Electrolyte disturbances in icu
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Electrolyte disturbances in icu

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Electrolyte disturbances in icu Electrolyte disturbances in icu Presentation Transcript

  • Electrolyte Disturbances In ICU Dr. Fathia Hassan Khalil
  • Body Fluids • The average body water is 60% of TBW • 65% in males & 55% in females • In obese patient it decrease 5%
  • Sodium
  • Sodium • Sodium is the major ion in ECF • Normal value in blood is 135 : 145 mMol/L
  • Sodium 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.
  • Sodium concentration is regulated by: • Renal system • Endocrine system
  • • 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).
  • Hyponatremia
  • Hyponatremia • 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 Hyponatremia I- Hyponatremia with normal serum osmolality II- Hyponatremia with high serum osmolality III- Hyponatremia with low serum osmolality
  • I-Hyponatremia with normal serum osmolality • 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 Osmolality 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 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 Hypoosmolality • 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- osmolality • 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 Hyponatremia • 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 Hypoosmolar Hyponatremia • Intra vascular volume depletion • Hypotension • Orthostatic hypotension • Tachycardia • Skin dehydration
  • Management of Hypovolemic Hypoosmolar 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
  • 2- Hypervolemic Hypoosmolar Hyponatremia • It is called dilutional hyponatremia • Causes: • CHF • Liver cirrhosis • Nephrotic syndrome
  • Manifestations of Hypervolemic Hypoosmolar 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 Hypoosmolar 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 Hyponatremia * 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 inappropriate 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 Hyponatremia • 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 Hyponatremia • In acute hyponatremia: • -CNS manifestations: • begin by lethargy & confusion up to seizures, cerebral edema & coma • GI symptoms • Muscle cramps & weakness
  • Management of Hyponatremia
  • Management Based on: *Treatment of the cause *Restoration of serum sodium concentration *Normalization of serum osmolality
  • Correction 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
  • Hypernatremia
  • Hypernatremia • 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: • 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 Hypernatremia I- Hypernatremia with hypovolemia II- Hypernatremia with hypervolemia III- Hypernatremia with euvolemia
  • I-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 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 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 Insipidus • I- Central DI • Idiopathic DI • Following head trauma • Neurological disease
  • • 2-Nephrogenic DI • Sickle cell nephropathy • Chronic pyelonephritis • Multiple Myeloma
  • Clinical Features 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 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: 1- Treatment of the underlying cause 2- Volume repletion with isotonic saline Hypotonic 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
  • Potassium
  • Potassium • 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 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
  • Hypokalemia
  • Hypokalemia • 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 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
  • 3- Renal 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 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 Hypokalemia • General measures: -Treatment of underlying disease - Correction of other electrolyte disturbance -Discontinue offending drug -Correction of acid base imbalance. Monitoring for arrhythmias.
  • Potassium 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 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.
  • Hyperkalemia
  • Hyperkalemia • 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 Hyperkalemia • I- Decreased excretory capacity • II-Excess intake of potassium • III- Translocation from ICF to ECF
  • I- 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 potassium 1- Iatrogenic excess potassium supplement 2- Stored blood 3- Salt substitutes
  • III- 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 Hyperkalemia * Cardiovascular: 1- Arrhythmias mainly VT & VF 2- Heart block 3- Delayed conduction 4- Ventricular standstill
  • Clinical features of Hyperkalemia • *Neuromuscular manifestations 1- Paresthesia 2- Muscle weakness 3- Flaccid paralysis 4- Mental confusion
  • Treatment of Hyperkalemia • General Measures: – Treatment of underlying disease – Restriction of exogenous potassium – Removal of offending drugs
  • Treatment of Hyperkalemia • Mild Hyperkalemia: • Restriction of potassium and liberalization of sodium and water are enough.
  • Treatment 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 Hyperkalemia 6- In resistant cases: Potassium-binding resins in 50ml sorbitol 20: 30 g orally/4h 7- Inhaled or infused B2 blocker 8- Dialysis