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

Traumatology deals with two different types of shock - the early hypovolemic-traumatic, and the late, so called septic shock, which is often associated with multi-organ failure. Both types of shock are triggered by several mediator systems of humoral and cellular origin, with numerous interactions between each other. In hypovolemic-traumatic shock central events are a perfusion deficit (ischemia with reperfusion injury via the xanthine-xanthine oxidase system) and activation of the humoral axis - of coagulation, of fibrinolysis, of the complement and kallikrein-kinin system by injured tissue. Coagulation and complement are responsible for the activation of platelets and granulocytes respectively. These cells further interact with each other e.g. via platelet activation factor, which finally causes tissue damage. Granulocytes play a central role because of their ability to release oxygen radicals and neutral proteinases, which can be monitored (elastase) and probably used to predict organ failure. The gut area is less resistant to the events of shock and therefore is a "locus minoris resistentiae" for further development of endotoxemia, bacteremia, septic shock and multi-organ failure without a typical septic focus. By this "septic challenge" further mediator systems get involved, especially those of macrophages like interleukin-1 or cachectin. Similar to the activation marker of PMN-elastase, we could demonstrate that it was possible to use neopterin for monitoring macrophage activation in sepsis and organ failure. By the action of these cellular elements in microcirculation at the endothelial and interstitial level tissue damage occurs, which finally leads to individual and multi-organ failure.
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PMID:[Current findings in the pathogenesis of the shock process in traumatology]. 328 34

Bacterial hepatic abscesses are a rare but serious disease. They develop either secondary to injuries or ischemia of the liver, infections in the drainage area of the portal vein, systemic sepsis or biliary infections. An abscess secondary to injuries or ischemia of the liver or infections in the drainage area of the portal vein, is usually caused by a mixed flora consisting of gramnegative aerobes and anaerobic bacteria. Hepatic abscesses secondary to systemic sepsis contain Staphylococci or Streptococci, while in abscesses on the basis of biliary infections gramnegative organisms are found. Clinically, one can find signs of systemic sepsis, pain in the right upper quadrant and a tender enlarged liver. Jaundice is absent unless a biliary obstruction is present simultaneously. The diagnosis is confirmed by ultrasonography or computerized tomography. An uncertain diagnosis can be confirmed by aspiration under ultrasonographic or computertomographic guidance. The therapy consists of administration of antibiotics and surgical or percutaneous drainage. Surgical drainage via laparotomy is always mandatory if one suspects a primary infectious focus within the abdomen. The mortality of multiple liver abscesses is 20 per cent, that of single abscesses 10 per cent. Amebic abscesses have been observed in nonendemic regions sporadically after travel or spontaneously. Clinical and radiological manifestations are the same as for bacterial abscesses. They are differentiated from bacterial abscesses by positive serology for amebiasis or aspiration which yields the typical anchovy paste. Most important complications are hepato-bronchial fistulae, empyema and amebic pericarditis. The therapy consists of a nitroimidazole and a luminal amebicide. Except for diagnostic reasons aspiration is only indicated for large abscesses of the left lobe of the liver. Mortality of an uncomplicated amebic liver abscess should be under one per cent.
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PMID:[Pathology, diagnosis and therapy of liver abscess]. 330 50

Recent experimental studies have demonstrated that gastric mucosal blood flow is an essential factor in mucosal defense against acute ulceration. Clinically, most patients who develop stress ulcers have experienced an episode of shock from hemorrhage, sepsis, or cardiac dysfunction. Diminished mucosal blood flow is also a common denominator in animal experiments that employ restraint, hemorrhage, or endotoxemia for the production of acute lesions. The mechanisms by which ischemia produces ulceration have been examined extensively. The leading hypothesis is that gastric mucosal blood flow plays an important role in the disposal, or buffering, of the H+ entering the tissue. Ischemia reduces the capacity of the gastric mucosa to neutralize acid that enters the tissue. This, in turn, leads to accumulation of H+ within the tissue, mucosal acidification, and ulceration. Ischemia may also render the stomach more susceptible to acute ulceration by a severe energy deficit of the gastric mucosa. Using a rat hemorrhagic shock model, a series of experiments demonstrated a profound reduction in mucosal ATP and other high-energy phosphate intermediates that coincided with the development of epithelial cell necrosis. In recent years, many of these experimental observations have been applied clinically in the management of critically ill patients at high risk for development of stress lesions. These include the correction of abnormalities in cardiac output and intravascular volume, careful attention to systemic acid-base balance, adequate nutritional support, and the use of antacids or antisecretory agents. As a result of these preventive measurements, the incidence and prevalence of stress ulcers have decreased significantly in recent years.
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PMID:Gastric blood flow and mucosal defense mechanisms. 330 51

Pylethrombosis is thrombosis of the portal vein or any of its branches. Five cases have been serendipitously detected, four by computed tomography and one by ultrasonography. Two patients had abdominal sepsis. A third patient had apparent acute cholecystitis with choledocholithiasis. The last two patients had a hypercoagulable state, mesenteric venous thrombosis, and enteric infarction that required resection. The newer diagnostic modalities of computed tomography and ultrasound may document unsuspected pylethrombosis. Surgery may be required because of signs of peritonitis, enteric ischemia, or unresolved sepsis. Anticoagulation is indicated for acute thrombosis of the portal or superior mesenteric veins to prevent further extension and enteric ischemia.
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PMID:Pylethrombosis. Serendipitous radiologic diagnosis. 331 Sep 61

The development of metabolic acidosis during neonatal sepsis with group B streptococci (GBS) has been attributed to progressive tissue ischemia resulting from reduced oxygen delivery (QO2). Using an animal model of GBS disease, we attempted to test this hypothesis by comparing the development of metabolic acidosis in two groups of piglets with comparably diminished systemic QO2, one septic and one not. Eighteen anaesthetized piglets were instrumented to observe aortic pressure, cardiac output, arterial and mixed venous blood gases, oxygen content, and hemoglobin concentration. QO2, oxygen consumption, and oxygen extraction ratio were calculated. Six piglets (group 1) received continuous infusion of live GBS organisms; six piglets (group 2) received continuous infusion of phenylephrine (PE), beginning with 10-micrograms/kg/min and increasing as required to match the PE-induced reduction in QO2 to the fall observed in the group 1 (GBS) piglets at each 30-min interval. Group 3 piglets (n = 6) received 0.9% saline and served as controls. No differences in either cardiac output or QO2 were noted comparing GBS and PE piglets at any time interval from 0-180 minutes. At 120, 150, and 180 minutes, both QO2 and cardiac output were lower in GBS and PE piglets compared to controls. Despite equivalent reductions in cardiac output and QO2, only GBS piglets developed significant metabolic acidosis, while pH and base deficit for PE piglets did not differ from controls. Oxygen consumption did not differ significantly among the three experimental groups at any observation time. Oxygen extraction ratio did not differ comparing PE and GBS piglets at any observation time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen delivery, oxygen consumption, and metabolic acidosis during group B streptococcal sepsis in piglets. 331 60

Nonpenetrating injury to the subclavian vessels is uncommon. During a 6-year period we have treated 167 patients with injuries to the subclavian and superior mediastinal arteries. Fifteen of these injuries (9%) occurred after blunt trauma. In 10 patients the proximal segment (first and second parts) of the artery was involved. No patient had an isolated injury; the most frequent associated injuries were rib fractures (n = 11), with the first rib being involved in four of these. Total brachial plexus disruption was found in nine patients. All patients with distal artery involvement had a clavicular fracture. All had an absent radial pulse and eight had critical ischemia of the hand. Four patients were treated nonoperatively and the remainder were treated along standard lines. Brachial plexus reconstruction was not feasible in any patient. Within 2 weeks of operation, one patient died as a result of head injuries and one required amputation because of sepsis. During a 12-month period, five regained full function, one additional patient requested above-elbow amputation after 6 months, and seven had a flail anesthetic limb. Twelve of these patients were involved in automobile accidents, eight of whom were wearing lap-shoulder harness seat belts with a loose-fitting shoulder strap component that created a characteristic abrasion pattern on the torso and chest. We conclude that the torsionshearing motion allowed by this situation contributed significantly to the pattern of injury and a plea is made for correctly fitted restraining devices.
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PMID:Nonpenetrating subclavian artery trauma. 338 81

Neuropathy, peripheral ischemia, and an altered host defense make the diabetic patient particularly prone to the development of infected foot ulcers. Successful treatment must be directed at these three primary pathologic situations. Since a limb-threatening infection carries a 25% risk of major amputation, early and prompt recognition and reporting of all foot problems are essential. Neuropathy requires total rest of the injured part. An altered host defense requires knowledge of the bacteria involved and proper use of antibiotics. It requires strict adherence to sound surgical principles that ensure debridement of all necrotic material and adequate dependent drainage of the wound while conserving as much viable skin and tissue for later revision or conservative amputations. Once sepsis is controlled, ischemic extremities can be revascularized. Because of the peculiar nature of the diabetic's vascular disease, revascularization procedures require the maximum skill and experience of the operating vascular surgeon. After revascularization, revisions or more conservative distal amputations can be achieved. Patient and physician education and understanding still remain essential not only to prevention but to successful management of all diabetic foot-related problems.
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PMID:The diabetic foot: amputations and drainage of infection. 355 24

Visceral hypoperfusion with local accumulation of lactate in the ischemic tissues has been reported in a septic rat model despite a hyperdynamic systemic circulation. This visceral ischemia is felt to contribute to the multiple system organ failure (MSOF) syndrome associated with sepsis. The purpose of this study was to determine whether a similar redistribution of blood flow existed in rats after a severe thermal injury as it too is associated with MSOF. Twenty-four hours after animals were subjected to either a resuscitated 50% scald burn (BURN) or sham treatment (SHAM), thermodilution cardiac output (CO), effective hepatic blood flow (EHBF) by galactose clearance at low concentrations, effective renal plasma flow (ERPF) by para-aminohippurate clearance, and blood, liver, and skeletal muscle pyruvate (P), and lactate (L) concentrations were determined. CO increased 52% in BURN (46.5 +/- 2.8 ml/min/100 g, n = 21) versus SHAM (30.7 +/- 1.0 ml/min/100 g, n = 22; P less than 0.001) while EHBF increased only 18% (BURN: 6.81 +/- 0.36 ml/min/100 g, n = 8 vs SHAM: 5.77 +/- 0.29 ml/min/100 g, n = 8; P less than 0.025) and ERPF showed an insignificant 24% increase (BURN: 2.98 +/- 0.32 ml/min/100 g, n = 6 vs SHAM: 2.40 +/- 0.40 ml/min/100 g, n = 6; P less than 0.10), demonstrating a redistribution of flow. There was no local accumulation of lactate in blood, liver, or skeletal muscle and no derangement in P/L ratios. This study when compared to previous observations in sepsis suggests that (1) the flow redistribution of sepsis has features differentiating it from solely a "stress response".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flow redistribution in a hyperdynamic small animal burn: comparison to patterns in sepsis. 359 83

Posttraumatic acute cholecystitis is an often unrecognized and potentially fatal complication seen among patients hospitalized for trauma, and differs in etiology from cholecystitis which develops de novo. The cause, although not yet clearly defined, is believed to be related to bile stasis, ischemia, bacterial infection, sepsis, the activation of factor XII, and the Shwarzman reaction. A case is described in which a 53-year-old man with pelvic fractures developed acute acalculous cholecystitis and died of multiple organ failure 3 weeks following cholecystectomy. The histopathological findings are also reported; these are most likely attributed to the Shwarzman reaction or the activation of the factor XII pathways. There has been a tendency to regard posttraumatic acute acalculous cholecystitis as induced by trauma, and calculous as mere coincidence. We believe, however, that it is not calculous but histopathological findings that determine whether acute cholecystitis following trauma was more than coincidence or just mere coincidence. Although progress in clinical care has improved the chances of survival of severely traumatized patients, posttraumatic acute cholecystitis has been increasing in frequency. We cannot be careful enough in judging the relationship of this fatal complication to the initial trauma.
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PMID:Posttraumatic acute cholecystitis. Relationship to the initial trauma. 360 14

The authors report a case of necrotizing enterocolitis which appeared in the first hours of life of a full-term neonate without signs of sepsis. This neonate presented with a severe hypoplasia of the horizontal aorta and very tight coarctation responsible for hepatic, renal and mesenteric ischemia. Reports of enterocolitis as a complication of congenital heart disease are rare and related most often to hypoplastic left heart than to coarctation of the aorta.
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PMID:[A rare cause of neonatal ulcero-necrotizing enterocolitis: aortic coarctation syndrome]. 361 70


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