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

To amplify recent interest in anaerobic infections following abdominal disease, trauma, or surgery, 512 consecutive patients subjected to emergency celiotomy had both aerobic and anaerobic cultures taken of peritoneal fluid as well as all complicating wound and intra-abdominal infections. Average time between peritoneal entry of abscess drainage and specimen incubating under anaerobic conditions was less than two minutes. During 4 of the seven study months, patients had antibiotic therapy randomized, with clindaymcin or cephalothin being sole parenteral agents and given intravenously prior to operation and for 5 days thereafter. Results demonstrated that anaerobes uniformly contaminate the peritoneal cavity whenever distal or obstructed intestine has been perforated, irrespective of the cause. Although all but one of the 123 complicating wound and intra-abdominal infections were due solely or at least in part to aerobic pathogens, 2/3 of such infections also contained one or more different anaerobic species acting in synergism with the aerobes. No significant difference in incidence of postoperative infection or in infecting bacteria could be found with respect to antibiotic administered or etiology of perforation. Indeed, duration of bacterial exposure to atmospheric oxygen was the most critical factor influencing culture recoverability of anaerobic organisms, likelihood of ensuing wound or peritoneal sepsis participated in by an anaerobe, and success in control of established infections harboring anaerobes.
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PMID:Incidence and significance of intraperitoneal anaerobic bacteria. 113 Aug 85

Tissue perfusion was determined by cardiac index (Cl) and skeletal muscle capillary blood flow (MBF), and arteriovenous oxygen difference (AVD) and oxygen uptake were compared in seven patients with severe spesis and eight nonseptic patients. Skeletal capillary muscle blood flow also was measured before and after a 2 day fast in 14 normal volunteers. In both septic and nonseptic patients, MBF varied directly with Cl. The average muscle blood flow was greater in septic than in nonseptic patients and, in addition, was greater per unit Cl. AVD in septic patients was narrower than in nonseptic patients. Septic patients with an AVD of less than 4 ml. of O2 had markedly higher MBF and Cl than did septic patients with an AVD greater than 4 ml. of O2. Fasting normal volunteers who, like the septic patients, would be catabolic had a significant increase in MBF during the fast. Although peripheral shunts are not ruled out ans an explanation of the hyperdynamic circulation in sepsis, the evidence is against their existence, at least in skeletal muscle, since capillary flow increases in direct proportion to cardiac output. If capillary flow is increased in fact in sepsis, then flow like blood pressure becomes less of a critical factor in explaining the demise of the septic patient. It might be postulated that the increased capillary flow seen in sepsis is secondary to the mobilization of amino acids from the body cell mass for gluconeogenesis and energy.
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PMID:Capillary muscle blood flow in human sepsis. 113 2

The relationship of glucogenesis and other energy-requiring functions of the liver to the proteolysis which is characteristic of trauma and sepsis was studied in conscious pigs following laporotomy and after the induction of intraperitoneal sepsis. By means of appropriately placed thermal dilution catheters, portal and hepatic arterial blood flows, hepatic oxygen consumption, glucogenesis, and uptake of the fuel, substrates were measured. No animal was in shock. Despite significant increases of lactate and aminoacids delivered to the liver, the blood concentrations were maintained in the normal range. The rate of glucogenesis was proportional (r equals 0.71) to the sum of the glucogenic precursors (lactate, pyruvate, glycerol, and alanine) taken up by the liver. Higher rates of glucose production were accompanied by elevated blood insulin values. Hepatic oxygen consumption and the uptake of free fatty acids also were related directly to the glucogenic rate, the correlation coefficients being 0.69 and 0.74, respectively. In the absence of shock, the liver function and hepatic energy production remained normal in post-traumatic and septic states. Under the conditions insulin-resistant muscle in the presence of reduced free fatty acid availability mobilize protein to satisfy local energy requirements. Skeletal muscle can oxidize only branch chain aminoacids; other aminoacids, including alanine, are transported to the liver for glucogenesis or other purposed. This concept accounted for failure of glucose infusion to eliminate post-traumatic and septic proteolysis, since alanine is cleared only from blood by conversion in the liver to glucose. Thus it is concluded that in sepsis the release of glucogenic substrates because of altered metabolism in peripheral tissues determines the rate of hepatic glucogenesis. This relationship constitutes an important metabolic homeostatic mechanism.
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PMID:Liver metabolism and glucogenesis in trauma and sepsis. 114 47

Total hepatic and portal blood flow as well as hepatic and splanchnic oxygen consumption was measured in pigs in the normal fasted state and in the septic fasted state induced experimentally by cecal ligation. Pigs in the septic state were divided into two groupds, a septic high output state and a septic low output state, according to whether or not a pig showed a higher or lower cardiac output in the septic state than in the normal fasted state. In the septic high output state, the average cardiac output was 155 per cent of that during fasting; hepatic arterial flow increased 96 per cent, while portal flow decreased 19 per cent. Total hepatic blood flow increased slightly, 14 per cent. The ratio of total hepatic blood flow to cardiac output decreased from 42 per cent in the normal fasted state to 30 per cent. The total hepatic oxygen consumption increased 26 per cent because of significantly elevated oxygen transport by hepatic arterial flow. In the low output state, hepatic arterial flow significantly dropped, 74 per cent, while portal flow decreased slightly, 23 per cent, and total hepatic blood flow decreased 38 per cent. The decrease of cardiac output was less, 18 per cent. The ratio of total hepatic blood flow to cardiac output was 31 per cent. Total hepatic oxygen consumption decreased remarkably, 29.1 per cent, due chiefly to the decrease of hepatic arterial flow, and splanchnic oxygen consumption also decreased significantly, 22 per cent. Dissociation of hepatic arterial response to sepsis from the other gastrointestianl vessels caused a great difference in the hepatic oxygen consumption between the septic high output and the septic low output state, contributing in part to the difference in mortality between these two states.
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PMID:Hepatic blood flow and oxygen consumption in starvation, sepsis and septic shock. 115 9

Nine variables were studied in 56 patients to analyze hemodynamic patterns of critically ill and shock patients. The variables were central venous pressure, mean arterial pressure, heart rate, cardiac index, left ventricular stroke work, strok index, total peripheral resistance, arteriovenous oxygen difference, and oxygen consumption. We observed six patterns; three with low cardiac index (hypodynamic) and three with high cardiac index (hyperdynamic). Group IA: Low cardiac index with increased central venous pressure and arteriovenous oxygen differences associated with myocardial infarction, cardiac insufficiency, and postoperative cardiac surgery: Group IB: Low cardiac index with normal arteriovenous oxygen difference associated with myocardial infarction or hypovolemia. Group IC: Low cardiac index and decreased arteriovenous oxygen difference in patients with hypodynamic septic shock. Group IID: High cardiac index and increased arteriovenous oxygen difference in patients with sepsis and stable hemodynamic conditions. Groups IIE and IIF: Increased cardiac index and normal or increased arteriovenous oxygen difference in septic patients, who were hemodymamically unstable or in shock. These hemodynamic observations were found to be useful for understanding physiological compensations, for deciding on therapy, and in evaluating the effectiveness of therapy.
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PMID:Hemodynamic patterns in shock and critically ill patients. 120 57

Acute RDS is a clinical and pathologic phenomenon with many causes. Some of the pulmonary problems are iatrogenic, resulting from the overuse of blood, crystalloids, oxygen, vasopressors, sedation, and immobility. Some are related to the blast effects of injuries at sites distant from the thorax. Other causative factors are metabolic, secondary to diminished peripheral perfusion. The pulmonary capillary bed is a principal target organ in shock--affected by the toxic action of vasoactive substances, gastric aspirates, and fat; by the obstructive action of platelet, fibrin, and leukocyte clots; and by changes in balance between perfusion pressures and oncotic pressures. The rationale of prevention and therapy presented here has resulted (except in those patients with prolonged sepsis) in almost complete disappearance of RDS as a cause of death in our institution.
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PMID:The respiratory distress syndrome. 124 60

Hospital and anesthesia records of 39 patients who had hepatic artery ligation for severe hepatic trauma were analyzed retrospectively to acquire information on any relationships between choice of anesthetic, preoperative physical condition of the patient, type and incidence of complications, and mortality. Patients who had lost the most blood received neuroleptanalgesia, ketamine, or cyclopropane; those with more stable cardiovascular status received halothane; those in severe circulatory compromise received only oxygen and muscle relaxants. Trends in results of postoperative liver function tests were not related to type of anesthesia. Of the 12 deaths, seven were due to massive bleeding, three to septicemia, one to multiple complications, and one to hepatorenal failure 18 days postoperatively. Choice of anesthetic agent appeared to have no significant influence on postoperative morbidity and mortality; rather, the choice of anesthesia depended on the preoperative physical (especially hemodynamic) status of the patient, which in turn reflected the apparent blood loss estimated at induction.
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PMID:Anesthesia and hepatic artery ligation. 125 Dec 34

Automatically stepwise driven pO2 electrodes were transcutaneously inserted into muscle tissue of severely ill septic shock patients. The pO2 profile was plotted from 200 individual measurements registered during 5 minutes and a histogram plotted for documentation. Arterial and venous blood gases, cardiac output, systemic and pulmonary vascular resistance were measured continuously on-line. In septicemia multiple drug schemes are suggested all intending to increase oxygen supply to the tissue and to improve oxygen demand/supply mismatch. So far the attending physician is bound to conclude and continue respectively change the treatment scheme according to the above described macrophysiological parameters. Perfusion distribution and local inhomogenities of tissue oxygen supply remain undetected. In the described study pretreatment pO2 profiles in musculus quadriceps femoris were obtained and measurements repeated in intervals of 10 minutes after start of pharmacological treatment. The changes of pO2 profiles of 20 patients, monitored in such a way over days and weeks, were carefully correlated to the described cardiocirculatory parameters and blood gas analyses. Dopamine was used to improve cardiac function and tissue oxygen supply as well. The investigations show that resulting changes of cardiovascular and blood gas parameters do not always indicate that tissue oxygen supply has really improved. On the other hand there was never an improvement in tissue oxygen supply when no changes of the other parameters had occurred. It is advised to add as a further diagnostic parameter tissue pO2 measurements to get insight if improvement in cardiac and pulmonary function really has the intended effect of improvement of tissue oxygen supply.
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PMID:pO2-profiles in human muscle tissue as indicator of therapeutical effect in septic shock patients. 128 15

Major thermal injury is associated with extreme hypermetabolism and catabolism as the principal metabolic manifestations encountered following successful resuscitation from the shock phase of the burn injury. Substrate and hormonal measurements, indirect calorimetry, and nitrogen balance are biochemical metabolic parameters which are useful and more readily available biochemical parameters worthy of serial assessment for the metabolic management of burn patients. However, the application of stable isotopes with gas chromatography/mass spectroscopy and more recently, new immunoassays for growth factors and cytokines has increased our understanding of the metabolic manifestations of severe trauma. The metabolic response to injury in burn patients is biphasic wherein the initial ebb phase is followed by a hypermetabolic and catabolic flow phase of injury. The increased oxygen consumption/metabolic rate is in part fuelled by evaporative heat loss from wounds of trauma victims, but likely also by a direct central effect of inflammation upon the hypothalamus. Although carbohydrates in the form of glucose appear to be an important fuel source following injury, a maximum of 5-6 mg/kg/min only is beneficial. Burn patients have accelerated gluconeogenesis, glucose oxidation, and plasma clearance of glucose. Additionally, considerable futile cycling of carbohydrate intermediates occurs which includes anaerobic lactate metabolism and Cori cycle activity arising from wound metabolism of glucose and other substrates. Similarly, accelerated lipolysis and futile fatty acid cycling occurs following burn injury. However, recent evidence suggests that lipids in the diet of burned and other injured patients serve not only as an energy source, but also as an important immunomodulator of prostaglandin metabolism and other immune responses. Amino acid metabolism in burn patients is characterized by increased oxidation, urea synthesis, and protein breakdown which is prolonged and difficult to reduce with current nutritional therapy. However, the current goal of nutritional support is to optimize protein synthesis. Specific unique requirements may exist for supplemental glutamine and arginine following burn injury but further research is needed before enhanced branched chain amino acids supplements can be recommended for burn patients. Recent research investigations have revealed the importance of enteral feeding to enhance mucosal defense against gut bacteria and endotoxin. Similarly, research has demonstrated that many of the metabolic perturbations of burns and sepsis may be due, at least in part, to inflammatory cytokines. Investigation of their pathogenesis and mechanism of action both at a tissue and a cellular level offer important prospects for improved understanding and therapeutic control of the metabolic disorders of burn patients.
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PMID:The metabolic effects of thermal injury. 129 Feb 69

Natural surfactant (Surfactant TA, Survanta, CLSE, SF-RI 1, Curosurf and human surfactant obtained from amniotic fluid) therapy for RDS in very premature infants has been evaluated in 17 controlled clinical trials. Uniformly intratracheal surfactant administration caused a decreased intensity of mechanical ventilation during the first hours (reduced inspiratory pressure, reduced oxygen requirements) as an immediate effect of surfactant administration. Metanalysis reveals barotraumatic pulmonary complications mainly, pneumothorax and pulmonary interstitial emphysema to occur less frequently in surfactant-treated infants in virtually all trials; an increased incidence of survival without bronchopulmonary dysplasia following surfactant treatment was observed in 10 controlled clinical trials. The incidence of other complications of prematurity (intracranial hemorrhage, patent ductus arteriosus and necrotizing enterocolitis) was unchanged following natural surfactant treatment. Dosing of natural surfactant is still under investigation, however recent data indicate that the initial dose should not be less than 100 mg/kg b.w. and retreatment should be given to infants with unsatisfactory response (i.e. fraction of inspired oxygen (FiO2) > 40%). Timing of surfactant treatment still remains controversial. Prophylactic treatment shortly following birth has been compared with rescue-treatment, i.e. surfactant administration to infants suffering from manifest RDS in most studies 4-8 h after birth. Conflicting data from 5 controlled trials may be interpreted as follows: prophylactic treatment seems to be favourable for extremely premature infants (GA < or = 26 weeks) and rescue treatment seems to be adequate for infants of 27-30 weeks of gestation. Intratracheal surfactant instillation in very premature infants did not result in an improved lung function for 24 h to 48 h in all patients. Ten--25% of study infants were reported to be "non-responders", i.e. infants without sustained decrease in oxygen requirements (i.e. FiO2 > 40%). Various factors may be operative including congenital bacterial infections (sepsis or pneumonia), lung hypoplasia and cardiac failure. Inactivation of surface properties of natural surfactant caused by a leakage of proteins across the alveolar-capillary membrane was observed in experimental and clinical studies. Current investigations focus on a combination of postnatal steroids and surfactant treatment to improve lung function and outcome in "non-responders". As long as any controlled clinical studies are being published, this approach remains experimental. Up to now, any controlled clinical trials have been performed to assess different modes of artificial ventilation (e.g. high frequency oscillating ventilation versus conventional ventilation) combined with surfactant therapy. Data obtained from premature animals given natural surfactant indicate any advantage with respect to gas exchange and lung histology to result from high frequency ventilation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Natural surfactant for neonatal respiratory distress syndrome in very premature infants: a 1992 update. 129 66


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