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Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
Water n electrolytes iii
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Water n electrolytes iii

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  • 1. DR. SHRADDHA THOURANI
  • 2. ASSESSMENT OF THE PATIENT  The diagnosis and treatment of fluid and electrolyte disorders are based on (1) careful history, (2) physical examination for volume status (3) serum electrolyte concentrations, (4) urine electrolyte concentrations, and (5) serum and urine osmolality.  The pathophysiology of electrolyte disorders is rooted in basic principles of total body water and its distribution across fluid compartments
  • 3. INTRODUCTION  Water is the most abundant constituent comprising approximately 60% of body weight in an adult.  Total body water (40L) is distributed in two major compartments: more than half is intracellular [intracellular fluid (ICF)], and remaining is extracellular [extracellular fluid (ECF)].  The ECF is further subdivided into intravascular (plasma water) and extravascular (interstitial) spaces in a ratio of 1:3.  The dominant cation in ICF is K+ with phosphates  The dominant cation in ECF is Na+ with Cl- and HCO3-
  • 4. WATER AND ELECTROLYTE DISTRIBUTION
  • 5.  Water may be lost from either or both compartments (intracellular and extracellular).  Effective circulating volume may be assessed by physical examination (eg, blood pressure, pulse, jugular venous distention).  Quantitative measurements of effective circulating volume and intravascular volume may be invasive (ie, central venous pressure or pulmonary wedge pressure)  or noninvasive (ie, right atrial pressure by echocardiography)
  • 6. HOMEOSTASIS  Balance between water, electrolytes and acid and bases.  Depends on vasopressin secretion, water intake and renal water transport.  Differential movement within the compartments to achieve osmotic equilibrium.  Kidney plays an important role in homeostasis.
  • 7. DISORDERS OF VOLUME STATUS  HYPOVOLEMIA generally refers to a state of combined salt and water loss exceeding intake, leading to ECF volume contraction.  HYPERVOLEMIA excessive retention of water into the extracellular space leading to increased ECF volume
  • 8. ETIOLOGY OF HYPOVOLEMIA RENAL CAUSES (Increased Na & H2o loss)  High filter load of glucose and urea  Mannitol  Diuretics  Mineralocorticoid deficiency  Tubulointerstitial injury (interstitial nephritis,ATN)  Excessive excretion of free water (diabetes incipidus)  Drugs like acetazolamide, trimethoprim
  • 9. EXTRARENAL CAUSES • Fluid loss from GI tract –vomiting, diarrhea. • Loss from skin – excessive sweating, burns • Insensible loss by respiratory tract – fever, hyperventilation • Excessive accumulation of fluid in interstitial or peritoneal space –sepsis, burns, peritonitis, bowel obstruction, pancreatitis • INADEQUATE intake of salt
  • 10. Clinical features SYMPTOMS  Fatigue ,weakness ,thirst and dizziness on standing. SIGNS  Low JVP  Postural hypotension  Tachycardia  Reduced skin turgor and dry m.m  Reduced urine output In severe form – hypotension, peripheral vasoconstriction, cyanosis, cold extremities, confusion, stupor and shock
  • 11. INVESTIGATIONS  Serum Creatinine – Normal in early hypovolemia  Plasma urea conc- increased  Plasma uric acid- increased  Urine osmolality increases due to increased excretion of Na and water.  Plasma conc. of sodium - normal
  • 12. TREATMENT  Goal is to restore normal volume and replace fluid lose.  Mild hypovolemia is treated with oral hydration  Severe hypovolemia requires intravenous hydration 1. Isotonic normal saline (0.9% NaCl) 2. Hypotonic saline (0.45% or 0.25% NaCl) 3. Hartmann’s solution ( compound sodium lactate solution) Plasma expanders and synthetic colloids can also be given
  • 13. HYPERVOLAEMIA  Hypervolemia associated with sodium excess leads to expansion of the ECFV predominantly interstitial fluid.  In the presence of normal function of the heart and kidneys, an excessive intake of salt and water is compensated for by increased excretion and so is unlikely to lead to clinically obvious features of hypervolaemia.  However, diseases affecting the heart, kidneys or liver can lead to hypervolaemia
  • 14. Causes of sodium and water excess  Impaired renal function- Primary renal disease  Primary hyperaldosteronism-e.g. Conn’s syndrome  Secondary hyperaldosteronism  Congestive cardiac failure  Cirrhotic liver disease  Nephrotic syndrome  Other hypoalbuminaemic states  Protein-losing enteropathy  Malnutrition
  • 15. S/S of ECF volume overload  Total body salt and water are increased due to increased renal retention of Na+ and water.  peripheral edema appears when ECF vol. increases by about 15%. Symptoms of hypervolemia  Ankle swelling  Abdominal swelling, ascites  Breathlessness, due to pulmonary edema
  • 16.  SIGNS of hypervolemia  Peripheral oedema  Raised JVP  Pulmonary crepitations  Pleural effusion  Ascites  Weight gain  Sometimes Hypertension
  • 17. M/M of ECFV overload  Restriction of dietary sodium to < 100mmol/day.  Diuretics  Specific treatment:  Cardiac failure – ACE inhibitors  Corticosteroids in minimal change nephropathy
  • 18. Hyponatremia  Defined as plasma sodium concentration < 135 mEq/L    Hyponatremia usually reflects excess water retention relative to sodium rather than sodium deficiency.  Most cases of hyponatremia reflect water imbalance and abnormal water handling, not sodium imbalance, indicating the primary role of ADH in the pathophysiology of hyponatremia    Hypotonic fluids commonly cause hyponatremia in hospitalized patients.     To determine the etiology - Volume status and serum osmolality are essential
  • 19.  Hyponatraemia can be classified based on the ECF volume status of the patient. 1. Hypovolemic hyponatraemia – body water↓,and total body sodium ↓↓(sod. deficite with relatively smaller water deficite) 2. Euvolemic hyponatraemia – body water ↑, total body sodium is normal(water retention alone) 3. Hypervolemic hyponatraemia- body water ↑↑, total body sodium ↑
  • 20. HYPOVOLEMIC HYPONATRAEMIA (TBW↓ & Na ↓↓) • Extra renal causes – diarrhea, vomiting, burns, pancreatitis • Renal causes – diuretics, osmotic diuresis, tubulo interstitial disease • Clinical features will be same as ECFV depletion – dizziness, weakness, hypotension, low JVP • Treated by volume replacement with isotonic normal saline
  • 21. EUVOLEMIC HYPONETRAEMIA ( dilutional hyponatraemia) (TBW ↑ & Na is normal) Causes • Polydipsia or psychogenic water drinking • Iatrogenic water excess – IV dextrose • Post op. bladder irrigation after prostatectomy • SIADH secretion – renal water retention
  • 22. • Clinical features – No signs of ECFV depletion, • JVP will be N • Plasma conc. Of sodium –low • Plasma osmolality is low • Urine osmolality is high • Urine sodium conc.is >30meq/l • Treatment – water restriction to < 1 lit/day
  • 23. HYPERVOLEMIC HYPONATRAEMIA – sodium retention with vol. expansion (TBW↑↑ & Na ↑) • Causes are cardiac failure, • renal failure, • liver failure or • nephrotic syndrome • Clinical features – tissue oedema is common - JVP is raised in cardiac failure  Plasma sodium conc –low Treatment – Diuretic therapy - fluid restriction
  • 24. Symptoms and Signs  Mild symptoms of nausea and malaise progress to  headache,  lethargy, and disorientation as the sodium concentration drops.  The most serious symptoms are respiratory arrest,  seizure, coma,  permanent brain damage, and death.
  • 25. SYMPTOMS and signs of hyponatraemia occur when plasma sodium level goes below 120meq/l  Slow developing hyponatraemia usually have no symptoms and can be treated by water restriction alone.  Rapidly developed hyponatreamia requires urgent correction by giving 3% hypertonic saline solution and the rise in plasma sodium should not be > 10 meq/24 hr, as it may lead to extrapontine myelinolysis  For this serum sodium levels should be checked every 4-6 hrs.
  • 26. Diagnosis of hyponatraemia  Detail history  Clinical assessment of volume status  Lab investigations  Plasma osmolality  Urine osmolality  Plasma sodium conc.  BUN  S. Creatinine
  • 27. TREATMENT OF HYPONATREMIA  Regardless of the patient’s volume status, it is necessary to restrict free water and hypotonic fluid intake, since these solutions will exacerbate hyponatremia.  Hypovolemic patients require adequate fluid resuscitation from isotonic fluids like  normal saline or lactated Ringer solution  Asymptomatic to mild forms – treated with hypertonic saline  Acute symptomatic hyponatremia – hypertonic 3% saline.
  • 28. Hypernatremia  Hypernatraemia occurs when a decreased water intake or increased water excretion or both leads to a decreased TBW.  Plasma sodium>148meq/l  Produced by either administration of hypertonic fluids or much more frequently, loss of thirst  hypernatremia generally occurs only in people with prolonged lack of thirst mechanism, elderly people  Patients with loss of ADH (Diabetes Insipidus)
  • 29. Causes of Hypernatremia  Lack of water intake  Insensible and sweat losses  GI losses  Diabetes Insipidus - no ADH release  Osmotic Diuresis – DKA  Hypothalamic lesions which affect thirst function – Causes include tumors, granulomatous diseases or vascular disease  Sodium Overload – Infusion of Hypertonic sodium bicarbonate for metabolic acidosis
  • 30. Symptoms of Hypernatremia  Initial symptoms include lethargy, weakness and irritability  Can progress to twitching, seizures, obtundation or coma  Diagnosis :  Serum osmolality,  urine osmolality and  urine sodium  TREATMENT – With appropriate hypotonic solution 0.45% saline or isotonic 5% dextrose
  • 31. DYSKALAEMIAS  Disorder of potassium metabolism  K+ is the major intracellular cation  Imp role in neuromuscular transmission and membrane potentials  In the kidney about 90% of the filtered K+is reabsorbed in the PCT and thick ascending limb. K+ is further secreted in cortical collecting duct under influence of aldosteron  Normal plasma K+ conc. Is 3.3-4.7meq/l
  • 32. HYPERKALAEMIA • Due to shift of K+ out of the cell or ↓ renal excretion of K+ • Normal plasma K+ conc. is 3.7-5.2meq/l Causes of hyperkalaemia 1. High intake of K+ • High K+ food • IV K+ therapy 2. Intravascular hemolysis 3. Catabolic states like fasting, tissue necrosis 4. Shift of K+ out of cells  acidosis • Insulin deficiency  hyperglycemia
  • 33. 5. decrease excretion of K+ by kidneys.  Renal failure – ARF,CRF  Tubular secretory failure
  • 34. C/F of hyperkalaemia  Most patients may be asymptomatic  Symptoms appear when plasma K+ level is >7meq/l  Tingling around lips or in the fingers  Severe muscular weakness leading to flaccid paralysis,  Loss of tendon jerks  Abdominal distension and ileus.  Cardiac arrhythmias or cardiac arrest  Diagnosis is by ECG – Tall T waves with prolonged PR interval and widening of QRS complex  Plasma electrolytes, bicarbonates and creatinine
  • 35. TREATMENT  Dietary restriction of K+ rich foods in renal failure  Metabolic acidosis is corrected by giving sodium bicarbonate.  Calcium gluconate infusion stabilizes conductive tissue membranes by reopening the sodium channels.  Insulin helps the re entry of K+ ions intracellularly.  If hyperkalaemia is secondary to renal failure; hemodialysis or peritoneal dialysis.
  • 36. HYPOKALAEMIA • Caused by shift of K+ into the cells or by K+ depletion FACTORS CAUSING k+ DEPLETION • Inadequate intake • GI loss – diarrhea, vomiting, aspiration of GI contents • Intestinal obstruction, ileus • Increased loss in urine due to ↓ reabsorption of K+ • Diuretics  Primary and sec. aldosteronism • Metabolic alkalosis (shift of K+ into the cells) • Insulin excess
  • 37. Mild hypokalemia Plasma K+ conc. <3.0-3.5 meq/l) are usually asymptomatic CLINICAL FEATURES • Tiredness and muscular weakness • ↓ intestinal motility or paralytic ileus • Ventricular arrhythmias or asystole • Long standing hypokalemia may lead to failure of antidiuretic response to ADH leading to nocturia, polyuria and polydipsia LAB : Plasma electrolytes, bicarbonates,& urine K+ MANAGEMENT • Oral K+ salt (potasium bicarbonate) or K+ rich diet(banana, citrus fruits) • IV KCl • Potasium sparing diuretics
  • 38. THANK YOU

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