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Disorders of Electrolytes(in surgical patients)

Textbook Reading

TAV/ARZ

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Pendahuluan

Penatalaksanaan cairan dan elektrolit sangatesensial dalam perawatan kasus bedah(perioperative care)

Gangguan keseimbangan tersebut dapat terjadipre,intra&post (operasi)

Sering menyertai pada kasus2critical ill(trauma & sepsis)

Topik ini dikhususkan hanya pada gangguankeseimbangan elektrolit

Na dan K merupakan elektrolit utama yangperlu pembahasan

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Komposisi Cairan Tubuh

TOTAL BODY WEIGHT 100%

ICF 40% ECF 20%

IVF

5%

TOTAL BODY WATER 60%

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Kompartemen cairan tubuh

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Komposisi elektrolit dalam cairan

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Natrium

Fungsi Natrium

Regulasi osmolalitas plasma

Mengatur permeabilitas membran sel

Berperan dalam konduksi impuls dan saraf

Kadar normal : 135 -145 mEq/L

Kebutuhan per hari: 2-4 mEq/kgBB/hari

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Hyponatremia

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Sistem organ Hyponatremia

Central nervous system Nyeri kepala, confusion, hyper-or hypoactive deep tendon

reflexes, kejang, koma, peningkatan TI

!usculoskeletal elemahan, kelelahan otot, muscle cramps"t#itching

$astrointestinal %norexia, nausea, vomiting, diare

Cardiovascular Hypertension and &radycardia

Tissue 'acrimation, salivation

(enal )liguria

!anifestasi klinis

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DiagnosticApproach

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Terapi Hiponatremia (basic principles)

Osmolalitas

Osmolalitas

Osmolalitas

N

ECF

ECF

ECF N

Volume expansion dg 0,9%

saline

Restriksi cairan dg diuretik

No spesific therapy

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13Treatment

Urea(antinatriuretic&osmotic diuresis):40mg in 150cc

normal saline IV every 8hHypertonic salineLoop diuretikVasopressin antagonis(aquaresis than diuresis):conivaptan

20-40 mg daily

Severe hiponatremi (Na

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13Rapid correction of

hyponatremia

central Pontine myelinolysis

Seizures, weakness/paresis,akinetic movements,unresponsiveness

Permanent brain damage

Death

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Hypernatremia

Iatrogenic

Selalu hiperosmolerRespon tubuh: haus dan release ADH

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Etiologi

Free waterloss

Sodium

intake

Renal

Non

Renal

Hiperglikemia, manitol, diet

tinggi protein (produksi urea),

diabetes incipidus

Diare

Insensible losses(fever &

burn)

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13Manifestasi klinis

Cent!" ne#$& &'&te( Re&t"e&&ne&&) "et*!+') !t!,-!)--t!.-"-t') t$n- &!&(&)e"--()&e-e&) $(!

3&"$&e"et!" e!ne&&

C!-$#!&"! T!*'!-!) *'$ten&-$n)&'n$e

T-&&e D' &t-' ($& (e(.!ne&)

e &$""en t$n+e)ee!&e&!"-#! !n te!&

Ren!" O"-+-!

3et!.$"- Fe#e

*ody system hypernatremia

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DiagnosticApproach

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Terapi Hipernatremia

Free water

loss

Sodium

intake

D5% atau NaCl 0,45% iv/oral

Water defisit =[left (serum sodium-140)/140] x TBW (liters)Or:Chane in serum !a" # (infusate !a" -

serum !a") $ (TBW " 1)

Diuretik (furosemide)

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13

The rate of fluid administration:

1. Acute hypernatremia: a decrease inserum sodium of no more than 1meq/h and

12meq/d

1. Chronic hypernatremia: a decrease inserum sodium of no more than 0.7meq/L/h

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Kalium

Kation terbanyak di tubuh(98% intraseluler)

Keseimbangannya diatur oleh Na-K ATPase

pump

Ekskresi terbanyak melalui ginjal

Uptake-nya di intraseluler dipengaruhi oleh

insulin dan beta2 reseptor

Fungsi Kalium: eksitabilitas membran danfungsi sel

Kadar normal kalium: 3,5 5 mEq/L

Kebutuhan per hari : 1 mEq/kgBB/hr

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Kalium

Rata-rata kebutuhan K per hari: 50-100meq/d

Rata-rata ekskresi melalui ginjal: 10-700meq/d

Kadar K dipengaruhi oleh:

Surgical stress

Injury

Acidosis

Tissue catabolism

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Penyebab hipokalemia

Intake yg inadekuat:Diet yang kurang

Pemberian cairan infus yg tdk mengandung K

Pemberian TPN yg tdk mengandung K

Ekskresi K yang berlebihan:Hyperaldosteronism

obat2an

GI / renal losses:Direct loss (diarrhea)

Renal loss (gastric fluid, either as vomiting or high nasogastric output)

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Gejala klinis hipokalemia

System hypokalemia

Gastrointestinal Ileus, constipation

Neuromuscular Decreased reflexes, fatigue, weakness,

paralysisCardiovascular Arrest

ECG changes !waves

"!wave flattening

#"!segment changes

Arrhythmias

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De!t(ent $ 7+-!" E!t-$n) O"!n$ Re+-$n!"3e-!" Cente/!"t e"et"'t e"!e(ent $t$$"&

2008

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De!t(ent $ 7+-!" E!t-$n) O"!n$ Re+-$n!"3e-!" Cente/!"t e"et"'t e"!e(ent $t$$"&

2008

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Penyebab hiperkalemia

Peningkatan intake:Potassium supplementation

Blood transfusions

Endogenous load/destruction:

Hemolysis atau rhabdomyolysisCrush injury

Gastrointestinal hemorrhage

peningkatan release:Acidosis

Rapid rise of extracellular osmolality (hyperglycemia or mannitol)

Impaired excretion:Potassium-sparing diuretics

Renal insufficiency/failure

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13Gejala klinis hiperkalemia

System hyperkalemia

Gastrointestinal Nausea/vomiting ,colic, diarrhea

Neuromuscular weakness, paralysis, respiratory ailure

!ardiovascular Arrhythmia, arrest

"!G changes #eaked T waves $early change%

&lattened # wave

#rolonged #' interval $irst(degree block% )idened *'S comple+

Sine wave ormation

entricular ibrillation

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13

Treatment of symptomatic hyperkalemia

+otassium removal

$ayexalate

%ral administration is &'!() g in ')!&)) m*of +) sor-itol

.ectal administration is ') g in +)) m* +) sor-itol

Dialysis

Shift potassium

Glucose & vial of D') and regular insulin '!&) units intravenous

/icar-onate & vial intravenous

Counteract cardiac effects

Calcium gluconate '!&) m* of &) solution

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Calcium

Fungsi utama:

Transmisi impuls saraf

Kontraksi otot jantung

Faktor pembekuan darah

Pembentukan gigi dan tulang

Kontraksi otot

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()

*tt9//"-:$e+$n&t!te:e/-n$ente/(-ne!"&/!"-(/!t*:*t("

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Kalsium

;e.t*!n *!-!n9 1en'e.!.9 H-e!!t-$--&( !n (!"-+n!n&-

Ge?!"!9 G!n++!n ne$"$+-&) e"e(!*!n $t$t !n n'e-) -&n+&- en!") (!")

(nt!*) n'e- et) *-eten&-) !-t(-!) en-n+!t!n t$&-&-t!& te*!! $.!t2!n

-+-t!"-&

E;G 9e(ene!n @T -nte#!") e(!n?!n+!n >R@R7 -nte#!") en-n+!t!n @R7

#$"t!+e) T !#e "!tten-n+ -en-n+) AV ."$

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1

ipokalsemia

en'e.!.9 !ne!t-t-&) -ne&- &$t t-&&e '!n+ "!&) +!+!"

+-n?!")-&t"! ente!") *'$!!t*'$--&() t($ "'&-& &'n$(e)

(!&&-#e ."$$ t!n&&-$n -t* -t!te .-n-n+

Ge?!"!9!e&te&-! !?!* !n e&te(-t!&) !( $t$t) &t-$)

tet!n-) e?!n+) *'ee"e,-!) T$&&e!& &-+n) C*#$&te& &-+n)

enn!n $nt!t-"-t!& ?!ntn+) +!+!" ?!ntn+

E;G9 $"$n+e @T -nte#!") T !#e -n#e&-$n) *e!t ."$) V