Cases reported "Hyperkalemia"

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1/442. 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. ( info)

2/442. Pseudo myocardial infarct--electrocardiographic pattern in a patient with diabetic ketoacidosis.

    diabetic ketoacidosis is an extremely serious complication of diabetes mellitus. It arises because of a complex disturbance in glucose metabolism. There is usually a precipitating cause such as sepsis or myocardial infarction. If not recognised and appropriately treated, it can have devastating consequences. This is a case report of a patient with severe diabetic ketoacidosis and interesting electrocardiographic findings. The initial electrocardiographic (ECG) findings were suggestive of an acute myocardial infarction. The ECG changes normalised remarkably following initial management of the diabetic ketoacidosis. There have been only occasional reports of hyperkalemia causing electrocardiographic changes, closely resembling those of acute myocardial infarction. ( info)

3/442. adrenal insufficiency in smith-lemli-opitz syndrome.

    We describe three unrelated patients with adrenal insufficiency and RSH or smith-lemli-opitz syndrome (SLOS), a disorder due to deficient synthesis of cholesterol. These patients presented with hyponatremia, hyperkalemia, and decreased aldosterone-to-renin ratio, which is a sensitive measure of the renin-aldosterone axis. All patients had profound serum total cholesterol deficiency (14-31 mg/dl) and marked elevation of 7-dehydrocholesterol (10-45 mg/ dl). Two patients were newborn infants with 46, XY karyotypes and complete failure to masculinize; one of these patients also had cortisol deficiency. Both patients died within 10 days of birth of cardiopulmonary complications while on adrenal replacement therapy. The third patient diagnosed with SLOS at birth presented at age 7months with fever and diarrhea and was noted to have profound hyponatremia. This patient is maintaining normal serum electrolytes on mineralocorticoid replacement. We conclude that adrenal insufficiency may be a previously undetected and treatable manifestation in SLOS. We hypothesize that deficiency of cholesterol, an adrenal hormone precursor, may lead to insufficient synthesis of adrenal steroid hormones. ( info)

4/442. succinylcholine induced hyperkalemia and cardiac arrest death related to an EEG study.

    Changes in EEGs during cardiac arrest have been described in detail by many authors; however, mortality because of an EEG has never been reported. The authors report the case of a patient who developed cardiac arrest causally related to administration of succinylcholine for reduction of excessive amounts of myogenic artifact during an EEG. This case indicates the need for caution when doing an EEG study in an intensive care unit setting. ( info)

5/442. hyperkalemia unresponsive to massive doses of aldosterone in a patient with renal tubular acidosis.

    In a 53-year-old male patient aldosterone-refractory hyperkalemia was associated with renal tubular acidosis (RTA) due to chronic interstitial nephritis accompanied by peritubular hyaline deposits in the distal nephron. The hyperkalemia was not caused by an adrenal disorder or acidosis and could not be abolished by diuretics, cortisone, longacting synthetic ACTH, excessive doses of DOCA and aldosterone. The results of our experimental studies carried out on the hyperkalemic RTA patient as well as on various control subjects and patients suggested the presence of a specific defect in renal K excretion associated with a decreased aldosterone responsiveness of the renal tubules presumably due to the peritubular pathology. ( info)

6/442. University of Miami Division of Clinical pharmacology therapeutic rounds: drug-induced hyperkalemia.

    Drug-induced hyperkalemia is an important but often overlooked problem encountered commonly in clinical practice. It may occur in the ambulatory as well as the impatient setting. Every evaluation of a hyperkalemic patient should include a careful review of medications to determine if a drug capable of causing or aggravating hyperkalemia is present. Medications generally produce hyperkalemia either by causing redistribution of potassium (beta2 -adrenergic blockers, succinylcholine, digitalis overdose, hypertonic mannitol) or by impairing renal potassium excretion. Drugs cause impaired renal potassium excretion by (1) interfering with the production and/or secretion of aldosterone (nonsterodial anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin-II receptor antagonists, heparin, cyclosporine, and FK 506) or (2) blocking the kaliuretic effects of aldosterone (potassium-sparing diuretics, trimethoprim, pentamidine, and nefamostat mesilate). Because severe renal insufficeiency is generally required to cause hyperkalemia, an elevated serum potassium concentration in a patient with mild-to-moderate renal failure should not be ascribed to renal failure alone. A careful search for "hidden" potassium loads and for causes of impaired tubular secretion of potassium (including drugs) is necessary. Finally, it is important to recognize that the causes of hyperkalemia may be additive. patients may have more than one cause of hyperkalemia at the same time. Therefore, all potential causes of hyperkalemia, including drugs, should be systematically evaluated in every hyperkalemic patient. ( info)

7/442. Transient pseudo-hypoaldosteronism following resection of the ileum: normal level of lymphocytic aldosterone receptors outside the acute phase.

    Pseudo-hypoaldosteronism (PHA) is due to mineralocorticoid resistance and manifests as hyponatremia and hyperkalemia with increased plasma aldosterone levels. It may be familial or secondary to abnormal renal sodium handling. We report the case of a 54-year-old woman with multifocal cancer of the colon, who developed PHA after subtotal colectomy, ileal resection and jejunostomy. She was treated with 6 g of salt daily to prevent dehydration, which she stopped herself because of reduced fecal losses. One month later she was admitted with signs of acute adrenal failure, i.e. fatigue, severe nausea, blood pressure of 80/60 mmHg, extracellular dehydration, hyponatremia (118 mmol/l); hyperkalemia (7.6 mmol/l), increased blood urea nitrogen (BUN) (200 mg/dl) and creatininemia (2.5 mg/dl), and decreased plasma bicarbonates level (HCO3-: 16 mmol/l; N: 27-30). However, the plasma cortisol was high (66 microg/100 ml at 10:00 h; N: 8-15) and the ACTH was normal (13 pg/ml, N: 10-60); there was a marked increase in plasma renin activity (>37 ng/ml/h; N supine <3), active renin (869 pg/ml; N supine: 1.120), aldosterone (>2000 pg/ml; N supine <150) and plasma AVP (20 pmol/l; N: 0.5-2.5). The plasma ANH level was 38 pmol/l (N supine: 5-25). A urinary steroidogram resulted in highly elevated tetrahydrocortisol (THF: 13.3 mg/24h; N: 1.4 /-0.8) with no increase in tetrahydrocortisone (THE: 3.16 mg/24h; N: 2.7 /-2.0) excretion, and with low THE/THF (0.24; N: 1.87 /-0.36) and alpha THF/THF (0.35; N: 0.92 /-0.42) ratios. The number of mineralocorticoid receptors in mononuclear leukocytes was in the lower normal range for age, while the number of glucocorticoid receptors was reduced. Small-bowel resection in ileostomized patients causes excessive fecal sodium losses and results in chronic sodium depletion with contraction of the plasma volume and severe secondary hyperaldosteronism. Nevertheless, this hyperaldosteronism may be associated with hyponatremia and hyperkalemia suggesting PHA related to the major importance of the colon for the absorption of sodium. In conclusion, this case report emphasizes 1) the possibility of a syndrome of acquired PHA with severe hyperkalemia after resection of the ileum and colon responding to oral salt supplementation; 2) the major increase in AVP and the small increase in ANH; 3) the strong increase in urinary THF with low THE/THF and alpha THF/THF ratios; 4) the normal number of lymphocytic mineralocorticoid receptors outside the acute episode. ( info)

8/442. Acute hyperkalemia associated with intravenous epsilon-aminocaproic acid therapy.

    Epsilon-aminocaproic acid (Amicar) is used to treat severe hemorrhage refractory to usual medical management. This antifibrinolytic drug has been associated with a number of renal complications. However, there are no descriptions of this medication causing hyperkalemia. This report describes the development of hyperkalemia in a patient with underlying chronic renal insufficiency treated with intravenous epsilon-aminocaproic acid. The patient, who underwent coronary artery bypass grafting, had no other obvious cause for the acute increase in serum potassium concentration. Based on data in animals and humans, the cationic amino acids lysine and arginine have been shown to enter muscle cells in exchange for potassium and lead to hyperkalemia through a shift of potassium from the intracellular to the extracellular space. Epsilon-aminocaproic acid, a synthetic amino acid structurally similar to lysine and arginine, also has been noted to cause an acute increase in serum potassium in anephric dogs infused with this medication. It is probable that the mechanism underlying the increase in serum potassium with epsilon-aminocaproic acid is also based on the shift of potassium from the intracellular to the extracellular space. Hence, it appears that intravenous epsilon-aminocaproic acid can also cause hyperkalemia in humans. ( info)

9/442. Familial pseudohyperkalemia maps to the same locus as dehydrated hereditary stomatocytosis (hereditary xerocytosis).

    Familial pseudohyperkalemia is a "leaky red blood cell" condition in which the cells show a temperature-dependent loss of potassium (K) from red blood cells when stored at room temperature, manifesting as apparent hyperkalemia. The red blood cells show a reduced lifespan in vivo but there is no frank hemolysis. Studies of cation content and transport show a marginal increase in permeability at 37 degrees C and a degree of cellular dehydration, qualitatively similar to the changes seen in dehydrated hereditary stomatocytosis (hereditary xerocytosis). Physiological studies have shown that the passive leak to K has an abnormal temperature dependence, such that the leak is less sensitive to temperature than that in normal cells. We performed genetic mapping on the original family and found that the condition in this kindred maps to the same locus (16q23-ter) that we have previously identified for an Irish family with dehydrated hereditary stomatocytosis, which does not show the same temperature effects. ( info)

10/442. A case of aldosterone-producing adenoma with severe postoperative hyperkalemia.

    It is known that some patients with primary aldosteronism show postoperative hyperkalemia, which is due to inability of the adrenal gland to secrete sufficient amounts of aldosterone. However, hyperkalemia is generally neither severe nor prolonged, in which replacement therapy with mineralocorticoid is seldom necessary. We report a case of a 46-year-old woman with an aldosterone-producing adenoma associated with severe postoperative hyperkalemia. After unilateral adrenalectomy, the patient showed episodes of severe hyperkalemia for four months, which required not only cation-exchange resin, but also mineralocorticoid replacement. Plasma aldosterone concentration (PAC) was low, although PAC was increased after rapid ACTH test. Histological examination indicated the presence of adrenocortical tumor and paradoxical hyperplasia of zona glomerulosa in the adjacent adrenal. immunohistochemistry demonstrated that the enzymes involved in aldosterone synthesis, such as cholesterol side chain cleavage (P-450scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), and 21-hydroxylase (P-450c21), or the enzyme involved in glucocorticoid synthesis, 11beta-hydroxylase (P-450c11beta), were expressed in the tumor, but they were completely absent in zona glomerulosa of the adjacent adrenal. These findings were consistent with the patterns of primary aldosteronism. serum potassium level was gradually decreased with concomitant increase in PAC. These results suggest that severe postoperative hyperkalemia of the present case was attributable to severe suppression of aldosterone synthesis in the adjacent and contralateral adrenal, which resulted in slow recovery of aldosterone secretion. It is plausible that aldosterone synthesis of adjacent and contralateral adrenal glands is severely impaired in some cases with primary aldosteronism, as glucocorticoid synthesis in cushing syndrome. ( info)
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