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)

Axillofemoral bypass (AXB) was performed on 100 patients who had claudication (19), pain at rest (42), gangrene or ulcer (22), aortic sepsis (14), or unresectable abdominal aneurysm (3). Unilateral (27 grafts), double unilateral (1), or axillobifemoral (72) grafts with Dacron (58), polytetrafluoroethylene (PTFE) (28), ring-supported Dacron or PTFE (12), or other material (2) were performed by 13 surgeons. Eight patients died within 30 days and three major amputations were necessary. Fifty-two (57%) of the 92 survivors had a total of 92 graft complications during a mean follow-up period of 21.5 months. Thirty-two patients underwent 57 reoperations of various types, incurring an additional three deaths and three amputations. Sixty (65%) of the original 92 survivors of AXB avoided reoperation. The 89 patients who survived the original and repeat procedures were followed up through the end of 1984 (62 patients), to late death (23), or to late graft removal (4), whichever occurred first. At these end points, 83 of the 89 (93%) patients had patent grafts. The graft patency rate of the original 100 AXBs by life table was 54% at 36 months; but with reoperation, it was 72%. Among those patients who left the hospital after AXB, the survival rate at 36 months was 69%. Statistically insignificant trends toward improved early patency were noted with bilateral femoral anastomoses, total iliac occlusion, and less severe ischemia. AXB provided safe palliation of severe arterial disease, with overall graft patency exceeding postoperative patient survival according to life-table analysis. However, the safety of AXB was tempered by frequent complications and the necessity for many reoperations to provide maximum efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Axillofemoral bypass: a tool with a limited role. 293 65

An unusual manifestation of a large bowel ischemia was observed in two patients. Both had a left flank tubular fluid collection demonstrated respectively by computed tomography (CT) and ultrasonography (US). At surgery, pyocolon (i.e. ischemic, dilated large bowel segments filled with pus) was discovered and resected. Pyocolon should be suspected in patients with ischemic colitis and sepsis. US, although useful, may be misleading; CT is the investigation of choice to establish the diagnosis.
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PMID:Pyocolon: an unusual manifestation of colon ischemia. 297 Oct 65

Between 1983 and 1986, four newborns who had primary closure of gastroschisis had postoperative ischemic bowel. Suspicion was raised almost immediately after closure that something was wrong inside the abdomen when there was persistent acidosis, sepsis, abdominal wall redness, and a generalized worsening condition. All four neonates were re-explored. Necrotic bowel was found, and three required silon pouch closure. The two survivors were left with a temporary short gut. Whether the cause of the bowel ischemia in the four babies was due to excessive intraabdominal pressure, volvulus, or the intestines being too vigorously manipulated, is speculative. Therefore, excessive manipulation and compression of gastroschisis contents seem unwise; if such a newborn has persistence of the above signs and symptoms, immediate reoperation and decompression are warranted.
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PMID:Ischemic bowel after primary closure for gastroschisis. 297 92

We report a case of a mixed sensorimotor, predominantly axonal mononeuritis multiplex that developed after a severe meningococcal septicemia and disseminated intravascular coagulation (DIC) with associated distal limb necrosis. Ischemia resulting from the DIC-induced multiple vascular occlusions is suggested as the leading cause of this neuropathy.
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PMID:Peripheral neuropathy in meningococcal septicemia. 299 4

The aim of this chapter was to highlight the major components of PAF actions which lead to a state of shock, i.e. inadequate perfusion of essential organs which if sustained over a critical period of time, leads to irreversible damage in essential organs and eventually death. The heart, the pulmonary vessels and the microcirculation seem to be the primary target organs to PAF-induced hypotension. The effects of PAF on the pulmonary airways in some species (bronchoconstriction) might lead to hypoxemia and further exacerbate organ function. Thrombocytopenia, leukopenia and activation of the complement system are also important in PAF-induced shock by promoting thrombi formation and generation of multiple secondary mediators (e.g. histamine kinins, TXA2, leukotrienes, oxygen radicals). Identification of PAF production during specific or generalized pathophysiological processes is a critical step to implicate this vasoactive lipid in disease processes. So far, only limited information has been derived from studies involving immune responses (anaphylaxis) or bacterial endotoxins. Yet, the growing number of selective and potent PAF antagonists provide important information on the potential role of PAF in shock states. Such evidence, summarized in table I, is of great importance in designing new therapeutic strategies to a highly complex and lethal disease such as septicemia. However, the data summarized in table I clearly show that little is known on the mechanism of action of the various PAF antagonists. It is also important to note that PAF-induced shock and death can be prevented by drugs which are not necessarily PAF antagonists. For example, dexamethasone is extremely efficient in preventing PAF-induced shock and death in the mouse [24, 39] and thyrotropin releasing hormone in the guinea pig [15]. Therefore, it is conceivable that pathological conditions in which PAF might play a fundamental role might be reversed by pharmacological interventions which activate physiological mechanisms which can overcome and reverse the pathological processes activated by PAF. In conclusion, PAF is a powerful vasoactive lipid which can produce severe derangements in essential biological functions which can lead to death. The role of PAF in pathological processes in vivo is well supported in conditions such as anaphylaxis and endotoxemia. Yet, direct proof for PAF production in other shock states, such as multiple trauma, ischemia, inflammation and hemorrhage, is still missing. Furthermore, it is important to keep in mind that in shock, trauma or inflammation, multiple mediators in addition to PAF are formed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Platelet-activating factor and shock. 304 32

An experimental model using surface-induced (20 degrees C) deep hypothermia and total circulatory arrest instead of cardiopulmonary bypass was developed for the study of growth of the transplanted heart. Autotransplantation of the heart was performed in 42 young dogs weighing from 4.4 to 9.0 kg (mean, 6.9 kg). Time of ischemia ranged from 26.0 to 60 minutes (mean, 43.4 minutes). Return of satisfactory cardiac function occurred in all but one animal. An early high mortality rate was due primarily to pulmonary complications, but with modifications to the technique, long-term survival increased to 70%. Early deaths (5 days to 13 weeks) of five dogs during preliminary trials were due to pleural effusion (2), sepsis (1), endocarditis (1), and ascites (1). There have been 14 long-term survivors (range, 194 to 498 days; mean, 264 days). Long-term survivors appear well, are active, and show satisfactory growth. This experimental model eliminates the need for heparinization and reduces the potential for complications associated with cardiopulmonary bypass in the dog. It avoids cannulations that might impinge on anastomotic sites. This model appears to be suited for studying growth of the transplanted heart.
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PMID:Cardiac transplantation without cardiopulmonary bypass: experimental model to study growth of the transplanted heart. 304 27

Free radicals generated during purine catabolism or by activated granulocytes cause tissue injury by peroxidation of lipid membranes. In a canine model of sepsis initiated by intravenous live Escherichia coli, fluorescent products of lipid peroxidation (FP) were measured in serum. Four groups of five dogs infused with 10(9)E. coli/kg were analyzed--I: no further treatment; II: prior depletion of granulocytes with a cytotoxic antibody; III: pre-treatment with superoxide dismutase and catalase; and IV: resuscitation after bacterial infusion to maintain cardiac output greater than 80% of pre-bacteremic levels. In Groups I, II, and III, cardiac output fell to less than 50% of baseline within 1 hr and remained there throughout the study. FP in Groups I and II rose to greater than 200% of baseline (P less than .02 and less than .03). In Groups III and IV, FP did not rise significantly from baseline. The rise in serum FP and the prevention of this rise by-treatment with antioxidants indicate generation of oxygen radicals. Their presence had no effect on hemodynamic parameters. Granulocyte depletion did not alter appearance of FP; however, prevention of low cardiac output blocked FP formation. These data suggest that oxygen free radicals were generated by tissue ischemia, rather than by granulocytes, in this model of septic shock.
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PMID:Oxygen free radical activity during live E. coli septic shock in the dog. 304 73

Necrotizing enterocolitis is the most common digestive emergency in neonatal units. Several factors are involved in their pathogenesis: intestinal ischemia, bacterial colonization and feeding. To analyse these factors, 25 cases of NEC are compared to a control group of 48 newborns. Results showed an incidence of NEC about 1.6 0/00 live newborns, without a greater mortality in respect to other pathologic newborns. Ischemic factors influence significatively in appearance of ECN (p less than 0.001). None of them received maternal feeding. By this reason it seems to be a protective factor against bottle feeding (p less than 0.05). Enteral feeding its main influence upon mature newborns. No common bacterial findings have been found, but 68% of children developed clinical findings compatible with sepsis. Severity of abdominal sings in clinical examination in the acute phase of NEC is positively correlated with the presence of complications. Individual considerations are needed in sight to the different severity and prognosis of NEC.
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PMID:[Etiopathogenic factors in neonatal necrotizing enterocolitis]. 314 23

Complement, activated during infection and injury, has been implicated as a mediator of microvascular injury and obstruction. This study examines how two potent activators of complement, zymosan, and cobra venom factor (CVF), affect systemic and visceral perfusion. Rats were injected with either saline (1 ml/kg), zymosan (5 mg/kg) or CVF (5 units/kg) at t = 0 and 30 minutes. Thermodilution cardiac output, mean arterial pressure, heart rate, systemic vascular resistance, and hematocrit were determined at t = 2 hours. Effective hepatic and renal blood flows, by clearance of galactose and p-aminohippurate respectively, were determined over the next hour. The per cent change in total hemolytic complement from t = 0 to t = 3 hours was determined by immune hemolysis of sheep erythrocytes. There was no difference in systemic hemodynamic parameters between the three groups. Hepatic blood flow was depressed in both the zymosan (3.83 +/- 0.23 ml/min/100 g) and CVF (3.72 +/- 0.20 ml/min/100 g) groups compared with controls (4.62 +/- 0.19 ml/min/100 g, P less than 0.05). Renal blood flow in the zymosan-treated group (6.40 +/- 0.24 ml/min/100 g) increased over control (4.80 +/- 0.40 ml/min/100 g, P less than 0.05) but was unchanged in the CVF group (5.06 +/- 0.23 ml/min/100 g). The amount of complement activated correlated with the change in hepatic (r = -0.419, P less than 0.05) but not renal (r = -0.008, P = 0.917) flow. Complement activation may occupy a proximal position in the pathogenesis of hepatic ischemia associated with trauma and sepsis.
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PMID:Visceral perfusion abnormalities following complement activation. Clues to the mediators of organ ischemia in trauma and sepsis. First place winner: Conrad Jobst Award. 319 44

Terminal complement complex (TCC) and anaphylatoxin formation in 18 patients with sepsis and 20 patients with acute limb ischemia were studied before the start of treatment and seven days later. The septic or ischemic patients had elevated levels of plasma TCC before start of therapy. In successfully treated patients these concentrations were within the normal range one week later. Similarly, the plasma anaphylatoxin level was increased before therapy and returned to the normal range within seven days. Escherichia coli incubated in vitro in fresh human serum at body temperature started formation of TCC in a dose-related manner. As complement will induce cellular lysis via TCC and edema via anaphylatoxins, anemia and impaired respiration in these patients may be influenced by increased concentrations of terminal complement complexes and of C3a and C5a.
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PMID:Terminal complement complexes and anaphylatoxins in septic and ischemic patients. 327 84


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