SLIDE BIMBINGAN SEM.1 ggn elektrolit.pptx

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About This Presentation

Ganggu elektrolit


Slide Content

Manajemen Terapi Cairan pad pasien Interna dengan Rasional Soraya Wildhani

Reddi AS. (2018). Electrolyte and Acid - Base Disorders. Seconf Edition . Springer International Publishing; 2018. p 1–503. Kadri A, Kiksal O, Kose A, Armagan E, Ozdemir F, Inal T, et al. General characteristics of patients with electrolyte imbalance admitted to emergency department. World J Emerg Med . 2013;4(2):113–6. A substance that dissociates in water into charged particles called ions Important electrolyte Protecting cellular function, tissue perfusion and acid-base balance. Electrolyte Sodium (Na + ) potassium (K + ) calcium (Ca 2+ ) magnesium (Mg 2+ ) chloride (Cl - ) bicarbonate (HCO 3 - ) and phosphate (H 2 PO 4 - ) Function Introduction Definition

Electrolytes are involved in many metabolic and homeostatic functions, including : enzymatic and biochemical reactions maintenance of cell membrane structure and function Neurotransmission nerve signal conduction hormone function muscle contraction cardiovascular function bone composition fluid and acid–base regulation

Fluid compartment are seperated by membranes that are freely permeable to water. Movement of fluids due to hydrostatic pressure and osmotic pressure Body fluid distribution Body fluids are distributed in two distinct area: intracellular fluid (ICF) 40% body weight Extracellular fluid (ECF) 20% body weight Interstitial fluid -15% body weight Plasma -5% body weight

Fluid and electrolyte homeostasis is maintained in the body neutral balance: input = output positive balance: input > output negative balance: input < output

Zat terlarut dalam tubuh... Zat terlarut dlm cairan tubuh  elektrolit & molekul 2 lainnya Elektrolit (ion) terdisosiasi dlm cairan membentuk 1/> partikel yg bermuatan Molekul 2 lain ( glu kosa , protein,urea,la ktat , & as.organik lain) tetap stabil dlm larutan Elektrolit utama dlm tubuh : sodium , potassium, calcium , magnesium, chloride, bicarbonate, phosphate, & sulfate . Kation = ion dgn muatan positif Anion = ion dgn muatan negatif

Komposisi ionik major kompartemen cairan tubuh

Electrolyte imbalance

Sodium imbalance

Hyponatremia Sodium  most abundant extracellular cation has a normal serum concentration of 135–145 meq /L Normal homeostatic mechanisms  keep the serum sodium concentration and serum osmolality (275–290 mosm /kg water) within narrow therapeutic ranges Hyponatremia  serum sodium concentration of <135 meq /L may reflect increased, decreased, or normal total body sodium concentrations  necessitates assessment of serum osmolality. As hypoosmolar (hypotonic) hyponatremia  develop in the presence of hypovolemia , isovolemia , or hypervolemia the patient’s fluid volume must also be assessed.

Nefrologia . 2018; 38(5) :558–572 Urine osmolality can vary in healthy person from 80 -1200 mOsm /kg H2O Most important osmols in the urine are Na+, K+, NH4 + with their corresponding anions and urea. It can be calculated: Uosm = 2 x (Na + + K + + NH 4 +) + (urea) + (glucose)

Clinical Manifestation Figure 5. Risk factors and clinical symptoms of hyponatremia. Table 4. Symptoms of hyponatremia based on Severity Symptoms of hypoNa + can vary from nonspecific, mild, severe and life-threatening. Rasyid H, Nilasari D, Hustrini NM. (2014). Panduan Praktik Klinis dan Tatalaksana Hiponatremia . p1–24. Spasovski G, Vanholder R, Allolio B, Annane D, Ball S, Bichet D, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia . Intensive Care Med . 2014;40(3):320–31. Spasovski G, Vanholder R, Allolio B, Annane D, Ball S, Bichet D, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia . Eur J Endocrinol . 2014;170(3):1-47. Moritz ML, Ayus JC. Management of Hyponatremia in Various Clinical Situations. Vol. 16, Curr Treat Options Neurol . 2014;16:1–14. Kulkarni M, Bhat A. Asymptomatic hyponatremia: is it time to abandon this entity? J Nephropharmacol . 2015;4(2):78–80.

Penanganan hiponatremia Mencari penyebab terjadinya hiponatremia Melakukan pengobatan tepat sasaran - bedakan akut atau kronik - kenali tanda atau penyakit yg menyertai hiponatremia (deplesi volume, dehidrasi, gagal jantung, gagal ginjal) Akut : koreksi cepat dengan larutan natrium hipertonik intravena Kronik : koreksi lambat dgn larutan natrium hipertonik intravena atau natrium oral Jumlah Na dlm larutan Na hipertonik = 0.6 x BB (kg) x (Na target – Na awal)

Management of severe/symptomatic hyponatremia Administration of bolus 3% NaCl (513 mEq /L Na+) is proposed for both severe and moderate symptoms ( 150 ml over 20 min for 2–3 times as needed or only once, respectively ). 100 ml bolus 3% NaCl over 10 min should be given for severely symptomatic patients. The dose cannot be repeated more than three times. The European Guidelines The American Guidelines Limiting the increase in serum sodium concentration to a total of 10 mmol/L during the first 24 h and an additional 8 mmol/L during every 24 h thereafter until the serum concentration reaches 130 mmol/L. In both European and United States guidelines the intravenous administration of hypertonic saline is considered the treatment of choice for the management of acute or symptomatic hypoNa + . Spasovski G, Vanholder R, Allolio B, Annane D, Ball S, Bichet D, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia . Intensive Care Med . 2014;40(3):320–31. Sterns RH. Treatment of severe hyponatremia. Clin J Am Soc Nephrol . 2018;13(4):641–9. Hoorn EJ, Zietse R. Diagnosis and treatment of hyponatremia: Compilation of the guidelines. J Am Soc Nephrol . 2017;28:1340–9. Sirota JC, Berl T. (2013). Physiology of water balance and pathophysiology of hyponatremia. In: Simon E, editor. Hyponatremia: Evaluation and Treatment. New Orleans: Springer International Publishing. p. 23–49. Filippatos T, Elisaf M, Liamis G. Pharmacological management of hyponatremia. Expert Opin Pharmacother . 2018;19(12):1337–44.

Management of chronic hyponatremia and minimal neurologic symptoms Restoration of plasma volume either with isotonic saline (154 mEq / L Na+) or balanced crystalloid solution (according to European guidelines) is the treatment of choice in patients with hypovolemic hypoNa + We recommend restoring extracellular volume with intravenous infusion of 0.9 % saline or a balanced crystalloid solution at 0.5–1.0 mL/kg/h. Hypovolemic hyponatremia Spasovski G, Vanholder R, Allolio B, Annane D, Ball S, Bichet D, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia . Eur J Endocrinol . 2014;170(3):1-47. Filippatos T, Elisaf M, Liamis G. Pharmacological management of hyponatremia. Expert Opin Pharmacother . 2018;19(12):1337–44.

Complication Hyponatremia is associated with significant morbidity and mortality Acute hypoNa + causes severe cerebral edema which can cause permanent disability or death. Chronic hypoNa + causes attention deficits, gait instability, osteoporosis, increases the risk of falls and fractures. Rapid correction of chronic hypoNa + is an osmotic stress on astrocytes, causing apoptosis which is clinically seen as an osmotic demyelinating syndrome. Sterns RH, Silver SM. Complications and management of hyponatremia. Curr Opin Nephrol Hypertens . 2016;25:114–9.

Hypernatremia Hypernatremia  serum sodium concentration of >145 meq /L reflects a water deficit relative to total body sodium levels associated with serum hypertonicity . can be further classified as acute or chronic and symptomatic or asymptomatic Patients are more likely to be symptomatic when hypernatraemia develops acutely (usually <48 hours). Acute hypernatraemia  brain cell shrinkage due to a shift of water from the intracellular to the extracellular fluid compartment . Generally, hypernatremia develops when the thirst mechanism is not functioning normally or if access to free water is limited or controlled. Clinical manifestations of hypernatremia in adult patients can include : lethargy , irritability, restlessness, thirst, muscle irritability and spasticity, hyperreflexia , seizures, coma, and death Evidence of hypovolemia or hypervolemia may be present.

2. HIPERNATREMIA Dlm keadaan normal, manusia tdk akan mengalami hipernatremia krn respon haus yg timbul akan dijawab dgn asupan air yg me ↑  hipernatremia tdk terjadi

Penanganan HIPERNATREMIA Tentukan etiologi Me nurunkan kadar Na dlm plasma ke arah normal

Potassium imbalane

Potassium/kalium Potassium is the second most abundant cation in the body. Approximately 98% of total body potassium is found in the intracellular space, with approximately 2% in the extracellular space. The normal serum potassium concentration is 3.5–5.0 meq /L Physiological functions, including cellular metabolism, glycogen and protein synthesis, and regulation of the electrical action potential across cell membranes, especially in the myocardium. The rate-limiting step for potassium entry into the cells is the sodium– potassium-adenosine triphosphatase pump that maintains a higher intracellular potassium level. Several factors affect the activity of this pump, including insulin, glucagon, cathecholamines , aldosterone, acid-base status, plasma osmolality, and intracellular potassium levels.

HIPOKALEMIA Defined as plasma concentration of K+ < 3.5 mEq /L Mild Hypokalemia : 3.0 – 3.5 mEq /L : asymptomatic Moderate Hypokalemia < 3.0 mEq /L : symptomatic Severe Hypokalemia <2.5 mEq /L Clinical manifestations of hypokalemia vary greatly between individual patients their severity depends on degree of hypokalemia Signs and symptoms of hypokalemia include nausea, vomiting, weakness, constipation, paralysis, respiratory compromise, and rhabdomyolysis

Hypokalemia Clinical Manifestations ECG Early: Flat or inverted T wave, Prominent U wave, DT segment depression, prolonged QU interval. Late: Prolonged PR interval, decreased voltage and widening of QRS interval, increased risk of ventricular dysrhythmias .

Referensi : ANTHONY J. VIERA, MD, MPH, and NOAH WOUK, MD, 2015- Potassium Disorders: Hypokalemia and Hyperkalemia, Am Fam Physician. 2015;92(6):487-495)

Penanganan HIPOKALEMIA Indikasi Mutlak : Sdg dlm th/ digitalis Ketoasidosis diabetik Kelemahan otot pernapasan Hipokalemia berat (K + <2 mEq/L) Indikasi kuat : Insufisiensi koroner / iskemia otot jantung Ensefalopati hepatikum Indikasi sedang : Hipokalemia ringan (K + 3-3.5 mEq/L)

TH/ HIPOKALEMIA Pemberian K + per oral  mudah : 40-60 mEq dpt menaikkan kadar K + 1-1.5 mEq/L Pemberian iv. ORAL POTTASIUM CHLORIDE SOLUTION 15 ML  20 mEq/L IV 15%POTTASIUM CHLORIDE 1ml  2 mEq/L 10 ml  20 mEq/L

Rumus untuk menghitung defisit kalium: K = K1 - (K0 x 0,25 x BB) K = kalium yang dibutuhkan K1 = serum kalium yang diinginkan K0 = serum kalium yang terukur BB = berat badan (kg)

PENGOBATAN K deficit= ( desired k- actual k ) x 100% 0.27 Estimation of K+ deficit 3.0 meq/L= total body K+ deficit of 200-400 meq/70kg 2.5 meq/L = 500 meq/70kg 2.0 meq/L = 700 meq/70kg ATAU K = K1 - (K0 x 0,25 x BB) K = kalium yang dibutuhkan K1 = serum kalium yang diinginkan K0 = serum kalium yang terukur BB = berat badan (kg)

Pemberian kalium Oral  Pemberian 40-60 meq dapat meningkatkan kadar kalium sebesar 1-1,5 meq/L . Pemberian 135-160 meq dapat meningkatkan kadar kalium 2,5-3,5 meq/L . IV (vena perifer)  K ecepatan pemberian KCl adalah 10 meq /jam . Konsentrasi cairan infus : KCl maksimal 60 meq dilarutkan dalam NaCl isotonic 1000 ml karena bila melebihi dapat menimbulkan rasa nyeri dan menyebabkan sclerosis vena IV (vena sentral)  K ecepatan pemberian KCl adalah 20 meq /jam atau lebih pada keadaan tertentu . Konsentrasi cairan infus : KCl maksimal 40 meq dilarutkan dalam NaCl isotonic 100 ml . Pada keadaan aritmia yang berbahaya atau adanya kelumpuhan otot pernapasan , KCl dapat diberikan dengan kecepatan 40-100 meq /jam. KCl dilarutkan sebanyak 20 meq dalam 100 ml NaCl isotonic .

Hyperkalemia Hyperkalemia (serum potassium concentration of >5.0 meq/L) can become life threatening when the serum potassium concentration exceeds 6.5 meq/L Clinical manifestations of hyperkalemia are related to changes in neuromuscular and cardiac function. muscle twitching, cramping, weakness, ascending paralysis, ECG changes (e.g., tall peaked T-waves, prolonged PR-interval, widened QRS complex, shortened QT-interval) and arrhythmias (e.g., bradyarrhythmias, ventricular fibrillation, asystole). Hyperkalemia is most commonly seen in the setting of renal insufficiency, and acute renal failure is frequently seen in ICU patients.

Pathogenesis of Hyperkalemia Best Practices in Managing Hiperkalemia, NKF Hiperkalemia

Electrocardiograph Changes Seen in Patients With Hyperkalemia* 1. Slovis C, Jenkins R. BMJ . 2002;324:1320. EKG features of hyperkalemia: 1 5.5-6.5 mEq/L: Tall peaked T waves 6.5-7.5 mEq/L: Loss of P waves 7.0-8.0 mEq/L: Widening of QRS complexes 8.0-10.0 mEq/L: Sine wave, ventricular arrhythmias, asystole *EKG changes not always present

Management Approaches to Hyperkalemia Stabilize: Evaluate patient for life-threatening toxicities Initiate EKG monitoring Ca- Gluconate Shift : Augment the shift of potassium from extra- to intracellular space Dextrose and/or insulin infusion Beta-adrenergic agonists Sodium bicarbonate Remove : Renal replacement therapy Hemodialysis CRRT Potassium binders Acute Management Remove or manage any ongoing contributors to hyperkalemia Diet Medications Co-morbid conditions Increase excretion of potassium Loop diuretics (furosemide) Mineralocorticoid accentuation Potassium binders Chronic Management CRRT, Continuous Renal Replacement Therapy Kovesdy C. Nat Rev Nephrol . 2014;10:653-662. Viera A, Wouk N. Am Fam Physician . 2015;92:487-495. Dunn J, et al. Am J Manag Care . 2015;21:s307-s315.

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