Electrolyte imbalance

Beirut arab university

5th year medical school
Salamtak workshop
Done by Dr. Ahmad Al-kouzi
Composition of Body
Fluids
 • 50% of body weight is water in
women
• 60% of body weight is water in men
• ICF:55-75%
• ECF:25-45% including intavascular
and extravascular in a ratio of 1:3
Major ECF particles: Major ICF
particles:
1-sodium 1-
potassium
2-chloride 2-ATP
 Water Balance
• Plasma osmolality:275-
290mosmol/kg
• Obligate water loss :Urine-Stool-skin
and respiratory tract.
• Minimum urine output of 500 ml/day
is required for neutral solute balance
• Water intake must equal water
excretion
 Water intake

• Thirst increase in effective

osmolality
or decrease in ECF
volume or
blood pressure

Sensed by
osmoreceptors
 Water excretion

A V P=ADH

Binds to V2 receptors of principal cells

in the collecting duct
The major stimulus for secretion is
hypertonicity sensed by the
osmoreceptors in antrolateral
hypothalamus
 Non osmotic factors that regulate AVP
1-effective circulating arterial volume
2-nausea,pain,stress,hypoglycemia
3-Pregnancy
 Hypovolemia
• Definition:”state of combined salt
and water loss exceeding intake
leading to ECF volume contraction”
NB:The loss of Sodium may be renal or
extrarenal
Eg renal: diuretics-glucose-urea-
mannitol-
diuretic phase of acute
tubular
• Eg of Extrarenal:
1-GIT
2-SKIN
3-THIRD space accumulation
 Pathophysiology
• ECF volume contraction

Hypotension and diminished cardiac

output
Stimulates baroreceptors in carotid
sinus and aortic arch
sympathetic activation
maintenance of cerebral and
• In respect to the Kidney:
1-increase PCT reabsorption of Sodium
2-Decrease GFR
3-increase reabsorption of Sodium by
the collecting duct
 Clinical Features:
• Symptoms
Signs:
2. Fatigue 1. JVP
3. Weakness 2.Postural
hypotension
4. Thirst 3.postural
tachycardia
5. Postural dizziness
6. If
 Diagnosis:
1-BUN:creatinine=20:1(decreased GFR)
However high BUN realtive to creatinine
occurs in hyperalimentation and
glucocorticoid therapy.
2-Urine sodium < 20 mmol/L
However in ATN there is impaired Sodium
reabsorption or in case of vomitting:see
Cl
3-urine osmolality>450 mosmol/kg
and specific gravity>1.015
However in DI SG and urine osmolalityare
 Treatment
• Mild:correct via the oral route
• Severe:IV normal saline(154 mmol/L)
However in Hypenatremia use half
normal saline or 5% dextrose
Patients with significant
hemorrhage,anemia may require
blood transfusion or dextran
 Hyponatremia
• Definition:Plasma sodium
concentration<135 mmol/L
Plasma Osmolality may be
Decreased(hypotonic)
Increased (hypertonic)
Normal(isotonic)
 Hypotonic hyponatremia
• Primary water gain and secondary
sodium loss:eg:1-Primary polydipsia
2-beer potomania
3-SIADH
4-Addison disease and
hypothyroidism

• Primary sodium loss and secondary

water gain
• Renal:
1-Diuretics(Thiazides) rarely loop.
2-Hypoaldosteronism
3-Salt wasting nephropathy
• Extrarenal:
1-Intergumentary
2-GIT
 Hyponatremia in ECF volume
Expansion
• By this there is Primary Na gain
exceeded by secondary water gain
1-Heart Failure
2-Hepatic cirrhosis
3-Nephrotic Syndrome
 Clinical features
Mainly neurological:
Brain cell swelling and cerebral edema
Symtoms depend on :
The severity of onset and the absolute
decrease in plasma Na
• Nausea and Malaise
• Headache,lethargy,confusion
• Stupor,seizures and coma(plasma Na
<120mmol/L or decreases rapidly)
 Diagnosis

1-Plasma osmolality
2-Urine osmolality
3-Urine Na
4-Urine K
 Treatment
1-Raise plasma Na by restricting water
intake and promoting water loss
2-Correct the underlying disorder

2 protocols

In ECF volume In ECF

volume
contraction
 In ECF volume contraction
• Na repletion in the form of isotonic
saline
The direct effect on the plasma Na is
trivial however there is restoration of
euvolemia and hence removing the
hemodynamic stimulus of AVP
allowing the excess free water to be
excreted
 In Edematous state
• Restriction of Na and water
• Correction of Hypokalemia
• Promotion of Water loss in excess of
Na
 Correction
(Desired plasma Na –Measured Plasma
Na)
X
Weight
X
0.6 in man or 0.5 in woman
 Important:
• Do not raise plasma Na more than
0.5 to 1 mmol/L/hour
And no more than 10-12 mmol/L/day
Except in altered mental status and
seizures you are allowed up to 2
mmol/L/hour
For fear of developping ODS
 Osmotic demyelination
syndrome
• Flaccid paralysis
• Dysarthria
• Dysphagia
Diagnosis:Clinically+neuroimaging
studies
Treatment:No treatment+high
morbidity and mortality
 Hypernatremia
• Definition:plasma Na concentration
>145mmol/L
• Hypernatremia is a state of
hyperosmolality which is usually mild
unless impaired thirst(Primary
hypodipsia) or limited access to
water is present.
• Causes:Primary Na gain(rare) or
water deficit(common)
 Non renal loss of water
• In Profuse prespiration there is
increase in solute free water loss
• Diarrhea:osmotic not
secretory(presents usually with
hyponatremia or normal Na).
• Mechanically ventilated patients and
severe burns
 Renal loss of water
• Most common osmotic
diuresis (DM)
Diabetes
insipidus

CDI
NDI
 Clinical features:
• Contracted ICF volume
• Decreased brain cell volume
increasing risk of subarachnoid or
intracerebal hemorrhage .
• Neurologic manifestations:
1-altered mental status
2-weakness
3-seizures and coma
 Treatment
• Stop the ongoing water loss
• And correct the water deficit
• Correction:
water deficit=[(Plasma Na concentration-140)/140]X TBW
• TBW is 40% in women and 50%in men

• Do not correct more than 0.5

mmol/L/h
• AND no more than 12mmol/L/h over
the 24 hours
• The safest route is by mouth or via
nasogastric tube
• Half normal saline or dextrose can be
given IV
• CDI:desmopressin nasally
• NDI:Thiazide.
 Potassium
• Major intracellular cation
• Normal:3.5-5mmol/L
• For balance:matching ingestion with
excretion.
• Immediately following a meal K⁺
enters cells as result of insulin and
initial elevation of plasma K⁺.
• Eventually however excess is
excreted in urine
 Potassium excretion
• 90% of filtered K⁺ is reabsorbed by
PCT and loop of Henle.(TALH)

• K⁺ delivery to the distal nephron

approximated dietary intake
• Regulation by ALDOSTERONE and
HYPERKALEMIA
 Hypokalemia
• Definition:plasma potassium
concentration<3.5mmol/L
• Causes
1-decreased intake
2-shift into cells
3-increased net loss
 Redistribution into cells
• In metabolic alkalosis
• Insulin treatment of DKA
• Uncontrolled DM from osmotic diuresis
• ß₂ adrenergic agonist
• Anabolic states
• Transfusion of frozen RBCs

NB:hypokalemic periodic paralysis is a

rare condition in which there is
recurrent episodic weakness or
paralysis
 Loss of Potassium
• Non renal:
1-Excessive sweating(renal)
2-ECF contraction and
hyperaldosteronism
3-Secretory diarrhea
4-Vomitting due to metabolic alkalosis
and volume depletion
• Renal:
1-Primary hyperaldosteronism
2-Hyperreninemia in Malignant
hypertension(+tumors)
3-Liddle’s syndrome(rare)
4-Bartters syndrome.
5-Most important:Diuretic abuse.
 Clinical features
• Fatigue ,myalgias and muscular weakness of
the lower extremities.
• Progressive weakness,hypoventilation and
complete paralysis
• ECG changes:
1-flattening or inversion of T wave
2-Prominent U wave
3-ST depression
4-Prolonged QU interval
If severe:
Prolonged PR and widening QRS
Hypokalemia
Metabolic
alkalosis
 Diagnosis
• Diuretic and laxative abuse
• Surreptitious vomitting
• Marked leucocytosis(AML)
Pseudohypokalemia
• TTKG
 Treatment
• Correct K⁺ deficit and minimize
losses
• In intracellular shifts use oral
preparations.
• In DKA there may be an
underestimation of the K⁺ deficit.
• Use KCl and rarely Bicarbonate
formulas.
 Hyperkalemia
• Definition: plasma K⁺ concentration
> 5 mmol/L
• Causes:
1-Decreased renal loss
2- increased potassium release from
the cells.
Pseudohyperkalemia:PROLONGED use
of a tourniquet-hemolysis-marked
leucocytosis and thrombocytosis.
• Renal failure
• Decreased distal flow
• Decreased K⁺ secretion :
A-Impaired Na reabsorption
1-Primary hypoaldosteronism
2-secondary hypoaldosteronism
3-Resistance to aldosterone
B-Enhanced Chloride reabsorption:
1-Gordon’s syndrome(Cl shunt)
2-Cyclosporine
 Clinical features
• Weakness,flaccid paralysis and
respiratory arrest
• Metabolic acidosis
• Cardiac toxicity ECG changes:
1-increased T wave amplitude or
tented T wave
2-increased PR interval and widening
of QRS
3-loss of P wave
ECG
 Diagnosis
• Exclude pseudohyperkalemia
• Symptoms
• Plasma K
• ECG
 Treatment
• Depends on Plasma K conc +ECG
changes+associated muscular
weakness
• If >7.5 severe and may be fatal so
emergency treatment:
1-Administration of Ca gluconate(rule of
10) dose may be repeated if no
changes in ECG
2-insulin +GLUCOSE
3-IV NaHCO3 (specifically in metabolic
acidosis)
 Removal of K⁺
• If renal function is adequate:
Loop and thiazide diuretics
• Na polystyrene sulfonate(SPS)
• If renal function is impaired
:Hemodialysis
 Calcium
• Normal calcium level:8.9-10.1 g/dl
• Regulation by PT glands+VitD
• Regulating diverse physiological
processes
 Hypercalcemia
• Causes:
1- Excess PTH
2-FHH (CaSR mutations)
3-PTHrP
4-Sarcoidosis
5-Hyperthyroidism
6-Osteolytic metastasis
 Clinical manifestations
• If mild asymptomatic however be
careful of neuropshychiatric changes.
• PUD
• Nephrolithiasis
• If severe >12-13 mg/dl lethargy
stupor or coma+GIT symptoms
• ECG changes:AV block-bradycardia-
short QT interval
 Diagnosis
• Note the albumin concentration
50% ionized-50% bound to albumin
If there is hypoalbuminemia add
0.8mg/dl for every 1g/dl albumin
decrement and opposite for increase
in albumin
• PTH level
• Renal function
 Treatment
• In severe hypercalcemia :
1-Hydration 4-6 L IV saline in 24 hours
2-Loop diuretics
3-Bisphosphonates
4-Calcitonin
5-Dialysis
6-IV phosphate
 In sarcoidosis and other
granulomatous disease:
• Glucocorticoids IV or oral
• Ketoconazole,chloroquine may be
occasionally used
 Hypocalcemia
• PTH levels:

If High:
If LOW
Secondary
Hypoparathyroidism
Renal failure
 Clinical manifestaions
• Paresthesias:finger,toes,circumoral
regions
• Carpopedal spasm
• Chvostek sign
• Trousseau sign
• QT prolongation