Dyselectrolytemia in icu

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By: Dr. Muhammad Asim Fazal
ICU Doctor.Meeqat Hospital,Madina, KSA

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Dyselectrolytemia in icu

  1. 1. By: Dr. Muhammad Asim Fazal
  2. 2. Definition  An electrolyte disorder is an imbalance of certain ionized salts (i.e., bicarbonate, calcium, chloride, magnesium, phos phate, potassium, and sodium) in the blood.
  3. 3. Electrolytes  Electrolytes are ionized molecules found throughout the blood, tissues, and cells of the body.  · · Cations Anions + ve - ve
  4. 4. General Functions of Electrolytes • • Help to balance pH and acid-base levels in the body. Facilitate the passage of fluid between and within cells through osmosis • Play a part in regulating the function of the neuromuscular, endocrine, and excretory systems.
  5. 5. Specific Electrolytes – Functions •      Sodium (Na) • Helps to balance fluid levels in the body and • Facilitates neuromuscular functioning. • Potassium (K) • Main component of cellular fluid • Helps to regulate neuromuscular function and osmotic pressure.
  6. 6. • • • • • • • Calcium (Ca) Affects neuromuscular performance and Contributes to skeletal growth Blood coagulation. Magnesium (Mg) Influences muscle contractions and Intracellular activity
  7. 7.           • • Chloride (CI-) Regulates blood pressure. • • • • Phosphate (HPO4) Impacts metabolism and regulates acid-base balance and calcium levels. • • Bicarbonate (HCO3) Assists in the regulation of blood pH levels
  8. 8. Normal levels of electrolytes • • • • • • Sodium. 135-145 mEq/L (serum) Potassium. 3.5-5.5 mEq/L (serum) Calcium(Serum) 8.8-10.4 mg/dL (total Ca) Magnesium (Plasma) 1.4-2.1 mEq/L Chloride(Serum) 100-108 mEq/L Phosphate (Plasma) 2.5-4.5 mg/dL (adults)
  9. 9. Sodium • Normal : 135-145 mEq/L  • Sodium helps the kidneys to regulate the amount of water the body retains or excretes.
  10. 10. HYPERNATREMIA (Serum sodium > 145 mEq/L) • • • • • • • Inadequate water intake Increased sodium intake Excessive free water loss: Extra-renal Burns Sweating Tachypnoea
  11. 11. • • • • • Renal Central diabetes insipidus Nephrogenic diabetes insipidus Craniophariangioma Post-operative
  12. 12. Symptoms of hypernatremia               • • • • • • • • • • • • • • Non-specific, Restlessness, Irritability, Muscular twitching, Hyperreflexia, Spasticity, and Seizures With hypotonic losses - signs of volume loss Tachycardia, Hypotension, Decreased JVP, Dry mucosa, Reduced skin turgor and Thick doughy skin
  13. 13. Treatment of Hypernatremia  Acute Hypernatremia can be corrected rapidly  Chronic Hypernatremia (more than 48 hours) should be corrected slowly.  If hypernatremia is rapidly corrected, the osmotic imbalance may cause cerebral edema and potentially severe neurologic impairment.  Aim for serum sodium correction of approximately 12 mol/L/24h (0.5 mmol/L/h)
  14. 14. Volume in (L) to be replaced = Current TBW × [Na] – 140 / 140 where TBW is typically 50% of total mass in women and 55% of total mass in men.
  15. 15. Hypernatremia with hypovolemia  Patients should receive isotonic 0.9% normal saline to restore euvolemia and to treat hyperosmolality  After adequate volume resuscitation with normal saline, 0.45% saline or 5% dextrose (or both) can be used to replace any remaining free water deficit.
  16. 16. Hypernatremia with euvolemia  Water ingestion or intravenous 5% dextrose will result in the excretion of excess sodium in the urine.
  17. 17. Hypernatremia with hypervolemia  Furosemide (1mg/kg) to get rid of sodium + Free water replacement as 5% D/W  • (* furosemide alone will aggravate the hypernatremia  • Dialysis may be required for patients with oliguric renal failure
  18. 18. HYPONATREMIA (Serum sodium less than 135 mEq/L)of all hospitalized patients develop  Up to 1% hyponatremia, making it one of the most common electrolyte disorders.  Hyponatremia usually reflects excess water retention relative to sodium rather than sodium deficiency.  The clinician should be wary about hyponatremia since mismanagement can result in neurologic catastrophes from cerebral osmotic demyelination.
  19. 19. Symptoms andis Signs depends on its  Whether hyponatremia symptomatic severity and acuity.  Chronic disease can be severe (sodium concentration < 110 mEq/L), yet remarkably asymptomatic because the brain has adapted by decreasing its tonicity over weeks to months.  Acute disease that has developed over hours to days can be severely symptomatic with relatively modest hyponatremia.
  20. 20.           Nausea • Abdominal cramping, and/or vomiting • Headache • Edema (swelling) • Muscle weakness and/or tremor • Paralysis • Disorientation • Slowed breathing • Seizures • Coma
  21. 21. Complications  The most serious complication of hyponatremia is iatrogenic cerebral osmotic demyelination from overly rapid sodium correction.  Also called central pontine myelinolysis.  Demyelination may occur days after sodium correction or initial neurologic recovery from hyponatremia.  The neurologic effects are generally catastrophic and irreversible.
  22. 22. Correction of Hyponatremia  Treatment depends on:  Etiology and types of hyponatremia  Clinical Condition  Serum Na level  Ongoing loss
  23. 23.  Regardless of the patient’s volume status, another common feature is to restrict free water and hypotonic fluid intake, since these solutions will exacerbate hyponatremia.  Free water intake from oral intake and intravenous fluids should generally be < 1–1.5 L/d.
  24. 24. Hypovolemic patients  Require adequate fluid resuscitation from isotonic fluids (either normal saline or lactated Ringer solution) to suppress the hypovolemic stimulus for ADH release.  Patients with cerebral salt wasting may require hypertonic saline to prevent circulatory collapse; some may respond to fludrocortisone.
  25. 25. Hypervolemic patients  May require loop diuretics or dialysis, or both, to correct increased total body water and sodium.  To treat the basic CAUSE.
  26. 26. Euvolemic patients  May respond to free water restriction alone.
  27. 27. Formula for Correction
  28. 28. For Example  a non edematous, severely symptomatic 70 kg woman with a serum sodium of 122 mEq/L should have her serum sodium corrected to approximately 132 mEq/L in the first 24 hours. Her sodium deficit is calculated as:
  29. 29.  3% hypertonic saline has a sodium concentration of 514 mEq/1000 mL. The delivery rate for hypertonic saline can be calculated as:
  30. 30.  Hypertonic saline in hyper-volemic patients can be hazardous, resulting in worsening volume overload, pulmonary edema, and ascites.
  31. 31. Potassium • Normal : 3.5-5.5 mEq/L  Main component of cellular fluid • Helps to regulate neuromuscular function and osmotic pressure
  32. 32. Hyperkalemia S. Potassium > 5.5 m Eq/L  Signs and Symptoms • • • • • • Fatigue Weakness Tingling, numbness, or other unusual sensations Paralysis Palpitations Difficulty breathing
  33. 33. ECG Changes  ECG changes in hyperkalemia include bradycardia, PR interval prolongation, peaked T waves, QRS widening, and biphasic QRS–T complexes.  Conduction disturbances, such as bundle branch block and atrioventricular block, may occur.  Ventricular fibrillation and cardiac arrest are terminal events.
  34. 34. Hyperkalemia - Etiology  What Causes It? •     Inadequate Excretion : • Renal failure • Addison’s disease • Excessive intake • Diet high in potassium (bananas, oranges, tomatoes, dates, high protein diets, salt substitutes, potassium supplements)
  35. 35. •       Shifting of potassium from tissues • Trauma, especially crush injuries or burns • Hemolysis • Acidosis • Insulin deficiency • Drugs • Digoxin, scuuinyl choline, beta agonists, potassium sparing diuretics
  36. 36. Treatment of Hyperkalemia  Mild: (Serum K+ = 5.5 to 6.0 m Eq/L) • Stop intake of potassium  • Stop offending drugs  Restrict potassium rich diet
  37. 37.  Moderate to Severe: (in addition to above..) • (Serum K+ = 6.0 to 8.0 m Eq/L or peaked T waves)  • Glucose Insulin Infusion : (0.5g/kg with 0.3 U regular insulin / g of glucose)  • Sodabicarb infusion (2 mEq/kg of NaHCO3 over 5 – 10 min)
  38. 38.  IV Calcium gluconate 0.5 mEq/kg – to reverse cardiac effects  • Dialysis in cases of resistant hyperkalemia  • Nebulized salbutamol  • Sodium polyesterene sulphate - ion exchange resin for long term management
  39. 39. Hypokalemia (Serum K+ < 3.5 mEq/L)  Increased Potassium Loss: • • • • • • • • Extrarenal – Diarrhoea Renal – RTA, polycystic kidneys, Drugs Endocrine – Cushing’s disease, hyperaldosteronism Decreased Stores Malnutrition Shift into intracellular compartment Alkalosis hyperinsulinemia
  40. 40. Symptoms and Signs  Muscular weakness, fatigue, and muscle cramps are frequent complaints in mild to moderate hypokalemia.  Gastrointestinal smooth muscle involvement may result in constipation or ileus.  Flaccid paralysis, hyporeflexia, hypercapnia, tetany, and rhabdomyolysis may be seen with severe hypokalemia (< 2.5 mEq/L).
  41. 41. Laboratory Findings  Urinary potassium concentration is low (< 20 mEq/L) as a result of extrarenal loss (eg, diarrhea, vomiting) and inappropriately high (> 40 mEq/L) with renal loss (eg, mineralocorticoid excess, Bartter syndrome, Liddle syndrome)
  42. 42. Electrocardiogram  The electrocardiogram (ECG) shows decreased amplitude and broadening of T waves, prominent U waves, premature ventricular contractions, and depressed ST segments.
  43. 43. Treatment of Hypokalemia  Oral potassium supplementation is the safest and easiest treatment for mild to moderate deficiency.  Intravenous potassium is indicated for patients with severe hypokalemia and for those who cannot take oral supplementation.  For severe deficiency, potassium may be given through a peripheral intravenous line in a concentration up to 40 mEq/L and at rates up to 10 mEq/h.
  44. 44.  Concentrations of up to 20 mEq/h may be given through a central venous catheter.  Continuous ECG monitoring is indicated, and the serum potassium level should be checked every 3–6 hours.  Magnesium deficiency should be corrected, particularly in refractory hypokalemia.
  45. 45. Formula for correction of Potassium  Required K+ in mmol = 0.3 × Weight × [ Desired K+ level – Measured K+ level]  Deficit corrected over 24 hour period.
  46. 46. HYPERCALCEMIA (Serum Ca++ > 12 mg/dL)  Parathyroid excess • • • • • • • Multiple myeloma, Vitamin D excess Sarcoidosis Subcutaneous fat necrosis William’s syndrome Thyrotoxicosis Prolonged immobilization
  47. 47.  Metastatic cancer, •      Multiple bone fractures, • Milk-alkali syndrome, and • Paget's disease. • Drugs • Excessive use of calcium-containing supplements • Certain over-the-counter medications (i.e., Antacids) may also cause hypercalcemia.
  48. 48. HYPERCALCEMIA - Symptoms              Nonspecific • fatigue • constipation • depression • confusion • muscle pain • nausea and vomiting • dehydration • increased urination • irregular heartbeat (arrhythmia) • Urinary stones • Nephrocalcinosis • Stupor & coma – S.Ca > 15 mg/dL)
  49. 49. HYPERCALCEMIA - Management  Forced saline diuresis with fruesemide • Treat primary cause  Bisphosphonates are the treatment of choice for hypercalcemia of malignancy. Although they are safe, effective, and normalize calcium in > 70% of patients, bisphosphonates may require up to 48–72 hours before reaching full therapeutic effect.  Calcitonin may be helpful in the short-term until bisphosphonates reach therapeutic levels.
  50. 50.  In emergency cases, dialysis with low calcium dialysate may be needed.
  51. 51. HYPOCALCEMIA (Serum Calcium < 8 mg/dL)           Vitamin D deficiency • Malabsorption • Abnormal metabolism • Prolonged phynetoin medication • Increased Losses • Idiopathic hypercalcuria • Renal tubular necrosis • Frusemide therapy • Hypomagnesemia • Hyperphosphatemia
  52. 52. • • • • • Metabolic causes Hypoparathyroidism Pseudohyperthyroidism Hypoprotenemia Acute pancreatitis
  53. 53. HYPOCALCEMIA - Symptoms  Muscle cramps and spasms • • • • • • • • Tetany and/or convulsions Mood changes (depression, irritability) Dry skin Brittle nails Facial twitching Latent Tetany Trousseu’s sign Chvostek’s sign
  54. 54. HYPOCALCEMIA - Management  Tetany, laryngospasm, seizures • 2 ml/kg of 10 5 Calcium gluconate slow IV under cardiac monitoring  • Later  • Oral calcium supplementation – 40 to 80 mg/kg/d  • Treat Vit. D def.
  55. 55. HYPERMAGNESEMIA  End-stage renal disease, • • Addison's disease, or An overdose of magnesium salts.
  56. 56.  Lethargy • • • • Hypotension Decreased heart and respiratory rate Muscle weakness Diminished tendon reflexes
  57. 57. Treatment  Exogenous sources of magnesium should be discontinued.  Calcium antagonizes Mg2+ and may be given intravenously as calcium chloride, 500 mg or more at a rate of 100 mg (4.1 mmol) per minute.  Hemodialysis or peritoneal dialysis may be necessary to remove magnesium, particularly with severe kidney disease.
  58. 58. HYPOMAGNESEMIA           Inadequate dietary intake • Chronic alcoholism • Malnutrition • Malabsorption syndromes, • Pancreatitis, • Aldosteronism, • Burns, • Hyperparathyroidism, • Digestive system disorders, and • Diuretic use.
  59. 59. Signs and symptoms  Leg and foot cramps • • • • • • Weight loss Vomiting Muscle spasms, twitching, and tremors Seizures Muscle weakness Arrthymia
  60. 60. Treatment  Symptomatic hypomagnesemia requires intravenous magnesium sulfate 1–2 g over 5–60 minutes mixed in either dextrose 5% or 0.9% normal saline.
  61. 61. THANKYOU

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