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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathophysiology, symptoms and treatment of paraquat intoxication, primarily from oral ingestion, and the pharmacology and pharmacokinetics of paraquat are reviewed. Toxicity has occurred after topical application, oral ingestion or inhalation of paraquat. Systemic toxicity has not been reported from smoking of paraquat-contaminated marijuana but heavy abusers of contaminated marijuana may experience coughing, hemoptysis and mouth irritation. Following ingestion of 30 mg/kg or 50 ml of a 21% (w/w) solution of paraquat (as the base), hepatic, cardiac or renal failure or death may occur. Smaller doses (greater than or equal to 4 mg/kg of paraquat base) may cause respiratory distress, renal dysfunction or, occasionally, jaundice or adrenal cortical necrosis. When paraquat ingestion is suspected, the drug should be removed immediately from the gastrointestinal tract by gastric lavage or by whole-gut irrigation. Adsorbents such as Fuller's earth, bentonite or activated charcoal may be used during gastric lavage. Combined use of forced diuresis (with furosemide, mannitol and i.v. dextrose in water or normal saline), hemodialysis or hemoperfusion is recommended until the compound cannot be detected in body fluids or the dialysate. Immediate and effective treatment is necessary to prevent systemic toxicity or death from paraquat intoxication.
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PMID:Paraquat poisoning: a review. 36 Aug 33

It was examined, whether by intraamnial applicated lecithine an approaching respiratory distress syndrome could be prevented. This possibility of therapy was tested on a fetus unviable of life. It was shown by examining the lavage-fluid of the fetal lung, as well as the organ homogenates of lung; liver and gut, that the intraamnial applicated lecithine was metabolised and resynthesised in the organism. In the lung the lecithine was present as a complete molecule.
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PMID:[Intraamnial application of 14C-labeled lecithine at man 13 hrs. ante partum (author's transl)]. 57 12

A rat model is described in which animals develop respiratory cryptosporidiosis, a disease which is well documented in immunocompromised patients, especially those with AIDS. Our present lack of knowledge of the pathophysiology and immunology of Cryptosporidium parvum respiratory infections warrants the development of a laboratory animal model. Lewis rats immunosuppressed by subcutaneous injection of methylprednisolone acetate and inoculated intratracheally with 10(6) C. parvum oocysts developed a reproducible infection consisting of all known developmental stages in the epithelium lining airways from the trachea to the terminal bronchioles. Developmental stages were morphologically indistinguishable from those seen in gut epithelium. Infections were apparent at 4 days post-inoculation, and at 10-14 days post-inoculation, rats exhibited respiratory distress and severe weight loss and had enlarged, elastic lungs. Increased mucus production and exfoliative necrosis of the epithelium resulted in accumulation of large amounts of mucocellular exudate throughout the airways and patchy alveolitis involving alveoli emerging from respiratory bronchioles.
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PMID:An immunosuppressed rat model of respiratory cryptosporidiosis. 181 28

Multiple organ failure continues to be the primary cause of death after trauma and sepsis. This clinical syndrome represents the transition from a hypermetabolic response to injury to a syndrome of progressive organ failures and death. Risk factors include: perfusion deficits, persistent foci of dead or injured tissue, an uncontrolled focus of infection, the presence of the respiratory distress syndrome, persistent hypermetabolism, and preexisting fibrotic liver disease. Once initiated, most treatment modalities for the organ failure syndrome become progressively ineffective including: ventilation, antibiotics, nutrition, and surgery. The best treatment remains prevention and rapid control of risk factors including restoration of oxygen transport and aggressive nutrition support. There seems to be no treatment "magic bullet" either experimentally or clinically once the syndrome has occurred. The metabolic response to injury involves alterations in physiology and in the metabolism of carbohydrate, fat and amino acids. These changes seem to reflect the modulation of the end-organs by the mediator systems activated in response to the stress stimuli. The transition from hypermetabolism to organ failure appears to reflect the clinical appearance of liver failure. It is hypothesized that this liver failure may represent a state of regulatory dysfunction induced in large part by the activated hepatic macrophage, the Kupffer cell. The activation of these macrophages is hypothesized to represent the final stage of a series of stimulating events, eg. hypoxia, endotoxin, bacteria, and gut translocated toxins. The precise monokine(s) responsible are not yet completely characterized, although Interleukin-1 (IL-1) and tumor necrosis factor (TNF) appear to be involved as do prostaglandins (Pg) such as PgE2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of monokines in altering hepatic metabolism in sepsis. 264 13

Times of first stool passage were studied in 171 infants who weighed less than 1,500 g at birth. Delayed passage (greater than 48 hours) was noted in 20.4% of this group. Significant differences were noted between the delayed and nondelayed groups for gestational age, presence of severe respiratory distress syndrome, and the time of the first enteral feeding. In very low birth weight infants, delay in the passage of the first stool is a common occurrence. This delay is probably due to physiologic immaturity of the motor mechanisms of the gut, lack of triggering effect of enteral feeds on gut hormones, and the presence of severe respiratory distress syndrome, which may singly or in concert adversely affect gastrointestinal motility.
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PMID:Passage of the first stool in very low birth weight infants. 310 45

Multiple organ failure continues as the main cause of death after burns, trauma and sepsis. This clinical syndrome represents the transition from a hypermetabolic response to injury to a setting of clinical organ failures and death. Risk factors include: perfusion deficits, persistent foci of dead or injured tissue, an uncontrolled focus of infection, the presence of the respiratory distress syndrome, persistent hypermetabolism, and preexisting fibrotic liver disease. Once in the organ failure syndrome, most treatment modalities become progressively ineffective, including: ventilation, antibiotics, nutrition, and surgery. The best treatment remains prevention with rapid control of the source and restoration of oxygen transport. The response to injury involves alterations in physiology and in the metabolism of carbohydrate, fat and amino acids. These changes seem to reflect the modulation of the end-organs by the mediator systems activated in response to the stress stimulus. The transition from hypermetabolism to organ failure appears to reflect the clinical appearance of liver failure. It is currently hypothesized that this liver failure represents a state of regulatory dysfunction induced by the activated hepatic macrophage, the Kupffer cell. This same process may also influence metabolic failure in other organs where this cell-cell regulation can occur, e.g. kidney, lung. The activation of these macrophages is hypothesized to represent the final stage of a series of continuous stimulating events, eg. hypoxia, endotoxin, bacteria, and gut translocated toxins. The precise monokine(s) responsible are not yet completely characterized. Treatment consists of the modalities outlined above and the employment of aggressive metabolic (nutritional) support.
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PMID:Hypermetabolism/organ failure: the role of the activated macrophage as a metabolic regulator. 328 26

Pancuronium bromide treatment in severely ill, mechanically ventilated infants has been shown to result in lower peak transpulmonary pressure, with an accompanying lower-than-expected incidence of pneumothorax. Infants, treated with pancuronium often demonstrate an ominous abdominal roentgenographic finding: the "gasless abdomen." Of 38 mechanically ventilated infants, 22 of 24 pancuronium-treated infants (as compared with four of 14 untreated infants) had diminished or absent bowel gas. There was no significant difference between the two groups with regard to birth weight, mortality, or incidence of respiratory distress syndrome. Pancuronium prevents swallowing of air but does not inhibit gut peristalsis, thus accounting for the evacuation of abdominal gas three hours or more after administration of the drug. Clinicians who treat infants with pancuronium should be aware of the phenomenon, to avoid needless roentgenographic studies.
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PMID:Pancuronium and abnormal abdominal roentgenograms. 741 4

Neuroenteric cysts are uncommon congenital malformations that can require early surgical treatment. The authors report on an unusual treatment of a very large neuroenteric cyst that involved most of the small bowel and extended into the chest. A 1-day-old boy was admitted because of abdominal distension. The prenatal ultrasound results at 8 and 36 weeks had been normal. Examination showed right upper quadrant fullness and mild respiratory distress. A malformed sternum and asymmetric upper thoracic vertebra were seen on the initial x-rays. The possibility of a midthoracic right paravertebral mass was raised. Abdominal ultrasound findings were consistent with a large bowel duplication cyst. Laboratory results were all normal except the bilirubin level, which was (59 mmol/L). During laparotomy, the second part of the duodenum was found to enter a dilated cyst, and the terminal ileum arose from the cyst. The total length of the intact small bowel was 20 cm including a competent ileocecal valve. The site of the biliary duct entering the cyst was not clear. The surgical procedure involved partial resection of the anterior wall of the cyst, creation of an enteric tube from the posterior cyst wall to communicate between the duodenum and the ileum, and addition of another 25 cm of length to the small bowel. An enterocutaneous fistula was created with the proximal portion of the cyst because the site of the papilla of Vater was suspected to enter this part of the cyst. A postoperative HIDA scan showed good uptake with no excretion into the gut or the proximal pouch.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unconventional treatment of neuroenteric cyst in a newborn. 772 13

We have used rats with epidermal growth factor (EGF) autoantibodies to study the role of EGF deficiency during perinatal development. The study was focused on organs known to contain EGF or its receptor. Compared with controls, the offspring of autoimmune rats had a higher perinatal mortality and a lower birth weight. The weight of the lungs was particularly low in the offspring of EGF-immunized rats, and morphologically the lungs from the surviving pups seemed atelectatic and had alveolar duct dilatation, which indicates mild respiratory distress syndrome. Judged from immunohistochemical studies, the amount of surfactant protein-A was decreased, suggesting a delayed lung maturation. The offspring of EGF-immunized rats had dry and wrinkled skin. The skin was thin and the hair follicles were immature. This suggests a role for EGF in the growth and development of the skin. The liver/body weight ratio was lower in pups from EGF-immunized rats. This difference was, however, not significant (p = 0.07), but flow cytometric analyses showed a significantly lower proportion of the liver cells from newborn EGF-deficient pups to be in S-phase and indicated that these cells were larger than liver cells from controls. To study possible alterations in EGF binding, 125I-EGF was injected i.v. in newborn rats. 125I-EGF bound in all the organs investigated. The binding is listed in decreasing order: liver, gut, skin, kidney, and lungs. In the pups from EGF-immunized rats, the lungs and the skin bound a significantly higher amount than the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fetal effects of epidermal growth factor deficiency induced in rats by autoantibodies against epidermal growth factor. 773 54

Extremely low birthweight (ELBW) infants are unique in many developmental characteristics that determine nutritional requirements, including: low energy reserves (both carbohydrate and fat); higher metabolic rate (intrinsically, due to a higher body content of more metabolically active organs, e.g. brain, heart, liver); higher protein turnover rate (especially when growing); higher glucose needs for energy and brain metabolism; higher lipid needs to match the in utero rate of fat deposition, and for essential fatty acids for brain, neural and vascular development; excessive evaporative rates, and occasionally very high urinary water and solute losses; low rates of gastrointestinal peristalsis; limited production of gut digestive enzymes and growth factors; high incidence of stressful events (e.g. hypoxemia, respiratory distress, sepsis); and abnormal neurological outcome if not fed adequately. Postnatally, ELBW infants do not grow well, or at all, often for weeks. This leads to a virtual "growth deficit", which has unknown consequences (which for the most part are not good) and requires excessive feeding later on to catch up to normal growth rates and body composition. The major future challenge for the nutrition of these infants is to define more accurately their nutritional requirements, particularly in the early postnatal period, in order to feed them more appropriately, to reduce to a minimum the nutritional and growth deficits that they so commonly develop and to prevent neurodevelopmental handicaps that are the result of nutritional deficiencies.
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PMID:Nutritional requirements of extremely low birthweight infants. 784 30


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