Dr Stella Palar, SpPD-KGHDivision of Nephrology and HypertensionDepartment of Internal Medicine Faculty of Medicine Sam Ratulangi University

HYPOKALEMIA

Serum K level < 3.5 mmol/L (normal: 3.5 5.0 mmol/L)

True hypokalemia : decreased of serum K level

False (spurious) hypokalemia : false in laboratory result in extreme leucocytosis (in vitro), wbc uptake kalium in the test tube

DIAGNOSTIC APPROACH OF HYPOKALEMIAHypokalemiaKalium depletionTranscelular shiftinsulin therapybeta2 agonistsalkalosisUrine K 20 meq/L renal lossesViarable PHpost obstructive ATN recoveryaminoglycosideMetabolic acidosis RTA Diabetic ketoacidosis

CLINICAL MANIFESTATIONS

Cardiacventricular irritabilityabnormal ECGpredisposition of digitalis intoxicationcoronary artery spasmNeuromuscularmuscle spasm, tetany, paralysisgastrointestinal (constipation, ileus) Renalpolyuriaincreased amoniogenesisEndocrenecarbohydrate intolerance

MANAGEMENT

Emergency or not emergenny ?clinical manifestationECGdegree of hypo K Estimated degree of decreases in total body kaliumdecreased in average of 0,3 mmol/L for each 100 mmol of kalium depletion

Serum K levelDeficitMild3.00 3.4 meq/L150 200 meq/LModerate2.00 3.0 meq/L200 400 meq/LSevere< 2 meq/L500 1000 meq/L

Treat the underlying causes

In mild hypo K : oral K preparation 600 -1200 meq/day- small risk of hyper KMANAGEMENT

Moderate and severe hypo K : intravenous administration do not give direct i.v injection : CRIMEintravenous drips peripheral or central venous line 10 20 meq/hr : into peripheral vein> 40 meq/hr : into central vein with ECG monitor

Monitoring K level carefully (every 4-6 hrs)

Definition :Plasma potassium consentration > 5. meq/L(N. 3.5 -.5 meq/L) ----- excess concentration K ion in extracellular fluidHYPERKALEMIA

Causes of Hyper KExtrarenalRenal

Extrarenal causes of hyper K

A. Increased intakeExogenous sourcespotassium supplementstored PRCsalt substituteEndogenous sourcerhabdomyolysistumor lysis syndromecatabolic state

B. Compartment shift a. inhibition of Na/K ATPaseinsulin resistance/deficiencyB2 adrenergic deficiency/resistanceFamilial hyperkalemic periodic paralysisb. Altered transcellular electrochemical K gradientinorganic metabolic acidosisECF hypertonicity/hyperosmolar state :(hyperglycemia, mannitol

2. Renal causes of hyper KAKICKDHypoaldosteronism (secondary/primary)

Clinical feature often asymptomaticneuromuscular disturbance (K>6.5 meq/L)distal parasthesiageneralized muscle weaknessascending flaccid paralysisventilatory failuresudden cardiac death (K>7-7.5 meq/L)

ECG changesK+, 5-6 meq/L50% no ECG changespeaked T, shortened QT K+, 6-7 meq/LProlonged QR, AV dissociation flattening and loss Pwidening QRS complexK+ > 7 8 meq/L - VT

Pseudo Hyper KCaused by released of K from damage cell in vitro ------ 1-2 meq/L artifactual releasehemolysisthrombocytosis leukocytosisfamilial psudohyper K

MANAGEMENTHyper K >6.5 meq/L : medical emergency- therapy should begin immediately1. Stabilization of cardiac membrane - 10 ml Ca gluconas 10% over 2-3 min into large vein - evident within minutes and lasts for 30 to 60 min - represents a temporizing measure only - plasma K concentration is unaltered

Management2. Transcellular redistribution a. insulin and dextrose --- activated insulin receptor stimulates N+/K+-ATPase driving cellular uptake of K - 1 iu insulin setiap 5 gr glukosa - each 10 iu insulin can expected to lower K by 0.5-1.5 meq/l within 15 min, lasting 2-4 hrs b. sodium bicarbonate - increasing the pH of ECF (100 mmol over 1-2 hrs) - when hyper K associated by severe inorganic acidosis c. Salbutamol - meter dose inhaler, nebulized, intravenous

Management3. Removal of excess - loop diuretic - cation exchange resin (kayexilate) - hemodialysis or CRRT - laxantia (MgS04)

Plasma sondium (Na+) concentration : the ratio between sodium and water in the plasma

Normal : 135 145 mmol/LHyponatremia : < 135 mmol/LIs, Na+ loss or water gain

HYPONATREMIA

Types and Causes of Hyponatremia

Pseudohyponatremia A rare measurement artefact caused by reduced plasma water, as a result of excess lipids (triglycerides) or abnormal proteins (e.g. IgM)Hyperosmolar (iso-osmolar and other) hyponatremiaHyperglycaemia (and other impairment solutes, but not urea)Surgical (e.g. transurethral prostatectomy) irrigation fluids (mannitol, sorbitol, glycine)Subarachnoid haemorrhageTrue (hypo-osmolar) hyponatremia ECF ( TBNa+) reduced effective arterial volume (Na+ loss) ECF ( TBNa+) reduced effective arterial volume (oedema) ECF ( TBNa+) normal effective arterial volume (no oedema), SIADH, drugs, stress, cortisol, thyroxine)

The formula of osmolalityPosm = 2[Na+] + [glucose]/18 + [BUN]/2.8

HiponatremiaTranslocational hyperglycemiairrigation fluids (mannitol, sorbitol)surgical (transurethral prostatectomy)Normal or high osmoticLow osmotic(true hyponatremia)Pseudohyponatremia

proteinlipidUrinary osmolality *)> 100 mosm/kgUrinary osmolality

A Clinical Approach to HyponatremiaHypo-osmotic hyponatremiaUrinary sodium concentrationUrinary osmolalityTreatmentNormal salineWater restrictionTreat + restrict waterHypovolaemiaEuvolaemiaHypervolaemiaRenal lossDiureticNa+ lossExtra Renal lossGastrointestinal tractSkinHeart failureLiver failureNephrotic syndromeSyndrome of inappropriate antidiureticPsychogenicHypothyroidDrugs(Robert U, NEPHROLOGY Medical Progress December 2003)

SALT LOSING NEPHRITIS

Nephritis with an excessive urinary loss of Nahypovolemic hyponatremiaurinary Na+ >20 mmol/Lmostly without hypertensionmedullary cystic diseasechronic interstitial nephritispolycystic kidney diseaseanalgetic nephropathypartial urinary tract obstructionchronic glomerulonephritis (rarely)

Diagnosis criteria for SIADH(Syndrome of inappropriate ADH secretion

EssentialECF effective osmolality below 270 mosmol/kg waterInappropriate urinary concentration (> 100 mosmol/kg)Clinical euvolemiaIncreased urinary [Na+] while on a normal salt and water intakeAbsence of adrenal, thyroid, pituitary or renal insufficiency or diuretic useSupplementalAbnormal water load test (inability to excrete at least 90% of 20 mL/kg water load in 4 h and/or failure to dilute urinary osmolality to below 100 mosmol/kg)Plasma ADH level inappropriately raised relative to plasma osmolalityNo significant correction of plasma [Na+] with volume expansion but improvement after fluid restrictionTHE LANCET, Vol 352, July 18, 1998)

CLINICAL MANIFESTATION:Symtoms of hyponatremia due to the consequences of plasma hypoosmolalityNote: Permanent neurologic damage may be occur in premenopausal womenthe cause is not well understoodso: hyponatremic women must be watched carefullyLauriat, SM. J. Am Soc Nephrol. 8 : 1997

HypoosmolalityMove of water from extra to intracellularintracellular edema

Particularly in CNSSymptoms:Lethargyconfusion nausea-vometingmuscle cramps seizures- coma

postoperative menstrual womenelderly women in thiazide diureticschildrenpsychiatric polydipsic patientshypoxemic patientsPATIENTS AT RISK FOR PERMANENT NEUROLOGIC COMPLICATION

MANAGEMENT

Important questions must be answered : Is the patients symptomatic ?Symptomatic patients have to treat aggressively but promptly 2. is the hyponatremia acute (before 48 hrs) ? chronic (after 48 hrs) ?Acute hyponatremic, carries a greater risk of permanent neurologic sequelae if the correction is not expeditiously3. Whats the Na+ level ?Severe hypoNa+ is Na level

SEVERE HYPONATREMIA(Na+

HypoN+ present for

HypoNa+ present for >48 hrs or the duration is unknownincrease the serum Na+ by 10% with hypertonic saline infusion at rate 1,5 -2 ml/kg/hr (or in 4-6 hrs)after the initial correction, do not exceed a correction rate of 1-1,5 ml/kg/hrcoadministration of loop diureticuntil the symptoms resolved or Na+ level 130 mmol/Ldo not increase the serum Na+ by more than 15 mmol/L 24 hrsserum Na+ should be carefully monitored (every 4-6 hrs) SEVERE CHRONIC SYMPTOMATIC HYPONa+

THE LANCET, Vol 352, July 18, 1998)CHRONIC ASYMPTOMATIC HYPONa+

No immediate therapy is required and underlying disease can be soughtNo urgency to coorect the serum Na+

TreatmentMechanismFluid restrictionDecreases free waterPharmacological inhibition of ADHLithiumInhibits renal response to ADHDemeclocyclineInhibits renal response to ADHV2 receptor antagonistAntagonises vasopressinIncreased solute intakeFurosemideIncreases free water clearanceUreaOsmotic diuresis

DefinitionSerum Na consentration > 145 meq/LHYPERNATREMIA

Classification1. Decreased total body sodiumExtracelular water and sodium loss with excess water loss

Extra renal lossVomitingDiarrheaExcessive sweatingDialysisRenal lossOsmotic diuretics (e.g., glucose, urea, mannitol)

2. Normal total body sodiumExtracellular water deficiency associated with minimal sodium loss

Extra renal lossUnconscious stateThirst center dysfunctionMechanical obstructionInappropriate intravenous therapyNo access to waterRenal lossCranial diabetes insipidusNephrogenic diabetes insipidus

3. Increased total body sodiumExtracellular water and sodium gain with relatively excess sodium gain

High sodium intakeSea water ingestionAccidental / intentional salt ingestionHypertonic salineSodium bicarbonate infusionLow sodium outputMineralocorticoid excess

Clinical presentationnot seen until serum Na >155 meq/Lfever, restlessness, lethargy, confusion

Treatmenttreat the underlying causefluid therapy with pure water or nasogastricallyintravenous therapy with dextrose 5% or pure water through central vein Note A rapid decreased of serum Na could be detrimental--- decrease of serum Na by 2 meq/L/hr

TAKE- HOME MESSAGE :

In diagnostic and treatment of water and electrolyte dysbalance :knowledge of basic renal physiology is useful for understanding.a promptly management and monitoring is needed

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