bluuebunny/crossref_metadata_2025_split huggingface dataset:
Benchmarks and control charts for surgical site infections
Authors: Gustafson T L 
Published: March 2003

Abstract

Background
Although benchmarks and control charts are basic quality improvement tools, few surgeons use them to monitor surgical site infection (SSI). Obstacles to widespread acceptance include: (1) small denominators, (2) complexities of adjusting for patient risk and (3) scepticism about their true purpose (cost cutting, surgical privilege determination or improving outcomes).

Methods
The application of benchmark charts (using US national SSI rates as limits) and control charts (using facility rates as limits) was studied in 51 hospitals submitting data to the AICE National Database Initiative. SSI rates were risk adjusted by calculating a new statistic, the standardized infection ratio (SIR), based on the risk index suggested by the Centers for Disease Control National Nosocomial Infection Surveillance Study. Fourteen different types of control chart were examined and 115 suspiciously high or low monthly rates were flagged. Participating hospital epidemiologists investigated and classified each flag as ‘a real problem’ (potentially preventable) or ‘not a problem’ (beyond the control of personnel at this facility).

Results
None of the standard, widely recommended, control charts studied showed practical value for identifying either preventable rate increases or outbreaks (clusters due to a single organism). On the other hand, several types of risk-adjusted control chart based on the SIR correctly identified most true opportunities for improvement. Sensitivity, specificity and receiver–operator characteristic (ROC) analysis revealed that the XmR chart of monthly SIRs would be useful in hospitals with smaller surgical volumes (ROC area = 0·732, P = 0·001). For larger hospitals, the most sensitive and robust SIR chart for real-time monitoring of surgical infections was the mXmR chart (ROC area = 0·753, P = 0·0005).
Role of tumour necrosis factor in lung injury caused by intestinal ischaemia–perfusion
Authors: Kuzu M A , Köksoy C , Kuzu I , Ergün H , Gürhan I 
Published: March 2003

Abstract

Background
Despite the well known inflammatory effects of tumour necrosis factor (TNF), the mechanism of TNF-mediated lung injury following ischaemia–reperfusion (IR) is still unclear. In this study, the role of TNF in the development of acute lung injury following intestinal IR was investigated.

Methods
Male Wistar rats underwent either sham operation (n = 10) or 1 h of superior mesenteric artery occlusion and 2 h of reperfusion (IR; n = 10) or pretreatment with anti-TNF polyclonal antibody 2 mg kg−1 and IR (n = 6). Lung injury was evaluated by Evans blue dye concentration, immunohistochemical staining and morphometric analysis. Intestinal injury was assessed by Evans blue dye concentration and histological examination.

Results
Intestinal IR resulted in lung injury characterized by an increase in Evans blue dye concentration, polymorphonuclear neutrophil (PMN) sequestration, and obvious staining for expression of pulmonary CD11b and CD18. Pretreatment of animals with anti-TNF antibodies led to a reduction in the sequestration of PMNs (P &lt; 0·05), a decrease in expression of pulmonary intercellular adhesion molecule 1 and CD18 (P &lt; 0·01), and a diminished histological grade compared with the IR-only group. Anti-TNF antibody pretreatment also reduced the intestinal microvascular injury after intestinal IR.

Conclusion
Treatment with an anti-TNF antibody resulted in significant attenuation of lung injury following intestinal IR, which is at least partially TNF mediated. The data indicate that TNF is an important trigger for upregulation of pulmonary endothelial and neutrophil adhesion molecules after intestinal IR.
Luminal endotoxin modifies reaction to gut ischaemia–reperfusion injury in the pig
Authors: van der Hoven B , Groeneveld A B J , Thijs L G 
Published: March 2003

Abstract

Background
Translocation of bacteria and their products through the intestinal mucosa during ischaemia–reperfusion (I/R) may contribute to gut I/R injury.

Methods
In order to study the role of luminal endotoxin in gut I/R injury, two groups of seven germ-free pigs each were studied by clamping of the superior mesenteric artery, with and without luminal administration of endotoxin. Two control groups of seven germ-free pigs, with and without endotoxin, were not clamped. Translocation of an inert indicator (polyethyleneglycol (PEG) 3350), mucosal ischaemia (measured by tonometry) and haemodynamics were assessed.

Results
Both clamped groups showed ischaemic injury as measured by raised PEG 3350 urinary levels, lowered intestinal pH, and increased intramucosal arterial and intramucosal portal partial pressure of carbon dioxide gradients. Luminal endotoxin application did not aggravate this I/R injury, nor did it influence haemodynamics. The PEG 3350 level in the clamped endotoxin group was significantly lower than that in the clamped control group (mean(s.d.) 0·55(0·37) versus 1·82(0·70); P = 0·001), suggesting a blunting influence of endotoxin on the I/R injury. This might be explained by a desensitizing effect on leucocytes in the gut wall by luminal endotoxin before clamping and diminishing the I/R-induced production of cytokines in the gut wall.

Conclusion
Endotoxin does not significantly mediate gut I/R injury in the pig and might desensitize the gut wall leucocytes, resulting in decreased translocation of large molecules, including bacterial products and endotoxin.
Two-hit model of haemorrhagic shock and Pseudomonas sepsis
Authors: Eissner B , von Engelhardt K , Röschmann A , Ungelenk B , Mertens A , Wudke J , Smorodschenko A , Valerio M , Hahn H , von Specht B U , Haberstroh J 
Published: March 2003

Abstract

Background
Shock or trauma is a frequent prerequisite of bacterial sepsis. This has not, however, been reported in connection with related animal models. Therefore a porcine two-hit model was established with haemorrhage and resuscitation followed by the induction of sepsis with Pseudomonas aeruginosa.

Methods
Thirteen pigs were anaesthetized and permanently catheterized. Seven were subjected to haemorrhagic shock (bleeding until a mean of 50 per cent of the estimated blood volume remained) for 45 min, and then resuscitated with crystalloid, colloid and shed blood. A further six animals without shock served as controls. All pigs were fully conscious. The following day a continuous intravenous infusion of P. aeruginosa (1·6 × 107 colony-forming units kg−1 h−1) was given for 24 h, followed by a reduced dose (1·6 × 106 colony-forming units kg−1 h−1) for a further 24 h. The animals were then observed for another 48 h.

Results
All animals fulfilled the criteria for sepsis. However, the initial fever, arterial pressure and systemic vascular resistance were significantly lower in the shock group. In contrast, the pulmonary pressure, pulmonary vascular resistance and cardiac index were raised (P &lt; 0·05, shock versus control group).

Conclusion
These data indicate that sepsis is aggravated by a preceding haemorrhagic shock. This two-hit model considers one important precondition of human sepsis and may contribute to the development of a better treatment for this condition.
Blockade of Kupffer cells by gadolinium chloride or dichloromethylene diphosphonate influences hepatic microcirculation after sepsis and haemorrhagic shock
Authors: Herzog C , Kuntz W , di Liberto A , Bauer C , Rooijen N , Marzi I 
Published: March 2003

Abstract

Background
The liver plays a key role in the host defence response after haemorrhagic shock–resuscitation (H/R) and sepsis. Kupffer cells (KCs) have been shown to be a trigger and motor of the subsequent inflammatory response syndrome. This may lead to hepatocellular dysfunction, microcirculatory alterations and liver injury involving, for example, tumour necrosis factor α, interleukin (IL) 1 and IL-6. In a double-blind study the effect of KC blockade with either gadolinium chloride or liposome-entrapped dichloromethylene diphosphonate (DMD) on hepatic microvascular flow after H/R and sepsis was investigated.

Methods
After pretreatment with intravenous gadolinium chloride 10 mg kg−1, DMD 1 mg kg−1 or saline 24 h before induction of shock, male Sprague-Dawley rats (n = 6–10 per group and time) were subjected to either haemorrhagic shock (mean arterial pressure 40 mmHg) for 60 min followed by resuscitation or lipopolysaccharide (LPS) 1 mg kg−1 intravenously. Microvascular flow was assessed by intravital microscopy of fluorescence-marked leucocytes in liver sinusoids at baseline, and 1, 6 and 12 h after shock induction.

Results
In saline groups, the mean(s.d.) leucocyte flow was significantly (P &lt; 0·05) higher at 1 h (20 759(2901) μm3 s−1) and 6 h (16 278(2916) μm3 s−1) after H/R as well as at 6 h after LPS (17 661(3949) μm3 s−1) compared with the baseline value (13 509(1580) μm3 s−1). Animals pretreated with gadolinium chloride showed a significant flow increase compared with baseline (11 797(1124) μm3 s−1) at l h following H/R (26 269(5909) μm3 s−1). In DMD-pretreated animals leucocyte flow showed no significant change over time, following either H/R or LPS treatment. However, flow was significantly higher at baseline (18 054(998) μm3 s−1) versus gadolinium chloride and saline groups. In addition, DMD-treated animals showed higher flow values 1 h after LPS challenge (20 665(2337) μm3 s−1) compared with gadolinium chloride (13 110(1224) μm3 s−1) and saline (15 311(800) μm3 s−1) groups. Similarly, at 12 h after H/R the DMD group (21 782(1887) μm3 s−1) had higher flow values than the gadolinium chloride (14 026(1616) μm3 s−1) and saline (15 999(3175) μm3 s−1) groups.

Conclusion
These results imply a significant influence of KCs on regulation of microvascular perfusion in liver sinusoids under normal conditions as well as after H/R and sepsis. The data indicate differential pathways and effects of blocking KCs by gadolinium chloride and DMD.
Alteration of inflammatory response following small-volume resuscitation
Authors: Gebhard F , Liener U C , Helm M , Lampl L , Kinzl L , Brückner U B 
Published: March 2003

Abstract

Background
Small-volume resuscitation is rather effective in the primary volume treatment of major trauma. Blood pressure stabilizing effects occur immediately but last for a limited period only. Influences on inflammatory reactions in humans have not been reported so far. This prospective randomized study therefore analysed the inflammatory response in the very early (pre)clinical period after administration of crystalloids plus starch, hyperosmolar/hyperoncotic starch and lyophilized plasma solutions.

Methods
Upon approval of the ethics committee, 41 patients were enrolled with multiple injuries (injury severity score (ISS) mean 34 (range 9–75)). The patients received randomly either standard solutions, i.e. starch plus crystalloids (group C (control); n = 14), hyperosmolar/hyperoncotic starch (group S (small volume); n = 14) or lyophilized plasma (group L (lyoplasma); n = 13). Subsets were performed according to the different solutions as well as to the severity of trauma (ISS below 17, 18–31, 32 or more) and survivors/non-survivors. The first blood sample was obtained at the scene of the accident before cardiopulmonary resuscitation, when appropriate. Subsequently, blood samples were collected hourly. All samples were spun immediately at 4°C and stored at −70°C. Interleukin (IL) 6 as well as several different prostaglandins (PGI2, thromboxane A2, PGE2) were determined to characterize the overall inflammatory response.

Results
Eleven casualties (seven men and four women, mean age 31 years) died because of major trauma within 24 h after the incident. In all patients IL-6 levels promptly increased within the first 2 h, most pronounced in patients with the severest trauma (ISS greater than 32) and non-survivors. Patients in groups C and S had a comparable time course of IL-6 plasma levels with a slightly higher release in minor injuries (ISS less than 30). The same was true for prostaglandins. In contrast, patients in group L had clearly higher IL-6 concentrations during the first 2–12 h, again most pronounced in those with the severest trauma (ISS greater than 32).

Conclusion
These results demonstrate that the early systemic inflammatory response after small-volume resuscitation is rather similar to that of patients infused with standard-volume therapy after trauma. In contrast, lyoplasma seems to increase the inflammatory response regardless of the injury severity.
Cytokine induction by non-lipopolysaccharide components of Neisseria meningitidis
Authors: Sprong T , Stikkelbroeck N , van der Ley P , Steeghs L , van der Meer J W M , van Deuren M 
Published: March 2003

Abstract

Background
Lipopolysaccharide (LPS), or endotoxin, is considered responsible for the pattern of cytokine activation and the subsequent pathophysiological events during Gram-negative septic shock. To determine whether non-LPS components of Neisseria meningitidis are able to induce cytokine activation, the cytokine-inducing capacities of serogroup B wild-type N. meningitidis H44/76, of an LPS-deficient mutant (Plak 33) and of meningococcal LPS in human peripheral blood mononuclear cells were studied.

Methods
2-Keto-3-deoxyoctanate spectrophotometry was used to obtain a molar-based quantitative comparison between LPS and bacteria.

Results
Whole meningococci H44/76 were more potent inducers of cytokine production than isolated LPS; the LPS-deficient meningococci, Plak 33, were also able to induce cytokine production. LPS-deficient meningococci supplemented with an amount of LPS equivalent to that present in the wild-type strain produced the same amount of cytokines as the wild-type meningococcus.

Conclusion
LPS is not the sole toxic element in meningococcal sepsis, because non-LPS components of N. meningitidis are able to induce cytokine activation substantially. Antiendotoxin therapy alone may not be sufficient to inhibit the pattern of cytokine activation and the subsequent pathophysiological events during meningococcal septic shock.
Role of resection and primary anastomosis of the left colon in the presence of peritonitis
Authors: Biondo S , Jaurrieta E , Ragué J Martí , Ramos E , Deiros M , Moreno P , Farran L 
Published: March 2003

Abstract

Background
Classically a primary colonic anastomosis is not performed in the presence of left colonic peritonitis. Recently there has been a trend towards resection and anastomosis in selected patients, but no prospective study concerning the safety of this approach has been published. The objective of this study was to define the role of intraoperative colonic lavage with resection and primary anastomosis (RPA) in left colonic peritonitis, and to evaluate the differences in outcome in patients with diffuse or localized peritonitis.

Methods
Between January 1994 and December 1998, 127 patients underwent emergency operation for a distal large bowel perforation. RPA was the operation of choice and was performed in 61 patients, 38 with localized and 23 with diffuse peritonitis. Septic shock, faecal peritonitis, immunocompromised status and American society of Anesthesiologists grade IV were contraindications to the one-stage procedure. Alternative operations used in high-risk patients were Hartmann's procedure in 55 patients, subtotal colectomy in eight and colostomy in three.

Results
There were two deaths (3 per cent) among 61 patients treated by RPA and one (2 per cent) case of clinical anastomotic dehiscence. Overall morbidity was 39 per cent and the overall mean(s.d.) hospital stay was 18(15) days. No statistical differences were observed between patients with localized and diffuse peritonitis treated by RPA.

Conclusion
RPA may be the operation of choice in selected patients with left colonic diffuse peritonitis.
Tacrolimus has less fibrogenic potential than cyclosporin A in a model of renal ischaemia–reperfusion injury
Authors: Jain S , Bicknell G R , Nicholson M L 
Published: March 2003

Abstract

Background
Cyclosporin is associated with significant chronic nephrotoxicity, manifest in the long term mainly as renal fibrosis. There have been claims that tacrolimus is a less fibrotic drug than cyclosporin, and this study was designed to determine the effect of the two drugs on the expression of fibrosis-associated genes.

Methods
Male Wistar rats underwent clamping of the right renal pedicle for 45 min together with left nephrectomy; this model has previously been shown to be associated with upregulation of fibrosis-associated genes. Experimental groups (six animals per group) received cyclosporin A 10 mg/kg daily, tacrolimus 0·2 mg/kg daily or no treatment. Animals were killed at 16 weeks, and the renal cortical expression of fibrosis-associated genes was studied by means of quantitative reverse transcriptase–polymerase chain reaction.

Results
Tacrolimus-treated animals developed significantly less proteinuria and had lower serum creatinine levels than those receiving cyclosporin. Tacrolimus administration also significantly reduced the expression of transforming growth factor β and tissue inhibitor of metalloproteinases 1, both the products of genes associated with fibrosis. Although cyclosporin treatment reduced levels of the matrix-degrading enzymes, matrix metalloproteinase (MMP) 2 and MMP-9, this was not statistically significant.

Conclusion
Tacrolimus has less nephrotoxicity than cyclosporin in this model. It also appears to have less fibrogenic potential, and this may have implications for the choice of long-term immunosuppressant in renal transplantation.
Mitogenic effects of oestrogen mediated by a non-genomic receptor in human colon
Authors: Winter D C , Taylor C , O'Sullivan G C , Harvey B J 
Published: March 2003

Abstract

Background
Oestrogens are important mitogens in epithelial cancers, particularly where tumours express complementary receptors. While the traditional model of oestrogen action involves gene-directed (genomic) protein synthesis, it has been established that more rapid, non-genomic steroid hormone actions exist. This study investigated the hypothesis that oestrogen rapidly alters cell membrane activity, intracellular pH and nuclear kinetics in a mitogenic fashion.

Methods
Crypts isolated from human distal colon and colorectal cancer cell lines were used as robust models. DNA replication and intracellular pH were measured by radiolabelled thymidine incorporation (12 h) and spectrofluorescence imaging respectively. Genomic protein synthesis, sodium–hydrogen exchanger (NHE) and protein kinase C (PKC) activity were inhibited with cycloheximide, ethylisopropylamiloride and chelerythrine chloride respectively.

Results
Oestrogen induced a rapid (less than 5 min) cellular alkalinization of crypts and cancer cells that was sensitive to NHE blockade (P &lt; 0·01) or PKC inhibition (P &lt; 0·01). Oestrogen increased thymidine incorporation by 44 per cent in crypts and by up to 38 per cent in cancer cells (P &lt; 0·01), and this was similarly reduced by inhibiting the NHE (P &lt; 0·01) or PKC (P &lt; 0·05).

Conclusion
Oestrogen rapidly activates cell membrane and nuclear kinetics by a non-genomic mechanism mediated by PKC but not gene-directed protein synthesis.
Primary hyperparathyroidism in India
Authors: Mishra S K , Agarwal G , Kar D K , Agarwal A , Gupta S K , Mithal A , Rastad J 
Published: March 2003

Abstract

Background
Primary hyperparathyroidism (PHPT) in Indians has some unique clinical features, such as early age of onset, extreme osteopenia, crippling bone involvement, large parathyroid tumours, higher proportion of malignancy and severe, prolonged postparathyroidectomy hungry bone syndrome. The current study aimed to study (1) whether these features of PHPT in Indians are due to a variant form of PHPT and (2) pathogenetic factors of such variant disease.

Methods
Clinical, investigative and pathological features of 29 consecutive patients with PHPT (24 females, five males) who underwent parathyroidectomy at 13–60 (mean 38) years of age were reviewed. Spearman's correlation coefficient was calculated between serum calcidiol levels and biochemical variables, bone mineral density (BMD) before surgery and parathyroid tumour weight.

Results
Median duration of symptoms was 2·5 (range 1–26) years. Mean total serum calcium, iPTH and ALP levels were 12·4 mg dl−1 (normal 8·5–10·8 mg dl−1), 955 pg ml−1 (normal 9–55 pg ml−1) and 850 units l−1 (normal 35–125 units l−1) respectively, while mean(s.d.) serum calcidiol and calcitriol concentrations were 14(6) ng ml−1 and 52(29) pg ml−1 (versus 9(9) and 30(14) pg ml−1 in matched controls). All patients had symptomatic osteitis fibrosa cystica and eight were bedridden. Single or multiple spontaneous fractures occurred in 14 patients, brown tumours in 20, and long bones were barely visible on plain films in four. BMD z-scores at distal radius and lumbar spine (mean) were −4·2 and −3·8. Palpable parathyroid tumours occurred in 14 patients and nine had renal damage, mainly nephrocalcinosis. Parathyroidectomy invariably resulted in long-standing severe hypocalcaemia, necessitating intravenous calcium infusion for 6 days on average, and long-term oral calcium and vitamin D supplementation. The mean parathyroid gland weight was 8·6 (range 2–36·6) g and signs of carcinoma were found in four. There was a negative correlation (P &lt; 0·05) between serum calcidiol and serum iPTH, and serum ALP and parathyroid gland weight.

Conclusion
PHPT in Indians manifests as severe, symptomatic musculoskeletal and renal disease. In spite of the severe hyperparathyroidism, the serum calcium levels are only moderately raised. These patients have signs of rapid parathyroid tumour growth resulting in large adenomas and a high proportion of parathyroid carcinomas. The signs of rapid cell proliferation, excessive calcium insensitivity of PTH release and peripheral PTH resistance may clarify roles of widely prevalent vitamin D deficiency in pathogenesis of this variant of PHPT.