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Electrolyte Disorders

Jai Radhakrishnan, MD

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Objectives

Diagnostic and therapeutic principles ofDisorders of osmolarity (Hypo/hypernatremia)PotassiumMagnesium

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Disorders of Osmolarity

Hyperosmolarity (Hypernatremia)

Hypoosmolarity (Hyponatremia)

Na Ξ OsmolalityFree Water Intake

Free Water Loss

P. Na

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Generation of Disorders of OsmolarityHypernatremia

If water intake is less than output

HyponatremiaIf free water intake is greater than output

Free Water Intake

Free Water Loss

P. Na

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Hyponatremia

Hypo-osmolar

Iso-osmolarlipid/protein

Hyper-osmolarOsmotically active subs

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Case

27 year old male alcoholic is admitted with altered mental status after a recent drinking spree.

P.E.: BP 100/70 HR=130 RR=40

Labs: 116|66|56 109

5.0|15 |2.8

A.G.=35 Ketones=neg

Measured Osm= 350

Calculated Osm=156

Urine= +++ oxalate crystals

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Hyperosmolar Hyponatremia: Osmolar Gap

Calculate:2Na + Glucose/18 + BUN/2.8

Measure:Freezing point depression (lab)

Gap: (Measured)-(Calculated) <10

Gap > 10 presence of an osmotic substance that is not Na, glucose or BUN

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Case: Hyperosmolar Hyponatremia

27 year old male alcoholic is admitted with altered mental status after a recent drinking spree.

P.E.: BP 100/70 HR=130 RR=40

Labs: 116|66|56 109

5.0|15 |2.8

A.G.=35 Ketones=neg

Measured Osm= 350

Calculated Osm=156

Urine= +++ oxalate crystals

Endogenous:AcetoneRenal failureLactate

Exogenous:MethanolEthylene GlycolEthanolGlycineMannitol

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Hypoosmolar Hyponatremia

Increased free water supplyDecreased free water excretion

Free Water Intake

Free Water Loss

P. Na

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Hyponatremia:1. Increased free water supply

Psychogenic polydipsia is the only situation where this mechanism is solely responsibleUosm low; <100mosm/L

Free Water Intake

Free Water Loss

P. Na

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"Drink at least eight glasses of water a day." Really? Is there scientific evidence for "8 × 8"?

Valtin H… Am J Physiol Regul Integr Comp Physiol 283: R993-R1004, 2002

12Sumit Kumar & Tomas Berl

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Hyponatremia-2. Impaired free water excretion by kidney

Too few nephronsrenal failure

Too much ADHVolume depletion

RealEffective (edema states)

EndocrineThyroidAdrenal

INAPPROPRIATE ADH

Free Water Intake

Free Water Loss

P. Na

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Evaluation of HyponatremiaIso/hyperosmolar states

Measure plasma osmolarity (calculate osmolar gap)Check Lipids/proteins

Psychogenic polydipsia?Urine Osm <100

Too few nephrons?Serum creatinine

Too much ADH?Volume depletion

Orthostatics etc., Urine Na+

Intravascular volume depl. (edematous states)Urine Na+, S. Uric acid

Thyroid/CortisolSIADH (by exclusion)

Chest, head, drugs.

Free Water Intake

Free Water Loss

P. Na

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Causes of SIADH

Tumours: bronchogenic carcinoma, lymphoma, pancreatic cancer, mesothelioma

Pulmonary: pneumonia, TB, lung abscess, COPDpneumothorax, HIV infection

CNS: head injury, meningitis, subduralhaematoma, subarachnoid hge, neurosurgery

Drugs: carbamazepine, chlorpropamide, cyclophosphamide, ‘ecstasy’, NSAID, tricyclic antidepressants, phenothiazines, SSRI

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Case

71 year old woman presented with fatigue and forgetfulness. PMHx: HTN on thiazides.

Physical exam: Systolic BP drop of 20mmHg

Plasma: 119|75| 4 UNa+=13

3.1|29|1.8 Uosm=422

Hyperosmolar?Psychogenic polydipsia?Too few nephrons?Too much ADH?

Volume depletionEdematous statesThyroid/CortisolSIADH (by exclusion)

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HyponatremiaClinical Effects

PNa+=139: Baseline

PNa+=119 in 2h

PNa+=122 (3.5 days)

PNa+= 99 (16 days)PNa+=140:

Day 5

320

340

360

380

400

420

440

460

Bra

in w

ater

g/1

00g

dry

wei

ght

139 139-119(2h)

140-122(3.5d)

139-99(16d)

Correction

18Sumit Kumar & Tomas Berl

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Clinical Course of Treated Hyponatremia

Arieff A.. NEJM 1986;314(24):1529-35

20Am J Med. 2006 Jan;119(1):71.e1-8

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Hyponatremia-Principles of Treatment

Treat vigorously if symptomatic/acute to reach a “safe” levelIf vigorous treatment planned do not increase PNa+ by >0.5meq/h.Use frequent monitoring of PNa+ to guide therapy.

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Treatment Modalities

All forms of hyponatremia will respond to water restriction.Primary polydipsiaRenal failure: DialysisTrue Volume depletion: Normal salineEffective volume depletion: treat cause, loop diuretics.Thyroid, cortisol: replacementSIADH

Asymptomatic/chronic: Water restrictSalt tablets, high protein dietFurosemide in divided dosesADH Antagonists

Acute/Mental status changeHypertonic saline until M.S. adequate (.5meq/hour)

Free Water Intake

Free Water Loss

P. Na

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Arginine Vasopressin

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Tolvaptan (SALT-1 & SALT-2)

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IV Conivaptan 40mg/d in Hypervolemic Hyponatremia

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Vasopressin v2-receptor blockade with tolvaptan in patients with chronic heart failure

Circulation. 2003 Jun 3;107(21):2690-6.

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Case

65 year old woman with no PMHx is admitted with unresponsiveness. Physical exam is normal.PNa+ = 115, Posm=240, Uosm=700, UNa+=70. Normal sugar/urea.

Hyperosmolar?Psychogenic polydipsia?Too few nephrons?Too much ADH?

Volume depletionEdematous statesThyroid/CortisolSIADH (by exclusion)

How would you treat this patient?

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Hypertonic saline-dose calculation

Current PNa+ = 115 Target PNa+ = 120Na+deficit = 5 meq/literTotal body Na+ deficit= 5 x total body water

= 5 x 0.5 x body wt (50kgs)= 125meq

Amount of 3% NaCl needed (Na=513meq/L) = 125/513= 240mlRate of infusion=0.5meq/hour=10 hours

=24ml/hour

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HYPERNATREMIA

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Case

60 year old male with ARDS/intubated/pressors/TPN

PNa= 150. Urine output 150ml/hr. Normal hemodynamics.

Uosm=504 UNa=40meq

Urine dip=2+ glucose

Serum glucose 400.

What is the cause of hypernatremia ?

How would you treat him?

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Pathogenesis of Hypernatremia

Decreased free water supplyWater loss

Osmotic diuresis, D.I.Osmotic diarrheaInsensible

Solute load

Free Water Intake

Free Water Loss

P. Na

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Workup of Hypernatremia

Why is the patient not drinking??Is there increased free water loss:

?PolyuriaUosm: if <250 – D.I.Uosm: if >300 – solute diuresis

? GI (osmotic diarrhea)Is the patient getting too much solute?

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Treatment of Hypernatremia

Provide free waterOral is optimalRate of correction <0.5meq/hourDose:

0.4 x body weight x [(PNa/140) – 1]

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Case

60 year old male with ARDS/intubated/pressors/TPN

PNa= 150. Urine output 150ml/hr. Normal hemodynamics.

Uosm=504 UNa=40meq

Urine dip=2+ glucose

Serum glucose 400.

What is the cause of hypernatremia ?

How would you treat him?

Why is the patient not drinking??Is there increased free water loss:

?PolyuriaUosm: if <250 – D.I.Uosm: if >300 – solute diuresis

? GI (osmotic diarrhea)Is the patient getting too much solute?

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Calculation of water deficitCalculate Amount of Water

0.4 x body weight x (PNa/140 – 1)0.4 x 50 x (150/140 – 1) = 1.4 litersInsensible losses= + 1 liter/24h

Total volume= 2.4 litersRate (0.5meq/hour)

For Na to go from 150->140=20 hoursPrescription: Rate of water repletion

= 2400/20=120ml/hr.

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Hyper- and Hypokalemia

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ICF ECF

Hyperkalemia- Etiology

Intake (never alone)

Shift (Acute)AcidosisInsulin lackTissue LysisBeta blockadeDigitalis o.d.Succinylcholine

Excretion (Chronic)Advanced renal failureHypoaldosteronismVolume depletion

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Hyperkalemia: Case50 year old male with NIDDM/ CRI has been prescribed a low Na

diet for HTN. He presents to the ER with marked weakness. Labs: 130|98|50 280

8.0 |17| 2.7

Is this pseudohyperkalemia ?What is causing the hyperkalemia?How would you treat ?

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Treatment of HyperkalemiaAntagonism of membrane action

Intravenous calciumShift

Insulin (Dextrose)NaHCO3ß-2 agonists

RemovalDiureticsCation exchange resinDialysis

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Hypokalemia- Etiology

Intake (never alone)

ShiftTreatment with insulinAlkalosisß-2 stimulationPeriodic paralysisTreatment of anemia

Increased ExcretionGIRenal

HyperaldosteronismDiuresisAmpho-BHypomagnesemia

ICF ECF

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Hypokalemia-Clinical Consequences

Cardiac arrhythmiasMuscle weaknessRhabdomyolysisRenal dysfunctionGlucose intolerance

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Hypokalemia-Treatment

Estimate of deficit is difficult~100-200 meq for 1 meq/liter

PO therapy usually adequateIV therapy if severe/symptomatic

Max conc. 40meq/literMax rate 20meq/hour Use in saline (not dextrose)

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Hypokalemia-case58 yr old cirrhotic is admitted with worsening ascitesMeds: Lasix 40mg bid, LactuloseEKG: Unifocal VPC’s, prominent U wavesAdmission labs: 125|87|32 80

2.2 |20|2.0How would you treat her hypokalemia ?

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Disorders of Magnesium

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Hypomagnesemia:Etiology

IntakeMalnutritionGI malabsorption

ShiftPancreatitisInsulin administrationPost-parathyroidectomy (hungry bone syndrome)

Excretion (Renal)Post-obstructive, Post ATNPost-renal transplantBartter’s/Gitelman’s syndromesDrugs: Diuretics, aminoglycosides, cisplatinum, amphotericinAlcohol (decreased intake contributing)

ICF ECF

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Hypomagnesemia:Clinical Effects

CardiovascularArrhythmia (prolonged QT)

MetabolicHypocalcemiaHypokalemia

NeurologicalTetanySeizures

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Hypomagnesemia: Treatment

Oral MgOMg-containing antacidsMilk of MagnesiaMg citrate, sulfate, lactate

Intravenous (avoid IM)BolusInfusion

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Hypermagnesemia:Etiology

INTAKEMg-containing antacids/laxativesIV magnesium replacement

SHIFTDKATissue injury

EXCRETION

ICF ECF

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Hypermagnesemia:Clinical Consequences

>4mEq/LInhibition of neuromuscular transmissionInhibition of cardiac conduction

> 7 mEq/LLethargyPR, QT and QRS prolongation

>10mEq/LRespiratory failure/voluntary muscle paralysisCHB/Asystole

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HypermagnesemiaTreatment

IV calciumDialysis

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END