Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 22 year-old man was brought to our hospital about twenty-three minutes following a high-speed motorbicycle accident in which he had blunt chest trauma. He was in severe respiratory distress with marked dyspnea and restless with extensive subcutaneous emphysema involving anterior chest wall, cervical and bilateral inguinal regions. A chest X-ray revealed bilateral pneumothorax involving mediastinal emphysema and also fracture of right submandibular and clavicula. In spite of orotracheal intubation and insertion of bilateral chest tube, continuous air leak and pneumothorax did not improve. Bronchoscopy revealed the disruption of mucosa of the right main bronchus at the bifurcation. Emergency right thoracotomy was performed and there was the complete disruption of the right main bronchus. Anastomosis of the right main bronchus with circumferential resection was undertaken on May 30, 1987 about two hours after trauma. About three months after reconstruction, bronchoscopic examination revealed stomal stenosis with deformation of tracheobronchial cartilage and granulation. The stenosis showed severe irregularity by deformed cartilage and thickened scar, so widening by Nd-YAG laser vaporization was inadequate in effect. Seven months after first reconstruction, we performed re-reconstructive operation, right upper sleeve lobectomy with partial resection of carcina and right wall of trachea for scar with severe deformation of cartilage. Following the operation, the patient suffered from sepsis with pneumonitis accompanied by lung edema. This complication was treated successfully. We considered that acute pneumonitis was caused by reventilation with increase of perfusion after tracheobronchial reconstruction. Consequently, we thought it important to treat such patients with long term IPPB postoperatively with adequate medication for respiratory system.
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PMID:[Successful re-reconstruction for complete disruption of the right main bronchus by blunt chest trauma]. 232 99

A 7-year-old Thoroughbred mare was examined because of persistent bilateral epistaxis and respiratory distress. Evidence of bilateral pleural effusion was found during physical examination, and a large amount of serosanguineous fluid was drained from the right side of the thorax. Cytologic examination and bacteriologic culture of the transtracheal aspirate and pleural fluid did not yield evidence of sepsis. A coagulation profile was unremarkable. Radiographic and echographic changes were seen in the lung parenchyma. Pleuroscopy, with the horse standing, revealed numerous dark nodules on the pleura, diaphragm, and lung surface. On the basis of biopsy and necropsy findings, the histopathologic diagnosis was disseminated hemangiosarcoma.
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PMID:Pleuroscopic diagnosis of disseminated hemangiosarcoma in a horse. 234 59

We report two cases of duodenal ulcer (DU) identified at endoscopy in a pair of dizygotic twins; their outstanding clinically recognizable features were a very early onset, a great familiar occurrence, a lack of triggering conditions (drugs, burns, stress, sepsis, respiratory distress), normal serum levels of gastrin and pepsinogen I, inadequate response to medical treatment with H2-receptor antagonists, but satisfactory response to associated therapy with H2-receptor antagonists and sucralfate. Results of this study show that examined twins were affected by a form of early-onset primary DU, probably inherited like an autosomal dominant disorder with high degree of penetrance, associated with normal serum pepsinogen I and gastrin; in this form of Du a decreased tissue resistance of duodenal mucosa is likely more important, pathogenically, than an increased peptic secretion. At present long-term prognosis of our patients is unknown.
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PMID:[Duodenal ulcer in 2 dizygotic twins]. 237 69

We evaluated the results of hemodialysis performed with 106 double lumen catheters in 87 patients (mean age 52, range 10-82). 46 patients had chronic and 38 acute renal failure; 2 had respiratory distress syndrome and one refractory heart failure. Catheter flow ranged from 100 to 250 ml/min (mean 207) and effective clearance from 64 to 171 ml/min (mean 125). Only one catheter was used in 75 patients (86%), 2 in 7 and more than 2 in 5. Causes of failure included inadequate flow (9), coagulation (6) and displacement (4). In nine instances, severe complications developed: sepsis (3), local infection (4), hematoma (1) and vagal reaction (1). Three patient with catheters located in the subclavian vein developed vein stenosis, requiring angioplasty in 2 and graft in 1. Thus, double lumen catheter is easy to place and helps preserve future vascular sites in chronic hemodialysis.
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PMID:[Hemodialysis: vascular access with double lumen catheter]. 251 82

The adult respiratory distress syndrome (ARDS) is the pulmonary manifestation of multiple organ failure. Respiratory distress, alveolar consolidation and hypoxemia refractory to oxygen are the result of uniform and unspecific morphological reactions of the alveolo capillary membrane. The development of ARDS is most commonly associated with risk factors such as sepsis, trauma, shock or pneumonia. A causal therapy for ARDS is not known. Treatment of the underlying disease, maintenance of arterial oxygenation and prevention of secondary complications are the most important therapeutic measures.
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PMID:[Pulmonary complications within the scope of multiple organ failure]. 257 46

We report two cases of neonatal pneumococcal septicemia, including one fatal case in a 32-week-gestational-age premature infant. Neonatal pneumococcal septicemias account for less than 1% of all neonatal infections. Diagnosis is provided by simple and rapid methods for identifying pneumococci. Clinical features have little specificity (respiratory distress) and resemble those found in B streptococcus infections. The mother rarely exhibits symptoms at delivery. The severity of the prognosis is not related to resistance to the antimicrobial agents currently used in neonatal infections but to the infectivity of the organism itself and to the specific immunologic characteristics of premature neonates. The current use of amoxicillin and aminoglycosides in neonatal infections does not therefore need to be revised.
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PMID:[Neonatal pneumococcal septicemia]. 262 83

A three-day-old female infant was transferred to the Pediatric Intensive Care Unit with chief presenting problems of progressive change of cyanosis and respiratory distress. Physical examination revealed tachypnea, acrocyanosis, hepatomegaly, undetectable pulse of extremities and oozing over the place of venous puncture. Chest roentgenograms revealed slight cardiomegaly; other X-rays were within normal limits. Complete electrocardiograms showed right axis deviation and right ventricular hypertrophy. Because of an impression of neonatal sepsis, the patient was put in an incubator with oxygen and antibiotics were given. Persistent anuria appeared associated with sighs of cardiac and renal failure; the ventilator was applied; dopamine and lasix were also given. Unfortunately, the cyanosis worsened progressive. Despite several attempts at resuscitations, the infant expired eight hours later. Pathology disclosed the heart size as normal; hypoplasia of ascending aorta as 0.4 cm in diameter; a PDA with 1 cm in diameter; a diminutive bean-sized left ventricle; hypertrophy of right ventricle and atresias of aortic and mitral valves. There was no evidence of septicemia.
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PMID:[Hypoplastic left heart syndrome due to aortic and mitral atresias: report of one case]. 263 9

Pulmonary complications secondary to postburn sepsis are a major cause of death in burned patients. Using an in vitro organotypic culture system, we examined the effect of E. coli endotoxin (LPS) on lung cell surfactant synthesis. Our results showed that E. coli endotoxin (1.0, 2.5, 10 micrograms LPS/ml) was capable of suppressing the incorporation of 3H-choline into de novo synthesized surfactant, lamellar bodies (LB), and common myelin figures (CMF) at 50%, 68%, and 64%, respectively. In a similar study, we were able to show that LPS also inhibited 3H-palmitate incorporation by cultured lung cells. LPS-induced suppression of surfactant synthesis was reversed by hydrocortisone. Our results suggest that LPS may play a significant role in reducing surfactant synthesis by rat lung cells, and thus contribute to the pathogenesis of sepsis-related respiratory distress syndrome (RDS) in burn injury.
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PMID:Endotoxin suppresses surfactant synthesis in cultured rat lung cells. 264 10

Phosphatidylglycerol (PG) in amniotic fluid is recognized as a good indicator of fetal lung maturity and is unaffected by moderate amounts of blood or meconium contamination. A rapid immunologic agglutination assay, Ultrasensitive AmnioStat-FLM (FLM), was compared with two-dimensional thin-layer chromatography (TLC) and an enzymic, colorimetric procedure (E-PG). Eighty amniotic fluid specimens were analyzed. FLM results were reported as high (H), intermediate (I), or low positive (L). TLC was compared with FLM:H (n = 27), mean 0.14 (fraction of total phospholipids); I (n = 7), mean 0.11; L (n = 9), mean 0.03; negative results had no detectable PG by TLC. In 33 cases E-PG was compared with FLM:H (n = 9), mean 7.0 mumol/L; I (n = 5), mean 8.1 mumol/L; L (n = 3), mean 3.0 mumol/L; negative (n = 16), mean 3.2 mumol/L. Records were reviewed in 70 cases. Thirty cases were excluded: sample to delivery time was greater than 72 hours; steroids were given or sepsis was documented. Fetal lung immaturity was clinically present in six cases: respiratory distress syndrome in three cases and transient tachypnea of the newborn (TTN) in three cases. One false positive result was identified (TTN, FLM:H). FLM sensitivity for fetal lung maturity was 85.3%, specificity was 83.3%, and the positive predictive value for fetal lung maturity was 96.7%. FLM is a fast, reliable indicator of fetal lung maturity.
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PMID:Phosphatidylglycerol in amniotic fluid. Comparison of an "ultrasensitive" immunologic assay with TLC and enzymatic assay. 264 6

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


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