electrolyte balance and siadh

8/19/2019 Electrolyte Balance and SIADH

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POSTGRADUATE OF BIOMEDICAL SCIENCE

FACULTY OF MEDICINE

UNIVERSITY SUMATERA UTARA

IRA ASTUTI HASIBUAN



ELECTROLYTE

A substance whose components dissociate in solution intopositively (cation) and negatively (anion) charged ions. For

example, sodium chloride in solution (saline), dissociates intoNa and Cl. Other electrolytes of physiological importanceinclude Ca, PO42-, etc.

Glucose is not an electrolyte since it does not dissociate insolution. At all times the total number of positive chargesbalances the number of negative charges to achieve electricalneutrality.



Non Electrolyte

dextrose

ureum

kreatinin

Electrolyte

Cation : Na, K,Ca, Mg

Anion : HCO3,Cl, HPO4



ELECTROLYTE

Kation/anion Ekstra selular ( mEq/L ) Intraselular ( mEq/L )Na + 142 15

K + 5 150

Ca ++ 5 2

Mg ++ 1 27

Total 154 194

HCO3- 24 10

Cl - 105105 1

HPO4 = 2 100

SO4 = 1 20

Asam Org 6

Protein 16 63

Total 154 194

142

105

150

100



Water and electrolyte in the body

The total body water is divided functionally into theextracellular (20% of body weight) and the intracellular

fluid spaces (40 of body weight) separated by the cellmembrane with its active sodium pump which ensures

that sodium remains largely in the ECF

The cell contains large anions such protein and glycogen, whichcannot escape and therefore draw in K ions to maintain

electrical neutrality.

These mechanism ensure that Na and its balance anions Cl andHCO, are the mainstay of ECF osmolality, and K has

corresponding function in the ICF



SODIUM

Normal range: 136–145 mEq/L or 136–145 mmol/L

The total body sodium is 3000-4000 mmol, of which only 60%is exchangeable, the remainder being locked mainly in bone

The principal role of sodium is to regulate serum osmolality as well as fluid balance.

Changes in body water and plasma volume can directly or

indirectly affect the serum sodium concentration.



As a result of changes in effective circulating volume,baroreceptors and osmoreceptors will respondaccordingly in an attempt to restore an isovolemic state of

the body.

Baroreceptors are located in the carotid sinus, aorticarch, cardiac atria,hypothalamus, and the

juxtaglomerular apparatus in the kidney.

Stimulation of these receptors will promote urinary loss of water and sodium.

PHYSIOLOGY OF SODIUM



Osmoreceptors are presentprimarily in the hypothalamus.

The Resultant Renal EffectsFrom These Three DistinctPathways Will Alter thehomeostasis Of Water andsodium.

The three major mediatorsinvolved include vasopressin orantidiuretic hormone (ADH),The renin-angiotensin-aldosterone System (RAAS),

And Natriuretic peptides.

PHYSIOLOGY OF SODIUM

H i h i i l d i di i



Homeostatic mechanisms involved in sodium, potassium,and water balance.



SIGN AND SYMPTOM OF HYPONATREMIA

AND HYPERNATREMIA

HYPONATREMIA HYPERNATREMIA

Abnormal sensor Agitation

Anorexia Apathy Cheyne-Stokes respirationDepressed deep-tendonreflexesDisorientation

HypothermiaLethargy Muscle crampsNauseaSeizures

ThirstRestlessness

Irritability Lethargy Muscle twitchingSeizuresHyperreflexia

ComaDeath



CAUSES OF HYPONATREMIA



SIADH

The syndrome of inappropriate antidiuretic hormone secretion(SIADH) is the most common cause of hyponatremia in

hospitalized patients

Normally, ADH is secreted from the posterior lobe of thepituitary gland in response to decrease in plasma volume or

increase in serum osmolality.

In SIADH, secretion of ADH is not caused by hemodynamicdisturbance and is mediated through nonosmotic receptors,

resulting in water retention and dilutional hyponatremia.



The key points in diagnosing SIADH are the serumsodium concentration, tonicity of plasma and urine,

urine sodium concentration and clinical volumestatus.

Finding of hyponatremia ( serum sodiumconcentration < 135 mEq/L ), hypotonicity plasma

osmolality ( <280 mOsm/kg) inappropriateconcentrated urine ( > 100 mOsm/kg ), elevated

urine sodium concentration (>20mEq/L) areconstant with SIADH

SIADH is a diagnosis of exclusion, and adrenal,cardiac, liver, kidney, and thyroid dysfunction

must be ruled out.



CAUSES OF HYPERNATREMIA

HYPERNATREMIA

Na > 145 mmol/L

EUVOLEMIA

Diabetic incipidus increasedinsensible water loss

fever,

extensive burns,

mechanical ventilation

HYPOVOLEMIA

profuse sweatingdiarrhea

HYPERVOLEMIA

Primaryhyperaldosteronism

Cushing disease

Sea water, neardrowning

Resuscitative effortsusing hypertonic

sodium bicarbonate



The total body K lies between 3000 and 3500 mmol and iscontained in the intracellular space at a concentrastion of 120-145 mmol/L

Only a very small proportion is in the ECF, where itsconcentration lies crucially in the narrow range 3.5-5.2mmol/L.

The major physiological role of potassium is in theregulation of muscle and nerve excitability. It also playimportant roles in control intracellular volume, protein

synthesis, enzymatic reaction, and carbohydrate metabolism

POTASSIUM



Na-K-ATPase pump is principally responsible for regulatingpotassium entry into cell. Potassium is primarily excreted by

the kidneys

Potassium homeostasis is altered by insulin, aldosterone,changes in acid-base balance, renal function, orgastrointestinal and skin loses

Although potassium may affect different body functions,its effect on cardiac muscle is the most important due to

the potential life threatening effect of arrhytmia as a resultof either high or low serum potassium concentration



The acute homeostatic sequence of events in the body to

maintain serum potassium within a narrow concentration range.

HYPOKALEMIA



HYPOKALEMIA

Hypokalemia is defined as a serum potassium concentration less

than 3.5 mEq/L (<3.5 mmol/L).ETIOLOGY : clinicians should determine whether hypokalemia isdue to intracellular shifting of potassium (apparent deficit) orincreased loss from the body (true deficit)

AlkalosisΒ2-

adrenergicstimulationinsulin

Decreased intake :Tea and toast diet, alcoholism,

indigence, potassium-free IV fluids,anorexia nervosa, bulimia

Increased output :Extrarenal : vomiting, diarrhea, laxative

abuse, intestinal fistulesRenal : corticosteroids, amphotericin B,diuretics, hyperaldosteronism, cushing’s

syndrome, licorice abuse

Apparentdeficit

Truedeficit



HYPERKALEMIA



HYPERKALEMIA

Hyperkalemia is defined as serum potassium concentrationgreater then 5.0 mEq/L (> 5.0 mmol/L )

Hypokalemia may indicate a true or apparent potassiumimbalance

Renal failure is the most common causes of hyperkalemia



ETIOLOGIES OF HYPERKALEMIA

Apparentexcess

( extracellularshifting )

True excess

Metabolicacidosis

INCREASED INTAKE

Endogenous causes :HemolysisRhabdomyolysisMuscle crush injuries

Burns

Exogenous causes :Salt subtitutesDrugs ( e.g. penicillinpotassium )

DECREASED OUTPUT

Chronic or acute renalfailureDrugs : potassium-sparing diuretics, ACE-

inhibitors, NSAID, Angiotensin II receptorantagonist, heparin,trimethoprimDeficiency of adrenalsteroids Addison’s disease

SIGN AND SYMPTOM OF HYPERKALEMIA



SIGN AND SYMPTOM OF HYPERKALEMIA

Symptom of hyperkalemia usually do not developed untilserum potassium concentration reach 5.5 mEq/L.

Symptoms are caused by changes in neuromuscular andcardiac function and include muscle twitching, cramping,

weakness and paralysis.

The most concerning symptoms are cardiac abnormalities :peaked T waves, widened QRS complexes, prolonged PRinterval, shortened QT interval, this can lead to cardiac

arrhytmias.



Normal range : 96-106 mEq/L or 96-106 mmol/L

Chloride is passively absorbed from the upper small intestine. In thedistal ileum and large intestine., its absorbtion is coupled withbicarbonate ion secretion

Chloride is influenced by the extracellular fluid balance and acid-base

balance.

The physiological role of chloride is primarily passive. It balances outpositive charges in the extracellular f luid and, by passively following

sodium, helps to maintain extracellular osmolality



Causes : A patient is on acid-suppressive therapy (e.g., high-doseH2-blockers or proton pump inhibitors)Patient who is receiving continuous or frequentnasogastric suction Person whose has profuse vomiting, a greater loss ofchloride than sodium can occur because gastric fluid

contains 1.5–3 times more chloride than sodium.Gastric outlet obstruction, protracted vomiting and self-induced vomitingMetabolic alkalosis

HYPOCHLOREMIA



The most causes : saline infusion in hospitalized patientparenteral nutrition solutions with high chlorideconcentrationsDrug : acetazolamideMetabolic and respiratoric acidosis

HYPERCHLOREMIA



CALCIUM

Ninety-nine percent of total body calcium resides inbone. Less than 1 % exist in the extracellular fluid.

Normal serum calcium concentration in the extracellularbetween 8.6 and 10.2 mg/dL. Nearly 50 % of serum calcium

is protein bound, primarily to albumin.

Calcium is essential to many body function, including bonemetabolism, neuromuscular activity, electrical conductionin the heart and smooth muscle, coagulation, and exocrine

and endocrine functions.

CALCIUM



HOMEOSTASIS

Calcium homeostasis is regulated by parathyroid hormone,calcitonin and vitamin D.

For every 1 g/dL decrease in serum albumin concentrationbelow 4 g/dl serum calcium concentration will decrease by

0,8 mg/dl, therefore serum calcium concentration should becorrected in patient with hypoalbuminemia

Corrected calcium = ( 0,8 ( 4 – albumin )) + serum calcium



source : https://quizlet.com/31186621/endocrine-06-bone-mineral-homeostasis-flash-cards/



HYPOCALCEMIA

Diminished intakeMedications : calcitonin

Ethylenediaminetetraacetic acid ( EDTA )GlucocorticoidLoop diuretics

Phosphate saltsPicamycin

HyperphosphatemiaHypoalbuminemiaHypomagnesemia

HypopharatiroidismPancreatitisRenal failureSecondary hyperpharathyroidism Vitamin D deficiency

CAUSES



HYPERCALCEMIA

CAUSESThe most causes is malignancy and primarilyhyperparathyroidism

Hypercalcemia can also result from:Excessive administrationOf IVcalcium saltsCalcium supplements

Chronic immobilizationPaget’sdiseaseSarcoidosisHyperthyroidism Acute adrenal insufficiency Somer espiratory diseases

Lithium-inducedrenalcalciumreabsorptionExcessivevitaminD,vitaminA,orthyroidhormone,which increasesintestinal absorptionTamoxifen AndrogenichormonesEstrogenProgesterone

SIGNS AND SYMPTOMS



HYPOCALCEMIA

Tetany → characteristic symptom

Neuromuscular disfunctionCardiovascular disfunctionCentral nervous system dysfunctionChronic hypocalcemia : hair loss,dermatitis, eczema, grooved nails

HYPERCALCEMIA

FatigueConfusionBradycardia

Arrhytmiachronic hypercalcemia :nephrolithiasis, metastatic calcification,renal failure



MAGNESIUM

Magnesium is found primarily in the bone,muscle and soft tissue. Approximately 1 % of total

body stores present in extracellular fluid

The normal serum magnesium concentration is1.5 to 2.4 mg/dl.

Magnesium is utilized throughout the body as acofactor for enzyme and is required in reaction

involving adenosine triphosphatase ( ATP )



REGULATION

Largely regulated by the kidney Other factors including :gastrointestinal function,parathyroid hormone activity,

patient condition

HYPOMAGNESEMIA



HYPOMAGNESEMIA

Defined as serum magnesium concentration less than 1.5mg/dl and is severe when the serum concentration is

below 1 mg/dl

CAUSES ExcessivegastrointestinallosesRenal losses

Surgery Trauma

BurnsSepsisPancreatitisMalnutrition

alcoholism

symptoms Arrhytmias, torsades de pointes, seizures,

coma and death

HYPERMAGNESEMIA



Defined as serum magnesium concentration greater than 2.4mg/dl. Most patients remain asymptomatic until serum

magnesium concentration exceed 4 mg/dl.

CAUSESRenal insufficiency

iatrogenic



SIGNS AND SYMPTOMS OF HYPERMAGNESEMIA

• Bradycardia, flushing, sweating,sensation of warmth, nausea, vomitting,decreased serum calcium and decreasedclotting mechanism

2-5 mEq/L

• Drowsiness and decreased deep tendonreflexes6 mEq/L

• Flaccid paralysis and increased PR andQRS intervals10-15mEq/L

> 15

mEq/LRespiratory distress and asystole

PHOSPHATE



PHOSPHATE

Normal range serum phosphate concentration : 2.6–4.5mg/dL or 0.84–1.45 mmol/L for adults

It is important for intracellular metabolism of proteins,

lipids, and carbohydrates and it is a major component inphospholipid membranes, RNAs, nicotinamide diphosphate(an enzyme cofactor), cyclic adenine and guanine nucleotides(second messengers), and phosphoproteins.

Phosphate absorption is diminished when a large amount ofcalcium or aluminum is present in the intestine due to the

formation of insoluble phosphate compounds.

PHOSPHATE REGULATION



Serum phosphate and calcium concentrations as well as PTH

and vitamin D levels are intimately related with each other.

Serum phosphate indirectly controls PTH secretion via anegative feedback mechanism. With a decrease in the serumphosphate concentration, the conversion of vitamin D to 1,25-DHCC increases (which increases serum concentrations of bothphosphate and calcium). Both the intestinal absorption andrenal reabsorption of phosphate is increased.

The concomitant increase in serum calcium then directlydecreases PTH secretion. This decrease in serum PTHconcentration permits a further increase in renal phosphate

reabsorption.

HOMEOSTASIS REGULATION OF CALCIUM ANDPHOSPHATE BY PTH VITAMIN D DAN FGF23



From the following article:The skeleton as an endocrine organ

Douglas J. DiGirolamo, Thomas L. Clemens & Stavroula Kousteni .Nature Reviews

Rheumatology 8, 674-683 (November 2012) doi:10.1038/nrrheum.2012.157

PHOSPHATE BY PTH, VITAMIN D DAN FGF23

HYPOPHOSPHATEMIA

http://www.nature.com/nrrheum/journal/v8/n11/full/nrrheum.2012.157.html

http://www.nature.com/nrrheum/journal/v8/n11/full/nrrheum.2012.157.html



Hypophosphatemia indicates a serum phosphate

concentrationless than 2.6 mg/dL (<0.84 mmol/L).

Common causes of decreased serum phosphate

concentrations:1. Increased renal excretion2. Intracellular shifting3. Decreased phosphate or vitamin D intake

Infusion of concentrated glucose solutions, especially whenaccompanied by insulin, can produce hypophosphatemiathrough intracellular phosphate shifting → refeeding

syndrome

SIGNS AND SYMPTOMS OF



Patients with moderate reduction in serum phosphate(2–2.5 mg/dL or 0.64–0.81 mmol/L) are often asymptomatic.Neurological irritability may occur as the serum phosphateconcentrationDrops below 2 mg/dL(<0.64 mmol/L )

Severe hypophosphatemia is often associated with muscle

weakness, rhabdomyolysis, paresthesia, hemolysis, plateletdysfunction, and cardiac and respiratory failure. CNS effectsoften include encephalopathy, confusion, obtundation,seizures, and ultimately, coma

HYPOPHOSPHATEMIA

HYPERPHOSPHATEMIA



Hyperphosphatemia indicates a serum phosphateconcentrationgreaterThan 4.5 mg/Dl (>1.45 mmol/L).There are three basic causes for elevated serumphosphate concentrations:

1.Decreased renal phosphate excretion2. Shift of phosphate from intracellular to extracellularfluid3. Increased intake of vitamin D or phosphate-containing

products (orally, rectally, or intravenously )

THE MOST CAUSERENAL

DYSFUNCTION

SIGNS AND SYMPTOMS



Signs and symptoms of hyperphosphatemia commonlyresult from the accompanying hypocalcemia andhyperparathyroidism

Renal function may diminish if hyperphosphatemia isleft untreated.

In the presence of renal dysfunction, phosphateexcretion is further reduced to cause an even greater

increase of serum phosphate concentration and a furtherdecline in serum calcium concentration

REFFERENCES



REFFERENCES

Lau A., Chan L., Electrolyte, Other minerals, andTrace Elements

Lobo D., Lewington A., Allison S., Basic Concepts of

Fluid and Electrolyte Therapy

Bartel B., Gau E., Fluid and Electrolyte Management

Balasubramanian A., Flareau B., Sourbeer J.,2007.,Syndrome of Inappropriate Antidiuretic Hormone

Secretion

electrolyte balance and siadh

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