Approach Considerations

The 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.

and causes for decreased cell uptake of

potassium. In most cases, all 3 of those
etiologic factors contribute to hyperkalemia. 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.

Initial Emergency
Management
In the prehospital setting, 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.[17] In patients with
hypotension or marked QRS widening, IV
bicarbonate, calcium, and insulin given
together with 50% dextrose may be
appropriate (see Medication). If digoxin
toxicity is suspected, avoid calcium; instead,
give magnesium sulfate (2 g over 5 minutes)
for patients with cardiac arrhythmias from
digitalis toxicity.
In the emergency department (ED), perform
continuous ECG monitoring with frequent
vital sign checks when hyperkalemia is
suspected or when laboratory values
indicative of hyperkalemia are received.
Measurement of potassium levels at least 1,
2, 4, 6, and 24 hours after identification and
treatment of hyperkalemia is recommended.
[57]

Discontinue any potassium-sparing drugs or

dietary potassium. If the patient is taking
digoxin, look for evidence of digitalis toxicity.
If the hyperkalemia is severe (potassium >7.0
mEq/L) or if the patient is symptomatic, begin
treatment before diagnostic investigation of
the underlying cause. Individualize treatment
in accordance with the patients presentation,
potassium level, and ECG findings. For
example, patients with mild hyperkalemia
may not need anything more than
enhancement of potassium excretion.
Medications such as calcium, insulin,
glucose, and sodium bicarbonate are
temporizing measures. Definitive loss of
excess potassium can be achieved only with
cation exchange resins, dialysis, or increased
renal excretion. Begin administration of a

pemeriksaan lebih lanjut harus dimulai

untuk menentukan penyebab menghasut
dan untuk mencegah episode masa
depan. pemeriksaan tersebut harus
mencakup evaluasi sumber asupan
kalium, menyebabkan untuk penurunan
ekskresi ginjal, dan menyebabkan untuk
penurunan penyerapan sel kalium. Dalam
kebanyakan kasus, semua 3 dari faktorfaktor etiologi berkontribusi hiperkalemia.
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.
Manajemen Darurat awal
Dalam pengaturan pra-rumah sakit,
pasien dengan hiperkalemia diketahui
atau pasien dengan gagal ginjal dengan
dugaan hiperkalemia harus memiliki
akses IV didirikan dan harus ditempatkan
pada monitor jantung. [17] Pada pasien
dengan hipotensi atau QRS ditandai
pelebaran, IV bikarbonat, kalsium, dan
insulin diberikan bersama-sama dengan
50% dextrose mungkin tepat (lihat Obat).
Jika toksisitas digoxin dicurigai, hindari
kalsium; sebaliknya, memberikan
magnesium sulfat (2 g lebih dari 5 menit)
untuk pasien dengan aritmia jantung dari
toksisitas digitalis.
Di departemen darurat (ED), melakukan
pemantauan EKG terus menerus dengan
sering cek tanda vital saat hiperkalemia
dicurigai atau ketika nilai-nilai
laboratorium menunjukkan hiperkalemia
diterima. Pengukuran kadar kalium
setidaknya 1, 2, 4, 6, dan 24 jam setelah
identifikasi dan pengobatan hiperkalemia
dianjurkan. [57]
Menghentikan setiap obat hemat kalium
atau potasium diet. Jika pasien
mengambil digoxin, mencari bukti
toksisitas digitalis.
Jika hiperkalemia parah (kalium> 7,0 mEq
/ L) atau jika pasien bergejala, memulai

cation exchange resin soon after the other

drugs have been administered.
Watch for overcorrection of potassium level.
For example, in diabetic ketoacidosis (DKA)
and many other types of metabolic acidosis,
the extracellular potassium level is elevated,
yet the patient may have a total body deficit
of potassium. Once the clinician initiates
therapy for DKA, the extracellular potassium
level decreases spontaneously.

Pharmacologic Therapy
and Dialysis
Medical treatment of hyperkalemia may be
conveniently divided into discrete
components. Although these different aspects
of hyperkalemia treatment are listed
sequentially below, in a step-by-step format,
they generally are addressed simultaneously.
Step 1
The first step is to administer IV calcium to
ameliorate cardiac toxicity, if present. Infuse
calcium chloride or calcium gluconate (10 mL
of a 10% solution over 2-3 minutes). Onset of
action occurs within minutes; duration of
action is 30 minutes to an hour.[58]
Step 2
The second step is to identify and remove
sources of potassium intake. Discontinue oral
and parenteral potassium supplements.
Remove potassium-containing salt
substitutes. Examine the patients diet.
Change the diet to a low-potassium tube feed
or a 2-g potassium ad-lib diet.
Step 3
The third step is to enhance potassium
uptake by cells to decrease the serum
concentration. IV glucose and insulin
infusions are very effective in enhancing
potassium uptake. A typical regimen is 10 U
of regular insulin and 50 mL of dextrose 50%
in water (D50W).The onset of action is within
20-30 minutes, and the duration is variable,
ranging from 2 to 6 hours. Continuous
infusions of insulin and glucose-containing IV
fluids can be used for prolonged effect.
IV insulin (even when administered with
dextrose) can cause hypoglycemia. Patients
with acute kidney injury and chronic kidney
disease are especially susceptible. Measure
glucose and potassium levels every 2 hours.

perawatan sebelum penyelidikan

diagnostik penyebab yang mendasari.
Individualize pengobatan sesuai dengan
presentasi pasien, tingkat kalium, dan
temuan EKG. Sebagai contoh, pasien
dengan hiperkalemia ringan mungkin
tidak perlu apa-apa lebih dari
peningkatan ekskresi kalium.
Obat-obatan seperti kalsium, insulin,
glukosa, dan natrium bikarbonat raguan
tindakan. hilangnya definitif kelebihan
kalium dapat dicapai hanya dengan resin
penukar kation, dialisis, atau meningkat
ekskresi ginjal. Mulailah administrasi dari
resin pertukaran kation segera setelah
obat lain telah diberikan.
Perhatikan overcorrection tingkat kalium.
Misalnya, di diabetic ketoacidosis (DKA)
dan jenis lain dari asidosis metabolik,
tingkat kalium ekstraseluler yang
ditinggikan, namun pasien mungkin
mengalami defisit tubuh total kalium.
Setelah dokter memulai terapi untuk DKA,
tingkat kalium ekstraseluler berkurang
secara spontan.
Terapi farmakologis dan Dialisis
perawatan medis hiperkalemia dapat
dengan mudah dibagi menjadi komponen
diskrit. Meskipun aspek-aspek yang
berbeda dari pengobatan hiperkalemia
tercantum secara berurutan di bawah ini,
dalam format langkah-demi-langkah,
mereka umumnya ditangani secara
bersamaan.
Langkah 1
Langkah pertama adalah untuk
mengelola kalsium IV untuk memperbaiki
toksisitas jantung, jika ada. Infus kalsium
klorida atau kalsium glukonat (10 mL
larutan 10% selama 2-3 menit). Onset
terjadi dalam beberapa menit; durasi
kerja adalah 30 menit sampai satu jam.
[58]
Langkah 2
Langkah kedua adalah untuk
mengidentifikasi dan menghapus sumber
asupan kalium. Hentikan suplemen

Continue monitoring glucose levels for at

least 6 hours after administering insulinglucose.[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.
Rates of hypoglycemia in the 10-U and 5-U
groups were 16.7% and 19.7%, respectively
(P = 0.79). Rates of severe hypoglycemia
were 8.9% and 7.0%, respectively (P =
0.90). [60]
Correct metabolic acidosis with sodium
bicarbonate. Because of the variable effect of
different forms of metabolic acidosis on the
serum potassium level, this therapeutic
modality is less effective and less predictable
in producing a hypokalemic response,
especially in patients with chronic renal
failure. Nonetheless, if the acidosis is severe,
then a trial of parenteral sodium bicarbonate
therapy is warranted.
Beta-adrenergic agonists also are quite
effective but are perhaps somewhat more
controversial and more likely to produce side
effects. In the United States, the most
commonly used preparation is nebulized
albuterol. The dose for treating hyperkalemia,
10 mg, is substantially higher than the usual
dose for the treatment of bronchospasm and
requires the assistance of a respiratory
therapist. The peak hypokalemic effect
occurs at 90 minutes. This therapy is highly
effective and is preferred to alkali therapy in
patients with renal failure.
Parenteral isoproterenol and albuterol also
decrease potassium. However, isoproterenol
is not commonly used, and parenteral
albuterol is not available in the United States.
Some investigators have reported
tachycardia and chest discomfort with the use
of beta-agonist therapy for hyperkalemia.
Discontinue beta-adrenergic antagonists.
Step 4
The fourth step is to increase potassium
excretion from the body. Renal excretion is
enhanced easily in patients with normal
kidney function by administering IV saline

kalium lisan dan parenteral. Hapus

pengganti garam kalium yang
mengandung. Periksa diet pasien.
Mengubah diet untuk feed tabung rendah
kalium atau potasium diet ad-lib 2-g.
Langkah 3
Langkah ketiga adalah untuk
meningkatkan penyerapan kalium oleh
sel untuk menurunkan konsentrasi serum.
glukosa IV dan infus insulin sangat efektif
dalam meningkatkan serapan kalium.
Sebuah rejimen khas adalah 10 U insulin
reguler dan 50 mL dekstrosa 50% dalam
air (D50W) .suatu timbulnya tindakan
dalam waktu 20-30 menit, dan durasi
yang bervariasi, mulai dari 2 sampai 6
jam. infus kontinu insulin dan cairan
glukosa yang mengandung IV dapat
digunakan untuk efek yang
berkepanjangan.
insulin IV (bahkan bila diberikan dengan
dextrose) dapat menyebabkan
hipoglikemia. Pasien dengan cedera ginjal
akut dan penyakit ginjal kronis sangat
rentan. Mengukur glukosa dan kalium
tingkat setiap 2 jam. Terus memantau
kadar glukosa selama minimal 6 jam
setelah pemberian insulin-glukosa. [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. Tarif hipoglikemia
dalam 10-U dan 5-U kelompok yang
16,7% dan 19,7%, masing-masing (P =
0,79). Tarif hipoglikemia berat adalah
8,9% dan 7,0%, masing-masing (P =
0,90). [60]
asidosis metabolik yang benar dengan
natrium bikarbonat. Karena efek variabel
bentuk yang berbeda dari asidosis
metabolik pada tingkat serum potassium,
modalitas terapi ini kurang efektif dan
kurang dapat diprediksi dalam

accompanied by a loop diuretic (eg,

furosemide). Discontinue potassium-sparing
diuretics, angiotensin-converting enzyme
(ACE) inhibitors, angiotensin-receptor
blockers (ARBs), and other drugs that inhibit
renal potassium excretion. Monitor volume
status and aim to maintain euvolemia.
Renal excretion can be enhanced by
administration of an aldosterone analogue,
such as 9-alpha fluorohydrocortisone acetate.
Fluorohydrocortisone is especially helpful in
patients with hyporeninemia or
hypoaldosteronism. It has been increasingly
used in solid-organ transplant recipients who
have chronic hyperkalemia from calcineurin
inhibitor use. Usually, serum potassium
returns to normal after about 48 hours.[61]
Sodium polystyrene sulfonate
Gastrointestinal (GI) excretion can be
increased through the use of cation exchange
resins such as sodium polystyrene sulfonate
(SPS). SPS can be administered orally or
rectally (as a retention enema). Because the
major site of action for this drug is the colon,
rectal administration is preferred for
hyperkalemic emergencies. The
effectiveness of SPS is enhanced if the
enema can be retained for 1 hour.
SPS is not useful for acute control of
hyperkalemia, because its effect on
potassium is delayed for at least 2 hours,
peaking at 4-6 hours. SPS can decrease
serum potassium by 2 mEq/L.
Oral SPS is useful in patients with advanced
renal failure who are not yet on dialysis or
transplant candidates. One or more daily
doses of 15 g can control mild to moderate
hyperkalemia effectively, with little
inconvenience to patients.
Although SPS has a long history of use for
hyperkalemia, its safety and efficacy have
been questioned.[59, 62, 63, 56] The US Food and
Drug Administration (FDA) advises against its
use in patients who do not have normal
bowel function (eg, postoperative patients
who have not had a bowel movement since
their procedure) or those who are at risk for
constipation or impaction.[64] SPS should be
discontinued in patients who become
constipated, and repeat doses should not be
given to patients who have not passed a

memproduksi respon hipokalemia,

terutama pada pasien dengan gagal
ginjal kronis. Meskipun demikian, jika
asidosis parah, maka uji coba terapi
natrium bikarbonat parenteral
dibenarkan.
agonis beta-adrenergik juga cukup efektif
tetapi mungkin agak lebih kontroversial
dan lebih mungkin untuk menghasilkan
efek samping. Di Amerika Serikat,
persiapan yang paling umum digunakan
adalah albuterol nebulasi. Dosis untuk
mengobati hiperkalemia, 10 mg, secara
substansial lebih tinggi dari dosis yang
biasa untuk pengobatan bronkospasme
dan membutuhkan bantuan dari seorang
terapis pernafasan. Efek hipokalemia
puncak terjadi pada 90 menit. Terapi ini
sangat efektif dan lebih disukai untuk
terapi alkali pada pasien dengan gagal
ginjal.
isoproterenol parenteral dan albuterol
juga menurunkan kalium. Namun,
isoproterenol tidak umum digunakan, dan
albuterol parenteral tidak tersedia di
Amerika Serikat. Beberapa peneliti telah
melaporkan takikardia dan
ketidaknyamanan dada dengan
penggunaan terapi beta-agonist untuk
hiperkalemia. Menghentikan antagonis
beta-adrenergik.
Langkah 4
Langkah keempat adalah untuk
meningkatkan ekskresi kalium dari tubuh.
ekskresi ginjal ditingkatkan dengan
mudah pada pasien dengan fungsi ginjal
yang normal dengan pemberian IV garam
disertai dengan loop diuretik (misalnya,
furosemide). Menghentikan diuretik
hemat kalium, enzyme (ACE) inhibitor
angiotensin-converting, blocker
angiotensin-receptor (ARB), dan obat lain
yang menghambat ekskresi potassium
ginjal. Memonitor status volume dan
bertujuan untuk mempertahankan
euvolemia.
ekskresi ginjal dapat ditingkatkan dengan
pemberian analog aldosteron, seperti 9-

bowel movement.
In addition, the FDA cautions that giving SPS
with sorbitol, an osmotic cathartic used to
prevent fecal impaction from SPS and to
speed delivery of resin to the colon, has been
associated with cases of intestinal necrosis,
some of them fatal.[64] Current evidence
indicates that this serious side effect can
occur with SPS even when preparation does
not contain any sorbitol.[65]
Patiromer
Patiromer sorbitex calcium (Veltassa) is a
nonabsorbed, cation exchange polymer that
contains a calcium-sorbitol counterion. It
increases fecal potassium excretion by
binding potassium in the lumen of the GI
tract. It is indicated for hyperkalemia. It
should not be used as an emergency
treatment for life-threatening hyperkalemia
because of its delayed onset of action.
FDA approval of patiromer was based on the
AMETHYST-DN trial. Results showed that
among patients with hyperkalemia and
diabetic kidney disease taking RAAS
inhibitors, patiromer resulted in statistically
significant decreases in serum potassium
level after 4 weeks of treatment, lasting
through 52 week.[72]
The OPAL-HK trial showed patiromer was
well tolerated, decreased serum K(+) , and,
compared with placebo, reduced recurrent
hyperkalemia in patients with chronic kidney
disease (CKD) and heart failure who were
hyperkalemic while taking renin-angiotensinaldosterone system inhibitors (RAASi). In the
study, patiromer was given to patients with
CKD who were taking RAASi and had serum
K(+) levels >5.1 mEq/L to <6.5 mEq/L
(n=243) for 4 weeks. Patients whose K(+)
levels were 3.8 mEq/L to <5.1 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. 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. The
median increase in serum K(+) from baseline
of the withdrawal phase was greater with
placebo (n = 22) than patiromer (n = 27) (P <
0.001). Recurrent hyperkalemia (serum K(+) ,

alpha fluorohydrocortisone asetat.

Fluorohydrocortisone sangat membantu
pada pasien dengan hyporeninemia atau
hypoaldosteronism. Telah semakin
digunakan dalam penerima transplantasi
solid-organ yang memiliki hiperkalemia
kronis dari penggunaan calcineurin
inhibitor. Biasanya, kalium serum kembali
normal setelah sekitar 48 jam. [61]
Sodium polystyrene sulfonate
Gastrointestinal (GI) ekskresi dapat
ditingkatkan melalui penggunaan resin
pertukaran kation seperti natrium
polistiren sulfonat (SPS). SPS dapat
diberikan secara oral atau rektal (sebagai
enema retensi). Karena situs utama
tindakan untuk obat ini adalah usus
besar, administrasi dubur lebih disukai
untuk keadaan darurat hyperkalemic.
Efektivitas SPS ditingkatkan jika enema
dapat dipertahankan selama 1 jam.
SPS tidak berguna untuk kontrol akut
hiperkalemia, karena efeknya pada
kalium tertunda selama minimal 2 jam,
memuncak pada 4-6 jam. SPS dapat
menurunkan kalium serum oleh 2 mEq /
L.
Oral SPS berguna pada pasien dengan
gagal ginjal canggih yang belum dialisis
atau transplantasi kandidat. Satu atau
lebih dosis harian dari 15 g dapat
mengontrol ringan sampai sedang
hiperkalemia efektif, dengan sedikit
ketidaknyamanan kepada pasien.
Meskipun SPS memiliki sejarah panjang
digunakan untuk hiperkalemia, keamanan
dan kemanjuran telah dipertanyakan. [59,
62, 63, 56] The US Food and Drug
Administration (FDA) menyarankan
terhadap penggunaannya pada pasien
yang tidak memiliki fungsi usus yang
normal (misalnya, pasien pasca operasi
yang belum memiliki buang air besar
karena prosedur mereka) atau mereka
yang berisiko untuk sembelit atau
impaksi. [64] SPS harus dihentikan pada
pasien yang mengalami konstipasi, dan

5.5 mEq/L) occurred in 52% on placebo and

8% on patiromer (P < 0.001).[73]
Step 5
The fifth step is emergency dialysis; 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. Initiation of dialysis can often
take several hours; therefore, even if dialysis
is contemplated, the other therapeutic
modalities should be instituted as a bridge to
dialysis.
The final step in the medical management of
hyperkalemia is to determine the cause of
hyperkalemia in order to prevent future
episodes. 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. Patients
with hyperkalemia due to rhabdomyolysis
may need surgical decompression of swollen,
ischemic muscle compartments. Patients
without end-stage renal disease who require
hemodialysis for control of hyperkalemia
require placement of a hemodialysis catheter
for emergency dialysis.[66]
In patients with solid tumors, tumor debulking
may be considered as a means of decreasing
the risk of hyperkalemia from tumor lysis
syndrome.[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.
Selain itu, FDA memperingatkan bahwa
pemberian SPS dengan sorbitol, sebuah
katarsis osmotik digunakan untuk
mencegah impaksi tinja dari SPS dan
untuk mempercepat pengiriman resin ke
usus, telah dikaitkan dengan kasus
nekrosis usus, beberapa dari mereka
yang fatal. [64] sekarang bukti
menunjukkan bahwa efek samping yang
serius ini dapat terjadi dengan SPS
bahkan ketika persiapan tidak
mengandung sorbitol apapun. [65]
Patiromer
Patiromer sorbitex kalsium (Veltassa)
adalah Selebihnya,, polimer tukar kation
yang berisi ion lawan kalsium-sorbitol. Hal
ini meningkatkan ekskresi kalium tinja
dengan mengikat kalium dalam lumen
saluran pencernaan. Hal ini diindikasikan
untuk hiperkalemia. Ini tidak boleh
digunakan sebagai pengobatan darurat
untuk hiperkalemia yang mengancam
jiwa karena onset tertunda aksi.
persetujuan FDA dari patiromer
didasarkan pada percobaan AMETHYSTDN. Hasil penelitian menunjukkan bahwa
di antara pasien dengan hiperkalemia
dan ginjal diabetes penyakit mengambil
Raas inhibitor, patiromer mengakibatkan
penurunan signifikan secara statistik
pada tingkat kalium serum setelah 4
minggu pengobatan, yang berlangsung
melalui 52 minggu. [72]
The OPAL-HK percobaan menunjukkan
patiromer ditoleransi, penurunan serum K
(+), dan, dibandingkan dengan plasebo,
mengurangi hiperkalemia berulang pada
pasien dengan penyakit ginjal kronis
(CKD) dan gagal jantung yang
hyperkalemic saat mengambil sistem
renin-angiotensin-aldosteron inhibitor
(RAASi). Dalam studi tersebut, patiromer
diberikan kepada pasien dengan CKD
yang mengambil RAASi dan memiliki

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, metabolic alkalosis, renal
insufficiency, hypocalcemia,
hypomagnesemia, and hypophosphatemia
due to aggressive loop diuretic use
Colon perforation due to exchange resin
administration
Treatment of pseudohyperkalemia may result
in hypokalemia; thus, treatment of nonlifethreatening hyperkalemia should be deferred
pending verification of hyperkalemia.

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. In particular, 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.

Prevention
Inform patients at risk for hyperkalemia about
dietary sources of potassium, including salt
substitutes. Adjust the diet to decrease
potassium dietary load. Adjust medications
that predispose to or exacerbate
hyperkalemia.
In a retrospective observational study of
27,355 patients with diabetes, 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.[12] The investigators found that for
monitored patients with diabetes alone, the
adjusted relative risk was 0.50, whereas for
monitored patients who also had chronic
kidney disease, the adjusted relative risk was
0.29.

Consultations
For patients with severe hyperkalemia or

serum K (+) tingkat> 5,1 mEq / L untuk

<6,5 mEq / L (n = 243) selama 4 minggu.
Pasien yang K (+) tingkat yang 3.8
mEq / L untuk <5,1 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. Peningkatan median di serum
K (+) dari awal dari fase penarikan lebih
besar dengan plasebo (n = 22) dari
patiromer (n = 27) (P <0,001).
hiperkalemia berulang (serum K (+), 5.5
mEq / L) terjadi pada 52% pada plasebo
dan 8% pada patiromer (P <0,001). [73]
Langkah 5
Langkah kelima adalah dialisis darurat; 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. Inisiasi dialisis sering
dapat memakan waktu beberapa jam;
Oleh karena itu, bahkan jika dialisis
direnungkan, modalitas terapi lainnya
harus dilembagakan sebagai jembatan
untuk dialisis.
Langkah terakhir dalam manajemen
medis hiperkalemia adalah untuk
menentukan penyebab dari hiperkalemia
untuk mencegah episode masa depan. 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. Pasien dengan
asidosis metabolik dan hiperkalemia
akibat karena usus iskemik jelas
membutuhkan eksplorasi. Pasien dengan
hiperkalemia karena rhabdomyolysis
mungkin perlu dekompresi bedah
bengkak, kompartemen otot iskemik.

renal failure, early consultation with a

nephrologist for aid in implementing efficient
therapy and plans for dialysis is highly
recommended. In addition, these patients
should be admitted to an intensive care unit
(ICU).
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 - For emergency pacemaker
placement in patients with refractory heart
block
Hematologist/oncologist For hyperkalemia
resulting from tumor lysis syndrome
Nutritional support specialist - For
hyperkalemia caused by renal failure, which
requires close regulation of potassium and
sodium intake
Endocrinologist For suspected
mineralocorticoid abnormalities (eg,
congenital adrenal hyperplasia)

Long-Term Monitoring
For patients whose hyperkalemia resulted
from a single, clearly defined episode (eg,
acute exertional rhabdomyolysis or druginduced hemolysis), infrequent monitoring of
serum potassium generally suffices.
However, for patients who have conditions or
medications that will continue to predispose
to hyperkalemia, more frequent monitoring of
serum potassium is required. For patients at
high risk, monthly measurements are
indicated.
Continuing care relates to the disease
process that led to the hyperkalemia. For
patients who have recurrent or constant
hyperkalemia (eg, those with diabetic
nephropathy and type IV renal tubular
acidosis), long-term therapy with an oral loop
diuretic and SPS may be indicated. For
pseudohypoaldosteronism type II, 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.
[66]
Pada pasien dengan tumor padat,
debulking tumor dapat dianggap sebagai
cara untuk mengurangi risiko
hiperkalemia dari sindrom lisis tumor.
[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, alkalosis metabolik,
insufisiensi ginjal, hipokalsemia,
hipomagnesemia, dan hypophosphatemia
karena penggunaan lingkaran diuretik
agresif
Colon perforasi karena administrasi resin
pertukaran
Pengobatan pseudohyperkalemia dapat
mengakibatkan hipokalemia; dengan
demikian, pengobatan hiperkalemia-nonmengancam nyawa harus ditangguhkan
verifikasi tertunda dari hiperkalemia.
Diet dan Aktivitas
Sebuah diet rendah kalium yang
mengandung 2 g kalium dianjurkan untuk
meminimalkan asupan kalium pada
pasien dengan risiko hiperkalemia.
Secara khusus, asupan kalium harus
diawasi secara ketat (dan mungkin

with acute kidney injury or end-stage renal

disease is heightened in patients with lower
body weight and creatinine clearance.
Sufficient dextrose in the patients treatment
regimen can minimize the risk.[68] In patients
with salt-wasting congenital adrenal
hyperplasia, corticosteroid and
mineralocorticoid supplementation are
necessary.

dibatasi) pada pasien dengan gagal

ginjal.
Tidak ada pembatasan aktivitas yang
diperlukan kecuali pemantauan terus
menerus untuk cardiotoxicity diperlukan.
Pencegahan
Menginformasikan pasien pada risiko
hiperkalemia tentang sumber makanan
kalium, termasuk pengganti garam.
Mengatur pola makan untuk mengurangi
beban diet kalium. Menyesuaikan obat
yang mempengaruhi atau memperburuk
hiperkalemia.
Dalam sebuah penelitian observasional
retrospektif 27.355 pasien dengan
diabetes, 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.
[ 12] para peneliti menemukan bahwa
pasien yang dipantau dengan diabetes
saja, risiko relatif disesuaikan adalah
0,50, sedangkan untuk pasien dipantau
yang juga memiliki penyakit ginjal kronis,
risiko relatif disesuaikan adalah 0,29.
konsultasi
Untuk pasien dengan hiperkalemia berat
atau gagal ginjal, awal konsultasi dengan
nephrologist untuk bantuan dalam
menerapkan terapi efisien dan rencana
untuk dialisis sangat dianjurkan. Selain
itu, pasien ini harus dirawat di unit
perawatan intensif (ICU).
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 - Untuk
hiperkalemia berkembang pada anak-

anak setelah ingestions disengaja atau

keracunan
Ahli jantung - Untuk penempatan alat
pacu jantung darurat pada pasien dengan
blok jantung refrakter
Hematologi / onkologi - Untuk
hiperkalemia akibat sindrom lisis tumor
Gizi dukungan spesialis - Untuk
hiperkalemia disebabkan oleh gagal
ginjal, yang membutuhkan regulasi dekat
asupan kalium dan natrium
Endokrinologi - Untuk dicurigai kelainan
mineralokortikoid (misalnya, hiperplasia
adrenal kongenital)
Pemantauan Jangka Panjang
Untuk pasien yang hiperkalemia
dihasilkan dari satu, episode yang jelas
(misalnya, rhabdomyolysis exertional
akut atau hemolisis obat-induced),
monitoring jarang kalium serum
umumnya sudah cukup. Namun, untuk
pasien yang memiliki kondisi atau obat
yang akan terus predisposisi
hiperkalemia, pemantauan lebih sering
kalium serum diperlukan. Untuk pasien
dengan risiko tinggi, pengukuran bulanan
ditunjukkan.
Melanjutkan perawatan berhubungan
dengan proses penyakit yang
menyebabkan hiperkalemia tersebut.
Untuk pasien yang memiliki berulang
atau konstan hiperkalemia (misalnya,
orang-orang dengan nefropati diabetik
dan tipe IV asidosis tubulus ginjal), terapi
jangka panjang dengan loop diuretik lisan
dan SPS dapat diindikasikan. Untuk
pseudohypoaldosteronism tipe II, pilihan
pengobatan adalah diuretik thiazide.
Risiko hipoglikemia berat untuk pasien
dengan cedera ginjal atau stadium akhir
penyakit ginjal akut meningkat pada
pasien dengan berat badan rendah dan
kreatinin. dekstrosa cukup dalam rejimen
pengobatan pasien dapat meminimalkan
risiko. [68] Pada pasien dengan
hiperplasia garam-buang adrenal
kongenital, kortikosteroid dan suplemen
mineralokortikoid yang diperlukan.

Medication Summary

The goals of pharmacotherapy are to reduce potassium levels and morbidity and
to prevent complications. Calcium protects the myocardium from the deleterious
effects of hyperkalemia. Beta-adrenergic agents, insulin, and loop diuretics
stimulate cellular uptake of potassium, lowering the serum potassium level.

Calcium salts
Class Summary
Calcium antagonizes the cardiotoxicity of hyperkalemia by stabilizing the cardiac
cell membrane against undesirable depolarization. Onset of effect is rapid ( 15
minutes) but relatively short-lived. These agents are the first-line treatment for
severe hyperkalemia (ie, >7 mEq/L), when the electrocardiogram (ECG) shows
significant abnormalities (eg, widening of QRS interval, loss of P wave, or cardiac
arrhythmias). Calcium usually is not indicated when the ECG shows only peaked
T waves.
Calcium has no effect on the serum level of potassium. For that reason,
administration of calcium should be accompanied by the use of other therapies
that actually help lower serum potassium levels.
Calcium chloride contains about 3 times more elemental calcium than an equal
volume of calcium gluconate: 1 g of calcium chloride has 270 mg (13.5 mEq) of
elemental calcium, whereas 1 g of calcium gluconate has 90 mg (4.5 mEq).
Therefore, when hyperkalemia is accompanied by hemodynamic compromise,
calcium chloride is preferred to calcium gluconate. Other calcium salts (eg,
glubionate and gluceptate) have even less elemental calcium than calcium
gluconate and generally are not recommended for therapy of hyperkalemia.
View full drug information

Calcium gluconate
Calcium increases the threshold potential, thus restoring the normal gradient
between threshold potential and resting membrane potential, which is abnormally
elevated in hyperkalemia. Onset of action is within 5 minutes, and duration of
action is about 30-60 minutes. Doses should be titrated with constant monitoring
of ECG changes during administration; repeat the dose if ECG changes do not
normalize within 3-5 minutes.
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. Because of its irritating
effects when administered parenterally, calcium chloride is generally considered
a second choice, after calcium gluconate.

Beta-adrenergic agonists
Class Summary
Through activation of cyclic adenosine monophosphate (cAMP), these agonists
stimulate the sodium-potassiumadenosine triphosphatase (Na+ -K+ -ATPase)
pump, thereby shifting potassium into the intracellular compartment. However,

these shifts in potassium occur primarily during exercise rather than at rest.
View full drug information

Albuterol (Proventil, Ventolin, Vospire ER)

Albuterol is an adrenergic agonist that has an additive effect with insulin and
glucose, which may in turn help shift potassium into the intracellular space. This
agent lowers the serum potassium level by 0.5-1.5 mEq/L. It can be very
beneficial in patients with renal failure when fluid overload is concern. Onset of
action is 30 minutes; duration of action is 4-6 hours for the immediate-release
product.

Antidiabetics, Insulins
Class Summary
Insulin is administered with glucose to facilitate the uptake of glucose into muscle
cells, bringing potassium with it, primarily by enhancing the activity of the Na+ -K+
-ATPase pump and thereby temporarily lowering serum potassium levels.
View full drug information

Insulin regular human (Novolin R, Humulin R)

Regular insulin stimulates cellular uptake of potassium within 20-30 minutes and
lasts for 4-6 hours. The serum potassium concentration typically drops by 0.5-1.2
mEq/L. Administer glucose along with insulin to prevent hypoglycemia. Monitor
blood sugar levels frequently. Although the effect is rapid, it is temporary;
therefore, insulin therapy should be followed by therapy that actually enhances
potassium clearance (eg, sodium polystyrene sulfonate [SPS]).

Diuretics, Loop
Class Summary
Loop diuretics markedly enhance renal potassium excretion and thus lower
serum levels. Parenterally administered drugs have a more rapid onset of action
and are preferable in emergency situations. Simultaneous administration of
saline can prevent severe volume depletion.
View full drug information

Furosemide (Lasix)
Furosemide increases excretion of water by interfering with the chloride-binding
cotransport system, which, in turn, inhibits sodium, potassium, and chloride
reabsorption in the ascending loop of Henle and distal renal tubule. Furosemide
has a slow onset of action (frequently 1 hour), and its effect on lowering the
potassium level is inconsistent. Large doses may be needed in renal failure.
Individualize the dose to the patient. For the treatment of edema, depending on
the response, administer in increments of 20-40 mg, no sooner than 6-8 hours
after the previous dose, until the desired diuresis occurs. When treating infants
and children, give 1-2 mg/kg every 6-12 hours. If the diuretic response is not
satisfactory, 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).

Oral absorption of furosemide varies from person to person. If the patient

requires rapid and effective therapy, the intravenous (IV) route is preferred.
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.
View full drug information

Bumetanide (Bumex)
Bumetanide increases excretion of water by interfering with the chloride-binding
cotransport system, which, in turn, inhibits sodium, potassium, and chloride
reabsorption in the ascending loop of Henle and distal renal tubule. Individualize
the dose to the patient.
For treatment of edema in adults, start at 0.5-1 mg IV or intramuscularly (IM); if
the desired response is not achieved, administer a second or third dose at 2-3
hour intervals. Titrate to a maximum dosage of 10 mg/day. Rarely, dosages as
high as 20 mg/day are used for edema in patients with renal impairment;
however, they generally are not required for treatment of hyperkalemia.
View full drug information

Ethacrynic acid (Edecrin)

Ethacrynic acid increases excretion of water by interfering with the chloridebinding cotransport system, which in turn inhibits sodium and chloride
reabsorption in the ascending loop of Henle and distal renal tubule. For treatment
of edema in adults, start at 0.5-1 mg/kg IV. Typically, 1 dose is all that is needed;
occasionally, however, a second dose may be given after 2-4 hours. For second
doses, a new injection site should be used so as to avoid possible
thrombophlebitis. Single IV doses higher than 100 mg are not recommended.

Potassium Binders
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Sodium polystyrene sulfonate (Kayexalate, Klonex, Kalexate, SPS)

SPS exchanges sodium for potassium and binds it in the gut, primarily in the
large intestine, decreasing the total body potassium level by approximately 0.5-1
mEq/L. Multiple doses are usually necessary.
Onset of action ranges from 2 to 24 hours after oral administration and is even
longer after rectal administration. The duration of action is 4-6 hours. Do not use
SPS as a first-line therapy for severe life-threatening hyperkalemia; use it in the
second stage of therapy.
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. Concomitant use of sorbitol with sodium polystyrene sulfonate
has been implicated in cases of colonic necrosis.[62]
View full drug information

Patiromer (Veltassa)
Patiromer sorbitex calcium is a nonabsorbed, cation exchange polymer that

contains a calcium-sorbitol counterion. It increases fecal potassium excretion by

binding potassium in the lumen of the GI tract. It is indicated for hyperkalemia. It
should not be used as an emergency treatment for life-threatening hyperkalemia
because of its delayed onset of action.

Alkalinizing Agents
Class Summary
In patients with severe metabolic acidosis, sodium bicarbonate IV is used as a
buffer that breaks down to water and carbon dioxide after binding free hydrogen
ions. By increasing the pH, sodium bicarbonate promotes a temporary potassium
shift from the extracellular to the intracellular environment. It also enhances the
effectiveness of insulin in patients with acidemia. These agents have been
successfully used in the treatment of acute overdose of slow-release oral
potassium preparations.
The use of sodium bicarbonate can be considered in treatment of hyperkalemia
even in the absence of metabolic acidosis, though it is less likely to be effective
in this context. This agent also increases sodium delivery to the kidney, which
assists in potassium excretion.
View full drug information

Sodium bicarbonate
The bicarbonate ion neutralizes hydrogen ions and raises urinary and blood pH.
Onset of action occurs within minutes; duration of action is approximately 15-30
minutes. Monitor blood pH to avoid excess alkalosis. Use the 8.4% solution in
adults and children and the 4.2% solution in children younger than 2 years. The
adult dose for hyperkalemia is 50 mEq IV over 5 minutes. Consider methods of
enhancing potassium removal or excretion, as appropriate.
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; however, 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.

Electrolytes
Class Summary
Magnesium sulfate is used for hyperkalemic patients with cardiac arrhythmias
from digitalis toxicity.
View full drug information

Magnesium sulfate
Magnesium is a cofactor in enzyme systems involved in neurochemical
transmission and muscular excitability. In adults, potassium 60-180 mEq/day,
magnesium 10-30 mEq/day, and phosphate 10-40 mmol/day may be necessary
for optimum metabolic response. Give IV for acute suppression of torsades de

pointes. Repeat doses are dependent on the continuing presence of patellar

reflex and adequate respiratory function.