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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In rats, a diet depleted of potassium caused a significant hypokalemia and hypermagnesemia, a diuresis and natriuresis, a decrease in urinary and fecal excretion of potassium, a magnesiuria, and a decrease in fecal excretion of magnesium. Balance studies revealed that potassium metabolism was negative in potassium-depleted rats and that magnesium metabolism was positive and higher than in control rats. In potassium-depleted rats, potassium and magnesium contents in muscle were reduced, whereas the sodium level was increased and plasma aldosterone was significantly lower. Therefore, the elevation in plasma concentration of magnesium induced by a diet poor in potassium is the result of a more positive metabolic balance of magnesium and of shifting of magnesium from the tissue into the plasma compartment. Results of additional preliminary studies support the possibility that the hypermagnesemia may be mediated through the depression in mineralocorticoid activity induced by the depletion of potassium.
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PMID:Magnesium metabolism in potassium-depleted rats. 66 73

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

This study was designed to determine the incidence, etiology and consequences of severe hypermagnesemia. We retrospectively reviewed all hospital admissions over a 5-year period from 1984 to 1989 and identified 8 cases of severe hypermagnesemia (serum Mg > or = 6.0 mg/dl) due to magnesium ingestion. All but 1 patient were elderly (mean age 70 +/- 6 years). The etiology when identified was due to magnesium-containing cathartics (n = 3) or antacids (n = 3). The total amount of magnesium ingested was not excessive, but bowel disorders that may have enhanced absorption (such as active ulcer disease, gastritis, colitis, perforated viscus, massive gastric dilatation) were present in 7 of the 8 patients. Unexpectedly, only 1 had preexisting renal failure. Renal function was found to be normal in 1, only mildly to moderately impaired in 5 (creatinine < 3.6 mg/dl) and severely impaired in 2 (creatinine 7.6, 15.7 mg/dl). Clinical sequelae of hypermagnesemia were hypotension (n = 7), bradycardia (n = 2), respiratory depression (n = 3), EKG abnormalities (n = 6), depressed mental status (n = 5). Hypocalcemia (range 5.7-7.4 mg/dl) more severe than could be attributed to either hypoalbuminemia or acute renal failure was present in 7. A low anion gap (range-2 to 9) was present in 5. Most striking was the fact that despite clinical sequelae, the hypermagnesemia was unsuspected in 6 of the 8 cases. Hypermagnesemia can occur without severe renal insufficiency in association with bowel disease, particularly in elderly individuals, and may be a clinically unrecognized cause of cardiovascular dysfunction, hypocalcemia and neurologic or respiratory depression.
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PMID:Unsuspected morbid hypermagnesemia in elderly patients. 148 3

Serum magnesium (Mg) was measured in 6,252 patients; in 1,246 (19.9%) the value was abnormal. Hypermagnesemia (serum Mg greater than or equal to 3.9 mg/dl) was observed in 51 patients (0.8%) and hypomagnesemia (Mg less than or equal to 1.5 mg/dl) in 165 (2.6%). Hypermagnesemia was found in patients with renal failure treated with Mg-containing antacids or cathartics, or with eclamptic convulsions treated with Mg sulfate. The most frequent clinical finding of hypermagnesemia was urinary disturbance, although various other neurological signs and symptoms were observed. Hypomagnesemia was seen in patients with various diseases such as cancer, hepatic cirrhosis, cerebrovascular disease, and generally poor condition. Abnormalities of electrolytes other than Mg were also frequently observed. The most common clinical findings of hypomagnesemia were personality changes and depression. The differentiation from psychiatric disease is important.
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PMID:An analysis of hypermagnesemia and hypomagnesemia. 227 20

The schema in Table 1 illustrates the inter-relationship between the major fluid and electrolyte disturbances with their primary site of involvement, that is, the CNS or peripheral nervous system (PNS), their primary effect (nervous system depression or irritability), and the major symptom complex associated with these sites and mechanisms (obtundation, seizures, muscle weakness, and tetany). As can be seen, a pattern emerges. Disorders of sodium and osmolality, whether hypernatremia (hyperNa), hyponatremia (hypoNa), hyperosmolality (hyperOsm), or hypo-osmolality (hypoOsm), all produce CNS depression with encephalopathy as the major clinical manifestation. Disorders of potassium, whether hyperkalemia (hyperK) or hypokalemia (hypoK), produce PNS depression with muscle weakness as the major clinical manifestation. On the other hand, disorders of magnesium and calcemia produce both CNS and PNS manifestations. Hypercalcemia (hyperCa) and hypermagnesemia (hyperMg) produce CNS and PNS depression with encephalopathy and muscle weakness, respectively, being the major clinical manifestations. Hypocalcemia (hypoCa) and hypomagnesemia (hypoMg) produce CNS and PNS irritability with seizures and tetany, respectively, being the major clinical manifestations.
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PMID:Neurologic manifestations of fluid and electrolyte disturbances. 267 34

A 39-year-old women was admitted to the hospital following a large ingestion of a tricyclic antidepressant. The administration of magnesium citrate in repeated doses with activated charcoal resulted in a striking increase in serum magnesium levels followed by acute neuromuscular deterioration and respiratory depression. The patient required dialysis for control of hypermagnesemia. Her clinical condition improved slowly without further complication and she was discharged to a rehabilitation center.
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PMID:Cathartic-induced magnesium toxicity during overdose management. 375 54

Beta-adrenergic agonists tocolysis is currently the most popular treatment modality in the United States. However, magnesium sulfate is receiving increasing attention as an alternating tocolytic agent in the presence of various clinical situations, such as the treatment of insulin-dependent diabetes. While there is an abundance of information about the maternal and fetal side effects associated with beta-adrenergic tocolysis, little information is available about maternal adverse side effects of magnesium sulfate treatment for preterm labor. Side effects such as pulmonary edema, respiratory depression, hypocalcemia, and hypermagnesemia have been reported in patients receiving this agent for either tocolysis or pre-eclampsia, though their occurrence is quite rare. One of the infrequent complications of beta-adrenergic agonist tocolysis is the occurrence of a paralytic ileus, which to our knowledge has not yet been reported in association with magnesium sulfate tocolysis. This article therefore concerns the development of a paralytic ileus in a patient receiving parenteral magnesium sulfate for tocolysis. The clinical features are described and the possible mechanisms involved discussed.
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PMID:Maternal paralytic ileus as a complication of magnesium sulfate tocolysis. 383 78

Hypermagnesemia developed in a patient as a result of excess antacid ingestion, bowel obstruction, and renal failure. Before the diagnosis was considered, refractory hypotension, respiratory depression, and coma developed, all of which were eventually reversed through the lowering of the serum magnesium concentration by hemodialysis.
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PMID:Hypermagnesemia as a cause of refractory hypotension, respiratory depression, and coma. 722 50

A preterm male infant born at 33 weeks of gestation developed respiratory depression and apnea at approximately 20 h after birth. Laboratory tests indicated severe hypermagnesemia, acidosis, and hypercalcemia. Cord blood and maternal blood concentrations of magnesium were normal. The effects and possible causes of hypermagnesemia are reviewed. The infant recovered with treatment, although the etiology of his hypermagnesemia remains unknown.
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PMID:Los Angeles County-University of Southern California Medical Center clinical pathology case conference: extreme hypermagnesemia in a neonate. 772 Feb 55

We present the case of a patient in whom hypotension, sudden cardiopulmonary arrest, and coma developed after a massive dose of a seemingly harmless cathartic agent. The diagnosis of hypermagnesemia was made 9 hours after the patient's admission, when the serum magnesium concentration was 21.7 mg/dL (8.9 mmol/L). The patient's condition improved with IV calcium, saline solution infusion, and cardiorespiratory support. The elimination half-life of magnesium in this case was 27.7 hours. Few cases have been reported in which patients have survived with serum levels greater than 18 mg/dL (7.4 mmol/L). This case provides evidence that hypermagnesemia may occur in patients with normal kidney function. The diagnosis of hypermagnesemia should be considered in patients who present with symptoms of hyporeflexia, lethargy, refractory hypotension, shock, prolonged QT interval, respiratory depression, or cardiac arrest.
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PMID:Acute hypermagnesemia after laxative use. 890 78


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