Cases reported "Hyperkalemia"

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1/9. syncope caused by nonsteroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors.

    A 85-year-old woman with diabetes mellitus and prior myocardial infarction was transferred to the emergency room with loss of consciousness due to marked bradycardia caused by hyperkalemia. The T wave during right ventricular pacing was tall and tent-shaped while the concentration of serum potassium was high, and its amplitude during pacing was decreased after correction of the serum potassium level. Simultaneously with the correction, normal sinus rhythm was restored. The cause of hyperkalemia was considered to be several doses of loxoprofen, a nonsteroidal anti-inflammatory drug (NSAID), prescribed for her lumbago by an orthopedic specialist, in addition to the long-term intake of imidapril, an angiotensin-converting enzyme inhibitor (ACEI), prescribed for her hypertension by a cardiologist. This case warns physicians that the combination of NSAID and ACEI can produce serious side effects in aged patients who frequently suffer from hypertension, diabetes mellitus, ischemic heart disease, and degenerative joint disease.
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2/9. Electrocardiographic manifestations of hyperkalemia.

    hyperkalemia is one of the more common acute life-threatening metabolic emergencies seen in the emergency department. early diagnosis and empiric treatment of hyperkalemia is dependent in many cases on the emergency physician's ability to recognize the electrocardiographic manifestations of hyperkalemia. The electrocardiographic manifestations commonly include peaked T-waves, widening of the QRS-complex, and other abnormalities of altered cardiac conduction. Peaked T-waves in the precordial leads are among the most common and the most frequently recognized findings on the electrocardiogram. Other "classic" electrocardiographic findings in patients with hyperkalemia include prolongation of the PR interval, flattening or absence of the P-wave, widening of the QRS complex, and a "sine-wave" appearance at severely elevated levels. A thorough knowledge of these findings is imperative for rapid diagnosis and treatment of hyperkalemia.
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3/9. Electrocardiographic manifestations of hypothermia.

    hypothermia is generally defined as a core body temperature less than 35 degrees C (95 degrees F). hypothermia is one of the most common environmental emergencies encountered by emergency physicians. Although the diagnosis will usually be evident after an initial check of vital signs, the diagnosis can sometimes be missed because of overreliance on normal or near-normal oral or tympanic thermometer readings. The classic and well-known electrocardiographic (ECG) manifestations of hypothermia include the presence of J (Osborn) waves, interval (PR, QRS, QT) prolongation, and atrial and ventricular dysrhythmias. There are also some less known (ECG) findings associated with hypothermia. For example, hypothermia can produce ECG signs that simulate those of acute myocardial ischemia or myocardial infarction. hypothermia can also blunt the expected ECG findings associated with hyperkalemia. A thorough knowledge of these findings is important for prompt diagnosis and treatment of hypothermia. Six cases are presented that show these important ECG manifestations of hypothermia.
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4/9. hyperkalemia-induced ECG abnormalities in patients with reduced renal function.

    hyperkalemia is a potentially lethal condition to be aware of in the presence of ECG abnormalities especially in patients with reduced renal function. However, ECG abnormalities are not always dependent on the degree ofhyperkalemia but may be aggravated by the rapidity of the development of hyperkalemia and by associated electrolyte disorders. We describe 3 patients with renal failure and different ECG changes induced by hyperkalemia. More severe changes were observed when hyperkalemia developed rapidly, but not in presence of electrolyte disorders. Even minor ECG abnormalities must alarm physicians in patients with renal failure since severe hyperkalemia is not always associated with critical ECG changes.
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5/9. hyperkalemia associated with intravenous labetalol therapy for acute hypertension in renal transplant recipients.

    Three renal transplant recipients developed potentially life-threatening hyperkalemia after receiving intravenous labetalol for postoperative hypertension. Even as beta-adrenergic agonists find increasing use in the therapy of acute hyperkalemia, physicians should be aware of the potential of beta blockers to cause profound elevations of serum potassium.
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6/9. thrombocytosis and hyperkalemia revisited.

    A major concern of physicians caring for patients is the development of hyperkalemia, a potentially life-threatening event requiring accurate determination of its etiology. After metabolic and iatrogenic causes have been excluded, factitious hyperkalemia must be considered, one cause of which may be the method of laboratory determination. hyperkalemia associated with thrombocytosis has been previously described but is a fact commonly overlooked in the evaluation of a patient with hyperkalemia. We compared the potassium levels in simultaneous serum and plasma samples from patients with normal and elevated platelet counts, since platelet activation during clot formation is associated with release of potassium. We found consistently higher potassium levels in serum (containing products of activated platelets) than in plasma (containing nonactivated platelets). The greatest discrepancy in potassium levels was in patients with thrombocytosis. This preliminary study suggests that if there is no obvious explanation for an elevated serum potassium the plasma potassium level should be measured, particularly in patients with elevated platelet counts.
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7/9. heparin-induced hyperkalemia.

    heparin sodium is routinely used in the prophylaxis against deep venous thrombosis in medical and surgical patients. While most physicians are aware of heparin-induced thrombocytopenia and skin necrosis, the association of heparin and hyperkalemia is less well recognized. We present four cases in which the use of heparin was associated with hyperkalemia and discuss the pathophysiology. Our findings suggest that hyperkalemia can develop with the use of low-dose heparin, within seven days of initiating heparin therapy, and that patients with diabetes mellitus or chronic renal insufficiency are especially predisposed to this complication.
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8/9. Reversible acute renal insufficiency and hyperkalemia following indomethacin therapy.

    We noted five cases of reversible acute deterioration of renal function in patients with very mild to moderate renal insufficiency who received indomethacin for an acute gouty attack. This decrease in renal function was consistent with a primary decrease in renal blood flow. In addition, hyperkalemia developed in the patients, which we attribute to a decrease in renin and aldosterone secretion, a decrease in distal tubular delivery of sodium, and, more importantly, to a decrease in urine flow. This report is intended to alert physicians to the possible complications of indomethacin therapy in patients with mild renal insufficiency.
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9/9. Prolonged asystolic hyperkalemic cardiac arrest with no neurologic sequelae.

    We report the case of a 70-year-old man who developed cardiac arrest secondary to hyperkalemia that complicated severe chronic renal failure due to obstructive uropathy. The patient experienced electromechanical dissociation and approximately 26 minutes of asystole after which the resuscitation was suspended. However, 8 to 10 minutes after declaration of death, the patient was noted to have developed spontaneous return of circulation as the emergency department personnel were preparing to transport him to the morgue. The patient survived and was discharged without apparent neurologic sequelae. This case demonstrates the challenges facing physicians to predict the outcome of hyperkalemic cardiac arrest based on usual parameters. It also highlights the relative paucity of resuscitation guidelines to assist in the management of this medical emergency.
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