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Fluid and electrolyte imbalance and management


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This presentation provides information about fluid balance in the body, various types of fluid and electrolyte imbalances and their management.

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Fluid and electrolyte imbalance and management

  1. 1. Seminar On Fluid and Electrolyte Imbalance Raksha Yadav 1st Year M.Sc. Nursing AIIMS Rishikesh
  4. 4. Water content of the body
  5. 5.  Body fluids are distributed in two distinct area: intracellular fluid (ICF) 40% body weight Extracellular fluid (ECF) 20% body weight Interstitial fluid - 15% body weight Plasma -5% body weight
  7. 7. Mechanisms controlling fluid & electrolyte movement  Diffusion  Facilitated diffusion  Active transport  Osmosis  Hydrostatic pressure  Oncotic pressure
  8. 8. Regulation of water balance
  9. 9.  Hypothalamic regulation  Pituitary regulation  Adrenal cortical regulation  Renal regulation  Cardiac regulation  Gastro-intestinal regulation
  10. 10. Aldosterone  Hormone secreted from the zona glomerulosa cells of adrenal cortex  Stimulates kidneys Retain sodium Retain water Secrete potassium
  11. 11. Antidiuretic hormone  Also called arginine vasopressin (AVP).  ADH is produced in neuron cell bodies in supraoptic and paraventricular nuclei of the Hypothalamus, and stored in posterior pituitary.  Physiological function  Promote the reabsorption of water in the collecting duct.
  12. 12. The natriuretic peptide family  Four peptides of this family have been identified, including: Atrial natriuretic peptide (ANP) Brain natriuretic peptide (BNP) C-type natriuretic peptide (CNP) Urodilatin  Function: Diuretic and natriuretic actions
  13. 13. Atrial Natriuretic Peptide: Function
  14. 14. The sensation of thirst  Conscious desire for water  Major factor that determines fluid intake  Initiated by the osmoreceptors in hypothalamus that are stimulated by increase in osmotic pressure of body fluids  Also stimulated by a decrease in the blood pressure through the baroreceptors.
  15. 15. The regulation of thirsty reaction  The stimulus sensed by osmoreceptor: • Not a change in the extracellular fluid osmolality • But a change in osmoreceptor neuron size or in the some intracellular substance.
  16. 16. Abnormalities in the Regulation of Body Fluid.  Fluid Volume Deficit (ECFVD)- Dehydration  Fluid Volume Excess- Over hydration
  17. 17. Extra Cellular Fluid Volume Deficit (ECFVD)  A decrease in intravascular and interstitial fluids.  It is a common and serious fluid imbalance that results in vascular fluid volume loss (hypovolemia).
  18. 18.  Risk Factors:  Diarrhea, vomiting  Fistula drainage  Diabetic ketoacidosis  Hemorrhage  Difficulty to swallowing  Aged  Severe mentally ill patient
  19. 19.  Degrees of dehydration: o Mild o Moderate o Severe  Types of dehydration: o Hyper-osmolar o Iso-osmolar o Hypo-osmolar
  20. 20.  Laboratory findings:  Increased Osmolality  Increased or normal serum sodium level  BUN (> 25 mg/d1)  Hyperglycaemia (>120 mg / dl)  Increased specific gravity of urine  Elevated hematocrit (>55%)
  21. 21. Management of Dehydration  Oral rehydration  IV fluids  Correction of the underlying problem  Dietary management  Nursing management
  22. 22. Falls Precautions:  Assess for orthostatic hypotension  Assess muscle strength in legs  Orient the client to the environment  Remind the client to call for help before getting out of bed or a chair  Help the client get out of bed or a chair  Provide, or remind the client to use, a walker or cane for ambulating
  23. 23.  Provide adequate lighting at all times, especially at night  Keep the call light within reach, and ensure that the client can use it  Place the bed in the lowest position with the brakes locked  Place objects that the client needs within reach  Ensure that adequate handrails are present in the client's room, bathroom, and hall  Encourage family members or significant other to stay with the client
  24. 24. Extra Cellular Fluid Volume Excess/ Overhydration  ECFVE is increased fluid retention in the intravascular & interstitial spaces (third spacing)
  25. 25. Etiology:  Administering fluids rapidly or in a large amount  Failure to excrete fluids: o Heart failure o Renal disorders o Venous obstructions o Decreased plasma proteins o Excessive fluid ingestion o Increased ADH & Aldosterone Decreased Excretion Increased absorption
  26. 26.  Laboratory findings:  Decreased Osmolality  Decreased or normal serum sodium level  BUN (<8 mg/dl)  Decreased specific gravity of urine  Decreased hematocrit (<45%)
  27. 27. Management of over hydration  ICFVE is treated by the addition of solutes to IV fluids.  Use of D5%, 0.45% Nacl will help to correct ICFVE when the cause is water excess.  Oral fluids such as water and soft drinks should be given in addition to water and ice chips.  IV therapy should be monitored every hour.
  28. 28.  Monitor vital signs and intake- output  Weight should be checked daily to measure fluid gain or loss.  Administer prescribed antiemetic as needed to allow food and fluids to be ingested.  Safety measures are necessary when the client displays behavioral changes.
  29. 29. NURSING INTERVENTIONS  Monitor cardiovascular, respiratory, neuromuscular, renal, integumentary, and gastrointestinal status.  Prevent further fluid overload and restore normal fluid balance.  Administer diuretics; osmotic diuretics typically are prescribed first to prevent severe electrolyte imbalances.
  30. 30.  Restrict fluid and sodium intake as prescribed.  Monitor intake and output; monitor weight.  Monitor electrolyte values, and prepare to administer medication to treat an imbalance if present.
  31. 31. Electrolyte Balance and Imbalance  Sodium: Hyponatremia Hypernatremia
  32. 32. Hyponatremia • Definition: – Commonly defined as a serum sodium concentration <135 mEq/L – Hyponatremia represents a relative excess of water in relation to sodium.
  33. 33. Hyponatremia is the most common electrolyte disorder Acute hyponatremia (developing over 48hr or less) are subject to more severe degrees of cerebral edema sodium level is less than 105 mEq/L, the mortality is over 50% Chronic hyponatremia (developing over more than 48hr) experience milder degrees of cerebral edema
  34. 34. Types of hyponatremia Hypovolemic hyponatremia Euvolemic hyponatremia Hypervolemic hyponatremia Redistributive hyponatremia
  35. 35. Hypovolemic hyponatremia  Develops as sodium and free water are lost and/or replaced by inappropriately hypotonic fluids  Sodium can be lost through renal or non-renal routes
  36. 36.  Nonrenal loss:  GI losses Vomiting, Diarrhea, fistulas, pancreatitis  Excessive sweating  Third spacing of fluids ascites, peritonitis, pancreatitis, and burns  Cerebral salt-wasting syndrome traumatic brain injury, aneurysmal subarachnoid hemorrhage, and intracranial surgery Must distinguish from SIADH
  37. 37.  Renal Loss: Acute or chronic renal insufficiency Diuretics
  38. 38. Euvolemic hyponatremia  Sodium deficit is more and the volume remains same.  Etiology: Psychogenic polydipsia, often in psychiatric patients Administration of hypotonic intravenous (5% DW) or irrigation fluids ( sorbitol, glycerin) in the immediate postoperative period
  39. 39. administration of hypotonic maintenance intravenous fluids Infants who may have been given inappropriate amounts of free water bowel preparation before colonoscopy or colorectal surgery
  40. 40. Hypervolemic hyponatremia  Total body sodium increases, and TBW increases to a greater extent.  Can be renal or non-renal acute or chronic renal failure dysfunctional kidneys are unable to excrete the ingested sodium load cirrhosis, congestive heart failure, or nephrotic syndrome
  41. 41. Redistributive hyponatremia Water shifts from the intracellular to the extracellular compartment, with a resultant dilution of sodium. The TBW and total body sodium are unchanged. This condition occurs with hyperglycemia Administration of mannitol
  42. 42. MEDICAL MANAGEMENT  Determine cause of hyponatremia and to correct it.  If client has hyponatremia due to fluid volume excess, intake of fluids will be restricted to allow the sodium to regain balance.  If the serum sodium level falls below 125 mEq/L, sodium replacement is needed.
  43. 43. PHARMACOLOGIC MANAGEMENT  For client with moderate hyponatremia 125 meq/ L I/V saline solution (0.9% Nacl) or lactated Ringer solution may be ordered.  When the serum sodium level is 115 meq / L or less, a concentrated saline solution such as 3 % Nacl is indicated.
  44. 44. NURSING INTERVENTIONS  Monitor cardiovascular, respiratory, neuromuscular, cerebral, renal, and gastrointestinal status of the client.  If hyponatremia is accompanied by a fluid volume deficit (hypovolemia), IV sodium chloride infusions are administered to restore sodium content and fluid volume.
  45. 45.  If hyponatremia is accompanied by fluid volume excess (hypervolemia), osmotic diuretics are administered to promote the excretion of water rather than sodium.  Instruct the client to increase oral sodium intake and inform the client about the foods to include in the diet.  If the client is taking lithium (Lithobid), monitor the lithium level, because hyponatremia can cause diminished lithium excretion, resulting in toxicity.
  46. 46. Hypernatremia  Hypernatremia is usually due to water deficit  Etiology:  Excess water loss : eg- heat exposure diabetes insipidus  Impaired thirst: eg - primary hypodypsia, comatose  Excessive Na+ retention
  47. 47. Clinical features of hypernatremia  Excessive thirst, polyuria, nausea  Muscular weakness, neuromuscular irritability  Altered mental status,focal neurological deficit occasionally coma or seizures
  48. 48. Treatment  correct water deficit  Rate of correction : -Acute hypernatremia- 1mEq/L/hr -Chronic hypernatremia-1mEq/L/hr or 10mEq/L over 24hr -rapid correction may lead to cerebral edema
  49. 49. Dietary management
  50. 50. HYPOKALEMIA Hypokalemia is a serum potassium level of less than 3.5 mEq /L
  51. 51. Etiological factors of hypokalemia
  52. 52. Clinical manifestations
  53. 53. Medical management  Determining & correcting the cause of the imbalance.  Extreme hypokalemia requires cardiac monitoring.
  54. 54. Pharmacological Management  Oral potassium replacement therapy is usually prescribed for mild hypokalemia.  Potassium is extremely irritating to gastric mucosa; therefore the drug must be taken with Glass of water or juice or during meals.  Potassium chloride can be administered intravenously for moderate or severe hypokalemia & must be diluted in IV fluids.
  55. 55.  Administration of potassium by IV push may result in cardiac arrests. Potassium can be given in doses of 10 to 20 mEq/ hour diluted in IV fluid if the client is on heart monitor.  High concentration of potassium is irritating to heart muscle. Thus correcting a potassium deficit may take several days.
  56. 56. Dietary management  The administration of foods that are high in potassium help to correct the problem as well as prevent further potassium losses.
  57. 57. HYPERKALEMIA Hyperkalemia is an Elevated potassium level over 5.0 mEq/L.
  58. 58. ETIOLOGY  Retention of Potassium- Renal insufficiency, renal failure, decreased urine output, potassium sparing diuretics.  Excessive release of Cellular Potassium - severe traumatic injuries. Severe burns, severe infection, metabolic acidosis.  Excessive IV infusions or Oral administration of potassium.
  61. 61. MEDICAL MANAGEMENT  When serum potassium level is 5.0 to 5.5 mEq/L restrict potassium intake.  If potassium Excess is due to metabolic acidosis, correcting the acidosis with sodium bicarbonate promotes potassium uptake into the cells.  Improving urine output decreases elevated serum potassium level.
  62. 62. DIETARY MANAGEMENT  When hyperkalemia is severe, immediate actions are needed to be taken to avoid severe Cardiac disturbances.  The administration of foods that are low in potassium help to correct the problem as well as prevent further potassium excess.
  63. 63. NURSING INTERVENTIONS  Monitor cardiovascular, respiratory, neuromuscular, renal, and gastrointestinal status; place the client on a cardiac monitor.  Discontinue IV potassium and hold oral potassium supplements.  Prepare to administer potassium-excreting diuretics if renal function is not impaired.
  64. 64.  Initiate a potassium-restricted diet.  If renal function is impaired, prepare to administer sodium polystyrene sulfonate (Kayexalate).  Prepare the client for dialysis if potassium levels are critically high.  Prepare for the IV administration of hypertonic glucose with regular insulin to move excess potassium into the cells.
  65. 65.  Monitor renal function.  Teach the client to avoid foods high in potassium.  Instruct the client to avoid the use of salt substitutes or other potassium-containing substances.
  66. 66. Calcium
  67. 67. HYPOCALCEMIA  Hypocalcemia is serum calcium below 4.5 meq/L or 8.5 mg/dl.
  68. 68. Etiology  Malabsorption of fat in intestine.  Metabolic alkalosis  Renal failure with hyperphsophatemia, acute pancreatitis, Burns, Cushing’s disease, hypoparathyrodism.  Medications – Magnesium sulfate.
  69. 69. CLINICAL MANIFESTATIONS  Neuromuscular: Tetany symptoms: Twitching around mouth, tingling and numbness of fingers, facial spasm, convulsions.  Respiratory: Dyspnea, laryngeal spasm.  Gastrointestinal: increased peristalsis, diarrhea.  Cardiovascular: Dysrhythmias, palpitations
  70. 70. MEDICAL MANAGEMENT  Determining & correcting the cause of hypocalcemia.  Asymptomatic hypocalcemia is usually corrected with oral calcium gluconate, calcium lactate or calcium chloride.  Administer calcium supplements 30 minutes before meals for better absorption and with glass of milk because vitamin D is necessary for absorption of calcium from the intestine.
  71. 71.  Intravenous calcium chloride or calcium gluconate (10%) is given slowly to avoid hypertension, bradycardia & other arrhythmias.  Chronic or mild hypocalcemia can be treated in part by having the client consume a diet high in calcium.
  72. 72. NURSING INTERVENTIONS  Monitor cardiovascular, respiratory, neuromuscular, and gastrointestinal status; place the client on a cardiac monitor.  Administer calcium supplements orally or calcium intravenously.  When administering calcium intravenously, warm the injection solution to body temperature before administration and administer slowly, monitor for electrocardiographic changes, and monitor for hypercalcemia.
  73. 73.  Administer medications that increase calcium absorption. i.e. Vitamin D aids in the absorption of calcium from the intestinal tract.  Initiate seizure precautions.  Keep 10% calcium gluconate available for treatment of acute calcium deficit.  Instruct the client to consume foods high in calcium.
  74. 74. HYPERCALCEMIA  Hypercalcemia is a serum level over 5.5 meq/L or 11 mg/L
  75. 75. ETIOLOGY  Metastatic malignancy-lung, breast, Ovarian, Prostatic, bladder, leukemia, Kidney.  Hyperparathyroidism.  Thiazide diuretic therapy.  Prolong immobilization.  Excessive intake of calcium supplements and vitamin D.
  76. 76. CLINICAL MANIFESTATIONS  Gastrointestinal: Anorexia, Vomiting, Constipation  Neuromuscular: Mild to moderate hypercalcemia state –weakness Severe hypercalcemic state-Extreme lethargy  Cardiovascular: Dysrhythmias  Electro-cardiographic Changes: Shortened ST Segment and lengthened QT interval.  Musculoskeletal: Bone pain, fracture.
  78. 78. MEDICAL MANAGEMENT  Treatment consists of correcting the underlying cause.  Intravenous normal saline (0.9% Nacl) given rapidly with furosemide to prevent fluid overload, Promote urinary calcium excretion.  Corticosteroid drugs decrease calcium levels by competing with vitamin D thus resulting in decreased intestinal absorption of calcium.
  79. 79.  If the cause is excessive use of calcium or vitamin D supplements or calcium containing antacids these agents should be either avoided or used in reduced dosage.  A newer form of drug therapy is etidronate di-sodium. This drug reduces serum calcium by reducing normal and abnormal bone reabsorption of calcium and secondarily by reducing bone formation.
  80. 80. NURSING INTERVENTIONS  Monitor cardiovascular, respiratory, neuromuscular, renal, and gastrointestinal status; place the client on a cardiac monitor.  Discontinue IV infusions of solutions containing calcium and oral medications containing calcium or vitamin D.  Discontinue thiazide diuretics and replace with diuretics that enhance the excretion of calcium.
  81. 81.  Administer medications as prescribed that inhibit calcium resorption from the bone, such as phosphorus, calcitonin, bisphosphonates, and prostaglandin synthesis inhibitors (aspirin, nonsteroidal anti-inflammatory drugs).  Prepare the client with severe hypercalcemia for dialysis if medications fail to reduce the serum calcium level.  Instruct the client to avoid foods high in calcium.
  82. 82. Phosphorus  Hypophosphatemia  Hyperphosphatemia
  83. 83. Hypophosphatemia  Hypophosphatemia is defined as plasma phosphorus <1.2mEq/L
  84. 84. Causes of hypophosphatemia  Malabsorption syndrome  TPN  Alcohol withdrawal  Phosphate binding anta-acids  Respiratory alkalosis  Recovery from DKA
  85. 85. Clinical manifestations  Muscle weakness  Osteomalacia  Rhabdomyolysis  Cadiac problems- Dysrhythmias, decreased stroke volume  CNS dysfunction
  86. 86. Management:  Mild cases- treated with dietary restrictions  Teach client about balanced diet  Severe cases: phosphate supplementation
  87. 87. Hyperphosphatemia  Hyperphosphatemia is defined as plasma phosphorus >3mEq/L
  88. 88. Causes of hyperphosphatemia  Excess intake of high phosphate foods  Excess vitamine D supplementation especially in renal insufficiency  Impaired colonic motility  Hypoparathyroidism  Addison’s disease
  89. 89. Clinical manifestations  Tachycardia, palpitations  Restlessness  Anorexia, nausea, vomiting  Hyper-reflexia, tetany  Dysrhythmias
  90. 90. Management:  Mild cases- limit phosphate rich foods ( milk, ice-cream, cheese, meat, fish)  Giving calcium, aluminium products that promotes binding & excretion of phosphate.  Dialysis is the TOC in case of hyperphosphatemia with renal failure.
  91. 91. Magnesium Hypomagnesemia Hypermagnesemia
  92. 92. Hypomagnesemia  Hypomagnesemia is defined as plasma magnesium <1.8mg/dl
  93. 93. Causes of hypomagnesemia  Diarrhea, vomiting  Chronic alcoholism  Prolonged malnutrition  Hyperaldosteronism  Impaired GI absorption  NG suction  Poorly controlled DM
  94. 94. Clinical manifestations  Myocardial irritability  Anorexia, nausea  Abdominal distention  Severe cases: Chvostek’s & Trousseau’s sign, tetany, convulsions, stroke
  95. 95. Management:  Oral magnesium replacement (anta-acids)  Parenteral magnesium sulphate  Increase dietary intake of magnesium (chili, tofu, wheat gram)  Initiate safety & seizure precautions in severe cases and monitor all electrolytes.  Keep watch on rising magnesium levels.
  96. 96. Hypermagnesemia  Hypermagnesemia is defined as plasma magnesium >3mg/dl
  97. 97. Causes of hypermagnesemia  Renal insufficiency  Excessive anta-acid use  Adrenal insufficiency  Ketoacidosis
  98. 98. Clinical manifestations Clinical amnifestations are related to blocked release of Acetylcholine from myoneronal junction which affects muscle cell activity.  Hypotension  Muscle weakness  Loss of DTR  Prolonged QT, PR interval  Lethargy, drowiness  Respiratory paralysis, loss of consiosness
  99. 99. Management:  Low magnesium diet (eat chicken, eggs, green peas, white bread, hamburger)  Decrease magnesium sulphate use  In severe cases saline infusion with diuretics is give to promote magnesium excretion  IV calcium (antagonistic action)  Drugs: Albuterol  If renal failure is also present than hemodialysis is done in severe cases
  100. 100. Bibliography  Priscilla Lemone, Karen Burke. “Medical surgical nursing, critical thinking in client care”. 4th edition (2008). Page no. 185-198  Ignatavicius Workman. “Medical surgical nursing, Patient centred collaborative care”. 6th edition (2010). Elsevier publication. Page no. 1022-1024  Brunner and Suddharth. “Text book of medical surgical nursing”. Page no. 249-255  Guyyton and Hall. “Text book of medical physiology”. 11th edition (2006). Elsevier publications. Page no. 642-650  Gerard.J.Tortora. “Principles of anatomy and physiology”. 11th edition (2006). Wiley publication. Page no. 1122-1130
  101. 101.  K. Sembulingam, Prema Sembulingam. “Essentials of medical physiology”. 5thedition (2010). Jaypee publications. Page no. 302- 309
  102. 102. 1. The type of fluid used to manipulate fluid shifts among compartments states is: A. Whole blood B. TPN C. Albumin D. Normal saline
  103. 103. 2. The balance of anions and cations as it occurs across cell membranes is known as: A. osmotic activity B. Electrical neutrality C. Electrical stability D. Sodium potassium pump
  104. 104. 3. A diet containing the minimum daily sodium requirement for an adult would be: A. no-salt diet B. diet including 2 gm sodium C. diet including 4 gm sodium D. 1500 calorie weight-loss diet
  105. 105. THANK YOU…………