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