Hyperkalemia Treatment - Emedicine

March 29, 2018 | Author: Rian Segal Hidajat | Category: Potassium, Pharmacology, Clinical Medicine, Medicine, Medical Specialties


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Approach ConsiderationsThe aggressiveness of therapy for hyperkalemia is directly related to the rapidity with which the condition has developed, the absolute level of serum potassium, and the evidence of toxicity. The faster the rise in the potassium level, the higher it has reached; the greater the evidence of cardiotoxicity, the more aggressive therapy should be. If the patient has only a moderate elevation in potassium level and no electrocardiographic (ECG) abnormalities, excretion can be increased by using a cation exchange resin or diuretics, and the source of excess potassium (eg, increased intake or inhibited excretion) can be corrected.[56] In patients with severe hyperkalemia, treatment focuses on immediate stabilization of the myocardial cell membrane, rapid shifting of potassium to the intracellular space, and total body potassium elimination. In addition, all sources of exogenous potassium should be immediately discontinued; including intravenous (IV) and oral potassium supplementation, total parenteral nutrition, and any blood product transfusion. Drugs associated with hyperkalemia should also be discontinued (see Etiology).[57] Definitive therapy is hemodialysis in patients with renal failure or when pharmacologic therapy is not sufficient. Any patient with significantly elevated potassium levels should undergo dialysis; pharmacologic therapy alone is not likely to bring about adequate reduction of potassium levels in a timely fashion. After emergency management and stabilization of hyperkalemia, the patient should be hospitalized. Once the potassium level is restored to normal, the potassiumlowering therapies can be discontinued, and the serum potassium level can be monitored. Continuous cardiac monitoring should be maintained. Further workup should be initiated to determine the inciting cause and to prevent future episodes. Such a workup should include evaluation of sources of potassium intake, causes for decreased renal excretion, Pertimbangan pendekatan Agresivitas terapi untuk hiperkalemia secara langsung berhubungan dengan kecepatan dengan yang kondisi telah mengembangkan, tingkat absolut kalium serum, dan bukti toksisitas. Semakin cepat kenaikan tingkat kalium, yang lebih tinggi telah mencapai; semakin besar bukti cardiotoxicity, terapi lebih agresif harus. Jika pasien hanya memiliki ketinggian moderat dalam tingkat kalium dan tidak ada elektrokardiografi (EKG) kelainan, ekskresi dapat ditingkatkan dengan menggunakan resin kation pertukaran atau diuretik, dan sumber kalium yang berlebih (misalnya, asupan meningkat atau ekskresi menghambat) dapat dikoreksi . [56] Pada pasien dengan hiperkalemia berat, pengobatan berfokus pada stabilisasi langsung dari membran sel miokard, pergeseran cepat kalium ke ruang intraseluler, dan jumlah tubuh kalium eliminasi. Selain itu, semua sumber kalium eksogen harus segera dihentikan akan; termasuk intravena (IV) dan suplemen kalium lisan, nutrisi parenteral total, dan setiap transfusi produk darah. Obat terkait dengan hiperkalemia juga harus dihentikan (lihat Etiologi). [57] Terapi definitif hemodialisis pada pasien dengan gagal ginjal atau ketika terapi farmakologis tidak cukup. Setiap pasien dengan kadar kalium meningkat signifikan harus menjalani cuci darah; Terapi farmakologis saja tidak mungkin untuk membawa pengurangan yang cukup kadar kalium secara tepat waktu. Setelah manajemen darurat dan stabilisasi hiperkalemia, pasien harus dirawat di rumah sakit. Setelah tingkat kalium dikembalikan ke normal, terapi kalium penurun dapat dihentikan, dan tingkat kalium serum dapat dipantau. monitoring jantung terus menerus harus dipertahankan. IV bikarbonat. 4. Di departemen darurat (ED). semua 3 dari faktorfaktor etiologi berkontribusi hiperkalemia. memberikan magnesium sulfat (2 g lebih dari 5 menit) untuk pasien dengan aritmia jantung dari toksisitas digitalis. or increased renal excretion. IV bicarbonate. [57] Menghentikan setiap obat hemat kalium atau potasium diet. look for evidence of digitalis toxicity. 2. calcium. If the hyperkalemia is severe (potassium >7. sebaliknya.[17] In patients with hypotension or marked QRS widening. Dalam kebanyakan kasus. dan 24 jam setelah identifikasi dan pengobatan hiperkalemia dianjurkan. dan insulin diberikan bersama-sama dengan 50% dextrose mungkin tepat (lihat Obat). In most cases. Manajemen Darurat awal Dalam pengaturan pra-rumah sakit. and ECG findings. Initial Emergency Management In the prehospital setting. In the emergency department (ED). Begin administration of a pemeriksaan lebih lanjut harus dimulai untuk menentukan penyebab menghasut dan untuk mencegah episode masa depan. dialysis. give magnesium sulfate (2 g over 5 minutes) for patients with cardiac arrhythmias from digitalis toxicity. begin treatment before diagnostic investigation of the underlying cause. kalsium.0 mEq / L) atau jika pasien bergejala. melakukan pemantauan EKG terus menerus dengan sering cek tanda vital saat hiperkalemia dicurigai atau ketika nilai-nilai laboratorium menunjukkan hiperkalemia diterima. 6. It is particularly important to reevaluate the use of potassium supplements (including salt substitutes) in patients with renal insufficiency or in patients taking medications that impair renal excretion of potassium. Definitive loss of excess potassium can be achieved only with cation exchange resins. all 3 of those etiologic factors contribute to hyperkalemia. Individualize treatment in accordance with the patient’s presentation. instead. patients with mild hyperkalemia may not need anything more than enhancement of potassium excretion. If digoxin toxicity is suspected. and 24 hours after identification and treatment of hyperkalemia is recommended. menyebabkan untuk penurunan ekskresi ginjal. Jika pasien mengambil digoxin. dan menyebabkan untuk penurunan penyerapan sel kalium. pasien dengan hiperkalemia diketahui atau pasien dengan gagal ginjal dengan dugaan hiperkalemia harus memiliki akses IV didirikan dan harus ditempatkan pada monitor jantung. Hal ini sangat penting untuk mengevaluasi kembali penggunaan suplemen kalium (termasuk pengganti garam) pada pasien dengan insufisiensi ginjal atau pada pasien yang memakai obat yang mengganggu ekskresi ginjal kalium. glucose. 4. hindari kalsium. For example. avoid calcium. Jika toksisitas digoxin dicurigai. pemeriksaan tersebut harus mencakup evaluasi sumber asupan kalium. potassium level. memulai . 6. mencari bukti toksisitas digitalis.0 mEq/L) or if the patient is symptomatic. 2. Measurement of potassium levels at least 1. Medications such as calcium. insulin. [57] Discontinue any potassium-sparing drugs or dietary potassium. perform continuous ECG monitoring with frequent vital sign checks when hyperkalemia is suspected or when laboratory values indicative of hyperkalemia are received. Jika hiperkalemia parah (kalium> 7. If the patient is taking digoxin. [17] Pada pasien dengan hipotensi atau QRS ditandai pelebaran. Pengukuran kadar kalium setidaknya 1.and causes for decreased cell uptake of potassium. a patient with known hyperkalemia or a patient with renal failure with suspected hyperkalemia should have IV access established and should be placed on a cardiac monitor. and insulin given together with 50% dextrose may be appropriate (see Medication). and sodium bicarbonate are temporizing measures. in diabetic ketoacidosis (DKA) and many other types of metabolic acidosis. Mulailah administrasi dari resin pertukaran kation segera setelah obat lain telah diberikan. tingkat kalium. Setelah dokter memulai terapi untuk DKA. Patients with acute kidney injury and chronic kidney disease are especially susceptible. the extracellular potassium level decreases spontaneously. Remove potassium-containing salt substitutes. insulin. Watch for overcorrection of potassium level. Terapi farmakologis dan Dialisis perawatan medis hiperkalemia dapat dengan mudah dibagi menjadi komponen diskrit. duration of action is 30 minutes to an hour. hilangnya definitif kelebihan kalium dapat dicapai hanya dengan resin penukar kation. Discontinue oral and parenteral potassium supplements. Infus kalsium klorida atau kalsium glukonat (10 mL larutan 10% selama 2-3 menit). Langkah 1 Langkah pertama adalah untuk mengelola kalsium IV untuk memperbaiki toksisitas jantung. dalam format langkah-demi-langkah. Meskipun aspek-aspek yang berbeda dari pengobatan hiperkalemia tercantum secara berurutan di bawah ini. Sebagai contoh. the extracellular potassium level is elevated. Examine the patient’s diet. Continuous infusions of insulin and glucose-containing IV fluids can be used for prolonged effect. Pharmacologic Therapy and Dialysis Medical treatment of hyperkalemia may be conveniently divided into discrete components. dan temuan EKG. Onset terjadi dalam beberapa menit. dan natrium bikarbonat raguan tindakan. and the duration is variable. Step 3 The third step is to enhance potassium uptake by cells to decrease the serum concentration. tingkat kalium ekstraseluler yang ditinggikan. atau meningkat ekskresi ginjal. Perhatikan overcorrection tingkat kalium. Although these different aspects of hyperkalemia treatment are listed sequentially below. For example. namun pasien mungkin mengalami defisit tubuh total kalium. A typical regimen is 10 U of regular insulin and 50 mL of dextrose 50% in water (D50W). Hentikan suplemen . Once the clinician initiates therapy for DKA. mereka umumnya ditangani secara bersamaan. durasi kerja adalah 30 menit sampai satu jam. Individualize pengobatan sesuai dengan presentasi pasien. Measure glucose and potassium levels every 2 hours. Infuse calcium chloride or calcium gluconate (10 mL of a 10% solution over 2-3 minutes). Step 1 The first step is to administer IV calcium to ameliorate cardiac toxicity.The onset of action is within 20-30 minutes. [58] Langkah 2 Langkah kedua adalah untuk mengidentifikasi dan menghapus sumber asupan kalium. in a step-by-step format. perawatan sebelum penyelidikan diagnostik penyebab yang mendasari. Change the diet to a low-potassium tube feed or a 2-g potassium ad-lib diet. they generally are addressed simultaneously. ranging from 2 to 6 hours. tingkat kalium ekstraseluler berkurang secara spontan. glukosa. pasien dengan hiperkalemia ringan mungkin tidak perlu apa-apa lebih dari peningkatan ekskresi kalium. IV glucose and insulin infusions are very effective in enhancing potassium uptake. IV insulin (even when administered with dextrose) can cause hypoglycemia. Misalnya. Obat-obatan seperti kalsium. jika ada. di diabetic ketoacidosis (DKA) dan jenis lain dari asidosis metabolik. Onset of action occurs within minutes. dialisis.cation exchange resin soon after the other drugs have been administered.[58] Step 2 The second step is to identify and remove sources of potassium intake. if present. yet the patient may have a total body deficit of potassium. and parenteral albuterol is not available in the United States. However. dan durasi yang bervariasi.90).suatu timbulnya tindakan dalam waktu 20-30 menit. Step 4 The fourth step is to increase potassium excretion from the body. glukosa IV dan infus insulin sangat efektif dalam meningkatkan serapan kalium. Some investigators have reported tachycardia and chest discomfort with the use of beta-agonist therapy for hyperkalemia. mulai dari 2 sampai 6 jam. Terus memantau kadar glukosa selama minimal 6 jam setelah pemberian insulin-glukosa. Karena efek variabel bentuk yang berbeda dari asidosis metabolik pada tingkat serum potassium. this therapeutic modality is less effective and less predictable in producing a hypokalemic response.0%.7%.9% and 7. Tarif hipoglikemia berat adalah 8. The dose for treating hyperkalemia. Mengubah diet untuk feed tabung rendah kalium atau potasium diet ad-lib 2-g. insulin IV (bahkan bila diberikan dengan dextrose) dapat menyebabkan hipoglikemia. Tarif hipoglikemia dalam 10-U dan 5-U kelompok yang 16. 10 mg. Rates of severe hypoglycemia were 8.79).Continue monitoring glucose levels for at least 6 hours after administering insulinglucose. masing-masing (P = 0. [59] Sebuah studi retrospektif oleh Pierce dkk dari 149 pasien dengan rendah perkiraan laju filtrasi glomerulus (eGFR) yang menerima IV insulin untuk hiperkalemia tidak menemukan perbedaan yang signifikan dalam tingkat hipoglikemia (gula darah ≤70 mg / dL) atau hipoglikemia berat (<50 mg / dL) dengan 10 U vs 5 U insulin. Langkah 3 Langkah ketiga adalah untuk meningkatkan penyerapan kalium oleh sel untuk menurunkan konsentrasi serum. modalitas terapi ini kurang efektif dan kurang dapat diprediksi dalam . Because of the variable effect of different forms of metabolic acidosis on the serum potassium level.7%. the most commonly used preparation is nebulized albuterol.0%. Renal excretion is enhanced easily in patients with normal kidney function by administering IV saline kalium lisan dan parenteral. [60] asidosis metabolik yang benar dengan natrium bikarbonat. respectively (P = 0. isoproterenol is not commonly used. In the United States. Nonetheless. Rates of hypoglycemia in the 10-U and 5-U groups were 16.79).7% dan 19.7% and 19. [60] Correct metabolic acidosis with sodium bicarbonate.[59] A retrospective study by Pierce et al of 149 patients with low estimated glomerular filtration rate (eGFR) who received IV insulin for hyperkalemia found no significant difference in the rate of hypoglycemia (blood glucose ≤70 mg/dL) or severe hypoglycemia (<50 mg/dL) with 10 U versus 5 U of insulin. Beta-adrenergic agonists also are quite effective but are perhaps somewhat more controversial and more likely to produce side effects. if the acidosis is severe. Pasien dengan cedera ginjal akut dan penyakit ginjal kronis sangat rentan. Periksa diet pasien. infus kontinu insulin dan cairan glukosa yang mengandung IV dapat digunakan untuk efek yang berkepanjangan. then a trial of parenteral sodium bicarbonate therapy is warranted.90). respectively (P = 0. is substantially higher than the usual dose for the treatment of bronchospasm and requires the assistance of a respiratory therapist. Parenteral isoproterenol and albuterol also decrease potassium.9% dan 7. Sebuah rejimen khas adalah 10 U insulin reguler dan 50 mL dekstrosa 50% dalam air (D50W) . especially in patients with chronic renal failure. Mengukur glukosa dan kalium tingkat setiap 2 jam. The peak hypokalemic effect occurs at 90 minutes. Discontinue beta-adrenergic antagonists. This therapy is highly effective and is preferred to alkali therapy in patients with renal failure. Hapus pengganti garam kalium yang mengandung. masing-masing (P = 0. ekskresi ginjal ditingkatkan dengan mudah pada pasien dengan fungsi ginjal yang normal dengan pemberian IV garam disertai dengan loop diuretik (misalnya. SPS can be administered orally or rectally (as a retention enema). blocker angiotensin-receptor (ARB). dan albuterol parenteral tidak tersedia di Amerika Serikat. 63. SPS is not useful for acute control of hyperkalemia. Renal excretion can be enhanced by administration of an aldosterone analogue. secara substansial lebih tinggi dari dosis yang biasa untuk pengobatan bronkospasme dan membutuhkan bantuan dari seorang terapis pernafasan. rectal administration is preferred for hyperkalemic emergencies. postoperative patients who have not had a bowel movement since their procedure) or those who are at risk for constipation or impaction. The effectiveness of SPS is enhanced if the enema can be retained for 1 hour.[61] Sodium polystyrene sulfonate Gastrointestinal (GI) excretion can be increased through the use of cation exchange resins such as sodium polystyrene sulfonate (SPS). Usually. angiotensin-receptor blockers (ARBs). and other drugs that inhibit renal potassium excretion. Namun. Fluorohydrocortisone is especially helpful in patients with hyporeninemia or hypoaldosteronism. 10 mg. 62. angiotensin-converting enzyme (ACE) inhibitors. Memonitor status volume dan bertujuan untuk mempertahankan euvolemia. SPS can decrease serum potassium by 2 mEq/L. Discontinue potassium-sparing diuretics. Menghentikan antagonis beta-adrenergik. Efek hipokalemia puncak terjadi pada 90 menit.accompanied by a loop diuretic (eg. because its effect on potassium is delayed for at least 2 hours. and repeat doses should not be given to patients who have not passed a memproduksi respon hipokalemia. Menghentikan diuretik hemat kalium. Although SPS has a long history of use for hyperkalemia. Monitor volume status and aim to maintain euvolemia. such as 9-alpha fluorohydrocortisone acetate. Meskipun demikian. isoproterenol tidak umum digunakan. persiapan yang paling umum digunakan adalah albuterol nebulasi. seperti 9- . ekskresi ginjal dapat ditingkatkan dengan pemberian analog aldosteron. Because the major site of action for this drug is the colon. 56] The US Food and Drug Administration (FDA) advises against its use in patients who do not have normal bowel function (eg. serum potassium returns to normal after about 48 hours. Dosis untuk mengobati hiperkalemia. Langkah 4 Langkah keempat adalah untuk meningkatkan ekskresi kalium dari tubuh. furosemide). dan obat lain yang menghambat ekskresi potassium ginjal.[64] SPS should be discontinued in patients who become constipated. jika asidosis parah. furosemide). with little inconvenience to patients. Di Amerika Serikat.[59. Beberapa peneliti telah melaporkan takikardia dan ketidaknyamanan dada dengan penggunaan terapi beta-agonist untuk hiperkalemia. Oral SPS is useful in patients with advanced renal failure who are not yet on dialysis or transplant candidates. It has been increasingly used in solid-organ transplant recipients who have chronic hyperkalemia from calcineurin inhibitor use. maka uji coba terapi natrium bikarbonat parenteral dibenarkan. isoproterenol parenteral dan albuterol juga menurunkan kalium. terutama pada pasien dengan gagal ginjal kronis. agonis beta-adrenergik juga cukup efektif tetapi mungkin agak lebih kontroversial dan lebih mungkin untuk menghasilkan efek samping. its safety and efficacy have been questioned. One or more daily doses of 15 g can control mild to moderate hyperkalemia effectively. Terapi ini sangat efektif dan lebih disukai untuk terapi alkali pada pasien dengan gagal ginjal. enzyme (ACE) inhibitor angiotensin-converting. peaking at 4-6 hours. memuncak pada 4-6 jam. reduced recurrent hyperkalemia in patients with chronic kidney disease (CKD) and heart failure who were hyperkalemic while taking renin-angiotensinaldosterone system inhibitors (RAASi). an osmotic cathartic used to prevent fecal impaction from SPS and to speed delivery of resin to the colon. SPS dapat diberikan secara oral atau rektal (sebagai enema retensi). dengan sedikit ketidaknyamanan kepada pasien. Patients whose K(+) levels were ≥3.[64] Current evidence indicates that this serious side effect can occur with SPS even when preparation does not contain any sorbitol. pasien pasca operasi yang belum memiliki buang air besar karena prosedur mereka) atau mereka yang berisiko untuk sembelit atau impaksi. It should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action. patiromer was given to patients with CKD who were taking RAASi and had serum K(+) levels >5. karena efeknya pada kalium tertunda selama minimal 2 jam. Karena situs utama tindakan untuk obat ini adalah usus besar. dan . It increases fecal potassium excretion by binding potassium in the lumen of the GI tract. SPS tidak berguna untuk kontrol akut hiperkalemia. alpha fluorohydrocortisone asetat. lasting through 52 week. Biasanya. In addition.1 mEq/L at the end of week 4 entered an 8-week randomized withdrawal phase and were randomly assigned to continue patiromer or switch to placebo. Telah semakin digunakan dalam penerima transplantasi solid-organ yang memiliki hiperkalemia kronis dari penggunaan calcineurin inhibitor. administrasi dubur lebih disukai untuk keadaan darurat hyperkalemic.1 mEq/L to <6. FDA approval of patiromer was based on the AMETHYST-DN trial. kalium serum kembali normal setelah sekitar 48 jam. decreased serum K(+) .[65] Patiromer Patiromer sorbitex calcium (Veltassa) is a nonabsorbed.001). The median increase in serum K(+) from baseline of the withdrawal phase was greater with placebo (n = 22) than patiromer (n = 27) (P < 0. The primary efficacy endpoint was the between-group difference in median change in the serum K(+) over the first 4 weeks of the withdrawal phase. Meskipun SPS memiliki sejarah panjang digunakan untuk hiperkalemia. Fluorohydrocortisone sangat membantu pada pasien dengan hyporeninemia atau hypoaldosteronism. Results showed that among patients with hyperkalemia and diabetic kidney disease taking RAAS inhibitors. In the study. Satu atau lebih dosis harian dari 15 g dapat mengontrol ringan sampai sedang hiperkalemia efektif. 63. [61] Sodium polystyrene sulfonate Gastrointestinal (GI) ekskresi dapat ditingkatkan melalui penggunaan resin pertukaran kation seperti natrium polistiren sulfonat (SPS). It is indicated for hyperkalemia.8 mEq/L to <5. Recurrent hyperkalemia (serum K(+) . cation exchange polymer that contains a calcium-sorbitol counterion. compared with placebo. [59. some of them fatal. patiromer resulted in statistically significant decreases in serum potassium level after 4 weeks of treatment. [64] SPS harus dihentikan pada pasien yang mengalami konstipasi. SPS dapat menurunkan kalium serum oleh 2 mEq / L. 62.5 mEq/L (n=243) for 4 weeks. the FDA cautions that giving SPS with sorbitol. has been associated with cases of intestinal necrosis. Oral SPS berguna pada pasien dengan gagal ginjal canggih yang belum dialisis atau transplantasi kandidat. and. 56] The US Food and Drug Administration (FDA) menyarankan terhadap penggunaannya pada pasien yang tidak memiliki fungsi usus yang normal (misalnya.[72] The OPAL-HK trial showed patiromer was well tolerated. Efektivitas SPS ditingkatkan jika enema dapat dipertahankan selama 1 jam. keamanan dan kemanjuran telah dipertanyakan.bowel movement. .[73] Step 5 The fifth step is emergency dialysis. polimer tukar kation yang berisi ion lawan kalsium-sorbitol. [64] sekarang bukti menunjukkan bahwa efek samping yang serius ini dapat terjadi dengan SPS bahkan ketika persiapan tidak mengandung sorbitol apapun. yang berlangsung melalui 52 minggu. Hasil penelitian menunjukkan bahwa di antara pasien dengan hiperkalemia dan ginjal diabetes penyakit mengambil Raas inhibitor. even if dialysis is contemplated.[67] Complications of Treatment Complications of therapy include the following: Failure to control hyperkalemia Hypokalemia due to excessively aggressive therapy Hypercalcemia due to excessive calcium administration Hypocalcemia from excessive bicarbonate therapy ulangi dosis tidak harus diberikan kepada pasien yang belum melewati buang air besar.5 mEq/L) occurred in 52% on placebo and 8% on patiromer (P < 0. persetujuan FDA dari patiromer didasarkan pada percobaan AMETHYSTDN. Patients without end-stage renal disease who require hemodialysis for control of hyperkalemia require placement of a hemodialysis catheter for emergency dialysis. tumor debulking may be considered as a means of decreasing the risk of hyperkalemia from tumor lysis syndrome. patiromer mengakibatkan penurunan signifikan secara statistik pada tingkat kalium serum setelah 4 minggu pengobatan. Selain itu. patiromer diberikan kepada pasien dengan CKD yang mengambil RAASi dan memiliki .[66] In patients with solid tumors. Hal ini meningkatkan ekskresi kalium tinja dengan mengikat kalium dalam lumen saluran pencernaan. Initiation of dialysis can often take several hours.≥5. dibandingkan dengan plasebo. This should include examination of the following: Sources of potassium intake Causes of decreased renal excretion Causes for impaired cellular uptake Surgical Therapy Surgical intervention generally is not needed for the care of a patient with hyperkalemia. Patients with metabolic acidosis and consequent hyperkalemia due to ischemic gut obviously require exploration. Ini tidak boleh digunakan sebagai pengobatan darurat untuk hiperkalemia yang mengancam jiwa karena onset tertunda aksi. Dalam studi tersebut. sebuah katarsis osmotik digunakan untuk mencegah impaksi tinja dari SPS dan untuk mempercepat pengiriman resin ke usus.001). beberapa dari mereka yang fatal. Patients with hyperkalemia due to rhabdomyolysis may need surgical decompression of swollen. [65] Patiromer Patiromer sorbitex kalsium (Veltassa) adalah Selebihnya. mengurangi hiperkalemia berulang pada pasien dengan penyakit ginjal kronis (CKD) dan gagal jantung yang hyperkalemic saat mengambil sistem renin-angiotensin-aldosteron inhibitor (RAASi). therefore. The final step in the medical management of hyperkalemia is to determine the cause of hyperkalemia in order to prevent future episodes. the other therapeutic modalities should be instituted as a bridge to dialysis. ischemic muscle compartments. telah dikaitkan dengan kasus nekrosis usus. FDA memperingatkan bahwa pemberian SPS dengan sorbitol. [72] The OPAL-HK percobaan menunjukkan patiromer ditoleransi. dan. Hal ini diindikasikan untuk hiperkalemia. this is a final recourse for patients who are experiencing potentially lethal hyperkalemia that is unresponsive to more conservative measures or for patients who have complete renal failure. penurunan serum K (+). In particular.50. Pasien dengan hiperkalemia karena rhabdomyolysis mungkin perlu dekompresi bedah bengkak.5 mEq / L) terjadi pada 52% pada plasebo dan 8% pada patiromer (P <0. Consultations For patients with severe hyperkalemia or serum K (+) tingkat> 5.[12] The investigators found that for monitored patients with diabetes alone.1 mEq / L pada akhir minggu 4 memasuki 8 minggu acak fase penarikan dan secara acak ditugaskan untuk melanjutkan patiromer atau beralih ke plasebo. Tujuan utama kemanjuran adalah perbedaan antara kelompok dalam perubahan median di K serum (+) selama 4 minggu pertama fase penarikan. potassium intake must be closely monitored (and possibly restricted) in patients with renal failure. No restrictions on activity are necessary unless continuous monitoring for cardiotoxicity is required. Pasien yang K (+) tingkat yang ≥3.355 patients with diabetes. Adjust medications that predispose to or exacerbate hyperkalemia. Pasien dengan asidosis metabolik dan hiperkalemia akibat karena usus iskemik jelas membutuhkan eksplorasi. Langkah terakhir dalam manajemen medis hiperkalemia adalah untuk menentukan penyebab dari hiperkalemia untuk mencegah episode masa depan. hiperkalemia berulang (serum K (+).001). metabolic alkalosis.1 mEq / L untuk <6.001). Raebel et al concluded that potassium monitoring can reduce the incidence of serious hyperkalemia-associated adverse events in patients with diabetes and chronic kidney disease who are undergoing reninangiotensin-aldosterone system inhibitor therapy. Peningkatan median di serum K (+) dari awal dari fase penarikan lebih besar dengan plasebo (n = 22) dari patiromer (n = 27) (P <0. including salt substitutes. Oleh karena itu.5 mEq / L (n = 243) selama 4 minggu. hypocalcemia.Chest discomfort or tachycardia due to betaagonist therapy Hypoglycemia or hyperglycemia complicating glucose and insulin administration Metabolic alkalosis and tetany due to excessive sodium bicarbonate administration Volume depletion.8 mEq / L untuk <5. and hypophosphatemia due to aggressive loop diuretic use Colon perforation due to exchange resin administration Treatment of pseudohyperkalemia may result in hypokalemia. Diet and Activity A low-potassium diet containing 2 g of potassium is recommended so as to minimize potassium intake in patients at risk for hyperkalemia. Inisiasi dialisis sering dapat memakan waktu beberapa jam. . thus. kompartemen otot iskemik. Ini harus mencakup pemeriksaan berikut: Sumber asupan kalium Penyebab ekskresi ginjal menurun Penyebab serapan seluler terganggu Terapi bedah intervensi bedah umumnya tidak diperlukan untuk perawatan pasien dengan hiperkalemia. whereas for monitored patients who also had chronic kidney disease. the adjusted relative risk was 0. bahkan jika dialisis direnungkan. treatment of non–lifethreatening hyperkalemia should be deferred pending verification of hyperkalemia. ≥5. hypomagnesemia. Adjust the diet to decrease potassium dietary load. the adjusted relative risk was 0. Prevention Inform patients at risk for hyperkalemia about dietary sources of potassium.29. In a retrospective observational study of 27. modalitas terapi lainnya harus dilembagakan sebagai jembatan untuk dialisis. [73] Langkah 5 Langkah kelima adalah dialisis darurat. renal insufficiency. ini adalah jalan terakhir bagi pasien yang mengalami berpotensi hiperkalemia mematikan yang tidak responsif terhadap langkah-langkah yang lebih konservatif atau untuk pasien yang mengalami gagal ginjal lengkap. dengan demikian. the treatment of choice is a thiazide diuretic. The risk of severe hypoglycemia for patients Pasien tanpa penyakit ginjal stadium akhir yang membutuhkan hemodialisis untuk menguasai hiperkalemia memerlukan penempatan kateter hemodialisis untuk cuci darah darurat. dan hypophosphatemia karena penggunaan lingkaran diuretik agresif Colon perforasi karena administrasi resin pertukaran Pengobatan pseudohyperkalemia dapat mengakibatkan hipokalemia. Diet dan Aktivitas Sebuah diet rendah kalium yang mengandung 2 g kalium dianjurkan untuk meminimalkan asupan kalium pada pasien dengan risiko hiperkalemia. hipomagnesemia. In addition. However. Secara khusus. those with diabetic nephropathy and type IV renal tubular acidosis). monthly measurements are indicated. which requires close regulation of potassium and sodium intake Endocrinologist – For suspected mineralocorticoid abnormalities (eg. these patients should be admitted to an intensive care unit (ICU). pengobatan hiperkalemia-nonmengancam nyawa harus ditangguhkan verifikasi tertunda dari hiperkalemia. insufisiensi ginjal. For pseudohypoaldosteronism type II. clearly defined episode (eg. infrequent monitoring of serum potassium generally suffices. [67] Komplikasi Pengobatan Komplikasi terapi meliputi berikut ini: Kegagalan untuk mengontrol hiperkalemia Hipokalemia karena terapi berlebihan agresif Hiperkalsemia karena administrasi kalsium yang berlebihan Hipokalsemia dari terapi bikarbonat yang berlebihan Dada ketidaknyamanan atau takikardia karena terapi beta-agonist Hipoglikemia atau hiperglikemia menyulitkan glukosa dan pemberian insulin alkalosis metabolik dan tetani karena administrasi bikarbonat natrium yang berlebihan deplesi volume. For patients at high risk.renal failure.For emergency pacemaker placement in patients with refractory heart block Hematologist/oncologist – For hyperkalemia resulting from tumor lysis syndrome Nutritional support specialist . acute exertional rhabdomyolysis or druginduced hemolysis). alkalosis metabolik. hipokalsemia. For patients who have recurrent or constant hyperkalemia (eg.For hyperkalemia caused by renal failure. asupan kalium harus diawasi secara ketat (dan mungkin . Consultations with the following specialists may be necessary in cases of hyperkalemia that result from certain conditions or disease states: Pediatric intensivist or neonatologist – For life-threatening hyperkalemia (hyperkalemia with ECG changes) in infants and children Social services specialist – For hyperkalemia developing in children after unintentional ingestions or poisonings Cardiologist . congenital adrenal hyperplasia) Long-Term Monitoring For patients whose hyperkalemia resulted from a single. early consultation with a nephrologist for aid in implementing efficient therapy and plans for dialysis is highly recommended. debulking tumor dapat dianggap sebagai cara untuk mengurangi risiko hiperkalemia dari sindrom lisis tumor. Continuing care relates to the disease process that led to the hyperkalemia. [66] Pada pasien dengan tumor padat. long-term therapy with an oral loop diuretic and SPS may be indicated. for patients who have conditions or medications that will continue to predispose to hyperkalemia. more frequent monitoring of serum potassium is required. dibatasi) pada pasien dengan gagal ginjal.[68] In patients with salt-wasting congenital adrenal hyperplasia. Pencegahan Menginformasikan pasien pada risiko hiperkalemia tentang sumber makanan kalium. risiko relatif disesuaikan adalah 0. Sufficient dextrose in the patient’s treatment regimen can minimize the risk. corticosteroid and mineralocorticoid supplementation are necessary.with acute kidney injury or end-stage renal disease is heightened in patients with lower body weight and creatinine clearance. pasien ini harus dirawat di unit perawatan intensif (ICU). awal konsultasi dengan nephrologist untuk bantuan dalam menerapkan terapi efisien dan rencana untuk dialisis sangat dianjurkan. [ 12] para peneliti menemukan bahwa pasien yang dipantau dengan diabetes saja. konsultasi Untuk pasien dengan hiperkalemia berat atau gagal ginjal. Tidak ada pembatasan aktivitas yang diperlukan kecuali pemantauan terus menerus untuk cardiotoxicity diperlukan.29. sedangkan untuk pasien dipantau yang juga memiliki penyakit ginjal kronis.355 pasien dengan diabetes. Mengatur pola makan untuk mengurangi beban diet kalium. Menyesuaikan obat yang mempengaruhi atau memperburuk hiperkalemia.50.Untuk hiperkalemia berkembang pada anak- . termasuk pengganti garam. Selain itu. Raebel et al menyimpulkan bahwa pemantauan kalium dapat mengurangi kejadian efek samping yang serius hiperkalemia terkait pada pasien dengan diabetes dan penyakit ginjal kronis yang menjalani terapi sistem inhibitor renin-angiotensin-aldosteron. Konsultasi dengan spesialis berikut mungkin diperlukan dalam kasus hiperkalemia akibat kondisi tertentu atau keadaan penyakit: intensivist pediatrik atau neonatologist Untuk yang mengancam jiwa hiperkalemia (hiperkalemia dengan perubahan EKG) pada bayi dan anak-anak spesialis layanan sosial . Dalam sebuah penelitian observasional retrospektif 27. risiko relatif disesuaikan adalah 0. terapi jangka panjang dengan loop diuretik lisan dan SPS dapat diindikasikan.Untuk hiperkalemia akibat sindrom lisis tumor Gizi dukungan spesialis . pengukuran bulanan ditunjukkan. pilihan pengobatan adalah diuretik thiazide. untuk pasien yang memiliki kondisi atau obat yang akan terus predisposisi hiperkalemia.Untuk dicurigai kelainan mineralokortikoid (misalnya. pemantauan lebih sering kalium serum diperlukan. hiperplasia adrenal kongenital) Pemantauan Jangka Panjang Untuk pasien yang hiperkalemia dihasilkan dari satu.anak setelah ingestions disengaja atau keracunan Ahli jantung . Untuk pasien dengan risiko tinggi. monitoring jarang kalium serum umumnya sudah cukup.Untuk hiperkalemia disebabkan oleh gagal ginjal.Untuk penempatan alat pacu jantung darurat pada pasien dengan blok jantung refrakter Hematologi / onkologi . Medication Summary . [68] Pada pasien dengan hiperplasia garam-buang adrenal kongenital. rhabdomyolysis exertional akut atau hemolisis obat-induced). episode yang jelas (misalnya. Melanjutkan perawatan berhubungan dengan proses penyakit yang menyebabkan hiperkalemia tersebut. Risiko hipoglikemia berat untuk pasien dengan cedera ginjal atau stadium akhir penyakit ginjal akut meningkat pada pasien dengan berat badan rendah dan kreatinin. kortikosteroid dan suplemen mineralokortikoid yang diperlukan. Untuk pseudohypoaldosteronism tipe II. Namun. dekstrosa cukup dalam rejimen pengobatan pasien dapat meminimalkan risiko. yang membutuhkan regulasi dekat asupan kalium dan natrium Endokrinologi . orang-orang dengan nefropati diabetik dan tipe IV asidosis tubulus ginjal). Untuk pasien yang memiliki berulang atau konstan hiperkalemia (misalnya. 5 mEq) of elemental calcium. However. whereas 1 g of calcium gluconate has 90 mg (4. Calcium has no effect on the serum level of potassium. these agonists stimulate the sodium-potassium–adenosine triphosphatase (Na+ -K+ -ATPase) pump. Other calcium salts (eg. Therefore. and duration of action is about 30-60 minutes. and loop diuretics stimulate cellular uptake of potassium. Beta-adrenergic agonists Class Summary Through activation of cyclic adenosine monophosphate (cAMP). Onset of effect is rapid (≤ 15 minutes) but relatively short-lived. calcium chloride is preferred to calcium gluconate. For that reason. calcium chloride is generally considered a second choice. Calcium usually is not indicated when the ECG shows only peaked T waves. widening of QRS interval.The goals of pharmacotherapy are to reduce potassium levels and morbidity and to prevent complications. repeat the dose if ECG changes do not normalize within 3-5 minutes. View full drug information Calcium gluconate Calcium increases the threshold potential. thus restoring the normal gradient between threshold potential and resting membrane potential. View full drug information Calcium chloride Calcium prevents the deleterious cardiac effects of severe hyperkalemia that may occur before the serum potassium level is corrected. which is abnormally elevated in hyperkalemia. Calcium salts Class Summary Calcium antagonizes the cardiotoxicity of hyperkalemia by stabilizing the cardiac cell membrane against undesirable depolarization. Beta-adrenergic agents. lowering the serum potassium level. >7 mEq/L). Because of its irritating effects when administered parenterally. after calcium gluconate.5 mEq). administration of calcium should be accompanied by the use of other therapies that actually help lower serum potassium levels. . when hyperkalemia is accompanied by hemodynamic compromise. glubionate and gluceptate) have even less elemental calcium than calcium gluconate and generally are not recommended for therapy of hyperkalemia. Doses should be titrated with constant monitoring of ECG changes during administration. thereby shifting potassium into the intracellular compartment. Calcium protects the myocardium from the deleterious effects of hyperkalemia. Calcium chloride contains about 3 times more elemental calcium than an equal volume of calcium gluconate: 1 g of calcium chloride has 270 mg (13. These agents are the first-line treatment for severe hyperkalemia (ie. when the electrocardiogram (ECG) shows significant abnormalities (eg. insulin. or cardiac arrhythmias). Onset of action is within 5 minutes. loss of P wave. Although the effect is rapid. Monitor blood sugar levels frequently. until the desired diuresis occurs. and its effect on lowering the potassium level is inconsistent. potassium. Diuretics. and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Humulin R) Regular insulin stimulates cellular uptake of potassium within 20-30 minutes and lasts for 4-6 hours. administer in increments of 20-40 mg. Vospire ER) Albuterol is an adrenergic agonist that has an additive effect with insulin and glucose. depending on the response. View full drug information Insulin regular human (Novolin R. primarily by enhancing the activity of the Na+ -K+ -ATPase pump and thereby temporarily lowering serum potassium levels. Large doses may be needed in renal failure. which may in turn help shift potassium into the intracellular space. Antidiabetics. Administer glucose along with insulin to prevent hypoglycemia. Parenterally administered drugs have a more rapid onset of action and are preferable in emergency situations. Insulins Class Summary Insulin is administered with glucose to facilitate the uptake of glucose into muscle cells. When treating infants and children.5-1. Simultaneous administration of saline can prevent severe volume depletion. insulin therapy should be followed by therapy that actually enhances potassium clearance (eg. Onset of action is 30 minutes. give 1-2 mg/kg every 6-12 hours.5 mEq/L. which. in turn. The serum potassium concentration typically drops by 0. This agent lowers the serum potassium level by 0. sodium polystyrene sulfonate [SPS]). Individualize the dose to the patient.5-1.these shifts in potassium occur primarily during exercise rather than at rest. . Ventolin. inhibits sodium. bringing potassium with it. it is temporary. duration of action is 4-6 hours for the immediate-release product.2 mEq/L. Furosemide has a slow onset of action (frequently 1 hour). If the diuretic response is not satisfactory. View full drug information Albuterol (Proventil. It can be very beneficial in patients with renal failure when fluid overload is concern. Loop Class Summary Loop diuretics markedly enhance renal potassium excretion and thus lower serum levels. View full drug information Furosemide (Lasix) Furosemide increases excretion of water by interfering with the chloride-binding cotransport system. therefore. furosemide may be titrated in increments of 1 mg/kg (no sooner than 2 hours after the previous dose) until a satisfactory effect is achieved (up to 6 mg/kg). For the treatment of edema. no sooner than 6-8 hours after the previous dose. a second dose may be given after 2-4 hours. decreasing the total body potassium level by approximately 0. they generally are not required for treatment of hyperkalemia. administer a second or third dose at 2-3 hour intervals. in turn. potassium. start at 0. Do not use SPS as a first-line therapy for severe life-threatening hyperkalemia. Potassium Binders View full drug information Sodium polystyrene sulfonate (Kayexalate. cation exchange polymer that .Oral absorption of furosemide varies from person to person. Typically. Kalexate. Concomitant use of sorbitol with sodium polystyrene sulfonate has been implicated in cases of colonic necrosis.5-1 mg/kg IV. which. The duration of action is 4-6 hours. a new injection site should be used so as to avoid possible thrombophlebitis. Klonex. Onset of action ranges from 2 to 24 hours after oral administration and is even longer after rectal administration. Individualize the dose to the patient.5-1 mg IV or intramuscularly (IM). which in turn inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. 1 dose is all that is needed. The US Food and Drug Administration (FDA) notes that SPS has been associated with intestinal necrosis and other serious gastrointestinal (GI) complications and advises against its use in patients who do not have normal bowel function. View full drug information Bumetanide (Bumex) Bumetanide increases excretion of water by interfering with the chloride-binding cotransport system. For second doses. Titrate to a maximum dosage of 10 mg/day. Multiple doses are usually necessary. however. Rarely. and chloride reabsorption in the ascending loop of Henle and distal renal tubule. For treatment of edema in adults. SPS) SPS exchanges sodium for potassium and binds it in the gut. if the desired response is not achieved. If the patient requires rapid and effective therapy. primarily in the large intestine.[62] View full drug information Patiromer (Veltassa) Patiromer sorbitex calcium is a nonabsorbed. however. dosages as high as 20 mg/day are used for edema in patients with renal impairment. Single IV doses higher than 100 mg are not recommended. Continuous infusion of furosemide (at rates as high as 40 mg/hr) is occasionally used for severe edema but rarely is required for the treatment of hyperkalemia. start at 0. occasionally. For treatment of edema in adults. the intravenous (IV) route is preferred. inhibits sodium. use it in the second stage of therapy. View full drug information Ethacrynic acid (Edecrin) Ethacrynic acid increases excretion of water by interfering with the chloridebinding cotransport system.5-1 mEq/L. magnesium 10-30 mEq/day. potassium 60-180 mEq/day. Alkalinizing Agents Class Summary In patients with severe metabolic acidosis. however. The adult dose for hyperkalemia is 50 mEq IV over 5 minutes.2% solution in children younger than 2 years. This agent also increases sodium delivery to the kidney. duration of action is approximately 15-30 minutes. Consider methods of enhancing potassium removal or excretion. as appropriate.contains a calcium-sorbitol counterion. which assists in potassium excretion. View full drug information Sodium bicarbonate The bicarbonate ion neutralizes hydrogen ions and raises urinary and blood pH. It is indicated for hyperkalemia. View full drug information Magnesium sulfate Magnesium is a cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. Use the 8. It also enhances the effectiveness of insulin in patients with acidemia. By increasing the pH. It should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action. These agents have been successfully used in the treatment of acute overdose of slow-release oral potassium preparations. sodium bicarbonate promotes a temporary potassium shift from the extracellular to the intracellular environment. though it is less likely to be effective in this context. The following formula may be used to estimate the dose that should be administered for metabolic acidosis: HCO3− (mEq) = 0.5 (L/kg) × weight (kg) × (24 − serum HCO3− [mEq/L]) This formula has many limitations. and phosphate 10-40 mmol/day may be necessary for optimum metabolic response.4% solution in adults and children and the 4. Onset of action occurs within minutes. Electrolytes Class Summary Magnesium sulfate is used for hyperkalemic patients with cardiac arrhythmias from digitalis toxicity. sodium bicarbonate IV is used as a buffer that breaks down to water and carbon dioxide after binding free hydrogen ions. In adults. It increases fecal potassium excretion by binding potassium in the lumen of the GI tract. Monitor blood pH to avoid excess alkalosis. Give IV for acute suppression of torsades de . The use of sodium bicarbonate can be considered in treatment of hyperkalemia even in the absence of metabolic acidosis. it allows the practitioner to make a rough determination of the amount of bicarbonate required and subsequently to titrate against the pH and anion gap. pointes. Repeat doses are dependent on the continuing presence of patellar reflex and adequate respiratory function. .
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