1. Fluids and Electrolytes Lea Marie Y. Angeles, M.D.

2. Composition of body fluids Total body water

3. Composition of body fluids Fluid compartments Total body water is divided into: Intracellular fluid (ICF) Extracellular fluid (ECF)

4. Composition of body fluids Electrolyte composition

5. Composition of body fluids Osmolality The ICF and ECF are in osmotic equilibrium Normal plasma osmolality: 285-295 mOsm/kg Effective osmolality (tonicity) Determines the osmotic force that is mediating the shift of water between the ICF and ECF Osmolal gap Present when the measured osmolality exceeds the calculated osmolality by >10 mOsm/kg

6. Regulation of Osmolality and Volume Regulation of osmolality ↑ effective osmolality ↓ Hypothalamus ↓ Secretion of ADH ↓ V2 receptors in collecting duct cells of kidneys ↓ ↑ cAMP ↓ ↑permeability to water ↓ ↑urine concentration, ↓water excretion

7. Regulation of osmolality and volume Regulation of osmolality ↑serum osmolality ↓ Hypothalamus ↓ Cerebral cortex ↓ Thirst stimulation

8. Regulation of osmolality and volume Regulation of volume Na balance Main regulator of volume status Kidney Determines Na balance Regulates Na balance by altering the percentage of filtered Na that is resorbed along the nephron Effective intravascular volume Most important determinant of renal Na excretion

9. Regulation of osmolality and volume Regulation of volume Na resorption Occurs throughout the nephron Proximal tubule and loop of Henle Sites where majority of filtered Na is resorbed Distal tubule and collecting ducts Main sites for precise regulation of Na balance

10. Renin-angiotensin system ↓effective intravascular volume ↓ Juxtaglomerular apparatus ↓ Renin ↓ Angiotensinogen ↓ Angiotensin I ↓angiotensin converting enzyme Angiotensin II ↑Na resorption ↑aldosterone ↓ ↑Na resorption ↑K excretion vasoconstriction ↓ ↑BP

11. Regulation of osmolality and volume Regulation of volume Volume expansion ↓ Atrial natriuretic peptide ↓ ↑GFR Inhibition of Na resorption (in collecting duct)

12. Sodium metabolism Sodium Dominant cation of ECF Principal determinant of extracellular osmolality Necessary for maintenance of intravascular volume

13. Sodium metabolism Intake Diet Presence of glucose enhances Na absorption due to the presence of a co-transport system Excretion Occurs in: Stool Sweat Kidney

14. Hypernatremia Na concentration >150 mEq/L Etiology Excessive sodium Improperly mixed formula Excess sodium bicarbonate Ingestion of sea water or NaCl Intentional salt poisoning (child abuse or Munchausen syndrome by proxy) Intravenous hypertonic saline Hyperaldosteronism

15. Hypernatremia Etiology Water deficit Nephrogenic diabetes insipidus Acquired X-linked Autosomal recessive Autosomal dominant Central diabetes insipidus Acquired Autosomal recessive Autosomal dominant Wolfram syndrome

16. Hypernatremia Etiology Water deficit Increased insensible losses Premature infants Radiant warmers Phototerapy Inadequate intake Ineffective breastfeeding Child neglect or abuse Adipsia

17. Hypernatremia Etiology Water and sodium deficits Gastrointestinal losses Diarrhea Emesis/nasogastric suction Osmotic cathartics (lactulose) Cutaneous losses Burns Excessive sweating Renal losses Osmotic diuretics (mannitol) Diabetes mellitus Chronic kidney disease (dysplasia and obstructive uropathy) Polyuric phase of acute tubular necrosis Postobstructive diuresis

18. Hypernatremia Clinical manifestations Dehydration Irritable, restless, weak, lethargic High-pitched cry, hyperpnea Very thirsty (if alert) May be febrile Hyperglycemia, mild hypocalcemia Brain hemorrhage

19. Hypernatremia Clinical manifestations Seizures and coma Central pontine myelinosis, extrapontine myelinosis Thrombotic complications Stroke Dural sinus thrombosis Peripheral thrombosis Renal venous thrombosis

20. Hypernatremia Treatment Goal Decrease serum Na by 12 mEq/L every 24 hours, rate of 0.5 mEq/L/hr

21. Hypernatremia Treatment In hypernatremic dehydration, 1st priority is restoration of intravascular volume with isotonic fluid Acute severe hypernatremia 20 to Na administration can be corrected rapidly Peritoneal dialysis Loop diuretic With Na overload – hypernatremia is corrected with Na-free IVF (D5W)

22. Hypernatremia Treatment Hyperglycemia from hypernatremia is usually not treated with insulin, rather, decrease the glucose concentration of IVF Treat underlying cause

23. Hyponatremia Serum Na level <135 mEq/L Etiology Pseudohyponatremia Hyperosmolality Hyperglycemia Mannitol

24. Hyponatremia Etiology Hypovolemic hyponatremia Extrarenal losses Gastrointestinal (emesis, diarrhea) Skin (sweating, burns) Third space losses Renal losses Thiazide or loop diuretics Osmotic diuresis Postobstructive diuresis Polyuric phase of acute tubular necrosis Juvenile nephronophthisis

25. Hyponatremia Etiology Hypovolemic hyponatremia Renal losses Autosomal recessive polycystic kidney disease Tubulointerstitial nephritis Obstructive uropathy Cerebral salt wasting Proximal (type II) renal tubular acidosis Lack of aldosterone effect (high serum potassium) Absent aldosterone Pseudohypoaldosteronism type Urinary tract obstruction and/or infection

26. Hyponatremia Etiology Euvolemic hyponatremia Syndrome of inappropriate antidiuretic hormone Nephrogenic syndrome of inappropriate diuresis Desmopressin acetate Glucocorticoid deficiency Hypothyroidism

27. Hyponatremia Etiology Euvolemic hyponatremia Water intoxication Iatrogenic (excess hypotonic intravenous fluid) Feeding infants excessive water products Swimming lessons Tap water enema Child abuse Psychogenic polydipsia Diluted formula Marathon running with excessive water intake Beer protomania

28. Hyponatremia Etiology Hypervolemic hyponatremia Congestive heart failure Cirrhosis Nephrotic syndrome Renal failure Capillary leak due to sepsis Hypoalbuminemia due to gastrointestinal disease (protein-losing enteropathy)

29. Hyponatremia Clinical manifestations Hyponatremia ->↑intracellular water ->cellular swelling Brain cell swelling -> ↑ICP Acute severe hyponatremia -> brainstem herniation and apnea

30. Hyponatremia Clinical manifestations Neurologic symptoms: Anorexia Nausea Emesis Malaise Lethargy Confusion Agitation Headache Seizures Coma Decreased reflexes

31. Hyponatremia Clinical manifestations Hypothermia Cheyne-Stokes respiration Muscle cramps, weakness Patients with hyponatremic dehydration have more manifestations of intravascular volume depletion than patients with equivalent water loss but with normal or increased serum Na concentration

32. Hyponatremia Treatment Avoid overly rapid correction Rapid correction may cause central pontine myelinosis Avoid correcting serum Na by >12 mEq/L/day (does not apply to acute hyponatremia) Severe symptoms (shock or sezures) Give a bolus of hypertonic saline to produce a small rapid increase in serum Na and the effect on serum osmolality leads to a decrease in brain edema

33. Hyponatremia Treatment Hypovolemic hyponatremia 1st step – restore intravascular volume with isotonic saline Hypervolemic hyponatremia Cornerstone of therapy – water and Na restriction Nephrotic syndrome – albumin and diuresis Congestive heart failure – improve cardiac output

34. Hyponatremia Treatment Isovolemic hyponatremia Acute symptomatic hyponatremia 20 to water intoxication give hypertonic saline to reverse cerebral edema Chronic hyponatremia because of poor solute intake give appropriate formula, eliminate excess water intake Non-physiologic stimuli for ADH production water restriction Hyponatremia of hypothyroidism or cortisol deficiency Specific hormone replacement

35. Hyponatremia Treatment Isovolemic hyponatremia SIADH Fluid restriction Furosemide + hypertonic saline Conivaptan V2-receptot antagonist Decreases permeability of collecting duct to water producing aquaresis Approved for short-term therapy of euvolemic patients with hyponatremia (usually SIADH)

36. Potassium Metabolism Intracellular K concentration: 150 mEq/L Na+K+-ATPase maintains high intracellular K concentration by pumping Na out of the cell and K into the cell Resulting chemical gradient is used to produce the resting membrane potential of cells

37. Potassium metabolism Potassium Necessary for electrical responsiveness of nerve and muscle cells and for contractility of cardiac, skeletal, and smooth muscles Intracellular concentration affects cellular enzymes Necessary for maintaining cell volume Majority of body K is in muscle

38. Potassium metabolism Substances that increase K movement into cells Insulin ↑pH β-adrenergic agonists Factors that increase extracellular [K] ↓pH α-adrenergic agonists Exercise ↑plasma osmolality

39. Potassium metabolism Intake Recommended: 1-2 mEq/L Most absorption occurs in small intestines Colon – exchanges body K for luminal Na Excretion Sweat Colon Urine Principal sites of K regulation: distal tubule and collecting duct

40. Potassium Excretion Aldosterone – principal hormone regulating K excretion Factors that increase urinary K excretion: Glucocorticoids ADH High urinary flow rate High Na delivery to distal nephron Loop and thiazide diuretics

41. Potassium metabolism Excretion Factors that decrease K excretion Insulin Catecholamines Urinary ammonia

42. Hyperkalemia Etiology Spurious laboratory value Hemolysis Tissue ischemia during blood drawing Thrombocytosis Leukocytosis Increased intake Intravenous or oral Blood transfusions

43. Hyperkalemia Etiology Transcellular shifts Acidosis Rhabdomyolysis Tumor lysis syndrome Tissue necrosis Hemolysis/hematomas/gastrointestinal bleeding Succinylcholine Digitalis intoxication Fluoride intoxication

44. Hyperkalemia Etiology Transcellular shifts β-adrenergic blockers Exercise Hyperosmolality Insulin deficiency Malignant hyperthermia Hyperkalemic periodic paralysis

45. Hyperkalemia Etiology Decreased excretion Renal failure Primary adrenal disease Acquired Addison disease 21-hydroxylase deficiency 3β-hydroxysteroid dehydrogenase deficiency Lipoid congenital adrenal hyperplasia Adrenal hypoplasia congenita Aldosterone synthase deficiency Adrenoleukodystrophy

46. Hyperkalemia Etiology Hyporeninemic hypoaldosteronism Urinary tract obstruction Sickle cell disease Kidney transplant Lupus nephritis Renal tubular disease Pseudohypoaldosteronism type I Pseudohypoaldosteronism type II Urinary tract obstruction Sickle cell disease Kidney transplant

47. Hyperkalemia Etiology Medications Angiotensin-converting enzyme inhibitors Angiotensin II blockers Potassium-sparing diuretics Calcineurin inhibitors Nonsteroidal anti-inflammatory drugs Trimethoprim Heparin Drug-induced potassium channel syndrome

48. Hyperkalemia Clinical manifestations Most important effects of hyperkalemia are due to the role of potassium in membrane polarization ECG changes Peaking of T waves Increased P – R interval Flattening of P wave Widening of QRS complex Ventricular fibrillation

49. Hyperkalemia Clinical manifestations Asystole Paresthesia, weakness, tingling

50. Hyperkalemia Treatment 1st step: stop all sources of additional K (oral or IV) If K level is >6-6.5mEq/L, obtain ECG Goals: To stabilize the heart to prevent life-threatening arrythmias To remove K from the body

51. Hyperkalemia Treatment Intravenous Ca NaHCO3 Insulin – must be given with glucose to prevent hypoglycemia Nebulized salbutamol

52. Hyperkalemia Treatment Measures that remove K from the body Loop diuretic Na polysterene sulfonate (Kayexelate) Dialysis Hemodialysis Peritoneal dialysis

53. Hypokalemia Etiology Spurious High white blood cell count Transcellular shifts Alkalemia Insulin β-adrenergic agonists Drugs/toxins (theophylline, barium, toluene, cesium chloride) Hypokalemic periodic paralysis Thyrotoxic periodic paralysis

54. Hypokalemia Etiology Decreased intake Anorexia nervosa Extrarenal losses Diarrhea Laxative abuse Sweating Sodium polystyrene sulfonate (Kayexelate) or clay ingestion

55. Hypokalemia Etiology Renal losses With metabolic acidosis Distal renal tubular acidosis Proximal renal tubular acidosis Ureterosigmoidostomy Diabetic ketoacidosis Without specific acid-base disturbance Tubular toxins: amphotericin, cisplatin, aminoglycosides Interstitial nephritis Diuretic phase of acute tubular necrosis Postobstructive diuresis Hypomagnesemia High urine anions (e.g. penicillin or penicillin derivatives)

56. Hypokalemia Etiology Renal losses With metabolic alkalosis Low urine chloride Emesis/nasogastric suction Chloride-losing diarrhea Cystic fibrosis Low-chloride formula Posthypercapnia Previous loop or thiazide diuretic use

57. Hypokalemia Etiology Renal losses High urine chloride and normal blood pressure Gitelman syndrome Bartter syndrome Autosomal dominant hypoparathyroidism Loop and thiazide diuretics

58. Hypokalemia Etiology Renal losses High urine chloride and high blood pressure Adrenal adenoma or hyperplasia Glucocorticoid-remedial aldosteronism Renovascular disease Renin-secreting tumor 17α-hydroxylase deficiency 11β-hydroxylase deficiency Cushing syndrome 11β-hydroxysteroid dehydrogenase deficiency

59. Hypokalemia Etiology Renal losses Licorice Liddle syndrome

60. Hypokalemia Clinical manifestations Affects heart and skeletal muscles ECG changes: Flattened T wave Depressed ST segment Appearance of a U wave Hypokalemia makes the heart susceptible to digitalis-induced arrythmias such as SVT, ventricular tachycardia and heart block

61. Hypokalemia Clinical manifestations Muscle weakness, cramps Paralysis Slowing of GI motility Impairment of bladder function -> urinary retention Polyuria and polydipsia Stimulation of renal ammonia production Kidney damage Poor linear growth

62. Hypokalemia Treatment IV potassium Dose:0.5-1mEq/kg given x 1 hr, max dose in adults: 40 mEq Oral potassium

63. Magnesium metabolism 4th most common cation and 3rd most common intracellular cation 50-60% of body Mg is in bone Most intracellular Mg is in muscle and liver Normal plasma concentration: 1.5-2.3 mg/dL or 1.2-1.9 mEq/L Necessary cation for hundreds of enzymes Important for membrane stabilization and nerve conduction

64. Magnesium metabolism Intake 30-40% of dietary Mg is absorbed Small intestine Major site of Mg absorption Absorption Decreases in the presence of substances that complex with Mg (free fatty acids, fiber, phytate, phosphate, oxalate) Decreases with increased intestinal motility and Ca Enhanced by vitamin D, PTH

65. Magnesium metabolism Excretion Renal excretion Principal regulator of Mg balance No defined hormonal regulatory system

66. Hypomagnesemia Etiology Gastrointestinal disorders Diarrhea Nasogastric suction or emesis Inflammatory bowel disease Celiac disease Cystic fibrosis Intestinal lymphangiectasia Small bowel resection or bypass Pancreatitis Protein calorie malnutrition Hypomagnesemia with secondary hypocalcemia

67. Hypomagnesemia Etiology Renal disorders Medications: amphotericin, cisplatin, cyclosporin, loop diuretics, mannitol, pentamidine, aminoglycosides, loop diuretics Diabetes Acute tubular necrosis (recovery phase) Postobstructive nephropathy Chronic kidney diseases: interstitial nephritis, glomerulonephritis, postrenal transplant Hypercalcemia Intravenous fluids

68. Hypomagnesemia Etiology Renal disorders Primary aldosteronism Genetic diseases Gitelman syndrome Bartter syndrome Familial hypomagnesemianwith hypercalciuria and nephrocalcinosis Autosomal recessive renal magnesium wasting Autosomal dominant renal magnesium wasting Autosomal dominant hypoparathyroidism Mitochondrial disorders

69. Hypomagnesemia Etiology Miscellaneous causes Poor intake Hungry bone syndrome Insulin administration Pancreatitis Intrauterine growth retardation Infants of diabetic mothers Exchange transfusion

70. Hypomagnesemia Clinical manifestations Usually occurs only at Mg levels <0.7 mg/dL Tetany, (+)Chvostek and Trosseau signs, seizures Rickets Hypokalemia

71. Hypomagnesemia Treatment Severe Parenteral Mg MgSO4 25-50 mg/kg (0.05-0.1 ml/kg of 50% solution; 2.5-5 mg/kg of elemental Mg); dose is repeated every 6 hours (every 8-12 hours in neonates) for 2-3 doses Long-term therapy Oral – dose is divided to decrease cathartic side effect Alternatives: IM injection and nighttime nasogastric infusion

72. Hypermagnesemia Almost always secondary to excessive intake Unusual except in neonates born to mothers receiving IV Mg for pre-eclampsia or eclampsia

73. Hypermagnesemia Etiology Mg is present in high amounts in certain laxatives, enemas, cathartics used to treat drug overdose and antacids Neonates may receive high amounts transplacentally if maternal levels are elevated Kidneys excrete excessive Mg but this is decreased in patients with chronic renal failure

74. Hypermagnesemia Etiology Conditions predisposing to hypermagnesemia Chronic renal failure Familial hypocalciuric hypercalcemia Diabetic ketoacidosis Lithium ingestion Milk alkali syndrome Tumor lysis syndrome

75. Hypermagnesemia Clinical manifestations Symptoms appear when plasma Mg level is >4.5 mg/dL Hypermagnesemia inhibits Ach release at neuromuscular junction -> hypotonia, hyporeflexia, weakness, paralysis Nausea, vomiting, hypocalcemia Direct CNS depression -> lethargy, sleepiness, poor suck

76. Hypermagnesemia Clinical manifestations Hypotension, flushing ECG changes Prolonged P-R, QRS and Q-T intervals Severe hypermagnesemia (>15 mg/dL) -> complete heart block and cardiac arrest

77. Hypermagnesemia Treatment IV hydration and loop diuretics Dialysis Exchange transfusion In acute emergencies: 100 mg/kg of IV Ca gluconate (transiently effective)

78. Phosphorus metabolism Most phosphorus is in bone or is intracellular, w/ <1% in plasma Phosphrous concentration varies with age Component of ATP and other trinucleotides, critical for cellular energy metabolism Necessary for nucleic acid synthesis Component of cell membranes and other structures Essential component of bone and is necessary for skeletal mineralization

79. Phosphorus metabolism Intake Readily available in food Best sources: milk and milk products High concentration: meat and fish Vegetables higher than fruits and grains 65% of intake is absorbed Absorption Almost exclusively in small intestines via a paracellular diffuse process and a vitamin D regulated transcellular pathway

80. Phosphorus metabolism Excretion Kidney – regulates phophorus balance Approximately 85% of filtered load is resorbed PTH – decreases resorption of phosphate, increasing urinary phosphate

81. Low plasma phosphorus ↓ 1α-hydroxylase (in kidney) ↓ Converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol) ↓ ↑ intestinal absorption of phosphorus Maximal renal resorption of phosphorus

82. Phosphorus metabolism Excretion Phosphatonin Inhibits renal resorption of phosphorus -> phosphaturia and hypophosphatemia Inhibits synthesis of calcitriol by decreasing 1α-hydroxylase activity

83. Serum phosphorus during childhood AGE 0-5 days 1-3 years 4-11 years 12-15 years 16-19 years PHOSPHORUS 4.-8.2 mg/dL 3.8-6.5 mg/dL 3.7-5.6 mg/dL 2.9-5.4 mg/dL 2.7-4.7 mg/dL

84. Hypophosphatemia Etiology Transcellular shifts Glucose infusion Insulin Refeeding Total parenteral nutrition Respiratory alkalosis Tumor growth Bone marrow transplantation Hungry bone syndrome

85. Hypophosphatemia Etiology Decreased intake Nutritional Premature infants Low phosphorus formula Antacids and other phosphate binders

86. Hypophosphatemia Etiology Renal losses Hyperparathyroidism Parathyroid hormone-related peptide X-linked hypophosphatemic rickets Tumor-induced osteomalacia Autosomal dominant hypophosphatemic rickets Fanconi syndrome Dent disease Hypophosphatemic rickets with hypercalciuria

87. Hypophosphatemia Etiology Renal losses Hypophosphatemia due to mutations in the sodium-phosphate cotransporter Volume expansion and intravenous fluids Metabolic acidosis Diuretics Glycosuria Glucocorticoids Kidney transplantation

88. Hypophosphatemia Etiology Multifactorial Vitamin D deficiency Vitamin D-dependent rickets type I Vitamin D-dependent rickets type 2 Alcoholism Sepsis Dialysis

89. Hypophosphatemia Clinical manifestations Long term phosphorus deficiency: rickets Severe hypophosphatemia: <1-1.5 mg/dL, may affect every organ Hemolysis and dysfunction of WBC Impaired release of oxygen to tissues Proximal muscle weakness and atrophy In ICU – slow weaning from ventilator or acute respiratory failure

90. Hypophosphatemia Clinical manifestations Rhabdomyolysis Cardiac dysfunction Neurologic symptoms Tremors Paresthesia Ataxia Seizures Delirium Coma

91. Hypophosphatemia Treatment Mild hypophosphatemia No treatment except if the situation suggests it’s a chronic depletion or if there are ongoing losses Oral phosphorus Intravenous phosphorus Increase dietary phosphorus

92. Hyperphosphatemia Etiology Renal insufficiency – most common cause Can occur because gastrointestinal absorption of large dietary intake of phosphorus is unguarded Develops when kidney function is <30% of normal

93. Hyperphosphatemia Etiology Transcellular shifts Tumor lysis syndrome Rhadomyolysis Acute hemolysis Diabetic ketoacidosis and lactic acidosis

94. Hyperphosphatemia Etiology Increase intake Enemas and laxatives Cow’s milk in infants Treatment of hypophosphatemia Vitamin D intoxication

95. Hyperphosphatemia Etiology Decreased excretion Renal failure Hypoparathyroidism or pseudohypoparathyroidism Acromegaly Hyperthyroidism Tumoral calcinosis with hyperphosphatemia

96. Clinical manifestations Principal clinical consequences: Hypocalcemia Systemic calcification Hypocalcemia Due to tissue deposition of Ca-P salt Inhibition of 1,25-dihydroxyvitamin D production Decreased bone resorption

97. Hyperphosphatemia Clinical manifestations Systemic calcification Occurs because solubility of phosphorus and calcium in plasma is exceeded Foreign body feeling in conjunctiva, erythema and injection More ominous manifestation: hypoxia from pulmonary calcification renal failure from nephrocalcinosis

98. Hyperphosphatemia Treatment Mild hyperphosphatemia in a patient with reasonable renal function resolves spontaneously Dietary phosphorus restriction Intravenous fluids

99. Hyperphosphatemia Treatment More significant hyperphosphatemia Add oral phosphorus binder Dialysis If unresponsive to conservative management or if renal insufficiency is supervening

100. Fluid therapy Degree of dehydration Mild (<5% in an infant; <3% in an older child or adult) Normal or increased pulse Decreased urine output Thirsty Normal physical activity

101. Fluid therapy Degree of dehydration Moderate (5-10% in an infant; 3-6% in an older child or adult) Tachycardia Little or no urine output Irritable/lethargic Sunken eyes and fontanel Decreased tears Dry mucous membranes Mild delay in elasticity (skin turgor) Delayed capillary refill (>1.5 sec) Cool and pale

102. Fluid therapy Degree of dehydration Severe (>10% in an infant; >6% in an older child or adult) Rapid and weak or absent peripheral pulses Decreased blood pressure No urine output Very sunken eyes and fontanel No tears Parched mucous membranes Delayed elasticity (poor skin turgor) Very delayed capillary refill (>3 sec) Cold and mottled Limp depressed consciousness

103. Fluid therapy Oral rehydration Preferred mode of rehydration and replacement of ongoing losses Risks associated with severe dehydration that may necessitate IV resuscitation Age <6 months Prematurity Chronic illness Fever >38 0C if <3 months or 39 0C if 3-36 months Bloody diarrhea Persistent emesis Poor urine output Sunken eyes Depressed level of consciousness

104. Fluid therapy Limitations to ORT Shock Ileus Intussusception Carbohydrate intolerance Severe emesis High stool output (>10ml/kg/hr)

105. Fluid therapy Guidelines for oral rehydration Mild dehydration 50 ml/kg of ORS given within 4 hours Moderate dehydration 100 ml/kg of ORS over 4 hours Additional 10 ml/kg of ORS for each watery stool Maintenance Volume of ORS ingested should equal volume of stool losses

106. Fluid therapy Intravenous therapy Fluid management of dehydration Restore intravascular volume Normal saline: 20 ml/kg over 20 min Repeat as needed Rapid volume repletion: 20 ml/kg normal saline or lactated ringer’s (max=1L) over 2 hours Calculate 24-hour fluid needs: maintenance + deficit volume Subtract isotonic fluid already administered from 24-hour fluid needs Administer remaining volume over 24 hours Replace ongoing losses as they occur

107. Fluid therapy Phases of fluid therapy Rehydration Also called deficit therapy Aimed at immediate correction o the abnormal losses of fluids and electrolytes which are reflected in the body composition by an acute loss in body weight Should be accomplished within 6 hours after initiation of treatment

108. Fluid therapy Phases of fluid therapy Maintenance Intended to stabilize internal milieu after it has been restored to normal during rehydration Normal daily requirement of fluid and electrolytes which is engendered by metabolic activity or expenditure is provided and simultaneously, all ongoing and abnormal losses should be actively replaced