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Fluid therapy
Fluid therapy in systemic disorders
Fluid therapy in electrolyte disturbances

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  3. 3.  2/3 (65%) of TBW is intracellular (ICF)  1/3 extracellular water ◦ 25 % interstitial fluid (ISF) ◦ 5- 8 % in plasma (IVF intravascular fluid) ◦ 1- 2 % in transcellular fluids – CSF, intraocular fluids, serous membranes, and in GI, respiratory and urinary tracts (third space) DR.RAHUL GARG
  5. 5. COMPOSITION OF COMMON IV FLUID(mEq/L DEXT. Na+ K+ Cl- mOsm Ca++ HPO4 ACET. Lact. /L 50 - - - - - - - 278 NS D5,. 45%NS 50 154 - 154 - - - - 308 77 - 77 - - - - 432 DNS 154 - 154 - - - - 586 130 4 109 3 - - 28 274 D5 50 RL ISO-G 50 63 17 150 - - - - 580 ISO-M 50 40 35 40 - 15 20 - 410 270 - 270 - - - - 540 513 - 513 - -DR.RAHUL GARG - - 1025 1.6%NS 3%NS -
  6. 6.    SODIUM BICARBONATE(NaHCO3): -Commonly available as7.5%w/v,10ml inj -each amp. contain 22.5 mEq Na+ and HCO3- 22.5mEq Amount of NaHCO3 req.(in mEq/l)= 0.5 * wt in Kg * (desired HCO3 - Actual HCO3) Approx 50% of calculated deficit is corrected in 4hr and rest gradually over 24hrs. DR.RAHUL GARG
  7. 7.  Special precaution with NaHCO3: -should not be given as iv bolous -in presence of renal failure it can cause tetany or pulmonary edema,so safer Tt will be dialysis if acidosis and renal failure are sever -never correct acidosis without correcting hypokalemia b/c this can aggravate K+ deficit. - do not mix inj Ca with NaHCO3 b/c it can ppt CaCO3 as white crystal DR.RAHUL GARG
  8. 8.  POTASSIUM CHLORIDE: -Inj KCl 15% 10 ml amp contain 20 mEq of K+. -Never give inj KCl as direct iv,always use in diluted infusion. -Never add more than 40mEq/l -Never in fuse more than 10mEq/hr -Never add KCl in ISOM. DR.RAHUL GARG
  9. 9. Fluid therapy in hypovolemia DR.RAHUL GARG
  10. 10.     Hypovolemia can be Mild (<2lit in adult): symptom can be thirst, conc. Urine Moderate (2-3 lit in adult): symp. Above plus dizziness ,weakness , oliguria(<400ml/day),postura hypotension, low jvp Severe(>3lit in adult): symp. Above plus cnfusion , stupor, syst BP<100, tachycardia, low vol pulse, cold extremities,reduced skin turgor. DR.RAHUL GARG
  11. 11.    Approx fluid deficit can be calculated by ECF deficit(L)=0.2*lean body wt *(current Hct/normal Hct - 1) Effective rate of fluid replacement per hr = 50 to 100 ml + U.O. per hr + ongoing loss(such as diarrhoea or tube drain) per hr DR.RAHUL GARG
  12. 12. DR.RAHUL GARG
  13. 13.    Isotonic saline is initial fluid of choice b/c 1 lit of NS will expend of intravascular vol. by 300ml ,sso rise in bp is much rapid. Once renal output is established preferred fluid is RL b/c its composition is almost idetical to ECF so large vol. can be infused without fear of electrolyte imbalance. Lactate in RL converted to HCO3 and can correct acidosis DR.RAHUL GARG
  14. 14.   RL avoided in initial treatment shock b/c -K+ in RL is unsafe till renal status is uncertain -In shock hepatic conversion of lactate to bicarbonate is uncertain Primary indication of use of albumin or other colloid is in hypovolemia with hypotension in protein losing state such burns. DR.RAHUL GARG
  15. 15.   Hypovolemic pt who are bleeding or have marked anemia require administration of blood in addition to fluid However with BT haematocrit should not be raised over 35% b/c increase PCV increase viscosity that can lead to stasis in already impaired capillary circulation. DR.RAHUL GARG
  16. 16. DR.RAHUL GARG
  17. 17. Vomiting Na loss Dehydration Aldosterone HCO3 absorption In proximal tubules Na absorpation K secretion & urinary loss Loss of Cl- loss of h+ Hypochloremia Metabolic alkalosis Hypokalemia When severe hypokalemia H+ secretion in DCT For increased Na absorption PARADOXICAL ACIDURIA DR.RAHUL GARG
  18. 18.   END RESULT :Hypokalemic Hypochlorimic Matabolic Alkalosis. Fluid use to correct deficit due to upper G.I. loss:1-Isolyte-G: this is specific fluid used for the replacement U.G.I. loss. By its ammonia(70mEq/L),high Cl (154mEq/L),K+(17mEq/L),& Na+ (63mEq/L) it correct H+,Cl-,K+&Na+ losses respectively. 2-Isotonic saline DR.RAHUL GARG
  19. 19. INFUSION OF ISOTINIC SALINE Vol. correction Renal HCO3- absorption Na+supplementation aldosterone Correct Hypochloremia Urinary H+ loss and K+ loss Correct metamolic acidosis Cl- supplementation Prevents Hypokalemia DR.RAHUL GARG Favours HCO3secretion
  20. 20.   Urinary pH is very imp. To assesss efficacy of fluid therapy Acidic pH suggest need for more vigerous Tt and Alkaline urine suggests response to therapy. DR.RAHUL GARG
  21. 21. DR.RAHUL GARG
  22. 22.   In diarrhea stool usually contain large amount of NaCl, K and HCO3 along with water. Fluid and Electrolyte abnormality in diarrhoea:Hypovolemia Sodium deficit Hypokalemia Hypochloremia Metabolic acidosis DR.RAHUL GARG
  23. 23. DIARRHOEA Rich in K+ & HCO3-,contain water &Na+ K loss Water loss Na loss Dehydration Aldosterone K seceretion& Urinary loss Na Absorption Associated Renal absorptio of Cl- H ypokalemia Hyperchloremia DR.RAHUL GARG HCO3 loss Intestinal lumina Exchange of HCO With Cl- G.I Cl- absorption Acidosis
  24. 24.   Oral rehydration therapy:- it preferred method of fluid replacement ORS provide Na,K,Cl and HCO3 along with glucose which effectively correct fluid and electrolyte abnormalities and also provide calories. DR.RAHUL GARG
  25. 25.   I/v fluid therapy :- indicated when -rapid correction of fluid required for severe dehydration & shock -inability of pt to take ORS due persistent vomiting -ORT fail to correct volume deletion due to greater loss. Preferred iv fluid in diarrhoea are RL & NS(but iv fluid is ideal) DR.RAHUL GARG
  26. 26. Preferred iv fluid in diarrhoea are RL & NS(but iv fluid is ideal)  RL- preferred solution b /c it provide adequate Na and also HCO3(by hepatic conversion of lactate) for correction of metabolic acidosis -K conc. Is low (4 mEq/L) and RL provide no glucose. so pt may require additional K and glucose  DR.RAHUL GARG
  27. 27.  NS-effectively correct hypovolemia and  provides Na along with water. -pt may require additional supplementation of K(10 to 20 mEq/L) and NaHCO3 (20-30 mEq/L) -altthough NS lacks K+ ,but adequate supply of Na & water prevent urinary loss of K+ by suppressing aldosterone. D5- not acceptable b/c it does not correct acidosis,hypokalemia,and Na deficit. DR.RAHUL GARG
  28. 28. DR.RAHUL GARG
  29. 29.   Avoid hypoglycemia:-pt are more prone to hypoglycemia due to glycogenolysis and gluconeogenesis. oral glucose supplementation(200gm/day approx.) or 10% or 20% dextrose should be given by slow iv infusion Avoid metabolic alkalosis:-overzealous use of diuretics ,vigorous paracentesis or vomiting can lead to metabolic alkalosis which can precipitate or aggravate HE. DR.RAHUL GARG
  30. 30.   Hypokalemia:- vomiting & diuretic therapy causes hypokalemia, and can precipitate or aggravate HE. It should be corrected by oral/iv supplement of K+ Hyponatremia:- only dextrose containing electrolyte free fluid can lead to hyponatremia,which can aggravate cerebral edema. DR.RAHUL GARG
  31. 31. Selection of iv fluid in HE:1-glucose containing fluid is preferred ,but avoid 5% dextrose as it is hypotonic. 2-avoid islyte-G as it contains ammonium chloride. 3-avoid RL as it contain lactate,which get converted into HCO3 by liver and can cause alkalosis,OR if lactate metabolism is impaired,it can cause lactic acidosis.  DR.RAHUL GARG
  32. 32. 4:-iv fluid preferred is D10,D25 & DNS. KCl(1amp of 15% KCl contain 20mEq of K+) may be added to iv fluid as per requirement. But oral supplement is preferred. 5:- vol of fluid infused depends on hydration status and urine output. edematous pt may require fluid restriction along with salt In cirrhotic pt salt should be restricted to 13gm/day.(N req. is about 6gm(100mEq)per day) DR.RAHUL GARG
  33. 33. DR.RAHUL GARG
  34. 34.  CHF -Edema in CHF is due to water and salt retention. so total body water & Na is more in these pt , but water retention of water is more than salt .so hyponatremia is seen usually dilutional DR.RAHUL GARG
  35. 35. DON’T Don’t correct hyponatremia with salt supplementation b/c it is dilutional and need fluid restriction and loop diuretics for correction. Don’t follow routine guidelines(i.e. total fluid required per day=U.O.+700ml) replacement.aim is to remove extra fluid from the body so restrict fluid intake despite good U.O. DON’T treat hypotension with Na rich fluid,  DR.RAHUL GARG
  36. 36.  Dos Give lrss fluid pt with severe anasarca require restriction of fluid as low as 500-600ml/day Restrict Na so avoid NS,DNS,&RL K+ should be corrected adequately as required DR.RAHUL GARG
  37. 37.  ESSENTIAL HYPERTENSION -Restrict Na intake to roughlt 50mEq/day -Avoid rapid correction of Na requirment within shorter duration -To deliver required Na use fluid with low Na conc.(ISOM ,ISOP) DR.RAHUL GARG
  38. 38. DR.RAHUL GARG
  39. 39.    Maintain euvolemia: avoid hypovolemia and hypotension. b/c hypovolemia can lead to decrease in cerebral perfusion pressure. Avoid hypotonic fluid (D5,RL) and hypoosmolality b/c it can induce or aggravate cerebral oedema NS(0.9% NaCl) best fluid especially when large volumes of fluid are to be infused. DR.RAHUL GARG
  40. 40.    Avoid hyperglycemia: immediate period after strok(i.e.for first 24 hr after a pt presents with an anterior circulation infract and for 72 hr after post. Circulation event) avoid dextrose containing fluid. Avoid hypovolemia during mannitol therapy Achive hypervolemia in vasospasm (like in SAH) DR.RAHUL GARG
  41. 41. DR.RAHUL GARG
  42. 42.   HEAT CRAMPS: -oral saline solution (1 teaspoon of salt in 500 ml of water) is adequate to replace both salt and water iv fluid rarely required HEAT SYNCOPE: - 1-2 lit of isotonic saline is given over 2-4 hr -serum electrolyete replaced accordin to need DR.RAHUL GARG
  43. 43.  HEAT STROKE: -Initially isotonic saline or RL is infused , subsequently 5%dextrose with 0-45%NS is used -Pt may need 1.2 to 1.4 lit or iv fluid during first 4 hr. -Initially there is marked vasdilatation , so vigorous fluid replacement is avoided b/c when temp fall and vasoconstrication occur it may lead to pulmonary oedema. DR.RAHUL GARG
  44. 44. DR.RAHUL GARG
  45. 45. DR.RAHUL GARG
  46. 46. • Definition: – Commonly defined as a serum sodium concentration <135 meq/L – Hyponatremia represents a relative excess of water in relation to sodium. DR.RAHUL GARG
  47. 47.  Hyponatremia is the most common electrolyte disorder  Acute hyponatremia (developing over 48 h or less) are subject to more severe degrees of cerebral edema ocw.jhsph.edu  sodium level is less than 105 mEq/L, the mortality is over 50%  Chronic hyponatremia (developing over more than 48 h) experience milder degrees of cerebral edema DR.RAHUL GARG
  48. 48.  Types ◦ ◦ ◦ ◦ ◦ Hypovolemic hyponatremia Euvolemic hyponatremia Hypervolemic hyponatremia Redistributive hyponatremia Pseudohyponatremia DR.RAHUL GARG
  49. 49.   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 www.grouptrails.com/.../0-Beat-Dehydration.jpg DR.RAHUL GARG
  50. 50.  Nonrenal loss ◦ GI losses  Vomiting, Diarrhea, fistulas, pancreatitis ◦ Excessive sweating ◦ Third spacing of fluids  ascites, peritonitis, pancreatitis, and burns www.jupiterimages.com ◦ Cerebral salt-wasting syndrome  traumatic brain injury, aneurysmal subarachnoid hemorrhage, and intracranial surgery  Must distinguish from SIADH DR.RAHUL GARG
  51. 51.  Renal Loss ◦ Acute or chronic renal insufficiency ◦ Diuretics www.ct-angiogram.com/images/renalCTangiogram2.jpg DR.RAHUL GARG
  52. 52.  Normal sodium stores and a total body excess of free water ◦ Psychogenic polydipsia, often in psychiatric patients ◦ Administration of hypotonic intravenous (5% DW) or irrigation fluids ( sorbitol, glycerin) in the immediate postoperative period DR.RAHUL GARG
  53. 53. ◦ administration of hypotonic maintenance intravenous fluids ◦ Infants who may have been given inappropriate amounts of free water ◦ bowel preparation before colonoscopy or colorectal surgery DR.RAHUL GARG
  54. 54.   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 DR.RAHUL GARG
  55. 55. ◦ 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 DR.RAHUL GARG
  56. 56.  Pseudohyponatremia ◦ The aqueous phase is diluted by excessive proteins or lipids. The TBW and total body sodium are unchanged.  hypertriglyceridemia  multiple myeloma DR.RAHUL GARG
  57. 57.  Clinical Manifestations ◦ most patients with a serum sodium concentration exceeding 125 mEq/L are asymptomatic ◦ Patients with acutely developing hyponatremia are typically symptomatic at a level of approximately 120 mEq/L ◦ Most abnormal findings on physical examination are characteristically neurologic in origin ◦ patients may exhibit signs of hypovolemia or hypervolemia DR.RAHUL GARG
  58. 58.  Diagnosis ◦ ◦ ◦ ◦ CT head, EKG, CXR if symptomatic Repeat Na level Correct for hyperglycemia Laboratory tests provide important initial information in the differential diagnosis of hyponatremia     Plasma osmolality Urine osmolality Urine sodium concentration Uric acid level DR.RAHUL GARG
  59. 59.  Laboratory tests Cont. ◦ Plasma osmolality  normally ranges from 275 to 290 mosmol/kg  If >290 mosmol/kg :  Hyperglycemia or administration of mannitol  If 275 – 290 mosmol/kg :  hyperlipidemia or hyperproteinemia  If <275 mosmol/kg :  Hypervolemic/ Euvolemic status/ hypovolemic DR.RAHUL GARG
  60. 60.  Laboratory tests Cont. ◦ Plasma osmolality < 275 mosmol /kg  Increased volume:  CHF, cirrhosis, nephrotic syndrome  Euvolemic  SIADH, hypothyroidism, psychogenic polydipsia, beer potomania, postoperative states  Decreased volume  GI loss, skin, 3rd spacing, diuretics DR.RAHUL GARG
  61. 61.  Laboratory tests Cont. ◦ Urine osmolality  Normal value is > 100 mosmol/kg  Normal to high:  Hyperlipidemia, hyperproteinemia, hyperglycemia, SIADH  < 100 mosmol/kg  hypoosmolar hyponatremia      Excessive sweating Burns Vomiting Diarrhea Urinary loss DR.RAHUL GARG
  62. 62.  Laboratory tests Cont. ◦ Urine Sodium  >20 mEq/L  SIADH, diuretics  <20 mEq/L  cirrhosis, nephrosis, congestive heart failure, GI loss, skin, 3rd spacing, psychogenic polydipsya ◦ Uric Acid Level  < 4 mg/dl consider SIADH DR.RAHUL GARG
  63. 63.  Treatment ◦ four issues must be addressed     Asyptomatic vs. symptomatic acute (within 48 hours) chronic (>48 hours) Volume status ◦ 1st step is to calculate the total body water  total body water (TBW) = 0.6 × body weight DR.RAHUL GARG
  64. 64.  Treatment Cont. ◦ next decide what our desired correction rate should be ◦ Symptomatic  immediate increase in serum Na level by 8 to 10 meq/L in 4 to 6 hours with hypertonic saline is recommended ◦ acute hyponatremia  more rapid correction may be possible  8 to 10 meq/L in 4 to 8 hours ◦ chronic hyponatremia  slower rates of correction  12 meq/L in 24 hours DR.RAHUL GARG
  65. 65.  Symptomatic or Acute ◦ Treatment Cont.  estimate SNa change on the basis of the amount of Na in the infusate  ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)  ΔSNa is a change in SNa  [Na + K]inf is infusate Na and K concentration in 1 liter of solution DR.RAHUL GARG
  66. 66.  Asypmtomatic or Chronic ◦ SIADH  Water restriction  0.5-1 liter/day  Salt tablets  Demeclocycline  Inhibits the effects of ADH  Onset of action may require up to one week DR.RAHUL GARG
  67. 67. PLASMA Na > 145mEq/L DR.RAHUL GARG
  68. 68.  Hypernatremia is usually due to water deficit Excess water loss :eg- heat exposure diabetes insipidus Impaired thirst:eg-primary hypodypsia, comatose Excessive Na retension DR.RAHUL GARG
  69. 69.  Clinical    feature- Excessive thirst,polyuria,nausea Muscular weakness, neuromuscular irritability Altered mental status,focal neurological deficit occasionally coma or seizures DR.RAHUL GARG
  70. 70.    Treatment correct water deficit water deficit = (plasma Na-140)/140*0.6*body wt in kg Rate of correction : -Acute hypernatremia- 1mEq/L/hr -Chronic hypernatremia-1mEq/L/hr or 10mEq/L over 24hr -rapid correction may lead to cerebral oedema DR.RAHUL GARG
  71. 71. Plasma K < 3.5 mmol/L DR.RAHUL GARG
  72. 72. Neuromuscular effects : - weakness, myalgia, fatigue - hypo/areflexia - paralyis, rhabodmyolysis, dyspnea Cardiac effects : delay in ventricular repolarization - ECG (T flat, depressed ST, U wave) - arrhythmia (reentry currents during prolonged repolarization) - ↑ sensibility to toxic drugs (digoxin) Renal effects : nephrogenic diabetes insipidus, Interstitial nephritis, ↑ ammoniagenesis Glucose intolerance : ↓ insulin secretion β-cell Blood pressure : ↑ (low K+ diet) or ↓ (Gitelmann) Growth defect : impaired protein metabolism – GH release DR.RAHUL GARG
  73. 73. Approx. K deficit ,normal plasma pH Serum K+ >3.5 (mEq/l) 3 2 Total K deficit (mEq) 300 450-600 0 DR.RAHUL GARG <2 >600
  74. 74. Serum K:Tt guidelines    3.5 to 4 mEq/L -no K+ supplement -Increase oral intake of K rich food -Add K sparing diuretics or decrease dose of diuretics 3 to 3.5 mEq/L: -Tt in selected high risk pt eg: CHF, DIGITALIS therapy ,IHD etc. <3 mEq/L -Need definativ Tt DR.RAHUL GARG
  75. 75. Oral supplementation : safer mode than iv  Avg dose of KCl is 60 to 80 mEq/day in divided doses  Iv therapy: reserved for severe symptomatic hypokaemia (<3mEq/l) -Never give inj. KCl as direct iv,always use in diluted infusion. -Never add more than 40mEq/l -Never in fuse more than 10mEq/hr -Never add KCl in ISOM.  DR.RAHUL GARG
  76. 76. Plasma K > 5 mmol/L DR.RAHUL GARG
  77. 77.  Cardiac  Neuromuscular  Renal electrolyte  Endocrine ◦ Abnormal electrocardiogram ◦ Atrial /ventricular arrhythmias ◦ Pacemaker dysfunction ◦ Paresthesias ◦ Weakness ◦ Paralysis ◦ Decreased renal NH4+ production ◦ Natriuresis ◦ Increased aldosterone secretion ◦ Increased insulin secretion DR.RAHUL GARG
  78. 78.  ECG changes -Tall peaked t wave - loss of p wave ,widening ofQRS complex -QRS merges with T wave forming sine waves - A-V dissociation -Ventricular tachycardia -fibrillation DR.RAHUL GARG
  79. 79.   Antagonize the cardiac effect of hyperkalemia ◦ 10% Calcium gluconate 10 cc over 5-10 min ◦ Can be repeated after 5 min if EKG changes persist ◦ Except if the patient on digoxin ◦ Onset 1-3 min, duration 30-60 min Induce intracellular K+ shift; ◦ Insulin 10-20 IU IV 25-50 cc D50%  Onset 30 min, duration 4-6 hrs ◦ Nebulized albuterol 10-20 mg or 0.5 mg IV  Onset 30 min, duration 2-4 hrs ◦ Na Bicarb IV if acidotic 50 mEq over 2 min DR.RAHUL GARG
  80. 80.  External removal; ◦ Renal  IVF + diuretics  Fludrocortisone 0.05 – 0.1 mg ◦ GI  Na or Ca resonium with tap water) sorbitol (15 gm PO or 50 gm rectal  Onset 1-2 hrs, duration 4-6 hrs ◦ Dialysis: immediate onset DR.RAHUL GARG
  81. 81. DR.RAHUL GARG
  82. 82.   Most common causes include primary hyperparathyroidism and malignancies ( more than 90% patients ) REMEMBER: as a general rule, primary hyperparathyroidism is the etiology in OPD patients who are asymptomatic and with a serum calcium level of <=11 mg/dl. Malignancy is often the cause in symptomatic patients with an abrupt onset of disease and serum calcium >=14 mg/dl DR.RAHUL GARG
  83. 83.      Clinical features are due to the underlying disorder causing hypercalcemia hypercalcemia per se CNS: weakness, fatigue, depression, confusion, stupor or coma GI: constipation, anorexia, nausea and vomiting. Abdominal pain, if present, is a result of the induced peptic ulcer or pancreatitis Renal: polyuria, nocturia and stone formation CVS: increased risk of digoxin toxicity, shortened QT interval DR.RAHUL GARG
  84. 84. A.    Measures to increase urinary excretion volume restoration, expansion and saline diuresis: the most useful and effective methods (the pt may need 4-6 L of fluid for the same, therefore to be used cautiously in the elderly and pts with heart disease) Furosemide: effective but avoid dehydration, hypokalemia and hypomagnesemia during treatment Hemodialysis: reserved for patients with severe hypercalcemia and little or no renal function DR.RAHUL GARG
  85. 85. B.    Measures to inhibit bone resorption Bisphosphonates: Pamidronate Calcitonin: also increases urinary calcium excretion. Has a rapid action and therefore mainly used as urgent therapy in life threatening hypercalcemia. Not useful for long term therapy Gallium Nitrate: not often used as it requires 5 days duration of infusion, has a potential for nephrotoxicity and the availability of better and safer alternatives DR.RAHUL GARG
  86. 86. C.    Measures to decrease intestinal absorption Glucorticoids: decreases intestinal absorption along with increasing urinary excretion in pharmacological doses. They are mainly used in the cases caused due to malignancies, sarcoidosis and vit d intoxication. Not useful in primary hyperparathyroidism or in a normal person Oral phosphate: promotes calcium deposition in the bone and soft tissue. Should only be used if serum phosphate is <3 mg/dl and renal function is normal Ketoconazole and hydroxychloroquine can also be used DR.RAHUL GARG
  87. 87. D.    Specific treatment Discontinue the drugs responsible Surgical removal of primary hyperparathyroidism Specific treatment for malignancy, thyroxicosis, etc DR.RAHUL GARG
  88. 88. DR.RAHUL GARG
  89. 89.   Hypoalbuminemia is the most common cause of hypocalcemia with normal ionised calcium. True hypocalcemia is caused due to decreased calcium absorption from the GI tract or decreased reabsorption from the bone, abnormalities of either PTH or Vit D DR.RAHUL GARG
  90. 90.      They vary with the degree and rate of onset and are caused due to increased neuromuscular excitability Pt usually complains of weakness, circumoral and distal extremity parasthesia, muscle spasm, carpopedal spasm, tetany and mental changes like irritability, psychosis and depression Chvostek’s sign and Trosseau’s sign positive ECG may show prolonged QT interval. Digitalis effect is reduced Severe forms may cause lethargy, confusion, laryngeal spasms, seizures or reversible heart failure DR.RAHUL GARG
  91. 91. ETIOLOGY SERUM CA TOTAL LCIUM SERUM PHOSPHATE SERUM PTH IONIZED Hypoalbuminemia Low Normal Normal normal Alkalosis Normal Low Normal Normal-high Vit-D deficiency Low Low Low high Chronic renal failure Low Low High high Hypoparathyroidis m Low Low High low DR.RAHUL GARG
  92. 92. Acute management Emergency treatment required with 10% calcium gluconate (90 mg elemental calcium/10 ml) 1020 ml i.v. slowly over 10 mins. Severe symptomatic hypocalcemia may require infusion of 60 ml of calcium gluconate in 500 ml of 5% dextrose. Calcium concentration of the drip is 1 mg/ml and its requirement is 0.5- 2 mg/kg/hour  If i.v. calcium does not relieve the tetany, rule out (and correct) hypomagnesemia DR.RAHUL GARG
  93. 93. Long term management: - Treat the underlying etiology - Calcium supplementation: an aymptomatic hypocalcemic pt needs 1-3 gm of calcium per day. Calcium is best absorbed when taken b/w meals  Vit D supplementation Calcitriol is the most potent of the vit D preparations and has the fastest onset and shortest duration of action. C Ergocalciferol requires several weeks to achieve full effect. Although cost is low, its long half life and storage in fat carry a high risk of vit D intoxication  DR.RAHUL GARG