HIPOKALEMIA

FSR
Hypokalemia
■ Hypokalemia is defined as serum
potassium level of less than 3.5 mEq/L(3.5
mmol/L)
Function of Potassium
Physiology of Renin-angiotensin-aldesterone mechanism.
From homeostasis to pathophysiological point of view
Pathophysiology of Potasium Depletion
Causes of hypokalemia
■ Decreased intake: kidney can conserve to 5-25
mEq K+ daily; normal intake 40-120 daily.
■ Shift into cells:
◻ Alkalosis
◻ Insulin
◻ Beta adrenergic stimuli
■ Stress
■ Beta agonists- e.g.: albuterol, ritodrine
Extra-renal losses of potassium:

Gastrointestinal losses of
potassium

■ Gastric juice contains 5 – 10 mEq K+/L.

■ Intestinal fluids contain 20 – 50 mEq/L
 Hypokalemia from loss of gastric
fluid.
■ >Diarrheal losses are usually
■ >Coexisting volume depletion accompanied by metabolic
acidosis
increases aldosterone
secretion. ◻ Villous adenoma
◻ Laxative abuse
■ >Increased delivery of
bicarbonate to the distal
nephron obligates a cation. In
the setting of increased
aldosterone levels, sodium is >Sweat losses- 5 – 10 mEq/L
retained and potassium
excreted.
The kidney and potassium
■ Nearly all potassium filtered at the glomerulus is
reabsorbed in the proximal nephron. Urinary
potassium is the result of distal potassium
secretion.
■ To excrete potassium, the kidney requires an
adequate number of nephrons, aldosterone, and
a circulation adequate to provide adequate distal
delivery of sodium for sodium/potassium
exchange.
Renal losses of potassium
■ Diuretics- activate the renin-angiotensin-
aldosterone cascade.
■ Primary aldosteronism/increased steroids.
■ Presentation of a non-resorbable anion distally,
obligating a cation, which will lead to increased
potassium excretion in the presence of
aldosterone.
Summary of genaral causes of hyperkalemia
 DIAGNOSIS
■ First line study include measurement of urine
potassium.
■ Serum magnesium assay
■ ECG
■ If urine potassium level is less than 20mEq/L,
consider the following:
• Diarhea and use of laxatives
• Total parentral nutrition
• The use of insulin
DDX
■ Pseudohypokalemia
■ Metabolic alkalosis
■ Bartter Syndrome
■ Hyperthyroidism and Thyrotoxicosis
■ Hypomagnesemia
■ Hypocalcemia
PATOFISIOLOGI

■ Results from a total body potassium deficit or shifting of serum potassium into the
intracellular compartment.
■ Many drugs can cause hypokalemia, and it is most commonly seen with use of loop
and thiazide diuretics. Other causes of hypokalemia include diarrhea, vomiting, and
hypomagnesemia.
MANIFESTASI KLINIS

■ Signs and symptoms are nonspecific and variable and depend on the degree of
hypokalemia and rapidity of onset. Mild hypokalemia is often asymptomatic.
■ Cardiovascular manifestations cardiac arrhythmias (eg, heart block, atrial flutter,
paroxysmal atrial tachycardia, ventricular fibrillation, and digitalis-induced
arrhythmias).
■ In severe hypokalemia (serum concentration <2.5 mEq/L; <2.5 mmol/L), ECG
changes include ST-segment depression or flattening, T-wave inversion, and U-wave
elevation.
■ Moderate hypokalemia is associated with muscle weakness, cramping, malaise, and
myalgias.
TREATMENT
■ In general, every 1 mEq/L (1 mmol/L) decrease in potassium below 3.5 mEq/L (3.5
mmol/L) corresponds with a total body deficit of 100 to 400 mEq (100–400 mmol).
To correct mild deficits, patients receiving chronic loop or thiazide diuretics generally
need 40 to 100 mEq (40–100 mmol) of potassium. Whenever possible, potassium
supplementation should be administered by mouth. Of the available salts, potassium
chloride is most commonly used because it is the most effective for common causes
of potassium depletion.
■ Limit IV administration to severe hypokalemia, signs and symptoms of hypokalemia,
or inability to tolerate oral therapy. IV supplementation is more dangerous than oral
therapy due to the potential for hyperkalemia, phlebitis, and pain at the infusion site.
Potassium should be administered in saline because dextrose can stimulate insulin
secretion and worsen intracellular shifting of potassium. Generally, 10 to 20 mEq
(10–20 mmol) of potassium is diluted in 100 mL of 0.9% saline and administered
through a peripheral vein over 1 hour. If infusion rates exceed 10 mEq/h (10
mmol/h), ECG should be monitored.
■ Evaluate serum potassium following infusion of each 30 to 40 mEq (30–40 mmol) to
direct further potassium supplementation.
STUDI KASUS.1
 CASE REPORT :
STEROID INDUCED
HYPOKALEMIA
SUBJECT
Ny. A. Wanita , Usia : 46 tahun , RA
Keluhan :
■ Nyeri Sendi
■ Kelelahan
■ Lemah
■ Baal (Mati rasa) pada bagian kaki dan tangan
Anamnesa :
■ Gelisah,
■ TTV dibawah Normal
Objective
Hasil Laboratorium :
Serum Urea, Serum Creatinine, Kalsium,
PO42-, AST, ALT ALP (Trans Aminase) dan
Creatine Kinase : NORMAL
Hasil Laboratorium : (3 hari kemudian)
Level Serum Potassium 4.5 meq/L (3.5 -
5.3 meq/L) , Level Serum Potassium 2.5 meq/L (3.5 -
5.3 meq/L)
Sodium 142 mEq/L (135 - 152 mEq/L)
Na , Urea dan Cr : NORMAL
HbA1c 6,1 % (4.6 - 6.2%)
Creatine Kinase : 495 IU/L ( 40 - 190 IU/L)
ESR 60 m
GRBS : 286 mg/dl
CRP 140 ( <1) ECG abnormal
RA positif
Cont’…. Objective
Riwayat pengobatan
■ Prednisolon 40 mg tablet (OD)
■ Methyl prednisolone 40 mg injeksi (OD)
■ MTX tablet 10 mg (once a week)
■ Folic acid tablet 5 mg (alternate days)
Riwayat pengobatan saat ini :
■ IV Potassium (Correction of the Potassium)
Obat pulang
■ MTX tablet 10 mg (once a week)
■ Folic acid tablet 5 mg (alternate days)
Assessment
■ Methyl Prednisolon (Prednison) digunakan untuk pengobatan inflamasi , serta
kondisi Auto imun, membatasi laju sintesis protein
■ Hipokalemia akibat penggunaan Steroid/Glucocorticoid (Methyl Prednisolon injeksi).
■ Skala probabilitas 8 (NARANJO menerangkan hubungan prednisolon dan
Hipokalemia)
■ Hipokalemia terjadi Karena kaliuresis yang diinduksi penggunaan Glucocorticoid
■ Rekomendasi Pemberian suplement Kalium
■ Gangguan ECG karena hipokalemia
Planning

■ Penghentian penggunaan Glucocorticoid

■ Rekomendasi Pemberian suplement Kalium
■ Monitoring kadar kalium setelah Koreksi HIpokalemia dengan Suplemen Kalium,
■ Monitoring gangguan Abnormalitas pada jantung akibat hipokalemia
STUDI KASUS.2
 CASE REPORT :
ORAL ACYCLOVIR INDUCED
HYPOKALEMIA AND ACUTE TUBULAR
NECROSIS
SUBJECT
Ny. B (Wanita) , Usia 54 tahun , Abses Gigi (Rajal)
Keluhan :
■ Kelemahan
■ Kelelahan ektremitas bawah paresis
■ N & V ( 3 kali) setelah minus obat
■ Merokok selama 20 tahun
■ Pemeriksaaan Fisik : Status hydras (Baik) , penurunan refleks osteotendinous patela
(++/++++)
■ Riwayat Alergi : AB Penisillin
■ Pasien disarankan menghentikan semua obat, mulai suplemen kalium oral , krn
peningkatan kelemahan (krn hipokalemia persisten) , lanjut Ranap
Objective
Riwayat pengobatan :
■ Klindamisin
■ Dicloxaciline
■ Asiklovir 400 mg / 8 jam
Objective
cont’…. Objective
Objective
■ Gbr. 1a . Glomeruli normal, atrofi
tubular 15-20% dari tubulus, túbulus
menunujukkan vakuolisasi terutama
sitoplasma granular, pengelupasan
fokus epitel, perubahan regerat sikta
tepi sel tubular dan gips hialin
■ Gbr. 1b & c. Intertitium 0-15% fibrosis,
dengan infiltrasi oleh limfosit, sel
plasma dan eosinofil menembus epitel
tubular
■ Gbr. 1d. Nefritis-interstitial infiltrasi sel
inflamasi
■ Gbr. 1e. Imunofluoresensi adalah
negatif IgM, IgG, IgA, C3c, C1q, ,
Fibrinogen dan Albumin
■ Interpretasi hasil histologi :
Konsistens dengan tubular necrosis
akut dan nefritis tubulointerstitial akut
Assessment
■ Asiklovir digunakan untuk pengobatan abses gigi
■ Hypokalemia disebabkan penggunaan asiklovir
■ Cedera ginjal akut disebabkan asiklovir
■ Switching kalium oral ke IV
Planning

■ IV asiklovir diberikan IV lambat (1-2 h)

■ Penyesuaian dosis IV asiklovir pada gangguan fungsi ginjal
■ HIndari pemberian agen nefrotoksis bersamaan , sebelum pemberian asiklovir
■ Monitoring kadar kalium setelah Koreksi hipokalemia dengan Suplemen Kalium,
■ Monitoring gangguan Abnormalitas pada jantung akibat hipokalemia
■ Monitoring gangguan fungsi ginjal dan tubular
STUDI KASUS 3
Kasus

Ny. A berusia 60 tahun HIV (+) , dalam terapi ARV (FTC/TDF +

RTV/Azatanavir) , mengalami Lymfoma Hodgkin. Pasien mulai kemoterapi
ABVD ( Doxorubicin, Bleomycin, Vinblastin dan Dacarbazine) dan mengalami
neutropenia dan Hipokalemia berat (severe) .
SUBJECT
Ny. B (Wanita) , Usia 60 tahun , HIV (+) , Limphoma Hodgkin
(10 tahun terakhir stage II-A)
Keluhan post Chemoterapi ABVD:
■ Neutropenia (grade 4)
■ Fever
■ Severe Hypokalemia
Objective
■ VL undetected
■ CD4 : 510 sel/uL
Setelah Chemotherapy :
■ K = 1.92 mEq/L
■ Perubahan ECG
■ Serum PH 7.44
■ pCO2 38,3
■ Bicarbonat 25.6 mEq/L
■ Normoglycemia dengan Glycosuria 204 mg/24 h
■ Serum Magnesium 2.4 mEq/L (Normal)
■ Hypophosphatemia 1.6 mEq/L
■ Gradient Transtubular Potassium elevated = 8.1
cont’…Objective
Riwayat penggunaan obat :
■ ARV : FTC+ TDF + Azatanavir/Ritonavir
■ ABVD (Doxorubicin, Bleomycin, Vinblastin dan Dacarbazine)
■ Piperacillin - Tazobactam
■ IV Potassium replacement
Objective
Assesment
■ Hypokalemia diduga adanya interaksi ARV dengan ABVD yaitu PI
dengan Vinblastine
■ Switching PI menjadi Dolutegravir
■ Piperacillin - Tazobactam digunakan untuk mengatasi demam (
Fever) akibat infeksi (WBC) meningkat
■ IV Potassium replacement digunakan untuk mengatasi
hipokalemia akibat interaksi obat (PI vs Vinblastin)
■ Pemberian Piperacillin - Tazobactam dan IV Potassium
replacement, berdampak WBC dan Level serum Potassium
(Normal)
Planning
■ Monitoring kadar Potassium akibet penggunaan ARV (TDF :
tubular damage agent) secara berkala khususnya selama
penggunaan Vinblastin
■ Monitoring gejala hypokalemia yang timbul selama rangkaian
kemoterapi (Vinblastin)
■ Monitoring fungsi ginjal secara ketat