Electrolyte Disorders

Jai Radhakrishnan, MD

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Objectives
„ Diagnostic and therapeutic principles of
„ Disorders of osmolarity (Hypo/hypernatremia)
„ Potassium
„ Magnesium

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 Disorders of Osmolarity

Na Ξ Osmolality
Free Water Intake
„ Hyperosmolarity (Hypernatremia)
„ Hypoosmolarity (Hyponatremia)

P. Na

Free Water Loss

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Generation of Disorders of Osmolarity
„ Hypernatremia
„ If water intake is less than
Free Water Intake output

„ Hyponatremia
„ If free water intake is
P. Na greater than output

Free Water Loss

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Hyponatremia
„ Hypo-osmolar

„ Iso-osmolar
„ lipid/protein

„ Hyper-osmolar
Osmotically 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 „ Endogenous:

with altered mental status after a recent
„ Acetone
drinking spree.
„ Renal failure
P.E.: BP 100/70 HR=130 RR=40 „ Lactate
Labs: 116|66|56 109 „ Exogenous:
5.0|15 |2.8 „ Methanol
„ Ethylene Glycol
A.G.=35 Ketones=neg
„ Ethanol
Measured Osm= 350 „ Glycine
Calculated Osm=156 „ Mannitol

Urine= +++ oxalate crystals 8

 Hypoosmolar Hyponatremia
„ Increased free water
supply
Free Water Intake
„ Decreased free water
excretion

P. Na

Free Water Loss

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Hyponatremia:
1. Increased free water supply
„ Psychogenic polydipsia is the
only situation where this
Free Water Intake
mechanism is solely responsible
„ Uosm low; <100mosm/L

P. Na

Free Water Loss

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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 11

Physiol 283: R993-R1004, 2002

 12
Sumit Kumar & Tomas Berl
Hyponatremia-
2. Impaired free water excretion by kidney

„ Too few nephrons

Free Water Intake
„ renal failure

„ Too much ADH

„ Volume depletion

ƒ Real
P. Na ƒ Effective (edema states)
„ Endocrine
ƒ Thyroid
ƒ Adrenal
Free Water Loss
„ INAPPROPRIATE ADH

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 Evaluation of Hyponatremia
„ Iso/hyperosmolar states
„ Measure plasma osmolarity (calculate osmolar gap)
„ Check Lipids/proteins
Free Water Intake„ Psychogenic polydipsia?
„ Urine Osm <100
„ Too few nephrons?
„ Serum creatinine
„ Too much ADH?
„ Volume depletion
P. Na
„ Orthostatics etc., Urine Na+
„ Intravascular volume depl. (edematous states)
„ Urine Na+, S. Uric acid
„ Thyroid/Cortisol
Free Water Loss
„ SIADH (by exclusion)
„ Chest, head, drugs.

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 Causes of SIADH
z Tumours: bronchogenic carcinoma, lymphoma,
pancreatic cancer, mesothelioma
z Pulmonary: pneumonia, TB, lung abscess, COPD
pneumothorax, HIV infection

z CNS: head injury, meningitis, subdural

haematoma, subarachnoid hge,
neurosurgery

z 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 depletion

‹ Edematous states

‹ Thyroid/Cortisol

‹ SIADH (by exclusion) 16

Hyponatremia
Clinical Effects
460

Brain water g/100g dry weight

440
420
400
PNa+=139:
380
Baseline
360
340
320
PNa+=119 in 2h 139 139-119 140-122 139-99
(2h) (3.5d) (16d)

PNa+=122 (3.5 days)

PNa+=140:
PNa+= 99 (16 days)
Day 5
Correction 17
 18
Sumit Kumar & Tomas Berl
Clinical Course of Treated
Hyponatremia

Arieff A.. NEJM 1986;314(24):1529-35 19

 20
Am J Med. 2006 Jan;119(1):71.e1-8
Hyponatremia-
Principles of Treatment
„ Treat vigorously if symptomatic/acute to
reach a “safe” level
„ If 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 polydipsia
Free Water Intake „ Renal failure: Dialysis
„ True Volume depletion: Normal saline
„ Effective volume depletion: treat cause, loop diuretics.
„ Thyroid, cortisol: replacement
„ SIADH
P. Na „ Asymptomatic/chronic:
„ Water restrict
„ Salt tablets, high protein diet
„ Furosemide in divided doses
„ ADH Antagonists
Free Water Loss
„ Acute/Mental status change
„ Hypertonic saline until M.S. adequate (.5meq/hour)

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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. 26

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 depletion

‹ Edematous states

‹ Thyroid/Cortisol

‹ SIADH (by exclusion)

„ How would you treat this
patient? 27
Hypertonic saline-
dose calculation
Current PNa+ = 115 Target PNa+ = 120
„ Na+deficit = 5 meq/liter
Total body Na+ deficit= 5 x total body water
= 5 x 0.5 x body wt (50kgs)
= 125meq
ƒ Amount of 3% NaCl needed (Na=513meq/L) =
125/513= 240ml
ƒ Rate 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

Free Water Intake „ Decreased free water supply

„ Water loss
„ Osmotic diuresis, D.I.
„ Osmotic diarrhea
P. Na
„ Insensible
„ Solute load

Free Water Loss

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Workup of Hypernatremia
„ Why is the patient not drinking??
„ Is there increased free water loss:
„ ?Polyuria
„ Uosm: 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 water
„ Oral is optimal
„ Rate of correction <0.5meq/hour
„ Dose:
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.
„ Why is the patient not drinking??
„ Is there increased free water loss:
„ ?Polyuria
Uosm: if <250 – D.I.
„

„ Uosm: if >300 – solute diuresis

Uosm=504 UNa=40meq „ ? GI (osmotic diarrhea)
„ Is the patient getting too much
Urine dip=2+ glucose solute?

Serum glucose 400.

‰What is the cause of
hypernatremia ?
‰How would you treat him?
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Calculation of water deficit
„ Calculate Amount of Water
ƒ 0.4 x body weight x (PNa/140 – 1)
0.4 x 50 x (150/140 – 1) = 1.4 liters
ƒ Insensible losses= + 1 liter/24h
ƒ Total volume= 2.4 liters
„ Rate (0.5meq/hour)
„ For Na to go from 150->140=20 hours
„ Prescription: Rate of water repletion
= 2400/20=120ml/hr.

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Hyper- and
Hypokalemia

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Hyperkalemia- Etiology

„ Intake (never alone)

„ Shift (Acute)
„ Acidosis
ICF ECF „ Insulin lack
„ Tissue Lysis
„ Beta blockade
„ Digitalis o.d.
„ Succinylcholine

„ Excretion (Chronic)
„ Advanced renal failure
„ Hypoaldosteronism
„ Volume depletion
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 Hyperkalemia: Case
50 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 Hyperkalemia
„ Antagonism of membrane action
„ Intravenous calcium
„ Shift
„ Insulin (Dextrose)
„ NaHCO3
„ ß-2 agonists
„ Removal
„ Diuretics
„ Cation exchange resin
„ Dialysis

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Hypokalemia- Etiology

„ Intake (never alone)

„ Shift
„ Treatment with insulin
„ Alkalosis
ICF ECF „ ß-2 stimulation
„ Periodic paralysis
„ Treatment of anemia

„ Increased Excretion
„ GI
„ Renal
„ Hyperaldosteronism
„ Diuresis
„ Ampho-B
„ Hypomagnesemia
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Hypokalemia-
Clinical Consequences
„ Cardiac arrhythmias
„ Muscle weakness
„ Rhabdomyolysis
„ Renal dysfunction
„ Glucose intolerance

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Hypokalemia-Treatment
„ Estimate of deficit is difficult
ƒ ~100-200 meq for 1 meq/liter
„ PO therapy usually adequate
„ IV therapy if severe/symptomatic
ƒ Max conc. 40meq/liter
ƒ Max rate 20meq/hour
ƒ Use in saline (not dextrose)

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Hypokalemia-case
„ 58 yr old cirrhotic is admitted with worsening ascites
„ Meds: Lasix 40mg bid, Lactulose
„ EKG: Unifocal VPC’s, prominent U waves
„ Admission labs: 125|87|32 80
2.2 |20|2.0
How would you treat her hypokalemia ?

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Disorders of
Magnesium

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 Hypomagnesemia:Etiology

„ Intake
„ Malnutrition
„ GI malabsorption
„ Shift
„ Pancreatitis
„ Insulin administration
ICF ECF „ Post-parathyroidectomy (hungry bone syndrome)
„ Excretion (Renal)
„ Post-obstructive, Post ATN
„ Post-renal transplant
„ Bartter’s/Gitelman’s syndromes
„ Drugs: Diuretics, aminoglycosides, cisplatinum,
amphotericin
„ Alcohol (decreased intake contributing)

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Hypomagnesemia:Clinical Effects
„ Cardiovascular
„ Arrhythmia (prolonged QT)
„ Metabolic
„ Hypocalcemia
„ Hypokalemia
„ Neurological
„ Tetany
„ Seizures

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Hypomagnesemia: Treatment
„ Oral
„ MgO
„ Mg-containing antacids
„ Milk of Magnesia
„ Mg citrate, sulfate, lactate
„ Intravenous (avoid IM)
„ Bolus
„ Infusion

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 Hypermagnesemia:Etiology

„ INTAKE
„ Mg-containing
antacids/laxatives
ICF ECF „ IV magnesium replacement
„ SHIFT
„ DKA
„ Tissue injury
„ EXCRETION

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Hypermagnesemia:
Clinical Consequences
„ >4mEq/L
„ Inhibition of neuromuscular transmission
„ Inhibition of cardiac conduction
„ > 7 mEq/L
„ Lethargy
„ PR, QT and QRS prolongation
„ >10mEq/L
„ Respiratory failure/voluntary muscle paralysis
„ CHB/Asystole

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Hypermagnesemia
Treatment
„ IV calcium
„ Dialysis

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END

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