The document provides a comprehensive overview of electrolyte imbalances, focusing on potassium, calcium, phosphorus, and magnesium. It elaborates on the causes, clinical manifestations, and treatment strategies for conditions such as hypokalemia, hyperkalemia, hyponatremia, and hypercalcemia, highlighting the importance of electrolyte homeostasis in various health conditions. The document emphasizes specific management protocols, including oral and intravenous replacements, to mitigate acute risks associated with severe imbalances.

1. Electrolyte
Imbalance
RS Mitra Keluarga Gading Serpong

2. Kebutuhan
basal Kalium
Intake K+ sehari antara 40-150 mEq
Homeostasis (kebutuhan minimum) 20-30
mEq/hari
Kebutuhan meningkat pada gagal jantung dan
hipertensi

3. Asupan Kalium rata-rata dewasa : 80 mEq
70 mEq
Urin
10 mEq
GI tract

5. 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

6. 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

7. 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

8. Hiperkalemia
K > 5,5 mEq/L
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
nefron, uremia
GFR < 5 biasanya hiperkalemia
3. ↑intake kalium / ↑pelepasan kalium dari organ yang
sebelumnya iskemik

9. Manifestasi klinis
Skeletal muscle weakness (plasma [K+> 8
mEq/L), fasikulasi, parestesi

10. Tatalaksana
Stabilize cardiac membrane with 10mL 10% calcium gluconate
Drive K+ into cells with 10units insulin in 50mL 20% glucose
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

11. Hypernatremia
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
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

12. 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 >>

13. Tatalaksana
Perbaiki deficit cairan dengan waktu >48 jam dengan D5%

14. Hyponatremia
etiologi
Hypovolemia
Euvolemia Hypervolemi
Renal Extrarenal
Diuretics GI loss SIADH Nephrotic Syndr
Cerebral Salt-wasting
Syndrome
Skin loss Hypothiroidism Hypoalbuminemia
Hyperaldosteronism Cystic fibrosis Sepsis Heart Failure
Malnutrition Renal Failure
Primary polydipsia Cirrhosis

15. Hyponatremia
[Na+] > 125  Tidak menunjukkan gejala neurologis
Tanda awal :
- Anoreksia
- Mual
- Kelemahan tubuh

16. Hyponatremia
Koreksi Na < 10mEq/hari
Koreksi Free Water Deficit (FWD) >48 jam untuk mengurangi risiko
edema cerebri

17. NaCl 3%
= 513mEq/L
=1meq/2cc

18. Calcium
Intake kalsium dewasa rata2 600-800mg/hari
Hingga 80% intake calcium harian dibuang melalui feses
Ekskresi kalsium renal rata-rata 100mg/hari , bervariasi antara 50-300mg/hari.
98% yang terfiltrasi bisa diabsorbsi Kembali
Di Tubulus distal, reabsorpsi kalsium bergantung pada sekresi hormone paratiroid, dimana
reabsorpsi natrium bergantung pada sekresi aldosterone.
Peningkatan PTH  Peningkatan reabsorpsi kalsium  Penurunan eksresi kalsium di urin

19. 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

20. 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).

21. 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

22. 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.

23. 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

24. Hypocalcemia
Should be diagnosed only on the basis of the plasma ionized calcium concentration.

25. 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.

26. 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.

27. 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

28. 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.

29. 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

30. 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

31. 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.

32. 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.

33. 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.

34. 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.

35. 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.

36. 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

37. Hypermagnesemia
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.

38. 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.

39. 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)

40. Hypomagnesemia

41. 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.

42. 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