOral phosphate 250-500 mg QID (decrease
absorption in gut)absorption in gut)
 Correcting or decreasing underlying diseaseCorrecting or decreasing underlying disease
 HyperparathyroidismHyperparathyroidism

44. Page, 12-Lead ECG for
Acute and Critical Care
Providers
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The QT IntervalThe QT Interval
 Measured from the start of the QRS complex toMeasured from the start of the QRS complex to
the end of the T wavethe end of the T wave
 Measures the total ventricular activity:Measures the total ventricular activity:
“refractory time”“refractory time”
 QTc is corrected for rateQTc is corrected for rate

45. Page, 12-Lead ECG for Acute and Critical Care Providers
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The QT/QTc TableThe QT/QTc Table
139

46. hypomagnesaemiahypomagnesaemia

47. Hypomagnesemia: SymptomsHypomagnesemia: Symptoms
 Symptoms:Symptoms:
 Refractory hypocalcemiaRefractory hypocalcemia
 DiarrheaDiarrhea
 Ventricular arrhythmiasVentricular arrhythmias
 Muscle weakness, tremors, tetanyMuscle weakness, tremors, tetany
 CausesCauses
 Decreased intake or malabsorptionDecreased intake or malabsorption
 Decreased renal reabsorption (familial, diuretics, amphotericin,Decreased renal reabsorption (familial, diuretics, amphotericin,
bartters’s, gitelman’sbartters’s, gitelman’s
 Transcellular shift (hyperaldosteronism, pancreatitis, respiratoryTranscellular shift (hyperaldosteronism, pancreatitis, respiratory
alkalosis, catecholamines)alkalosis, catecholamines)

48. HypomagnesemiaHypomagnesemia
 TreatmentTreatment
 Magnesium sulfate 25-50 mg/kgMagnesium sulfate 25-50 mg/kg
 Replace potassium and calciumReplace potassium and calcium
 Oral supplementationOral supplementation

49. hypophosphatemiahypophosphatemia

50. HypophosphatemiaHypophosphatemia
 SymptomsSymptoms
 Muscle weakness, paralysisMuscle weakness, paralysis
 Respiratory depressionRespiratory depression
 Leukocyte and platelet dysfunctionLeukocyte and platelet dysfunction
 HemolysisHemolysis
 CausesCauses
 Decreased intake or malabsorptionDecreased intake or malabsorption
 Decreased renal reabsorption (hyperparathyroidism, fanconi’s,Decreased renal reabsorption (hyperparathyroidism, fanconi’s,
vitamin D deficiency, medications)vitamin D deficiency, medications)
 Transcellular shift (catecholamines, theophylline, respiratory alkalosis)Transcellular shift (catecholamines, theophylline, respiratory alkalosis)

51. Hypophosphatemia: TreatmentHypophosphatemia: Treatment
 Determine underlying cause (many times it isDetermine underlying cause (many times it is
multifactorial)multifactorial)
 Replace using:Replace using:
 NaPhosNaPhos
 Kphos 0.08-0.32 mmol/kg over 4-6 hoursKphos 0.08-0.32 mmol/kg over 4-6 hours

52. Clinical Manifestations ofClinical Manifestations of
HyponatremiaHyponatremia
Plasma Na+ 125-130 meq/LPlasma Na+ 125-130 meq/L
nausea and malaisenausea and malaise
Plasma Na+ <115-120 meq/LPlasma Na+ <115-120 meq/L
headache, lethargy, and seizures, coma andheadache, lethargy, and seizures, coma and
respiratory arrestrespiratory arrest

53. HyponatremiaHyponatremia
Causes:Causes:
 Increased Free waterIncreased Free water
 Increased sodium lossIncreased sodium loss
 Decreased salt intakeDecreased salt intake
Most common cause in children is extra-renal GIMost common cause in children is extra-renal GI
losses like diarrhea.losses like diarrhea.

54. Hyponatremia- typesHyponatremia- types
Hypovolemic HyponatremiaHypovolemic Hyponatremia
 Renal Loss: Urine Na > 20 mEq/LRenal Loss: Urine Na > 20 mEq/L
 Diuretic UseDiuretic Use
 Urinary tract obstruction and/or urinary tract infectionUrinary tract obstruction and/or urinary tract infection
 Autosomal recessive polycystic kidney diseaseAutosomal recessive polycystic kidney disease
 Tubulointerstitial nephritisTubulointerstitial nephritis
 Cerebral salt wastingCerebral salt wasting
 Lack of aldosterone effect (serum ↑ K+, ↓ Na+) / Deficient aldosterone (CAH)Lack of aldosterone effect (serum ↑ K+, ↓ Na+) / Deficient aldosterone (CAH)
 Pseudohypoaldosteronism type IPseudohypoaldosteronism type I
 Extra-renal Loss: Urine Na < 20 mEq/LExtra-renal Loss: Urine Na < 20 mEq/L
 Gastrointestinal (emesis, diarrhea)Gastrointestinal (emesis, diarrhea)
 Skin (CF, sweating, or burns)Skin (CF, sweating, or burns)
 Third space losses (pancreatitis, burns, effusions, ascites)Third space losses (pancreatitis, burns, effusions, ascites)
Hypervolemic HyponatremiaHypervolemic Hyponatremia
 Hypoalbuminemia due to gastrointestinal disease/ Nephrotic syndrome/ CirrhosisHypoalbuminemia due to gastrointestinal disease/ Nephrotic syndrome/ Cirrhosis
 Congestive heart failureCongestive heart failure
 Renal failureRenal failure
 Capillary leak due to sepsisCapillary leak due to sepsis

55. Hyponatremia- typesHyponatremia- types
Euvolemic HyponatremiaEuvolemic Hyponatremia
 Syndrome of inappropriate antidiuretic hormoneSyndrome of inappropriate antidiuretic hormone
 Usually ADH secreted due to ↓ vol ↑ osm.Usually ADH secreted due to ↓ vol ↑ osm.
 Can be released due to pain, nausea, vomiting, morphineCan be released due to pain, nausea, vomiting, morphine
 Glucocorticoid deficiencyGlucocorticoid deficiency
 HypothyroidismHypothyroidism
 Water intoxication – diluted formula, swimming,Water intoxication – diluted formula, swimming,
 Water enemasWater enemas
PseudohyponatremiaPseudohyponatremia
 HyperglycemiaHyperglycemia
 MannitolMannitol

56. Hyponatremia- DiagnosisHyponatremia- Diagnosis
Cause of Hyponatremia by Urine Specimen
Cause Urine Na Urine
Volume
Osmolarity Specific
Gravity
Hypovolemic renal Na loss ↑ >20mEq/L ↑ ↓ ↓
Hypovolemic extrarenal loss ↓ ↓ ↑ ↑
Hypervolemic HypoNa- CHF,edema ↓<20mEq/L ↓ ↑ ↑
Hypervolemic HypoNa- Renal Failure varies ↓ varies varies
SIADH-like syndrome ↑ >20mEq/L ↓ ↑ ↑
History can tell you most of the story
Laboratory studies: Urine Na and Osm compared to Serum Na and Osm
Calculate Osmolar Gap: Difference between measured & calculated osm
Gap is high with mannitol, glycerol, lactate, methanol, EtOH,
ethylene glycol
Calc Osm= 2( Serum Na + serum K+) + (BUN/2.8) + (glucose/18)

57. Hyponatremia- TreatmentHyponatremia- Treatment
Correction: in chronic hypo Na- correct by no more than 8-12mEq/L each dayCorrection: in chronic hypo Na- correct by no more than 8-12mEq/L each day
 In acute hypoNa: brain doesn’t have time to adapt.In acute hypoNa: brain doesn’t have time to adapt.
 Active CNS symptoms often improve after receiving 4–6mL/kg of 3% sodium chloride.Active CNS symptoms often improve after receiving 4–6mL/kg of 3% sodium chloride.
Correction by TYPE of hyponatremiaCorrection by TYPE of hyponatremia
 HypovolemicHypovolemic hyponatremiahyponatremia: replace the Na and H20 deficit: replace the Na and H20 deficit
 restore the intravascular volume with isotonic saline- suppresses ADH which permits excretionrestore the intravascular volume with isotonic saline- suppresses ADH which permits excretion
of the excess water.of the excess water.
 monitoring of the sodium to avoid overly rapid correctionmonitoring of the sodium to avoid overly rapid correction
 HypervolemicHypervolemic hyponatremia:hyponatremia: excess H20 and Na.excess H20 and Na.
 Don’t give Na -causes volume overload and edema.Don’t give Na -causes volume overload and edema.
 Restrict water and sodium (2/3 maintenance)Restrict water and sodium (2/3 maintenance)
 DiureticsDiuretics
 Infusion of albumin if low albuminInfusion of albumin if low albumin
 CHF: improving cardiac output improves diuresis.CHF: improving cardiac output improves diuresis.
 Renal failure: fluid restriction or dialysis.Renal failure: fluid restriction or dialysis.
 IsovolemicIsovolemic hyponatremiahyponatremia: excess of water and a mild Na deficit.: excess of water and a mild Na deficit.
 Eliminate the excess water.Eliminate the excess water.
 For acute water intoxication, give 3% Na to reverse cerebral edema.For acute water intoxication, give 3% Na to reverse cerebral edema.
 For chronicFor chronic hyponatremiahyponatremia from poor solute intake, give appropriate formula, and eliminatefrom poor solute intake, give appropriate formula, and eliminate
excess waterexcess water

58. Hyponatremia- TreatmentHyponatremia- Treatment
IVF replacementIVF replacement
 3% NS: 513 mEq/L of Na3% NS: 513 mEq/L of Na
 1ml/kg of 3% Na increases serum Na by 1.6 mEq/L1ml/kg of 3% Na increases serum Na by 1.6 mEq/L
 NS: 154 mEq/ L of NaNS: 154 mEq/ L of Na
 ½ NS: 77 mEq/ L of Na½ NS: 77 mEq/ L of Na
 ¼ NS: 38.5 mEq/ L of Na¼ NS: 38.5 mEq/ L of Na
How much Na do you need to give?How much Na do you need to give?
 Maintenance needs: Sodium: 2–3mEq/kg/24hrMaintenance needs: Sodium: 2–3mEq/kg/24hr
 Deficit Replacement:Deficit Replacement:
 Estimate Water = % dehydration X patient's weightEstimate Water = % dehydration X patient's weight
 Calculated Na deficit from serumCalculated Na deficit from serum
 Serum Na Deficit= [0.6 x Wt(kg)] x [Desired Na- Actual Na]Serum Na Deficit= [0.6 x Wt(kg)] x [Desired Na- Actual Na]
 Ongoing Losses:Ongoing Losses:
 Diarrhea: Na content 55 mEq/LDiarrhea: Na content 55 mEq/L
 Gastric fluids: Na content 60mEq/LGastric fluids: Na content 60mEq/L
 Sweat: 5–40 mEq/L of NaSweat: 5–40 mEq/L of Na

59. Hyponatremia: ComplicationsHyponatremia: Complications
Physiology review: Hyponatremia= decreased plasma osmolarityPhysiology review: Hyponatremia= decreased plasma osmolarity
(except in extreme hyperglycemia)---Water flow from low solute(except in extreme hyperglycemia)---Water flow from low solute
(low osm) to high solute (high osm)---So water flow from(low osm) to high solute (high osm)---So water flow from
extracellular space into intracellular space ---Cells SWELL!extracellular space into intracellular space ---Cells SWELL!
Brain adapts to the decreased extracellular osmolality by decreasing itsBrain adapts to the decreased extracellular osmolality by decreasing its
internal osmolality. Initially, through loss of sodium, potassium,internal osmolality. Initially, through loss of sodium, potassium,
and chloride. Chronically there is loss of intracellular osmolesand chloride. Chronically there is loss of intracellular osmoles
such as amino acids.such as amino acids.
 Treatment complications: overly rapid correctionTreatment complications: overly rapid correction
 Central pontine myelinolysisCentral pontine myelinolysis
 Extrapontine myelinolysisExtrapontine myelinolysis
 Both = osmotic demyelination syndromeBoth = osmotic demyelination syndrome

60. HypernatremiaHypernatremia
Serum Na >145 mEq/L [deficit of (TBW) relative to Na]Serum Na >145 mEq/L [deficit of (TBW) relative to Na]
 Primarily hospital-acquired →in children who have restrictedPrimarily hospital-acquired →in children who have restricted
access to fluids.access to fluids.
 Incidence >1% in hospitalized patients.Incidence >1% in hospitalized patients.
CAUSES:CAUSES:
 Water deficitWater deficit
 Salt ExcessSalt Excess
 Water depletion exceeding sodium depletionWater depletion exceeding sodium depletion
Sodium is unique among electrolytes…
because water balance, not sodium balance, usually determines its concentration.

61. Hypernatremia: CausesHypernatremia: Causes
Water LossWater Loss
Water Loss/ DeficitWater Loss/ Deficit
 RenalRenal
 CentralCentral
 NephrogenicNephrogenic
 Insensible LossesInsensible Losses
 Fever/ Heat exhaustion/HeatstrokeFever/ Heat exhaustion/Heatstroke
 Respiratory IllnessRespiratory Illness
 Prematurity-large surface areaPrematurity-large surface area
 large evaporative water losseslarge evaporative water losses
 Phototherapy or radiant warmersPhototherapy or radiant warmers
 Inadequate IntakeInadequate Intake

62. Hypernatremia-CausesHypernatremia-Causes
Water and Sodium DeficitWater and Sodium Deficit
 Gastrointestinal losses Gastrointestinal losses
 Diarrhea Diarrhea
 Emesis/nasogastric suction Emesis/nasogastric suction
 Osmotic cathartics (lactulose)Osmotic cathartics (lactulose)
 Cutaneous losses Cutaneous losses
 Burns Burns
 Excessive sweatingExcessive sweating
 Renal losses Renal losses
 Osmotic diuretics (mannitol) Osmotic diuretics (mannitol)
 Diabetes mellitus Diabetes mellitus
 Chronic kidney disease (dysplasia and obstructive uropathy) Chronic kidney disease (dysplasia and obstructive uropathy)
 Polyuric phase of acute tubular necrosisPolyuric phase of acute tubular necrosis
 Postobstructive diuresisPostobstructive diuresis

63. Hypernatremia- CausesHypernatremia- Causes
Excessive SodiumExcessive Sodium
 Improperly mixed formula Improperly mixed formula
 Excess sodium bicarbonate Excess sodium bicarbonate
 Ingestion of seawater or sodiumIngestion of seawater or sodium
chloride chloride
 Intentional salt poisoningIntentional salt poisoning
 (child abuse) (child abuse)
 Intravenous hypertonic saline Intravenous hypertonic saline
 HyperaldosteronismHyperaldosteronism

64. Hypernatremia:Hypernatremia:
signs and symptomssigns and symptoms
Note ↓ skin turgor is a LATE signNote ↓ skin turgor is a LATE sign
(doughy)(doughy)
 Irritability or lethargyIrritability or lethargy
 Altered conscious levelAltered conscious level
 SeizuresSeizures
 Increased muscle toneIncreased muscle tone
 FeverFever
 RhabdomyolysisRhabdomyolysis
 OligouriaOligouria
Severe hypernatremic dehydrationSevere hypernatremic dehydration
induces brain shrinkageinduces brain shrinkage
 tears cerebral blood vesselstears cerebral blood vessels→→
cerebral hemorrhagecerebral hemorrhage
 venous sinus thrombosisvenous sinus thrombosis
 seizures, paralysis, andseizures, paralysis, and
encephalopathyencephalopathy
Brain cell volume canBrain cell volume can ↓↓10% to 15%10% to 15%
acutelyacutely
 Within 1 hour, the brainWithin 1 hour, the brain ↑↑
intracellular Na and K, amino acids,intracellular Na and K, amino acids,
& idiogenic osmoles& idiogenic osmoles
 Within 1 week, the brain regains 98%Within 1 week, the brain regains 98%
of its water content.of its water content.
In patients with prolonged hypernatremia, rapid rehydration with hypotonic fluids
may cause cerebral edema, which can lead to coma, convulsions, and death.

65. Categorizing hypernatremiaCategorizing hypernatremia

66. Hypernatremia: Work-upHypernatremia: Work-up Serum sodium, glucose, osmolality, BUN, and creatinine levels must be measured.Serum sodium, glucose, osmolality, BUN, and creatinine levels must be measured.
 Urine volume, urine osmolality and urine electrolyte levelsUrine volume, urine osmolality and urine electrolyte levels
 Assess renal concentrating abilityAssess renal concentrating ability
 Quantify the urinary free water lossesQuantify the urinary free water losses
 urine osm (<800 mmol/L) with serumurine osm (<800 mmol/L) with serum hypernatremiahypernatremia = renal= renal
concentrating defectconcentrating defect
 Urine tests of sodium concentration and osmolalityUrine tests of sodium concentration and osmolality
 Hypovolemic hypernatremiaHypovolemic hypernatremia
 Extrarenal losses show urine sodium levels of <20 mEq/LExtrarenal losses show urine sodium levels of <20 mEq/L
 Renal losses urine sodium values are >20 mEq/L.Renal losses urine sodium values are >20 mEq/L.
 In euvolemic hypernatremia, urine sodium data vary.In euvolemic hypernatremia, urine sodium data vary.
 In hypervolemic hypernatremia, the urine sodium level is >20 mEq/L.In hypervolemic hypernatremia, the urine sodium level is >20 mEq/L.
 Imaging studiesImaging studies
 In alert, severely hypernatremic patients: rule out a hypothalamic lesionIn alert, severely hypernatremic patients: rule out a hypothalamic lesion
 affecting the thirst center.affecting the thirst center.
 CT /MRI scans show intracranial pathologies.CT /MRI scans show intracranial pathologies.

67. Hypernatremia: TreatmentHypernatremia: Treatment
Correct fluid deficit firstCorrect fluid deficit first
Rapid correction can cause cerebral edema.Rapid correction can cause cerebral edema.
Dehydration should be corrected over 48-72 hours.Dehydration should be corrected over 48-72 hours.
The rate of sodium correction: 10-12 mEq/L in 24 hours.The rate of sodium correction: 10-12 mEq/L in 24 hours.
Calculation of body water deficit:Calculation of body water deficit:
In children, TBW is 60% of lean body weight. TBW = 0.6 X weight.In children, TBW is 60% of lean body weight. TBW = 0.6 X weight.
An exception is babies, with TBW around 80% of their body weight.An exception is babies, with TBW around 80% of their body weight.
1. Water deficit (L) = [(current Na1. Water deficit (L) = [(current Na mEq/LmEq/L ÷ 145÷ 145 mEq/LmEq/L) - 1] X 0.6 X Wt (kg)) - 1] X 0.6 X Wt (kg)
oror
2. Water deficit(L)= 4ml x Wt(kg) x (desired change in Na2. Water deficit(L)= 4ml x Wt(kg) x (desired change in Na mEq/LmEq/L))
 Example calculation: A child weighs 10 kg with Na= 160Example calculation: A child weighs 10 kg with Na= 160 mEq/LmEq/L..
 With first equation, water deficit (L) = [(160 mEq/L ÷ 145 mEq/L) - 1] X 0.6 X 10 = 0.62 L.With first equation, water deficit (L) = [(160 mEq/L ÷ 145 mEq/L) - 1] X 0.6 X 10 = 0.62 L.
 With second equation, water deficit (L)= 4ml x 10 kg x 15 mEq/L Na change = 600ml= 0.6 LWith second equation, water deficit (L)= 4ml x 10 kg x 15 mEq/L Na change = 600ml= 0.6 L

68. Cause Treatment*
A.Sodiumandwaterloss D5½NS
B.Primarywaterloss D5¼NS
C.Nephrogenicdiabetesinsipidus D2.51/8 NS (acutemanagement)
D.Centraldiabetesinsipidus Desmopressinacetate
E.Sodiumoverload D5W(mayneedDiureticsordialysis)
Hypernatremia treatmentHypernatremia treatment

69. Treatment of Hypernatremic Dehydration
RESTORE INTRAVASCULAR VOLUME
Normal saline: 20 mL/kg over 20 min
(Repeat until intravascular volume restored)
DETERMINE TIME FOR CORRECTION BASED ON INITIAL SODIUM
[Na]:145–157 mEq/L:24 hr
[Na]:158–170 mEq/L:48 hr
[Na]:171–183 mEq/L:72 hr
[Na]:184–196 mEq/L:84 hr
ADMINISTER FLUID AT CONSTANT RATE OVER TIME FOR CORRECTION
Typical fluid: D5 ½ normal saline (with 20 mEq/L KCl unless contraindicated)
Typical rate: 1.25–1.5 times maintenance
FOLLOW SERUM SODIUM CONCENTRATION EVERY 2-4 hrs
ADJUST FLUID BASED ON CLINICAL STATUS AND SERUM SODIUM
Signs of volume depletion: administer normal saline (20 mL/kg)
Sodium decreases too rapidly
Increase sodium concentration of IVF, or Decrease rate if IVF
Sodium decreases too slowly
Decrease sodium concentration of IVF, or Increase rate if IVF

70. ThanksThanks