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Electrolytes disorders
 

Electrolytes disorders

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by Elwaleed Ali MD

by Elwaleed Ali MD
Consultant Nephrologist, Detroit, MI

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    Electrolytes disorders Electrolytes disorders Presentation Transcript

    • Electrolyte Disorders Elwaleed Ali Mohamed Elhassan, FACP Khartoum February 2012
    • Talk Elements• Hyponatremia• Hypernatremia• Hyperkalemia• Hypokalemia• Hypercalcemia  Elhassan, FACP
    • The relation between salt and water Definitions• Too much salt – EDEMA – Appropriate response: increase sodium excretion• Tool little sodium – VOLUME DEPLETION – Appropriate response: reduce sodium excretion• Too much water – HYPONATREMIA – Appropriate  response: suppress ADH to increase water  excretion• Too little water – HYPENATREMIA – Appropriate response: enhance ADH release and thirst Elhassan, FACP
    • Osmo-regulation vs. Volume Regulation Osmo‐regulation  Volume regulationWhat is sensed Plasma osmolality, primarily Effective tissue perfusion Plasma NaSensors Hypothalamic osmoreceptors Glomerular AA Carotid sinus AtriaEffectors ADH Renin‐AII‐Aldo Thirst SAS ANP, BNPWhat is affected Water excretion Urine Na Water intake ADH, thirst Elhassan, FACP
    • Effect of Plasma Osmolality on ADH Release and ThirstElhassan, FACP
    • Hormonal and Urinary Responses to Cheese and Potato Chips• Salt intake raises the P Na, which initiates the following responses: – P Na increases, raising P osmolality – The increase in P osm pulls water out of cells, increasing the  extracellular fluid volume – The rise in Posm stimulates both ADH release and thirst, increasing  both urine osmolality and water intake  – The increase in ECF volume raises ANP and reduce the activity of the  renin‐angiotensin‐aldosterone system, raising Na excretion• The final urine has a lot of Na in a small volume, similar to intake  (steady state achievement) Elhassan, FACP
    • HyponatremiaElhassan, FACP
    • Major Causes• Intake of water that cannot be excreted – Hypovolemic states – True volume depletion – Diuretics, particularly thiazides – CHF and cirrhosis• SIADH – CNS disorders – Malignancy, primarily small cell ca – Drugs: SSRI, carbamazepine – Pulmonary infection – Post‐surgery – Adrenal insufficiency or hypothyroidism• Advanced renal failure• Primarily polydipsia, e.g marathon runners Elhassan, FACP
    • Initial evaluation of hyponatremia: Step 1• Measure P osm – largely determined by P Na – Low: • True hyponatremia – Normal or elevated: • Pseudohyponatremia (milky serum, hyperproteinemia) • Hyperglycemia • Renal Failure Elhassan, FACP
    • Initial evaluation of hyponatremia: Step 2• Urine osmolality – Less than 100 mosmol/L • Primary polydipsia with normal water excretion • Reset osmostat – Greater than 150 mosmol/L • Other causes of true hyponatremia in which water  excretion is impaired Elhassan, FACP
    • Initial evaluation of hyponatremia: Step 3• Volume status and urine Na concentration – Less than 10 mEq/L • True volume depletion • CHF or cirrhosis (EABV depletion) – Greater than 20 mEq/L • Other causes of hyponatremia in which euvolemia (SIADH)  or renal salt wasting is present Elhassan, FACP
    • Hyponatremia Workup Serum osmolality Normal Low High(280-295 mosm/kg) (<280 mosm/kg) (>295 mosm/kg)Isotonic hyponatremia Hypotonic Hypertonic (translocational)(pseudohyponatremia) hyponatremia hyponatremia hyperproteinemia, hyperglycemia, mannitol, hyperlipidemia radiocontrast agents Urine osmolality < 100 mosmol/L > 150 mosmol/L Primary polydipsia True hyponatremia with impaired water excretion Elhassan, FACP
    • Volume status Hypovolemic Euvolemic Hypervolemic Urine Na<20 Urine Na >20 oSIADH oPostop hyponatremia oHypothyroidism CHF Renal oPsychogenic polydipsia Cirrhosis failure Nephrotic syndrome Urine Na<10 Urine Na >20Extra-renal losses: Renal losses:Diarrhea DiureticsVomiting ACE inhibitors Nephropathies Mineralocorticoid deficiencies Elhassan, FACP Cerebral salt wasting
    • Presentation• Symptoms: – Nausea, malaise (120‐125 meq/L) – Headache, lethargy, obtundation ( 115‐120  meq/L) – Seizures, coma (<115 meq/L)• Chronic hyponatremia cause few if any symptoms Elhassan, FACP
    • Pathophysiology of Hyponatremia Normotremia: equilibrium Extracellular fluid ECF Acute hyponatremia Na/H2O K, Na, osmolytes / H2OECF hypo‐osmolality K, Na, osmolytes Na↓/H2O↑ H2O↑ Movement down  Chronic hyponatremia osmotic gradient ECF hypo‐osmolality K↓, Na↓, osmolytes↓ Na↓/H2O↑ H2O ↓ Brain adapted to new  osmotic equilibrium Elhassan, FACP
    • Rx of Hyponatremia• Hypovolemic hyponatremia:  – Volume replacement with isotonic (0.9%) saline• Hypervolemic hyponatremia:  – Water restriction (1‐1.5 L/d) and diuretics – Specific treatment for CHF, cirrhosis and advanced  renal failure Elhassan, FACP
    • Euvolemic Hyponatremia• Treat the underlying disease• Fluid restriction (~50‐60% of daily fluid intake to  achieve negative water balance)• Measures to augment water diuresis – Salt tablets  – Demeclocycline – Urea – V2 receptor antagonists Elhassan, FACP
    • Long term  management Identification and Rx of reversible etiologies Water restriction Demeclocycline mg BID (allow two weeks for full effect) Urea 15‐60 g/day  2 receptor antagonists VElhassan, FACP
    • Treating HyponatremiaBased on acuity and presence vs. absence of symptoms: – severe neurologic manifestations: (seizures, impaired  mental status or coma) • hypertonic saline – Less severe (fatigue, nausea, dizziness, gait disturbances,  forgetfulness, confusion, lethargy, muscle cramps): • measures above – “Asymptomatic" with subtle neurologic manifestations Elhassan, FACP
    • Treatment principles• Avoid overly rapid correction – (<10 meq/L 1st 24 hr/<18 meq/L 1st 48 hr)• Estimate Na deficit Na deficit = TBW x (desired serum Na ‐ actual serum Na)• Determine need for urgent correction, if using Hypertonic  saline: – Contains 513 mEq/L – 100 mL of as IV bolus to reduce cerebral edema.  – If neurologic symptoms persist or worsen, bolus can be  repeated  X1‐2 at 10 min intervals.  Elhassan, FACP
    • Elhassan, FACP
    • Example I• A 60 years old man has a tumor of the lung and is admitted to  the hospital with a 2 weeks history of progressive lethargy and  obtundation. The physical examination is within normal limits  except for obtundation. The following lab studies were  obtained:• Na= 105 meq/L, K= 4 meq/L, Cl=72 meq/L, HCO‐3=21 meq/L• POSM= 222mosmol/L• UOSM= 604 mosmol/L, UrineNa= 78 meq/L• What is the most likely diagnosis?• How would you correct it? Elhassan, FACP
    • Example II• A 68 years old diabetic man with congestive  heart failure is seen in the outpatient clinic  with mild peripheral edema. Lab  investigations revealed a plasma Na= 123  meq/L, K=3.7 meq/L and a plasma osmolality  of 268 mosm/kg.• What is correct therapy? Elhassan, FACP
    • HypenatremiaElhassan, FACP
    • Hypernatremia• Serum Na > 145 meq/L due to deficit of water  relative to sodium. • Almost always due to loss of hypotonic fluid  and impaired access to free. Elhassan, FACP
    • Hypernatremia• Symptoms:   Lethargy, Weakness, Irritability, Seizure, Coma, and Death• Severity of symptoms depends on: – The rate of rise in the POSM – Chronic hypernatremia is asymptomatic due to cerebral  adaptation Elhassan, FACP
    • Major causes of Hypernatremia• Impaired thirst or impaired access to water – Water loss:  • Insensible losses: most common. Seen primarily in  adults with impaired mental status • Central or nephrogenic DI: urine should be dilute unless  marked hypovolemia • Osmotic diuresis or osmotic diarrhea – Sodium retention • Administration of hypertonic solution Elhassan, FACP
    • Workup• Check volume status • Obtain urine osmolality• Determine why patient is not drinking  Elhassan, FACP
    • Determine volume status Hypovolemic or euvolemic Hypervolemic Water Loss Na retentionUrine osm <300 Urine osm 300- Urine osm 600 >600Complete DI Renal water losses: Extra-renal water Exogenous NaCl infusion Diuretics losses: Mineralocorticoid excess Osmotic diuresis: (glucose, GI mannitol) Insensible losses Partial DI Reset osmostat Elhassan, FACP
    • Treatment-I• In chronic hypernatremia, brain cells generate  osmoles to minimize intracellular dehydration.• Too rapid correction ‐> ↓s osm in se ng of  high brain osm ‐> water entrance/cereberal edema Elhassan, FACP
    • Treatment-II• Replace volume (based on clinical judgment) and replace free water  deficit:Free water deficit = 0.6 X BW [(Na /140) – 1] (x 0.85 in females)• D5W, or ½ or ¼ NS to simultaneously provide volume and free  water.• Replace free water deficit (50% in first 24 h) + ongoing free  water loss• Slow correction (0.5 meq/L per hour or 12 meq/L per day) Elhassan, FACP
    • Treatment-III• Hypervolemic hypernatremia: – Loop diuretics and dextrose 5% in water.• Diabetes insipidus (DI): – Central DI: desmopressin (dDAVP), a long‐acting vasopressin  analog. – Nephrogenic DI: treat underlying cause; salt and protein  restriction + thiazide diuretics (reduces delivery of filtrate to  diluting segments of kidney). Elhassan, FACP
    • Why salt/protein restriction in DI for polyuria and NOT water restriction? Patient A: extra‐ Patient B: DI renal water lossSerum Na 150 meq/L 150 meq/LDaily Osmole intake 1200 mOsm/d 1200 mOsm/dMaximum ability of  1200 mOsm/L Partial: 300‐800 mOsm/Lurine concentration  Complete: 0‐300 mOsm/L(Max C)UOP= daily Osm intake 1200/1200= 1 L P: 1200/300‐800= 1.5‐4 L Max C C: 1200/0‐300= ∞‐4 L Elhassan, FACP
    • DDx of Renal Water Loss/Polyuria Polyuria (UOP > 3 L/d) UOSM < 800 mOsm/Kg Osmolar excretion rate (UOP X Uosm) > 1000 mOsm/d < 1000 mOsm/d Osmotic diuresis Water diuresisNaCl, Glucose, Urea, Mannitol DI, Primary Polydipsia Elhassan, FACP
    • DDx of DI/polyuria Water deprivation test P OSM ≥295 mOsm/Kg U OSM300‐800 mOsm/kg < 300 mOsm/Kg Partial DI Complete DI Primary Polidipsia DDAVP ~ 50% rise in UOSM No change in UOSM Partial Central DI Nephrogenic DI Primary Polydipsia100‐800% rise in UOSM Complete Central DI Elhassan, FACP
    • HypokalemiaElhassan, FACP
    • K Homeostasis Net absorption  100 mEq/day Extracellular Fluid  Intracellular Fluid  (70 mEq) ‐ 90 mv (3500 mEq) (3.5‐5.5 mEq/L) (140‐150 mEq/L) Msucle 2700 mEq Liver 250 mEq Erythrocytes 250 mEq Bone 300 mEq ‐ 90 mvRenal Excretion 90 mEq/day GI excretion 10 mEq/day Elhassan, FACP
    • Factors Influencing the Distribution of K ↓K+ Cell ↑ K+ K +−Insulin * −Mineral Metabolic Acidosis−β2 Adrenergic Agonists* −Hypertonicity (Hyperglycemia)−Alkalosis −β2 Adrenergic Antagonists−α Adrenergic Antagonists −α Adrenergic Agonists−Anabolism (rapidly growing cells) −Glucagon−Aldosterone * Important in normal K homeostasis Elhassan, FACP
    • Elhassan, FACP
    • Transtubular K Gradient (TTKG) TTKG = UK/Pk X 300/Uosmo TTKG is one method to assess the renal response to  hypoK or hyperKo Distal tubule Na delivery is required for an appropriate  renal K response.o Therefore also check the urine Na; it should be  >20mEq/l for adequate interpretation TTKG should be >7 if pt is hyperkalemic TTKG should be <3 if pt is hypokalemic Elhassan, FACP
    • Unwin RJ. Nat Rev Nephrol. 2011;7(2):75‐84. Elhassan, FACP
    • HyperkalemiaElhassan, FACP
    • Hyperkalemia• Pseudohyperkalemia – Hemolysed Blood Sample (e.g. tourniquet effect)  – Leukocytosis/Thrombocytosis – Check out ECG, and plasma potassium• Redistribution – Severe hyperglycemia (d/t ↑osmolality) – Severe nonorganic acidosis – Rarely with β‐blockers Elhassan, FACP
    • HyperkalemiaDecreased urinary K+ excretion Cell shift Metabolic acidosisHypoaldosteronism Insulin deficiency, hyperglycemiaRenal failureEffective circulating volume  Increased tissue catabolismdepletion Β‐blockadeHyperkalemic type 1 renal tubular  Exerciseacidosis Digitalis overdoseSelective impairment of potassium excretion Hyperkalemic periodic paralysisUreterojejunostomy Elhassan, FACP
    • Tubular flow NSAIDs COX2‐I Type IV RTA ACE‐I/ARBs COX2 ↓GFR AA           PGE2   Renin            Angiotensin                   ↓ECV(actual or Aldosterone Addison’s effective) Principal Cell Heparin MCR Na+ ENaC Block: Na+ Amiloride K+ Trimetoprim Spironolactone Pentamidine K+ K+ K+ Digitalis K+ Intercalated Cell K+ H+ H+ Tubular lumen CCD/CNT Elhassan, FACP Blood
    • Decreased urinary K+ Excretion TTKG >7 <7 Decreased tubular flow Decreased CCD K+ secretionRenal failure ↓ECV ( ↓GFR) Meds Adrenal Hyporenin NSAIDs Insufficiency Hypoaldo RAAS ACEi/ARB Addison’s (Type IV RTA) Blockade Heparin 1° hypoaldo DM Spironolactone SLE Cyclosporine Obstruction Myeloma/Amyloid Amiloride HIV Na+ channel  Triamterene NSAIDs Blockade Trimethoprim Pentamidine Elhassan, FACP
    • ECG Changes? Elhassan, FACP
    • Signs and Symptoms of Hyperkalemia• Muscle weakness (rare)• ECG changes• Cardiac arrythmia• Metabolic acidosis by interfering with renal  ammonium (NH4+) excretionElhassan, FACP
    • Elhassan, FACP
    • Hyperkalemia (serum (K+)>5.5 meq/L in the  absence of hemolysis in the blood sample taken) Severe muscle  Serum (K+) 7.0 meq/L or  Marked ECG weakness greater changes Emergency treatment Calcium Gluconate NaHCO3, 44‐88  Regular insulin, 5‐ Nebulized salbutamol, 10‐20  10%, 5‐30 ml IV; or  meq (1‐2  10 units, plus  mg in 4 ml normal saline, Calcium Chloride 5%,  ampules) IV dextrose 50%, 50  inhaled over 10 minutes 5‐30 ml IV  ml if plasma  Increase K+  glucose is < 250  Increase K+ entry into cellsStabilize membrane  entry into cells mg/dl excitability Increase K+ entry  into cells Elhassan, FACP
    • Serum (K+) ≤6.5 Asymptomatic patient No ECG changes Non‐urgent treatment Furosemide, 40‐160  Cation‐exchange resin: Hemodialysis or  mg IV or orally Oral: 15‐30 g in 20% sorbitol (50‐100ml) Peritoneal dialysisRemoval of excess Rectal: 50 g in 20% sorbitol Removal of excess K+ Removal of excess K+ K+ Dietary K+ restriction (chronically helpful) Elhassan, FACP
    • HypokalemiaElhassan, FACP
    • Causes• R/O pseudo‐hypokalemia – Artifactual (↑↑ WBCs)• K shift from ECF to ICF – Alkalosis (small effect), insulin, stress release of  epinephrine, salbutamol, thyroid hormone,  hypokalemic p paralysis, chloroquine intoxication• Gastrointestinal losses (most common)• Renal losses• Inadequate intake (usually contributing factor) Elhassan, FACP
    • Tubular flow↑Na delivery: Renoma Bartter RAS Osmotic  Gitelman Renin Angiotensin diuresis Loop diuretics Thiazides 1° Hyperaldo Principal Cell Aldosterone GRA MCR Na+ Cushing Liddle Na+ syndrome K+ Cortisol K+ Nonabsorbable anion K+ K+ β-HSD K+ Cortisone Intercalated Cell Licorice Amphoterecin AME K+ Classic distal H+ RTA H+ CCD/CNT BloodTubular lumen Elhassan, FACP
    • Hypokalemia GI loss Urinary K+ wasting Cell shift<15 mEq/day 24 h urine K+ > 15 mEq Metabolic Alkalosis Vomiting Insulin excess Diarrhea β-agonist Hypokalemic periodic paralysis Elhassan, FACP
    • Urinary K+ wasting High BP Normal or low BP Aldosterone Plasma HCO3- High Low High Low Renin •Cushing •Liddle Synd •RTA U Cl- •Licorice ingestion •AME High Low Low High•Renal Artery •Primary Hyperaldo •Gastric loss: •Diuretic•Stenosis •GRA Vomiting •Mg Deficiency•Malignant HTN •Nonreabsorbable •Bartter Synd•Reninoma anion (e.g. Penicillin, •Giltelman Synd Cisplatin) Elhassan, FACP
    • Clinical Manifestations• Hypertension• Insulin resistance• Muscle weakness (voluntary and smooth)• Polyuria/Polydipsia (acquired nephrogenic DI)• Rhabdomyolysis• Hepatic Encephalopathy • Cardiac arrhythmiaElhassan, FACP
    • Elhassan, FACP
    • Treatment• Oral KCl supplements• IV KCl (no more than 10 mEq/hr through  peripheral line, 40 mEq/hr through central line)• Amiloride or spironolactone may be useful in  patients with hyperaldosteronismElhassan, FACP
    • Elhassan, FACP
    • HypercalcemiaElhassan, FACP
    • Elhassan, FACP
    • Elhassan, FACP
    • Clinical Presentation• Constipation • Polyuria• Azotemia • Stupor, coma• Ventricular arryrhytha Elhassan, FACP
    • Elhassan, FACP
    • S. Ca >12 mg/dL NS at 200 to 300  Calcitonin (4 IU/kg) Zoledronic acid  ml/hr Remeasure s.  (4 mg IV over 15  Adjust NS to  calcium in several  minutes) maintain UO at 100‐ hours Or 150 ml/hr  If a hypocalcemic  pamidronate Furoemide to  response is noted  (60 to 90 mg  patients who are, or  may repeated  over two hours) who get fluid‐ calcitonin every six  overloaded on this  to 12 hours regimen Check Ca frequently. If persistent or recurring  hypercalcemia consider Chemotherapy or  Hemodialysis with little or no  radiation therapy  calcium in the dialysate for malignant  Peritoneal dialysis  hypercalcemia Consider early dialysis in patients with  severe malignancy‐associated  hypercalcemia CKD or CHF where  hydration cannot be safely administeredElhassan, FACP
    • ‫واﳊﻤﺪ ﷲ أوﻻً وآﺧﺮاً،‬ ‫وﺻﻠﻰ اﷲ ﻋﻠﻰ ﻧﺒﻴﻨﺎ ﳏﻤﺪ،‬ ‫وﻋﻠﻰ آﻟﻪ وﺻﺤﺒﻪ وﺳﻠﻢ‬‫‪Elhassan, FACP‬‬