Electrolyte imbalance พญ.วราภรณ เล ยวนรเศรษฐ หน วยโรคไต

Electrolyte imbalance พญ.วราภรณ เล ยวนรเศรษฐ หน วยโรคไต

Content : Electrolyte Emergency!!

Serum sodium Normal serum sodium: 135-145 meq/l Normal serum osmolality: 285-295 mosm/l Normal urine sodium: 10-20 meq/kg Normal urine osmolality: 400-500 mosm/kg

Body Fluid Compartments: 2/3 ICF: 55%~75% X 50~70% lean body weight TBW Male (60%) > female (50%) Most concentrated in skeletal muscle TBW=0.6xBW ICF=0.4xBW ECF=0.2xBW 1/3 ECF 3/4 1/4 Extravascular Interstitial fluid Intravascular plasma

Hyponatremia Posm Nae + Ke TBW PNa < 135 mmol/l Posm Nae Translocational Hyponatremia PseudoHyponatremia True hyponatremia

Symptoms Serum Na + (meq/l) 135-130 130-125 125-120 < 120 Symptoms Decreased taste Thirst Anorexia, N + V Muscle cramps Weakness Lethargy Restlessness Confusion Delirium Coma Seizures

Workup for Hyponatremia 3 mandatory lab tests Serum Osmolality Urine Osmolality Urine Sodium Concentration Additional labs depending on clinical suspicion TSH, cortisol (Hypothryoidism or Adrenal insufficiency) Albumin, BM, triglycerides and SPEP (psuedohyponatremia, cirrhosis, MM)

Approach Hyponatremia : P Na<135 High Posm (>295) P osm เพ อย นย นภาวะ true hyponatremia Normal Posm (285-295) Translocation hypo-natremia glucose or manitol Hyponatremia + Hypo-osmolality Low(<285) True-hypoNatremia Uosm Pseudo-hypo-Natremia yes Inappropriate ADH Work >100 ADH Work Lipid or Protein เพ อย นย นว าม การหล งของ ADH (เม อ U osm.>100) Hypothyroidism Hypoadrenalism SIADH no primary polydipsia Appropriate ADH Work Volume depletion

Management Depend on: Acute or chronic Asymptomatic or symtomatic Rate of decrease in serum sodium Volume status

Severe hyponatremia (<125 mmol/l) Acute Acute Duration<48hr. symptomatic Chronic Chronic Duration>48hr. Asymptomatic Chronic rarely<48hr. Emegency correction Needed Emegency hypertonic correction saline Needed hypertonic 1-2 Saline ml/kg/h, 1-2 ml/kg/h, coadministration coadministration of of furosemide furosemide Some immediate Correction needed Hypertonic saline1-2 ml/kg/h Furosemide Water restriction F/U serum, urine electrolyte Not exceed 1.5 mmol/l/h or 20 mmol/d No No immediate correction needed Long term management

Severe hyponatremia (<125 mmol/l) symptomatic Asymptomatic Acute Acute Duration<48hr. Chronic Chronic Duration>48hr. Some Some immediate Correction needed Chronic Chronic rarely<48hr. No No immediate correction needed Emegency correction Long term management Treatment irreversible causes Water restriction Democloclocycline 300-600 mg bid Urea 15-60g/d VV2 2 receptor antagonists

Treatment 1.Corrected P Na level 2.Corrected Etiology(underlying) NaCl Restric water Volume depletion Diuretic Adrenal insufficiency Hypothyroid SIADH Edema Renal failure Primary polydipsia

Case consult A 75 year-old woman Watery diarrhea 10/day for 2 days orthostatic presyncope for 1 days drinking 1 litres of water/day Underlying HT on HCTZ (50 mg) 1X1 lab Na 125 meq/l K 3.3 meq/l Cl 110 meq/l HCO 3 18 meq/l # Hyponatremia

Hypo-osmolar hyponatremia Hypovolemic Non-hypovolemic GI Losses Renal Losses Skin Losses Vommitting diarrhea bleeding obstruction Diuretics hypoaldo saltwasting neph Burns GPP/eryth roderma SIADH Edematous States CNS Disease Pulmonary Drugs CHF NS Cirrhosis Slide courtesy of Adam Oster

Hypovolemic Hyponatremia Loss Na > Loss H 2 O Low ECF ---- ADH released increases tubular reabsorption of H 2 O low urine volume Renin released (low renal perfusion) kidneys retain sodium urine sodium low (<20 mmol/l)

What caused our patient s hyponatremia? GI losses HCTZ (impairs excretion of free water) as ECF decreases kidney exchanges K for Na to maintain volume - thus low K (Aldosterone)

How will you treat our patient off HCTZ Treat diarrhea oral rehydration salts IV NSS + KCl until no further postural drop oral potasium supplement Follow up electrolytes

SIADH Euvolemic Hyponatremia DDx hypothyroidism adrenal insufficiency psychogenic polydipsia

SIADH Diagnosis clinically euvolemic normal renal function normal thyroid (TSH) normal adrenal (cortisol stim test) no medications known to cause SIADH-like syndrome

SIADH causes Source: Yeates K, et al. CMAJ 2004;170(3):365-9

SIADH - Treatment acute hypertonic saline goal to increase Na by ~5 over 12 hours or until asymptomatic fluid restriction 750-1500 ml/d goal to increase Na by ~5 over 12 hours chronic fluid restriction Li (inhibits renal effects of ADH) demeclocycline 600 mg po od

Management Symptomatic hyponatremia Cause: SIADH W/U: serum osm, urine osm, Na deficit: calculate Form IV: 3%NaCl Rate: 1 meq/l

Calculation [Na] deficit = 10x0.6X50 = 300 meq/l Form IV: 3%NaCl (513 mosm/l) Volume: (300X1000)/513 = 584.8 ml(600 ml) Rate: 1 meq/l/hr(60ml/hr)x 5hr then 0.5 meq/l/hr(30 ml/hr) correct Na not excess 12 meq/l/day

Case consult A 58 year-old man BW 50 kg. Underlying: Non small cell lung cancer confusion & lethargy for 2 days P/E Euvolemia Nausea/vomiting no ascites / no edema no sign of hypothyroidism or hypoadrenalism Lab: Na 108 meq/l, K 3.9 meq/l,cl 88 meq/l,co 3 88 meq/l Cr 1.4 mg/dl, serum osm 220 mosm/l urine Na 44 meq/kg, urine osm 660 mosm/kg

Consult # Euvolemic hyponatremia----- SIADH

Hypervolemic hyponatremia Increased ECF CHF cirrhosis / ascites nephrotic syndrome low effective circulating volume body retains Na and H 2 0 low urine Na (<20) Treatment Na and free water restriction

Pathophysiology CPM central pontine myelinolysis Acute non-inflammatory demyelination in basis pontis and other CNS sites (in ~10%) Mechanism unknown; felt to occur due to rapid changes in cell volume Actual incidence is unknown Risk factors Na + <120 meq/l for > 48 hrs Aggressive IV resuscitation w/ hypertonic saline Most cases occurred with rates of correction > 12 mmol/l /24 hrs Hypernatremia during treatment

CPM central pontine myelinolysis Clinical Features Usually neurologic deterioration 48-72 hrs after rapid Na + correction Confusion, horizontal gaze paralysis, spastic quadriplegia, pseudobulbar palsy, encephalopathy coma, locked-in syndrome Dx MRI Tx supportive

Treatment summary Hypovolemic hyponatremia Correct with NS (0.9%) which is mildly hypertonic compared to pts serum Euvolemic hyponatremia: Restrict free water intake Identify underlying cause SIADH: Giving normal saline will worsen condition due to free water retention Can Tx with lithium and demeclocycline inhibit action of ADH Hypervolemic hyponatremia: Restrict free water intake +/- diuretics may worsen due to further Na+ loss dialysis if large amount of fluid needs to be taken off Slide courtesy of M Haager

Dry Source of Sodium loss? Hyponatremia Normovolemic (excess total body water but no edema) Fluid overloaded (excess water > excess Na + ) Renal: -Diuretics -Adrenal insufficiency -Salt-wasting nephritis -Bicarbonate loss -RTA -metabolic alkalosis -ketonuria -Osmotic diuresis -glucose -mannitol Extra-renal losses -GI losses -Third spacing Urine Na + <10 mmol/l SIADH Drugs Glucocorticoid deficiency Hypothyroidism Pain / emotion Urine Na + >20 mmol/l Nephrotic Syndrome Cirrhosis CHF Urine Na + <10 mmol/l Acute / Chronic Renal Failure Urine Na + >20 mmol/l Urine Na + >20 mmol/l Normal Saline Water restriction

Hypernatremia Symptoms anorexia N/V fatigue irritable Signs lethargy stupor coma muscle twitching hyperreflexia spasticity tremor ataxia focal neurological signs

Causes of Hypernatremia Reduced H 2 O intake disorders of thirst can t get H20 Increased H 2 O loss GI V&D NG 3rd spacing renal DI osmotic diuresis post-obstructive diuresis dermal burns perspiration Gain in Na exogenous Na intake NaCl NaHCO 3 hypertonic NS salt water drowning increased Na reabsorption hyperaldosteronism cushing s disease exogenous corticosteroids congenital adrenal hyperplasia

Management of hypernatremia Hypovolemic goal: restore volume deficits 0.9% NS Euvolemic DI oral fluids hypotonic saline (0.45%) vasopressin Hypervolemic increase renal sodium excretion > H20 diuretics +/- hypotonic saline may need dialysis

Case 93 year old man from nursing home, BW 40 kg Dementia, bed ridden not eating well Drowsiness P/E JVP flat, dry mouth Na = 160 meq/l BUN 40 mg/dl, Cr 0.8 mg/dl Urine sp.gr. 1.030

# Hypernatremia Dehydration Water deficit: TBWX(Na-normal Na)/normal Na 0.6X40X(160-140)/140 = 3.4 L Rate increase Na not excess 12 meq/l Duration: 48 hr

Potassium a precisely controlled cation Mostly intracellular Precise transcellular gradients required for neuronal transmission and cardiac conduction Also important in acid-base balance and buffering. K+/H+ pump Extracellular K controlled by serum ph change in ph of 0.1 0.6mEq change in K+ aldosterone insulin catecholamines

Hyperkalemia - etiology pseudohyperkalemia hemolysis increased intake impaired renal excretion renal failure hypoaldosteronism K-sparing diuretics Transcellular shifts acidosis insulin deficient drugs B-Blockers sux digitalis cellular injury rhabdomyolysis tumour lysis syndrome crush/burn

Hyperkalemia Mechanisms INCREASED INTAKE IMPAIRED EXCRETION TRANSCELLULAR SHIFT CELLULAR INJURY RENAL FAILURE NON RENAL FAILURE Slide courtesy of A. Oster

Hyperkalemia - etiology pseudohyperkalemia hemolysis increased intake impaired renal excretion renal failure hypoaldosteronism K-sparing diuretics Transcellular shifts acidosis insulin deficient drugs B-Blockers digitalis cellular injury rhabdomyolysis tumour lysis syndrome crush/burn

Hyperkalemia Clinical Features Cardiac 2/3 degree heart block wide complex tachycardias VF asystole ECG progression peaked T waves loss of P waves prolonged PR interval widening of QRS sine wave pattern ventricular fibrillation asystole

Non-specific muscle cramps weakness paralysis paresthesias tetany Hyperkalemia Neurological SSx focal neurological deficits

Management Principles Cardiac monitoring stabilize myocardium shift K into cells decrease GI absorption treat underlying cause

Immediate Management Calcium mechanism antagonises K and stabilizes myocardium indications dysrhythmia hypotension ECG changes onset 0-5 minutes duration 20-40 minutes dose 5-30ml 10% calcium gluconate IV

Immediate Management Ventolin Mechanism shifts K into cells onset 15 minutes duration 2-4 hours dose 5-10mg neb repeat prn

Immediate Management Glucose and Insulin mechanism shifts K into cells onset 15 minutes duration 4-6 hours dose 10-20 units of R 1 amp D50W (no D50W if hyperglycemic)

Immediate Management bicarbonate mechanism shifts K into cells only works if acidotic dose 1 amp (44 meq) IV push over 5 minutes onset 15 minutes duration 2 hours beware if hypertonic hypernatremic alkalotic

Delayed Therapy Exchange Resins kayelalate (polystyrene sulfonate) mechanism ion exchange resin removes K from body onset 1 hour duration dose 1-3 hours 1g binds 1mEq of K oral or rectal 20g in 70% sorbitol po (Rosen) 30g pr retained for 30 minutes

Mechanism removes K from blood Delayed Therapy hemodialysis can remove 200-300 meq Indications renal failure unstable patient unresponsive to other treatment

Hypokalemia Spectrum of Symptoms Asymptomatic K 3-3.5 Neuromuscular K usually < 2.5 lethargy confusion fasciculations weakness decreased DTRs paralysis (K<2) Cardiovascular usually no symptoms in patients without heart disease palpitations ectopy dysrhythmias 1-2 degree HB atrial fibrillation ventricular fibrillation

GI Hypokalemia Spectrum of Symptoms impairs intestinal smooth muscle N/V paralytic ileus Renal polyuria polydipsia

Hypokalemia Decreased Intake decreased dietary intake decreased absorption Transcellular Shifts alkalosis insulin B2 agonists eg: ventolin - lowers K ~ 0.4 mmol/l x 4 hours coffee Increased Loss renal hyperaldosteronism renal tubular defects mineralocorticoids glucocorticoids (alter GFR) +++diuretics drugs GI N/V/D Skin burns perspiration

Hypokalemia ECG findings small or absent T waves prominent U waves ST segment depression Slide courtesy A. Oster

Management Oral KCl elixir(20meq/15ml) K-Phos(4.4mEq/ml) useful if hypophosphatemic K-Citrate (0.9mEq/ml) useful in RTA IV KCl (10/20/40mEq/100cc) 10-20mEq/h >20mEq/h requires central line and cardiac monitor S/E s transient hyperkalemia burning at IV site

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