Micromethods for the simultaneous measurement of intracellular potassium and corticosterone output of isolated adrenal cortical cells.

1. A technique is described for the measurement of potassium and water spaces in less than 1 mul of packed cells. 2. The total potassium content of cell pellets is measured in a perchloric and nitric acid extract by flame spectrophotometry. The potassium in trapped medium is estimated from the distribution space of hydroxy[-14C]methylinulin and subtracted from the total potassium content to give intracellular potassium content. Corticosterone output was measured by radioimmunoassay. 3. The simultaneous measurement of total water from the [-3H]water space allows calculation of the intracellular water space. 4. Values obtained for intracellular potassium content, intracellular water space and calculated intracellular potassium concentration are presented for different preparations of isolated adrenal cortical cells.     

Concentration dependence of active potassium transport in the human red blood cell in the presence of inhibitors

The active potassium influx in the human red blood cell is inhibited by strophanthidin, ethacrynic acid, and MK-870 (a new diuretic), and the degree of inhibition is greater at low concentrations of extracellular potassium than at high. In the case of ethacrynic acid, potassium appears to diminish the rate of combination of the drug with the transport system. The kinetic behavior of the active potassium influx in the presence of the inhibitors strophanthidin and ethacrynic acid is consistent with a model in which the binding of potassium at one of the potassium-sensitive sites in the transport system reduces the affinity of the system for the drug, and binding of a second potassium ion further reduces the affinity. It is not possible to distinguish between the sites on the basis of the studies presented here.     

Potassium disturbances as a cause of metabolic neuromyopathy

We report two cases of ascending muscular weakness progressing to areflexic quadriplegia caused by severe derangement of potassium homeostasis. The first patient presented with a 17-alpha-hydroxylase deficiency and severe hypokalemia. The second case had primary adrenocortical deficiency (Addison's disease) and extreme hyperkalemia. Complete recovery ensued after correction of the metabolic disorder in both cases. The role of potassium in the pathophysiology of neuromuscular excitation is discussed. We conclude that when neuromyopathy is present, metabolic causes should be considered and the serum potassium determined.     

Disorders of potassium homeostasis. Hypokalemia and hyperkalemia

This article reviews the diagnosis and management of clinical disorders of potassium balance, with particular attention to the critically ill patient. The normal regulation of potassium balance is reviewed as a background for understanding these disorders, followed by a discussion of the causes and management of hypo- and hyperkalemia. Practical guidelines are presented for acute and chronic management.     

Slow-release potassium overdose: Is there a role for magnesium?

Slow-release potassium overdose is rare and often fatal. Recommended treatment is derived from that of other, more common, causes of hyperkalaemia and from the general principles of overdose management. We present a patient who survived after a massive slow-release potassium (Slow-K^®) ingestion resulting in a peak potassium concentration of 12 mmol/L, the highest yet reported. A review of previously reported cases of potassium overdose and a summary of recommended therapies for the treatment of hyperkalaemia are presented. Laboratory and current clinical evidence support the addition of magnesium to standard therapy for potassium overdose, particularly where there is concern about increasing doses of calcium; this suggestion requires further clinical research.     

Potassium Supplements in Patients Receiving Long-Term Diuretics for Oedema

Plasma, blood cell, and total body potassium levels were measuredserially in 21 patients receiving long-term diuretics for thetreatment of cardiac oedema and the results compared with similarmeasurements in 10 control subjects. Initially, all diureticrecipients received potassium chloride supplements. However,in 17 of the 21 subjects these were discontinued and measurementsof potassium status were repeated regularly thereafter. No significantfall in the measured indicators of potassium status were observedin the patients in whom potassium was withdrawn; however, inone subject with persistent cardiac failure who presented withhypokalaemia this was not corrected even after intensive potassiumsupplementation. It is concluded that for those taking a normaldiet who are free of any major gastro-intestinal disorder, routinepotassium supplementation is unnecessary, and might indeed occasionallyprove harmful.     

Hypokalemic hypoventilation complicating severe diabetic ketoacidosis

Hypokalemia has been previously reported as a cause for respiratory impairment complicating therapy for diabetic ketoacidosis. A case is presented with a short interval of hypoventilation documented by hypercapnia. A reversal from hypercapnia to hypocapnia occurred when the serum potassium level became normal after potassium replacement. Causes of muscular weakness other than hypokalemia were considered unlikely on the basis of clinical and laboratory data. The present report records the occurrence of hypoventilation associated with hypokalemia in diabetic ketoacidosis and serves to underscore the need for adequate potassium replacement during the treatment of this disorder.     

Saltpeter ingestion

A 37-year-old man presented to the emergency department after an attempt to self-treat his priapism with saltpeter (K+NO3). Initially he had a potassium of 7.6 with electrocardiographic changes and a markedly elevated CO2. The potassium and carbon dioxide normalized in less than 24 hours with standard treatment for hyperkalemia. Hyperkalemia is expected with large oral potassium ingestion; and the elevated CO2 was spurious, caused by the misreading of serum nitrates by the Ektachrom 700 system. Ingestion of K+NO3 should be added to the differential of hyperkalemia with a markedly elevated CO2.     

Effect of proportional reduction of sodium intake on the adaptive increase in glomerular filtration rate/nephron and potassium and phosphate excretion in chronic renal failure in the rat.

1. The influence of dietary sodium intake on the glomerular filtration rate (GFR/nephron) and potassium and phosphate excretion was examined at three stages of progressive chronic renal failure produced in rats by sequential partial nephrectomies. 2. The adaptive increased sodium excretion per nephron in the control group receiving a constant sodium intake did not occur in the experimental group that had a gradual reduction of dietary sodium in direct proportion to the fall in GFR. 3. Despite the difference in sodium excretion, the increase in GFR/nephron, the daily variation in the amount of potassium and phosphate excreted, the increase in potassium and phosphate excretion per unit nephron, and the plasma potassium and phosphate concentrations were the same in the two groups. 4. The concept of 'autonomous adaptation' in chronic renal failure is presented.     

Amiodarone-induced thyrotoxicosis presenting as hypokalemic periodic paralysis

Thyroid disorder is a well-recognized side effect of amiodarone therapy. Thyrotoxicosis is less common than hypothyroidism. Hypokalemic periodic paralysis is one manifestation of thyrotoxicosis, and is more often seen in Oriental and Latin American men than in other demographic groups. This phenomenon, however, has not been previously described in thyrotoxicosis due to amiodarone usage. We describe a case of amiodarone-induced thyrotoxicosis in a 34-year-old man who presented with sudden lower extremity weakness, heat intolerance, and weight loss. Physical examination demonstrated fine tremors. Serum potassium level was 2.2 mEq/L on admission. Gastrointestinal and renal causes of potassium loss were excluded by history and physical examination. Further biochemical testing demonstrated abnormal thyroid function. The urinary potassium and serum bicarbonate, magnesium, and calcium levels were within normal limits. Lower extremity weakness resolved immediately after potassium replacement therapy. Methimazole therapy was initiated, and the patient was clinically euthyroid on discharge.     

Potassium changes in megaloblastic anaemia.

1. Serial measurements of serum potasssium and total-body potassium were made on eighteen patients with megaloblastic anaemia before the start of therapy and during the period of recovery. 2. In those patients who presented with an initial packed cell volume of less than 25%, a mean decrease in serum potassium of 0.4 mmol/1 occurred on average with 2.5 days of the start of therapy. This was followed by a significant increase in serum potassium during the period of recovery. There was a significant increase in total-body potassium in these patients, but this could be explained by increases in erythrocyte mass, erythrocyte potassium concentration and lean body mass.     

Determination of ammonia in urine with an ammonium electrode and with a direct method

The results of ammonia determination in urine with an electrode method as well as with a direct method were strongly correlated (r = 0.998), the electrode method yielding somewhat lower values (p < 0.001). The electrode method is simple. It requires 20 ml of urine of a pH not exceeding 7. Correction of the potassium error is necessary, thus a nomogram is presented. The direct method is simple in skilled hands, it requires 1 μl of urine. Presumably it provides the exact urinary ammonia concentration. Calculation of urinary potassium by performing both ammonia methods on urine samples showed a close correlation (r = 0.926) to measured urinary potassium.     

Effect of Volume Expansion by Hyperosmolar and Hyperoncotic Solutions under Constant Infusion of Angiotensin II on Plasma Aldosterone in Man and its Counterbalance by Potassium Administration

Abstract. The influence on plasma aldosterone of plasma volume expansion by hyperosmolar and hyperoncotic solutions and its counterbalance by potassium administration was studied in man. All experiments were done during constant infusion of angiotensin II (All) which consequently excluded changes of the endogenous renin. Hyperosmolar infusion of NaCl, mannitol and NaHCO₃ provoked an immediate fall in plasma aldosterone levels and presumably a shift of intracellular potassium to the extracellular compartment. Hyperoncotic solutions of dextran in 0.9% NaCl provoked an immediate fall in plasma aldosterone while dextran in 5% glucose provoked a delayed fall. Administration of minute amounts of potassium could prevent the fall in plasma aldosterone which followed administration of dextran solutions. The same minute amount of potassium, administered without volume expansion, increased plasma aldosterone markedly above the high levels induced by AII. – The data presented add further evidence for the important role of potassium as a mediator in aldosterone regulation. They indicate that intracellular potassium changes at the adrenal level, rather than plasma potassium concentration, probably exert the regulatory function in aldosterone biosynthesis.     

Hypokalemia in acute theophylline poisoning

The frequency, severity, and time of occurrence of hypokalemia and their relationship with vomiting was studied in 40 patients with acute theophylline poisoning. The mean peak theophylline concentration was 58 micrograms/mL (range, 21 to 115), and the mean nadir of serum potassium was 3.0 mEq/L (range, 2.1 to 3.9). In 85% of the patients, the nadir of serum potassium was less than 3.5 mEq/L; 45% had potassium concentrations of less than 3 mEq/L. The severity of hypokalemia correlated with peak serum theophylline concentrations (p less than 0.001). Hypokalemia was observed early in the course of the overdose (mean, 5 hours after ingestion or administration of theophylline). The nadir in serum potassium concentrations was more severe among 25 patients who presented to the emergency department within 6 hours of the overdose than among 13 patients who presented later (mean +/- SE, 3.0 +/- 0.1 mEq/L vs 3.4 +/- 0.1 mEq/L, p less than 0.01), despite similar admission serum theophylline concentrations in both groups (49 +/- 5 and 55 +/- 5 micrograms/mL, respectively; p = not significant). Spontaneous or ipecac-induced emesis occurred in 95% of the patients; however, hypokalemia preceded vomiting in 13 patients. Its severity was similar whether patients did or did not vomit before its occurrence. Hypokalemia is a frequent manifestation of acute theophylline poisoning, has a very early onset, and occurs independently of vomiting, suggesting an intracellular shift of potassium.     

Profound muscle weakness and hypokalemia due to clay ingestion

We have presented the case of a 43-year-old woman with severe myositis due to clay ingestion and hypokalemia. EMG studies revealed a pattern consistent with myositis, and muscle biopsy showed a nonspecific diffuse myositis. The clay was shown to act as a potassium binder. With potassium replacement and discontinuance of clay ingestion, the symptoms and signs abated and laboratory values returned to normal.     

Dissociation Between Ion Permeability and the Lethal Action of Polyene Antibiotics on Candida albicans

Kinetic data on potassium release from and killing of Candida albicans by the four polyene antibiotics amphotericin B, amphotericin B methyl ester hydrochloride, nystatin, and nystatin methyl ester hydrochloride are presented. The nystatins were relatively more effective than the amphotericins in causing potassium release rather than killing. These data suggest that the aqueous channels or pores formed by the polyene antibiotics are not central to the lethal action of the drugs.     

Acute digoxin overdose: use of digoxin-specific antibody fragments

An acute ingestion of 6 to 7 mg digoxin as a suicidal gesture in a 76-year-old man with chronic heart disease is presented. The patient arrived in the emergency department approximately 5 hours after ingestion with a normal serum potassium and increasing numbers of multifocal premature ventricular contractions. Digoxin-specific antibody fragments were administered. The patient developed ventricular tachycardia and ventricular fibrillation and was eventually stabilized 35 minutes after the Fab fragments were infused. A review of the pharmacology and indications for use of digoxin-immune Fab fragments is also presented.     

Ectopic pregnancy: sonographically-guided transvaginal reduction.

The advanced modalities of vaginal ultrasonography and sensitive human chorionic gonadotropin assays have greatly facilitated the diagnosis of early ectopic pregnancy. The treatment spectrum for ectopic pregnancy ranges from a variety of conservative operative measures, including salpingectomy and operative laparoscopy, to various medical regimens or simply watchful observation alone. We report 12 cases in which the ectopic gestation was treated by transvaginal instillation of potassium chloride or methotrexate under sonographic guidance. Three of these, one of two patients receiving potassium chloride and two of six patients receiving methotrexate, later required a laparotomy. The level of beta-subunit of human chorionic gonadotropin was found to be unreliable in predicting the outcome in these patients. Ultrasound follow-up is mandatory. A protocol for treatment is presented.     

Endoscopic Removal of Pharmacobezoar in Case of Intentional Potassium Overdose

Background

Hyperkalemia is a potentially life-threatening electrolyte abnormality commonly seen in the emergency department (ED). Intentional overdose of potassium supplements is an uncommon occurrence.

Objective

This case illustrates a novel approach to treatment of pharmacobezoar with esophagogastroduodenoscopy (EGD) and demonstrates its effectiveness in the setting of extended-release potassium chloride overdose.

Case Report

A 44-year-old female presented to the ED with intentional ingestion of an unknown amount of extended-release potassium chloride (K-Dur®) tablets and alprazolam (Xanax®). The patient's serum potassium was initially 7.3 mmol/L and she was treated with standard treatments, including albuterol, calcium gluconate, insulin, dextrose, and sodium bicarbonate. Radiographic investigation showed a pharmacobezoar in the gastric fundus. Treatment was then augmented with whole bowel irrigation (WBI) using polyethylene glycol solution via nasogastric tube. Patient did not tolerate the nasogastric tube, became combative with increasing alteration in her level of consciousness, and WBI therapy was stopped. After discussion with the gastroenterologist, the patient was treated with EGD to remove the pharmacobezoar. The EGD was successful in the removal of the pharmacobezoar and the patient's potassium normalized without complications.

Conclusions

We recommend that in cases of suspected or confirmed potassium drug bezoar in the stomach, physicians consider EGD for removal. This allows for normalization of potassium level while preventing adverse sequelae.     

THYROTOXICOSIS PRESENTING AS A LIFE THREATENING HYPOKALAEMIC PARALYSIS: INVESTIGATION OF THE Na/K PUMP IN ISOLATED LEUCOCYTES

A 37-year-old Chinese man presented with the rapid onset of profound muscle weakness, and a serum potassium of 1.7 mmol/l. The intravenous infusion of undiluted potassium chloride (2 mmol/ml) through a central venous catheter resulted in rapid recovery. Further investigation revealed thyrotoxicosis. He was treated with carbimazole and subsequently remained well. We assessed Na/K pump activity in isolated leucocytes taken from the patient and found an exaggerated response to adrenaline which ceased after he became euthyroid.