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Electrolyte Electrolyte Disorders Disorders Resident Rounds Resident Rounds Aric Storck Aric Storck February 26, 2004 February 26, 2004

Electrolyte Disorders Resident Rounds Aric Storck February 26, 2004

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Electrolyte Electrolyte DisordersDisorders

Resident RoundsResident Rounds

Aric StorckAric Storck

February 26, 2004February 26, 2004

Case 1Case 1 75 yo woman75 yo woman

orthostatic presyncope x 2 daysorthostatic presyncope x 2 days diarrhea x 1 weekdiarrhea x 1 week drinking 2-3 litres of tea a daydrinking 2-3 litres of tea a day

PMHxPMHx HTNHTN

MedsMeds HCTZ 25 mg po odHCTZ 25 mg po od

O/EO/E JVP ASAJVP ASA significant orthostatic drop in BPsignificant orthostatic drop in BP

lablab Na 128Na 128 K 3.1K 3.1 Cr 125Cr 125

HyponatremiaHyponatremiaClinical SSxClinical SSx

Severity depends Severity depends on absolute value on absolute value ANDAND rate of rate of decreasedecrease

Source: Yeates K, et al. CMAJ 2004;170(3):365-9

SymptomsSymptoms

DeliriumDeliriumComa Coma

SeizuresSeizures

< 120< 120

WeaknessWeaknessLethargyLethargy

RestlessnessRestlessnessConfusionConfusion

125 - 120125 - 120

ThirstThirstAnorexia, N + VAnorexia, N + VMuscle crampsMuscle cramps

130 - 125130 - 125

Decreased tasteDecreased taste135 - 130135 - 130

SymptomsSymptomsSerum NaSerum Na++ (mEq/L) (mEq/L)

Approach to Approach to hyponatremiahyponatremia

Hypo-osmolar Iso-osmolar Hyper-osmolar

Hyponatremia

•Normal ECF osmolality

•Increased serum solids, lipids (nephrotic syndrome) , protein (multiple myeloma)

•Glucose / mannitol

•Draws H2O into ECF

•Vast majority

Hypo-osmolar Hypo-osmolar hyponatremiahyponatremia

Non-hypovolemicHypovolemic

GI Losses Renal Losses Skin Losses

SIADH Edematous States•Vommitting•diarrhea•bleeding•obstruction

•Diuretics•hypoaldo•salt-wasting neph

•Burns•GPP/erythroderma

CNS DiseasePulmonary Drugs

CHFnephrotic Syndcirrhosis

Slide courtesy of Adam Oster

Hypovolemic Hypovolemic HyponatremiaHyponatremia

Loss Na > Loss H2OLoss Na > Loss H2O

ADH released (low ECF)ADH released (low ECF) increases tubular reabsorption of H2Oincreases tubular reabsorption of H2O low urine volumelow urine volume

Renin released (low renal perfusion)Renin released (low renal perfusion) kidneys retain sodiumkidneys retain sodium urine sodium low (<20 mmol/L)urine sodium low (<20 mmol/L)

What caused our patient’s What caused our patient’s hyponatremia?hyponatremia? GI lossesGI losses HCTZ (impairs excretion of free HCTZ (impairs excretion of free

water)water) as ECF decreases kidney exchanges as ECF decreases kidney exchanges

K for Na to maintain volume - thus K for Na to maintain volume - thus low Klow K

How will you treat our patientHow will you treat our patient d/c HCTZd/c HCTZ oral rehydration saltsoral rehydration salts IV NS + KCl until no further postural IV NS + KCl until no further postural

dropdrop oral sodium and Koral sodium and K recheck lytes in a few daysrecheck lytes in a few days

Case 2Case 2

58 yo man58 yo man small cell lung small cell lung

cancercancer confusion & confusion &

lethargy x 2 dayslethargy x 2 days

No MedsNo Meds

O/EO/E JVP 3cmJVP 3cm MMMMMM no ascites / no no ascites / no

edemaedema no sign of no sign of

hypothyroidism or hypothyroidism or hypoadrenalismhypoadrenalism

lablab

Na 108Na 108 K 3.9K 3.9 Cr 44Cr 44 urine Na 44urine Na 44

Euvolemic HyponatremiaEuvolemic HyponatremiaDDxDDx

SIADHSIADH hypothyroidismhypothyroidism adrenal insufficiencyadrenal insufficiency psychogenic polydipsiapsychogenic polydipsia

SIADHSIADH

DiagnosisDiagnosis

clinically euvolemicclinically euvolemic normal renal functionnormal renal function normal thyroid (TSH)normal thyroid (TSH) normal adrenal (cortisol stim test)normal adrenal (cortisol stim test) no medications known to cause SIADH-no medications known to cause SIADH-

like syndromelike syndrome

SIADHSIADHcausescauses

Source: Yeates K, et al. CMAJ 2004;170(3):365-9

SIADH - TreatmentSIADH - Treatment acuteacute

hypertonic salinehypertonic saline goal to increase Na by ~5 over 12 hours or until goal to increase Na by ~5 over 12 hours or until

asymptomaticasymptomatic

fluid restrictionfluid restriction 750-1500 ml/d750-1500 ml/d goal to increase Na by ~5 over 12 hoursgoal to increase Na by ~5 over 12 hours

chronicchronic fluid restrictionfluid restriction Li (inhibits renal effects of ADH)Li (inhibits renal effects of ADH) demeclocycline 600 mg po od demeclocycline 600 mg po od

What happens if you use What happens if you use normal saline?normal saline?

More water retained than NaMore water retained than Na

worsening hyponatremiaworsening hyponatremia

How do you calculate How do you calculate amount of fluid amount of fluid

needed?needed?

Source: Adrogue H, et al. NEJM 2000: 342(1)1581--1589.

Sample calculationSample calculation

Change [Na] per litre 3% HTS = Change [Na] per litre 3% HTS =

(513-108) / (0.6x60 +1) (513-108) / (0.6x60 +1)

=10.8 mmol=10.8 mmol

thus 0.46 litres (5/10.8) over 12 hoursthus 0.46 litres (5/10.8) over 12 hours

==38ml/h x 12 hours38ml/h x 12 hours

Case 3Case 3

45 year old woman45 year old woman alcoholic, HCV, end stage hepatic alcoholic, HCV, end stage hepatic

diseasedisease gross ascites and peripheral edemagross ascites and peripheral edema Na 125Na 125

Hypervolemic Hypervolemic hyponatremiahyponatremia

Increased ECFIncreased ECF CHFCHF cirrhosis / ascitescirrhosis / ascites nephrotic syndromenephrotic syndrome

low effective circulating volumelow effective circulating volume body retains Na and H20body retains Na and H20 low urine Na (<20)low urine Na (<20)

TreatmentTreatment Na and free water restrictionNa and free water restriction

Source: Yeates K, et al. CMAJ 2004;170(3):365-9

PseudohyponatremiaPseudohyponatremia

= falsely low Na+ due to:= falsely low Na+ due to: high serum protein concentrationhigh serum protein concentration high serum lipidshigh serum lipids

was an issue w/ flame photometry but not was an issue w/ flame photometry but not w/ potentiometric measurment techniquesw/ potentiometric measurment techniques

Slide courtesy of Moritz Haager

Redistributive Redistributive HyponatremiaHyponatremia

= dilutional picture due to presence = dilutional picture due to presence of excess osmotically active of excess osmotically active substances drawing water out of substances drawing water out of cells into extracellular spacecells into extracellular space Hyperglycemia (e.g. DKA)Hyperglycemia (e.g. DKA)

Correction = ~3mmol NaCorrection = ~3mmol Na++ decrease for decrease for every 10 mmol increase in glucoseevery 10 mmol increase in glucose

MannitolMannitol

Slide courtesy of Moritz Haager

Case 4Case 4 Your med student saw the pt and Your med student saw the pt and

w/o discussing with you ordered a 1 w/o discussing with you ordered a 1 L bolus of NS X 2 and then 200 cc/hL bolus of NS X 2 and then 200 cc/h

The pts NaThe pts Na+ + corrects to 138 by next corrects to 138 by next AMAM

Pt is sent home asymptomatic 36 hrs Pt is sent home asymptomatic 36 hrs after admissionafter admission

Comes back 3 days later unable to Comes back 3 days later unable to stand, confused, with slurred speechstand, confused, with slurred speech

What’s going on?What’s going on?

Slide courtesy of Moritz Haager

CPMCPM central pontine myelinolysiscentral pontine myelinolysis

PathophysiologyPathophysiology Acute non-inflammatory demyelination in basis Acute non-inflammatory demyelination in basis

pontis and other CNS sites (in ~10%)pontis and other CNS sites (in ~10%) Mechanism unknown; felt to occur due to rapid Mechanism unknown; felt to occur due to rapid

changes in cell volumechanges in cell volume Actual incidence is unknownActual incidence is unknown Risk factorsRisk factors

NaNa++ <120 mEq/L for > 48 hrs <120 mEq/L for > 48 hrs Aggressive IV resuscitation w/ hypertonic salineAggressive IV resuscitation w/ hypertonic saline

Most cases occurred with rates of correction Most cases occurred with rates of correction >> 12 12 mmol/L /24 hrsmmol/L /24 hrs

Hypernatremia during treatmentHypernatremia during treatment

Slide courtesy of Moritz Haager

CPMCPM central pontine myelinolysiscentral pontine myelinolysis

Clinical FeaturesClinical Features Usually neurologic deterioration 48-72 Usually neurologic deterioration 48-72

hrs after rapid Nahrs after rapid Na++ correction correction Confusion, horizontal gaze paralysis, Confusion, horizontal gaze paralysis,

spastic quadriplegia, pseudobulbar palsy, spastic quadriplegia, pseudobulbar palsy, encephalopathy – coma, locked-in encephalopathy – coma, locked-in syndromesyndrome

DxDx MRIMRI

TxTx supportivesupportive

Slide courtesy of Moritz Haager

TreatmentTreatmentsummarysummary

Hypovolemic hyponatremiaHypovolemic hyponatremia Correct with NS (0.9%) which is mildly hypertonic Correct with NS (0.9%) which is mildly hypertonic

compared to pts serumcompared to pts serum

Euvolemic hyponatremia:Euvolemic hyponatremia: Restrict free water intakeRestrict free water intake Identify underlying causeIdentify underlying cause SIADH:SIADH:

Giving normal saline will worsen condition due to free Giving normal saline will worsen condition due to free water retentionwater retention

Can Tx with lithium and demeclocycline Can Tx with lithium and demeclocycline inhibit action inhibit action of ADHof ADH

Hypervolemic hyponatremia:Hypervolemic hyponatremia: Restrict free water intakeRestrict free water intake +/- diuretics +/- diuretics may worsen due to further Na+ loss may worsen due to further Na+ loss dialysis if large amount of fluid needs to be taken dialysis if large amount of fluid needs to be taken

offoffSlide courtesy of M Haager

Hyponatremia

“Dry” Normovolemic(excess total body

water but no edema)

Fluid overloaded(excess water >excess Na+)

Source of Sodium loss?

Renal:-Diuretics-Adrenal insufficiency-Salt-wasting nephritis-Bicarbonate loss -RTA -metabolic alkalosis -ketonuria-Osmotic diuresis -glucose -mannitol

Extra-renal losses-GI losses-Third spacing

Urine Na+ >20 mmol/L

Urine Na+ <10 mmol/L

Normal Saline

SIADHDrugs•Glucocorticoid deficiency•Hypothyroidism•Pain / emotion

•Nephrotic Syndrome•Cirrhosis•CHF

Acute / ChronicRenal Failure

Urine Na+ >20 mmol/L

Urine Na+

<10 mmol/LUrine Na+ >20 mmol/L

Water restrictionSlide courtesy of M Haager

Case 5Case 5

93 year old man from nursing home93 year old man from nursing home dementeddemented not eating wellnot eating well less perky than usual - in ER to be less perky than usual - in ER to be

“checked out”“checked out” O/EO/E

JVP down, dry mouthJVP down, dry mouth 97 16 87/53 99% 37.397 16 87/53 99% 37.3

Na = 157Na = 157

HypernatremiaHypervolemic•Iatrogenic (NaHCO3)•Cushing’s syndrome•Hyperaldosteronism

•Tx•Na restriction•Diuretics•H2O

Non-hypervolemic

Increased urine concentration•Dehydration•Tx: H2O

No increased urine concentrationDiabetes Insipidus

Give DDAVP

No response=nephrogenic DI

Tx: H2O +/- thiazides

Good response=central DITx: DDAVP

HypernatremiaHypernatremia

SymptomsSymptoms anorexiaanorexia N/VN/V fatiguefatigue irritableirritable

SignsSigns lethargylethargy stuporstupor comacoma muscle twitchingmuscle twitching hyperreflexiahyperreflexia spasticityspasticity tremortremor ataxiaataxia focal neurological focal neurological

signssigns

Causes of Causes of HypernatremiaHypernatremia

Reduced H2O intakeReduced H2O intake disorders of thirstdisorders of thirst can’t get H20can’t get H20

Increased H2O lossIncreased H2O loss GIGI

V&DV&D NGNG 3rd spacing3rd spacing

renalrenal DIDI osmotic diuresisosmotic diuresis post-obstructive diuresispost-obstructive diuresis

dermaldermal burnsburns perspirationperspiration

Gain in NaGain in Na exogenous Na intakeexogenous Na intake

NaClNaCl NaHCO3NaHCO3 hypertonic NShypertonic NS salt water drowningsalt water drowning

increased Na increased Na reabsorptionreabsorption

hyperaldosteronismhyperaldosteronism cushing’s diseasecushing’s disease exogenous exogenous

corticosteroidscorticosteroids congenital adrenal congenital adrenal

hyperplasiahyperplasia

Causes of DICauses of DI

CentralCentral idiopathicidiopathic head traumahead trauma cerebral hemorrhagecerebral hemorrhage suprasellar infectionsuprasellar infection granulomatous granulomatous

disordersdisorders

Systemic diseasesSystemic diseases sickle cellsickle cell sarcoidosissarcoidosis amyloidosisamyloidosis

NephrogenicNephrogenic congenital renal congenital renal

disordersdisorders obstructive uropathyobstructive uropathy polycystic diseasepolycystic disease

drugsdrugs amphotericin Bamphotericin B phenytoinphenytoin LiLi aminoglycosidesaminoglycosides methoxyfluranemethoxyflurane

Management of Management of hypernatremiahypernatremia

HypovolemicHypovolemic goal: restore goal: restore

volume deficitsvolume deficits 0.9% NS0.9% NS

EuvolemicEuvolemic DIDI

oral fluidsoral fluids hypotonic saline hypotonic saline

(0.45%)(0.45%) vasopressinvasopressin

HypervolemicHypervolemic increase renal increase renal

sodium excretion > sodium excretion > H20H20

diuretics +/- diuretics +/- hypotonic salinehypotonic saline

may need dialysismay need dialysis

Calculation of water Calculation of water deficitdeficit

Water deficit = Water deficit =

Weight (kg) x Weight (kg) x

( Normal [Na] / Measured [Na] - 1 )( Normal [Na] / Measured [Na] - 1 )

Case 6Case 6

53 year old man53 year old man DM 1, chronic renal DM 1, chronic renal

failurefailure presents via EMS presents via EMS

from homefrom home Wife tells you that Wife tells you that

he has had N/V/D he has had N/V/D for the last 4 days for the last 4 days with decreased po with decreased po intake.intake.

O/EO/E 140, 89/59, 26, 140, 89/59, 26,

94%, 37.394%, 37.3 JVP down, dry MMJVP down, dry MM Slightly tender Slightly tender

abdomenabdomen

What would you What would you like to order?like to order?

lablab

CBCCBC Hb 146Hb 146 WBC 35WBC 35

neutrophils 30neutrophils 30 0.3 bands0.3 bands

Platelets 223Platelets 223

LytesLytes Na 133Na 133 K 7.4K 7.4 HCO3 4HCO3 4 Cl 97Cl 97 Cr 223Cr 223 glucose 43glucose 43

Case 6Case 6ECGECG

HyperkalemiaHyperkalemiaClinical FeaturesClinical Features

CardiacCardiac 2/3 degree heart 2/3 degree heart

blockblock wide complex wide complex

tachycardiastachycardias VFVF asystoleasystole

ECG progressionECG progression peaked T wavespeaked T waves loss of P wavesloss of P waves prolonged PR prolonged PR

intervalinterval widening of QRSwidening of QRS sine wave patternsine wave pattern ventricular ventricular

fibrillationfibrillation asystoleasystole

HyperkalemiaHyperkalemiaNeurological SSxNeurological SSx

Non-specificNon-specific muscle crampsmuscle cramps weaknessweakness paralysisparalysis paresthesiasparesthesias tetanytetany focal neurological deficitsfocal neurological deficits

PotassiumPotassiuma precisely controlled cationa precisely controlled cation

Mostly intracellularMostly intracellular

Precise transcellular Precise transcellular gradients required for gradients required for neuronal transmission neuronal transmission and cardiac conductionand cardiac conduction

Also important in acid-Also important in acid-base balance and base balance and buffering.buffering. K+/H+ pumpK+/H+ pump

Extracellular K Extracellular K controlled by controlled by serum pHserum pH

change in pH of 0.1change in pH of 0.1 0.6mEq change in 0.6mEq change in

K+K+ aldosteronealdosterone insulin insulin catecholaminescatecholamines

Hyperkalemia Hyperkalemia MechanismsMechanisms

INCREASEDINTAKE

IMPAIREDEXCRETION

TRANSCELLULARSHIFT

CELLULARINJURY

RENALFAILURE

NON RENALFAILURE

Slide courtesy of A. Oster

Hyperkalemia - etiologyHyperkalemia - etiology pseudohyperkalempseudohyperkalem

iaia hemolysishemolysis

increased intakeincreased intake

impaired renal impaired renal excretionexcretion renal failurerenal failure hypoaldosteronismhypoaldosteronism K-sparing diureticsK-sparing diuretics

Transcellular shiftsTranscellular shifts acidosisacidosis insulin deficientinsulin deficient drugsdrugs

B-BlockersB-Blockers suxsux digitalisdigitalis

cellular injurycellular injury rhabdomyolysisrhabdomyolysis tumour lysis tumour lysis

syndromesyndrome crush/burncrush/burn

Management PrinciplesManagement Principles

Cardiac monitoringCardiac monitoring stabilize myocardiumstabilize myocardium shift K into cellsshift K into cells decrease GI absorptiondecrease GI absorption treat underlying causetreat underlying cause

Immediate Immediate ManagementManagement

CalciumCalcium mechanismmechanism antagonises K and stabilizes antagonises K and stabilizes

myocardiummyocardium indicationsindications

dysrhythmiadysrhythmia hypotensionhypotension ECG changesECG changes

onsetonset 0-5 minutes0-5 minutes

durationduration 20-40 minutes20-40 minutes

dosedose 5-30ml 10% calcium 5-30ml 10% calcium

gluconate IVgluconate IV

Slide courtesy of A. Oster

Immediate ManagementImmediate ManagementVentolinVentolin

MechanismMechanism shifts K into cellsshifts K into cells

onsetonset 15 minutes15 minutes

durationduration 2-4 hours2-4 hours

dosedose 5-10mg neb 5-10mg neb

repeat prnrepeat prn

Slide courtesy of A. Oster

Immediate Immediate ManagementManagementGlucose and InsulinGlucose and Insulin mechanismmechanism

shifts K into cellsshifts K into cells onsetonset

15 minutes15 minutes durationduration

4-6 hours4-6 hours dosedose

10-20 units of R10-20 units of R 1 amp D50W1 amp D50W (no D50W if hyperglycemic)(no D50W if hyperglycemic)

Immediate ManagementImmediate Managementbicarbonatebicarbonate

mechanismmechanism shifts K into cellsshifts K into cells only works if only works if

acidoticacidotic

onsetonset 15 minutes15 minutes

durationduration 2 hours2 hours

dosedose 1 amp (44 meq) IV 1 amp (44 meq) IV

push over 5 push over 5 minutesminutes

beware ifbeware if hypertonichypertonic hypernatremichypernatremic alkaloticalkalotic

Delayed TherapyDelayed TherapyExchange ResinsExchange Resins

kayelalate (polystyrene sulfonate)kayelalate (polystyrene sulfonate) mechanismmechanism

ion exchange resinion exchange resin removes K from bodyremoves K from body

onsetonset 1 hour1 hour

durationduration 1-3 hours1-3 hours

dosedose 1g binds 1mEq of K1g binds 1mEq of K oral or rectaloral or rectal 20g in 70% sorbitol po (Rosen)20g in 70% sorbitol po (Rosen) 30g pr retained for 30 minutes30g pr retained for 30 minutes

MechanismMechanism removes K from bloodremoves K from blood can remove 200-300 meqcan remove 200-300 meq

IndicationsIndications renal failurerenal failure unstable patient unresponsive to other unstable patient unresponsive to other

treatmenttreatment

Delayed TherapyDelayed Therapyhemodialysishemodialysis

Case 6Case 6K+ 7.4K+ 7.4

Slide courtesy of A. Oster

Case 6Case 6 K+6.2K+6.2

Slide courtesy of A. Oster

Case 6Case 6K+ 5.5K+ 5.5

Slide courtesy of A. Oster

Case 7Case 7

General surgery rotationGeneral surgery rotation 03:30 - you are awakened from a sound 03:30 - you are awakened from a sound

sleep by a nurse who tells you that Mr. sleep by a nurse who tells you that Mr. X’s potassium is only 3.0.X’s potassium is only 3.0.

Do you care?Do you care? Why do you care?Why do you care? What are you going to do about it?What are you going to do about it?

HypokalemiaHypokalemiaSpectrum of SymptomsSpectrum of Symptoms

AsymptomaticAsymptomatic K 3-3.5K 3-3.5

NeuromuscularNeuromuscular K usually < 2.5K usually < 2.5

lethargylethargy confusionconfusion fasciculationsfasciculations weaknessweakness decreased DTRsdecreased DTRs paralysis (K<2)paralysis (K<2)

CardiovascularCardiovascular usually no symptoms usually no symptoms

in patients without in patients without heart diseaseheart disease

palpitationspalpitations ectopyectopy dysrhythmiasdysrhythmias 1 - 2 degree HB1 - 2 degree HB atrial fibrillationatrial fibrillation ventricular fibrillationventricular fibrillation

GIGI impairs intestinal smooth muscleimpairs intestinal smooth muscle N/VN/V paralytic ileusparalytic ileus

RenalRenal polyuriapolyuria polydipsiapolydipsia

ApproachApproach

DECREASEDINTAKE

TRANSCELLULARSHIFT

INCREASEDLOSSES

GI RENAL

Slide courtesy A. Oster

HypokalemiaHypokalemia Decreased IntakeDecreased Intake

decreased dietary decreased dietary intakeintake

decreased absorptiondecreased absorption

Transcellular ShiftsTranscellular Shifts alkalosisalkalosis insulininsulin B2 agonistsB2 agonists

eg: ventolin - lowers K ~ eg: ventolin - lowers K ~ 0.4 mmol/L x 4 hours0.4 mmol/L x 4 hours

coffeecoffee

Increased LossIncreased Loss renalrenal

hyperaldosteronismhyperaldosteronism renal tubular defectsrenal tubular defects mineralocorticoidsmineralocorticoids glucocorticoids (alter glucocorticoids (alter

GFR)GFR) +++diuretics+++diuretics drugsdrugs

GIGI N/V/DN/V/D

SkinSkin burnsburns perspirationperspiration

His ECG...His ECG...

Slide courtesy A. Oster

HypokalemiaHypokalemia

ECG findingsECG findings small or absent T small or absent T

waveswaves prominent U wavesprominent U waves ST segment ST segment

depressiondepression

Slide courtesy A. Oster

How will you treat him?How will you treat him?

Potassium is an intracellular ionPotassium is an intracellular ion 1 mEq/L decrease in serum K may equal 1 mEq/L decrease in serum K may equal

up to 370 mEq total body deficitup to 370 mEq total body deficit

~50% of administered K excreted in ~50% of administered K excreted in urine - therefore several days to correct urine - therefore several days to correct deficitdeficit

OralOral K-Dur (20mmol/tab)K-Dur (20mmol/tab) KCl KCl

elixir(20mmol/15mlelixir(20mmol/15ml))

K-Phos(4.4mmol/K-Phos(4.4mmol/ml)ml)

useful if useful if hypophosphatemichypophosphatemic

K-Citrate K-Citrate (0.9mmol/ml)(0.9mmol/ml)

useful in RTAuseful in RTA

IVIV KCl KCl

(10/20/40mmol/100cc(10/20/40mmol/100cc))

10-20mEq/h10-20mEq/h >20mEq/h requires >20mEq/h requires

central line and central line and cardiac monitorcardiac monitor

S/E’sS/E’s transient transient

hyperkalemiahyperkalemia burning at IV siteburning at IV site

HypomagnesemiaHypomagnesemia

Magnesium required in Na-K ATP-Magnesium required in Na-K ATP-asease hypomag often co-exists with hypomag often co-exists with

hypokalemiahypokalemia Mg must be corrected along with KMg must be corrected along with K

Cofactor in PTH metabolismCofactor in PTH metabolism often coexists with low Caoften coexists with low Ca

HypomagnesemiaHypomagnesemia

Diuretic useDiuretic use thiazide and loop thiazide and loop

diureticsdiuretics decrease Mg ~25-50%decrease Mg ~25-50%

EtOH abuseEtOH abuse 30-80%30-80%

Renal lossesRenal losses GI lossesGI losses

V/DV/D short bowelshort bowel pancreatitispancreatitis

Endocrine disordersEndocrine disorders DMDM hyperaldosteronismhyperaldosteronism hyperthyroidismhyperthyroidism

PregnancyPregnancy DrugsDrugs

aminoglycosides, B-aminoglycosides, B-agonists, cyclosporine, agonists, cyclosporine, pentamidine, pentamidine, theophyllinetheophylline

Congenital disordersCongenital disorders

HypomagnesemiaHypomagnesemiaclinical featuresclinical features

Non-specificNon-specific

NeuromuscularNeuromuscular weaknessweakness tremortremor hyperreflexiahyperreflexia Chvostek/Chvostek/

TrousseauTrousseau seizuresseizures comacoma

CardiacCardiac supraventricular supraventricular

dysrhythmiasdysrhythmias ventricular ventricular

dysrhythmiasdysrhythmias

ECGECG non-specificnon-specific

long PR/QRS/QTlong PR/QRS/QT ST-T abnormalitiesST-T abnormalities flattened Tflattened T UwaveUwave

HypomagnesemiaHypomagnesemiaManagementManagement

Treat if Treat if Magnesium < 1.2 Magnesium < 1.2

mg/dlmg/dl or, symptomaticor, symptomatic

IVIV Magnesium sulfateMagnesium sulfate

1g = 8.3mEq 1g = 8.3mEq magnesiummagnesium

OralOral Magnesium Magnesium

RougierRougier multiple othersmultiple others cause diarrheacause diarrhea

HypermagnesemiaHypermagnesemia

Very rare …. especially in ERVery rare …. especially in ER

kidneys can excrete >6g / daykidneys can excrete >6g / day

generallygenerally iatrogeniciatrogenic renally insufficientrenally insufficient

HypermagnesemiaHypermagnesemiaClinical FeaturesClinical Features

>3 mg/dl>3 mg/dl N/VN/V weaknessweakness

>4mg/dl>4mg/dl hyporeflexiahyporeflexia loss of DTR’sloss of DTR’s

>5-6mg/dl>5-6mg/dl hypotensionhypotension ECG changesECG changes

QRS widenineQRS widenine QT/PR prolongationQT/PR prolongation conduction conduction

abnormalitiesabnormalities

>9mg/dl>9mg/dl repiratory depressionrepiratory depression comacoma complete heart blockcomplete heart block

HypermagnesemiaHypermagnesemiaTreatmentTreatment

Mild symptoms & Mild symptoms & normal renal normal renal functionfunction ObserveObserve

Moderate Moderate symptomssymptoms IV normal saline & IV normal saline &

furosemidefurosemide watch Kwatch K

Severe symptomsSevere symptoms IV CalciumIV Calcium

antagonizes antagonizes membrane effects of membrane effects of MgMg

reverses respiratory reverses respiratory depression/dysrhytmdepression/dysrhytmias, etcias, etc

DialysisDialysis refractory symptomsrefractory symptoms renal failurerenal failure

Case 8Case 8

55 woman with metastatic breast cancer55 woman with metastatic breast cancer Increasing weakness and confusion x 24 hoursIncreasing weakness and confusion x 24 hours Ataxic this morningAtaxic this morning HeadacheHeadache ThirstyThirsty

VitalsVitals 110 18 100/80 92% 37.0110 18 100/80 92% 37.0

O/E O/E alert but disoriented and confused, GCS 15 alert but disoriented and confused, GCS 15 otherwise unremarkableotherwise unremarkable

Case 8Case 8

LabsLabs CBC CBC

normalnormal electrolyteselectrolytes

normalnormal Calcium 4.5Calcium 4.5 Albumin 30Albumin 30

How do you How do you correct [Ca] for correct [Ca] for albumin?albumin? Add 0.2 for every Add 0.2 for every

10 units albumin is 10 units albumin is below 40below 40

ie: 47ie: 47

Case 8Case 8ECGECG

Characteristic changesCharacteristic changes Short QTShort QT prolongation or PRprolongation or PR QRS wideningQRS widening

Occasionally seeOccasionally see sinus bradycardiasinus bradycardia BBBBBB AV blockAV block cardiac arrestcardiac arrest

Calcium MetabolismCalcium Metabolism 1200g Ca in body1200g Ca in body

99% in bone99% in bone 1% in serum1% in serum

60% protein bound60% protein bound 40% free40% free

parathyroid hormoneparathyroid hormone bone resorptionbone resorption renal Ca reabsorptionrenal Ca reabsorption renal conversion renal conversion

vitamin D to 1,25DHCC)vitamin D to 1,25DHCC) renal phosphate renal phosphate

excretionexcretion

calcitonincalcitonin decreases osteoclastic decreases osteoclastic

activity and enhances activity and enhances skeletal depositionskeletal deposition

HypercalcemiaHypercalcemiaEtiologyEtiology

Most (~90%)Most (~90%) Primary Primary

hyperparathyroidishyperparathyroidismm

MalignanciesMalignancies

OthersOthers medicationsmedications

thiazidesthiazides LiLi Vitamin D toxicityVitamin D toxicity Ca ingestionCa ingestion

granulomatous granulomatous diseasedisease

other endocrine other endocrine disordersdisorders

HypercalcemiaHypercalcemiaClinical FeaturesClinical Features

NeurologicNeurologic fatigue, weaknessfatigue, weakness confusion, lethargyconfusion, lethargy ataxiaataxia comacoma hypotoniahypotonia

CVCV hypertensionhypertension sinus bradycardiasinus bradycardia AV blockAV block ECG abnormalities (short ECG abnormalities (short

QT, BBB)QT, BBB)

RenalRenal polyuria, polydipsiapolyuria, polydipsia pre-renal azotemiapre-renal azotemia nephrolithiasisnephrolithiasis nephrocalcinosisnephrocalcinosis

GIGI N/VN/V pancreatitispancreatitis constipationconstipation ileusileus

HypercalcemiaHypercalcemiaTreatment PrinciplesTreatment Principles

restore intravascular restore intravascular volumevolume Serum calcium will Serum calcium will

decrease with decrease with hydrationhydration

increase renal increase renal calcium eliminationcalcium elimination hydrationhydration fursosemide 40-80mg fursosemide 40-80mg

iv q6-8hiv q6-8h AVOID thiazidesAVOID thiazides

reduction of reduction of osteoclastic activityosteoclastic activity Etidronate/PamidronateEtidronate/Pamidronate PlicamycinPlicamycin calcitonin 4U/kg sc calcitonin 4U/kg sc

q12hq12h

treatment of primary treatment of primary disorderdisorder parathyroidectomyparathyroidectomy treat malignancytreat malignancy withdrawal of medswithdrawal of meds

Case 9Case 9

52 year old woman52 year old woman HTNHTN

B-Blocker, thiazideB-Blocker, thiazide diarrhea x 1 weekdiarrhea x 1 week tingling around mouth and in fingerstingling around mouth and in fingers cramps in arms and legscramps in arms and legs

When taking her blood When taking her blood pressurepressure

Source: Meininger et al. NEJM 2000:343 (25): 1855

Case 9Case 9ECGECG

HypocalcemiaHypocalcemiaEtiologyEtiology

PTHPTH PTH insufficiencyPTH insufficiency

primaryprimary secondarysecondary

neck surgeryneck surgery Mg disordersMg disorders pancreatitispancreatitis drugsdrugs

PTHPTH Vitamin D insufficiencyVitamin D insufficiency

malnutritionmalnutrition malabsorptionmalabsorption hepatic/renal diseasehepatic/renal disease

Calcium chelationCalcium chelation hyperphosphatemiahyperphosphatemia citratecitrate alkalosisalkalosis fluoride poisoningfluoride poisoning

HypocalcemiaHypocalcemiaClinical FeaturesClinical Features

NeuromuscularNeuromuscular confusion/anxietyconfusion/anxiety paresthesiasparesthesias weaknessweakness spasmsspasms tetanytetany

Chvostek/TrousseauChvostek/Trousseau hyperreflexiahyperreflexia seizuresseizures

CVCV bradycardiabradycardia decreased decreased

contractilitycontractility hypotensionhypotension CHFCHF

ECGECG QT prolongationQT prolongation

HypocalcemiaHypocalcemia

ManagementManagement IV calcium chlorideIV calcium chloride

10ml amps of 10%10ml amps of 10% 360mg elemental 360mg elemental

CaCa

IV calcium IV calcium gluconategluconate

10ml amps of 10%10ml amps of 10% 93mg elemental 93mg elemental

CaCa

recommended initial recommended initial adult dose is 100-adult dose is 100-300mg300mg pediatric dose is 0.5-pediatric dose is 0.5-

1.0mg/kg of Ca gluconate1.0mg/kg of Ca gluconate lasts 2hourslasts 2hours consider an infusionconsider an infusion

S/E’sS/E’s HTNHTN N/VN/V bradycardia/HBbradycardia/HB tissue necrosis if interstitialtissue necrosis if interstitial

the endthe end