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10. fluids and electrolytes

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  • 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

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