1.By: Dr. Muhammad Asim Fazal

2. Definition An electrolyte disorder is an imbalance of certainionized salts (i.e., bicarbonate, calcium, chloride, magnesium, phos phate, potassium, and sodium) in the blood. 3. Electrolytes Electrolytes are ionized molecules found throughoutthe blood, tissues, and cells of the body. Cations Anions+ ve - ve 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. 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. Calcium (Ca) Affects neuromuscular performance and Contributes to skeletal growth Blood coagulation. Magnesium (Mg) Influences muscle contractions and Intracellular activity 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. 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. Sodium Normal : 135-145 mEq/L Sodium helps the kidneys to regulate the amount of water the body retains or excretes. 10. HYPERNATREMIA (Serum sodium > 145 mEq/L) Inadequate water intake Increased sodium intake Excessive free water loss: Extra-renal Burns Sweating Tachypnoea 11. Renal Central diabetes insipidus Nephrogenic diabetes insipidus Craniophariangioma Post-operative 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. Treatment of Hypernatremia Acute Hypernatremia can be corrected rapidly Chronic Hypernatremia (more than 48 hours) shouldbe 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. 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. Hypernatremia with hypovolemia Patients should receive isotonic 0.9% normal saline torestore 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. Hypernatremia with euvolemia Water ingestion or intravenous 5% dextrose will resultin the excretion of excess sodium in the urine. 17. Hypernatremia with hypervolemia Furosemide (1mg/kg) to get rid of sodium + Free waterreplacement as 5% D/W (* furosemide alone will aggravate the hypernatremia Dialysis may be required for patients with oliguric renal failure 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. 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. Nausea Abdominal cramping, and/or vomiting Headache Edema (swelling) Muscle weakness and/or tremor Paralysis Disorientation Slowed breathing Seizures Coma 21. Complications The most serious complication of hyponatremia isiatrogenic 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. Correction of Hyponatremia Treatment depends on: Etiology and types of hyponatremia Clinical Condition Serum Na level Ongoing loss 23. Regardless of the patients volume status, anothercommon 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 < 11.5 L/d. 24. Hypovolemic patients Require adequate fluid resuscitation from isotonicfluids (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. Hypervolemic patients May require loop diuretics or dialysis, or both, tocorrect increased total body water and sodium. To treat the basic CAUSE. 26. Euvolemic patients May respond to free water restriction alone. 27. Formula for Correction 28. For Example a non edematous, severely symptomatic 70 kg womanwith 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. 3% hypertonic saline has a sodium concentration of514 mEq/1000 mL. The delivery rate for hypertonic saline can be calculated as: 30. Hypertonic saline in hyper-volemic patients can behazardous, resulting in worsening volume overload, pulmonary edema, and ascites. 31. Potassium Normal : 3.5-5.5 mEq/L Main component of cellular fluid Helps to regulate neuromuscular function and osmotic pressure 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. ECG Changes ECG changes in hyperkalemia include bradycardia, PRinterval prolongation, peaked T waves, QRS widening, and biphasic QRST complexes. Conduction disturbances, such as bundle branch block and atrioventricular block, may occur. Ventricular fibrillation and cardiac arrest are terminal events. 34. Hyperkalemia - Etiology What Causes It? Inadequate Excretion : Renal failure Addisons disease Excessive intake Diet high in potassium (bananas, oranges, tomatoes, dates, high protein diets, salt substitutes, potassium supplements) 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. 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. 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. IV Calcium gluconate 0.5 mEq/kg to reverse cardiaceffects Dialysis in cases of resistant hyperkalemia Nebulized salbutamol Sodium polyesterene sulphate - ion exchange resin for long term management 39. Hypokalemia (Serum K+ < 3.5 mEq/L) Increased Potassium Loss: Extrarenal Diarrhoea Renal RTA, polycystic kidneys, Drugs Endocrine Cushings disease, hyperaldosteronism Decreased Stores Malnutrition Shift into intracellular compartment Alkalosis hyperinsulinemia 40. Symptoms and Signs Muscular weakness, fatigue, and muscle cramps arefrequent 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. 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. Electrocardiogram The electrocardiogram (ECG) shows decreasedamplitude and broadening of T waves, prominent U waves, premature ventricular contractions, and depressed ST segments. 43. Treatment of Hypokalemia Oral potassium supplementation is the safest andeasiest 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. Concentrations of up to 20 mEq/h may be giventhrough a central venous catheter. Continuous ECG monitoring is indicated, and the serum potassium level should be checked every 36 hours. Magnesium deficiency should be corrected, particularly in refractory hypokalemia. 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. HYPERCALCEMIA (Serum Ca++ > 12 mg/dL) Parathyroid excess Multiple myeloma, Vitamin D excess Sarcoidosis Subcutaneous fat necrosis Williams syndrome Thyrotoxicosis Prolonged immobilization 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. 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. 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 4872 hours before reaching full therapeutic effect. Calcitonin may be helpful in the short-term until bisphosphonates reach therapeutic levels. 50. In emergency cases, dialysis with low calcium dialysatemay be needed. 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. Metabolic causes Hypoparathyroidism Pseudohyperthyroidism Hypoprotenemia Acute pancreatitis 53. HYPOCALCEMIA - Symptoms Muscle cramps and spasms Tetany and/or convulsions Mood changes (depression, irritability) Dry skin Brittle nails Facial twitching Latent Tetany Trousseus sign Chvosteks sign 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. HYPERMAGNESEMIA End-stage renal disease, Addison's disease, or An overdose of magnesium salts. 56. Lethargy Hypotension Decreased heart and respiratory rate Muscle weakness Diminished tendon reflexes 57. Treatment Exogenous sources of magnesium should bediscontinued. 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. HYPOMAGNESEMIA Inadequate dietary intake Chronic alcoholism Malnutrition Malabsorption syndromes, Pancreatitis, Aldosteronism, Burns, Hyperparathyroidism, Digestive system disorders, and Diuretic use. 59. Signs and symptoms Leg and foot cramps Weight loss Vomiting Muscle spasms, twitching, and tremors Seizures Muscle weakness Arrthymia 60. Treatment Symptomatic hypomagnesemia requires intravenousmagnesium sulfate 12 g over 560 minutes mixed in either dextrose 5% or 0.9% normal saline. 61. THANKYOU