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

A multiinstitutional review of 10 pregnancies complicated by septic shock was undertaken to identify the clinical characteristics and hemodynamic alterations associated with this condition. Prolonged rupture of membranes with the subsequent development of chorioamnionitis or postpartum endometritis were risk factors that commonly preceded the diagnosis of septic shock. The majority of septic shock cases occurred during the puerperium. There were two maternal deaths in this selected series. Associated complications included pulmonary edema, adult respiratory distress syndrome, disseminated intravascular coagulation, pulmonary emboli, and cardiac arrest. The primary hemodynamic derangements were reduced systemic vascular resistance with depressed myocardial function. The mean initial systemic vascular resistance index in eight surviving women was 885 +/- 253 dyne.sec/cm5.m2. Despite an overall presenting cardiac index of 4.20 +/- 2.01 L/min/m2, five patients (50%) had evidence of myocardial depression based on analysis of their left ventricular function curves. Mean arterial pressure, systemic vascular resistance, and left ventricular stroke work index all showed significant improvement after therapy. A hemodynamic algorithm based on volume therapy, inotropic agents, and peripheral vasoconstrictors is offered. This therapeutic approach is designed to optimize cardiac performance and maintenance of organ perfusion in the critically ill patient with septic hypotension during pregnancy.
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PMID:Septic shock during pregnancy. 340 99

The course of 177 consecutive patients with severe salicylate self-poisoning treated in an intensive care unit (ICU) during a period of 15 years is presented. On admission, cerebral depression was observed in 61% respiratory failure was present in 47%, acidosis in 36% and cardiovascular function was impaired in 14%. A mortality rate of 15% was observed, which was proportionally higher in patients more than 40 years old and in patients with delayed diagnosis. Twenty-seven patients died and an autopsy was performed on 26 patients. The main autopsy diagnosis was ulcers of the gastrointestinal tract in 46%, pulmonary oedema in 46%, cerebral oedema in 31% and cerebral haemorrhage in 23%.
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PMID:Acute salicylate self-poisoning in 177 consecutive patients treated in ICU. 359 Dec 55

There is evidence from pediatric tertiary care centers in the United States that childhood deaths from asthma in hospitalized patients are becoming increasingly rare, while asthma mortality outside the hospital appears to be on the rise. When a young outpatient with asthma dies, the event is apt to be sudden and unanticipated and the victim is likely to be a preadolescent or adolescent who has suffered from asthma most of his or her life and who, despite ongoing bronchodilator therapy, requires hospitalizations for treatment of status asthmaticus. Patients in this age cohort have a strong tendency to underuse, overuse, or neglect to use prescribed medications, possibly as a gesture of emerging independence or because of the depression engendered by a chronic illness. In some instances serious psychosocial pathology accounts for noncompliance. For a patient with chronic asthma with a high-risk profile, any departure from an ongoing treatment regimen may result in respiratory failure. Pathologic complications of asthma may also act to upset the precarious physiologic equilibrium these patients have established. Unsuspected chronic pneumonia may lead to further increases in a chronically high degree of oxygen desaturation. Hypoxic seizures during an asthma attack may precipitate pulmonary edema. Tension pneumothorax has an even greater fatality potential for high-risk patients with asthma than it has for other patients with asthma, and pulmonary hypertension with cor pulmonale may develop because of chronic hypoxia. Some sudden deaths in children with chronic, severe asthma are unassociated with any of the above, making it necessary to entertain still other hypotheses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An analysis of fifteen childhood asthma fatalities. 362

The clinical signs and lesions of Nubian goats and Desert sheep orally dosed with fresh and dry leaves and stems of Ipomoea carnea at 2.5, 5 and 10 g/kg/day were studied. The signs of Ipomoea poisoning were inappetence, depression, weakness of the hind limbs, dyspnea, staggering, and pallor of the visible mucous membranes. The main lesions were focal necrosis and fatty vacuolation of centrilobular hepatocytes, accumulation of fibroblasts in hepatic portal tracts, degeneration or necrosis of the cells of the renal proximal convoluted tubules, hemorrhage in renal cortices, in renal medullas and in cardiac muscle fibers, focal pulmonary edema, and emphysema and straw-colored fluid in serous cavities. Increased serum aspartate amino transferase and ammonia concentrations, and decreased concentrations of total protein, calcium and magnesium in the serum of Ipomoea-poisoned animals were detected. Hematological changes indicated the development of normocytic normochromic anaemia.
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PMID:The effects of Ipomoea carnea on goats and sheep. 362 12

Groups of male and female Fischer 344 rats, B6C3F1 mice, and Hartley guinea pigs were exposed once for 6 hr to mean concentrations of 10.5, 5.4, 2.4, 1.0, or 0 (control) ppm of methyl isocyanate (MIC) vapor. Rats and mice were also exposed to 20.4 ppm of MIC. No deaths occurred in animals exposed to 2.4 or 1.0 ppm. The majority of deaths for the 20.4- and 10.5-ppm groups occurred during postexposure Days 1 through 3, while at 5.4 ppm deaths were observed throughout the 14-day postexposure period. The 6-hr LC50 values (with 95% confidence limits) were 6.1 (4.6 to 8.2) ppm for rats, 12.2 (8.4 to 17.5) ppm for mice, and 5.4 (4.4 to 6.7) ppm for guinea pigs. Notable clinical observations during and immediately following MIC exposure were lacrimation, perinasal/perioral wetness, respiratory difficulty (e.g., mouth breathing), decreased activity, ataxia, and hypothermia. The frequency of clinical signs decreased during the second postexposure week. Body weight losses were common in all species following MIC exposures of 2.4 ppm or greater. At 1.0 ppm, only female mice had body weight depression. Recovery of body weight loss was observed in the 5.4- (guinea pigs only), 2.4- and 1.0-ppm concentration groups. The lungs of all animals that died were discolored. Following microscopic examination of the respiratory tract, deaths were attributed to pulmonary edema and congestion. In a separate study, Fischer 344 rats and Hartley guinea pigs were exposed once for 4 hr to mean concentrations of 36.1, 25.6, 15.2, or 5.2 ppm of MIC vapor. In general, the results were similar to those of the single 6-hr exposure study.
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PMID:Acute inhalation studies with methyl isocyanate vapor. I. Methodology and LC50 determinations in guinea pigs, rats, and mice. 371 40

The case of a man who injected turpentine intravenously in an attempt to kill himself is reported. The patient developed immediate pulmonary edema and hypoxia, followed later by cellulitis at the site of injection. Although only one death to date has been attributed to this form of chemical abuse, extensive local reactions, pulmonary involvement, central nervous system depression, and febrile reactions should be anticipated, and such patients should be admitted to the hospital. Patients should be observed for local reactions and myonecrosis around the site of injection, especially as these occur 12-24 hours later.
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PMID:Intravenous hydrocarbon abuse. 377 1

Pulmonary edema has been proposed as a stimulus for pulmonary C-fibers. Stimulation of pulmonary C-fibers causes depression of cardiovascular function and either tachypnea or apnea. Our objective was to determine whether pulmonary edema, induced by either increasing pulmonary vascular permeability with alloxan or hydrostatic challenges, would elicit depression of cardiovascular function or changes in frequency of inspiratory activity. Utilizing a preparation in which the left pulmonary vessels and left airway were isolated, we monitored systemic blood pressure (BP), heart rate (HR), and diaphragm contractions (DC) in 13 anesthetized dogs. Injection of alloxan into the left pulmonary artery (LPA) produced transient decreases in HR, BP, and frequency of DC within 20 s of injection with no subsequent cardiorespiratory changes up to 5 min. These alloxan injections also caused coagulation necrosis. Generation of hydrostatic pulmonary edema in the left lung caused no changes in HR, BP, or in the frequency and amplitude of DC. We conclude that alloxan does stimulate reflex cardiorespiratory depression consistent with C-fiber stimulation, but these reflex responses are probably caused by alloxan's caustic effect and not by the resultant edema. We also conclude that pulmonary edema induced by increased hydrostatic pressure does not evoke any reflex cardiovascular responses or changes in frequency of inspiratory activity.
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PMID:Pulmonary edema in dogs fails to cause reflex responses. 381 22

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

We studied the intrapleural and hemodynamic effects of positive end-expiratory pressure (PEEP) during high-frequency ventilation (HFV) with a Venturi high-frequency ventilator (Bird). Ten healthy mongrel dogs were anesthetized with sodium pentobarbital, catheterized with intrapleural and thermodilution pulmonary artery lines, and subjected to oleic acid-induced pulmonary edema. A mean PEEP of 16 +/- 6 (SD) cm H2O restored venous admixture to baseline in nine animals. Both mean airway pressure (Paw) and mean intrapleural pressure (Ppl) increased significantly with each increment of PEEP during HFV. Approximately 50% of Paw was transmitted to the intrapleural space. Cardiac index (CI) decreased with increments of PEEP in spite of constant transmural central venous and pulmonary capillary wedge pressures, so that oxygen delivery decreased despite increased PaO2. Possible mechanisms of PEEP-induced depression of CI during HFV are discussed. We conclude that both hemodynamic and intrapleural effects of PEEP during HFV are similar to those during conventional mechanical ventilation.
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PMID:Hemodynamic effects of positive end-expiratory pressure during high-frequency ventilation. 392 57

Sixteen Holstein cattle allotted into 4 groups (4 cattle/group) were each given a single oral dosage of 0.2 g of 3-methylindole (3MI)/kg of body weight. The groups were killed at 12, 24, 48, and 72 hours, respectively, after 3MI administration. Comparison of clinical signs, pathologic pulmonary lesions, and in vitro pulmonary artery responses to pharmacologic stimuli was made between the 4 treated groups and 8 control Holstein cattle of similar age. Clinical signs of pulmonary distress first appeared 8 to 12 hours after 3MI administration. After 20 hours, clinical signs included dyspnea, moderate depression, and a marked expiratory grunt. A partial remission of these clinical signs was seen between 30 and 45 hours after 3MI administration. After remission, the cattle had clinical signs of severe dyspnea and depression and expiratory grunts were more pronounced. Pathologic pulmonary lesions, including heavy rubbery lungs, dilated interlobular septae, and subplural air bullae characteristic of pulmonary edema and interstitial emphysema were observed. The lungs of treated cattle did not collapse when the thorax was incised at necropsy. In vitro pulmonary artery strips contracted dose dependently to norepinephrine (NE). Group I tissues (12 hours after 3MI administration) responded similarly to control samples. Group II tissues (24 hours after 3MI administration) had a significant inhibition (P less than 0.05) in response to NE stimulation as compared with controls.
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PMID:Impairment of sympathetic pulmonary vasoconstriction by 3-methylindole in cattle. 401 39


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