Electrolyte disorder for internist

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Electrolyte disorder for internist

  1. 1. Electrolyte disorders for internist
  2. 2. Contents • Water and sodium metabolism – Hypo- and hyper- osmolarity – Hypo- and hyper- natremia • Potassium – Hypo- and hyper- kalemia • Acid-base disorder
  3. 3. Contents • Water and sodium metabolism – Hypo- and hyper- osmolarity – Hypo- and hyper- natremia • Potassium – Hypo- and hyper- kalemia • Acid-base disorder
  4. 4. • Osmotic pressure – A function of the concentration of all the solutes in a fluid compartment Osmotic pressure = total solute total water Osmolarity = total solute ; mOsm/Kg H2O weight of water Osmolality = total solute ; mOsm / L H2O volume of water
  5. 5. Osmolality • Measurement • Calculation 2Na + Glucose + BUN 18 2.8
  6. 6. Total body water Depends on age, gender, body fat
  7. 7. Body water regulation Water gain Water loss Intake metabolism Insensible loss sweat, lung Feces kidney
  8. 8. HypotonicityHypotonicity HypothalamusHypothalamus OsmoreceptorsOsmoreceptors ADHADH Thirst OsmoregulationOsmoregulation StimulateStimulate HypertonicityHypertonicity ADHADH InhibitInhibit IsotonicityIsotonicity Thirst WaterWater intakeintake WaterWater intakeintake Renal water excretion Renal water retention
  9. 9. Hypothalamus Angiotensin Baroreceptor OC = osmoreceptor MnPO = median preoptic nuclei SFO = subfornical organ OVLT =organum vasculosum of the lamina terminalis Osmolality
  10. 10. Arginine vasopressin stimulation • Osmotic stimuli • Nonosmotic stimuli – Blood pressure and blood volume – Drinking – Nausea – Angiotensin II – Stress : pain, emotion – Hypoxia – drug
  11. 11. Renal regulation of sodium
  12. 12. Hyponatremia • Pseudohyponatremia (normal osmolality) – Hyperlipidemia – Hyperproteinemia • Translocational hyponatremia (hyperosmolality) – Hyperglycemia – Mannitol, sorbital, glycerol • True hyponatremia ( hypo-osmolality)
  13. 13. Approach Guideline of HypoNa True HyponatremiaTrue Hyponatremia (exclude hyperglycemia)(exclude hyperglycemia) Assess ECF volume statusAssess ECF volume status TBW , TBNaTBW , TBNa++ HypovolemiaHypovolemia TBW , TBNaTBW , TBNa++ HypervolemiaHypervolemia TBW , TBNaTBW , TBNa++ NormovolemiaNormovolemia Renal loss Extrarenal loss Renal failure Nephrotic syndrome Cirrhosis Cardiac failure SIADH Endocrinopathy Drugs UNa >20 <20 > 20 > 20 < 20
  14. 14. • Hypovolemic hyponatremia with UNa >20 (renal loss) – Diuretic use – Mineralocorticoid deficiency – Salt-losing nephropathy – Bicarbonaturia – Ketonuria • Hypovolemic hyponatremia with UNa <20 (extrarenal loss) – Vomiting – Diarrhea – Third space loss • Burn, pancreatitis
  15. 15. Causes of SIADH CARCINOMAS PULMONARY DISORDERS CNS DISORDERS OTHERS Bronchogenic CA Viral pneumonia Encephalitis AIDS Small cell lung CA Bacterial pneumonia Meningitis Prolonged exercise CA duodenum Tuberculosis Head trauma idiopathic CA pancreas Aspergillosis Brain abscess CA stomach Lung abscess Delerium tremens Thymoma Asthma Acute psychosis Lymphoma Pneumothorax Multiple sclerosis Ewing sarcoma Mesothelioma CVA CA bladder Cystic fibrosis Guillain-Barre syndrome Prostate CA Oropharyngeal tumor Positive pressure breathing
  16. 16. Symptoms of hyponatremia • Depend on – Age – Gender – Magnitude and acuteness • Gastrointestinal symptoms : nausea, vomiting • Neurological symptoms: headache, lethargy, muscle weakness, ataxia, psychosis, seizure, coma, brain herniation
  17. 17. Treatment of Hyponatremia 1. Level, duration of hyponatremia 2. Symptoms 3. Volume status 4. Risk of neurological damage
  18. 18. Hyponatremic patients at risk for neurological complications • Postoperative menstruating female • Elderly women on thiazide • Children • Hypoxemic patients • Psychiatric polydipsic patients • Alcholics • Malnourished patients • Hypokalemic patients
  19. 19. Treatment solution Depend on volume status (causes of hyponatremia) Hypovolemia - isotonic saline Euvolemia (EM) - hypertonic Hypervolemia - diuretic ± hypertonic
  20. 20. Treatment of hyponatremia • Acute symptomatic hyponatremia – Raise SNa 1-2 meq/L – Not more than 12 meq/L in 24 hours • Chronic symptomatic hyponatremia – Raise SNa 0.5-1 meq/L – Not more than 10 meq/L in 24 hours • Asymptomatic hyponatremia – Water restriction – Drug-induced water diuresis : democlocyclin, lithium, V2 antagonist – Increase solute intake : urea
  21. 21. • A 70-Kg man present diagnosed bronchogenic carcinoma. He presents with GTC. BP 130/80 mmHg. JVP 3 cm, lung- clear. His serum Na is 103 meq/L, Cr 0.7 mg/dl, BS 100 mg/dl • U/A : sp gr 1.020 Euvolemic hyponatremia Thyroid function test and cortisol level is normal SIADH
  22. 22. Desired Na = 110 mmol/l = TBW x (dNa – sNa) = 0.6 (70) (110 - 103) = 294 mmol Na 294 mmol = 3% NaCl 573 ml Correct Na 1 mmol/l/hr = 3% NaCl 573/7 = 80 ml/hr iv.drip
  23. 23. Approach guideline for hypernatremia Assess volume status Hypovolemia TBW TBNa Euvolemia TBW TBNa Hypervolemia TBW TBNa UNa >20 <20 variable >20 Renal loss Osmotic or loop diuretics Postobstructive diuresis Intrinsic renal disease Extrarenal loss Excessive sweating Burn Diarrhea fistula Renal loss DI hypodipsia Extrarenal loss Insensible loss Sodium gain Primary hyperaldosteronism Cushing’s syndrome Hypertonic dialysis Hypertonic sodium bicarbonate
  24. 24. Patients at risk of severe hypernatremia • Elderly patients or infants • Patients receiving – Hypertonic infusion – Osmotic diuresis – Lactulose – Mechanical ventilator • Third space water loss : rhabdomyolysis • Altered mental status • Uncontrolled diabetes mellitus • Unerlying polyuric disorder
  25. 25. Hypotonic polyuria Disorders Urine osmolality SNa Insufficient AVP Central diabetes insipidus + osmoreceptor dysfunction Diabetes insipidus in pregnancy Impaired renal response to AVP Nephrogenic diabetes insipidus Primary polydipsia Dipsogenic polydipsia psychogenic polydipsia
  26. 26. Water deprivation test • Patients with hypotonic polyuria – Urine > 50 ml/kg/day – UOsm < 300 mOsm/kg – Total osmole <15 mOsm/kg/day, no glucosuria or other osmoles
  27. 27. Protocol for water deprivation test • Initiation of the deprivation period • Baseline data – Body weight, BP – Serum osmolality, electrolyte – Urine osmolality – Serum AVP • Follow up BW, BP, urine osmolality hourly • Stop deprivation if BW decrease > 3%, orthostatic hypotension or urine osmolality changes < 10% in 2-3 consecutive measrement • Serum electrolyte, serum osmolality and serum AVP at the end point • If SOsm >295, DDAVP 1 ug or AVP 5 ug sc then measure urine output, urine osmolality 1-2 hours after injection
  28. 28. Treatment of hypernatremia • Reduction of ongoing loss • Correction of preexisting water deficit – Rate of correction depends on • Acuteness • Severity • Risk of neurological deficit
  29. 29. • If serum osmolality > 330 (SNa > 165), decrease Sosm to 320-330 mOsm/L in 24 hours then 0.5 meq/L/hour Water deficit = 0.6 x BW x (SNa – 140) SNa
  30. 30. Treatment of hypernatremia • Specific treatment – Central DI • DDAVP, vasopressin • Chlorpropamide – Nephrogenic DI • Correct cause • Low salt diet • Thiazide or amiloride • NSAIDs – Pregnancy-induced DI – DDAVP – Osmoreceptor dysfunction – schedule – Psychogenic polydipsia – psychotherapy, clozapine
  31. 31. Contents • Water and sodium metabolism – Hypo- and hyper- osmolarity – Hypo- and hyper- natremia • Potassium – Hypo- and hyper- kalemia • Acid-base disorder
  32. 32. Internal and external K balanceInternal and external K balance IntakeIntake (RBC, Muscle, Liver, Bone)(RBC, Muscle, Liver, Bone) ICFICF ExcretionExcretion KidneyKidney 90%90% ColonColon 10%10% KK 60-10060-100 mEq/daymEq/day DistributionDistribution 235235 30003000 200200 300 mEq300 mEq Sweat <Sweat <10%10% ECF 50-70 meq
  33. 33. Factors - transcellular distribution of KFactors - transcellular distribution of K NaNa++ KK++ KK++ InsulinInsulin bb22 -adrenergic-adrenergic agonistagonist AldosteroneAldosterone cAMPcAMP Na-KNa-K ATPaseATPase 1.1. HormoneHormone 2. Acid-base status2. Acid-base status 3. Plasma tonicity3. Plasma tonicity 4. Congenital diseases4. Congenital diseases ThyroidThyroid
  34. 34. Renal regulation of potassium
  35. 35. PosmPosm 300300 mOsmol/kgmOsmol/kg Serum [K]Serum [K] 4 mEq/L4 mEq/LCCT [K]CCT [K] 40 mEq/L40 mEq/L CCTCCT MCDMCD 1 L1 L 0.75 L0.75 L 0.25 L0.25 L Uosm 1200Uosm 1200 Uosm 300Uosm 300 HH22OO urine [K]urine [K] 160 mEq/L160 mEq/L TTKG = CCT[K] = urine[K] / (U/P)osmTTKG = CCT[K] = urine[K] / (U/P)osm Serum [K]Serum [K] Serum [K]Serum [K] Transtubular K gradientTranstubular K gradient
  36. 36. K CCT = K urine [K] CCT VCCT = [K]urine Vurine [K]CCT = [K]urine Vurine VCCT V = solute Vurine = K/ Uosm osmolarity VCCT K/Osm CCT  Posm TTKG = [K]CCT = [K]urine x Posm [K] P [K]P x Uosm
  37. 37. Symptoms • Hypokalemia – Skeletal and smooth muscle weakness – Rhabomyolysis – Nephrogenic DI – EKG; flattened T wave, U wave • Hyperkalemia – EKG; peak T wave, flattened P wave, widening QRS complex, sine wave – Muscle paralysis – Impaired urinary acidification – Stimulate aldosterone secretion
  38. 38. Approach Guideline of HypoK Decreased serum [K]Decreased serum [K] excretionexcretionRedistributionRedistribution -- AlkalosisAlkalosis - Insulin Rx- Insulin Rx - HypoK periodic paralysis- HypoK periodic paralysis - Drugs:- Drugs: ββ-agonists-agonists - Barium poisoning- Barium poisoning Renal K excretionRenal K excretion:: vary low high (>20 mmol/d)vary low high (>20 mmol/d) lowlow (<20 mmol/d)(<20 mmol/d) ExtrarenalExtrarenal - Diarrhea- Diarrhea - Cathartics- Cathartics RenalRenal - Diuretics- Diuretics - HypoMg- HypoMg - Hyperaldosteronism- Hyperaldosteronism - Inherited kidney dis- Inherited kidney dis - Drugs toxicity:- Drugs toxicity: Amphotericin BAmphotericin B Carbenicillin, etc.Carbenicillin, etc. Low intakeLow intake
  39. 39. Rx of hypokalemia Rx causes Potassium deficit, 100-200 mEq if S. [K] = 3-3.5 mEq/L 200-400 mEq if S. [K] < 3 mEq/L > 600 mEq if S. [K] < 2 mEq/L Caution in periodic paralysis
  40. 40. Form: Oral * Elix. KCl (20 mEq/15 ml) with metabolic alkalosis * M Pot Cit oral (10 mEq/15 ml) with metabolic acidosis IV * [K] < 60 mEq/L in glucose-free sol. with the rate of < 10 mEq/h unless ECG is monitored
  41. 41. Causes of hyperkalemia • Pseudohyperkalemia – hemolysis, thrombocytosis, severe leukocytosis, fist clenching • Decreased renal excretion  Acute and chronic renal failure  Aldosterone deficiency: DM, CTIN, obstructive uropathy  Addison’s disease  Drugs inhibit K+ secretion  Kidney diseases that impairdistal tubule function • Abnormal K+ distribution  Insulin defiency  β-blocker  Metabolic acidosis, respiratory acidosis  Familial hyperkalemic periodic paralysis • Abnormal potassium release from cells  Rhabdomyolysis  Tumor lysis syndrome
  42. 42. Treatment of hyperkalemia Agents Dosage Action Mechanism 10% calcium gluconate 10 ml IV in 1 min, repeat q 5 min immedialtely Stabilze myocardium insulin 5 units + 50% glucose 50 ml 15 min Intracellular K+ shift If BS >300 mg/dl, insulin alone Aware hypoglycemia Sodium bicarbonate 50-100 ml Renal K+ excretion Intracellular shift Severe metabolic acidosis (<10 meq/L) B2 agonist 20 mg albuterol NB in 10 min 30 min Intracellular shift diuretic Furosemide IV 30-60 min Remove K+ For patients with adequate renal function Exchange resin Kayexalate 50 gm or kallimate 2 hours Remove K+ dialysis Remove K+
  43. 43. Contents • Water and sodium metabolism – Hypo- and hyper- osmolarity – Hypo- and hyper- natremia • Potassium – Hypo- and hyper- kalemia • Acid-base disorder
  44. 44. METABOLIC ACIDOSIS • Anion gap = [Na+ ] – { [HCO3- ]+[Cl- ] } – Normal 9 -12 mEq/L – Each decline in serum albumin by 1 g/dL from the normal value of 4.5 g/dL, decreases the AG by 2.5 mEq/L
  45. 45. CAUSES OF METABOLIC ACIDOSIS • High anion gap – Ketoacidosis • Diabetic • Alcoholic • Starvation – Lactic acidosis • L-lactic acidosis (type A and B) • D-lactic acidosis – Drugs and toxin • Ethanol, Ethylene glycol, Methanol • Salicylate – Uremia • Normal anion gap – GI loss of HCO3 • Diarrhea • Fistula – Renal loss of HCO3 or failure to excrete NH4+ • Renal tubular acidosis • Acetazolamide – Miscellaneous • NH4Cl ingestion • Sulfur ingestion
  46. 46. Metabolic acidosis Anion gap ; Na – (Cl + HCO3) high normal Osmolol gap Measured osmolality – calculated osmolality high normal Ethanol Ethylene glycol Methanol Isopropyl alcohol Ketoacidosis Lactic acidosis uremic Serum potassium Hypo or normokalemia hyperkalemia Urine anion gap (Na + K) – Cl negative positive GI loss Drugs Proximal RTA Aldosterone resistance Aldosterone deficiency dRTA type IV >5.5 Urine pH <5.5
  47. 47. ACCUMULATION OF LACTATE Increase lactate production ischemia seizure extreme exercise leukemia alkalosis Decrease lactate utilization poor blood flow defective active transport of lactate into cell inadequate metabolic conversion of lactate to pyruvate Liver 70%, kidneys 30% Muscle, gut, brain, skin, RBC
  48. 48. LACTIC ACIDOSIS • TYPE A – Poor tissue perfusion – Shock – Hypoxemia – Carbon monoxide poisoning • TYPE B – Liver disease – Leukemia, lymphoma, large tumor – Anemia – Diabetes mellitus – Drugs : metformin, NRTIs, sorbital, isoniazid, salicylate etc – Inborn error metabolism – Intravenous fructose
  49. 49. Symptoms • Respiratory symptoms – Kussmaul respiration – Oxyhemoglobin dissociation curve • Left shift in chronic acidosis • Right shift in acute acidosis • Cardiovascular systems – Negative inotropic effect – Peripheral arterial vasodilatation – Central venoconstriction • Neurological systems – Headache, lethargy, stupor and coma
  50. 50. Treatment of metabolic acidosis • Get rid of cause – DKA : IV fluid + insulin – Alcoholic ketoacidosis, starvation : IV fluid (5%D) – Shock : IV fluid – Toxin : increase excretion ( kidney, dialysis), antidote • Bicarbonate replacement – Causes are not corrected in short period – Ongoing loss of HCO3 – Severe metabolic acidosis

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