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Fluids & electrolytes seminar [autosaved]

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fluids and electrolytes

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Fluids & electrolytes seminar [autosaved]

  1. 1. PRESENTER – DR AVINASH RATHORE FLUIDS AND ELECTROLYTES
  2. 2. CONTENTS • Basic Terminologies And Definitions • Introduction • Body Fluids And Fluid Balance • Regulation Of Fluids • Principals Of Fluid Therapy • Classification Of I.V Fluids • Fluids in specific conditions • Acid – base disorders • Electrolyte disorders • Clinical implications • Refrences
  3. 3. Basic Terminologies And Definitions • Fluid :- [Latin fluidus - flowing freely] A substance, such as a liquid or gas, that can flow, has no fixed shape, and offers little resistance to an external stress • Electrolyte : A substance that ionizes when dissolved in suitable ionizing solvents such as water.
  4. 4. OSMOSIS
  5. 5. • Osmolality : Is the amount of solute dissolved in a solvent measured in weight(per kg of solvent) • Osmolarity: Is the amount of solute dissolved in a solvent measured in volume (per litre of solvent). • Osmotic Pressure : Is the distribution of water among the different fluid compartments,particularly between ECF & ICF.
  6. 6. TONICITY • The ability of an extracellular solution to make water move into or out of a cell by osmosis is know as its tonicity. A solution's tonicity is related to its osmolarity, which is the total concentration of all solutes in the solution. • RULE OF OSMOLARITY- movement of solvent from LOW concentration to HIGH concentration.
  7. 7. • Plasma osmolality :- 275-290mosm/kg • Plasma osmolality = 2 × Na + glucose(mg/dl) + BUN(mg/dl) 18 2.8 • Effective osmolarity :- = 2 × Na + glucose(mg/dl) 18
  8. 8. INTRODUCTION “Intravenous fluids have a range of physiologic effects and should be considered to be drugs with indications, dose ranges, cautions, and side effects.” In 1861 ,Thomas Graham’s investigated and classified substances as crystalloids and colloids depending on their ability to diffuse through a parchment membrane. • Crystalloids are fluids that pass through a semipermeable membrane • Colloids are fluids that do not pass through semipermeable membrane
  9. 9. • The administration of intravenous (IV) fluid is a core expertise for surgeons and an area in which we have an important role in advising clinical colleagues. • The aims of IV fluid administration should be to- – avoid dehydration – maintain an effective circulating volume – prevent inadequate tissue perfusion during a period when the patient is unable to achieve these goals through normal oral fluid intake.
  10. 10. • Knowledge of the composition and the clinical effects of different fluids has increased substantially in recent years. • The choice of fluid type in a variety of clinical situations can be rationally guided by an understanding of the physicochemical and biologic properties of the various crystalloid and colloid solutions available in combination with the available clinical trial data.
  11. 11. BODY FLUIDS AND FLUID BALANCE
  12. 12. Composition of Body Fluids • Water is the universal solvent • Solutes – Electrolytes – Inorganic salts, all acids and bases,and some proteins. – Non-electrolytes –Most non electrolytes are organic molecules – glucose lipids,creatinine and urea. •Electrolytes have greater osmotic power than non electrolytes •Water moves according to osmotic gradients
  13. 13. • Elderly: Have lower % of total body fluid than younger adults • Women: Have lower % total body fluid than men. • Infants : Have 80% of body water in relation to weight and declines with age.
  14. 14. Regulation Of Fluids • Hypothalmus –Thirst receptors (osmoreceptors) continuosly monitor serum osmolarity (concentration). If it rises, thirst mechanism is triggered • Pituitary regulation- posterior pituitary releases ADH (antidiuretic hormone) in response to increasing serum osmolarity.Causes renal tubules to retain H20. • Thirst is a late sign of water deficit
  15. 15. • Renal regulation:- Nephron receptors sense decreased pressure (low osmolarity) and kidney secretes RENIN. • Renin from kidney undergoes renin angiotensin aldosterone system (RAAS System).
  16. 16. • Four major stimuli to thirst: 1.hypertonicity 2.hypovolaemia 3.hypotension 4.angiotensin2
  17. 17. Principles of Fluid Therapy
  18. 18. PRINCIPLES OF FLUID THERAPY
  19. 19. Five ‘Rs’ of intravenous fluid administration Resuscitation Routine maintenance Replacement Redistribution Reassessment
  20. 20. RESUSCITATION IV fluids may need to be given urgently to restore circulation to vital organs following loss of intravascular volume due to bleeding, plasma loss, or excessive external fluid and electrolyte loss, usually from the gastrointestinal (GI) tract, or severe internal losses (e.g. from fluid redistribution in sepsis).
  21. 21. ROUTINE MAINTENANCE IV fluids are sometimes needed for patients who simply cannot meet their normal fluid or electrolyte needs by oral or enteral routes but who are otherwise well in terms of fluid and electrolyte balance and handling i.e. they are essentially euvolaemic, with no significant deficits, ongoing abnormal losses or redistribution issues.
  22. 22. REPLACEMENT In some patients, IV fluids are used to treat losses from intravascular and or other fluid compartments, are not needed urgently for resuscitation, but are still required to correct existing water and/or electrolyte deficits or ongoing external losses. These losses are usually from the GI or urinary tract, although high insensible losses occur with fever, and burns patients can lose high volumes of what is effectively plasma.(e.g. cautious, slow replacement to reduce risks of pontine demyelinosis)
  23. 23. REDISTRIBUTION In addition to external fluid and electrolyte losses, some hospital patients have marked internal fluid distribution changes or abnormal fluid handling. This type of problem is seen particularly in those who are septic, otherwise critically ill, post-major surgery or those with major cardiac, liver or renal co-morbidity. Many of these patients develop oedema from sodium and water excess and some sequester fluids in the GI tract or thoracic/peritoneal cavities.
  24. 24. REASSESMENT If patients are receiving IV fluids for resuscitation, reassess the patient using the ABCDE approach (Airway, Breathing, Circulation, Disability, Exposure), monitor their respiratory rate, pulse, blood pressure and perfusion continuously, and measure their venous lactate levels and/or arterial pH and base excess according to guidance on advanced life support (Resuscitation Council [UK], 2011)
  25. 25. INDICATIONS • Fluid therapy is used to maintain homeostasis when enteral intake is insufficient (eg, when a patient is “nil by mouth” or has reduced absorption), and to replace any additional losses. These losses may occur from the gastrointestinal tract (due to vomiting, diarrhoea or a fistula) or the urinary tract (eg, diabetes insipidus), or be caused by blood loss from trauma or surgery. • In addition, insensible losses can increase during fever or after suffering from burns because the barrier function of the skin is impaired.
  26. 26. Fluids can accumulate into spaces that normally contain minimal fluid volumes (eg, the peritoneal or pleural cavities) during surgery, anaesthesia or as a result of inflammatory conditions (eg, sepsis).This is known as “third spacing” and is caused by vasodilation and “leakage” of vascular epithelial walls. This breakdown of normal compartment integrity can result in loss of circulating intravascular volume.  Total parenteral nutrition.  As a vehicle for various i.v medications.
  27. 27. CLASSIFICATION Blood and Products I V Fluids Non blood I V Fluids Crystalloids •Glucose Containing •Electrolyte solutions •Mixed Colloids Proteino us Non proteinous Gelatins •Haemacc el •Gelofusin Album in 20% & 5% Starch Dextra ns  HES  PentaSt arch  Tetrast arch
  28. 28. CRYSTALLOIDS
  29. 29. CRYSTALLOIDS Definition : Crystalloid are electrolyte solutions with small molecules that can diffuse freely from intravascular to interstitial fluid compartments. Crystalloids distributes uniformly in extracellular fluid . only 25% of transfused crystalloids remains in the intravascular space.  75% diffuses into interstitial space  Hence Crystalloids mainly useful to expand the interstitial space.
  30. 30. CRYSTALLOIDSCRYSTALLOIDS HYPOTO NIC HYPOTO NIC ISOTONI C ISOTONI C HYPERTO NIC HYPERTO NIC IONICIONIC NON- IONIC NON- IONIC • D5W • ½ NS(0.45%) • D5W • ½ NS(0.45%) • NS • RL • Plasmaly te • NS • RL • Plasmaly te • Hypertoni c saline • 10%, 25% & 50% dextrose. • Hypertoni c saline • 10%, 25% & 50% dextrose. • NS • Dextrose saline (DNS) • Ringer’s lactate • NS • Dextrose saline (DNS) • Ringer’s lactate • 5% Dextrose • 25% Dextrose • 5% Dextrose • 25% Dextrose
  31. 31. NORMAL SALINE • One of the most commonly administered crystalloids . • Using in vitro red cell lysis experiments , Hamburger ascertained that 0.9% was the NaCl concentration that was isotonic with human plasma. • It was not initially developed with the aim of in vivo administration, yet has entered widespread clinical use despite having a Na+ and Cl− concentration far in excess of that of plasma. • Infusion of 0.9% NaCl leads to an increase in ECF volume , more persistent than balanced crystalloids, dilutional decrease in hematocrit and albumin, increase in Cl− and K+ concentrations, and decrease in plasma HCO3−.
  32. 32. •1 N sodium chloride solution = 58 grams per litre •0.9% sodium chloride = 9 grams per litre •Composition : Na 154 mEq/L, Cl 154 mEq/L , pH 4-5 - Hence it affects the acid base balance of the body. •.
  33. 33. • Pharmacological basis :  provide major extracellular electrolytes.  corrects both water and electrolyte deficit.  increase the intravascular volume substantially  It causes more expansion of extracellular volume because of hypertonicity due to increased Na+ in relation to ECF. • Acid base effect causes hyperchloremic metabolic acidosis caused by high concentration of chloride in 0.9% NaCl
  34. 34. STRONG ION DIFFERENCE • Hyperchloremic metabolic acidosis occurs because 0.9% saline contains strong cations and strong anions in the same quantity (SID equal to zero). When the plasma chloride concentration increases after 0.9% saline infusion, the net positive charge of plasma (SID) is reduced. Conversely, compensatory mechanisms designed to maintain the plasma electro-neutrality are activated, thus increasing the plasma positive charge (H+ ) while decreasing the arterial pH.
  35. 35. Indications : Water and salt depletion – diarrhoea, vomiting, excessive diuresis. Hypovolemic shock- distributed in extracellular space expanding the intravascular volume. Ideal fluid to increase blood pressure. Preferred in case of brain injury, hypochloraemic metabolic alkalosis , hyponatraemia. Initial fluid therapy in DKA. In patients with hyperkalemia eg: renal failure. Irrigation – washing of body fluids. Vehicle for certain drugs.
  36. 36. Limitations : • Avoid in patients with sodium overload : Eg: CCF. • Dehydration with severe hypokalaemia – deficit of intracellular potassium – NS without additional K+ supplementation can aggravate electrolyte imbalance. • Large volume may lead to hyperchloremic metabolic acidosis.
  37. 37. RINGER'S FLUIDS • In 1880, Sydney Ringer , a British physician studied the contraction of isolated frog heart. • He introduced a solution that contained calcium and potassium in sodium chloride solution to promote cardiac contraction and cell viability. This is known as Ringer`s injection • In early 1930, an American pediatrician named Alex Hartmann added sodium lactate to Ringer`s solution as a buffer to metabolic acidosis. • This is known as Hartmann`s solution or Ringer`s lactate
  38. 38. Composition Sodium:131mEq/Lt ; chloride – 111mEq/Lt ; Potassium – 5mEq/Lt; Calcium – 4mEq/Lt ; Bicarbonate – 29 mEq/Lt. •(per 100ml) Sodium lactate 320 mg, NaCl 600mg ,KCl 40mg ,CaCl2 27mg. •RL contains k+ and ca2+ in concentrations that appropriate free (ionic) concentrations in plasma. •Addition of these cations reduces Na+ requirement to maintain electrical neutrality.
  39. 39. Advantage of Ringer’s lactate over normal saline is lack of significant acid base imbalance Disadvantage: •Presence of calcium in ringer’s lactate binds to situated anticoagulant of stored blood. •In critically ill patients with impaired lactate clearance due to circulatory shock or hepatic insufficiency, Ringer’s lactate infusion can increase serum lactate levels.
  40. 40. PHARMACOLOGICAL BASIS • Ringer`s lactate is the most physiological fluid as the electrolyte content is similar to that of plasma. Larger volumes can be infused without the risk of electrolyte imbalance . • Sodium content rapidly expands intravascular volume effective in treatment of hypovolemia. • Sodium lactate in RL is metabolized to bicarbonate in the liver useful in correction of metabolic acidosis.
  41. 41. Indications :Indications : •Correction in severe hypovolaemia. •Replacing fluid in post operative patients, burns , fractures. •Diarrhoea induced hypokalemic metabolic acidosis and hypovolemia. •Fluid of choice in diarrhoea induced dehydration in paediatric patients. •In DKA , provides glucose free water, correct metabolic acidosis and supplies potassium •Maintainance fluid during surgery/paediatrics also.
  42. 42. Limitations : •Severe liver disease, severe hypoxia •Severe CHF - lactic acidosis takes place. •Vomiting or NGT induced alkalosis. •Simultaneous infusion of RL and blood. •Certain drugs – amphotericin, thiopental, ampicillin, doxycycline should not be mixed with RL – calcium binds with these drugs and reduces bioavailability and efficiency.
  43. 43. DEXTROSE SOLUTIONS • D5 water • Dextrose with 0.9% NS ( DNS ). • Dextrose with 0.45% NS (D1/2NS ) • 10% dextrose. • 25% dextrose EFFECT OF DEXTROSE IN FLUID : Protein sparing effects Volume effect Lactate production. Effect of hyperglycemia
  44. 44. EFFECT OF DEXTROSE IN FLUID Protein sparing effect : •Earlier it was used to provide calories in patients who were Nil by mouth •50 grams of dextrose provides 170 kcal. •Hence , infusion of 3 litres of D5W at 125 ml per hour per day provides 510 kcal per day •It provides energy and prevents endogenous protein breakdown •It is no longer used frequently as most patients with long-term Nil by mouth have enteral tube feedings or TPN.
  45. 45. 5% Dextrose Composition : Glucose 50 gms/ltr Pharmacological Basis : •Corrects Dehydration And Supplies Energy( 170kcal/L) •Administered safely at the rate of 0.5gm/kg/hr without causing glycosuria. METABOLISM : Dextrose is metabolised leaving free water  distributed in all compatments of the body. A proportion of dextrose load contributes to lactate formation –  5% in healthy subjects  85% in critically ill patients. = not the preferred fluid.
  46. 46. Indications : • Prevention and treatment of intracellular dehydration. • IV administration of various drugs • Prevention of ketosis in starvation, vomiting, diarrhoea. •Adequate glucose infusion protects liver against toxic substances. •Correction of hypernatraemia –slow IV- provides free water.
  47. 47. LIMITATIONS • Neurosurgical procedures- can cause Cerebral oedema • Acute ischaemic stroke- – hyperglycemia aggravates cerebral ischaemic brain damage. – Dextrose metabolism aggravates tissue acidosis in ischaemic areas. • Hypovolemic shock – Poor expansion of intracellular volume. – Faster rate of infusion causes osmotic diuresis  worsens shock and false impression of the hydration status  reduced fluid replacement. • Hyponatremia , water intoxication • Blood transfusion – haemolysis , clumping seen due to hypotonicity of the solution. • Uncontrolled DM / severe hyperglycemia.
  48. 48. DEXTROSE SALINE (DNS) Composition : 5% dextrose with 0.9% NS NaCl– 154 meq/lt each, glucose 50 gm/ltr. Pharmacological basis : • supply major extracellular electrolytes, energy and fluid to correct dehydration Indications : • Conditions with salt depletion ,hypovolaemia- not the ideal fluid though. Faster rate of infusion causes osmotic diuresis  worsens shock and false impression of the hydration status  reduced fluid replacement. • Correction of vomiting or NGT aspiration induced alkalosis and hypochloremia along with supply of calories.
  49. 49. Limitations : • Anasarca – cardiac, hepatic or renal cause • Severe hypovolemic shock – rapid correction is needed. Faster infusion can cause osmotic diuresis and worsen the condition.
  50. 50. 10% DEXTROSE & 25% DEXTROSE 1 liter of fluid has 100 gms glucose and 250 gms glucose respectively. Pharmacological basis: • It is hypertonic crystalloid fluid. • Supplies energy and prevents catabolism  useful when faster replacement of glucose is needed. Indications : • Rapid correction of hypoglycaemia . • In liver disease, if given as first drip, it inhibits glycogenolysis and gluconeogenesis • Nutrition to patients on maintainance fluid therapy. • Treatment of hyperkalemia .
  51. 51. Limitations : •In patients with dehydration , anuria , intracranial hemorrhage. •Avoided in patients with diabetes unless there is hypoglycemia. •Rapid infusion of 25D can cause glycosuria . Hence in the absence of hypoglycemia it should be infused slowly over 45 - 60 min.
  52. 52. HYPEROSMOLAR FLUIDS MANNITOL HYPERTONIC SALINE
  53. 53. MANNITOL • 6 carbon sugar • Osmotic diuretic • Freely filterable at glomerulus • Limited reabsorption from renal tubules • Resist metabolism • Pharmacologically inert • Not absorbed from GIT • Doesn’t enter cells • Clearance from plasma by glomerular filtration
  54. 54. Increases plasma osmolarity Draws fluid from intracellular to extra cellular spaces Acute expansion of intravascular fluid volume Decreases brain bulk ,ICP, increases renal blood flow to medulla Oxygen radical scavenger Prevents cellular swelling Reduces renal tubular obstruction
  55. 55. Limitations:- •Anuria due to severe renal disease. •Severe pulmonary congestion or frank pulmonary edema. •Active intracranial bleeding except during craniotomy. •Severe dehydration. •Progressive renal damage or dysfunction after institution of mannitol therapy, including increasing oliguria and azotemia.
  56. 56. HYPERTONIC SALINE • Available as 1.8%, 3% , 5%, and 7.5%
  57. 57. PHARMACOLOGICAL PROPERTIES: The hypertonic nature of these solutions draws water out of the intracellular compartment into the extracellular compartment . USES: – Plasma volume expansion: The hypertonic nature of these solutions draws water out of the intracellular compartment and into the extracellular (including plasma) volume and may therefore achieve plasma volume expansion while minimizing the volume of fluid administered. However, clinical trials have not shown any benefits. •Correction of hypo osmolar hyponatremia – •Treatment of raised ICT- superior to mannitol. •7.5% - endothelial injury  used as sclerosant
  58. 58. Isolyte G,M,P,E ISOLYTE G ISOLYTE M ISOLYTE P ISOLYTE E DEXTROSE 50 50 50 50 Na 63 40 25 140 K 17 35 20 10 Cl 150 40 22 103 Acetate --- 20 23 47 Lactate --- --- --- --- NH4CL 70 --- --- --- Ca --- --- --- 5 Mg --- --- --- 3 HPo4 --- 15 3 --- Citrate --- --- 3 8 Mosm/L 580 410 368 595
  59. 59. INDICATIONS AND LIMITATIONS Isolyte G : Vomiting / NGT induced hypochloremic , hypokalemic metabolic alkalosis. NH4 gets converted to H+ and urea in the liver. Treatment of metabolic alkalosis. Limitations : hepatic failure , renal failure , metabolic acidosis. ISOLYTE M: Richest source of potassium (35mEq) correction of hypokalaemia. LIMITATIONS : Renal failure ,burns, adrenocortical insufficiency.
  60. 60. ISOLYTE P: Maintenance fluid for children. Excessive water loss or inability to concentrate urine LIMITATIONS : hyponatremia , renal failure. ISOLYTE E: Extracellular replacement fluid, additional potassium and acetate. Corrects Mg deficiency. Treatment of diarrhoea and metabolic acidosis. LIMITATIONS : metabolic alkalosis.
  61. 61. COLLOID SOLUTION A colloid is defined as a high molecular weight (MW) substance that largely remains in the intravascular compartment, thereby generating an oncotic pressure. Colloids are of two types: Natural - Human albumin Plasma protein factor Fresh frozen plasma Immunoglobin solution Artificial - Gelatin and dextran solutions, hydroxyethyl starches (HES).
  62. 62. INDICATIONS • SHOCK • BURNS • HYPO-ALBUMINAEMIA CONDITIONS - Paracentesis Liver cirrhosis After liver transplantation In conjuction with crystalloids Critically ill patients-ICU,pulmonary oedema, congestive cardiac failure
  63. 63. Albumin • Heat treated preparation of human serum albumin available as 5% solution (50 gm/L) and 25% solution (250 gm/L).  Pharmacologic basis – 5% albumin has a colloid osmotic pressure of 20 mmHg and expands the plasma volume to the same as the volume infused. Whereas, 25% albumin solution has a colloid osmotic pressure of 70 mmHg and expands the plasma volume to almost 4 to 5 times the volume infused.
  64. 64. • Indications :- 1. Plasma volume expansion 2. Correction of hypoprotenemia 3. In therapeutic plasmapheresis as a plasma expander.  Precautions and Contraindications :- 1. Fast infusion will rapidly increase circulatory volume with resultant volume overload and pulmonary oedema. 2. Contraindicated in patients with severe anemia and cardiac failure.
  65. 65. 3. Dehydrated patients may require additional fluids along with albumin infusion. 4. Albumin infusion should not be used for parenteral nutrition. Rate of administration –  For adults, an initial infusion of 25 gm of albumin is suggested.( 500 ml of 5% solution or 100 ml of 25% solution).  The suggested rate is 2 ml /min for 5% solution and 1 ml/min for 25% solution.
  66. 66. Dextran • These are glucose polymers produced by bacteria (leucohostoc) incubated in a sucrose medium. It is available in two forms- Dextran 40 ( molecular wt. 40,000) Dextran 70 ( molecular wt 70,000)  Pharmacologic basis – Plasma volume expansion- D-40 as 10% solution produces greater expansion than D-70 as 6% solution. But, duration of expansion is shorter than D-70.
  67. 67. Indications:- 1. Correction of hypovolemia in conditions such as shock, burns, haemorrhage or trauma. 2. Prophylaxis of deep vein thrombosis. 3. To improve microcirculation and blood flow in threatened vascular gangrene. 4. Improvement of thromboembolism.
  68. 68. • Side Effects :- 1. Acute renal failure 2. Hypersensitivity reactions 3. It may interfere with blood grouping and cross matching. • Contraindications :- 1. Severe oliguria and renal failure. 2. Known hypersensitivity reactions. 3. Severe CHF or circulatory overload. 4. Bleeding disorders such as thrombocytopenia. 5. Severe dehydration
  69. 69. • Administration :- 1. Dextran 40 :- It is given as 10% infusion in 0.9% NaCl or glucose. Adults with shock requires 500ml rapid infusion. In first 24 hours, dose not to exceed 20 ml/kg and subsequently 10 ml/kg/day for 5 days. 2. Regime for thromboembolism:- Day 1 – 500-1000 ml over 4 to 6 hrs. Day 2 – 500 ml over 4 to 6 hrs. Upto 10 days – 500 ml over 4 to 6 hrs on alternate days.
  70. 70. Gelatin Polymers (Haemaccel) • It is available in 3.5% solution in a 500 ml bottle.  Composition – Each litre contains :- Gelatin polymer 35 gms Sodium 145 mEq Chloride 145 mEq Calcium 12.5 meq Potassium 5.1 mEq
  71. 71. • Indications – 1. For rapid expansion of intravascular volume. 2. Prophylactic use in major surgeries to reduce total volume of fluid replacement. 3. For priming of heart lung machine. • Advantages – 1. Does not interfere with coagulation , blood grouping. 2. Remains in blood for 4-5 hours and expands the plasma volume by about 50% of infused volume.
  72. 72. Hetastarch ( Hydroxyethyl starch) • It is a synthetic colloid available as 6% solution in isotonic solution.  Pharmacologic basis – 1. It has a osmolarity of about 30 mm Hg 2. It produces greater plasma volume expansion as compared to dextran. 3. The expanded volume may last for 24 hours.
  73. 73.  Advantages :- 1. Fewer antigenic properties as compared to dextran 2. It does not interfere with blood grouping and cross matching. 3. Less expensive. 4. Plasma volume expansion greater than albumin. 5. Effect last for about for 24 hours.
  74. 74. • Disadvantages :- 1. Increase in serum amylase concentration. 2. Decreased oxygen carrying capacity. • Indications, Contraindications, administration :- 1. Similar to dextran.
  75. 75. Colloid Vs. crystalloid for volume resuscitation in the critically ill patients • The safety of colloids was first questioned by a rudimentary meta analysis performed by Velanovich in 1989. • The SAFE (Saline versus Albumin Fluid Evaluation) trial randomized 7000 critically ill patients requiring fluid resuscitation to receive iso oncotic albumin or isotonic crystalloid. • In this study, there was no overall difference in outcome according to whether patients received colloids or crystalloids.
  76. 76. A problem-based approach • The colloid-crystalloid controversy is fueled by the premise that one type of fluid is optimal in all cases of hypovolemia. • This seems unreasonable , since no single resuscitation fluid will perform optimally in all conditions associated with hypovolemia. • Example: – life threatening hypovolemia due to blood loss – blood products / albumin – Hypovolemia due to dehydration – crystalloid resuscitation • Tailoring the type of resuscitation fluid to the specific cause and severity of hypovolemia is a more reasoned approach than using the same type of fluid for all cases of hypovolemia.
  77. 77. Routine fluid calculation • Holliday and Segar formula-1957 • 4-2-1 rule derived from 100-50-20 rule determines hourly rate  Depends upon pts weight Both are effective in normal weight pts 0-10kgs-4ml/kg/hr 10-20kg-2ml/kg/hr >20kg- 1ml/kg/hr
  78. 78. ACID BASE BALANCE AND DISORDERS
  79. 79. Importance of pH 1. Normal cellular enzymatic reactions 2. Normal ionic concentrations 3. Change in pH can cause cardiac arrhythmias. 4. Act as a marker of an underlying diseases.
  80. 80. Basic Terminology Clinical terminology Criteria Normal pH 7.4(7.35-7.45) Acidosis pH < 7.35 Alkalosis pH > 7.45 Normal PaCO2 40 mm of Hg Respiratory acidosis PaCO2 > 45 mm of Hg Respiratory alkalosis PaCO2 < 35 mm of Hg Normal HCO3 24 mEq/L Metabolic acidosis HCO3 < 22 mEq/L Metabolic alkalosis HCO3 > 26 mEq/L
  81. 81. Regulation of Acid-Base Balance 1. Buffers - These are the chemical systems which maintain the acid base balance in the body. Eg:bicarbonate, phosphate, proteins and haemoglobin. 2. Respiratory regulation :- by excretion of volatile acids and maintaining PaCO2 at optimum concentrations , it has a double buffering system. 3. Renal regulation :- It acts by balancing the excretion of hydrogen ions and net reabsorption and production of bicarbonate ions.
  82. 82. Primary Acid-Base Disorders  If initial disturbance affects HCO3, 1. Metabolic Acidosis ( fall in bicarbonate). 2. Metabolic Alkalosis ( rise in bicarbonate).  If initial disturbance affects PaCO2, 1. Respiratory Acidosis (rise in PaCO2). 2. Respiratory Alkalosis (fall in PaCO2).
  83. 83. Compensation in Acid-Base disorders :- The body’s response to neutralize the effect of the initial insult on pH homeostasis is called as compensation. o To maintain normal pH, primary metabolic disorders leads to compensatory respiratory responses. o Same direction rule :- In each case, the compensatory changes are in the same direction as the primary change. This is known as Same direction rule.
  84. 84. Disorder Expected compensation Metabolic Acidosis ( Fall in HCO3) Fall in PaCO2 = 1.5 × HCO3 + 8 Metabolic Alkalosis(Rise in HCO3) Rise in PaCO2 = 0.5 × Rise in HCO3 Respiratory Acidosis Rise in PaCO2 Acute:Rise in HCO3 = 0.1 × Rise in PaCO2 Fall in pH 0.01 × Rise in PaCO2 Chronic: Rise in HCO3 = 0.4 × Rise in PaCO2 Fall in pH = 0.003 × Rise in PaCO2 Respiratory Alkalosis Fall in PaCO2 Acute : Fall in HCO3 = 0.2 × Fall in PaCO2 Rise in pH = 0.01 × Fall in PaCO2 Chronic : Fall in HCO3 = 0.4 × Fall in PaCO2 Rise in pH = 0.002 × Fall in PaCO2
  85. 85. Metabolic Acidosis • It is characterized by fall in plasma HCO3 and fall in pH (below 7.35). • Etiology :- (A) Normal Anion gap - (B) Increased Anion gap – - Loss of HCO3 : - Metabolic disorders : diarrhea, proximal RTA lactic acidosis, DKA - Failure to excrete H+ : - Addition of acids : distal RTA Salicylate poisoning - Addition of H+ - Renal failure NH4Cl infusion
  86. 86. Treatment • It is subdivided into two types – A. Specific management of underlying disorder :- Firstly, underlying disorder should be treated meticulously, and is the only required treatment in most of the cases. B. Alkali therapy :– Bicarbonate administration should be reserved for selective patients with severe acidosis. Treatment of all acidotic patients is not only unnecessary but can also be detrimental.
  87. 87. Sodium Bicarbonate  Composition- 7.5% sodium bicarbonate 25ml ampoule each ampoule contains 22.5 mEq sodium and 22.5mEq bicarbonate.  Indications –  Treatment of metabolic acidosis  Cardiopulmonary resuscitation and shock.  Treatment of hyperkalemia.  Alkaline forced diuresis along with diuretics in treatment of barbiturates and salicylates.
  88. 88. When to use? Mild to moderate acidosis can be treated with Ringer’s lactate or Isolyte E in addition to treatment of underlying disorders. Severe metabolic acidosis can be treated with sodium bicarbonate. How much to give? Amount of NaHCO3 = 0.6 × Weight × (Desired HCO3 – Actual HCO3).
  89. 89. • How to infuse? 50% of the deficit is corrected in 4 hours and the rest gradually over 24 hours. To avoid irritation of vein and sudden sodium loading , it is added to D5% and infused at desired rate for correction.
  90. 90. Special Precautions :- It should not be given as bolus except in emergency cases. As it is very irritant, establish a proper large i.v line for infusion. Never treat acidosis without treating the etiology. Avoid in cases of renal failure as it can lead to pulmonary oedema and tetany. Never correct acidosis without treating the associated hypokalemia. Do not mix with calcium in the same syringe as it can lead to calcium carbonate crystals.
  91. 91.  Complications:-  Post treatment metabolic alkalosis.  Hypokalemia  Volume overload  Hypocalcaemia  Contraindications :-  Respiratory alkalosis, metabolic alkalosis and hypokalemia.  Cautious use in congestive heart failure, chronic renal failure, cirrhosis of liver or hypertension.
  92. 92. Metabolic Alkalosis • It is characterized by increase in serum HCO3 levels , high pH and compensatory increase in PaCO2 due to alveolar hypoventilation.  Pathogenesis :- 1. Generation of metabolic alkalosis – loss of hydrogen ions, addition of alkali and disproportionate loss of chloride. 2. Maintenance of metabolic alkalosis – volume/chloride depletion, hypokalemia and aldosterone excess.
  93. 93. • Etiology :- Saline responsive Urine chloride < 15 mEq/L Saline resistant Urine chloride > 20 mEq/L ECF volume depletion Vomiting Diuretics Hypercapnia correction Normal or increased ECF Hypertensive Hyperaldosteronism Cushing’s syndrome No ECF volume depletion NaHCO3 infusion Multiple transfusions Normotensive Bartter’s syndrome Severe K+ depletion
  94. 94. Clinical Features 1. CNS symptoms :- Neuromuscular irritability, paresthesia, headache and carpopedal spasm. 2. CVS symptoms :- Hypotension and arrhythmias. 3. Respiratory symptoms – Hypoxia due to compensatory mechanism in patients with pre-existing lung diseases. 4. Others – Weakness, muscle cramps, dizziness.
  95. 95. Treatment 1. Correction of volume deficit with isotonic saline along with potassium and chloride supplementation. 2. Treatment with H2 inhibitors which reduces H+ ions secretion and further minimizes H+ loss. 3. Discontinue exogenous source of alkali such as NaHCO3 , Ringer’s lactate etc. 4. Dilute HCl can be given I.V to lower HCO3 concentration, can be corrosive and produce thrombophlebitis.
  96. 96. • Saline resistant metabolic alkalosis :-  It requires specific treatment of the underlying etiology-  Surgical treatment of pituitary tumour or adrenal adenoma in Cushing’s syndrome.  Supportive treatment such as spironolactone, correction of hypokalemia and sodium restriction.
  97. 97. Respiratory Acidosis • It is a clinical disorder characterized by an elevation in the PaCO2 leading to decrease in pH and compensatory increase in plasma HCO3.
  98. 98. Clinical Features • Acute Hypercapnia:– • Anxiety, headache, • dyspnea,confusion,psychosis, • hallucination and coma. • Chronic Hypercapnia:– Sleep disturbances, loss of memory, daytime somnolence, personality changes and tremors. • Fall in CSF pH is greater in respiratory acidosis than in metabolic acidosis. • CVS manifestations,vasculature.
  99. 99. Treatment General Measures :- 1. Treat the underlying cause promptly. 2. Establish patent airway and restore adequate oxygenation. 3. In patient with chronic hypercapnia, search for aggravating factors, vigorous treatment of pulmonary infection, bronchodilator therapy can be used.
  100. 100. OXYGEN THERAPY:- • In Acute Respiratory Acidosis: Major threat is hypoxia and not hypercapnia or acidosis,so oxygen supplementation is required. • In Chronic Hypercapnia : Oxygen therapy be instituted cautiously and in lowest possible concentration. Since hyoxemia may be the primary and only stimulus to respiration.
  101. 101. Mechanical Ventilatory Support : Indications :–  Unstable, symptomatic or progressively hypercapnic patients.  Patients exhibiting signs of muscle fatigue.  Refractory severe hypoxia or apnea.  Depression of respiratory centre.
  102. 102. • Alkali Therapy :- Avoid alkali therapy except in patients with – A) Associated metabolic acidosis. B) Severe acidaemia C) Severe bronchospasm.
  103. 103. Respiratory Alkalosis • When hyperventilation reduces the PaCO2 and leads to increased pH. • Etiology :- Hypoxemia Pulmonary Diseases – pneumonia, interstitial fibrosis, edema, emboli. CHF, hypotension or severe anaemia. High altitude residence. Stimulation of Respiratory centre Psychogenic or voluntary , pain , pregnancy Hepatic failure Salicylate intoxication Rapid correction of metabolic acidosis Neurological disorders.
  104. 104. Clinical Features It varies with the severity, rate of onset and underlying disorders. 1.It may be the only sign of the underlying sepsis or hepatic failure. 2.Common features are light headache, tingling of the extremities, circumoral paresthesia and cardiac arrhythmias. 3.PaCO2 below 20 mm of Hg carries a grave prognostic sign.
  105. 105. Treatment 1. Vigorous treatment of the underlying cause. 2. Oxygen supplementation , as hypoxia is a common cause of hyperventilation. 3. In absence of hypoxia, patient needs reassurance and rebreathing in a paper bag. 4. Pre-treatment with acetazolamide minimizes symptoms due to hyperventilation at high altitudes.
  106. 106. Electrolyte Disturbances
  107. 107. Sodium • Sodium is the major ECF cation (sodium value 140 mEq/l. • Total body sodium is about 5,000 mEq in a normal adult person • 85-90% of sodium is present in ECF and it is responsible for more than 90% of total osmolality of extracellular fluids. • Major function of sodium is to maintain ECF volume and therefore maintain blood pressure. • ECF volume is the reflection of total body sodium content. • Daily requirement of sodium is about 100mEq or 6gm of sodium chloride.
  108. 108. Hyponatremia • It is defined as a plasma conc. of less than 135mEq/L. • Etiology – I. Pseudo hyponatremia - A. Normal osmolality – Hyperlipidemia, Hyperproteinemia. B. High osmolality - Hyperglycemia, Mannitol.
  109. 109. Hyponatremia can be further subclassified according to effective osmolality, as follows: •Hypotonic hyponatremia •Isotonic hyponatremia •Hypertonic hyponatremia
  110. 110. Clinical Features Mild Moderate Severe Anorexia Personality changes Drowsiness Headache Muscle cramps Diminished reflexes Nausea Muscular weakness Convulsions Vomiting Confusion Coma Lethargy Ataxia Death
  111. 111. • Initial evaluation of Hyponatremia – 1. Plasma osmolality-(280-295mosm/kg) 2. Urine osmolality (500-800mosm/kg) 3. Urine sodium concentration.(20mEq)
  112. 112. • Treatment :- I. To raise the plasma sodium at a safe rate. II. To replace sodium or potassium deficit or both. III.To correct underlying etiology.  Specific treatment :- 1. Removal of specific drugs.eg- diuretics, cyclophosohomide. 2. Management of physical stress, post- operative pain. 3. Specific treatment for adrenal insufficiency, hypothyroidism etc.
  113. 113. • Chronic asymptomatic hyponatremia :-  The targeted rate of plasma sodium correction should not be greater than 0.5 to 1 mEq/L/hour.  A targeted rate of correction should not exceed 8 mEq/L/day.  A rate of correction higher than the above mentioned can cause central pontine myelinosis.
  114. 114. • Acute hyponatremia with neurological symptoms :-  Initial rate of correction for plasma sodium should be 1.5-2 mEq/L/hour for the first 3-4 hours or until the neurological symptoms subside.  The initial correction should not exceed 10-12 mEq in first 24 hours.  Patient may also require anticonvulsant therapy and adequate ventilation.
  115. 115. • Change in serum sodium concentration for a given infusate :- Sodium defecit(mEq)=total body weight x (140-ser.sodium)
  116. 116. Hypernatremia • It is defined as the plasma concentration of sodium more than 145 mEq/L . • Hypernatremia ([Na] > 145 mEq/L) is less common than hyponatremia, but may affect up to 10% of critically ill patients. • If severe ([Na] > 160 mEq/L), a 75% mortality may occur depending on the severity of the underlying disease process.
  117. 117. Clinical features :- These are primarily neurological, this is state in which dry sticky mucous membrane is characteristic and also elevated body temperature is present. Nausea Muscular weakness altered mental status neuromuscular irritability focal neurological deficit Coma or seizures
  118. 118. • Treatment :- 1. To diagnose and treat specific etiology 2. Correct the fluid deficit = plasma Na – 140 × TBW(kg)×0.6 140 3.Rate of correction – acute: 1 mEq/L/hr, chronic : 1 mEq/L/2 hrs. 4.Deterioration of neurological symptoms(cerebral edema). 5. Usually used fluids are isotonic saline, 0.45% saline and 5% dextrose.
  119. 119. Potassium • It is the major intracellular cation present in the body. • Total body potassium is about 3500 mEq. • Serum potassium concentration is about 3.5 to 5 mEq/L. • Intracellular concentration is about 150 mEq/L. • Normal requirement of potassium is about 50-80 mEq/day. • It plays an important role in the normal cellular functions and neuromuscular transmission.
  120. 120. Hypokalemia • This is defined as persistent decrease of the serum potassium levels below 3.5 mEq/L. • Responsible for regulation of electrical action potential across cell membrane specially in cardiac tissues,cellular metabolism,glycogen/protein synthesis.
  121. 121. • Etiology:– 1.Poor intake – low dietary intake or potassium free I.V fluids,refeeding syndrome 2.Intracellular k+ shift- albuterol,insulin,theophylline,caffeine 3.K+ loss-amphotericinB,loop and thiazide diuretics. 4.Non renal loss – vomiting, diarrhea, large naso-gastric aspiration. 5.Renal loss – Diuretics, mineralocorticoid excess, Cushing’s syndrome, magnesium deficiency
  122. 122. Clinical features • It is mainly neuromuscular and cardiac in origin 1. Fatigue, myalgia and muscular weakness are the common symptoms. 2. Smooth muscle involvement results in constipation, ileus and urinary retention. 3. Hyporeflexia, hypoventilation and virtually complete paralysis. 4. Increased risk of arrhythmia in patients on chronic digitalis toxicity. 5. Hepatic encephalopathy in patients with hepatic failure.
  123. 123. Diagnosis of etiology of hypokalemia 1. History 2. Urinary potassium excretion – - Hypokalemia with low renal potassium excretion - Hypokalemia with high renal potassium excretion : - metabolic acidosis - variable pH - metabolic alkalosis with or without hypertension.
  124. 124. TREATMENT
  125. 125. • In mild to moderate hypokalemia(3-3.4), average dose of potassium is 60-80 mEq/day along with treatment of underlying etiology. • In severe hypokalemia(<3), more rapid correction is required and can be done orally. Usual dose is 40-80 mEq/ 6 hourly under ECG monitoring. • I.V potassium supplementation is reserved for patients with severe symptomatic hypokalemia or who cannot ingest oral potassium.
  126. 126. Potassium chloride Composition – Inj. KCl 15% 10 ml ampoule 1 amp = 1.5 gm KCl = 20 mEq. Pharmacological basis –  Important for neuromuscular regulation  Inability of kidneys to retain potassium  Potassium is lost in certain conditions to maintain conc. Of sodium. Normal requirement of potassium is 50-60 mEq
  127. 127.  Indications –  Added to various maintenance fluids to counteract hypokalemia.  Added to potassium free peritoneal dialysis to maintain potassium level.  During Cardiac bypass surgery for achieving cardiac standstill after heart lung bypass.
  128. 128. Basic rules in use of KCl :- Never give Inj. KCl directly. Never give more than 40 mEq per litre. Never infuse more than 10 mEq per hour. Monitor constantly the levels of potassium and if possible ECG monitor too. Contraindications – Cautious use in renal failure. Never infuse KCl without knowing the potassium status.
  129. 129. Hyperkalemia • It is the serum potassium levels greater than 5.5 mEq/L is termed as hyperkalemia. Although, not as common as hypokalemia , it can lead to severe complications. • Etiology :- 1. Increased intake 2. Tissue breakdown 3. Shift of potassium out of cells 4. Impaired excretion 5. Pseudohyperkalemia
  130. 130. TREATMENT
  131. 131. Calcium  It is essential for bone formation and neuromuscular co- ordination.  Contains 1.2 to 1.4 kg of calcium in the body.  Serum calcium – 10 mg/dl.  40% is in ionized form and remaining bound to protein.  Small amount complexed with anions of organic acids.  Regulated by parathormone,Vitamin D and calcitonin.
  132. 132. Hypercalcaemia • Etiology :- 1. Increased bone turnover - Primary hyperparathyroidism Tertiary hyperparathyroidism Malignancy Thyrotoxicosis Lithium therapy
  133. 133. 2. Increased intestinal absorption : vitamin D intoxication Milk alkali syndrome granulomatous diseases 3. Decreased renal excretion : thiazide diuretics acute adrenal insufficiency hypocalciuric hypercalcaemia
  134. 134. Clinical features :- A.Central nervous system – neurologic depression B.GIT System – constipation C.Renal system- osmotic diuresis, renal stones D.CVS – increased heart rate and blood pressure.
  135. 135. Treatment A. Measures to increase urinary excretion - volume expansion and saline diuresis. Haemo-dialysis B. Measures to inhibit the bone resorption - Palmidronate Mithramycin Calcitonin Gallium nitrate. C. Measures to decrease intestinal absorption :- Glucocorticoids Oral phosphate
  136. 136. Hypocalcaemia • Decrease in the serum calcium level below 10 mg/dl  Etiology – 1. Hypoparathyroidism 2. Post surgical – hungry bone syndrome Hypomagnesemia Idiopathic 3. Hypoalbuminemia
  137. 137. 3. Defect in vitamin D metabolism – nutritional , lack of exposure to sunlight mal-absorption liver diseases, renal failure vitamin D dependent rickets 4. Miscellaneous – metabolic or respiratory alkalosis sepsis, toxic shock syndrome
  138. 138. • Clinical features :- - Weakness, circumoral and distal extremity paresthesia - muscle spasm, carpopedal spasm - mental changes( irritability, depression, psychosis) - lethargy, confusion , laryngeal spasm - chvostek’s sign, trousseau’s sign - chronic hypocalcaemia can lead to calcification of basal ganglia.
  139. 139. • Treatment :-  10% calcium gluconate (10 to 20 ml) I.V over 10 minutes is the usual treatment in emergency conditions.  Severe symptomatic conditions may require infusion of 60 ml of calcium gluconate in 500 ml of 5% dextrose.  To rule out hypomagnesemia  In long term management of hypocalcaemia, oral elemental calcium 1 to 3 grams per day is given.  Vitamin D supplementation
  140. 140. Phosphorus • It is critical in bone formation and cellular energy metabolism.  Chiefly intracellular and 1% in ECF.  Serum phosphate level is 3 to 4.5 mg/dl.  Major regulatory factors include parathormone, vitamin D and insulin.
  141. 141. Hypophosphatemia  Etiology – 1. Decreased intestinal phosphate absorption - vitamin D deficiency vitamin D dependant rickets malabsorption, phosphate binding antacids. 2. Increased renal phosphate excretion. 3. Shift of phosphate in intracellular fluid.
  142. 142. • Clinical features :- I. Muscular abnormalities – proximal muscle weakness, rhabdomyolysis, impaired diaphragmatic function. II. Neurological abnormalities – paresthesia, dysarthia, confusion, seizures and coma. III.Haematological abnormalities :- Tissue hypoxia, impaired phagocytosis and opsonization , mineralization defects which leads to rickets in children and osteomalacia in adults.
  143. 143. • Treatment :-  In cases where , serum phosphate levels are greater than 1 mg/dl, oral phosphate replacement is enough.  Severe hypophosphatemia requires I.V phosphate therapy.  Care should be taken to avoid hyperphosphatemia which can lead to varied complications.
  144. 144. Hyperphosphatemia • It is serum levels greater than 5 mg/dl is defined as hyperphosphatemia.  Etiology :- 1. Decreased renal excretion 2. Acute tissue destruction 3. Increased renal phosphate reabsorption ( hormonal changes) 4. Miscellaneous - vitamin D intoxication Metabolic or respiratory acidosis.
  145. 145. • Clinical features – 1. Neurological manifestations – muscular weakness, loss of deep tendon reflexes, muscular paresis. 2. Cardiac – hypotension, bradyarrhythmia and cardiac asystole. 3. Hypocalcaemia may result.
  146. 146. • Treatment :- 1. Correction of underlying etiology 2. Restriction of dietary phosphate to 600-900 mg/day. 3. Oral phosphate binders – calcium acetate and calcium carbonate. 4. Correct hyperphosphatemia before correcting hypocalcaemia. 5. Saline diuresis 6. Dialysis.
  147. 147. CLINICAL IMPLICATIONS
  148. 148. TRAUMA
  149. 149. Goal=> Hemostasis then restoration of normal circulating volume and tissue perfusion Permit hypovolemia to achieve cerebration rather than normotension, maintain SBP of 70 to 80 mm Hg in penetrating trauma, or 90 mm Hg in blunt trauma.  Large volumes of IV crystalloids or colloids in early resuscitation will cause hemodilution and dilute clotting factors, and saline-based fluids may aggravate the acidosis . pRBCs, FFP and platelets replaced early. “High” ratios of FFP to pRBC (e.g., 1:1 to 1:2) are associated with the best outcomes  Avoidance hyponatremia and hypoosmolality to minimize cerebral edema in isolated head injuries with a MAP >90 mm Hg.
  150. 150. NEUROSURGERY
  151. 151. • Rational management => maintain baseline blood volume and cerebral perfusion avoid decreases in serum Na+, osmolality, and oncotic pressure. • Specific management may be required in: • 1. Increased ICP: Mannitol and hypertonic saline given by bolus. Hypertonic saline superior to mannitol. • Restrictive fluid strategies advocated in severe traumatic brain injury. • 2.Cerebral vasospasm: “triple-H” therapy Hypervolemia, Hemodilution, Hypertension • 3.Intracranial pathologic condition CAUSE cerebral salt wasting, diabetes insipidus, SIADH. Albumin is => increase in mortality in traumatic brain injury.
  152. 152. PAEDIATRIC • General measures that should be applied to all patients, as follows: – Returning to oral fluids as early as possible – Ensuring euvolemia to minimize the ADH response – Not confusing maintenance requirements with the variable amounts of fluid required because of ongoing losses (e.g., GI or blood), which should typically be replaced by isotonic crystalloids, colloids, or blood – Checking electrolytes at least daily in those still receiving IV fluids
  153. 153. • Intraoperative – 20-40ml/kg of balanced salt solution. • Postoperative fluid management should be reduced to a 2, 1, 0.5 rule; that is, – 2 mL/kg for the first 10 kg – 1 mL/kg for the next 10 kg – 0.5 mL/kg for each kg above 20 kg with an isotonic fluid. • If after 12 hours the child is unable to convert to oral intake, then a standard hypotonic solution (D5 0.45% saline) is initiated at the 4- 2-1 rule rate to avoid hypernatremia.
  154. 154. REFERENCES Miller’s Anaesthesia (8th edition ) – Ronald Miller. Practical guidelines on Fluid Therapy(2nd edition) –Dr. Sanjay Pandya. Textbook of Physiology – Guyton and Hall. Textbook of General Surgery – Bailey and Love. SHAILA SHODHAN KAMAT-IV FLUIDS IN SURGICAL PATIENTS. WARD PROCEDURES-PATEL AND UPADHYAY

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