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Background: Contemporary emergency department (ED) standard-of-care treatment of hyperkalemia is poorly described., Objective: Our aim was to determine the treatment patterns of hyperkalemia management in the ED., Methods: This multicenter, prospective, observational study evaluated patients aged ≥ 18 years with hyperkalemia (potassium [K + ] level ≥ 5.5 mmol/L) in the ED from October 25, 2015 to March 30, 2016. K + -lowering therapies and K + were documented at 0.5, 1, 2, and 4 h after initial ED treatment. The primary end point was change in K + over 4 h., Results: Overall, 203 patients were enrolled at 14 U.S.-based sites. The initial median K + was 6.3 (interquartile range [IQR] 5.7-6.8) mmol/L and median time to treatment was 2.7 (IQR 1.9-3.5) h post-ED arrival. Insulin/glucose (n = 130; 64%) was frequently used to treat hyperkalemia; overall, 43 different treatment combinations were employed within the first 4 h. Within 4 h, the median K + for patients treated with medications alone decreased from 6.3 (IQR, 5.8-6.8) mmol/L to 5.3 (4.8-5.7) mmol/L, while that for patients treated with dialysis decreased from 6.2 (IQR 6.0-6.6) mmol/L to 3.8 (IQR 3.6-4.2) mmol/L. Hypoglycemia occurred in 6% of patients overall and in 17% of patients with K + > 7.0 mmol/L. Hyperkalemia-related electrocardiogram changes were observed in 23% of all patients; 45% of patients with K + > 7.0 mmol/L had peaked T waves or widened QRS. Overall, 79% were hospitalized; 3 patients died., Conclusions: Hyperkalemia practice patterns vary considerably and, although treatment effectively lowered K + , only dialysis normalized median K + within 4 h., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Hyperkalemia is a common electrolyte disorder that can result in morbidity and mortality if not managed appropriately., Objectives: This review evaluates the classic treatments of hyperkalemia and discusses controversies and new medications for management., Discussion: Potassium (K+) plays a key role in determining the transmembrane potentials of "excitable membranes" present in nerve and muscle cells. K+ is the predominant intracellular cation, and clinical deterioration typically ensues when patients develop sufficiently marked elevation in extracellular fluid concentrations of K+ (hyperkalemia). Hyperkalemia is usually detected via serum clinical laboratory measurement. The most severe effect of hyperkalemia includes various cardiac dysrhythmias, which may result in cardiac arrest and death. Treatment includes measures to "stabilize" cardiac membranes, to shift K+ from extracellular to intracellular stores, and to promote K+ excretion. Calcium gluconate 10% dosed 10 mL intravenously should be provided for membrane stabilization, unless the patient is in cardiac arrest, in which case 10 mL calcium chloride is warranted. Beta-agonists and intravenous insulin should be given, and some experts recommend the use of synthetic short-acting insulins rather than regular insulin. Dextrose should also be administered, as indicated by initial and serial serum glucose measurements. Dialysis is the most efficient means to enable removal of excess K+. Loop and thiazide diuretics can also be useful. Sodium polystyrene sulfonate is not efficacious. New medications to promote gastrointestinal K+ excretion, which include patiromer and sodium zirconium cyclosilicate, hold promise., Conclusions: Hyperkalemia can be deadly, and treatment requires specific measures including membrane stabilization, cellular shift, and excretion., (Published by Elsevier Inc.)

Background: In severe hyperkalemia, neurologic symptoms are described more rarely than cardiac manifestations. We report a clinical case; present a systematic review of available literature on secondary hyperkalemic paralysis (SHP); and also discuss pathogenesis, clinical effects, and therapeutic options., Case Report: A 75-year-old woman presented to the emergency department complaining of tetraparesis. Her serum potassium level was 11.4 mEq/L. Electrocardiogram (ECG) showed a pacemaker (PMK)-induced rhythm, with loss of atrial capture and wide QRS complexes. After emergency treatment to restore cell membrane potential threshold and lower serum potassium, neurologic and ECG signs completely disappeared. An acute myocardial infarction subsequently occurred, possibly linked to tachycardia induced by salbutamol therapy. We reviewed 99 articles (119 patients). Mean serum potassium was 8.8 mEq/L. In most cases, ECG showed the presence of tall T waves; loss of PMK atrial capture was documented in 5 patients. In 94 patients, flaccid paralysis was described and in 25, severe muscular weakness; in 65 patients, these findings were associated with other symptoms. Concurrent renal failure was often documented. The most frequent treatments were dialysis and infusion of insulin and glucose. Eighty-seven percent of patients had complete resolution of symptoms. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Severe hyperkalemia is always a life-threatening medical emergency, as it can precipitate fatal dysrhythmias and paralysis. SHP should be considered in the differential diagnosis of neurologic signs and symptoms of uncertain etiology, especially in a subject with kidney failure or who is taking medications that may worsen renal function. The presence of a PMK does not necessarily impede hyperkalemic cardiac toxicity., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Cephalhematomas rarely lead to serious complications such as infection, osteomyelitis and skull fractures. However, we present a newborn infant with hyperkalemia in the context of a serious complication believed to be caused by hemolysis of a large cephalhematoma. The patient was treated with urgent peritoneal dialysis and discharged with a successful outcome. In conclusion, neonates with massive cephalhematoma should be closely examined in terms of bilirubin counts as well as electrolyte counts.

Hyperkalemia is a common cause of electrolyte induced cardiac conduction disturbance. A well-defined series of changes at the cellular level leads to characteristic evolutionary changes in the surface electrocardiogram. Initial high T waves and shortened intervals give way to prolongation of conduction and lethal dysrhythmias as the serum potassium level rises. The patterns of electrocardiographic changes associated with hyperkalemia are reviewed and an outline of appropriate therapeutic interventions.

The management of medical emergencies in hemodialysis patients is not simple and is best carried out in consultation with experienced nephrologists. However, emergency staff who are likely to encounter such emergencies must be familiar with the principles of their diagnosis and treatment and have practical management strategies at their disposal.