Electrolyte Electrolyte Disturbances In ICU Disturbances In ICU Dr. Fathia Hassan Khalil Dr. Fathia Hassan Khalil
May 24, 2015
Electrolyte Disturbances Electrolyte Disturbances In ICUIn ICU
Dr. Fathia Hassan KhalilDr. Fathia Hassan Khalil
Body FluidsBody Fluids
• The average body water is 60% of TBW
• 65% in males & 55% in females
• In obese patient it decrease 5%
SodiumSodium
SodiumSodium
• Sodium is the major ion in ECF
• Normal value in blood is 135 : 145 mMol/L
Sodium is responsible forSodium is responsible for::
• 1- Maintaining plasma & ECF osmolality
• 2- Maintaining i.v. & ECF volume
• 3- Has physiologic role in generation of
• Membrane resting potential
• Action potential
• Glucose & a. a. transport.
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• Renal system
• Endocrine system
Sodium concentration is regulated by:
• Renal excretion of sodium is adjusted to equal the amount ingested.
• Urine sodium output 1 - 400 mEq/day
• The normal is 90 mEq/d
• In the kidney 96-99 % of the filtered sodium is reabsorbed– 67% in PCT by active process– 25% in thick ascending loop of Henel
passively (loop diuretics acted upon)– 5% in DCT & 3% in CD in exchange with K &
Cl (controlled by aldosteron).
HyponatremiaHyponatremia
HyponatremiaHyponatremia
• Hyponatremia means serum sodium less than 130 mEq/L
Less than 130 Mild
• Less than 125 Moderate
• Less than 115 Severe
• No linear correlation between degree of hyponatremia and symptoms.
• Symptoms depend upon the rapidity of occurrence of hyponatremia.
Because of difference between the regulation of total body volume and
sodium concentration, it is possible to have hypo- or hypernatremia in face of
hypo-, hyper-, or euvolemia.
Classification of HyponatremiaClassification of Hyponatremia
I- Hyponatremia with normal serum osmolality
II- Hyponatremia with high serum osmolality
III- Hyponatremia with low serum osmolality
I-Hyponatremia with normal serum I-Hyponatremia with normal serum osmolalityosmolality
• S. Osmolality: 280-295 mOsm/kg water
• Called Pseudohyponatremia
• Causes:– 1- Hyperlipidemia (every 4-6 gm/L increase in
lipids leading to 1mEq/L decrease in sodium.– 2- Hyperproteinemia e.g. multiple myeloma
(every 10gm/dl increase leading to 1mEq/L decrease in serum sodium).
II-Hyponatremia with High Serum II-Hyponatremia with High Serum OsmolalityOsmolality
S. Osmolality: > 295mosm/kg water
• Called Hypertonic Hyponatremia
Caused by increase impermeant solutes replacing sodium in the blood
• Causes:
1-Non sodium solutes e.g. glucose, mannitol, and some toxins (ethanol & urea).
2- Renal failure due to impaired water excretion.
Management of Hyponatremia with Management of Hyponatremia with normal & High S. Osmolality normal & High S. Osmolality
- Restoration of volume and free water deficit
- Treatment of non-sodium salts e.g. toxins
- Treatment of hyperglycemia or mannitol level
- Treatment of hyperlipidemia or hyperprotenemia.
III-Hyponatremia with III-Hyponatremia with HypoosmolalityHypoosmolality
• S. Osmolality : < 280 mosm/kg water
• It is the most common type
• It means that free water intake more than water loss
Types of Hyponatremia with Hypo-Types of Hyponatremia with Hypo-osmolalityosmolality
• Based on clinical assessment of total body water and sodium content it is classified into:
1. Hypovolemic hypoosmolar hyponatremia
2. Hypervolemic hypoosmolar hyponatremia
3. Euvolemic hypoosmolar hyponatremia
1-Hypovolemic Hypoosmolar 1-Hypovolemic Hypoosmolar HyponatremiaHyponatremia
• Causes:
• 1- Renal causes
• Diuretic use
• Renal tubular dysfunction
• Hypoaldosteronism
Urine sodium > 30mEq/L
Urine osmolality normal (300:400)
• 2- Non renal causes:
• G.I. loss
• Skin loss
• Dietery sodium restriction
• Third spacing
Urine sodium < 15mEq/L
Urine osmolality > 400 mosm/kg w
Manifestations of Hypovolemic Manifestations of Hypovolemic Hypoosmolar HyponatremiaHypoosmolar Hyponatremia
• Intra vascular volume depletion
• Hypotension
• Orthostatic hypotension
• Tachycardia
• Skin dehydration
Management of Hypovolemic Management of Hypovolemic Hypoosmolar HyponatremiaHypoosmolar Hyponatremia
• - Replace the volume depletion to depress ADH by isotonic crystalloid, or colloids and blood if not enough.
• -Replace free water with sodium by Water restriction and Furosemide
• Replace urine output by isotonic or hypertonic saline
22 - -Hypervolemic Hypoosmolar Hypervolemic Hypoosmolar HyponatremiaHyponatremia
• It is called dilutional hyponatremia
• Causes:
• CHF
• Liver cirrhosis
• Nephrotic syndrome
Manifestations of Hypervolemic Manifestations of Hypervolemic Hypoosmolar HyponatremiaHypoosmolar Hyponatremia
• Total body water increased and the patient is edematous but
• The effective circulatory volume is low.
• Urine sodium < 15 mEq/L
• Urine osmolality > 400 mosm/kg w
Management of Hypervolemic Management of Hypervolemic Hypoosmolar HyponatremiaHypoosmolar Hyponatremia
• The aim of management is to improve
• The effective circulating volume
• Renal function
• Cardiac function
• Distal tubular delivery of sodium*Combination of furosemide & ACE
Inhibitor.
3-Euvolemic Hypoosmolar 3-Euvolemic Hypoosmolar HyponatremiaHyponatremia
* Syndrome of inappropriate ADH secretion• Excess ADH secretion• Secretion stimulated by non-osmotic,
non-volumic factors e.g.:– Emotional stress– Endocrine disorders– CNS diseases– Excess hypotonic fluids– Drugs e.g. NSAID & Carbamezapine
• Urine Na > 30mEq/L, U. Osm > 400mosm
Management of Syndrome of Management of Syndrome of inappropriate ADH secretioninappropriate ADH secretion
• Treatment of the cause e.g. brain tumor resection
• Free water restriction
• Furosemide to get –ve water balance
• Replace fluid by isotonic or hypertonic saline
• Measure serum sodium every 6:12 h.
• * Water intoxication: e.g.
• Psychosis
• Heavy beer drinking
• Absorption of hypoosmolar fluids during prostate resection.
• Urine osmolality < 100 mosm/kg w
• Treated by water restriction
General Manifestations of General Manifestations of HyponatremiaHyponatremia
• Serum osmolality and cellular dehydration are the main insult done
• CNS cells are the most affected by changes in osmolality.
• CNS compensate for slow changes in osmolality affected severely in acute changes.
General Manifestations of General Manifestations of HyponatremiaHyponatremia
• In acute hyponatremia:
• -CNS manifestations:
• begin by lethargy & confusion up to seizures, cerebral edema & coma
• GI symptoms
• Muscle cramps & weakness
Management of HyponatremiaManagement of Hyponatremia
Management Based onManagement Based on::
*Treatment of the cause
*Restoration of serum sodium concentration
*Normalization of serum osmolality
Correction of Serum SodiumCorrection of Serum Sodium
Acute changes in sodium concentration should be treated rapidly, but
• Chronic changes should be treated more slowly.
In acute hyponatremia (<2 days):
Correct by no faster than 1 : 2 mMol/L/h
Serum sodium not increased more than 130 mEq/L and avoid hypernatremia
In presence of seizures or increase ICP the correction could be in 3 :4 mMol/L in the first hour or even 8 mMol/L
In chronic hyponatremia:
Correct by less than 12 mMol/L/day
The rapid correction may leads to:
Osmotic Demyelination Syndrome
Severe neurological deterioration after one to several days of rapid correction.
• The amount of sodium required to increase serum sodium concentration is calculated as the equation:
• Na required=
(Desired Na – Present Na) * TB Water
• TB Water =
• BW * 0.6 in male (0.5 in female)
• The desired sodium should not exceed 130mEq/L
• Hypertonic saline used only in severe hyponatremia
• Hypertonic saline should be stopped when:• Pt become asyptomatic• Plasma sodium increased by 20 mmol/L• Plasma sodium reached to 120:125mmol/L
HypernatremiaHypernatremia
HypernatremiaHypernatremia
• It means s. sodium >150 mEq/L
• It results from loss of free water or
• Gain of sodium ions in excess of water
Risky patients are:Risky patients are:
• The extreme of age for inability to drink
• Very sick patient
• Comatosed patient
• Severe vomiting
• Severe hypernatremia producing:
• Cellular dehydration
• Hyperosmolality in most cases
Classification of HypernatremiaClassification of Hypernatremia
I- Hypernatremia with hypovolemia
II- Hypernatremia with hypervolemia
III- Hypernatremia with euvolemia
I-Hypernatremia with hypovolemiaI-Hypernatremia with hypovolemia
• Causes:
• 1-Renal water loss e.g.
• Osmotic diuretics in excess
• Tubular renal disease
• Adrenal failure
• Impaired response to ADH & DI– U Na>20 mMol/L– U Osm<300:400 mOsm/kg water
• 2- Non-renal water loss e.g.
• GI loss e.g. diarrhea
• Skin loss, severe sweating
• Peritoneal dialysis– U Na < 15 mMol/L– U Osm > 400 mOsm/kg water
II-Hypernatremia with hypervolemiaII-Hypernatremia with hypervolemia
• Causes:
• 1- Iatrogenic (Na containing compounds)
• 2- Mineralocorticoid in excess e.g.
• Aldosteronism
• Cushing disease
• CAH– U Na >20 mMol/L– U Osm >300 mOsm/kg water
III- Hypernatremia with euvolemiaIII- Hypernatremia with euvolemia
• Causes:
• 1-Renal water loss e.g.
• DI
• Renal disease
• Diuretics– U Na variable– U Osm <290 mOsm/kg water
• 2- Non renal water loss e.g.
• Diarrhea
• Fever– U Na variable
– U Osm > 400 mOsm/kg water
Diabetes InsipidusDiabetes Insipidus
• I- Central DI
• Idiopathic DI
• Following head trauma
• Neurological disease
• 2-Nephrogenic DI
• Sickle cell nephropathy
• Chronic pyelonephritis
• Multiple Myeloma
Clinical Clinical FeaturesFeatures of Hypernatremia of Hypernatremia
• Neurological features:– Begin by irritability, to focal deficit up to
cerebral dehydration & hemorrhage
• Cardiovascular features– Manifestations of volume depletion up to
shock
• Renal features– Polyuria or oliguria up to renal insufficiency
Management of HypernatremiaManagement of Hypernatremia
• Acute hypernatremia treated rapidly
• While chronic state should be treated slowly to avoid neurological insults as seizures and cerebral edema
• Correction should not exceed 2mMol/L/h
Management of Hypernatremia:Management of Hypernatremia:
1- Treatment of the underlying cause
2- Volume repletion with isotonic salineHypotonic fluid used after volume repletion
Water deficit replaced over 24 : 48 h
3- Sodium overload :Removed by loop diuretics & renal dialysis in severe cases
4- Treatment of DI
- Hormonal replacement (Desmopressin)
- In nephrogenic DI desmopressin is not completely beneficial but
- Limitation of salt and water intake and
- Thiazide diuretics are the treatment of choice
PotassiumPotassium
PotassiumPotassium
• Serum potassium (k) range is
3.5 to 5mMol/L• But 98 % of total body k is intracellular
• Then decrement of 1 mMol of serum potassium concentration means a loss of about 200 : 300 mMol/L in body potassium store.
Functions of PotassiumFunctions of Potassium
• The main function is the stability of the action potential of the cell membrane.
• Then the main effect of serum hypokalemia is hyperpolarization of resting membrane potential affecting mainly:
• The heart producing arrhythmias and
• The brain affecting the nerve conduction
-Potassium also play a role as a cofactor in enzymatic reactions
-It maintain the normal cell volume
-It affects the IC hydrogen ion concentrations and participate in regulation of intracellular PH
HypokalemiaHypokalemia
HypokalemiaHypokalemia
• Hypokalemia means serum level less than 3.5 mMol/L
• Because potassium is primarily an intracellular ion, hypokalemia may occur in low, normal, or high total body potassium.
Causes of HypokalemiaCauses of Hypokalemia
• 1- Redistribution e.g.–Shift of potassium from ECF to ICF
– Insulin – Metabolic alkalosis– Catecholamines e.g. aldosteron – Periodic paralysis– Anabolism– Vitamin B12
• 2- Non-renal loss of potassium e.g.
– Gastrointestinal loss mainly diarrhea and repeated suction
– Discontinued diuretics with alkalosis
– Skin loss
33 - -Renal loss of potassiumRenal loss of potassium
The most common causes e.g.
* Diuretics:
It leads to increase renal tubular flow, aldosteron secretion & alkalosis
*Aldosteron: Causing potassium waisting in pressence of sodium ions
* Renal tubular damage:
From nephrotoxin drugs
*Diabetic ketoacidosis:
As a result of osmotic diuresis, and increased excretion of non-reabsorbable ketoacid anions.
Clinical Effect of HypokalemiaClinical Effect of Hypokalemia
1- Cardiovascular:
arrhythmias then conduction defects
2- Vascular: postural hypotension
3- Muscular: weakness up to cramps
4- Neurological:
hyporeflexia up to impaired mentation
5- Renal features:
Reduced glomerular filtration to renal damage
6- Gastrointestinal:
Paralytic ileus, nausea & vomiting
7- Metabolic features:
Glucose intolerance, metabolic alkalosis
Management of HypokalemiaManagement of Hypokalemia
• General measures:
-Treatment of underlying disease
- Correction of other electrolyte disturbance
-Discontinue offending drug
-Correction of acid base imbalance.
Monitoring for arrhythmias.
Potassium ReplacementPotassium Replacement
• Precautions:
• The maximal infusion in 10 : 40 mMol/h
• The minimal concentration given in peripheral big vessel is 60 mMol/liter fluid
• Potassium should be diluted in nonglucose solutions
• Avoid over infusion & hyperkalemia
Potassium ReplacementPotassium Replacement
• In severe cases i.e. s.k < 2 mMol/L, or ECG changes or muscle weakness:
• Give up to 40mMol/h in one litter normal saline iv.
• In mild to moderate cases i.e. s.k >2 mMol/L and no ECG changes:
• Give up to 10mMol/h iv.
HyperkalemiaHyperkalemia
HyperkalemiaHyperkalemia
• Hyperkalemia means serum potassium more than 5 mMol/L
• It may occur with low, normal or elevated total body potassium stores
• Pseudohyperkalemia results if potassium is released from cells in the test tube.
Most Common Causes of HyperkalemiaMost Common Causes of Hyperkalemia
• I- Decreased excretory capacity
• II-Excess intake of potassium
• III- Translocation from ICF to ECF
I- Decreased excretory capacityI- Decreased excretory capacity
1- Renal failure when GFR decreases below 10ml/min
2- Potassium sparing diuretics
3- Hypoaldosteronism
4 ACE inhibitors
5- NSAID
II-Excess intake of potassiumII-Excess intake of potassium
1- Iatrogenic excess potassium supplement
2- Stored blood
3- Salt substitutes
III- Translocation from ICF to ECFIII- Translocation from ICF to ECF
1- Acidosis
2- Severe catabolism & Rabdomyolysis
3- Insulin deficiency
4- Aldosteron antagonists
5- Digitalis toxicity
6-Hyperosmolality
Clinical features of HyperkalemiaClinical features of Hyperkalemia
* Cardiovascular:
1- Arrhythmias mainly VT & VF
2- Heart block
3- Delayed conduction
4- Ventricular standstill
Clinical features of HyperkalemiaClinical features of Hyperkalemia
• *Neuromuscular manifestations
1- Paresthesia
2- Muscle weakness
3- Flaccid paralysis
4- Mental confusion
Treatment of HyperkalemiaTreatment of Hyperkalemia
• General Measures:
– Treatment of underlying disease
– Restriction of exogenous potassium
– Removal of offending drugs
Treatment of HyperkalemiaTreatment of Hyperkalemia
• Mild Hyperkalemia:
• Restriction of potassium and liberalization of sodium and water are enough.
Treatment of HyperkalemiaTreatment of Hyperkalemia
• Severe Hyperkalemia:
1-Calcium 5 mMol IV over 5 min.
2-Sodium Bicarb. 50: 100 mMol over 5min.
3-Loop diuretics
4-Glucose and insulin
5-Hypertonic saline
Treatment of HyperkalemiaTreatment of Hyperkalemia
6- In resistant cases:
Potassium-binding resins in 50ml sorbitol 20: 30 g orally/4h
7- Inhaled or infused B2 blocker
8- Dialysis