10. fluids and electrolytes


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10. fluids and electrolytes

  1. 1. Fluids and Electrolytes<br />Lea Marie Y. Angeles, M.D.<br />
  2. 2. Composition of body fluids<br />Total body water<br />
  3. 3. Composition of body fluids<br />Fluid compartments<br />Total body water is divided into:<br />Intracellular fluid (ICF)<br />Extracellular fluid (ECF)<br />
  4. 4. Composition of body fluids<br />Electrolyte composition<br />
  5. 5. Composition of body fluids<br />Osmolality<br />The ICF and ECF are in osmotic equilibrium<br />Normal plasma osmolality: 285-295 mOsm/kg<br />Effective osmolality (tonicity) <br />Determines the osmotic force that is mediating the shift of water between the ICF and ECF<br />Osmolal gap<br />Present when the measured osmolality exceeds the calculated osmolality by >10 mOsm/kg<br />
  6. 6. Regulation of Osmolality and Volume<br />Regulation of osmolality<br />↑ effective osmolality<br />↓<br />Hypothalamus<br />↓<br />Secretion of ADH<br />↓<br />V2 receptors in collecting duct cells of kidneys<br />↓<br />↑ cAMP<br />↓<br />↑permeability to water<br />↓<br />↑urine concentration, ↓water excretion<br />
  7. 7. Regulation of osmolality and volume<br />Regulation of osmolality<br />↑serum osmolality<br />↓<br />Hypothalamus<br />↓<br />Cerebral cortex<br />↓<br />Thirst stimulation<br />
  8. 8. Regulation of osmolality and volume<br />Regulation of volume<br />Na balance<br />Main regulator of volume status <br />Kidney<br />Determines Na balance<br />Regulates Na balance by altering the percentage of filtered Na that is resorbed along the nephron<br />Effective intravascular volume<br />Most important determinant of renal Na excretion<br />
  9. 9. Regulation of osmolality and volume<br />Regulation of volume<br />Na resorption <br />Occurs throughout the nephron<br />Proximal tubule and loop of Henle<br />Sites where majority of filtered Na is resorbed<br />Distal tubule and collecting ducts<br />Main sites for precise regulation of Na balance<br />
  10. 10. Renin-angiotensin system<br />↓effective intravascular volume<br />↓<br />Juxtaglomerular apparatus<br />↓<br />Renin<br />↓<br />Angiotensinogen<br />↓<br />Angiotensin I<br /> ↓angiotensin converting enzyme<br />Angiotensin II<br />↑Na resorption<br />↑aldosterone<br />↓<br />↑Na resorption<br />↑K excretion<br />vasoconstriction<br />↓<br /> ↑BP<br />
  11. 11. Regulation of osmolality and volume<br />Regulation of volume<br />Volume expansion<br />↓<br />Atrial natriuretic peptide<br />↓<br />↑GFR<br />Inhibition of Na resorption (in collecting duct)<br />
  12. 12. Sodium metabolism<br />Sodium<br />Dominant cation of ECF<br />Principal determinant of extracellular osmolality<br />Necessary for maintenance of intravascular volume<br />
  13. 13. Sodium metabolism<br />Intake<br />Diet<br />Presence of glucose enhances Na absorption due to the presence of a co-transport system<br />Excretion<br />Occurs in:<br />Stool<br />Sweat<br />Kidney<br />
  14. 14. Hypernatremia <br />Na concentration >150 mEq/L<br />Etiology<br />Excessive sodium<br />Improperly mixed formula<br />Excess sodium bicarbonate<br />Ingestion of sea water or NaCl<br />Intentional salt poisoning (child abuse or Munchausen syndrome by proxy)<br />Intravenous hypertonic saline<br />Hyperaldosteronism<br />
  15. 15. Hypernatremia <br />Etiology<br />Water deficit<br />Nephrogenic diabetes insipidus<br />Acquired<br />X-linked<br />Autosomal recessive<br />Autosomal dominant<br />Central diabetes insipidus<br />Acquired<br />Autosomal recessive<br />Autosomal dominant<br />Wolfram syndrome<br />
  16. 16. Hypernatremia <br />Etiology <br />Water deficit<br />Increased insensible losses<br />Premature infants<br />Radiant warmers<br />Phototerapy <br />Inadequate intake<br />Ineffective breastfeeding<br />Child neglect or abuse<br />Adipsia <br />
  17. 17. Hypernatremia <br />Etiology<br />Water and sodium deficits<br />Gastrointestinal losses<br />Diarrhea<br />Emesis/nasogastric suction<br />Osmotic cathartics (lactulose)<br />Cutaneous losses<br />Burns<br />Excessive sweating<br />Renal losses<br />Osmotic diuretics (mannitol)<br />Diabetes mellitus<br />Chronic kidney disease (dysplasia and obstructive uropathy)<br />Polyuric phase of acute tubular necrosis<br />Postobstructive diuresis<br />
  18. 18. Hypernatremia <br />Clinical manifestations<br />Dehydration<br />Irritable, restless, weak, lethargic<br />High-pitched cry, hyperpnea<br />Very thirsty (if alert)<br />May be febrile<br />Hyperglycemia, mild hypocalcemia<br />Brain hemorrhage<br />
  19. 19. Hypernatremia <br />Clinical manifestations<br />Seizures and coma<br />Central pontine myelinosis, extrapontine myelinosis<br />Thrombotic complications<br />Stroke<br />Dural sinus thrombosis<br />Peripheral thrombosis<br />Renal venous thrombosis<br />
  20. 20. Hypernatremia <br />Treatment <br />Goal <br />Decrease serum Na by 12 mEq/L every 24 hours, rate of 0.5 mEq/L/hr<br />
  21. 21. Hypernatremia <br />Treatment <br />In hypernatremic dehydration, 1st priority is restoration of intravascular volume with isotonic fluid<br />Acute severe hypernatremia 20 to Na administration can be corrected rapidly<br />Peritoneal dialysis<br />Loop diuretic<br />With Na overload – hypernatremia is corrected with Na-free IVF (D5W)<br />
  22. 22. Hypernatremia <br />Treatment<br />Hyperglycemia from hypernatremia is usually not treated with insulin, rather, decrease the glucose concentration of IVF<br />Treat underlying cause<br />
  23. 23. Hyponatremia <br />Serum Na level <135 mEq/L<br />Etiology<br />Pseudohyponatremia<br />Hyperosmolality<br />Hyperglycemia<br />Mannitol<br />
  24. 24. Hyponatremia <br />Etiology<br />Hypovolemic hyponatremia<br />Extrarenal losses<br />Gastrointestinal (emesis, diarrhea)<br />Skin (sweating, burns)<br />Third space losses<br />Renal losses<br />Thiazide or loop diuretics<br />Osmotic diuresis<br />Postobstructive diuresis<br />Polyuric phase of acute tubular necrosis<br />Juvenile nephronophthisis<br />
  25. 25. Hyponatremia <br />Etiology<br />Hypovolemic hyponatremia<br />Renal losses<br />Autosomal recessive polycystic kidney disease<br />Tubulointerstitial nephritis<br />Obstructive uropathy<br />Cerebral salt wasting<br />Proximal (type II) renal tubular acidosis<br />Lack of aldosterone effect (high serum potassium)<br />Absent aldosterone<br />Pseudohypoaldosteronism type<br />Urinary tract obstruction and/or infection<br />
  26. 26. Hyponatremia <br />Etiology<br />Euvolemic hyponatremia<br />Syndrome of inappropriate antidiuretic hormone<br />Nephrogenic syndrome of inappropriate diuresis<br />Desmopressin acetate<br />Glucocorticoid deficiency<br />Hypothyroidism <br />
  27. 27. Hyponatremia <br />Etiology<br />Euvolemic hyponatremia<br />Water intoxication<br />Iatrogenic (excess hypotonic intravenous fluid)<br />Feeding infants excessive water products<br />Swimming lessons<br />Tap water enema<br />Child abuse<br />Psychogenic polydipsia<br />Diluted formula<br />Marathon running with excessive water intake <br />Beer protomania<br />
  28. 28. Hyponatremia <br />Etiology<br />Hypervolemic hyponatremia<br />Congestive heart failure<br />Cirrhosis <br />Nephrotic syndrome<br />Renal failure<br />Capillary leak due to sepsis<br />Hypoalbuminemia due to gastrointestinal disease (protein-losing enteropathy)<br />
  29. 29. Hyponatremia <br />Clinical manifestations<br />Hyponatremia ->↑intracellular water ->cellular swelling<br />Brain cell swelling -> ↑ICP<br />Acute severe hyponatremia -> brainstem herniation and apnea<br />
  30. 30. Hyponatremia <br />Clinical manifestations<br />Neurologic symptoms:<br />Anorexia<br />Nausea<br />Emesis<br />Malaise<br />Lethargy<br />Confusion<br />Agitation<br />Headache<br />Seizures<br />Coma<br />Decreased reflexes<br />
  31. 31. Hyponatremia <br />Clinical manifestations<br />Hypothermia<br />Cheyne-Stokes respiration<br />Muscle cramps, weakness<br />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<br />
  32. 32. Hyponatremia <br />Treatment<br />Avoid overly rapid correction<br />Rapid correction may cause central pontine myelinosis<br />Avoid correcting serum Na by >12 mEq/L/day (does not apply to acute hyponatremia)<br />Severe symptoms (shock or sezures) <br />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 <br />
  33. 33. Hyponatremia <br />Treatment<br />Hypovolemic hyponatremia<br />1st step – restore intravascular volume with isotonic saline<br />Hypervolemic hyponatremia<br />Cornerstone of therapy – water and Na restriction<br />Nephrotic syndrome – albumin and diuresis<br />Congestive heart failure – improve cardiac output<br />
  34. 34. Hyponatremia <br />Treatment <br />Isovolemic hyponatremia<br />Acute symptomatic hyponatremia 20 to water intoxication <br />give hypertonic saline to reverse cerebral edema<br />Chronic hyponatremia because of poor solute intake<br /> give appropriate formula, eliminate excess water intake<br />Non-physiologic stimuli for ADH production <br />water restriction<br />Hyponatremia of hypothyroidism or cortisol deficiency<br />Specific hormone replacement<br />
  35. 35. Hyponatremia <br />Treatment<br />Isovolemic hyponatremia<br />SIADH<br />Fluid restriction<br />Furosemide + hypertonic saline<br />Conivaptan <br />V2-receptot antagonist<br />Decreases permeability of collecting duct to water producing aquaresis<br />Approved for short-term therapy of euvolemic patients with hyponatremia (usually SIADH)<br />
  36. 36. Potassium Metabolism<br />Intracellular K concentration: 150 mEq/L<br />Na+K+-ATPase maintains high intracellular K concentration by pumping Na out of the cell and K into the cell<br />Resulting chemical gradient is used to produce the resting membrane potential of cells<br />
  37. 37. Potassium metabolism<br />Potassium<br />Necessary for electrical responsiveness of nerve and muscle cells and for contractility of cardiac, skeletal, and smooth muscles<br />Intracellular concentration affects cellular enzymes<br />Necessary for maintaining cell volume<br />Majority of body K is in muscle<br />
  38. 38. Potassium metabolism<br />Substances that increase K movement into cells<br />Insulin<br />↑pH<br />β-adrenergic agonists<br />Factors that increase extracellular [K]<br />↓pH<br />α-adrenergic agonists<br />Exercise<br />↑plasma osmolality<br />
  39. 39. Potassium metabolism<br />Intake <br />Recommended: 1-2 mEq/L<br />Most absorption occurs in small intestines<br />Colon – exchanges body K for luminal Na<br />Excretion<br />Sweat<br />Colon<br />Urine<br />Principal sites of K regulation: distal tubule and collecting duct<br />
  40. 40. Potassium <br />Excretion <br />Aldosterone – principal hormone regulating K excretion<br />Factors that increase urinary K excretion:<br />Glucocorticoids<br />ADH<br />High urinary flow rate<br />High Na delivery to distal nephron <br />Loop and thiazide diuretics<br />
  41. 41. Potassium metabolism<br />Excretion<br />Factors that decrease K excretion<br />Insulin<br />Catecholamines<br />Urinary ammonia<br />
  42. 42. Hyperkalemia <br />Etiology<br />Spurious laboratory value<br />Hemolysis<br />Tissue ischemia during blood drawing<br />Thrombocytosis<br />Leukocytosis<br />Increased intake<br />Intravenous or oral<br />Blood transfusions<br />
  43. 43. Hyperkalemia <br />Etiology<br />Transcellular shifts<br />Acidosis<br />Rhabdomyolysis<br />Tumor lysis syndrome<br />Tissue necrosis<br />Hemolysis/hematomas/gastrointestinal bleeding<br />Succinylcholine<br />Digitalis intoxication<br />Fluoride intoxication<br />
  44. 44. Hyperkalemia <br />Etiology <br />Transcellular shifts<br />β-adrenergic blockers<br />Exercise<br />Hyperosmolality<br />Insulin deficiency<br />Malignant hyperthermia<br />Hyperkalemic periodic paralysis<br />
  45. 45. Hyperkalemia <br />Etiology<br />Decreased excretion<br />Renal failure<br />Primary adrenal disease<br />Acquired Addison disease<br />21-hydroxylase deficiency<br />3β-hydroxysteroid dehydrogenase deficiency<br />Lipoid congenital adrenal hyperplasia<br />Adrenal hypoplasia congenita<br />Aldosterone synthase deficiency<br />Adrenoleukodystrophy <br />
  46. 46. Hyperkalemia <br />Etiology <br />Hyporeninemic hypoaldosteronism<br />Urinary tract obstruction<br />Sickle cell disease<br />Kidney transplant<br />Lupus nephritis<br />Renal tubular disease<br />Pseudohypoaldosteronism type I<br />Pseudohypoaldosteronism type II<br />Urinary tract obstruction<br />Sickle cell disease<br />Kidney transplant<br />
  47. 47. Hyperkalemia <br />Etiology <br />Medications<br />Angiotensin-converting enzyme inhibitors<br />Angiotensin II blockers<br />Potassium-sparing diuretics<br />Calcineurin inhibitors<br />Nonsteroidal anti-inflammatory drugs<br />Trimethoprim<br />Heparin<br />Drug-induced potassium channel syndrome<br />
  48. 48. Hyperkalemia <br />Clinical manifestations<br />Most important effects of hyperkalemia are due to the role of potassium in membrane polarization<br />ECG changes<br />Peaking of T waves<br />Increased P – R interval<br />Flattening of P wave<br />Widening of QRS complex<br />Ventricular fibrillation<br />
  49. 49. Hyperkalemia <br />Clinical manifestations<br />Asystole<br />Paresthesia, weakness, tingling<br />
  50. 50. Hyperkalemia <br />Treatment <br />1st step: stop all sources of additional K (oral or IV)<br />If K level is >6-6.5mEq/L, obtain ECG<br />Goals:<br />To stabilize the heart to prevent life-threatening arrythmias<br />To remove K from the body<br />
  51. 51. Hyperkalemia <br />Treatment<br />Intravenous Ca<br />NaHCO3<br />Insulin – must be given with glucose to prevent hypoglycemia<br />Nebulized salbutamol<br />
  52. 52. Hyperkalemia <br />Treatment<br />Measures that remove K from the body<br />Loop diuretic<br />Na polysterene sulfonate (Kayexelate)<br />Dialysis<br />Hemodialysis<br />Peritoneal dialysis<br />
  53. 53. Hypokalemia <br />Etiology<br />Spurious<br />High white blood cell count<br />Transcellular shifts<br />Alkalemia<br />Insulin<br />β-adrenergic agonists<br />Drugs/toxins (theophylline, barium, toluene, cesium chloride)<br />Hypokalemic periodic paralysis<br />Thyrotoxic periodic paralysis<br />
  54. 54. Hypokalemia <br />Etiology<br />Decreased intake<br />Anorexia nervosa<br />Extrarenal losses<br />Diarrhea<br />Laxative abuse<br />Sweating<br />Sodium polystyrene sulfonate (Kayexelate) or clay ingestion<br />
  55. 55. Hypokalemia <br />Etiology<br />Renal losses<br />With metabolic acidosis<br />Distal renal tubular acidosis<br />Proximal renal tubular acidosis<br />Ureterosigmoidostomy<br />Diabetic ketoacidosis<br />Without specific acid-base disturbance<br />Tubular toxins: amphotericin, cisplatin, aminoglycosides<br />Interstitial nephritis<br />Diuretic phase of acute tubular necrosis<br />Postobstructive diuresis<br />Hypomagnesemia<br />High urine anions (e.g. penicillin or penicillin derivatives)<br />
  56. 56. Hypokalemia <br />Etiology<br />Renal losses<br />With metabolic alkalosis<br />Low urine chloride<br />Emesis/nasogastric suction<br />Chloride-losing diarrhea<br />Cystic fibrosis<br />Low-chloride formula<br />Posthypercapnia<br />Previous loop or thiazide diuretic use<br />
  57. 57. Hypokalemia <br />Etiology<br />Renal losses<br />High urine chloride and normal blood pressure<br />Gitelman syndrome<br />Bartter syndrome<br />Autosomal dominant hypoparathyroidism<br />Loop and thiazide diuretics <br />
  58. 58. Hypokalemia <br />Etiology <br />Renal losses<br />High urine chloride and high blood pressure<br />Adrenal adenoma or hyperplasia<br />Glucocorticoid-remedial aldosteronism<br />Renovascular disease<br />Renin-secreting tumor<br />17α-hydroxylase deficiency<br />11β-hydroxylase deficiency<br />Cushing syndrome<br />11β-hydroxysteroid dehydrogenase deficiency<br />
  59. 59. Hypokalemia <br />Etiology<br />Renal losses<br />Licorice<br />Liddle syndrome<br />
  60. 60. Hypokalemia <br />Clinical manifestations<br />Affects heart and skeletal muscles<br />ECG changes:<br />Flattened T wave<br />Depressed ST segment<br />Appearance of a U wave<br />Hypokalemia makes the heart susceptible to digitalis-induced arrythmias such as SVT, ventricular tachycardia and heart block<br />
  61. 61. Hypokalemia <br />Clinical manifestations<br />Muscle weakness, cramps<br />Paralysis<br />Slowing of GI motility<br />Impairment of bladder function -> urinary retention<br />Polyuria and polydipsia<br />Stimulation of renal ammonia production <br />Kidney damage<br />Poor linear growth<br />
  62. 62. Hypokalemia <br />Treatment<br />IV potassium<br />Dose:0.5-1mEq/kg given x 1 hr, max dose in adults: 40 mEq<br />Oral potassium<br />
  63. 63. Magnesium metabolism<br />4th most common cation and 3rd most common intracellular cation<br />50-60% of body Mg is in bone<br />Most intracellular Mg is in muscle and liver<br />Normal plasma concentration: <br />1.5-2.3 mg/dL or 1.2-1.9 mEq/L<br />Necessary cation for hundreds of enzymes<br />Important for membrane stabilization and nerve conduction<br />
  64. 64. Magnesium metabolism<br />Intake<br />30-40% of dietary Mg is absorbed<br />Small intestine<br />Major site of Mg absorption<br />Absorption<br />Decreases in the presence of substances that complex with Mg (free fatty acids, fiber, phytate, phosphate, oxalate)<br />Decreases with increased intestinal motility and Ca<br />Enhanced by vitamin D, PTH<br />
  65. 65. Magnesium metabolism<br />Excretion<br />Renal excretion<br />Principal regulator of Mg balance<br />No defined hormonal regulatory system<br />
  66. 66. Hypomagnesemia <br />Etiology <br />Gastrointestinal disorders<br />Diarrhea<br />Nasogastric suction or emesis<br />Inflammatory bowel disease<br />Celiac disease<br />Cystic fibrosis<br />Intestinal lymphangiectasia<br />Small bowel resection or bypass<br />Pancreatitis<br />Protein calorie malnutrition<br />Hypomagnesemia with secondary hypocalcemia<br />
  67. 67. Hypomagnesemia <br />Etiology <br />Renal disorders<br />Medications: amphotericin, cisplatin, cyclosporin, loop diuretics, mannitol, pentamidine, aminoglycosides, loop diuretics<br />Diabetes <br />Acute tubular necrosis (recovery phase)<br />Postobstructive nephropathy<br />Chronic kidney diseases: interstitial nephritis, glomerulonephritis, postrenal transplant<br />Hypercalcemia<br />Intravenous fluids<br />
  68. 68. Hypomagnesemia <br />Etiology<br />Renal disorders<br />Primary aldosteronism<br />Genetic diseases<br />Gitelman syndrome<br />Bartter syndrome<br />Familial hypomagnesemianwith hypercalciuria and nephrocalcinosis<br />Autosomal recessive renal magnesium wasting<br />Autosomal dominant renal magnesium wasting<br />Autosomal dominant hypoparathyroidism<br />Mitochondrial disorders<br />
  69. 69. Hypomagnesemia <br />Etiology <br />Miscellaneous causes<br />Poor intake<br />Hungry bone syndrome<br />Insulin administration<br />Pancreatitis<br />Intrauterine growth retardation<br />Infants of diabetic mothers<br />Exchange transfusion<br />
  70. 70. Hypomagnesemia <br />Clinical manifestations<br />Usually occurs only at Mg levels <0.7 mg/dL<br />Tetany, (+)Chvostek and Trosseau signs, seizures<br />Rickets<br />Hypokalemia <br />
  71. 71. Hypomagnesemia <br />Treatment <br />Severe <br />Parenteral Mg<br />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<br />Long-term therapy<br />Oral – dose is divided to decrease cathartic side effect<br />Alternatives: IM injection and nighttime nasogastric infusion<br />
  72. 72. Hypermagnesemia <br />Almost always secondary to excessive intake<br />Unusual except in neonates born to mothers receiving IV Mg for pre-eclampsia or eclampsia<br />
  73. 73. Hypermagnesemia <br />Etiology<br />Mg is present in high amounts in certain laxatives, enemas, cathartics used to treat drug overdose and antacids<br />Neonates may receive high amounts transplacentally if maternal levels are elevated<br />Kidneys excrete excessive Mg but this is decreased in patients with chronic renal failure<br />
  74. 74. Hypermagnesemia <br />Etiology <br />Conditions predisposing to hypermagnesemia<br />Chronic renal failure<br />Familial hypocalciuric hypercalcemia<br />Diabetic ketoacidosis<br />Lithium ingestion<br />Milk alkali syndrome<br />Tumor lysis syndrome<br />
  75. 75. Hypermagnesemia <br />Clinical manifestations<br />Symptoms appear when plasma Mg level is >4.5 mg/dL<br />Hypermagnesemia inhibits Ach release at neuromuscular junction -> hypotonia, hyporeflexia, weakness, paralysis<br />Nausea, vomiting, hypocalcemia<br />Direct CNS depression -> lethargy, sleepiness, poor suck<br />
  76. 76. Hypermagnesemia <br />Clinical manifestations<br />Hypotension, flushing<br />ECG changes<br />Prolonged P-R, QRS and Q-T intervals<br />Severe hypermagnesemia (>15 mg/dL) -> complete heart block and cardiac arrest<br />
  77. 77. Hypermagnesemia <br />Treatment<br />IV hydration and loop diuretics<br />Dialysis<br />Exchange transfusion<br />In acute emergencies:<br />100 mg/kg of IV Ca gluconate (transiently effective)<br />
  78. 78. Phosphorus metabolism<br />Most phosphorus is in bone or is intracellular, w/ <1% in plasma<br />Phosphrous concentration varies with age<br />Component of ATP and other trinucleotides, critical for cellular energy metabolism<br />Necessary for nucleic acid synthesis<br />Component of cell membranes and other structures<br />Essential component of bone and is necessary for skeletal mineralization<br />
  79. 79. Phosphorus metabolism<br />Intake<br />Readily available in food<br />Best sources: milk and milk products<br />High concentration: meat and fish<br />Vegetables higher than fruits and grains<br />65% of intake is absorbed<br />Absorption<br />Almost exclusively in small intestines via a paracellular diffuse process and a vitamin D regulated transcellular pathway<br />
  80. 80. Phosphorus metabolism<br />Excretion<br />Kidney – regulates phophorus balance<br />Approximately 85% of filtered load is resorbed<br />PTH – decreases resorption of phosphate, increasing urinary phosphate<br />
  81. 81. Low plasma phosphorus<br />↓<br />1α-hydroxylase (in kidney)<br />↓<br />Converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol)<br />↓<br />↑ intestinal absorption of phosphorus<br />Maximal renal resorption of phosphorus<br />
  82. 82. Phosphorus metabolism<br />Excretion <br />Phosphatonin<br />Inhibits renal resorption of phosphorus -> phosphaturia and hypophosphatemia<br />Inhibits synthesis of calcitriol by decreasing 1α-hydroxylase activity<br />
  83. 83. Serum phosphorus during childhood<br />AGE<br />0-5 days<br />1-3 years<br />4-11 years<br />12-15 years<br />16-19 years<br />PHOSPHORUS<br />4.-8.2 mg/dL<br />3.8-6.5 mg/dL<br />3.7-5.6 mg/dL<br />2.9-5.4 mg/dL<br />2.7-4.7 mg/dL<br />
  84. 84. Hypophosphatemia <br />Etiology<br />Transcellular shifts<br />Glucose infusion<br />Insulin<br />Refeeding<br />Total parenteral nutrition<br />Respiratory alkalosis<br />Tumor growth<br />Bone marrow transplantation<br />Hungry bone syndrome<br />
  85. 85. Hypophosphatemia <br />Etiology<br />Decreased intake<br />Nutritional<br />Premature infants<br />Low phosphorus formula<br />Antacids and other phosphate binders<br />
  86. 86. Hypophosphatemia <br />Etiology<br />Renal losses<br />Hyperparathyroidism<br />Parathyroid hormone-related peptide<br />X-linked hypophosphatemic rickets<br />Tumor-induced osteomalacia<br />Autosomal dominant hypophosphatemic rickets<br />Fanconi syndrome <br />Dent disease<br />Hypophosphatemic rickets with hypercalciuria<br />
  87. 87. Hypophosphatemia <br />Etiology <br />Renal losses<br />Hypophosphatemia due to mutations in the sodium-phosphate cotransporter<br />Volume expansion and intravenous fluids<br />Metabolic acidosis<br />Diuretics<br />Glycosuria<br />Glucocorticoids<br />Kidney transplantation<br />
  88. 88. Hypophosphatemia <br />Etiology<br />Multifactorial<br />Vitamin D deficiency<br />Vitamin D-dependent rickets type I<br />Vitamin D-dependent rickets type 2<br />Alcoholism<br />Sepsis<br />Dialysis <br />
  89. 89. Hypophosphatemia <br />Clinical manifestations<br />Long term phosphorus deficiency: rickets<br />Severe hypophosphatemia: <1-1.5 mg/dL, may affect every organ<br />Hemolysis and dysfunction of WBC<br />Impaired release of oxygen to tissues<br />Proximal muscle weakness and atrophy<br />In ICU – slow weaning from ventilator or acute respiratory failure<br />
  90. 90. Hypophosphatemia <br />Clinical manifestations<br />Rhabdomyolysis<br />Cardiac dysfunction<br />Neurologic symptoms<br />Tremors<br />Paresthesia<br />Ataxia<br />Seizures<br />Delirium<br />Coma<br />
  91. 91. Hypophosphatemia <br />Treatment <br />Mild hypophosphatemia<br />No treatment except if the situation suggests it’s a chronic depletion or if there are ongoing losses<br />Oral phosphorus<br />Intravenous phosphorus<br />Increase dietary phosphorus <br />
  92. 92. Hyperphosphatemia <br />Etiology<br />Renal insufficiency – most common cause<br />Can occur because gastrointestinal absorption of large dietary intake of phosphorus is unguarded<br />Develops when kidney function is <30% of normal<br />
  93. 93. Hyperphosphatemia <br />Etiology<br />Transcellular shifts<br />Tumor lysis syndrome<br />Rhadomyolysis<br />Acute hemolysis<br />Diabetic ketoacidosis and lactic acidosis<br />
  94. 94. Hyperphosphatemia <br />Etiology<br />Increase intake<br />Enemas and laxatives<br />Cow’s milk in infants<br />Treatment of hypophosphatemia<br />Vitamin D intoxication<br />
  95. 95. Hyperphosphatemia <br />Etiology<br />Decreased excretion<br />Renal failure<br />Hypoparathyroidism or pseudohypoparathyroidism<br />Acromegaly<br />Hyperthyroidism<br />Tumoral calcinosis with hyperphosphatemia<br />
  96. 96. Clinical manifestations<br />Principal clinical consequences:<br />Hypocalcemia<br />Systemic calcification<br />Hypocalcemia<br />Due to tissue deposition of Ca-P salt<br />Inhibition of 1,25-dihydroxyvitamin D production<br />Decreased bone resorption<br />
  97. 97. Hyperphosphatemia <br />Clinical manifestations<br />Systemic calcification<br />Occurs because solubility of phosphorus and calcium in plasma is exceeded<br />Foreign body feeling in conjunctiva, erythema and injection<br />More ominous manifestation:<br /> hypoxia from pulmonary calcification <br /> renal failure from nephrocalcinosis <br />
  98. 98. Hyperphosphatemia <br />Treatment<br />Mild hyperphosphatemia in a patient with reasonable renal function resolves spontaneously<br />Dietary phosphorus restriction<br />Intravenous fluids<br />
  99. 99. Hyperphosphatemia <br />Treatment<br />More significant hyperphosphatemia<br />Add oral phosphorus binder<br />Dialysis <br />If unresponsive to conservative management or if renal insufficiency is supervening<br />
  100. 100. Fluid therapy<br />Degree of dehydration<br />Mild (<5% in an infant; <3% in an older child or adult)<br />Normal or increased pulse<br />Decreased urine output<br />Thirsty<br />Normal physical activity<br />
  101. 101. Fluid therapy<br />Degree of dehydration<br />Moderate (5-10% in an infant; 3-6% in an older child or adult)<br />Tachycardia<br />Little or no urine output<br />Irritable/lethargic<br />Sunken eyes and fontanel<br />Decreased tears<br />Dry mucous membranes<br />Mild delay in elasticity (skin turgor)<br />Delayed capillary refill (>1.5 sec)<br />Cool and pale<br />
  102. 102. Fluid therapy<br />Degree of dehydration<br />Severe (>10% in an infant; >6% in an older child or adult)<br />Rapid and weak or absent peripheral pulses<br />Decreased blood pressure<br />No urine output<br />Very sunken eyes and fontanel<br />No tears<br />Parched mucous membranes<br />Delayed elasticity (poor skin turgor)<br />Very delayed capillary refill (>3 sec)<br />Cold and mottled<br />Limp depressed consciousness<br />
  103. 103. Fluid therapy<br />Oral rehydration<br />Preferred mode of rehydration and replacement of ongoing losses<br />Risks associated with severe dehydration that may necessitate IV resuscitation<br />Age <6 months<br />Prematurity<br />Chronic illness<br />Fever >38 0C if <3 months or 39 0C if 3-36 months<br />Bloody diarrhea<br />Persistent emesis <br />Poor urine output<br />Sunken eyes<br />Depressed level of consciousness<br />
  104. 104. Fluid therapy<br />Limitations to ORT<br />Shock<br />Ileus<br />Intussusception<br />Carbohydrate intolerance<br />Severe emesis<br />High stool output (>10ml/kg/hr)<br />
  105. 105. Fluid therapy<br />Guidelines for oral rehydration<br />Mild dehydration<br />50 ml/kg of ORS given within 4 hours <br />Moderate dehydration<br />100 ml/kg of ORS over 4 hours<br />Additional 10 ml/kg of ORS for each watery stool<br />Maintenance<br />Volume of ORS ingested should equal volume of stool losses<br />
  106. 106. Fluid therapy<br />Intravenous therapy<br />Fluid management of dehydration<br />Restore intravascular volume<br />Normal saline: 20 ml/kg over 20 min<br />Repeat as needed<br />Rapid volume repletion: 20 ml/kg normal saline or lactated ringer’s (max=1L) over 2 hours<br />Calculate 24-hour fluid needs: maintenance + deficit volume<br />Subtract isotonic fluid already administered from 24-hour fluid needs<br />Administer remaining volume over 24 hours<br />Replace ongoing losses as they occur<br />
  107. 107. Fluid therapy<br />Phases of fluid therapy<br />Rehydration<br />Also called deficit therapy<br />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<br />Should be accomplished within 6 hours after initiation of treatment<br />
  108. 108. Fluid therapy<br />Phases of fluid therapy <br />Maintenance<br />Intended to stabilize internal milieu after it has been restored to normal during rehydration<br />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<br />