electrolyte disorder for internist

Electrolyte disorders for internist

Contents

• Water and sodium metabolism – Hypo- and hyper- osmolarity– Hypo- and hypernatremia

• Potassium– Hypo- and hyperkalemia

• Acid-base disorder

• Osmotic pressure – A function of the concentration of all the

solutes in a fluid compartment

Osmotic pressure = total solute total water

Osmolarity = total solute ; mOsm/Kg H2O weight of water

Osmolality = total solute ; mOsm / L H2O volume of water

Osmolality

• Measurement

• Calculation

2Na + Glucose + BUN 18 2.8

Total body water Depends on age, gender, body fat

Body water regulation

Water gain Water loss

Intakemetabolism

Insensible loss sweat, lungFeceskidney

HypotonicityHypotonicity

HypothalamusHypothalamusOsmoreceptorsOsmoreceptors

ADHADH

Thirst

OsmoregulationOsmoregulation

Stimulate Stimulate

HypertonicityHypertonicity

ADHADH

Inhibit Inhibit

IsotonicityIsotonicity

Thirst

Water Water intakeintake

Water Water intakeintake

Renal water excretion

Renal water retention

HypothalamusAngiotensin

Baroreceptor

OC = osmoreceptorMnPO = median preoptic nucleiSFO = subfornical organOVLT =organum vasculosum of the lamina terminalis

Osmolality

Arginine vasopressin stimulation

• Osmotic stimuli• Nonosmotic stimuli

– Blood pressure and blood volume– Drinking– Nausea– Angiotensin II– Stress : pain, emotion– Hypoxia– drug

Renal regulation of sodium

Hyponatremia

• Pseudohyponatremia (normal osmolality)– Hyperlipidemia– Hyperproteinemia

• Translocational hyponatremia (hyperosmolality)– Hyperglycemia– Mannitol, sorbital, glycerol

• True hyponatremia ( hypo-osmolality)

Approach Guideline of HypoNa

True HyponatremiaTrue Hyponatremia(exclude hyperglycemia) (exclude hyperglycemia)

Assess ECF volume statusAssess ECF volume status

TBW , TBNaTBW , TBNa++

HypovolemiaHypovolemia


HypervolemiaHypervolemia


NormovolemiaNormovolemia

Renalloss

Extrarenalloss

Renalfailure

Nephrotic syndrome

CirrhosisCardiac failure

SIADHEndocrinopathy

Drugs

UNa >20 <20 > 20 > 20 < 20

• Hypovolemic hyponatremia with UNa >20 (renal loss)– Diuretic use– Mineralocorticoid

deficiency– Salt-losing

nephropathy– Bicarbonaturia– Ketonuria

• Hypovolemic hyponatremia with UNa <20 (extrarenal loss)– Vomiting– Diarrhea– Third space loss

• Burn, pancreatitis

Causes of SIADH

CARCINOMAS PULMONARY DISORDERS

CNS DISORDERS OTHERS

Bronchogenic CA Viral pneumonia Encephalitis AIDS

Small cell lung CA Bacterial pneumonia Meningitis Prolonged exercise

CA duodenum Tuberculosis Head trauma idiopathic

CA pancreas Aspergillosis Brain abscess

CA stomach Lung abscess Delerium tremens

Thymoma Asthma Acute psychosis

Lymphoma Pneumothorax Multiple sclerosis

Ewing sarcoma Mesothelioma CVA

CA bladder Cystic fibrosis Guillain-Barre syndrome

Prostate CA

Oropharyngeal tumor

Positive pressure breathing

Symptoms of hyponatremia

• Depend on – Age– Gender– Magnitude and acuteness

• Gastrointestinal symptoms : nausea, vomiting

• Neurological symptoms: headache, lethargy, muscle weakness, ataxia, psychosis, seizure, coma, brain herniation

Treatment of Hyponatremia

1. Level, duration of hyponatremia

2. Symptoms

3. Volume status

4. Risk of neurological damage

Hyponatremic patients at risk for neurological complications

• Postoperative menstruating female• Elderly women on thiazide• Children• Hypoxemic patients• Psychiatric polydipsic patients• Alcholics• Malnourished patients• Hypokalemic patients

Treatment solution

Depend on volume status(causes of hyponatremia)

Hypovolemia - isotonic saline

Euvolemia (EM) - hypertonic

Hypervolemia - diuretic

hypertonic

Treatment of hyponatremia

• Acute symptomatic hyponatremia– Raise SNa 1-2 meq/L – Not more than 12 meq/L in 24 hours

• Chronic symptomatic hyponatremia– Raise SNa 0.5-1 meq/L – Not more than 10 meq/L in 24 hours

• Asymptomatic hyponatremia– Water restriction– Drug-induced water diuresis : democlocyclin, lithium, V2 antagonist– Increase solute intake : urea

• A 70-Kg man present diagnosed bronchogenic carcinoma. He presents with GTC. BP 130/80 mmHg. JVP 3 cm, lung- clear. His serum Na is 103 meq/L, Cr 0.7 mg/dl, BS 100 mg/dl

• U/A : sp gr 1.020

Euvolemic hyponatremia

Thyroid function test and cortisol level is normal

SIADH

Desired Na= 110 mmol/l

= TBW x (dNa – sNa)

= 0.6 (70) (110 - 103)

= 294 mmol

Na 294 mmol = 3% NaCl 573 ml

Correct Na 1 mmol/l/hr

= 3% NaCl 573/7 = 80 ml/hr iv.drip

Approach guideline for hypernatremia

Assess volume status

Hypovolemia TBW TBNa

EuvolemiaTBW TBNa

Hypervolemia TBW TBNa

UNa >20 <20 variable >20

Renal lossOsmotic or loop diureticsPostobstructive diuresisIntrinsic renal disease

Extrarenal lossExcessive sweatingBurnDiarrheafistula

Renal lossDIhypodipsia

Extrarenal lossInsensible loss

Sodium gainPrimary hyperaldosteronismCushing’s syndromeHypertonic dialysisHypertonic sodium bicarbonate

Patients at risk of severe hypernatremia

• Elderly patients or infants • Patients receiving

– Hypertonic infusion– Osmotic diuresis– Lactulose– Mechanical ventilator

• Third space water loss : rhabdomyolysis• Altered mental status• Uncontrolled diabetes mellitus• Unerlying polyuric disorder

Hypotonic polyuria

Disorders Urine osmolality SNa

Insufficient AVP

Central diabetes insipidus

+ osmoreceptor dysfunction

Diabetes insipidus in pregnancy

Impaired renal response to AVP

Nephrogenic diabetes insipidus

Primary polydipsia

Dipsogenic polydipsia

psychogenic polydipsia

Water deprivation test

• Patients with hypotonic polyuria– Urine > 50 ml/kg/day– UOsm < 300 mOsm/kg– Total osmole <15 mOsm/kg/day, no

glucosuria or other osmoles

Protocol for water deprivation test

• Initiation of the deprivation period• Baseline data

– Body weight, BP– Serum osmolality, electrolyte– Urine osmolality– Serum AVP

• Follow up BW, BP, urine osmolality hourly• Stop deprivation if BW decrease > 3%, orthostatic hypotension

or urine osmolality changes < 10% in 2-3 consecutive measrement

• Serum electrolyte, serum osmolality and serum AVP at the end point

• If SOsm >295, DDAVP 1 ug or AVP 5 ug sc then measure urine output, urine osmolality 1-2 hours after injection

Treatment of hypernatremia

• Reduction of ongoing loss

• Correction of preexisting water deficit– Rate of correction depends on

• Acuteness• Severity• Risk of neurological deficit

• If serum osmolality > 330 (SNa > 165), decrease Sosm to 320-330 mOsm/L in 24 hours then 0.5 meq/L/hour

Water deficit = 0.6 x BW x (SNa – 140) SNa

Treatment of hypernatremia• Specific treatment

– Central DI • DDAVP, vasopressin• Chlorpropamide

– Nephrogenic DI• Correct cause• Low salt diet • Thiazide or amiloride• NSAIDs

– Pregnancy-induced DI – DDAVP– Osmoreceptor dysfunction – schedule– Psychogenic polydipsia – psychotherapy, clozapine

Contents




Internal and external K balanceInternal and external K balance

IntakeIntake

(RBC, Muscle, Liver, Bone)(RBC, Muscle, Liver, Bone)

ICFICF

ExcretionExcretion

Kidney Kidney 90%90%

Colon Colon 10%10%

K K 60-100 60-100 mEq/daymEq/day

DistributionDistribution

235235 3000 3000 200 200 300 mEq 300 mEq

Sweat <Sweat <10%10%

ECF50-70 meq

Factors - transcellular distribution of Factors - transcellular distribution of KK

NaNa++

KK++KK++

InsulinInsulin

bb22-adrenergic -adrenergic agonistagonist

AldosteroneAldosterone

cAMPcAMP

Na-KNa-K ATPaseATPase

1. 1. HormoneHormone

2. Acid-base status2. Acid-base status

3. Plasma tonicity3. Plasma tonicity

4. Congenital 4. Congenital diseasesdiseases

ThyroidThyroid

Renal regulation of potassium

PosmPosm 300300

mOsmol/kgmOsmol/kg

Serum [K]Serum [K] 4 mEq/L4 mEq/LCCT [K]CCT [K] 40 mEq/L40 mEq/L

CCTCCT

MCDMCD

1 L1 L

0.75 L0.75 L

0.25 L0.25 L

Uosm 1200Uosm 1200

Uosm 300Uosm 300

HH22OO

urine [K]urine [K] 160 mEq/L160 mEq/L

TTKG = CCT[K] = urine[K] / (U/P)osm TTKG = CCT[K] = urine[K] / (U/P)osm Serum [K] Serum [K] Serum [K] Serum [K]

Transtubular K gradientTranstubular K gradient

K CCT = K urine

[K] CCT VCCT = [K]urine Vurine

[K]CCT = [K]urine Vurine

VCCT

V = solute Vurine = K/ Uosm

osmolarity VCCT K/Osm CCT Posm

TTKG = [K]CCT = [K]urine x Posm

[K] P [K]P x Uosm

Symptoms

• Hypokalemia– Skeletal and smooth muscle

weakness– Rhabomyolysis– Nephrogenic DI– EKG; flattened T wave, U

wave• Hyperkalemia

– EKG; peak T wave, flattened P wave, widening QRS complex, sine wave

– Muscle paralysis– Impaired urinary acidification– Stimulate aldosterone

secretion

Approach Guideline of HypoKDecreased serum [K]Decreased serum [K]

excretionexcretionRedistributionRedistribution

- - AlkalosisAlkalosis - Insulin Rx- Insulin Rx - HypoK periodic paralysis- HypoK periodic paralysis - Drugs: - Drugs: -agonists-agonists - Barium poisoning- Barium poisoning

Renal K excretionRenal K excretion: : vary low high (>20 mmol/d)vary low high (>20 mmol/d) lowlow (<20 mmol/d)(<20 mmol/d)

ExtrarenalExtrarenal - Diarrhea- Diarrhea - Cathartics- Cathartics

RenalRenal - Diuretics- Diuretics - HypoMg- HypoMg - Hyperaldosteronism- Hyperaldosteronism - Inherited kidney dis- Inherited kidney dis - Drugs toxicity:- Drugs toxicity: Amphotericin BAmphotericin B Carbenicillin, etc. Carbenicillin, etc.

Low intakeLow intake

Rx of hypokalemia

Rx causes

Potassium deficit,

100-200 mEq if S. [K] = 3-3.5 mEq/L

200-400 mEq if S. [K] < 3 mEq/L

> 600 mEq if S. [K] < 2 mEq/L

Caution in periodic paralysis

Form:

Oral * Elix. KCl (20 mEq/15 ml)

with metabolic alkalosis

* M Pot Cit oral (10 mEq/15 ml)

with metabolic acidosis

IV * [K] < 60 mEq/L in glucose-free sol.

with the rate of < 10 mEq/h

unless ECG is monitored

Causes of hyperkalemia• Pseudohyperkalemia

– hemolysis, thrombocytosis, severe leukocytosis, fist clenching• Decreased renal excretion

Acute and chronic renal failure Aldosterone deficiency: DM, CTIN, obstructive uropathy Addison’s disease Drugs inhibit K+ secretion Kidney diseases that impairdistal tubule function

• Abnormal K+ distribution Insulin defiency -blocker Metabolic acidosis, respiratory acidosis Familial hyperkalemic periodic paralysis

• Abnormal potassium release from cells Rhabdomyolysis Tumor lysis syndrome

Treatment of hyperkalemia

Agents Dosage Action Mechanism

10% calcium gluconate

10 ml IV in 1 min, repeat q 5 min

immedialtely Stabilze myocardium

insulin 5 units + 50% glucose 50 ml

15 min Intracellular K+ shift If BS >300 mg/dl, insulin alone

Aware hypoglycemia

Sodium bicarbonate

50-100 ml Renal K+ excretion

Intracellular shift

Severe metabolic acidosis (<10 meq/L)

B2 agonist 20 mg albuterol NB in 10 min

30 min Intracellular shift

diuretic Furosemide IV 30-60 min Remove K+ For patients with adequate renal function

Exchange resin Kayexalate 50 gm or kallimate

2 hours Remove K+

dialysis Remove K+

Contents




METABOLIC ACIDOSIS

• Anion gap = [Na+] – { [HCO3-]+[Cl-] }– Normal 9 -12 mEq/L– Each decline in serum albumin by 1 g/dL from

the normal value of 4.5 g/dL, decreases the AG by 2.5 mEq/L

CAUSES OF METABOLIC ACIDOSIS

• High anion gap– Ketoacidosis

• Diabetic • Alcoholic• Starvation

– Lactic acidosis• L-lactic acidosis (type A

and B)• D-lactic acidosis

– Drugs and toxin• Ethanol, Ethylene glycol,

Methanol• Salicylate

– Uremia

• Normal anion gap– GI loss of HCO3

• Diarrhea• Fistula

– Renal loss of HCO3 or failure to excrete NH4+

• Renal tubular acidosis• Acetazolamide

– Miscellaneous• NH4Cl ingestion• Sulfur ingestion

Metabolic acidosisAnion gap ; Na – (Cl + HCO3)

high normal

Osmolol gapMeasured osmolality – calculated osmolality

high normal

EthanolEthylene glycolMethanolIsopropyl alcohol

KetoacidosisLactic acidosisuremic

Serum potassium

Hypo or normokalemia

hyperkalemia

Urine anion gap (Na + K) – Cl

negative positive

GI lossDrugsProximal RTA

Aldosterone resistanceAldosterone deficiency

dRTA type IV

>5.5

Urine pH

<5.5

ACCUMULATION OF LACTATE

Increase lactate productionischemiaseizureextreme exerciseleukemiaalkalosis

Decrease lactate utilizationpoor blood flowdefective active transport of lactate into cellinadequate metabolic conversion of lactate to pyruvate

Liver 70%, kidneys 30%

Muscle, gut, brain, skin, RBC

LACTIC ACIDOSIS

• TYPE A– Poor tissue perfusion– Shock– Hypoxemia– Carbon monoxide

poisoning

• TYPE B– Liver disease– Leukemia, lymphoma,

large tumor– Anemia– Diabetes mellitus– Drugs : metformin, NRTIs,

sorbital, isoniazid, salicylate etc

– Inborn error metabolism– Intravenous fructose

Symptoms

• Respiratory symptoms– Kussmaul respiration– Oxyhemoglobin dissociation curve

• Left shift in chronic acidosis• Right shift in acute acidosis

• Cardiovascular systems– Negative inotropic effect– Peripheral arterial vasodilatation– Central venoconstriction

• Neurological systems– Headache, lethargy, stupor and coma

Treatment of metabolic acidosis

• Get rid of cause– DKA : IV fluid + insulin– Alcoholic ketoacidosis, starvation : IV fluid (5%D)– Shock : IV fluid– Toxin : increase excretion ( kidney, dialysis), antidote

• Bicarbonate replacement– Causes are not corrected in short period

– Ongoing loss of HCO3

– Severe metabolic acidosis

electrolyte disorder for internist

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