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PubMed1987

Hyperkalemia as a complication of drug therapy.

A wide array of drugs in common use can produce hyperkalemia. We reviewed our experience with severe hyperkalemia (potassium levels greater than 5.9 mEq/L [greater than 5.9 mmol/L]) in adult inpatients during a one-year period, to evaluate the extent to which drugs could be implicated in this electrolyte disorder. Excluding hemolyzed samples, single unexplained values, and measurements obtained during cardiopulmonary bypass or resuscitation, drug therapy was a probable contributing factor in more than 60% of the hyperkalemic episodes; in 25%, drugs were temporally linked to the onset of the hyperkalemia. In declining order of frequency, the drugs associated with hyperkalemia were potassium chloride, captopril, nonsteroidal anti-inflammatory agents, and potassium-sparing diuretics. In more than 80% of the drug-related hyperkalemic episodes, potassium regulation was compromised by underlying disease states. The most common was renal insufficiency, followed by diabetes mellitus and metabolic acidosis. This review underscores the dictum that caution should be exercised when drugs with hyperkalemic potential are used in patients with impaired potassium homeostasis.

Acidosis↗
PubMed1982

[Hyporeninemic hypoaldosteronism and the differential diagnosis of hyperkalemia].

Selective hypoaldosteronism is defined as diminished production of aldosterone, and sometimes also of 18-hydroxycorticosterone, with otherwise intact adrenal function. A decrease in the secretion of potassium and H+-ions and in the reabsorption of sodium in the distal nephron may result and lead to hyperkalemia, hyperchloremic acidosis, and impaired renal sodium conservation. The form of hypoaldosteronism which occurs in the adult is characterized by the following additional features: the aldosterone deficiency is due in the majority of cases to a decrease in enzymatically active plasma renin ("hyporeninemic hypoaldosteronism"), while various endogenous mechanisms as well as certain drugs (prostaglandin inhibitors, beta-blockers) may contribute. Other disturbances of the renin-angiotensin system (e.g. during treatment with converting-enzyme inhibitors) may rarely be responsible. Abnormalities in adrenal cortical synthesis may sometimes coexist, but proof that adrenal enzymatic defects play a primary pathogenic role in selective hyperaldosteronism in the adult is lacking. Such patients are frequently older (greater than 50 years), and often have diabetes mellitus and/or nephropathy (diabetic, interstitial, or hydronephrosis). Hyperkalemia and acidosis tend particularly to develop in association with mild to moderate impairment of renal function. The differential diagnosis should include other causes of impaired renal potassium secretion (Addison's disease, renal resistance to mineralocorticoids, potassium-sparing diuretics). Moreover, possible extrarenal factors contributing to hyperkalemia (oral potassium intake and redistribution of intracellular/extracellular space, particularly with associated insulin deficiency) should also be considered. For treatment, dietary potassium restriction is recommended as a general step. Replacement with the mineralocorticoid fludrocortisone acetate usually reverses the hyperkalemia and acidosis, but may sometimes induce sodium retention and hypertension. Loop diuretics, potassium-exchanging preparations and/or bicarbonate may also be useful as alternatives or additives.

Acid-Base Equilibrium↗
PubMed1981

Hyperkalemia associated with indomethacin.

Substantial hyperkalemia with ECG abnormalities developed in a patient. None of the common causes of hyperkalemia was found, eg, acidosis, hemolysis, rhabdomyolysis, renal failure, hypoadrenalism, leukocytosis, or thrombocytosis. The patient had been receiving indomethacin, a drug known to inhibit renin production, aldosterone excretion, and prostaglandin synthetase. The patient was rechallanged with indomethacin, and measurements of serum potassium and renin, urinary potassium, aldosterone, and creatinine levels were done. The study period clearly showed a hyporeninemic-hypoaldosterone states with diminished renal potassium excretion, leading to hyperkalemia associated with the indomethacin therapy. The development of hyperkalemia caused by indomethacin is probably unusual; however, we believe it is important to report this potentially serious pathophysiologic occurrence associated with a commonly used medication.

Adult↗
PubMed1996

[Influence of hyperkalemia on clinical decision making].

INTRODUCTION: In our hospital, extreme values are promptly reported in routine test, one of three kinds of reporting system. We investigated the influence of hyperkalemia on clinical decision making and discussed critical levels of hyperkalemia and the significance of prompt report of it. MATERIALS AND METHODS: One hundred eighty six patients with more than 6 mmol/l of blood potassium detected during 1993 were studied. Each episode in a patient with different causes was classified as a separated case and finally 194 cases were studied. Cause of hyperkalemia, clinical symptoms, electrocardiogram, outcome and treatment were investigated. RESULTS AND DISCUSSION: The mortality was 14% in 6 approximately 7 mmol/l, 42% in 7 approximately 8 mmol/l and 100% in more than 8 mmol/l. Electrocardiograms showed high peaked T wave in 6 approximately 7 mmol/l, widening of QRS complex and bradycardia in 7 approximately 8 mmol/l, and ventricular fibrillation and flatter in more than 8 mmol/1. These results supported that 7 mmol/l was acceptable as a critical value. One hundred percent of outpatients and 79% of inpatients undergoing emergency tests were promptly treated by doctors, and 61% and 35% undergoing urgent tests, and 52% and 30% undergoing routine tests (prompt report) were done respectively. Prompt reports of extreme values were more useful in decision making for outpatients than inpatients. Urea-N was more important than potassium as a factor influencing decision making in both patients, because most patients had renal failure or heart failure. CONCLUSION: The mortality and electrocardiogram studies supported that 7 mmol/l was an acceptable critical value. Prompt reports of hyperkalemia were more significant to clinical decision making for medical care for outpatients than for inpatients.

Clinical Laboratory Techniques↗
PubMed1998

Hyperkalemia: treatment options.

Although extracellular potassium accounts for only 1% to 2% of total body potassium, its concentration, [K+], is critical because it affects the depolarization of electrically excitable tissues such as heart and skeletal muscle. Renal failure is a predisposing factor in three-quarters of cases of hyperkalemia. Drugs contribute to the development of hyperkalemia in half of the cases, and most cases are multifactorial. Because hyperkalemia can lead to fatal arrhythmias, it deserves respect as a genuine electrolyte emergency. Nonetheless, recent data highlight the poor correlation of the EKG with [K+]. When present, however, EKG changes should be rapidly antagonized by infusion of calcium salts. Additional measures include shifting potassium from the extracellular to the intracellular compartment, removing potassium from the body, and eliminating risk factors for recurrence. Insulin is the most reliable agent for promoting transcellular shift of potassium. Albuterol can be used alone or to augment the effect of insulin. Alkalinization with bicarbonate, although formerly recommended as a mainstay of therapy, is not efficacious. Hemodialysis rapidly and reliably removes potassium and lowers [K+]. Exchange resins are also useful in removing potassium. Precise data on the quantity of potassium removed with current hemodialysis techniques or with resin are lacking. Although effective, rapid, and convenient means of treating hyperkalemia are available, physicians frequently fail to use them effectively.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Hyperkalemia associated with rapid infusion of conventional and lipid complex formulations of amphotericin B.

A child developed hyperkalemia and cardiac arrest with infusion of an amphotericin B lipid complex 5.0 mg/kg over 1 hour. Another child, with chronic renal failure, developed hyperkalemia after infusion of conventional amphotericin B deoxycholate 1.0 mg/kg over 2 hours. Rapid infusion of the agent causes hyperkalemia in dogs and humans that is exacerbated in the setting of renal failure. A lipid formulation of amphotericin B is commercially available, and no reports of hyperkalemia are associated with its administration.

Amphotericin B↗
PubMed1987

Suppression of plasma renin activity in a boy with chronic hyperkalemia.

Chronic hyperkalemia (6.8 mmol/L [6.8 mEq/L]) was discovered in a boy, aged 13 years 7 months, with short stature, delayed puberty, and normal blood pressure. Additional studies revealed hyperchloremic metabolic acidosis (serum values: sodium ion, 139 mmol/L [139 mEq/L]; chloride, 113 mmol/L [113 mEq/L]; bicarbonate, 18 mmol/L [18 mEq/L]), a normal glomerular filtration rate, a subnormal renal threshold for bicarbonate reabsorption, and normal serum thyroxine, growth hormone, and cortisol values. Renal excretion of potassium ion was subnormal for the prevailing serum concentration of potassium ion but was increased normally by infusion of sodium sulfate. The serum aldosterone concentration was appropriate for a normokalemic subject, despite marked suppression of plasma renin activity (PRA) (supine/upright: aldosterone, 140/580 pmol/L [5/21 ng/dL]; PRA, 0.0/0.03 ng/L X s [0.0/0.1 ng/mL/h]). Treatment with chlorothiazide and sodium chloride resulted in correction of the abnormal electrolyte concentrations and an increase in linear growth velocity. Serum aldosterone concentrations did not change significantly during treatment, even though the PRA had increased (supine/upright: aldosterone, 110/920 pmol/L [4/33 ng/dL]; PRA, 0.89/2.17 ng/L X s [3.2/7.8 ng/mL/h]). In this patient, we conclude that (1) hyperkalemia was due to inadequate renal excretion of potassium ion; (2) the serum potassium ion concentration was the major stimulus to aldosterone secretion before treatment; (3) suppression of PRA was more likely due to hyperkalemia than to extracellular volume expansion.

Acidosis↗
PubMed2000

Elderly heart failure patients with drug-induced serious hyperkalemia.

We report four cases of hyperkalemia induced by the association of spironolactone with ACE inhibitor in geriatric patients. Over a period of one year, four elderly patients treated for congestive heart failure with this association were admitted to the Geriatric Ward with serious hyperkalemia. These occurrences represented one third of all-cause severe hyperkalemia cases admitted during this one-year period. A common observation in our cases was that the dose of spironolactone employed far exceeded the recommended dosages. These cases illustrate that spironolactone dosage must be kept low in the setting of chronic congestive heart failure treatment, as well as the need for close monitoring of frail elderly patients who are given this combination.

Aged↗
PubMed2003

Variations of serum potassium level and risk of hyperkalemia in inpatients receiving low-molecular-weight heparin.

OBJECTIVES: To observe the variations of serum potassium level in patients receiving low-molecular weight heparin, assess the consequent risk of hyperkalemia and evaluate the clinical contributory factors. METHODS: A prospective study was performed on consecutive inpatients treated with low-molecular-weight heparin as indicated by the attending physicians. The changes of serum potassium level observed within 5-8 days were tested by univariate and multivariate analysis according to demographic and clinical variables and concomitant pharmacological therapy. RESULTS: Four hundred and sixteen patients (mean age 73 years; 64% female) were enrolled in the study over 15 months. After receiving nadroparin or enoxaparin (mean daily dosage: 76.3 anti-factor Xa unit/kg) for a median 6-day period, their mean (+/-SD) serum potassium level increased from 4.2+/-0.5 mmol/l to 4.5+/-0.5 mmol/l ( P<0.0001). This change was significantly correlated with baseline potassium, interval between potassium samplings, history of hypertension or renal insufficiency, and marginally with aldosterone antagonist treatment. Hyperkalemia, defined as potassium exceeding 5.5 mmol/l, developed in ten patients (2.4%) and the highest value observed was 7.6 mmol/l; by multivariate logistic-regression analysis, history of diabetes was the only significant independent predictor (odds ratio 6.5; 95% C.I.=1.7-24.8). CONCLUSION: Short-term treatment with low-molecular-weight heparin induces a significant increase in serum potassium level but the related incidence of relevant hyperkalemia is low. However, given the high absolute number of patients currently exposed to the risk in many clinical settings and the limitation of risk prediction, clinicians should prevent this life-threatening complication by a high index of suspicion and, accordingly, a quite routine monitoring of serum potassium.

Adult↗
PubMed2005

Hypokalemia causing rhabdomyolysis resulting in life-threatening hyperkalemia.

Hyperkalemia is commonly associated with renal failure and is rare if renal function is normal. It is rarely caused by rhabdomyolysis and can be life threatening if unrecognized. Rhabdomyolysis is caused by many disorders, including hypokalemia. The available literature, both for human beings and experimental animals, contains evidence of hypokalemia causing rhabdomyolysis and rhabdomyolysis leading to hyperkalemia. Hypokalemia as a cause of rhabdomyolysis often goes unnoticed, because of the counteracting effect of rhabdomyolysis on serum potassium. There are no pediatric reports showing hypokalemia as a cause of rhabdomyolysis leading to life-threatening hyperkalemia. This case emphasizes the vigilance required toward the occurrence of rhabdomyolysis, which if not detected promptly may prove fatal.

Humans↗
PubMed1996

Effect of hydrochlorothiazide in pseudohypoaldosteronism with hypercalciuria and severe hyperkalemia.

Severe hyperkalemia resistant to treatment with sodium chloride (NaCl) supplements plus cation exchange resins can be found in pseudohypoaldosteronism type I. In a patient with the multiple target organ variant of this condition, hyperkalemia persisted at dangerous levels (8.5 mmol/l) despite large doses of NaCl (50 mmol/kg per day) and cation exchange resins (6 g/kg per day). Hypercalciuria was also present. The total volume of fluids and supplements required was not tolerated orally. Indomethacin (2 mg/kg per day) and later hydrochlorothiazide (2 mg/kg per day) were tried to further correct imbalance. Plasma potassium (K) and Na levels, the urinary Na/K ratio, transtubular potassium gradient (TTKG), and urinary calcium/creatinine (Ca/Cr) ratio were used to evaluate the effect of hydrochlorothiazide. Under treatment, plasma Na was stable (137-144 mmol/l), K levels decreased from 8.5 to 5 mmol/l, urinary Na/K from 90 to 24, and TTKG increased from 0.3 to 1.8. Ca/Cr decreased from 3.5 to 1.5 mmol/mmol. The dosage of cation exchange resins was decreased, oral fluids were tolerated, and the patient's general condition improved. Hence: hydroclorothiazide can be useful in the treatment of severe hyperkalemia and hypercalciuria of pseudohypoaldosteronism type I.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1978

Electrocardiographic changes simulating acute myocardial infarction caused by hyperkalemia: report of a patient with normal coronary arteriograms.

A patient is described with severe diabetic ketoacidosis and hyperkalemia who presented with an ECG resembling an acute anterior wall myocardial infarction. Treatment of hyperkalemia resulted in prompt return of the ECG towards normal. Subsequent work-up including exercise testing and selective coronary arteriography ruled out any significant coronary artery disease suggesting that the ECG changes were probably caused by hyperkalemia. While similar changes have rarely been described in the past, this would appear to be the first such case in whom coronary artery disease was ruled out by a negative exercise testing and coronary arteriography.

Coronary Angiography↗
PubMed1975

Atrioventricular and intraventricular conduction in hyperkalemia.

Twelve patients exhibited electrocardiographic evidence of fascicular block during hyperkalemia. Isolated left posterior hemiblock occurred in four, isolated left anterior hemiblock in two, right bundle branch block with left anterior hemiblock in two, right bundle branch block with left posterior hemiblock in one, left bundle branch block with abnormal left axis deviation in two and advanced atrioventricular block in one. In all seven patients with sinus rhythm the P-R interval shortened after correction of hyperkalemia. Electrophysiologic studies using His bundle recording and atrial pacing in one patient revealed intraatrial conduction delay and marked prolongation of conduction time in the His-Purkinje system. It is concluded that conduction defects in the specialized intraventricular conduction system are common in hyperkalemia and result in electrocardiographic patterns of fascicular block.

Adolescent↗
PubMed1990

Fatal refractory hyperkalemia due to tumor lysis during primary resection for hepatoblastoma.

Infants with large, rapidly growing tumors of the liver who exhibit preoperative signs of tumor necrosis (elevated uric acid or K+), having received no prior chemotherapy or radiation therapy, may be at risk for acute hyperkalemia during operative manipulation of the mass. In these patients, consideration should be given to careful monitoring of serum potassium throughout operative manipulation; cardiopulmonary bypass, to protect the heart from acute hyperkalemia; or to primary biopsy of the tumor with resection planned after chemotherapy. A case of fatal refractory hyperkalemia due to tumor lysis during a trisegmentectomy for hepatoblastoma in a 7-month-old girl who presented with a large, rapidly growing tumor and hyperuricemia is described.

Carcinoma, Hepatocellular↗
PubMed1989

Usefulness of transesophageal atrial pacing in hyperkalemia-induced impulse formation and conduction disturbances.

This report describes the usefulness of transesophageal atrial pacing in the treatment of five patients with hyperkalemia-induced bradycardias. Three patients had marked sinus bradycardia while the other two had a regular rhythm with QRS of left bundle branch block morphology, with no P waves visible on the surface electrocardiogram. Four patients were in chronic hemodialysis three times a week, and one had severe post-traumatic hemorrhage. In three patients, hyperkalemia had been precipitated by food intoxication. In one case the cause was unknown while, in the last case, hyperkalemia was due to rapid infusion of stored blood and solutions containing high concentrations of potassium. Transesophageal atrial pacing was performed in all cases utilizing a bipolar catheter introduced into the esophagus and a constant current generator delivering square wave pulses of 10 msec duration and 19-28 mA intensity. Atrial capture, followed by impulse conduction to the ventricles, was constant in all cases, being performed for between 15 and 35 minutes until a normal sinus rhythm was restored. The procedure was well tolerated. The advantages of this procedure as opposed to invasive ventricular pacing are discussed.

Aged↗
PubMed1988

Fluoride-induced hyperkalemia: the role of Ca2+-dependent K+ channels.

Acute fluoride poisoning is associated with sudden cardiac death by an unknown mechanism. Because F- binds to Ca2+ to cause marked hypocalcemia, lowered serum Ca2+ concentrations have been thought to be a major underlying factor in the ventricular irritability of F(-)-toxic patients. However, correction of the hypocalcemia does not prevent sudden death. Paradoxically, while decreasing extracellular Ca2+ levels, in vitro studies have shown F- increases intracellular Ca2+, which is thought to trigger Ca2+-dependent K+ channels and produce a K+ efflux. The K+ efflux may be important clinically, as patients with F- overdose can exhibit hyperkalemia shortly before cardiovascular collapse. In erythrocyte suspensions, we found that propranolol, which increases the sensitivity of the Ca2+-dependent K+ channels, exacerbates the efflux, and quinidine, which blocks the channel, prevents the efflux. In six dogs, 35 mg/kg of sodium fluoride given intravenously produced intractable ventricular fibrillation within 140 minutes. Four dogs given 200 mg of quinidine sulfate with the sodium fluoride developed no ventricular arrhythmias. The data indicate that F--induced hyperkalemia is important in sudden cardiac death following acute fluoride toxicity and that this hyperkalemia is mediated by Ca2+-dependent K+ channels.

Animals↗
PubMedDate not supplied

Pseudomyocardial infarction and hyperkalemia: a case report and subject review.

A case of diabetic ketoacidosis with hyperkalemia and ECG evidence of pseudomyocardial infarction is presented. Electrocardiogram abnormalities resolved shortly after treatment of the elevated potassium. The electrophysiology of hyperkalemia and theories to explain observed ECG changes are discussed. Pseudoinfarction changes that may be peculiar to patients with diabetic ketoacidosis and hyperkalemia are examined.

Diabetes Mellitus, Type 1↗
PubMedDate not supplied

Hyperkalemia during human cardiopulmonary resuscitation: incidence and ramifications.

Although hypokalemia has been reported after cardiac arrest and successful resuscitation, experimental data indicate that potassium is released from cells during ischemia. The purpose of this investigation was to study serum potassium concentration ([K+]) during closed chest cardiopulmonary resuscitation (CC-CPR) in humans. Twenty-two patients presenting to the emergency department (ED) in cardiopulmonary arrest had simultaneous measurement of central venous and arterial [K+] and blood gases during CC-CPR utilizing current advanced cardiac life support protocols and a pneumatic chest compressor and ventilator. Mean arterial and central venous [K+] were 5.0 +/- 1.3 and 5.6 +/- 2.9 mEq/L, respectively, (p greater than .05) with 7 patients having [K+] of greater than 6 mEq/L. Significant hyperkalemia does occur in some patients during cardiac arrest and CC-CPR. Because poor tissue perfusion during CC-CPR impairs exchange between the interstitial and intravascular compartments, increases in interstitial [K+] would be expected to be even greater. Interstitial hyperkalemia may play a role in the genesis of wide complex electromechanical dissociation (EMD) seen after prolonged cardiac arrest. Since calcium has long been known to be beneficial in the treatment of hyperkalemia-induced dysrhythmias, the success of calcium chloride in treating wide complex EMD may be on the basis of this phenomenon.

Aged↗