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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Three infants with infant botulism are presented to illustrate how atypical, early, and severe features may obscure or delay diagnosis. Two boys aged 6 weeks and 20 days, respectively, presented with rapid deterioration after brief periods of poor feeding, one with an apparent life-threatening event at home and the other with a full cardiopulmonary arrest. Initial abnormal laboratory findings of coagulopathy suggested sepsis in the first infant. In the second infant, severe acidosis and hypoglycemia suggested an underlying metabolic disorder. A third infant, aged 1 month, was hospitalized originally with an admitting diagnosis of "pharyngitis" resulting from his inability to take adequate feedings. He received intravenous fluids and antibiotics. One week later he suffered a respiratory arrest. Laboratory findings of severe hyponatremia and acidosis at the time of his arrest suggested a metabolic etiology. Even retrospectively, none of these infants had the typical initial complaint of constipation, and none were noted to have ptosis or facial weakness before catastrophic collapse. However, in each case, the parent had initially brought the child to the physician for "poor feeding" or "poor suck," which was not recognized by medical personnel as a result of bulbar weakness. Ultimately, all 3 infants were found to have infant botulism. All 3 had received antibiotics before catastrophic collapse, possibly contributing to the rapidity of the deterioration. Each recovered, although the delay in diagnosis made them ineligible for treatment with botulism immunoglobulin.
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PMID:Catastrophic presentation of infant botulism may obscure or delay diagnosis. 1614 Jun 90

A case report of a 67-year-old man who suffered a hypersensitivity reaction to atorvastatin is described. He suffered collapse and was in shock characterised by marked hypotension, facial oedema and eosinophilia. His initial condition led the surgeons to think he might have had an abdominal sepsis. The reaction with angio-oedema reoccurred on rechallenge. The literature on statin hypersensitivity reactions which can occur several months after commencing therapy is reviewed. Although the estimated prevalence is rare (0.1%), prescribers and pharmacists should be aware of this important reaction which can be quite debilitating.
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PMID:Hypotension and eosinophilia with atorvastatin. 1622 23

Respiratory dysfunction during sepsis is common. However, although lung function can often be adequately supported, death frequently results from cardiovascular collapse. Despite intense investigation, the mechanism underlying the myocardial dysfunction of sepsis remains unclear. Macrophage migration inhibitory factor (MIF), an important cytokine released in sepsis and the acute respiratory distress syndrome, is a known cardiac depressant. We hypothesized that MIF released from the lung results in myocardial dysfunction during sepsis. In murine models of polymicrobial sepsis, we demonstrate a significant increase in the lungs of total and lavagable MIF between 20 and 30 h post induction of sepsis. At 30 h post sepsis, the lungs released MIF into the pulmonary circulation, increasing the plasma concentration by up to 51% in a single pass. Exogenous MIF, instilled into the lungs, increased alveolar keratinocyte-derived chemokine (KC), Macrophage inflammatory protein-2 (MIP2), and tumor necrosis factor alpha (TNFalpha) at 3 h, and plasma KC and MIP2 at 6 h postinstillation. This was associated with an increase in p38 mitogen-activated protein kinase and c-Jun N-terminal kinase phosphorylation. Because changes in mitogen-activated protein kinase activation can lead to myocardial depression, these data suggest that MIF released from the lungs may be responsible, at least in part, for the cardiac dysfunction seen in the late stages of sepsis.
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PMID:Macrophage migration inhibitory factor within the alveolar spaces induces changes in the heart during late experimental sepsis. 1631 87

This article presents a case study of a 49-year-old male admitted to the Intensive Care Unit (ICU) via Accident and Emergency following a collapse at home with a diagnosis of severe sepsis. The pathophysiology of sepsis is discussed together with a physiological assessment of the patient's cardiovascular, respiratory and renal systems, coagulation and metabolic responses. The discussion focuses on the period from ICU admission to commencement of drotrecogin alpha (activated) treatment (also known as recombinant human activated protein C). The management of sepsis and the treatment the patient received are outlined with particular focus on the strategic and procedural issues of the drug administration. The article concludes by presenting nursing clinical guidelines which will provide helpful guidance for nurses when caring for patients receiving drotrecogin alpha (activated) treatment. This is especially welcome, as drotrecogin alpha (activated) is internationally recommended in the treatment of severe sepsis.
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PMID:Severe sepsis: patient management focusing on administration of drotrecogin alpha (activated) infusion. 1647 Dec 93

Babesia (canis) rossi infection is common in dogs in South Africa, and frequently causes severe, life-threatening disease. Acidemia, persistent hyperlactatemia, hemoconcentration, elevated creatinine, cerebral babesiosis, pulmonary edema and pancreatitis are all associated with mortality rates above 30%, compared with overall mortality of 12% in admitted cases. Although half the admitted cases are severely anemic, hemoconcentration is associated with far higher mortality. Cerebral babesiosis is uncommon, but carries a poor prognosis. The pathological mechanism has been suggested to be endothelial cell damage and necrosis, followed by segmental microvascular necrosis with perivascular edema and hemorrhage. Renal involvement in babesiosis resembles the functional renal failure of sepsis. Hypotension is common, and other cardiovascular disturbances have been documented. Cerebellar ataxia, rhabdomyolysis and pancreatitis are recently identified complications. While the previous categorization into "severe" (life-threatening anemia) and "complicated" (complications not directly attributable to anemia) disease has proved useful, the distinction is artificial and probably unnecessary. An updated approach to classification is suggested, aimed at grouping animals by severity and prognosis, and using simple measures, such as clinical collapse and abnormal breathing, as much as possible. Although inflammatory mechanisms are undoubtedly important in the pathophysiology of babesiosis, there can be little doubt that tissue hypoxia plays a major role in the disease process.
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PMID:The South African form of severe and complicated canine babesiosis: clinical advances 1994-2004. 1650 90


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