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

A prospective neoadjuvant trial utilizing chemotherapy (CTX) and radiotherapy (XRT) prior to pancreatectomy was established to determine the feasibility of resection after aggressive pretreatment and its effect on survival. Fifteen patients with pancreatic cancer (14 head, 1 body) and 1 patient with duodenal cancer, (with paraaortic adenopathy), were subjected to combination treatment with infusional 5-FU, bolus injection of mitomycin-C, and XRT (4 patients were treated off the protocol). Patients were restaged 3 wk after XRT, and those deemed resectable underwent a pancreatic resection. Three patients did not undergo exploration after the neoadjuvant therapy, although two of these were deemed resectable by CT scan. The remaining 13 patients underwent exploration and 10 underwent resection. Three did not undergo resection because of extrapancreatic disease, although their primary tumors were resectable. One patient had no residual tumor in the specimen. The others had residual tumor with evidence of necrosis and hyalinization, but all margins were free of tumor. There were two perioperative deaths from sepsis. Of the remaining patients who underwent resection, one died of a myocardial infarction at 9 mo. One patient died with recurrent disease at 19 mo. The remaining patients are alive 40, 32, 11, 11, 10, and 4 mo since diagnosis and are currently free of disease. Aggressive neoadjuvant chemoradiotherapy can be performed safely, allows successful resection, and may yield long-term survival or curve.
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PMID:Increased resectability of locally advanced pancreatic and periampullary carcinoma with neoadjuvant chemoradiotherapy. 208 23

Delayed spontaneous rupture of the urinary bladder following augmentation enterocystoplasty is a serious life-threatening complication of uncertain etiology. Multiple factors are believed to contribute to the mechanism of bladder perforation. Ruptured augmented bladders share a common urodynamic pattern of high leak point pressure of the urethra, with sensory and mechanical tolerance of high filling pressure. This combination seems to be the main predisposing factor for spontaneous perforation. Other risk factors, including catheter trauma during intermittent self-catheterization, urinary retention due to mucus retention or noncompliance with the catheterization protocol, chronic infection, and decreased sensation of bladder filling, may play roles in the mechanism of rupture. Clinically, patients present with sepsis, abdominal pain and distension, ileus, fever, oliguria and peritoneal irritation. The diagnosis is made on low pressure cystography, although failure of cystography to demonstrate extravasation is not unusual. Aggressive surgical treatment consists of immediate exploration, primary repair of the perforation, drainage of the perivesical space, suprapubic cystostomy and broad-spectrum antibiotics. Longterm management includes a strict intermittent catheterization schedule, anticholinergic therapy and urodynamic evaluation. Failure to achieve a low pressure storage reservoir by conservative means entails an increased risk of recurrent perforation. In such cases further surgical intervention should be considered. We present a 21-year-old paraplegic man 5 months after augmentation enterocystoplasty who required operation because of spontaneous rupture of the augmented bladder. Spontaneous delayed rupture of the bladder should be considered in the differential diagnosis of acute abdomen in patients after augmentation enterocystoplasty. Early surgical treatment and subsequent monitoring of the low pressure reservoir are recommended.
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PMID:[Delayed spontaneous rupture of the bladder following augmentation enterocystoplasty]. 222 70

Septicaemia frequently presents without "classic" signs of infection--tachypnoea, hypotension and confusion are the commonest features. The mortality rate is 40 to 80% and in intensive care units, septicaemia accounts for 70% of all deaths. Despite the use of antimicrobial drugs to which the offending organism is sensitive, patients are still dying. Effects on distant organ systems are due to "Mediators". "Microvascular Failure" resulting in tissue hypoxia is the unifying hypothesis of multiple organ failure in septicaemia. Mortality is correlated with the number of organ system failures. Supportive management is aimed at prevention of organ failure--manipulation of the circulation being the central key. Intravascular volume expansion, vasoactive drugs, mechanical ventilation and invasive monitoring are the means. Antimicrobial therapy must be guided by 'best guess' approach with multiple agents until isolation of the offending organism can recommend specific therapy. Aggressive surgical drainage or excision, is particularly applicable in abdominal sepsis. Several adjunctive therapies aimed at mediators of sepsis, are as yet experimental.
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PMID:Septicaemia and the prevention of multiorgan failure--the intensive care perspective. 222 36

When esophageal disruption occurs in the presence of preexisting esophageal disease or is associated with sepsis or fluid and electrolyte imbalance, aggressive and definitive therapy often provides the only chance for patient salvage. Twenty-four adults (average age, 59 years) with intrathoracic esophageal perforations underwent esophagectomy: 15, transhiatal esophagectomy without thoracotomy; and 9, transthoracic esophagectomy. Restoration of alimentary continuity with an immediate cervical esophagogastric anastomosis was carried out in 13 patients. Eleven underwent a cervical or anterior thoracic esophagostomy, and 10 of them had a subsequent colonic (7) or gastric (3) interposition from 4 to 32 weeks (average time, 8.6 weeks) later. The perforations were due to esophageal instrumentation (9 patients), acute caustic ingestion (2), emesis (2), intrathoracic esophagogastric anastomotic disruption (2), and other causes (9). Preexisting esophageal disease in 20 patients included chronic strictures (10 patients), reflux esophagitis (3), esophageal cancer (3), achalasia (2), diffuse spasm (2), and monilial esophagitis (1 patient). Ten patients were operated on within 12 hours after the injury; 3, within 12 to 24 hours; and 11, within three to 45 days (average interval, 6.6 days). There were three hospital deaths (13%). Nineteen of the 21 survivors were able to swallow comfortably until the time of death or latest follow-up. Aggressive diagnosis and aggressive treatment of life-threatening esophageal perforations are advocated. Conservative procedures (repair, diversion, or drainage) for a perforation with preexisting esophageal disease often inflict more morbidity than esophageal resection, which eliminates the perforation, the source of sepsis, and the underlying esophageal disease. The decision to restore alimentary continuity in a single stage must be individualized.
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PMID:Esophagectomy for esophageal disruption. 229 75

Nasogastric tube-feeding was inadvertently administered parenterally to a 65-year-old woman with chronic lymphocytic leukemia. Administration was discontinued after approximately 8 hr of infusion. The patient manifested acute renal failure, respiratory failure, hepatic insufficiency, and high-output septic shock requiring invasive hemodynamic monitoring, peritoneal dialysis, mechanical ventilation, and broad spectrum intravenous antibiotics. Blood cultures were positive for alpha-hemolytic Streptococcus, Staphylcoccus epidermidis, and Enterobacter cloacae while cultures of the enteral solution grew alpha-hemolytic Streptococcus, S. epidermidis, Pseudomonas vesiculare and unidentifiable coliforms. Aggressive management resulted in hospital discharge, although she eventually died of recurrent pneumonia and septicemia 111 days after the infusion. It is of paramount importance to be cognizant of this potential complication in any patient receiving enteral feeding who presents with the clinical picture of high-output septic shock. We discuss clinical features as well as treatment modalities necessary for a positive outcome.
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PMID:Multiorgan failure from the inadvertent intravenous administration of enteral feeding. 251 14

A recent experience with infrainguinal graft infections was reviewed in an effort to identify factors related to limb loss and mortality. The records of 32 patients who had operative treatment of 33 episodes of infrainguinal graft infection between 1978 and 1985 were reviewed to evaluate the effects of 20 factors possibly affecting outcome. The amputation rate was 79%. Of the 20 factors studied, only the presence of overt limb sepsis was associated with the need for amputation, with 100% of patients having limb sepsis requiring amputation vs. 72% of patients without limb sepsis (p = 0.03). The in-hospital mortality rate was 22%. Eighty-six percent of the deaths were due to ongoing sepsis. Again, a single factor was associated with death. Five of the 12 patients (42%) in whom preservation of axial flow was attempted died in contrast to only 2 of 20 patients (10%) who did not have attempted arterial reconstruction (p = 0.04). Limb salvage did not occur in any of the patients in whom preservation of axial flow was attempted and nine required above-knee amputation. Thirteen of the remaining 20 patients had occluded femoral vessels either because of operative ligation (nine) or previous thrombosis (four). Above-knee amputations healed in all but one of these 13 patients. Determined attempts at increasing limb preservation were associated with no improvement in amputation rate or level and were accompanied by an unacceptably high mortality rate. Aggressive control of sepsis through the early amputation of septic limbs after graft removal may improve survival without further detriment to limb preservation.
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PMID:Mortality and limb loss with infected infrainguinal bypass grafts. 295 30

A patient with acquired immunodeficiency syndrome (AIDS) who required aggressive nutritional intervention via home parenteral nutrition therapy is described, and nutritional status, etiology and therapeutic management of AIDS-associated malnutrition, role of nutrition support, and factors for consideration in using parenteral nutrition in AIDS patients are discussed. Parenteral nutrition therapy was initiated in a 30-year-old AIDS patient with Kaposi's sarcoma lesions of the gastrointestinal tract because of rapid weight loss, low serum protein levels, and malnutrition. He had previously undergone a small-bowel resection and a jejunojejunostomy, and radiation and antineoplastic-drug therapy was planned. During parenteral nutrition therapy, the patient demonstrated increased physical strength and was able to care for himself during most of the time spent at home or in a long-term-care facility. Aggressive measures, including parenteral nutrition therapy, were discontinued 11 days before the patient's death. Complications of therapy included one episode of sepsis and a tear in the external catheter tubing. Malabsorption and diarrhea mainly caused by gastrointestinal disease, reduced food intake because of oral and esophageal infections, adverse effects from medication, and depression are factors that can contribute to AIDS-associated malnutrition. Also, hypermetabolism resulting from infections and fevers may contribute to malnutrition in AIDS. The extent to which this malnutrition affects the underlying immune dysfunction occurring in the syndrome and the response to other more direct drug therapies in AIDS is not known. Available methods for nutritional intervention are based on clinical experience and anecdotal reports. Because of gastrointestinal disease, an oral diet, supplements, and enteral tube feedings may not meet nutritional goals for an AIDS patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parenteral nutrition in the management of gastrointestinal Kaposi's sarcoma in a patient with AIDS. 313 64

Aggressive control of intragastric pH in the burn patient has essentially eliminated upper gastrointestinal bleeding. The recent spectrum of complications in the thermally injured patient has shifted. Vascular occlusion and missed associated injury were the most frequent early complications in this review. Those complications occurring late in the course were attributed to sepsis originating in the burn wound. The common diagnostic error was to blame the burn injury for the patient's signs and symptoms. A high index of suspicion of an occult process must be exercised when caring for the burn patient who has burn shock with a decreasing hematocrit value or a compartment syndrome that does not respond to escharotomy or fasciotomy or the septic patient with a clean burn wound.
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PMID:Surgical complications of thermal injury. 320 73

There is no one operative treatment for acute pancreatitis. Surgery is indicated to resolve diagnostic uncertainty and perhaps to modify the early course of gallstone pancreatitis. Peritoneal lavage is useful in reversing early-phase systemic circulatory effects mediated by toxins in the ascitic fluid, but does not modify the underlying pancreatitis. When pancreatitis progresses to pancreatic and peripancreatic necrosis, the ultimate outcome is determined by a) the amount of necrosis, b) the extent of extrapancreatic necrosis, and c) bacterial contamination of necrosis. The amount of pancreatic regional necrosis that can be safely observed for healing is unknown; large collections tend to become infected secondarily and thus should be evacuated. Computed tomographic scanning is the best current means of detecting pancreatic necrosis and abscesses. Only percutaneous aspiration can reliably differentiate sterile from infected collections. As sepsis is the most common cause of death in acute pancreatitis, adequate surgical drainage is essential, while antibiotic therapy is only adjunctive. Aggressive treatment directed at the two principal causes of death, early-phase shock and late-phase sepsis, should reduce mortality to about 1% overall and to about 5% in cases complicated by regional necrosis and sepsis.
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PMID:Surgical intervention in acute pancreatitis. 333 82

In a retrospective study of 300 children who underwent placement or revision of cerebrospinal fluid (CSF)-peritoneal shunts during a 10-year period, 15 (5%) developed shunt-related abdominal complications with ventricular sepsis and two developed acute perforated appendicitis. Abdominal complications and associated shunt infections suggested two potential modes of development: (1) descent of contaminated CSF from an infected shunt into the abdomen (CSF ascites--four patients, CSF pseudocysts--four patients, and shunt-induced abscess/peritonitis--five patients); and (2) ascent of bacteria into the shunt from an abdominal source (visceral perforation by the shunt catheter--two patients and acute perforated appendicitis--two patients). Three types of shunt systems were placed during the study period; five of the seven (71%) most serious septic complications were associated with the use of Raimondi spring-reinforced catheters. Bacteria isolated in this series were associated with differing modes of sepsis: those involving descent of bacteria into the abdomen from an infected shunt were predominantly gram-positive, cutaneous microorganisms, whereas those associated with ascent of bacteria from the abdomen into the shunt were mixed, gram-negative intestinal microorganisms. Appendicitis did not result in shunt infections. Aggressive treatment resulted in no operative or complication-related deaths. Removal of the shunt catheter from the abdomen and intravenous antibiotics were essential for eradication of sepsis; laparatomy was required only for cases with suspected peritonitis. In eight of the 17 (47%) patients, reestablishment of CSF-peritoneal shunts was performed after resolution of shunt-related complications. In recent years improved shunting materials and supportive care have reduced the incidence of the most serious of these complications.
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PMID:Ventricular sepsis and abdominally related complications in children with cerebrospinal fluid shunts. 398 17


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