Treatment of hyperkalemia in children with intravenous salbutamol

The aim of this study is to investigate the efficacy and safety of intravenous salbutamol in hyperkalemia. Fourteen children with chronic renal failure, three with acute renal failure and hyperkalemia were treated by intravenous infusions of 4μg/kg salbutamol. Reductions in the mean plasma potassium (K⁺) concentrations obtained at 40 and 120 min after therapy were statistically significant when compared with the mean plasma K⁺ concentration at the beginning of therapy (P < 0.01).     

Clinical Management in Systemic Type Pseudohypoaldosteronism Due to SCNN1B Variant and Literature Review

Systemic pseudohypoaldosteronism (PHA) is a rare, salt-wasting syndrome that is caused by inactivating variants in genes encoding epithelial sodium channel subunits. Hyponatremia, hyperkalemia, metabolic acidosis, increased aldosterone and renin levels are expected findings in PHA. Clinical management is challenging due to high dose oral replacement therapy. Furthermore, patients with systemic PHA require life-long therapy. Here we report a patient with systemic PHA due to SCNN1B variant whose hyponatremia and hyperkalemia was detected at the 24^th hour of life. Hyperkalemia did not improve with conventional treatments and dialysis was required. He also developed myocarditis and hypertension in follow-up. Challenges for diagnosis and treatment in this patient are discussed herein. In addition, published evidence concerning common features of patients with SCNN1B variant are reviewed.     

Amiodarone Attenuates Fluoride-induced Hyperkalemia in Vitro

Poisoning by hydrofluoric acid or fluoride salts results in hypocalcemia, hypomagnesemia, and hyperkalemia with subsequent cardiac dysrhythmias. In previous studies, quinidine attenuated fluoride-induced hyperkalemia in vitro, and enhanced survival in animals. Like quinidine, amiodarone is a potassium channel blocker, although amiodarone is more familiar to clinicians due to its recent inclusion in advanced cardiac life support (ACLS) protocols. OBJECTIVES: This in-vitro study of human erythrocytes was designed to determine whether amiodarone could attenuate fluoride-induced hyperkalemia. METHODS: Six healthy volunteers each donated 60 mL of blood on three occasions. Each specimen was divided into 12 tubes, incubated at 37 degrees C, and oxygenated with room air. An aqueous sodium fluoride (F(-)) solution was added to tubes 1-9. Incremental amounts of quinidine were added to tubes 1-4 (Q(1)-Q(4)) to attain calculated concentrations of 0.73 microg/mL, 1.45 microg/mL, 2.9 microg/mL, and 5.8 microg/mL, respectively. Incremental amounts of amiodarone were added to tubes 5-8 (A(1)-A(4)) to attain calculated concentrations of 0.38 microg/mL, 0.75 microg/mL, 1.5 microg/mL, and 3.0 microg/mL, respectively. Tubes 9-12 were controls for each of F(-), amiodarone, quinidine alone, and no additive, respectively. Extracellular potassium concentration ([K(+)]) was followed, and an objective endpoint was defined as the rise in potassium concentration at 6 hours. RESULTS: Fluoride produced a significant change in [K(+)] by 6 hours in all samples. Quinidine produced a J-shaped curve in its ability to attenuate the rise in [K(+)], with only one concentration, Q(3), demonstrating significance versus tube 9 (control). Amiodarone also demonstrated a J-shaped dose-response effect, with statistical significance at A(1), A(2), and A(3) versus tube 9 (control). There was no significant difference among the effective concentrations (Q(3), A(1), A(2), and A(3)) of both drugs. CONCLUSIONS: In this in-vitro model using human blood, amiodarone and quinidine both attenuated F(-)-induced hyperkalemia. Further study is indicated to determine whether amiodarone enhances survival in F(-)-poisoned animals.     

经典非转流肝移植术中下腔静脉血酸碱及电解质变化

目的:探讨非转流经典原位肝移植术中患者下腔静脉血血气和电解质变化及其原因。方法:26例行经典非转流原位肝移植患者,采用气管内插管静吸复合麻醉。经右颈内静脉和右股静脉穿刺置入中心静脉导管。于开腹前(T0)、无肝期前5min(T1)、新肝开放前5min(T2)、新肝期15min(T3)、新肝期30min(T4),分别从右颈内静脉、右股静脉导管抽取上、下腔静脉血,进行血气、电解质分析。结果:与上腔静脉比较,下腔静脉血氧分压[p(O2)]在T2时降低(P<0.01),pH、剩余碱(BE)、二氧化碳分压[p(CO2)]、血钾、血糖和乳酸水平与上腔静脉血差异无统计学意义(均P>0.05)。与T0比较,下腔静脉pH、BE在T2时下降,新肝期15min分别降达最低值[7.283±0.060、(-5.4±3.1)mmol/L],而p(CO2)于T2、T3升高。结论:无肝期阻断远端下腔静脉血除出现明显的低氧血症外,未见严重的高钾血症和酸中毒表现,提示再灌注综合征与下腔静脉血钾水平和酸碱状态无关。     

Effects of Ca channel blockers on Ca loading induced by metabolic inhibition and hyperkalemia in cardiomyocytes

The effects of the L-type (nifedipine and verapamil) and the T-type (mibefradil) Ca²⁺ channel blockers on the increase in intracellular Ca²⁺ concentration ([Ca²⁺]_i) induced by NaCN metabolic inhibition and hyperkalemia were examined in chicken cardiomyocytes using fluorescence imaging with Fura-2. NaCN induced a slow and sustained rise in [Ca²⁺]_i, which was not affected by pretreating the cells for 5 min with nifedipine, verapamil, or mibefradil at 100 nM or 10 μM. Pretreatment of the cells with 10 μM nifedipine, verapamil, or mibefradil for 5 min remarkably inhibited the K⁺-induced increase in [Ca²⁺]_i. These inhibitory effects diminished after 48-h pretreatment with nifedipine or verapamil but not with mibefradil. Ryanodine also induces an increase in [Ca²⁺]_i, and this effect was enhanced by 48-h pretreatment of the cells with 10 μM verapamil but not with 10 μM mibefradil. We conclude that the NaCN-induced increase in [Ca²⁺]_i is independent of the Ca²⁺ influx though the L-type or T-type Ca²⁺ channels. Chronic inhibition of the L-type Ca²⁺ channels but not T-type channels may enhance the ryanodine receptor-mediated Ca²⁺ release, which may be responsible for the development of tolerance to their inhibitory effects on K⁺-induced increase in [Ca²⁺]_i.     

The postoperative cardiovascular arrest of a 5-year-old male: an initial presentation of Duchenne's muscular dystrophy

Anesthesia may be administered to patients with Duchenne's muscular dystrophy, but cases are reported in which apparently healthy children suffer hyperkalemic cardiac arrest. We present the case of a 5-year-old boy whose muscular dystrophy was discovered following a fatal, perioperative cardiac arrest in the postanesthesia care unit.     

大鼠实验性高钾血症的解救方法的改进

目的:探讨硫化氢对大鼠实验性高钾血症的解救作用及机制。方法:32只Sprague-Dawley大鼠随机分成正常对照组(A组)、正常硫化钠组(B组,Na2S)、模型组(C组,KCl+NaCl)与硫化钠解救组(D组,KCl+Na2S),每组8只,腹腔注射10%KCl溶液复制高钾血症模型,在大鼠心电图发生显著变化时,硫化钠解救组大鼠立即腹腔注射2 g/L的硫化钠溶液,观察40 min后心脏采血,离心分离,取上清测定K+、Na+、Ca2+等离子水平。结果:模型组大鼠血清钾离子浓度较正常对照明显升高,心电图异常(T波高尖QT间期延长);给予硫化钠治疗后,解救组大鼠血清钾离子浓度显著降低,心电图逐渐恢复正常。结论:硫化钠对KCl所复制的大鼠高钾血症模型具有很好的解救作用。     

Comparison of the Effects of Regional Ischemia and Hyperkalemia on the Membrane Action Potentials of the In Situ Pig Heart

APD During Ischemia. Introduction: This study was designed to determine the role of increased extracellular potassium [K⁺]_e on action potential duration (APD) in the in situ porcine heart during acute regional no-flow ischemia.
Methods and Results: In open chest, anesthetized swine, an arterial shunt from the carotid artery to the mid-left anterior descending coronary artery was created through which a solution of KCl was infused to raise [K⁺]_e, Myocardial [K⁺]_e, was determined by potassium-sensitive electrodes, and transmembrane action potential was recorded by floating glass microelectrode. During the first 2 minutes of ischemia, APD at 90% repolarization (APD₉₀) lengthened by 31.2 ± 1.1 msec (P < 0.05). The comparable increase in [K⁺]_e alone shortened APD₉₀, During the next 6 minutes of ischemia. [K⁺]_e, rose to 11.3 ± 0.3 mM and APD₉₀, showed a decrease. However, the comparable increase in |K⁺]_e, by infusion of KCl caused further shortening of APD₉₀, at similar levels of [K⁺]_e.
Conclusions: Acutely ischemic myocardium showed a brief increase in APD₉₀, during the first 2 minutes of ischemia, followed by a fall in APD₉₀, after 2 minutes of ischemia, but the shortening is less than anticipated by the rise in [K⁺]_e. Thus, we hypothesize that other component(s) of ischemia may inhibit action potential repolarization.     

Evaluating the Utility of Rapid Point-of-Care Potassium Testing for the Early Identification of Hyperkalemia in Patients with Chronic Kidney Disease in the Emergency Department

Purpose

Severe hyperkalemia leads to significant morbidity and mortality if it is not immediately recognized and treated. The concentration of potassium (K⁺) in the serum increases along with deteriorating renal function. The use of point-of-care K⁺ (POC-K⁺) in chronic kidney disease (CKD) could reduce the time for an accurate diagnosis and treatment, saving lives. We hypothesized that POC-K⁺ would accurately report K⁺ serum level without significant differences compared to reference testing, regardless of the renal function of the patient.

Materials and Methods

The retrospective study was performed between January 2008 and September 2011 at an urban hospital in Seoul. The screening program using POC was conducted as a critical pathway for rapid evaluation and treatment of hyperkalemia since 2008. When a patient with CKD had at least one warning symptom or sign of hyperkalemia, both POC-K⁺ and routine laboratory tests were simultaneously ordered. The reliability of the two assays for serum-creatinine was assessed by intra-class correlation coefficient (ICC) analysis using absolute agreement of two-way mixed model.

Results

High levels of reliability were found between POC and the laboratory reference tests for K⁺ (ICC=0.913, 95% CI 0.903-0.922) and between two tests for K⁺ according to changes in the serum-creatinine levels in CKD patients.

Conclusion

The results of POC-K⁺ correlate well with values obtained from reference laboratory tests and coincide with changes in serum-creatinine of patients with CKD.