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Water and electrolytes 2013 final
- 1. Dr Alan Richardson 26 April 2013
- 2. Learning Objectives Logically investigate the causes of high and low levels of electrolytes through case study review Compare and contrast the principles of vapour pressure and freezing point osmometry Evaluate the use of the water deprivation test in the investigation of diabetes insipidus
- 3. Total Body Water 50-70% of body weight is water (lower in females, higher in males) – about 42L 2/3rds is intracellular (about 28L) Remaining 14L is spread between interstitial compartments (3/4), plasma compartments and transcellular compartments
- 4. Vander’s Renal Physiology. Eaton and Pooler 6th Ed 2004 *
- 5. Body Fluid Compartments How do we work out total body water and its distribution? TBW – deuterated or tritiated water ECF – sucrose, mannitol, inulin Plasma – 131I-albumin, 31Cr-erythrocytes Interstitial – ECW – plasma Intracellular – TBW - ECW *
- 6. Changes to ECF volume Decreased Acute blood loss Vomiting and diarrhoea Diuretics Salt wasting diseases of renal or adrenal origin Increased Congestive heart failure Hepatic cirrhosis Nephrotic syndrome Iatrogenic
- 7. Third Space Losses Loss of volume to compartments of the body at the expense of intravascular volume This can include interstitial and transcellular compartments Bowel obstruction Peritonitis Pancreatitis Burns Sepsis Multitrauma *
- 8. Vander’s Renal Physiology. Eaton and Pooler 6th Ed 2004
- 9. Osmolality What is osmolality? Osmolality is a measure of the number of dissolved particles per kg of water Essentially a measure of the osmotic pressure exerted by a solution How do we measure it? *
- 10. Freezing Point Depression Solution supercooled below its freezing point with gentle stirring Rapid stirring or vibration initiated to start freezing process Heat of fusion warms the solution Freezing completes * http://www.iupui.edu/~cletcrse/380/ch3suppos.htm
- 11. Loser Messtechnik Osmometers product application website. Accessed 12/04/13
- 12. Vapour Pressure Depression Change in vapour pressure measured indirectly through a decrease in dew point Sample placed in a vaporisation/condensation chamber Temperature is then manipulated to establish thermal and vapour equilibrium Cooling of the sample then occurs to below the dew point of the sample causing condensation to occur This increases the temperature of the sample until the dew point is achieved *
- 13. ©Wescor Biomedical Systems. Accessed from http://panza.uchicago.edu/Phys.261/mat erials/Osmometer/ on the 12/04/13
- 14. Vapour Pressure Depression Relies on the vapour released by a liquid condensing again as the temperature is manipulated within a narrow range Thus volatiles within a sample will easily become gaseous but will not condense again at the temperatures we are using Volatiles include ethanol, methanol, ethylene glycol and even dissolved CO2
- 15. Calculated osmolality Osm(calc) = 1.86 (Na+) + Glu + Urea + 9 Osmolal gap (measured – calculated) Alcohols – methanol, ethanol, ethylene glycol Sugars – mannitol, sorbitol Ketoacidosis, lactic acidosis Lipids – hypertriglyceridaemia Proteins – multiple myeloma, Waldentrom’s macroglobulinaemia Dorwart and Chalmers Clin Chem 1975 21:190-194 *
- 16. Sodium and Water Water balance in adults Intake Oral fluid 1200ml Dietary 1000ml Metabolism 300ml 2500ml Output Insensible 700ml Sweat 100ml Faeces 200ml Urine 1500ml 2500ml
- 17. Sodium and Water Total body sodium 70kg human contains about 4200 mmol of sodium 50% in ECF 40% in bones 10% in ICF Abnormal plasma sodium concentrations are most usually related to an abnormality in water balance, rather than a primary abnormality in sodium balance
- 18. Sodium and Water Water balance is maintained primarily by sensation of thirst (intake) and production of anti-diuretic hormone (output) Control of ADH (vasopressin) is through two primary triggers Osmolality Blood pressure Other less important factors include nausea, atrial natriuretic peptide and angiotensin II Drugs including nicotine (stimulates) and ethanol (inhibits) also affect its release
- 19. Sodium and Water Osmotic control of ADH secretion Changes in plasma osmolality are sensed by osmoreceptor cells in the hypothalamus which respond by either swelling or shrinking Osmoreceptor cells do not respond to all molecules equally (respond well to changes in sodium, do not respond at all to changes in urea) ADH has a half-life of 15-20 minutes so is rapidly broken down when secreted *
- 20. * Physiology. Berne et al.5th Ed 2004
- 21. Sodium and Water Haemodynamic control of ADH secretion Baroreceptors located both in the high pressure circulation (aortic arch and carotid sinus) and the low pressure circulation (left atrium and large pulmonary vessels) Signals sent by Vagus and Glossopharyngeal nerves to the brain stem which then relays the signal to the hypothalamic neuroendocrine cells Signals from these baroreceptors change both the set point and the sensitivity of the neuroendocrine cells to osmoreceptors *
- 22. Physiology. Berne et al.5th Ed 2004 *
- 23. Principles of Anatomy and Physiology. Tortora and Grabowski. 9th Ed 2000 *
- 24. Sodium and Water Actions of ADH Primary action is to increase the permeability of the renal collecting ducts to water (and the medullary portion of the collecting duct to urea) Acts via a G-protein coupled receptor to cause intracellular vesicles containing specific water channels (aquaporin type 2) to fuse with the apical cell membrane (basolateral membranes are freely permeable to water) Also has the long term effect of altering the expression of the aquaporin 2 gene
- 26. Sodium and Water Thirst Perception of thirst initiated by changes in plasma osmolality, blood volume and arterial pressure Hyperosmolality is more potent (2-3% increase in osmolality) than a decrease in blood volume (10-15% decrease) Thirst centre is located in the hypothalamus Angiotensin II also acts on the hypothalamus to evoke a sensation of thirst Sensors in the oropharynx and upper GIT detect the ingestion of liquid and temporarily decrease the thirst impulse *
- 27. Syndrome of Inappropriate ADH Continued ADH secretion in the presence of decreased plasma osmolality causing the body to retain water inappropriately Causes a euvolaemic hyponatraemia and an inappropriately concentrated urine Aetiology CNS pathology – infections, stroke, tumours, trauma, Guillain- Barre Syndrome Lung disease – infections, cystic fibrosis, tuberculosis Malignancy – SCLC, oropharynx, GI tumours Drugs – antiepileptics, anticonvulsants, antipsychotics, MDMA Transient – nausea, pain, stress (HOSPITAL PATIENTS!) Hereditary – 4 different types of ADH problems - A (high ADH), B (high basal ADH), C (low setpoint) and D (active receptor) *
- 28. Diabetes Insipidus Inadequate effect of ADH results in the excretion of large volumes of dilute urine (polyuria) which causes the individual to consume large quantities of fluid (polydipsia) Several forms Neurogenic – decreased ADH production Causes - hypothalamic or pituitary stalk lesion, idiopathic and inherited forms Nephrogenic – defect in the renal receptor causing decreased response to ADH Causes – genetic defects, metabolic abnormalities, drugs, heavy metals, chronic kidney disease *
- 29. Water Deprivation Test Used to investigate a patient with polyuria and polydipsia to determine if the cause is psychogenic (primary) polydipsia, neurogenic DI or nephrogenic DI Check thyroid, adrenal function and ensure K+ and Ca2+ are normal Patient deprived of fluid for up to 8 hours and the following parameters are measured Body weight Urine output Serum and Urine osmolality
- 30. Water Deprivation Test Diagnosis Fluid deprivation Desmopressin Primary polydipsia >600 >600 Neurogenic DI <300 >50% increase Nephrogenic DI <300 <300 Primary polydipsia – low plasma osmolality at the start of the test and will concentrate their urine appropriately during water deprivation Diabetes insipidus – confirmed by a plasma osmolality of >300 and a urine osmolality of <300 *
- 32. Hyponatraemia Normal plasma sodium is 135-145 mmol/L By definition, any plasma sodium value below 135 mmol/L is considered to constitute hyponatraemia Severity Mild 130-135 mmol/L Moderate 125-130 mmol/L Severe <125 mmol/L *
- 33. Hyponatraemia Clinical presentation No symptoms Lethargy, fatigue Loss of appetite Restlessness and irritability Muscle weakness Neurological symptoms (hyponatraemic encephalopathy) Headache, nausea, vomiting, confusion Seizures, cardiac and/or respiratory arrest Coma *
- 34. Hyponatraemia Mrs YR is a 78 yr old female who presented blurred vision but on further questioning admitted to a 2 month history of weakness, anorexia and weight loss. Analyte Result Analyte Result Na 119 (↓↓↓) TP 118 (↑↑↑) K 5.7 (↑) Alb 24 (↓) Cl 87 (↓) TBil 18 HCO3 - 23 ALP 97 Urea 17.2 (↑) GGT 44 Creat 197 (↑) AST 40
- 35. Hyponatraemia Pseudohyponatraemia In normal plasma 93% of the sample is water and the rest is solute In patients with significant increases in proteins or lipids there is a decrease in the percentage of the sample that is water Direct ISEs measure correctly but indirect methods are misled by the increased proportion of the sample that is dissolved solid rather than water
- 36. [Na+ ] 140 mmol/L 7% dissolved solids (protein or lipids) [Na+ ] 140 mmol/L 22% dissolved solids (protein or lipids) Measured [Na+ ] = 119 mmol/L Richardson A 2013
- 37. Hyponatraemia Hyperglycaemia Glucose in the serum is osmotically active and when it accumulates to very high levels has two effects Osmotic diuresis – which results in a loss of water (with a smaller sodium loss) Shift of water from ICF to ECF Rule of thumb: For every 3.5 mmol/L of glucose in the serum, the serum sodium decreases by 1 mmol/L i.e. blood glucose of 70 mmol/L means that a sodium of 120 mmol/L is actually normal and will self correct when the glucose is controlled *
- 38. Hyponatraemia Classification based on ECF volume Hypovolaemic hyponatraemia Euvolaemic hyponatraemia Hypervolemic hyponatraemia
- 39. Hyponatraemia Hypovolemic hyponatraemia Renal sodium loss Diuretics Osmotic diuresis Adrenal insufficiency Renal tubular acidosis Extra-renal sodium loss Diarrhoea/vomiting Excessive sweating Third space sequestration *
- 40. Hyponatraemia Euvolemic hyponatraemia Thiazide diuretics Hypothyroidism Adrenal insufficiency SIADH Decreased salt intake Beer potomania Tea and toast diet Psychogenic (primary) polydipsia *
- 41. Hyponatraemia Hypervolemic hyponatraemia Congestive heart failure Hepatic cirrhosis Nephrotic syndrome Renal failure (acute or chronic) Pregnancy *
- 42. Hyponatraemia Really? Pseudohyponatraemia Lipids Protein (Glucose) Is the patient dehydrated? Yes Urine Na >20 mmol/L Renal Losses (diuretics, aldosterone deficiency, renal tubular acidosis, osmotic diuresis) Urine Na <10 mmol/L Extra-Renal Losses (vomiting, diarrhoea, 3rd space losses) Isotonic saline No Is the patient hypervolemic? No Euvolemic Hyponatraemia Urine osmolality >500 mOsm/kg SIADH Water restriction Urine osmolality <500 mOsm/kg Psychogenic polydipsia Water overload Hypothyroidism Glucocorticoid deficiency Water restriction Yes Heart failure Nephrotic syndrome Cirrhosis Renal Failure Salt and water restriction * Richardson A 2010
- 43. Is the hyponatraemia severe? (Na<125 mmol/L) Yes Are there symptoms? (confusion, ataxia, headache, seizures, obtundation) Yes What is the duration of the hyponatraemia? Acute (<48 hr) Emergency correction with hypertonic saline Chronic/Unknown (>48 hr) Urgent correction with normal saline or hypertonic saline until symptoms resolve thereafter correct slowly No Hyponatraemia likely to be chronic Urgent intervention unnecessary Assess volume status and correct slowly No Significant sequelae unlikely * Richardson A 2010
- 44. Hyponatraemia Treatment aimed at correcting serum sodium by no more than 0.5 mmol/L per hour Rapid correct of hyponatraemia carries a risk of osmotic demyelination of pontine and extrapontine neurons *
- 45. Central Pontine Myelinolysis. Fleming and Babu. NEJM 2008 *
- 46. Hyponatraemia Mrs VD is an 83 yo with dementia, hypertension and type 2 diabetes mellitus. She takes paroxetine (SSRI), metformin and ramipril. She has been sent in by her GP for investigation and management of her hyponatraemia Analyte Result Analyte Result Na 118 (↓↓↓) U Osm 548 K 5.1 U Na 69 Cl 83 (↓) HCO3 - 21 Urea 5.1 Creat 83 *
- 47. Hyponatraemia Really? Pseudohyponatraemia Lipids Protein (Glucose) Is the patient dehydrated? Yes Urine Na >20 mmol/L Renal Losses (diuretics, aldosterone deficiency, renal tubular acidosis, osmotic diuresis) Urine Na <10 mmol/L Extra-Renal Losses (vomiting, diarrhoea, 3rd space losses) Isotonic saline No Is the patient hypervolemic? No Euvolemic Hyponatraemia Urine osmolality >500 mOsm/kg SIADH Water restriction Urine osmolality <500 mOsm/kg Psychogenic polydipsia Water overload Hypothyroidism Glucocorticoid deficiency Water restriction Yes Heart failure Nephrotic syndrome Cirrhosis Renal Failure Salt and water restriction Richardson A 2010 *
- 48. Hypernatraemia Normal plasma sodium is 135-145 mmol/L By definition, any plasma sodium value above 145 mmol/L is considered to constitute hypernatraemia Less common because of the thirst impulse Clinical presentation Lethargy Weakness Irritability Neuromuscular excitability Seizures and coma *
- 49. Hypernatraemia Aetiology Hypovolemic hypernatraemia Renal sodium loss Diuretics Osmotic diuresis Extra-renal sodium loss Diarrhoea Excessive sweating Euvolemic hypernatraemia Diabetes insipidus Hypervolemic hypernatraemia Increased oral or IV salt Chronic renal failure (during water restriction) *
- 50. Hypernatraemia Mrs MH, a 79yo female nursing home resident with mild dementia presents with worsening confusion over the last 3 days. She has recently been treated with antibiotics for a urinary tract infection but is otherwise healthy and on no other medications. On examination, she is febrile (38.1oC), HR 90, RR 18 and BP 118/60
- 51. Hypernatraemia Analyte Result Analyte Result Na 165 (↑) U Osm 700 K 4.6 U Na 93 Cl 118 (↑) HCO3 - 28 Urea 14.6 (↑) Creat 115 (↑) *
- 52. Hypernatraemia Hypovolemic hypernatraemia Renal sodium loss Diuretics Osmotic diuresis Extra-renal sodium loss Diarrhoea Excessive sweating Euvolemic hypernatraemia Diabetes insipidus Hypervolemic hypernatraemia Increased oral or IV salt Chronic renal failure (during water restriction) *
- 53. Hypokalaemia Normal plasma potassium is 3.5-5.0 mmol/L By definition, any plasma potassium value below 3.5 mmol/L is considered to constitute hypokalaemia Important to remember that K+ is the major intracellular cation so there is a major concentration gradient across the cell membrane K+ can be driven into cells by ECF alkalosis Hormones – insulin, catecholamines, aldosterone *
- 54. Hypokalaemia 90% of the dietary load of K+ is excreted by the kidneys Aldosterone is the single most important factor in determining K+ excretion Clinical presentation Muscle weakness, myalgia, muscle cramps Constipation Flaccid paralysis and hyporeflexia ECG changes Arrhythmias *
- 55. Hypokalaemia Factitious? Redistribution into cells? Excessive potassium losses Renal losses Alkalosis Insulin excess Catecholamine Hypokalaemic periodic paralysis Richardson A 2013 ↓ potassium intake? Dietary IV fluids Non-renal losses Hyperaldosteronism Corticosteroid therapy Cushing’s syndrome Liquorice Diuretics RTA Hypomagnesaemia Vomiting Diarrhoea Laxative abuse Bowel obstruction Ureterosigmoidostomy
- 56. Hypokalaemia Factitious? Redistribution into cells? Excessive potassium losses Renal losses Alkalosis Insulin excess Catecholamine Hypokalaemic periodic paralysis Drip arm? * Richardson A 2013 ↓ potassium intake? Dietary IV fluids Non-renal losses Hyperaldosteronism Corticosteroid therapy Cushing’s syndrome Liquorice Diuretics RTA Hypomagnesaemia Vomiting Diarrhoea Laxative abuse Bowel obstruction Ureterosigmoidostomy
- 57. Hypokalaemia Mr PR is a 58 yr old male with a history of paranoid schizophrenia, hypertension and her GP had sent him in by ambulance for investigation and management of severe hypokalaemia. Medications included olanzepine and an oral potassium supplement prescribed by his GP. Examination was unremarkable and the only abnormality was a BP of 192/112. ECG showed early changes consistent with hypokalaemia
- 58. Hypokalaemia Analyte Result Analyte Result Na 142 Glu 5.7 K 1.8 (↓↓↓) Mg 1.1 Cl 103 Urine Na 68 HCO3 - 43 (↑) Urine K 33 Urea 3.1 Creat 83
- 59. Hypokalaemia Factitious? Redistribution into cells? Excessive potassium losses Renal losses Alkalosis Insulin excess Catecholamine Hypokalaemic periodic paralysis Drip arm? Richardson A 2013 ↓ potassium intake? Dietary IV fluids Non-renal losses Hyperaldosteronism Corticosteroid therapy Cushing’s syndrome Liquorice Diuretics RTA Hypomagnesaemia Vomiting Diarrhoea Laxative abuse Bowel obstruction Ureterosigmoidostomy Mr PR K 1.8 Bicarb 43 Mg 1.1 Urine K 33
- 60. Hypokalaemia Further history from Mr PR He takes a range of herbal supplements including Animal adrenal extract Black liquorice oil *
- 61. Hyperkalaemia Normal plasma potassium is 3.5-5.0 mmol/L By definition, any plasma potassium value above 5.0 mmol/L is considered to constitute hyperkalaemia Clinical presentation Often asymptomatic Malaise Palpitations Muscle weakness Cardiac arrhythmia or sudden death *
- 62. Hyperkalaemia Factitious? Redistribution out of cells? Renal retention of potassium Renal failure Acidosis Insulin deficiency (DKA) Catecholamine deficiency ( -blockers) Hyperkalaemic periodic paralysis Richardson A 2013 ↑ potassium into ECF? Exogenous – diet, IV fluids Endogenous – damaged tissues, intravascular haemolysis, rhabdomyolysis, chemotherapy, crush injury Renal tubule dysfunction Acute Chronic Addison’s disease Drugs (NSAIDs, ACE inhibitors, -blockers) Pseudohypoaldosteronism Tubulointerstitial disease (SLA, amyloidosis, infection) RTA Potassium sparing diuretics (amiloride, spironolactone)
- 63. Hyperkalaemia Factitious? Redistribution out of cells? Renal retention of potassium Renal failure Acidosis Insulin deficiency (DKA) Catecholamine deficiency ( -blockers) Hyperkalaemic periodic paralysis Richardson A 2013 ↑ potassium into ECF? Exogenous – diet, IV fluids Endogenous – damaged tissues, intravascular haemolysis, rhabdomyolysis, chemotherapy, crush injury Renal tubule dysfunction Haemolysis, very high WBC/Plt, drip arm, long torniquet times, EDTA contamination, Acute Chronic Addison’s disease Drugs (NSAIDs, ACE inhibitors, -blockers) Pseudohypoaldosteronism Tubulointerstitial disease (SLA, amyloidosis, infection) Potassium sparing diuretics (amiloride, spironolactone) *
- 64. Hyperkalaemia Mr KG is a 78 yr old man who lives alone. He was last seen 3 days ago and was just found by his son on the floor of his apartment. He is complaining of pain in his left hip and is acutely confused. He has a history of poorly controlled type 2 diabetes mellitus, hypertension and osteoarthritis. His normal medications are metformin, ramipril and celebrex. His vital signs were HR 96, BP 78/54, RR 34, T38.2 ECG is consistent with hyperkalaemia
- 65. Hyperkalaemia Analyte Result Analyte Result Na 132 (↓) Glu 32.7 (↑) K 8.7 (↑↑↑) Arterial pH 7.12 (↓) Cl 93 (↓) HCO3 - 8 (↓) Urea 21.2 (↑) Creat 160 (↑)
- 66. Hyperkalaemia Factitious? Redistribution out of cells? Renal retention of potassium Renal failure Acidosis Insulin deficiency (DKA) Catecholamine deficiency ( -blockers) Hyperkalaemic periodic paralysis Richardson A 2013 ↑ potassium into ECF? Exogenous – diet, IV fluids Endogenous – damaged tissues, intravascular haemolysis, rhabdomyolysis, chemotherapy, crush injury Renal tubule dysfunction Haemolysis, very high WBC/Plt, drip arm, long torniquet times, EDTA contamination, Acute Chronic Addison’s disease Drugs (NSAIDs, ACE inhibitors, -blockers) Pseudohypoaldosteronism Tubulointerstitial disease (SLA, amyloidosis, infection) Potassium sparing diuretics (amiloride, spironolactone) * Mr KG K 8.7 Bicarb 8 Urea 21.2 Creat 160 Glu 32.7
- 67. Questions?