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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the first case of a girl born to a diabetic mother who was found to have Down syndrome and prune-belly anomalies (bilateral gross hydronephrosis, megaureter, and megacystis with abdominal muscle deficiency). The girl also had an atrioventricular septal defect. Diagnoses were confirmed with a cytogenetic study and micturating cystourethrography. She died at 29 days of age with a sudden collapse, most likely due to sepsis.
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PMID:Prune-belly anomalies in a girl with Down syndrome. 1368 Mar 26

Anthrax, a disease of mammals (including humans), is caused by a spore-forming Gram-positive bacilli called Bacillus anthracis. Anthrax is one of the oldest threats to humanity, and remains endemic in animals in many parts of the world. The incidence of anthrax has decreased in developed countries, but it remains a considerable health problem in developing countries. The disease is transmitted to humans by contact with sick animals or their products, such as wool, skin, meat etc. Capsular polypeptide and anthrax toxin are the principal virulence factors of B. anthracis. Anthrax toxin consists of three proteins called protective antigen, edema factor, and lethal factor, each of which is nontoxic but acts synergistically. Human anthrax has three major clinical forms: cutaneous, inhalational, and gastrointestinal. The diagnosis is easily established in cutaneous cases, characterized by black eschar. Severe intoxication and collapse during the course of bronchopneumonia or hemorrhagic enteritis should prompt suspicion of anthrax. Treatment with antibiotics is mandatory. If untreated, anthrax in all forms can lead to septicemia and death. Recently, considerable attention has been focused on the potential for B. anthracis to be used in acts of biological terrorism. The ease of laboratory production and its dissemination via aerosol led to its adoption by terrorists, as shown by recent events in the USA. A good knowledge of anthrax, its epidemiology, pathogenesis, clinical forms and potential as a biological weapon is essential for timely prevention and treatment. This review summarizes the current knowledge on anthrax.
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PMID:Anthrax--an overview. 1458 93

The virulence of pathogenic bacteria is critically dependent on their ability to produce toxins that attack eukaryotic target cells. Microbial toxins are either structural components of the bacterial cell wall (endotoxins) or actively secreted proteins (exotoxins). Sepsis and septic shock, which represent major causes of mortality in modern intensive care medicine, are caused by an inadequate inflammatory and immunological host response to bacterial infection. Emerging evidence suggests that the systemic spread of microbial toxins, rather than bacteremia itself, is the crucial event in the pathogenesis of this dramatic dysregulation. The endothelium, with its diversity of physiological functions is a main target of bacterial toxins. The resulting endothelial dysfunction is believed to contribute to the underlying pathomechanisms and the collapse of homeostasis of organ function. In vitro, bacterial toxins induce subtle alterations of endothelial cell function rather than massive cell damage. Furthermore, bacterial toxins targeting endothelial cells severely alter the behavior of extravascular cells and circulating leukocytes via excessive formation of vasoactive mediators and overexpression of adhesion molecules. Research on the effects of microbial toxins on vascular endothelium has broadened our general understanding of microbial strategies to induce organ damage, even in the absence of viable bacteria. Combining antitoxin strategies with antibiotic therapy may prove to be of benefit to patients suffering from bacterial sepsis in the future.
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PMID:Endothelial responses to bacterial toxins in sepsis. 1470 Feb 71

Between January 1997 and June 2002, we retrospectively reviewed the records of all premature infants (birth weight less than 2000 g) admitted to the newborn intensive care unit (NICU) at Chi Mei Medical Center. Among the 399 premature infants (birth weight less than 2000 g) surviving more than one week, 111 infants were diagnosed with patent ductus arteriosus (PDA). Seventeen premature infants underwent surgical closure of PDA after failure of indomethacin treatment. The indication for surgical closure of PDA was ventilator dependence and/or congestive heart failure in infants with echocardiographic evidence of a ductus arteriosus. The mean gestational age and birth weight were 26.9 +/- 2.4 weeks (range 23-32 weeks) and 978.8 +/- 360.1 g (range 494-1920 g), respectively. The mean age and weight at the time of operation were 28.1 +/- 12.4 days (range 13-61 days) and 950.8 +/- 390.4 g (range 402-2120 g), respectively. All the operation procedures were performed in our NICU, using operating room personnel, thus eliminating the risks of patient transport. There was no intraoperative death. Three infants died in hospital due to other problems. One died of sepsis and the other two died due to bronchopulmonary dysplasia (BPD) and suspected sepsis. There were only two infants who had complications after surgical closure of PDA. One infant had left pneumothorax with subcutaneous emphysema and the other one had right upper lung collapse. We conclude that surgical closure of the PDA for the premature infant can be a safe and effective procedure performed in the NICU, when indomethacin closure is ineffective or contraindicated.
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PMID:Surgical closure of patent ductus arteriosus in preterm infants at neonatal intensive care unit. 1496 85

Sepsis is the clinical syndrome that results from a host's inflammatory response to infection via activation of the innate immune system. This response involves a complex network of inflammatory mediators that is self-reinforcing. When this immune response progresses uncontrollably, it can ultimately result in cardiovascular collapse and death. This complex inflammatory response is comprised of multiple mediators including cytokines such as TNF-alpha and IL-1beta, that are synthesized and secreted in response to signaling by receptors of the Toll-like receptor (TLR) family of pattern recognition receptors (PRR) that bind to pathogen associated molecules. A central downstream element of TLR-dependent signaling is the pleiotropic transcription factor NF-kappaB. NF-kappaB has been implicated in the regulation of multiple biological phenomena and disease states, including apoptosis, cell growth, stress response, innate immunity and septic shock. NF-kappaB-dependent genes are numerous and several have been implicated in the pathogenesis of sepsis and associated with cardiac dysfunction in sepsis. NF-kappaB activation occurs in multiple organs and cell types, and may be primarily protective in one tissue but injurious in another. Thus, a detailed understanding of the molecular basis of the pathophysiology of sepsis is needed in order to specifically block pro-inflammatory and pro-apoptotic signaling in the heart, while avoiding adverse effects in other organs.
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PMID:NF-kappaB action in sepsis: the innate immune system and the heart. 1497 37

Besides being one of the mechanisms responsible for ventilator-induced lung injury, atelectasis also seems to aggravate the course of experimental pneumonia. In this study, we examined the effect of reducing the degree of atelectasis by natural modified surfactant and/or open lung ventilation on bacterial growth and translocation in a piglet model of Group B streptococcal pneumonia. After creating surfactant deficiency by whole lung lavage, intratracheal instillation of bacteria induced severe pneumonia with bacterial translocation into the blood stream, resulting in a mortality rate of almost 80%. Treatment with 300 mg/kg of exogenous surfactant before instillation of streptococci attenuated both bacterial growth and translocation and prevented clinical deterioration. This goal was also achieved by reversing atelectasis in lavaged animals via open lung ventilation. Combining both exogenous surfactant and open lung ventilation prevented bacterial translocation completely, comparable to Group B streptococci instillation into healthy animals. We conclude that exogenous surfactant and open lung ventilation attenuate bacterial growth and translocation in experimental pneumonia and that this attenuation is at least in part mediated by a reduction in atelectasis. These findings suggest that minimizing alveolar collapse by exogenous surfactant and open lung ventilation may reduce the risk of pneumonia and subsequent sepsis in ventilated patients.
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PMID:Reducing atelectasis attenuates bacterial growth and translocation in experimental pneumonia. 1598 Jan 12

The stove-in chest is a rare form of flail chest in which there is collapse of a segment of the chest wall, associated with a high immediate mortality. A 65-year-old male pedestrian was admitted with severe chest pain and dyspnoea, after being struck by a car. The initial chest radiograph demonstrated multiple right-sided rib fractures and pulmonary contusion. His gas exchange was good, and after pain relief via an epidural catheter was achieved, an intercostal drain was inserted into the right hemi-thorax. Clinically apparent deformation of the chest then occurred. A further chest radiograph confirmed the stove-in chest. The patient remained well initially, but on day 5 he deteriorated precipitously with respiratory failure, and signs of systemic sepsis. He died despite maximal ventilatory and inotropic support on the Intensive Care Unit (ICU). Post-mortem examination demonstrated congested, oedematous lungs with a right-sided empyema. The management of complex flail chest injuries requires treatment to be tailored to the individual patient. Early ventilatory support, despite good gas exchange, may have closed down the pleural space prevented the empyema. Prophylactic ventilation and possibly surgical stabilisation of the chest wall should be considered early in the course of admission, even when the conventional parameters to indicate ventilation are not met.
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PMID:The stove-in chest: a complex flail chest injury. 1508 26

The authors report their experience with eight patients (11 hips) with Down syndrome who sustained a slipped capital femoral epiphysis (SCFE). Six patients were diagnosed with hypothyroidism. All patients were greater than the 85th percentile for body mass index. Initial treatment was by in situ pinning in all hips. Six of the 11 slips progressed, 2 had collapse consistent with avascular necrosis, and 1 developed collapse secondary to joint sepsis and osteomyelitis. Additional surgery was necessary on seven hips. Four of eight hips followed until maturity had substantial femoral head deformity. Three of these patients had a noticeable limp and pain. Treatment of SCFE in patients with Down syndrome is difficult and the prognosis is guarded. These patients should be screened for hypothyroidism.
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PMID:Slipped capital femoral epiphysis in patients with Down syndrome. 1510 22

Septic shock, a severe form of sepsis, is characterized by cardiovascular collapse following microbial invasion of the body. The progressive hypotension, hyporeactivity to vasopressor agents and vascular leak leads to circulatory failure with multiple organ dysfunction and death. Many inflammatory mediators (e.g. TNF-alpha, IL-1 and IL-6) are involved in the pathogenesis of shock and, among them, nitric oxide (NO). The overproduction of NO during septic shock has been demonstrated to contribute to circulatory failure, myocardial dysfunction, organ injury and multiple organ failure. We have previously demonstrated with in vitro and in vivo studies that methylguanidine (MG), a guanidine compound deriving from protein catabolism, significantly inhibits iNOS activity, TNF-alpha release and carrageenan-induced acute inflammation in rats. The aim of the present study was to evaluate the possible anti-inflammatory activity of MG in a model of septic shock induced by lipopolysaccharide (LPS) in mice. MG was administered intraperitoneally (i.p.) at the dose of 30 mg/kg 1 h before and at 1 and 6 h after LPS-induced shock. LPS injection (10 mg/kg in 0.9% NaCl; 0.1 ml/mouse; i.p.) in mouse developed a shock syndrome with enhanced NO release and liver, kidney and pancreatic damage 18 h later. NOx levels, evaluated as nitrite/nitrate serum levels, was significantly reduced in MG-treated rats (78.6%, p < 0.0001; n = 10). Immunohistochemistry revealed, in the lung tissue of LPS-treated group, a positive staining for nitrotyrosine and poly(adenosine diphosphate [ADP] ribose) synthase, both of which were reduced in MG-treated mice. Furthermore, enzymatic evaluation revealed a significant reduction in liver, renal and pancreatic tissue damage and MG treatment also improved significantly the survival rate. This study provides evidence that MG attenuates the degree of inflammation and tissue damage associated with endotoxic shock in mice. The mechanisms of the anti-inflammatory effect of MG is, at least in part, dependent on the inhibition of NO formation.
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PMID:Effect of methylguanidine in a model of septic shock induced by LPS. 1562 90

A 3-month-old male infant presented with intermittent low-grade fever from the age of 1 month. On investigation, a non-homogenous opacity was found in the upper lobe of the right lung. A computerized tomographic scan revealed loss of aeration of the right upper lobe and partial collapse of the middle lobe. A provisional diagnosis of congenital cystic adenomatoid malformation of the lung (with episodes of infection) was made. We describe the use of a single lumen tracheal tube (TT) for thoracotomy and lobectomy in this infant. The surgical procedure was complicated by a flood of thick, semisolid caseous material from the TT tube causing hypoxia and inability to ventilate the infant. The problem was managed appropriately in the circumstances. The infant died on the 10th postoperative day after two episodes of pneumothorax and, finally, sepsis, and multiorgan failure. Histopathological examination of the tissues and smears revealed acid-fast bacilli in all fields and confirmed the diagnosis of perinatal tuberculosis. This appears to be the first report of its kind of an anesthetic complication of perinatal tuberculosis. A brief update on this condition and the importance of lung separation in infants undergoing thoracotomy is discussed.
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PMID:Perinatal tuberculosis: implications of failure to isolate the lungs in an infant undergoing thoracotomy. 1602 5


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