Electrolytes

Made Easy !

Dr. Mahmoud W. Qandeel

Outlines
• Hyponatremia
• Hypernatremia
• Hypokalemia
• Hyperkalemia
• Hypochloremia
• Hyperchloremia
• Hypocalcemia
• Hypercalcemia

Dr. Mahmoud W. Qandeel

A 63 year old man is restless and ataxic and has tonic
spasm. Serum osmolality 330 mOsm/l. The most likely
diagnosis ? (7/2016)

a) Hyponatremia
b) Hypercalcemia
c) Hyperkalemia
d) Hypernatremia
e) Hypermagnesemia
Dr. Mahmoud W. Qandeel
Hyponatremia

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
P osm (mOsmol/L) = 2 * serum Na + K + glucose/ 18 +BUN/2.8

P osmolality = 290 – 310 mOsmol / L

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
Dr. Mahmoud W. Qandeel
 Body System Hyponatremia
CNS Headache, confusion, hyper or hypo active deep tendon reflexes,
seizures, coma, increased intracranial pressure
Musculoskeletal Weakness, fatigue, muscle cramps, twitching
GIT Anorexia, nausea, vomiting, watery diarrhea
CVS Hypertension & bradycardia if significant increase in intracranial
pressure
Tissue Lacrimation, salivation
Renal Oliguria

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
Acute hyponatremia: associated with acute cerebral edema,
seizures, and coma. (<48 H)

Chronic hyponatremia: Well tolerated to Na concentrations 110

mEq/L; symptoms generally include in confusion/decreased mental
status, irritablity, and decreased deep tendon reflexes. (> 48 H)

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
 Isotonic (Normo-osmolar) hyponatremia
• Pseudohyponatremia
➢hyperlipidemia,
➢hyperproteinemia
• Isotonic infusions glucose, mannitol & glycine
• TURP

Dr. Mahmoud W. Qandeel

 Hypertonic (Hyper-osmolar) hyponatremia
➢Hyperglycemia
➢Hypertonic infusions glucose mannitol glycine
➢TURP

• For each 100 mg/dl glucose increment above 200 Na decrease

1.3-1.6 mmol/l

Dr. Mahmoud W. Qandeel

 Hypotonic (Hypo-osmolar) hyponatremia
✓Hypovolemic hypotonic hyponatremia like GIT loss , skin loss ,
lung loss , third space loss & renal loss, ‘tea and toast
syndrome’.
✓Hypervolomic hypotonic hyponatremia like CHF , cirrhosis &
Nephrotic syndrome.
✓Euvolemic hypotonic hyponatremia water intoxication , K
losses , SIADH, glucocorticoid deficiency, hypothyroidism.

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
Dr. Mahmoud W. Qandeel
 SIADH
• Na less than 135
• Low plasma osmolality less than 280
• Low urine output
• But concentrated more than 100 mosm/kg
• Elevated urine Na more than 200 meq/l
• SIADH initially by fluid restriction then diuretics.

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
Dr. Mahmoud W. Qandeel
 Treatment
• Isotonic & Hypertonic hyponatremia treat the cause.
• Hypovolemic by normal saline
• Water intoxication by fluid restriction
• Hypervolemic if odema & symptomatic loop diuretics + NaCl 3%
• Replace 25% of hourly urine output by 3% NaCl.
• BNP (brain natriuretic peptide) inhibit Na reabsorption & inhibit vassopressin
action on water.

Dr. Mahmoud W. Qandeel

• If symptomatic or less than 110
– 3% NaCl to the level of 120 (desired Na level)
– Na deficit =
TBW * (Desired Na - measured serum Na)
– Furosemide 20-200 mg IV / 6hr increase the effectiveness of 3%
saline

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
• The Adrogué-Madias formula
Increase in SNa = (Infusate [Na] – SNa) ÷ (TBW + 1)

Dr. Mahmoud W. Qandeel

 Central pontine demyelination
• The risk controversial
• Appear related to chronicity more than 48 hr and to the rate of correction
• Na correction not more than 12 mmol/day Or 0.5 mmol/hr
• If acute can corrected rapidly 1-2 mmol/hr
• Na monitoring every 2hr
• Until level 120mmol/l then discont. 3% N.S.

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
Dr. Mahmoud W. Qandeel
Dr. Mahmoud W. Qandeel
 Hypernatremia
Hypovolemic hypernatremia
• Hypotonic fluid loss
• Common causes:
✓Diuresis
✓GIT losses
✓Respiratory losses
✓Cut. Losses
✓CRF

Dr. Mahmoud W. Qandeel

 Hypervolemic hypernatremia
• Result from the parenteral administration of hypertonic fluids
✓Saline
✓Sodium bicarbonate
✓Medication( mineralocorticoids excess)
✓Nutrition

Dr. Mahmoud W. Qandeel

 Isovolemic hypernatremia

• Loss of water

• Hypotonic losses

• Skin losses

• Diabetes insipidus

• Therapeutic

Dr. Mahmoud W. Qandeel

 Symptoms
• Those of volume depletion
– (e.g., tachycardia, hypotension) Big and Bloated
• As well as other signs of dehydration
– (e.g., dry mucus membranes, decreased skin turgor); lethargy,
– Result from water shifts from the intracellular compartment in CNS.
• CNS: confusion, and coma.
• Skin: flush, edema and low grade fever
• Polydepisia
• Serious : swollen dry tongue, N&V, increased muscle tone
Dr. Mahmoud W. Qandeel
 Treatment
• Water deficit
TBW * (( serum Na in mmol/ l / 140) – 1)
• Rapid correction = cerebral odema
• Only ½ of water deficit should be corrected over 24hr.
• The reminder over 2-3 days
• I.V dextrose 5 w, dextrose saline, normal S

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
 Diabetes insipidus

• Central D.I :

• Treated by desmopressin intranasally 10-40 microgramdaily

• Nephrogenic D.I :

• Diatery Na restriction + thiazide diuretics 50-100 mg/day orally

Dr. Mahmoud W. Qandeel

 Sodium
Equations of
Clinical use

Dr. Mahmoud W. Qandeel

 Potassium
• Only 2% is extracellular
• Serum K is 3.3 - 5 mmol/l
• 50-100 mmol ingested & absorbed daily
• 90% is excreted renally
• 10% is eliminated in stool
• Cardiac and muscle contraction

Dr. Mahmoud W. Qandeel

 Hypokalemia
• GIT losses ( diarrhea, vomiting, NG,…)
• Renal losses ( diuretics, …)
• Cutaneous Losses ( burn )
• Acute intracellular K uptake ( insulin, metabolic alkalosis, M.
infarction, hypothermia,…)
• TPN ( refeeding syndrome)
• Medical disease: hyperaldosteronism, Cushing syndrome

Dr. Mahmoud W. Qandeel

 Manifestation
• Primarily cardiovascular
• Heart: ECG increasing order severity
✓T-wave flattening or inversion, Low and Slow
✓Depressed ST segments,
✓Development of U wave
✓Prolonged QT nterval
✓Ventricular tachycardia
• GI: Ileus, constipation, hypoactive bowel sounds
• Muscular: Muscle weakness, flaccid paralysis, depressed DTR
Dr. Mahmoud W. Qandeel
 Treatment
• Oral replacement in mild hypokalemia
• 50-100mmol KCl single or divided doses/d
• Parenterally in severe hypokalemia
• Not more than 40 mmol/l
• Good renal function
• Cardiac monitoring for high doses
• Correct hypomagnesaemia

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
 Hyperkalemia
• High intake
• Pseudokyperkalemia (laboratory)
• Spurious hyperkalemia (hemolysis)
• Redistributional hyperkalemia
✓ Insulin def., B.blocker,
✓ Acute acidemia, Rhabdomyolysis,
✓ Cell lysis, Reperfusion syndrome,
✓ Digitalis, succinylcholine

Dr. Mahmoud W. Qandeel

 Manifestation (S&S)
• Heart :
– ECG changes
Tight and contracted
• GI:
– Diarrhea and
– Hyperactive bowel sounds
• Muscular:
– Paralysis in extremities,
– Increased DTR,
– Muscle weakness
Dr. Mahmoud W. Qandeel
 Manifestation

• ECG increasing order of severity:

✓Symmetrical peaking t-wave
✓ST elevation
✓Reduce p-wave voltage
✓Widening of QRS complex
✓If severe untreated sinusoidal ECG pattern

Dr. Mahmoud W. Qandeel

 Treatment
Mild hyperkalemia 5-6 mmol/l
• Reduction of daily intake
• Possible loop diuretics
• Discontinued any drugs

Dr. Mahmoud W. Qandeel

 Severe hyperkalemia
• Temporizing measures ( shifting K )
1. NaHCO3 1mmol/kg iv over3-5min can be repeated after 15 min
2. Dextrose 0.5g/kg infuse w regular insulin 0.3 unit / g dextrose (usual dose 25 g
dextrose w 6-10 unit insulin iv bolus)
3. Inhaled B. agonist ( Alubuterol sulfate 2-4 ml of 0.5 ml solution via nebulizer )
4. Calcium gluconate 10% , 5-10 ml, iv over 2 min. with severe ECG changes
– Protection of the heart not for – K
– Stabilizes cardiac myocyte membranes and can prevent dysrhythmias

Dr. Mahmoud W. Qandeel

 Therapeutic measures

• To promote K excretion
➢Kayexalate Na-K exchange resin
Orally (20-50g in100-200 ml of 20% sorbitol/ 4 hr)
Or rectally (50g in 50ml of 70% sorbitol added to 100-200ml water / 2 hr)

➢Hydration (normal saline w loop diuretics)

➢Dialysis ( definitive therapy for life threatening)

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
 Chloride
• Function as Na; maintain:
– Blood volume
– Blood pressure
– pH balance

Dr. Mahmoud W. Qandeel

 Hypochloremia
• Cl < 90 mEq/L
• Symptoms: dehydration or hypokalemia due to vomiting or other GI loss
• Stomach HCl is lost from vomiting, leading to low chloride and a buildup
of bicarbonate, causing a metabolic alkalosis.
• It is often associated with paradoxic aciduria.
– Normally, the kidneys would excrete bicarbonate to reduce pH; however, as the
dehydration worsens, the kidneys’ drive to retain sodium predominates, and the
kidney excretes both K and H to conserve sodium.

Dr. Mahmoud W. Qandeel

 Hyperchloremia
• Cl > 110 mEq/L
• The most common cause in surgical patients is the adminstration of
large amounts of chloride in IV solutions.

• Excess chloride decreases the strong ion deference, thereby

causing more water to dissociate and more H ions to be present, leading
to metabolic acidosis.

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
 Calcium
• Level 8.5-10.5 mg/dl
• Ionized 45%
• Protein bound 40%
• Complexed 15%
• Daily intake 500-1000 mg
• PTH & Vitamin D

Dr. Mahmoud W. Qandeel

 Hypocalcemia
• Calcium sequestration (pancreatitis) or vit.D deficiency
• Chronic renal failure, intestinal malabsorption, laxatives, mercury
• Transient hypocalcemia (thyroidectomy)
• Lactate, citrate from blood transfusions
• Parathyroidectomy
• Hypomagnesemia
• Acute alkalemia (affect the ionized form)
• Hypoalbuminemia
( each 1 gm fall decrease Ca 0.8 mg/dl )
Dr. Mahmoud W. Qandeel
 Manifestations
• Tetany
• Chovestek’s sign & trousseau sign
• Perioral numbness & tingling
• QT interval prolongation
• Ventricular arrhythmias

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
 Treatment
• Parenteral therapy in symptomatic one
✓ 200 mg is needed to abort tetany
✓ Initial bolus of Ca is ( 10-20ml of 10% Ca-gluconate over 10 min. iv.)
✓ Then maintenance infusion 1-2 mg/kg/ hr.
• Ca. chloride 3 times more Ca gluconate
✓ Normalize in 6-12 hours then decrease to 0.3-0.5 mg/kg/hr.
✓ Mg & Phosphorus should be checked
✓ Be careful w digitalis

Dr. Mahmoud W. Qandeel

 Oral therapy
• Carbonate each 1250 mg contain 500mg elemental Ca
• Gluconate each 1000 mg contain 90mg
• In chronic 1000-2000 mg daily is enough
• If severe Ca salt with vitamin D
✓ 50 000 IU of calciferol or
✓ 0.4 mg of dihydrotachysterol or
✓ 0.25-0.50 microgram of 1,25 dihydroxy vit.D3

Dr. Mahmoud W. Qandeel

 Hypercalcemia
• Malignancy (Most common inpatient cause)
• Hyperparathyroidism (Most common outpatient cause)
• Hyperthyroidism
• Vitamin D intoxication
• Prolonged immobilization
• TPN
• Thiazide diuretics
• Granulomatous disease.
Dr. Mahmoud W. Qandeel
Dr. Mahmoud W. Qandeel
 Manifestations
• Bone disease
• Nephrolithiasis
• If severe
✓Altered mental level
✓Diffuse weakness, dehydration, N&V
✓Adynamic ileus & severe constipation
✓QT interval shortening & arrhythmias

Dr. Mahmoud W. Qandeel

 Treatment
• If less than 12 mg/dl
• Restricted Ca intake
• Treat the cause
• Correct dehydration
• Correct vitamin D deficiency
• Stop thiazide

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
 If severe hypercalcemia
1. Normal saline & loop diuretics
• In good cardiovascular & renal function
• 250-500 ml/ hr with furosemide 20mg/4 hr
• Adjusted to maintained UOP 200-300ml/hr
• Mg , Phosphorus & K should monitered
• This promote Ca loss 2 gm / day

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel
2. Salmon calcitonin
• With good hydration
• Subcutaneous or intramuscular
• Skin test first by 1 IU
• Then 4 IU / kg every 12 hours
• Hypocalcemic effect occur after 6-10 hr
• Doubled if unsuccessful after 48 hrs
• Maximum dose 8 IU / kg

Dr. Mahmoud W. Qandeel

3. Sodium pamidronate (bisphosphonate)
• Decrease osteoclastic activity
• With good hydration
• For moderate 12-13 mg/dl
• 60 mg diluted in liter fluid infuse over 24 hrs
• For severe 90 mg
• If recurrence repeat the dose after 7 days

Dr. Mahmoud W. Qandeel

4. Plicamycin

• 25 microgram/kg diluted in liter fluid over 4 hrs daily for 3

days
• The onset of action is 1-2 days
• The duration of action is up to 1 week
• No longer available in US

5. Glucocorticoids

Dr. Mahmoud W. Qandeel