Hypokalemia and hyperkalemia are the most commonly encountered electrolyte abnormalities in hospitalized patients. Because untreated hypokalemia or hyperkalemia is associated with high morbidity and mortality, it is important to recognize and treat them immediately. Hypokalemia and hyperkalemia can result from disruptions in transcellular homeostasis or in the renal regulation of K+ excretion. Although the recognition is simple, appropriate management requires an understanding of normal K+ homeostasis and pathophysiology. In this article, normal K+ homeostasis, pathophysiology, diagnosis and management of hypokalemia and hypokalemia are discussed.
Diagnosis ; Homeostasis ; Humans ; Hyperkalemia* ; Hypokalemia* ; Mortality ; Potassium

An 18-day-old male infant was admitted to the hospital due to recurrent hyperkalemia for more than 10 days. The neonate had milk refusal and dyspnea. The blood gas analysis revealed recurrent hyperkalemia, hyponatremia and metabolic acidosis. Adrenocortical hormone replacement therapy was ineffective. Additional tests showed a significant increase in aldosterone levels. Family whole exome sequencing revealed that the infant had compound heterozygous in the SCNNIA gene, inherited from both parents. The infant was diagnosed with neonatal systemic pseudohypoaldosteronism type I. The infant's electrolyte levels were stabilized through treatment with sodium polystyrene sulfonate and sodium supplement. The infant was discharged upon clinical recovery. This study provides a focused description of differential diagnosis of salt-losing syndrome in infants and introduces the multidisciplinary management of neonatal systemic pseudohypoaldosteronism type I.
Infant ; Infant, Newborn ; Humans ; Male ; Pseudohypoaldosteronism/genetics* ; Hyperkalemia/etiology* ; Hyponatremia/diagnosis* ; Diagnosis, Differential

Acute hyperkalemia may result from many causes, i.e. excessive load, transcellular shift, decreased renal excretion, and so on, and may be associated with irreversible and fatal cardiac manifestations, muscle weakness, ventilatory and adrenal insufficiency, etc. We experienced a case of acute hyperkalemia probably due to red cell lysis which was evident immediately after the induction of general anesthesia with thiopental sodium and succinylcholin in 1 33 year-old female patient with common bile duct obstructive jaundice. In spite of active management during anesthesia and posoperative period, eventually she died of cardiac arrest. For the successful management of the acute hyperkalemia, the anesthesiologist should be aware of its etiologies, pathophysiology, diagnosis & treatment.
Adrenal Insufficiency ; Adult ; Anesthesia ; Anesthesia, General* ; Common Bile Duct ; Diagnosis ; Female ; Heart Arrest ; Humans ; Hyperkalemia* ; Jaundice, Obstructive ; Muscle Weakness ; Thiopental

Pseudohypoaldosteronism type 1 is a genetic renal tubular disease of salt wasting, presenting in young infants. Tubular unresponsiveness to elevated endogenous and exogenous aldosterone is the suggested pathogenetic mechanism. Oral sodium chloride supplementation relieve the clinical symptoms and electrolyte distrubances. We experienced 2 cases of PHA type 1 in 38-day and 45-day old male infants who were presented with failure to thrive, vomiting and/or dehydration. Laboratory data showed hyponatremia, hyperkalemia, hypochloremia and metabolic acidosis. Renal and adrenal functions were normal. Plasma renin activity and plasma aldosterone concentration were markedly elevated. Under the diagnosis of pseudohypoaldosteronism type 1, oral supplementation of NaCl and/or kayexalate improved the clinical states of the patients.
Acidosis ; Aldosterone ; Dehydration ; Diagnosis ; Failure to Thrive ; Humans ; Hyperkalemia ; Hyponatremia ; Infant ; Male ; Plasma ; Pseudohypoaldosteronism* ; Renin ; Sodium Chloride ; Vomiting

PURPOSE: It is to examine clinical manifestations, early biochemical indicators, and risk factors for non-oliguric hyperkalemia (NOHK) in extremely low birth weight infants (ELBWI). MATERIALS AND METHODS: We collected clinical and biochemical data from 75 ELBWI admitted to Ajou University Hospital between Jan. 2008 and Jun. 2011 by reviewing medical records retrospectively. NOHK was defined as serum potassium > or =7 mmol/L during the first 72 hours of life with urine output > or =1 mL/kg/h. RESULTS: NOHK developed in 26.7% (20/75) of ELBWI. Among NOHK developed in ELBWI, 85% (17/20) developed within postnatal (PN) 48 hours, 5% (1/20) experienced cardiac arrhythmia and 20% (4/20) of NOHK infants expired within PN 72 hours. There were statistically significant differences in gestational age, use of antenatal steroid, and serum phosphorous level at PN 24 hours, and serum sodium, calcium, and urea levels at PN 72 hours between NOHK and non-NOHK groups (p-value <0.050). However, there were no statistical differences in the rate of intraventricular hemorrhage, arrhythmia, mortality occurred, methods of fluid therapy, supplementation of amino acid and calcium, frequencies of umbilical artery catheterization and urine output between the two groups. CONCLUSION: NOHK is not a rare complication in ELBWI. It occurs more frequently in ELBWI with younger gestational age and who didn't use antenatal steroid. Furthermore, electrolyte imbalance such as hypernatremia, hypocalcemia and hyperphosphatemia occurred more often in NOHK group within PN 72 hours. Therefore, more use of antenatal steroid and careful control by monitoring electrolyte imbalance should be considered in order to prevent NOHK in ELBWI.
Gestational Age ; Humans ; Hyperkalemia/diagnosis/drug therapy/*epidemiology ; *Infant, Extremely Low Birth Weight ; Infant, Newborn ; Infant, Premature ; Infant, Premature, Diseases/diagnosis/drug therapy/*epidemiology ; Republic of Korea ; Risk Factors

Boerhaave's syndrome, spontaneous esophageal rupture, is lethal and associated with a 70% survival rate despite emergent surgical management in recent reports. Early diagnosis and management is critical for more favorable outcome. But, it is difficult to diagnose early because of the low incidence and lack of specific symptoms and signs. We experienced 37 year-old male patient with Boerhaave's syndrome who was heavy drinker, and suffered from chronic renal failure. He visited a hospital because of hematemesis and severe back pain. He was transferred to our hospital with a nasogastric tube insertion, which was penetrating the distal esophagus. A radiologic examination revealed that the distal tip was located in the left pleural cavity. It was assumed that the tube had passed through the preexisting perforation site. Operation was not performed emergently due to delay in diagnosis and severe hyperkalemia. The patient was in a septic condition, but had recovered slowly after systemic broad spectrum antibiotic therapy, pleural drainage and intrapleural antibiotic injections. An esophagography revealed no leakage of gastro-grafin on the 14th hospital day, and he later completely recovered from sepsis.
Adult ; Back Pain ; Diagnosis ; Drainage ; Early Diagnosis ; Esophageal Perforation ; Esophagus ; Hematemesis ; Humans ; Hyperkalemia ; Incidence ; Kidney Failure, Chronic ; Male ; Pleural Cavity* ; Rupture ; Sepsis ; Survival Rate

The ST segment corresponds to the plateau phase of ventricular repolarization, i.e., phase 2 of the action potential. Heightened awareness of the characteristic patterns of ST segment changes is vital to quickly identifying life-threatening disorders. The differential diagnosis of ST segment elevation includes four major processes: ST segment elevation myocardial infarction (STEMI); early repolarization; pericarditis; and ST elevation secondary to an abnormality of the QRS complex (left bundle branch block, left ventricular hypertrophy, or preexcitation). Other processes that may be associated with ST elevation include hyperkalemia, pulmonary embolism, and Brugada syndrome. Two particular patterns of ST segment depression reflect STEMI rather than non-ST-segment elevation acute coronary syndrome: ST segment depression that is reciprocal to a subtle and sometimes overlooked ST-segment elevation, and ST segment depression that is maximal in leads V₁-V₃, suggesting true posterior infarction. The clinical setting and specific electrocardiographic criteria often allow identification of the cause.
Action Potentials ; Acute Coronary Syndrome ; Brugada Syndrome ; Bundle-Branch Block ; Depression ; Diagnosis, Differential ; Electrocardiography ; Hyperkalemia ; Hypertrophy, Left Ventricular ; Infarction ; Myocardial Infarction ; Pericarditis ; Pulmonary Embolism

OBJECTIVE: The biochemical data of 10 patients admitted with diabetic ketoacidosis(DKA) during the last 2 years were analyzed for the disturbances of serum potassium(K) and acid-base balance with a special interest to look for the underlying causes of potassium(K) disorder, retrospectively. METHODS: Arterial blood gas analysis was done and electrolytes, serum glucose, serum osmolality, BUN, creatinine were checked on admission and recovery in 10 patients with diabetic ketoacidosis. RESULTS: The mean(+/-SE) serum K at diagnosis and on recovery was 4.9+/-0.9mEq/L(range, 3.2-6.5 mEq/L) and 3.8+/-0.2mEq/L(range, 3.0-4.3mEq/L), respectively. Hyperkalemia(>5.0mEq/L) in 30%(3/10) and hypokalemia(<3.5mEq/L) in 10%(1/10) was noted on admission, whereas, on recovery, hyperkalemia in none and hypokalemia in 40%(4/10). Initial K levels showed a negative correlation with pH(gamma= -0.62, P=0.05) but no significant correlation was found between the initial K levels with anion gap (AG), with serum glucose value and with blood osmolality. Only 40%(4/10) had a simple metabolic acidosis while 60%(6/10) had a mixed acid-base disorder DKA with respiratory alkalosis, mostly(5/6). The ratio of delta AG over delta HCO3 was not significantly different between patients with a simple metabolic acidosis(0.95) and with a mixed acid-base disorder(0.92). CONCLUSION: The degree of acidosis must be one of the predominant factors in the pathogenesis of the initial hyperkalemia rather than hyperglycemia resulting from insulinopenia itself. Also, we observed that patients with DKA commonly develop mixed acid- base disorders, and delta AG/delta HCO3 ratio would not be an useful tool to look for a mixed acid-base disorder.
Acid-Base Equilibrium* ; Acidosis ; Alkalosis, Respiratory ; Blood Gas Analysis ; Blood Glucose ; Creatinine ; Diabetic Ketoacidosis ; Diagnosis ; Electrolytes ; Humans ; Hyperglycemia ; Hyperkalemia ; Hypokalemia ; Osmolar Concentration ; Potassium* ; Retrospective Studies

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.
Blood Chemical Analysis/methods ; Emergency Service, Hospital ; Humans ; Hyperkalemia/*diagnosis ; Point-of-Care Systems ; Potassium/*blood ; Renal Insufficiency, Chronic/*blood ; Reproducibility of Results ; Retrospective Studies ; Sensitivity and Specificity

Hypokalemia is a common clinical problem. The kidney is responsible for long term potassium homoeostasis, as well as the serum potassium concentration. The main nephron site where K secretion is regulated is the cortical collecting duct, mainly via the effects of aldosterone. Aldosterone interacts with the mineralocorticoid receptor to increase sodium reabsorption and potassium secretion; the removal of cationic sodium makes the lumen relatively electronegative, thereby promoting passive potassium secretion from the tubular cell into the lumen through apical potassium channels. As a result, any condition that decreases the activity of renal potassium channels results in hyperkalemia (for example, amiloride intake or aldosterone deficiency) whereas their increased activity results in hypokalemia (for example, primary aldosteronism or Liddle's syndrome). The cause of hypokalemia can usually be determined from the history. If there is no apparent cause, the initial step is to see if hypokalemia is in associated with systemic hypertension or not. In the former group hypokalaemia is associated with a high mineralocorticoid effect or hyperactive sodium channel as in Liddle's syndrome. In hypertensive hypokalemic patients, measurement of the renin, aldosterone, and cortisol concentrations would be of help in differential diagnosis.
Aldosterone ; Amiloride ; Diagnosis, Differential ; Humans ; Hydrocortisone ; Hyperaldosteronism ; Hyperkalemia ; Hypertension ; Hypokalemia ; Kidney ; Mineralocorticoids ; Nephrons ; Potassium ; Potassium Channels ; Receptors, Mineralocorticoid ; Renin ; Sodium ; Sodium Channels