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      • Association between ED crowding and delivery of medications to critical patients with hyperkalemia

        ( Sun Hee Moon ),( Ki Jeong Hong ),( Jong Hwan Shin ),( Jin Kim ),( Kyoung Hwa Lim ),( Chun Sun Ham ),( Jin A Choi ),( Ji Hee Kang ),( Jung Mee Han ),( Su Yong Shin ),( Sun Young Kim ),( Sung Wook Son 대한응급의학회 2013 대한응급의학회 학술대회초록집 Vol.2013 No.2

        Background: The effect of ED crowding on delay of treatment to critically ill patients is controversial. Few investigations have been evaluated whether ED crowding delayed delivery of medications to critically ill patients with hyperkalemia. The purpose of this study is to investigate association between ED crowding and delay in managing critically ill patients with hyperkalemia. Methods: This study was conducted at the emergency department located in metropolitan area. We retrospectively reviewed medical records from Jan to Dec 2011. Inclusion criteria was critically ill adult patient (ESI level with 1, 2) with hyperkalemia (initial electrolyte test: potassium >5.0 mmol/L) who was given regular insulin via IV access during ED stay. ED crowding was measured by hourly number of ED visits. Crowed ED was defined by upper quartile of hourly ED visits. Delivery time of medications was measured by minutes from ED visit to infusion time of regular insulin to the patients in nursing records. We performed descriptive analysis and multivariate linear regression adjusted for age, sex, EMS use, nursing duty time, injury. Results: During study period, 45,520 adults visited ED and 1,098 cases showed laboratory result of hyperkalemia. Among them, 123 hyperkalemia cases were triaged by ESI 1, 2 and given regular insulin. 35(28.5%) of enrolled cases visited crowded ED and 88(71.5%) visited non-crowded ED. There was no significant difference of demographics, EMS use and presence of injury between two groups. Delivering time of regular insulin to hyperkalemia case was significantly longer in crowded group than non-crowded (124.7±145.0 vs 76.0±83.3, p<0.01, minutes). In multivariate linear regression, visiting crowded ED delayed delivery time of regular insulin (43.0 minutes, 95% CI: 3.3-82.7). Conclusion: ED crowding delayed delivery of medications to critically ill patients with hyperkalemia. ED crowding could affect quality of medical care for emergency patients with high acuity.

      • KCI등재후보

        Study design of Real World Evidence for Treatment of Hyperkalemia in the Emergency Department (REVEAL-ED): a multicenter, prospective, observational study

        Zubaid Rafique,Mikhail Kosiborod,Carol L. Clark,Adam J. Singer,Stewart Turner,Joseph Miller,Douglas Char,W. Frank Peacock IV 대한응급의학회 2017 Clinical and Experimental Emergency Medicine Vol.4 No.3

        Objective Hyperkalemia affects up to 10% of hospitalized patients and, if left untreated, can lead to serious cardiac arrhythmias or death. Although hyperkalemia is frequently encountered in the emergency department (ED), and is potentially life-threatening, standard of care for the treatment is poorly defined, with little supporting evidence. The main objectives of this observational study are to define the overall burden of hyperkalemia in the ED setting, describe its causes, the variability in treatment patterns and characterize the effectiveness and safety of ED standard of care therapies used in the United States. Methods This is an observational study evaluating the management of hyperkalemia in the ED. Two hundred and three patients who presented to the ED with a potassium value ≥5.5 mmol/L were enrolled in the study at 14 sites across the United States. Patients were treated per standard of care practices at the discretion of the patient’s physician. In patients who received a treatment for hyperkalemia, blood samples were drawn at pre-specified time points and serum potassium values were recorded. The change in potassium over 4 hours and the adverse events after standard of care treatment were analyzed. Results and Conclusion This article describes the background, rationale, study design, and methodology of the REVEAL-ED (Real World Evidence for Treatment of Hyperkalemia in the Emergency Department) trial, a multicenter, prospective, observational study evaluating contemporary management of patients admitted to the ED with hyperkalemia.

      • KCI등재

        고칼륨혈증에서 심전도의 진단적 의의

        윤수영,박원녕,정성필,김승호,이한식 대한응급의학회 2000 대한응급의학회지 Vol.11 No.3

        Background: Hyperkalemia is a common and potentially life-threatening metabolic disorder. The electrocardiogram(ECG) is known to be a relatively sensitive diagnostic tool for hyperkalemia. However many exceptions, in which patients showed normal ECG findings even though hyperkalemic, have been reported. The purpose of this study was to determine the extent of correlation between the ECG findings and hyperkalemia and to determine when the ECG has value for diagnosing hyperkalemia. Methods: Patients who had been diagnosed as having hyperkalemia at two university hospitals during three years were enrolled in this study. We reviewed the medical records of the patients and evaluated the following 6 ECG abnormalities: tall T waves, narrow T waves, QRS widening, atrioventricular block, loss of P waves, and sine waves. We defined tall T waves and narrow T waves as 20 percentiles of heights and widths of the T waves from the 100 patients with normokalemia. Results: During the study period, there were 100 hyperkalemic patients, and we analyzed 69 available electrocardiograms. Abnormal ECG findings were revealed in 67%of 69 patients. The higher the serum potassium level, the more abnormal ECG findings. The common ECG abnormalities were tall T waves and loss of P waves. The patients with normal ECGs even though hyperkalemic had relatively low potassium levels. And whether chronic renal disease was not correlated to the ECG abnormality. Conclusion: The electrocardiogram is a good diagnostic tool for hyperkalemia if it is used with accurate diagnostic criteria. Thus, hyperkalemia should be considered when the ECG shows tall T waves or loss of P waves.

      • 산혈증 유발 고칼륨혈증과 고칼륨혈증 유발 산혈증의 비교 연구

        윤준오(Yoon, Jun-Oh),박춘옥(Park, Choon-Ok),황상익(Hwang, Sang-Ik),김종환(Kim, Chong-Whan),김우겸(Kim, Woo-Gyeum) 대한생리학회 1990 대한생리학회지 Vol.24 No.1

        A comparative study of acid-base balance has been made between acidemia-induced hyperkalemia and hyperkalemia-induced acidemia. A group of rabbits was infused 0.1 N hydrochloric acid solution and metabolic acidosis was induced. Another group was administered 20 mM potassium chloride solution and hyperkalemia was induced. The third group was infused 0.1 N hydrochloric acid and 20 mM potassium chloride solution, simultaneously. Acid-base data and plasma potassium ion concentration were monitored every thirty minutes in these three groups of rabbits. Following results were obtained: 1 ) Along with the infusion of hydrochloric acid, acute metabolic acidosis was induced in the rabbits. Plasma bicarbonate ion concentration decreased primarily in this group. As a respiratory compensation, there was a tendency of reduction of arterial Pco<sub>2</sub>. The alteration of data became larger along with the amount of administration and the time elapsed. However, hyperkalemia was not so severe compared with the second group. 2) In potassium chloride infused group, plasma potassium ion concentration increased along with the time elapsed and the amount of infusion. And the alteration of acid-base data was parrallel to the level of potassium ion concentration, above all depression of pH was prominent. 3) Above data suggest that when acute metabolic acidosis was induced, exchange of intracellular potassium ion with extracellular hydrogen ion seems significant for the regulation of extracellular acid-base balance. And when hyperkalemia was induced with the infusion of potassium chloride solution, the exchange of intracellular hydrogen ion with extracellular potassium ion also seems significant for the regulation of extracellular potassium balance. 4) In the group of rabbits infused hydrochloric acid and potassium simultaneously, disturbances of acid-base balance and potassium balance were much more severe than two other groups. In these mixed disturbances, the process of compensatory mechanism might be inhibited and one disturbance might aggregate each other. 5) Through above data it has been postulated that in acid-base disturbance potassium balance can be sacrificed as a compensatory mechanism, and vice versa in disturbance of potassium balance. And our data also suggest that hydrogen ion and potassium ion are compensatory pair, one another.

      • KCI등재

        Sulodexide 유발 고칼륨 혈증: 증례 보고

        박인일 ( In Il Park ),최명진 ( Myung Jin Choi ),윤종우 ( Jong Woo Yoon ),김수진 ( Soo Jin Kim ),박태진 ( Tae Jin Park ),송영수 ( Young Soo Song ),이영기 ( Young Ki Lee ),김형직 ( Hyung Jik Kim ),노정우 ( Jung Woo Noh ),구자룡 ( Ja 대한신장학회 2009 Kidney Research and Clinical Practice Vol.28 No.3

        Sulodexide is composed of two glycosaminoglycans (fast-moving heparin 80%, dermatan sulfate 20%) that are capable of preventing diabetic nephropathy by correcting abnormal glycosaminoglycan metabolism. Considering heparin-like propertyof sulodexide, side effect profiles of sulodexide are expected to be similar with those of heparin. Among those side effects, we remarked on heparin-induced hyperkalemia and hereby report a case of severe hyperkalemia during the use of sulodexide. A 52-year-old man with diabetic nephroapthy and hypertension was admitted to our hospital because of severe hyperkalemia up to 7.5 meq/L. His clinical condition was stable and medications including losartan and furosemide had not been changed for last 6 months except the addition of sulodexide, which was started 30 days prior to admission. Despite intensive use of Kayexalate and immediate discontinuation of losartan, hyperkalemia aggravated up to 8.0 meq/L. After recognition of possible sulodexide-induced hyperkalemia, sulodexide was discontinued, which resulted in rapid correction of hyperkalemia. In view of the above discussed clinical consideration, we suspect sulodexide as a major cause of hyperkalmia and report this case with a review of literature.

      • KCI등재

        Voriconazole-induced Severe Hyperkalemia Precipitated by Multiple Drug Interactions

        Jae Young Choi,Seong Geun Cho,Ki-Seok Jang,Gheun-Ho Kim 전해질고혈압연구회 2020 Electrolytes & Blood Pressure Vol.18 No.1

        Voriconazole, a triazole antifungal agent used to treat serious fungal infections, has a pharmacokinetic characteristic of undergoing hepatic metabolism by the cytochrome P450 system. Few cases of hyperkalemia have been reported, which presented only when the serum voriconazole level was exceptionally elevated by drugdrug interactions. Additionally, azole antifungals may interfere with the biosynthesis of adrenal steroids and therefore can predispose patients to aldosterone deficiency. However, it is unclear whether voriconazole itself can induce hypoaldosteronism or hyperkalemia. Here, we report a case of voriconazole-induced hyperkalemia in a patient administered concurrent medications to treat comorbidities. Voriconazole was orally administered for pulmonary aspergillosis, and three episodes of severe hyperkalemia recurred, which improved with emergency treatment. In the first episode, renin-angiotensin-aldosterone system inhibitors were associated. We found that dronedarone might have increased the voriconazole level in the second episode. At that time, severe hypercalcemia was concurrent, which improved with acute hemodialysis and eliminating dronedarone. Finally, severe hyperkalemia recurred without concurrent medications known to interact with voriconazole. Upon switching from voriconazole to itraconazole, the hyperkalemia was resolved. Drug level monitoring is necessary when voriconazole is used. Genetic susceptibility, such as through CYP2C19 polymorphism, may be investigated for patients with adverse reactions to voriconazole.

      • KCI등재후보

        일차진료에서 흔히 접하는 수분 전해질 문제 ; 안지오텐신 전환효소 억제제/안지오텐신 수용체 차단제 사용과 고칼륨혈증

        정성진 ( Sung Jin Chung ),박철휘 ( Cheol Whee Park ) 대한내과학회 2011 대한내과학회지 Vol.80 No.1

        Therapeutic manipulation of the renin-angiotensin-aldosterone system (RAAS) is an important strategy for improving hypertension, diabetes, cardiovascular disease, and chronic kidney disease. Development of hyperkalemia after the administration of RAAS inhibitors is of particular concern because patients at highest risk for this complication are often the same patients who derive the greatest cardiovascular or renoprotective benefit. Based on an overview of the incidence of hyperkalemia during treatment with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers alone and in combination, this review suggests approaches for monitoring, detecting, and managing hyperkalemia in patients treated with RAAS inhibitors. Although the incidence of hyperkalemia with RAAS inhibitors is generally low, hyperkalemia can be associated with increased mortality. When using RAAS inhibitors, it is important to monitor on-treatment electrolyte levels and renal function parameters in patients with a high risk for hyperkalemia. (Korean J Med 2011;80:20-30)

      • KCI등재

        칼륨 대사 장애

        이주훈,Lee, Joo-Hoon 대한소아신장학회 2010 Childhood kidney diseases Vol.14 No.2

        저칼륨혈증의 경우 약제 또는 백혈구 증가증 등에 의해서 칼륨이 일시적으로 세포내로 이동하는 재분포에 의해서 생기는 저칼륨혈증을 먼저 감별한다. 칼륨소실에 의한 결핍의 경우 소변 칼륨 농도 또는 TTKG를 구하고, 감소되어 있는 경우에는 칼륨의 신외성 손실, 칼륨 섭취의 부족 등을 감별한다. 증가되어 있는 경우 신장을 통한 칼륨의 소실을 생각하고, 고혈압이 동반되어 있지 않을 경우 산증과 관련된 경우, 구토에 의한 경우, 세뇨관에서의 칼륨 재흡수 장애 또는 칼륨의 분비가 증가되는 경우를 생각할 수 있다. 고혈압이 동반되어 있을 경우 혈장 레닌과 알도스테론을 측정하여 레닌이 증가되어 있을 경우, 혈장 레닌이 정상 또는 낮으면서 혈장 알도스테론만 증가한 경우, 혈장 알도스테론은 증가되어 있지 않지만 알도스테론 이외에 광물부신겉질호르몬의 작용이 증가하는 경우를 감별한다. 증상은 무기력, 경련, 근육통, 횡문근 융해증, 변비, 장폐쇄, 부정맥, 지각이상 등이 있다. 치료는 원인 질환의 치료 및 칼륨공급이다. 고칼륨혈증은 재분포에 의한 경우, 가성 고칼륨혈증, 진성 고칼륨혈증을 감별해야 한다. 진성 고칼륨혈증이면서 사구체 여과율이 감소되어 있는 경우 신부전 또는 체내 칼륨 부하가 증가하는 경우를 감별한다. 사구체 여과율이 15 mL/min/$1.73m^2$ 이상인 경우에는 혈장 레닌과 알도스테론을 검사한다. 모두 낮을 경우, 혈장 레닌은 정상이지만 알도스테론만 낮은 경우, 혈장 알도스테론의 농도는 정상이지만 알도스테론의 작용을 저해되는 경우 등을 감별해야 한다. 증상은 부정맥, 감각 이상, 허약 등이 있다. 치료는 calcium gluconate, 인슐린, 베타2작용제, 중탄산염, furosemide, resin, 투석 등이 있으며, 칼륨을 제한하고 원인 약물이 있을 경우 이를 중단해야 한다. Hypokalemia usually reflects total body potassium deficiency, but less commonly results from transcellular potassium redistribution with normal body potassium stores. The differential diagnosis of hypokalemia includes pseudohypokalemia, cellular potassium redistribution, inadequate potassium intake, excessive cutaneous or gastrointestinal potassium loss, and renal potassium wasting. To discriminate excessive renal from extrarenal potassium losses as a cause for hypokalemia, urine potassium concentration or TTKG should be measured. Decreased values are indicative of extrarenal losses or inadequate intake. In contrast, excessive renal potassium losses are expected with increased values. Renal potassium wasting with normal or low blood pressure suggests hypokalemia associated with acidosis, vomiting, tubular disorders or increased renal potassium secretion. In hypokalemia associated with hypertension, plasam renin and aldosterone should be measured to differentiated among hyperreninemic hyperaldosteronism, primary hyperaldosteronism, and mineralocorticoid excess other than aldosterone or target organ activation. Hypokalemia may manifest as weakness, seizure, myalgia, rhabdomyolysis, constipation, ileus, arrhythmia, paresthesias, etc. Therapy for hypokalemia consists of treatment of underlying disease and potassium supplementation. The evaluation of hyperkalemia is also a multistep process. The differential diagnosis of hyperkalemia includes pseudohypokalemia, redistribution, and true hyperkalemia. True hyperkalemia associated with decreased glomerular filtration rate is associated with renal failure or increased body potassium contents. When glomerular filtration rate is above 15 mL/min/$1.73m^2$, plasma renin and aldosterone must be measured to differentiate hyporeninemic hypoaldosteronism, primary aldosteronism, disturbance of aldosterone action or target organ dysfunction. Hyperkalemia can cause arrhythmia, paresthesias, fatigue, etc. Therapy for hyperkalemia consists of administration of calcium gluconate, insulin, beta2 agonist, bicarbonate, furosemide, resin and dialysis. Potassium intake must be restricted and associated drugs should be withdrawn.

      • KCI등재후보

        Trimethoprim / Sulfamethoxazole ( TMP / SMX ) 을 복용 중인 외래 환자에서 발생하는 경구 칼륨 투여 후 칼륨 대사 장애

        최춘식(Chun Sik Choi),유영조(Young Jo Yoo),김태영(Tae Young Kim),민경환(Kyung Hwan Min),한상웅(Sang Woong Han),노광호(Kwang Ho Roh),양성규(Seong Kyu Yang),유준호(Jun Ho Yoo),오석중(Suk Joong Oh),문중돈(Jung Don Mun),김호중(Ho Jung Ki 대한내과학회 1999 대한내과학회지 Vol.57 No.1

        TMP/SMX has been shown to cause hyperkalemia in a few outpatients on standard-dose. This prospective study was aimed at investigating other associated factors inducing clinically important hyperkalemia in outpatients on standard-dose of TMP/SMX. Methods : Age-matched diabetic(n=22) and non-diabetic (n=20) patients with UTI on standard dose of TMP/SMX for 5 days were given acute oral intake of 40 mEq of potassium chloride(KCl). Results : Before the intake of TMP/SMX, basal levels of serum potassium(K), serum BUN and creatinine, plasma renin activity(PRA), aldosterone(PA), and transtubular potassium gradient(TTKG) were comparable between diabetic and non-diabetic subjects. Also after TMP/SMX was taken, all parameters didnt reveal any overt changes except a slightly increased serum K but not significantly (from 4.20±0.15 to 4.14±0.21mEq/L in non-diabetics; from 4.13±0.18 to 4.25±0.13mEq/L in diabetics). Following acute oral KCl load, however, the peak increases of serum K changes were significantly higher in diabetics compared to non-diabetics(0.34 0.06 vs 0.62 0.09mEq/L, p<0.01). Furthermore, 8 out of 22 diabetics but none of non-diabetics after acute KCl load developed hyperkalemia(> 5.0 mEq/L). After KCl load, PRA did not show any significant changes, whereas PA was increased simultaneously with the increments of serum K in both diabetic subgroups hyperkalemic(n=8) and normokalemic (n=14) diabetics. But increment was blunted in hyperkalemic diabetic subgroup. TTKG was increased prominently in normokalemic diabetic subgroup(9.20 from 4.50), while it was slightly increased in hyperkalemic diabetic subgroup(4.63 from 3.79mEq/L). There was statistical difference between two subgroups(p < 0.05). In conclusion, Besides the known effect of blocking sodium channels in distal K secreting cells by TMP/SMX, insulinopenia(DM). Hypoaldosteronism with its decreased tubular bioactivity, and increased exogenous K intake in concert could cause clinically overt hyperkalemia on standard-dose of TMP/SMX. When standard- dose of TMP/SMX is administered to patients with deranged K homeostasis, especially to diabetics with hypoaldosteronism, blood K level should be monitored meticulously to avoid hyperkalemia.

      • Wide QRS complex as a predictor of hyperkalemia during pulseless electrical activity (PEA) cardiac arrest

        김영민,신태건,박종은,황승연,심민섭,조익준,이건탁 대한응급의학회 2020 대한응급의학회 학술대회초록집 Vol.2020 No.2

        Introduction The aim of this study was to evaluate the association between hyperkalemia and the QRS widening in cardiac arrest patients showing initial electrocardiogram (ECG) rhythm of pulseless electrical activity (PEA). Material & Method This was a retrospective observational study of patients whose initial ECG rhythm was PEA among patients treated for cardiac arrest at a tertiary referral hospital. We reviewed the cardiac arrest registry which has been prospectively collected for cardiopulmonary resuscitation (CPR) quality improvement in our hospital. Out-of-hospital cardiac arrest (OHCA) and in-hospital cardiac arrest (IHCA) patients over the age of 18 were included in this study, and those with no measured potassium levels, no ECG rhythm strip records, or inability to clarify readings were excluded. The QRS interval of electrocardiogram in cardiac arrest patients was measured separately by two emergency physicians if the two physicians agreed, the initial rhythm was considered as wide QRS PEA. Result 111 episodes in the wide QRS complex group and 506 episodes in the narrow QRS complex group were included. The wide QRS group showed significantly more diabetes patients, lower blood pH and higher creatinine than the narrow QRS group. The potassium level in the wide QRS group was significantly higher than in the narrow QRS group (5.4 mmol/L [IQR, 4.4-6.7] vs. 4.6 mmol/L [IQR, 4.0-5.6] p<0.001). This trend remained in similar trends regardless of the presence of CKD or dialysis. In patients who were unable to excrete potassium well due to poor renal function, probability of having hyperkalemia at the time of PEA cardiac arrest was significantly higher in the wide QRS group than in the narrow QRS group. Conclusion The width of the QRS complex showed a significant correlation with the serum potassium level. In the presence of kidney dysfunction, wide QRS complex tended to have a stronger association with hyperkalemia. To better evaluate the effectiveness of these treatments in the clinical setting, a larger scale multicenter trials is needed.

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