Electrolyte Disorders

Jai Radhakrishnan, MD

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

Disorders of Osmolarity
Na Osmolality
Free Water Intake

Hyperosmolarity
(Hypernatremia)

P. Na

Hypoosmolarity
(Hyponatremia)

Free Water Loss

Generation of Disorders of Osmolarity

Free Water Intake

Hypernatremia
If water intake is less than output

P. Na

Hyponatremia
If free water intake is greater than output

Free Water Loss

Hyponatremia
Hypo-osmolar Iso-osmolar lipid/protein Hyper-osmolar
Osmotically active subs

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

Case:

Hyperosmolar Hyponatremia
Endogenous:
Acetone Renal failure Lactate

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

Exogenous:
Methanol Ethylene Glycol Ethanol Glycine Mannitol
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Hypoosmolar Hyponatremia
Free Water Intake

Increased free water supply Decreased free water excretion

P. Na

Free Water Loss

Hyponatremia:
1. Increased free water supply
Free Water Intake

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

P. Na

Free Water Loss

"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

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Sumit Kumar & Tomas Berl

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HyponatremiaFree Water Intake

2. Impaired free water excretion by kidney

Too few nephrons
renal failure

Too much ADH

Volume depletion
P. Na

Real Effective (edema states)

Endocrine
Free Water Loss

Thyroid Adrenal

INAPPROPRIATE ADH
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Evaluation of Hyponatremia
Free Water Intake

P. Na

Iso/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+

Free Water Loss

Intravascular volume depl. (edematous states)

Urine Na+, S. Uric acid

Thyroid/Cortisol SIADH (by exclusion)

Chest, head, drugs. 13

Causes of SIADH
Tumours: Pulmonary: CNS:
bronchogenic carcinoma, lymphoma, pancreatic cancer, mesothelioma pneumonia, TB, lung abscess, COPD pneumothorax, HIV infection head injury, meningitis, subdural haematoma, subarachnoid hge, neurosurgery carbamazepine, chlorpropamide, cyclophosphamide, ecstasy, NSAID, tricyclic antidepressants, phenothiazines, SSRI

Drugs:

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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 3.1|29|1.8
Hyperosmolar? Psychogenic polydipsia? Too few nephrons? Too much ADH? Volume depletion Edematous states Thyroid/Cortisol SIADH (by exclusion)
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UNa+=13 Uosm=422

Hyponatremia Clinical Effects

Brain water g/100g dry weight

460 440 420 400 380 360 340 320 139 139-119 (2h) 140-122 (3.5d) 139-99 (16d)

PNa+=139: Baseline

PNa+=119

in 2h

PNa+=122 (3.5 days) PNa+= 99 (16 days)

PNa+=140: Day 5
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Correction

Sumit Kumar & Tomas Berl

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Clinical Course of Treated Hyponatremia

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

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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

Free Water Loss

Acute/Mental status change

Hypertonic saline until M.S. adequate (.5meq/hour)

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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 depletion Edematous states Thyroid/Cortisol SIADH (by exclusion)

How would you treat this patient?

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Hypertonic salinedose 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 Amount of 3% NaCl needed (Na=513meq/L) = 125/513= 240ml Rate of infusion=0.5meq/hour=10 hours =24ml/hour
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HYPERNATREMIA

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Pathogenesis of Hypernatremia
Free Water Intake

Decreased free water supply Water loss

Osmotic diuresis, D.I. Osmotic diarrhea Insensible

P. Na

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. 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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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?

Calculation of water deficit

Calculate Amount of Water
0.4 x body weight x (PNa/140 1) 0.4 x 50 x (150/140 1) = 1.4 liters Insensible losses= + 1 liter/24h 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) ICF ECF
Acidosis 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 -2 agonists

Removal
Diuretics Cation exchange resin Dialysis
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Intractable life-threatening hyperkalaemia in a diabetic patient

Nephrol Dial Transplant (2000) 15: 113-114

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Hypokalemia- Etiology
Intake (never alone) Shift ICF ECF
Treatment with insulin Alkalosis -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
~100-200 meq for 1 meq/liter

PO therapy usually adequate IV therapy if severe/symptomatic

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

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Hypokalemia-case
28 yr old type 1 diabetic is admitted with DKA Persistent vomiting EKG: Unifocal VPCs, prominent U waves Admission labs: 125|87|32 570 3.0 |20|2.0 Ketones=3+ How would you treat her hypokalemia ?

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Disorders of Magnesium

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Hypomagnesemia:Etiology
Intake
Malnutrition GI malabsorption

Shift ICF ECF

Pancreatitis Insulin administration Post-parathyroidectomy (hungry bone syndrome)

Excretion (Renal)
Post-obstructive, Post ATN Post-renal transplant Bartters/Gitelmans 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 IV magnesium replacement

ICF

ECF

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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