Electrolyte

Imbalance
RS Mitra Keluarga Gading Serpong
Kebutuhan Intake K+ sehari antara 40-150 mEq
Homeostasis (kebutuhan minimum) 20-30
basal mEq/hari
Kebutuhan meningkat pada gagal jantung dan
Kalium hipertensi
 Asupan Kalium rata-rata dewasa : 80
mEq

70 mEq 10 mEq
Urin GI tract
Hipokalemia
[K+] < 3,5 mEq/L, karena :
1. Intercompartmental shift kalium: terapi insulin, alkalosis, hipotermia, ↑uptake K
dari eritrosit pada pengobatan asam folat/B12 pada anemia megaloblastik
2. ↑ Kehilangan kalium : peningkatan aktivitas mineralocorticoid, renal tubular
acidosis, ketoacidosis, amphotericin B, muntah/diare persisten, Keringat berlebih
(jika intake K+ kurang),
3. Intake kalium inadekuat
Hipokalemia
Manifestasi klinis :
Aritmia
Disfungsi miokard
Penurunan kontraksi otot 
Otot halus : konstipasi
Otot skeletal : weakness, keram, paralisis flaccid
Otot pernapasan : Depresi napas
Otot jantung : Aritmia, cardiac arrest
Hipokalemia (Koreksi)
Paling aman : Oral replacement beberapa hari (60-80mEq/hari)
IV replacement dengan KCl biasanya untuk pasien dengan risiko jantung atau severe
muscle weakness.
Tujuan terapi IV untuk mencegah bahaya bukan untuk mengkoreksi deficit kalium
Kalium  iritatif pada vena perifer  koreksi tidak boleh > 8mEq/jam (1
mEq/kg/jam pada anak)

Cairan yang mengandung dextrose dan sekresi insulin sekunder harus dihindari 
menyebabkan hiperglikemia
 Disebabkan karena :
1. Intercompartmental shift Kalium : asidosis, lisis sel
(kemoterapi, hemolisis, trauma massif jaringan, digitalis
overdose,
2. ↓ekskresi kalium pada urin : ↓ filtrasi glomerulus,
↓aktivitas aldosterone, defek sekresi kalium pada distal
Hiperkalemia nefron, uremia
K > 5,5 mEq/L GFR < 5 biasanya hiperkalemia

3. ↑intake kalium / ↑pelepasan kalium dari organ yang

sebelumnya iskemik
 Manifestasi klinis

Skeletal muscle weakness (plasma [K+> 8

mEq/L), fasikulasi, parestesi
Tatalaksana
Calcium : 5-10 mL 10% calcium glukonas ATAU 3-5cc 10% calcium chloride
IV dengan 30-50g glucose : 10 U insulin
Sodium polystyrene Sulfonate (SPS) /6jam PO (FDA? Peningkatan nekrosis
intestinal), dilarang pada yg akut
Pada keadaan asidosis  NaHCO3 untuk meningkatkan uptake Kalium
Beta agonis (Epinefrin, NE, Salbutamol) untuk peningkatan intake kalium ke sel
Loop diuretic jika fungsi ginjal adekuat.
Patiromer  mengikat Kalium pada GI tract  u/ hiperkalemi kronik
 Table 28–4. Major Causes of Hypernatremia.
Impaired thirst 
  Coma
  Essential hypernatremia
Solute diuresis 
  Osmotic diuresis: diabetic ketoacidosis, nonketotic hyperosmolar coma,
mannitol
administration
Excessive water losses 
Hypernatremia   Renal (Na Concentration in urine >20mEq/L)
     Neurogenic diabetes insipidus
     Nephrogenic diabetes insipidus
  Extrarenal (Na Concentration in urine <10mEq/L)
     Sweating, diarrhea
Combined disorders 
  Coma plus hypertonic nasogastric feeding
Manifestasi Klinis
Predominan gejala neurologi -> umumnya disebabkan dehidrasi seluler
Gelisah, letargi, hiperreflex  kejang, koma, kematian

Air keluar dari sel otak  rupture vena cerebral  fokal intraserebral/perdarahan
subarachnoid

Pada anak, Na > 158 mEq/LKejang dan kerusakan neurologis >>

Tatalaksana
Perbaiki deficit cairan dengan waktu >48 jam dengan D5%
Hyponatremia
etiologi

Hypovolemia
Euvolemia Hypervolemi
Renal Extrarenal
Diuretics GI loss SIADH Nephrotic Syndr

Cerebral Salt-wasting Skin loss Hypothiroidism Hypoalbuminemia

Syndrome
Hyperaldosteronism Cystic fibrosis Sepsis Heart Failure
Malnutrition Renal Failure
Primary polydipsia Cirrhosis
Hyponatremia
[Na+] > 125  Tidak menunjukkan gejala neurologis
Tanda awal :
- Anoreksia
- Mual
- Kelemahan tubuh
- Jika edema cerebri pro
Hyponatremia
Koreksi Na < 10mEq/hari
Koreksi Free Water Deficit (FWD) >48 jam untuk mengurangi
risiko edema cerebri
Calcium
Calcium intake in adults averages 600 to 800 mg/d, and calcium absorption occurs primarily
in the proximal small bowel.

Up to 80% of the daily calcium intake is normally lost in feces

Renal calcium excretion averages 100 mg/d but may vary from as low as 50 mg/d to more
than 300 mg/d. Normally, 98% of the filterable calcium is reabsorbed.

In the distal tubules, however, calcium reabsorption is dependent on parathyroid hormone

(PTH) secretion, whereas sodium reabsorption is dependent on aldosterone secretion.
Increased PTH levels enhance distal calcium reabsorption and thereby decrease urinary
calcium excretion.
Calcium
Normal plasma calcium concentration : 8.5 to 10.5 mg/dL (2.1–2.6 mmol/L)
50% is in the free, ionized form, 40% is protein bound (mainly to albumin), and 10% is
complexed with anions such as citrate and amino acids.
The free, ionized calcium concentration ([Ca 2+]) is physiologically most important. Plasma
[Ca 2+ ] is normally 4.75 to 5.3 mg/dL (1.19–1.33 mmol/L).

Tiap ↑/↓ 1g/dL albumin  total plasma calcium concentration ↑/↓ 0.8-1 mg/dL
Tiap ↑/↓ pH 0,1  Ca 2+ ↑/↓ 0.16 mg/dL
Hypercalcemia
In primary hyperparathyroidism, secretion of
PTH is inappropriately increased in relation to
[Ca 2+ ].
In contrast, in secondary hyperparathyroidism
(eg, chronic kidney failure or malabsorption
syndromes), PTH levels are elevated in response
to chronic hypocalcemia.
Prolonged secondary hyperparathyroidism,
however, can occasionally result in autonomous
secretion of PTH, resulting in a normal or
elevated [Ca 2+ ] (tertiary
hyperparathyroidism).
Clinical Manifestations
Anorexia, nausea, vomiting, weakness, and polyuria.
Ataxia, irritability, lethargy, or confusion can rapidly progress to coma. Hypertension
is often present initially before hypovolemia supervenes.
ECG signs include a shortened ST segment and shortened QT interval.
Hypercalcemia increases cardiac sensitivity to digitalis.
Hypercalcemia may promote pancreatitis, peptic ulcer disease, and kidney failure
Treatment
Acute : ↑UOP and Ca2+ excretion w/ NS maintenance rate (if glomerular filtration
rate and blood pressure are stable)
Chronic : loop diuretic  hati2 penurunan K dan Mg

Severe hypercalcemia (>15 mg/dL) usually requires additional therapy after saline
hydration and furosemide calciuresis. Bisphosphonates or calcitonin are preferred
agents. Intravenous administration of pamidronate (Aredia) or etidronate (Didronel)
is often utilized in this setting. Hemodialysis is very effective in correcting severe
hypercalcemia and may be necessary in the presence of kidney or heart failure.
 Approximately 90% of all hypercalcemia is due to either
malignancy or hyperparathyroidism. The best laboratory test for
discriminating between these two main categories of
hypercalcemia is the PTH assay
Hypocalcemia
Should be diagnosed only on the basis of the plasma ionized calcium concentration.
Clinical Manifestations
Paresthesias, confusion, laryngeal stridor (laryngospasm), carpopedal spasm (Trousseau sign),
masseter spasm (Chvostek sign), and seizures.
Biliary colic and bronchospasm have also been described.
ECG may reveal cardiac irritability or QT interval prolongation, which may not correlate in
severity with the degree of hypocalcemia.
Decreased cardiac contractility may result in heart failure, hypotension, or both. Decreased
responsiveness to digoxin and β-adrenergic agonists may also occur.
Treatment
Symptomatic hypocalcemia is a medical emergency and should be treated
immediately with intravenous calcium chloride (3–5 mL of a 10% solution) or
calcium gluconate (10–20 mL of a 10% solution).
10 mL of 10% CaCl2 contains 272 mg of Ca 2+ , whereas 10 mL of 10% calcium
gluconate contains 93 mg of Ca 2+ .
To avoid precipitation, intravenous calcium should not be given with bicarbonate- or
phosphate-containing solutions. Serial ionized calcium monitoring is mandatory.
Repeat intravenous boluses or a continuous infusion (Ca 2+ 1–2 mg/kg/h) may be
necessary.
Plasma magnesium concentration should be checked to exclude hypomagnesemia. In
chronic hypocalcemia, oral calcium (CaCO3 ) and vitamin D replacement are usually
adequate.
Phosphorous
(1) the phospholipids and phosphoproteins in cell membranes and intracellular
organelles
(2) the phosphonucleotides involved in protein synthesis and reproduction
(3) ATP used for the storage of energy
Phosphorous
Phosphorus intake averages 800 to 1500 mg/d in adults, and 80% of that amount is
normally absorbed in the proximal small bowel.
Vitamin D increases intestinal absorption of phosphorus.
The kidneys are the major route for phosphorus excretion and are responsible for
regulating total body phosphorus content.
Urinary excretion of phosphorus depends on both intake and plasma concentration.
Secretion of PTH promotes urinary phosphorus excretion by inhibiting proximal
tubular reabsorption.
Phosphorous
Normal plasma phosphorus concentration is 2.5 to 4.5 mg/dL (0.8– 1.45 mmol/L) in
adults and up to 6 mg/dL in children.
Plasma phosphorus concentration is usually measured during fasting, because
recent carbohydrate intake transiently decreases plasma phosphorus concentration
Hypophosphatemia increases vitamin D production, whereas hyperphosphatemia
depresses it
Hyperphosphatemia
Major cause:
1. Increased phosphorus intake (abuse of phosphate laxatives or excessive potassium
phosphate administration)
2. decreased phosphorus excretion (chronic kidney disease), or tumor lysis syndrome
Hyperphosphatemia
Clinical manifestation :
Although hyperphosphatemia per se does not appear to be directly responsible for
any functional disturbances, significant hyperphosphatemia may produce
hypocalcemia via phosphate chelation with plasma [Ca 2+ ] and may also produce
acute kidney injury via parenchymal and tubular deposits of calcium-phosphate salts.
Hyperphosphatemia is associated with increased mortality in chronic kidney
disease and kidney failure patients, and is managed in this patient population by
dietary restriction, the use of phosphate binders, dialysis, or a combination of these
methods.
Treatment:
Hyperphosphatemia is generally treated with phosphate-binding antacids such as
aluminum hydroxide or aluminum carbonate.
Hypophosphatemia
Intercompartmental shifts of phosphorus can occur during alkalosis and following
carbohydrate ingestion or insulin administration
Large doses of aluminum- or magnesium-containing antacids, severe burns,
insufficient phosphorus supplementation during total parenteral nutrition, diabetic
ketoacidosis, alcohol withdrawal, and prolonged respiratory alkalosis can each
produce negative phosphorus balance and lead to severe hypophosphatemia.
Clinical Manifestations
1.5 – 2.5 mg/dL  asymptomatic
< 1.0 mg/dL  morbidity and mortality in critically ill patients.
Cardiomyopathy, impaired oxygen delivery (decreased 2,3-diphosphoglycerate levels),
hemolysis, impaired leukocyte function, platelet dysfunction, encephalopathy,
arrhythmia, skeletal myopathy, respiratory failure, rhabdomyolysis, skeletal
demineralization, metabolic acidosis, and hepatic dysfunction have all been associated
with severe hypophosphatemia.

It is uncertain whether hypophosphatemia is a direct and independent contributor to

these major morbidities or to mortality, or is merely a marker of illness severity.
Treatment
Oral phosphorus replacement is generally preferable to parenteral replacement
because of the increased risk of phosphate precipitation with calcium, resulting in
hypocalcemia, and also because of the increased risks of hyperphosphatemia,
hypomagnesemia, and hypotension. Accordingly, intravenous replacement therapy is
usually reserved for instances of symptomatic hypophosphatemia and extremely low
phosphate levels.
Magnesium
Intake averages 20 to 30 mEq/d (240–370 mg/d) in adults. Of that amount, only 30% to
40% is absorbed, mainly in the distal small bowel. Renal excretion is the primary route
for elimination, averaging 6 to 12 mEq/d.
Magnesium reabsorption by the kidneys is very efficient. Twenty-five percent of filtered
magnesium is reabsorbed in the proximal tubule and 50% to 60% is reabsorbed in the
thick ascending limb of the loop of Henle.
Factors known to increase magnesium reabsorption in the kidneys include
hypomagnesemia, PTH, hypocalcemia, ECF depletion, and metabolic alkalosis. Factors
known to increase renal excretion include hypermagnesemia, acute volume expansion,
aldosterone, hypercalcemia, ketoacidosis, diuretics, phosphate depletion, and alcohol
ingestion.
Magnesium
Plasma [Mg 2+ ] is closely regulated between 1.7 and 2.1 mEq/L (0.7–1 mmol/L or 1.7–
2.4 mg/dL) through interaction of the gastrointestinal tract (absorption), bone (storage),
and the kidneys (excretion).
Approximately 50% to 60% of plasma magnesium is unbound and diffusible
Hypermagnesia
Increases in plasma [Mg 2+ ] are nearly always due to excessive intake (magnesium-
containing antacids or laxatives: magnesium hydroxide, Milk of Magnesia), kidney
impairment (GFR <30,L/min), or both

Less common causes include adrenal insufficiency, hypothyroidism, rhabdomyolysis, and

lithium administration. Magnesium sulfate therapy for preeclampsia and eclampsia can
result in maternal and fetal hypermagnesemia.
Clinical Manifestations
Hyporeflexia, sedation, muscle weakness, and respiratory depression.
Vasodilation, bradycardia, and myocardial depression may cause hypotension. ECG signs
may include prolongation of the P–R interval and widening of the QRS complex.
Severe hypermagnesemia can lead to respiratory and cardiac arrest.
Treatment
Discontinue source(s) of magnesium intake (usually antacid or laxa
In cases of relatively high [Mg 2+ ] OR presence of clinical signs of magnesium toxicity,
intravenous calcium can temporarily antagonize most of the effects of clinical toxicity.
Forced diuresis with a loop diuretic and intravenous fluid replacement enhances
urinary magnesium excretion in patients with adequate renal function.
Dialysis will be necessary in such patients with significant kidney impairment or kidney
failure. Ventilatory or circulatory support, or both, may be necessary)
Hypomagnesemia
Clinical Manifestations
Most patients with hypomagnesemia are asymptomatic, but weakness,
fasciculation, paresthesias, confusion, ataxia, and seizures may be encountered.
Hypomagnesemia is frequently associated with both hypocalcemia (impaired PTH
secretion) and hypokalemia (due to renal K+ wasting). Cardiac manifestations
include arrhythmias and potentiation of digoxin toxicity; both are worsened by
hypokalemia.
Hypomagnesemia is associated with an increased incidence of atrial fibrillation.
Prolongation of the P–R and QT intervals may also be present.
Treatment
Asymptomatic hypomagnesemia can be treated orally or intramuscularly.
Serious manifestations such as seizures should be treated with
intravenous magnesium sulfate, 1 to 2 g (8–16 mEq or 4–8 mmol) given
over 10 to 60 min