1/26. Severe hyperkalemia with minimal electrocardiographic manifestations: a report of seven cases.Severe hyperkalemia with minimal or nonspecific electrocardiographic (ECG) changes is unusual. We report data on seven patients with renal failure, metabolic acidosis, and severe hyperkalemia (K > or =8 mmol/L) without typical ECG changes. Initial ECGs revealed sinus rhythm and PR and QT intervals in the normal range. QRS intervals were slightly prolonged in two patients (110 ms), and incomplete right bundle branch block was evident in one. Thus, the absence of typical ECG changes does not preclude severe hyperkalemia.- - - - - - - - - - ranking = 1keywords = hyperkalemia (Clic here for more details about this article) |
2/26. neuroleptic malignant syndrome due to promethazine.A 42-year-old man came to our emergency room hyperthermic (oral temperature, 42.4 degrees C), diaphoretic, and delirious. Other findings included labile blood pressure, sinus tachycardia (heart rate, 138/min), tachypnea (respiratory rate 34/min), muscle rigidity, and incontinence. Two days earlier, he had gone to a local clinic with complaints of abdominal pain, nausea, and vomiting. promethazine was prescribed, and this was the patient's only medication on admission. Laboratory studies showed leukocytosis, hypernatremia, metabolic acidosis, elevated creatinine phosphokinase level, elevated transaminase levels, azotemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobulinuria. The clinical and laboratory findings were characteristic of the neuroleptic malignant syndrome, with promethazine as the offending agent.- - - - - - - - - - ranking = 0.14285714285714keywords = hyperkalemia (Clic here for more details about this article) |
3/26. ventricular flutter in a neonate--severe electrolyte imbalance caused by urinary tract infection in the presence of urinary tract malformation.male infants under the age of 3 months presenting with pyelonephritis in the presence of urinary tract malformation (UTM) are prone to transient pseudohypoaldosteronism. This may resemble congenital adrenal hyperplasia (CAH). hyponatremia, hyperkalemia, dehydration, and metabolic acidosis are the primary findings that permit the diagnosis of CAH. We report a case of transient pseudohypoaldosteronism resulting from pyelonephritis and vesicouretric reflux. The 17-day-old boy presented with a salt-losing episode simulating adrenal insufficiency. An initial diagnosis of CAH was made. The severe metabolic imbalance resulted in ventricular flutter that resolved after correction of the metabolic acidosis and the electrolyte and volume depletion. early diagnosis is essential because both conditions are potentially fatal and treatment differs significantly. Differential diagnosis may be achieved by urinalysis and abdominal ultrasound scan.- - - - - - - - - - ranking = 0.14285714285714keywords = hyperkalemia (Clic here for more details about this article) |
4/26. Acute tumor lysis syndrome with choriocarcinoma.A 52-year-old man with retroperitoneal nodal, lung, and liver metastases from choriocarcinoma received chemotherapy with etoposide, cisplatin, and bleomycin. Within 48 hours of starting treatment, he had hypotension, hypoxemia, and anuria. Laboratory values showed hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis. He was placed on mechanical ventilation, and hemodialysis was instituted, with marked improvement in renal function. A second, shortened course of chemotherapy with carboplatin and etoposide was given 21 days later. However, on hospital day 48, the patient died of progressive pulmonary insufficiency and cardiac arrest. This represents the first reported case of acute tumor lysis syndrome after systemic chemotherapy for advanced nonseminomatous germ cell cancer.- - - - - - - - - - ranking = 0.14285714285714keywords = hyperkalemia (Clic here for more details about this article) |
5/26. citric acid ingestion: a life-threatening cause of metabolic acidosis.We present a case that illustrates the acute (<6 hours) metabolic and hemodynamic effects of the ingestion of a massive oral citric acid load. The principal findings included metabolic acidosis accompanied by an increase in the plasma anion gap that was not caused by L -lactic acidosis, hyperkalemia, and the abrupt onset of hypotension. A unique feature was a dramatic clinical improvement when ionized calcium was infused. The case illustrates the importance of considering the properties of the conjugate base (anion) of the added acid because, in this instance, the citrate anion had a unique and life-threatening consequence (lower ionized calcium level) that was rapidly reversible.- - - - - - - - - - ranking = 0.14285714285714keywords = hyperkalemia (Clic here for more details about this article) |
6/26. Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion.The authors present the hospital course of a 13-year-old girl with a closed head injury who received a prolonged infusion of propofol for sedation and, subsequently, died as a result of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse. The patient had been treated for 4 days at a referring hospital for a severe closed head injury sustained in a fall from a bicycle. During treatment for elevations of intracranial pressure, she received a continuous propofol infusion (100 microg/kg/min). The patient began to exhibit severe high anion gap/low lactate metabolic acidosis, and was transferred to the pediatric intensive care unit at the authors' institution. On arrival there, the patient's glasgow coma scale score was 3 and this remained unchanged during her brief stay. The severe metabolic acidosis was unresponsive to maximum therapy. Acute renal failure ensued as a result of rhabdomyolysis, and myocardial dysfunction with bizarre, wide QRS complexes developed without hyperkalemia. The patient died of myocardial collapse with severe metabolic acidosis and multisystem organ failure (involving renal, hepatic, and cardiac systems) approximately 15 hours after admission to the authors' institution. This patient represents another case of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse observed after a prolonged propofol infusion in a pediatric patient. The authors suggest selection of other pharmacological agents for long-term sedation in pediatric patients.- - - - - - - - - - ranking = 0.14285714285714keywords = hyperkalemia (Clic here for more details about this article) |
7/26. Acute renal failure following ingestion of manganese-containing fertilizer.fertilizers are used to promote the survival and growth of plants and crops and have a good safety record when used properly. The basic elements in fertilizer include phosphorus, nitrite, and potassium. In addition, there are additive agents that vary for different crops and which may include some metals. Acute intoxication by ingesting fertilizer includes damage to various organ systems as well as severe cardiovascular or respiratory distress. We report the case of a 64-year-old man who ingested about 700 mL of fertilizer and suffered acute renal failure, hyperkalemia, and mild methemoglobinemia. After supportive care and emergent hemodialysis for hemodynamic instability due to hyperkalemia, the renal function of the patient recovered in four days.- - - - - - - - - - ranking = 0.28571428571429keywords = hyperkalemia (Clic here for more details about this article) |
8/26. Pseudo-hypo aldosteronism Type II.A 50-day-old infant diagnosed as meningitis had persistently elevated serum potassium, low serum bicarbonate and normal serum sodium. She had metabolic acidosis with low TTKG, low serum renin and low normal serum aldosterone with no renal failure or extra renal causes of hyperkalemia. Hence a diagnosis of Type II pseudo-hypoaldosteronism was made. She was started on oral thiazide following which her serum electrolytes normalized.- - - - - - - - - - ranking = 0.14285714285714keywords = hyperkalemia (Clic here for more details about this article) |
9/26. Electrocardiographic changes predicting sudden death in propofol-related infusion syndrome.BACKGROUND: The occurrence of metabolic acidosis, rhabdomyolysis, hyperkalemia, and sudden cardiac death after long-term, high-dose propofol infusion has been referred to as propofol infusion syndrome (PRIS). OBJECTIVES: The purpose of this study was to explore the ECG abnormalities observed in a patient with PRIS in order to identify possible pathophysiologic mechanisms of the syndrome. methods: ECG changes in the index case were characterized by down-sloping ST-segment elevation in precordial leads V1 to V3 (Brugada-like ECG pattern). We subsequently assessed the relationship between this ECG pattern and the propofol infusion rate, the development of arrhythmias, and the occurrence of sudden death in a previously described cohort of 67 head-injured patients, seven of whom had been identified as having PRIS. RESULTS: Six of the PRIS patients developed the ECG pattern of ST-segment elevation in leads V1 to V3 and died within hours of irrecoverable electrical storm. This ECG pattern was the first aberration recorded hours before the death of these patients. ECGs that were available for 30 of 60 unaffected patients exhibited a normal pattern. None of the 60 patients developed ventricular arrhythmias. CONCLUSION: Our findings indicate that development of an acquired Brugada-like ECG pattern in severely head-injured patients is a sign of cardiac electrical instability that predicts imminent cardiac death. Future studies will determine whether such an ECG pattern also predicts imminent cardiac arrhythmia in other patient populations.- - - - - - - - - - ranking = 0.14285714285714keywords = hyperkalemia (Clic here for more details about this article) |
10/26. Role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism.We studied the relative importance of hyperkalemia and mineralocorticoid deficiency in the metabolic acidosis of a patient with proved isolated hyporeninemic hypoaldosteronism and moderate kidney failure. The hyperkalemia and acidosis were severe in relation to the slight azotemia. Despite the systemic acidosis and urinary pH of 4.9, urinary ammonium excretion was distinctly blunted. Correction of the hyperkalemia by potassium-sodium exchange resin alone resolved the acidosis and restored the previously diminished urinary ammonium excretion to normal. Administration of mineralocorticoids only partially corrected the hyperkalemia and the acidosis. hyperkalemia by itself, rather than hypoaldosteronism per se, caused the acidosis in this patient. hyperkalemia apparently suppresses urinary ammonium excretion and thus interferes with urinary acidification.- - - - - - - - - - ranking = 1.1428571428571keywords = hyperkalemia (Clic here for more details about this article) |
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