Electrolyte Imbalance slide explanations

1

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

4. 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

5. 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

6. 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

7. Hiperkalemia K > 5,5 mEq /L Disebabkan karena : Intercompartmental shift Kalium : asidosis , lisis sel ( kemoterapi , hemolisis , trauma massif jaringan , digitalis overdose, ↓ 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

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

9. 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

10. 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

11. 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 >>

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

13. 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

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

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

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

17. 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

18. 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

19. 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 ).

20. 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

21. Treatment Acute : ↑UOP and Ca 2+ 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.

22. 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

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

24. 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.

25. 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.

26. 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

27. 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.

28. 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

29. 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

30. 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.

31. 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.

32. 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.

33. 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.

34. 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.

35. 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

36. 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 .

37. 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.

38. Treatment D iscontinue 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 )

39. Hypomagnesemia

40. 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.

41. 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