8a Fluid and Electrolyte Disorders Year 4 Internal Medicine

8a Fluid and Electrolyte Disorders Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / IMED 4.2 / Mogere -- Slide 1 FLUID AND ELECTROLYTE DISORDERS DR ALEX MOGERE Consultant physician Slide 2 WATER 60% of Body Weight 55% - 75% Intra cellular 25 – 45% Extracelluar\n⅔ interstitial (extravascular)\n⅓ intravascular (Plasma) Slide 3 Rule of “Thirds” Slide 4 Effective Circulating Volume (ECV) Intravascular volume essential to maintain organ perfusion pressures ECV jealously protected Slide 5 ECV SENSOR Slide 6 BARORECEPTORS (BP ) Slide 7 BARORECEPTORS (Cont’d) Slide 8 BARORECEPTORS (Cont’d) Slide 9 OSMO RECEPTOR ≥ 2%  in effective Osmolality Stimulation anterolateral hypothalamus  AVP Enhanced water conservation Vaso contriction\n  Renal perfusion\nRAAS stimulation Slide 10 CHEMO RECEPTOR Intrarenal – Maculadensa cells (distal nephron)\n Na+ delivery\n RAAS stimulation Slide 11 EFFECTOR MECHANISMS NEURO-HUMORAL SYSTEMS SYMPATHETICS RAAS ANP AVP Each system is interlinked with the other Rapid responses (minutes) have hemodynamic effects Slow responses (hrs) may alter Na+/H2O balance Slide 12 CLINICAL SITUATIONS ASSOCIATED WITH  ECV Slide 13 DIAGNOSIS OF VOLUME LOSS Slide 14 MANAGEMENT PRINCIPLES REPLENISH INTRAVASCULAR VOLUME Slide 15 HYPONATRAEMIA Serum [Na+] < 135 mmol/L Marker of hypo-osmolar/hypotonic state Plasma 93% water/Na+ Pseudo hyponatraemia Plasma is normoosmolar\nor Hyperosmolar Slide 16 HYPONATRAEMIA Serum Osmolality = = 2[Na] + [Glucose,in mmol/l] + [Urea,in mmol/l] n/b- Na is multiplied by 2 to take into a/c the accompanying anions Slide 17 Pseudohyponatraemic states Hypertonic hyponatraemia\n- hyperglycaemia\n- IV mannitol Isotonic hyponatraemia\n- hyperproteinaemia\n- hyperlipidemia\n- post TURP bladder irrigation Slide 18 CLINICAL STATES HYPONATRAEMIA] Oedema state Volume depleted state Isovolaemic state or (mild oedema) – normal Na stores and total body excess of free water Slide 19 I. Oedema States Interstitial volume expansion ECV  thirst,  RAAS\n AVP,  GFR Primary Na+ gain, 2° Excess water gain Conditions e.g. \n● Heart failure\n● Nephrotic syndrome\n● Hepatic cirrhosis Slide 20 II. Volume depleted State ECF Volume depletion  Thirst,  AVP Primary Na+ loss with secondary water gain Conditions – i) skin loss, ii) Git loss\niii) renal loss Slide 21 III. Isovolaemic State Primary H2O gain (2° Na+ loss) Conditions 1° Polydipsia AVP release (pain, nausea, drugs) Glucocorticoid deficiency(glucocorticoids increase H2O diuresis, GFR,& renal plasma flow) Hypothyroidism Chronic renal insufficiency Syndrome of inappropriate anti-diuretic hormone secretion (SIADH) Slide 24 CLINICAL MANIFESTATIONS Hyponatraemia  osmotic H2O shift\n[intracellular] Brain cell swelling ● brain oedema Symptoms depend on: \ni) Rapidity of development of \nhyponatraemia \nii) Degree of hyponatraemia Slide 25 CT. Clinical manifestation Asymptomatic Mild symptoms (nausea, malaise) Headache, Lethargy, confusion\nStupor, seizure, coma More severe with rapid [Na+] Slide 26 Chronic hyponatraemia Adaptive mechanisms protect\nbrain cell volume Less severe symptoms Loss of Na+ and K+ Slide 27 MANAGEMENT PRINCIPLES 1] Restrict Free water intake 2] Promote water loss (diuretics) 3] Raise plasma Na+ concentration\nHypertonic saline (symptomatic) 4] correct underlying disorder Slide 28 HYPER NATRAEMIA Plasma [Na+] 145 mmol/L Hyper natraemia is a Hyper osmolality state Causes 1° Na+ GAIN H2O DEFICIT [MAJORITY] Slide 29 Appropriate response to Hypernatraemia Hypernatraemia [Hyperosmolar]  Thirst, AVP\nExcretion of max conc. Urine Degree of hyperosmolality mild except if thirst mechanism abnormal\nor \nAccess to water is restricted or limited Slide 30 Commoner Clinical Condition Infants Physically handicapped Impaired mental status Post operative Elderly Slide 31 CLINICAL CONDITIONS Free H2O Loss Skin insensible loss Lung (, fever, burns ventilation) Git – diarrhoea Renal loss – (commonest)\nDrugs (loop diuretics)\nOsmotic (manitol, hyperglycemia\nUrea, high protein diet)\nDiabetes insipidus Slide 32 CLINICAL CONDITIONS (Cont’d) Primary Na+ gain (infrequent) Hypertonic saline (3%) NaHCo3 (resuscitation) Infant formula\n(sugar replaced by salt) Slide 33 Clinical Features H2O shift from cells Brain cell volume Risk of Subarachnoid bleed Risk of Intracerebral bleed Slide 34 Ct.Clinical features Altered mental status Weakness ● neuromuscular irritability Focal deficits ● coma Seizures ● polyuria Polydipsia Signs/symptoms of volume depletion High mortality with plasma [Na+]\n 180 mmol/L Slide 35 Chronic Hypernatraemia Less symptomatic Adaptive mechanisms protect cell volume Na+, K+ salts, Organic osmolytes\n(eg. Inositol) taken intracellular Slide 36 PRINCIPLES OF MANAGEMENT 1] Manage underlying cause 2] Stop H2O loss 3] Correct H2O deficit:\nPlasma Conc – 140 x TBW\n140\nCorrect slowly Safest oral/N-G water Varying strengths of saline\nto 5% Dextrose-water Slide 37 POTASSIUM Major intracellular cation Normal