Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven cases of submersion in the Dead Sea are described. The clinical picture varied in severity and consisted of signs of pulmonary edema, chemical bronchitis, hypermagnesemia and hemoconcentration. Two of the patients died of hypotension and cardiac arrhythmia. The clinical findings were similar to those found in cases of drowning in seawather, but the presence of hypermangesemia is unique to this entity. The amount of aspirated water causing severe clinical signs seemed to be much smaller than is seen with ordinary seawater. Therapeutic guidelines, including assisted respiration, infusion of hypotonic solutions and corticosteroid therapy, are suggested.
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PMID:Near drowning in the Dead Sea. 85 66

Aluminum phosphide (ALP) is highly toxic to the lungs, heart and blood vessels causing pulmonary edema, shock and arrhythmias. There is massive focal myocardial damage resulting in raised cardiac enzymes. This study included 92 patients of proven ALP poisoning. The age varied between 20-50 years and the majority (74) were females. Clinical manifestations were nausea and vomiting (92), dyspnea and palpitation (72 each), cyanosis (54), hypotension (32) and shock (46) etc. Cardiac arrhythmias were present in 80 cases and hypermagnesemia in 78 patients. Mean serum magnesium level (1.95 +/- 0.18 mE/l) was significantly (p less than 0.01) raised compared to mean magnesium level in control subjects (1.62 +/- 0.26 mEq/l). Hypermagnesemia results from myocardial and liver damage and to our knowledge has not been described in the literature. Of 92 cases studied, 66 died, 60 of whom died within 24 hours of ALP ingestion. Treatment is supportive.
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PMID:Hypermagnesemia following aluminum phosphide poisoning. 202 69

With 2 groups of 10 patients the influence of an additional therapy with 1 g magnesium sulfate/h during i.v. tocolysis with the betamimetic fenoterol (2 micrograms/min) upon parameters of water and electrolyte balance has been investigated. The whole of the magnesium administered during the 24 hours investigational period has been eliminated via the kidneys. Most probably due to a competition within the distal tubulus hypermagnesemia was associated with hypocalcemia and hypercalciuria, followed by a rise in parathyroid hormone. As PTH is able to compensate hypocalcemia not only by means of bone mobilisation but also by an increase in enteral Ca absorption, estimated losses of calcium are minimal. These may be neglected, as additional therapy with magnesium sulfate--besides the advantages yet known (cardioprotection, saving of betamimetic dosage, reduction of drug tolerance development)--reduces betamimetic induced water retention, thus significantly diminishing lung edema hazard during tocolytic therapy.
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PMID:[Effect of co-medication with magnesium sulfate in beta-mimetic tocolysis on parameters of water-electrolyte balance]. 231 70

Aluminium phosphide (ALP) a major suicidal agent in the developing countries is freely available as grain fumigant. It is highly toxic to lungs, heart and blood vessels causing pulmonary oedema, shock and arrhythmias. There is massive focal myocardial damage resulting in raised cardiac enzymes. Clinical manifestations were nausea and vomiting (32), dyspnoea and palpitations (25 each), cyanosis (12), hypotension (12) and shock (15). Cardiac arrhythmias were present in 28 cases and hypermagnesaemia in 13 patients. Mean serum magnesium level (1.95 +/- 0.2O, mEq/L) was significantly raised compared to mean magnesium level in control subjects (1.62 +/- 0.23 mEq/L). Hypermagnesaemia occurs due to myocardial and liver damage. Out of 32 cases studied, 22 died 18 within 24 hours of ALP ingestion. Thirty two cases of ALP were studied.
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PMID:Cardiovascular manifestations of aluminium phosphide intoxication. 238 68

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

To determine the effects of Tityus serrulatus scorpion toxin on lung compliance and resistance, ionic equilibrium and acid-base balance over time in anesthetized and mechanically ventilated rats, we measured air flow, tracheal and esophageal pressure. Lung volume was obtained by electronic integration of airflow signal. Arterial blood samples were collected through a catheter at baseline (before) and 5, 15, 30 and 60 min after scorpion toxin injection for arterial blood gases, bicarbonate, and alkali reserve levels as well as for, sodium, potassium, magnesium, glucose, lactate, hematocrit, and osmolality analysis. Injection of the gamma fraction of the T. serrulatus scorpion venom in rats under mechanical ventilatory support leads to a continuous decrease in lung compliance secondary to pulmonary edema, but no change in airway resistance. The changes in arterial blood gases characterizing metabolic acidosis were accompanied by an increase in arterial lactate and glucose values, suggesting a scorpion toxin-induced lactic acidosis, in association with poor tissue perfusion (hypotension and low cardiac output). Moreover, scorpion toxin injection resulted in hyperosmolality, hyperkalemia, hypermagnesemia and an increase in hematocrit. The experiments have shown a clinically relevant animal model to study severe scorpion envenoming and may help to better understand the scorpion envenoming syndrome.
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PMID:Lung compliance, plasma electrolyte levels and acid-base balance are affected by scorpion envenomation in anesthetized rats under mechanical ventilation. 1531 52