Outcomes of fracture-related infections - do organism, depth of involvement, and temporality count?

Purpose: To determine mortality and outcomes of patients diagnosed with fracture-related infections (FRIs).Methods: FRI patients treated at a trauma centre between 2001 and 2020 were analysed. The primary outcome was 1-year mortality; mortality associations with FRI organism, depth of involvement, and temporality were investigated with multivariable survival analysis. Healthcare-associated and serological outcomes were reported as secondary outcomes. Results: 311 FRIs with mean age of 67.0 and median Charlson comorbidity index of 0 were analysed. Methicillin-sensitive Staphylococcus aureus (MSSA) (29.9%) was the most frequently implicated organism. The majority of FRIs were deep infections (62.7%). FRIs were diagnosed at a median of 40 (IQR 15-200) days post index surgery. The mean follow-up was 5.9 years. One-year mortality amounted to 17.7%. MSSA FRIs were associated with better survival (adj HR 0.34, 95%CI 0.15-0.76, p = 0.008). There was no difference in survivorship between deep or superficial FRI (adj HR 0.86, 95%CI 0.62-1.19, p = 0.353) or in relation to onset time (adj HR 1.0, 95%CI 0.99-1.00, p = 0.943). Implant removal or debridement alone was performed in 61.7% and 17% respectively. Antibiotics was prescribed for 53 (IQR 23-110) days, and patients were hospitalised for 39 (IQR 19-78) days. CRP and ESR normalised in 70.3% (median 46 days) and 53.8% (median 86 days) patients respectively. Conclusion: Fracture-related infections are associated with significant mortality and morbidity regardless of depth and temporality. Non-MSSA FRIs are associated with inferior survival.

Acceptance, attitudes, and beliefs of Singaporean Chinese toward an ocular implant for glaucoma drug delivery.

PURPOSE: We investigated patients' attitudes and perceptions toward a subconjunctival implant as a novel ocular drug delivery method for glaucoma. METHODS: We recruited 344 Chinese patients with primary open angle or angle closure glaucoma currently on topical antiglaucoma medication for a minimum of six months from specialist glaucoma clinics. Sociodemographic data, and information about patients' general and ocular health were collected. Beliefs about medicines, glaucoma, eye drops, and self-reported adherence were assessed by trained interviewers using validated questionnaires. A description about the implant was provided and patients subsequently were assessed on their understanding and acceptance. RESULTS: Of the 344 Chinese patients enrolled, 216 (62.8%) would accept the implant as a replacement for their current eye drops. Of those who accepted the implant, 99 (45.8%) were willing to accept it at similar costs, while 40 (18.5%) and 20 (9.3%) patients were willing to pay 1.5 and 2 times the cost of their present medication, respectively. Patients who accepted the implant had more severe glaucoma (P = 0.015) and felt that the implant was more helpful than eye drops (P < 0.001). Beliefs toward medicines, glaucoma, eye drops, self-reported adherence, and sociodemographic factors did not have a significant impact on the patients' decisions. CONCLUSIONS: An ocular drug implant would be an acceptable alternative to topical eye drops for subgroups of glaucoma patients.

Na(+)-dependent neutral amino acid transporter ATB(0) is a rabbit epithelial cell brush-border protein.

System B(0) activity accounts for the majority of intestinal and kidney luminal neutral amino acid absorption. An amino acid transport system, called ATB(0) (also known as ASCT2), with functional characteristics similar to those of system B(0), has been recently cloned. We generated polyclonal antibodies to human and rabbit ATB(0) COOH-terminal peptides and used Western blot analysis to detect ATB(0) protein in rabbit tissues, rabbit ileal brush-border membrane vesicles (BBMV), and HeLa cells transfected with plasmids containing ATB(0) cDNAs. Immunohistochemistry was used to localize ATB(0) in rabbit kidney and intestine. In Western blots of rabbit tissues, ATB(0) was a broad smear of 78- to 85-kDa proteins. In transfected HeLa cells, ATB(0) appeared as a smear consisting of 57- to 65-kDa proteins. The highest expression was found in the kidney. ATB(0) was enriched in rabbit ileal BBMV and in HeLa cells transfected with ATB(0) cDNAs. In the kidney and in the intestine, ATB(0) was confined to the brush-border membrane (BBM) of the proximal tubular cell and of the enterocyte, respectively. Tissue and intracellular distribution of ATB(0) protein parallels that of system B(0) activity. ATB(0) protein could be the transporter responsible for system B(0) in the BBM of epithelial cells.

Detection of mutated K12-ras in histologically negative lymph nodes as an indicator of poor prognosis in stage II colorectal cancer.

Stage II colorectal carcinoma is characterized by negative lymph node pathology as determined by conventional microscopic examination. These patients generally do not receive adjuvant therapy although 20%-30% will die from metastatic disease. To determine whether K-ras mutations at codon 12 could be used as a sensitive indicator of occult lymph node metastasis in stage II colon carcinoma, a retrospective study was performed using restriction endonuclease-mediated selective polymerase chain reaction (REMS-PCR) amplification. Of 106 colonic tumors analyzed, 46 were identified as positive for a K12-ras mutation in the primary tumor. Multiple lymph node samples from 38 of these 46 patients were examined by a sensitive nested PCR protocol for the presence of a K12-ras mutation. Of these 38 patients, 14 had 1 or more positive lymph nodes by PCR (37%) and 24 were negative for the mutation (63%). Of the 14 patients with a K12-ras mutation detected in lymph nodes, 8 died of the disease within 5 years (57%) compared to only 4 of the 24 patients with ras-negative lymph nodes (17%). The difference in time to death from disease, stratified using K12-ras status of lymph nodes, was statistically significant (P = 0.036; log-rank test). These results suggest K-ras mutation status of lymph nodes in patients with stage II colon cancer might identify a subgroup of patients who are more likely to develop recurrent and/or metastatic disease and benefit from adjuvant therapy. Larger studies are indicated to determine whether detection of K-ras mutation positivity in histologically negative lymph nodes portends a poor prognosis and to determine whether more aggressive use of adjuvant therapy is warranted.

CD-20 expression in post-transplant lymphoproliferative disorders: treatment with rituximab.

B-cell lymphoproliferative disorders are rare but serious complications of solid organ and bone marrow transplantation. We report that these tumors frequently express the CD-20 antigen, and immunotherapy directed at this antigen may be a well-tolerated and effective treatment.

Multiple esophageal rings: an association with eosinophilic esophagitis: case report and review of the literature.

Esophagitis may present endoscopically with erythema, edema, loss of vascular pattern, friability, and ulceration of the esophageal mucosa. Left untreated, chronic esophagitis may result in stricture formation. The presence of multiple concentric rings involving the entire esophagus has been cited as a chronic form of esophagitis. We present a case of an 8-yr-old boy with multiple concentric esophageal rings and histological evidence of eosinophilic esophagitis, who failed medical antireflux treatment and responded to an elimination diet.

Effects of 5-fluorouracil on flexor tendon repair.

This study was performed to assess the effects of a single 5-minute exposure of 5-fluorouracil (5-FU) applied topically at the time of flexor tendon repair in an attempt to reduce postoperative adhesions. The flexor digitorum profundus tendon to the long and fourth toe of Leghorn chickens was lacerated and primarily repaired using a 2-strand technique. The repair site was then exposed to a single 5-minute application of 5-FU in concentrations of 5, 25, or 50 mg/mL. Legs were casted for 3 weeks. After death the tendon was examined for the work of flexion using a tensile testing machine and examined with light microscopy, scanning electron microscopy, and transmission electron microscopy for morphologic and histologic differences in adhesion formation. Forty-seven chickens were examined. Average work of flexion values were 0.12 J for normal tendon, 0.31 J for operative controls, 0.34 J for the 5 mg/mL group, 0.15 J for the 25 mg/mL group, and 0.19 J for the 50 mg/mL group. The work of flexion was significantly reduced in the 25 and 50 mg/mL groups compared with the operative controls (p =.008 and p =.03, respectively). Histologic sections as graded by a blinded pathologist revealed decreased adhesion formation in all the 5-FU-treated animals (p <.008). Histologic examination showed that the highest concentration of 5-FU was not as effective at reducing adhesions as the 25 mg/mL dose. This appeared to be due to increasing inflammatory changes seen around and within the tendons of the 50 mg/mL group. Overall, a single intraoperative application of 5-FU at concentrations of 25 mg/mL appears to be an effective mechanism for reducing postoperative flexor tendon adhesions.

Seven cases of complete and incomplete forms of Churg-Strauss syndrome not related to leukotriene receptor antagonists.

BACKGROUND: Various forms of Churg-Strauss syndrome have been reported in association with the use of leukotriene receptor antagonists in asthmatic patients. OBJECTIVE: Our purpose was to increase awareness that different forms of the Churg-Strauss syndrome occur in patients not receiving leukotriene modifiers. METHODS: We searched for all the cases of Churg-Strauss syndrome that were seen in the University of Rochester Medical Center, New York, in the past 4 years. RESULTS: We identified 7 patients, 6 of whom fulfilled the American College of Rheumatology criteria for the classification of Churg-Strauss syndrome. None of them used leukotriene receptor antagonists. All had asthma and sinus disease. The duration and severity of their asthma varied considerably. In the majority of the patients the features of Churg-Strauss syndrome became obvious as the systemic corticosteroid dose was being tapered or discontinued, although 3 patients had not been receiving maintenance oral corticosteroids at disease onset. Three patients had positive antineutrophil cytoplasmic antibodies test result (perinuclear pattern). There was histologic documentation of vasculitis in 4 patients. Five of 7 patients responded to high-dose corticosteroid treatment. CONCLUSION: Our 7 cases are similar to the various forms of Churg-Strauss syndrome that have been reported in association with the leukotriene receptor antagonists. Complete or incomplete forms of this syndrome can become apparent in asthmatic patients as systemic corticosteroids are being tapered but can also occur in patients with mild asthma of short duration who use only inhaled corticosteroids.

Gastric adenocarcinoma associated with fundic gland polyps in a patient with attenuated familial adenomatous polyposis.

Familial adenomatous polyposis (FAP) is a rare autosomal dominant precancerous condition of the colon caused by mutations in the adenomatous polyposis coli (APC) tumor suppressor gene. FAP is characterized by the appearance of innumerable adenomatous polyps throughout the large bowel. Fundic gland polyps are the most common gastric lesion in FAP. It is generally believed that fundic gland polyps have little or no potential for malignant transformation in the population at large, and only a few case reports describe the development of high grade dysplasia or gastric adenocarcinoma associated with diffuse fundic gland polyposis in patients with FAP. We report the second case of gastric adenocarcinoma intimately associated with fundic gland polyposis in a family with an attenuated form of FAP. The patient had undergone routine screening per current guidelines because of his known mutation in the APC gene. This suggests that malignant transformation of fundic gland polyps in patients with FAP occur more frequently than previously believed. Current screening recommendations may not be sufficient for patients with FAP or its attenuated forms.

Tolerance induction permits the development of graft-versus-host disease: donor-mediated attack following small bowel transplantation in mixed chimeras.

The induction of tolerance to organ allografts would eliminate acute and chronic rejection as well as the need for nonspecific immunosuppression. We have shown that tolerance induced through the creation of mixed allogeneic bone marrow chimeras allows for the long-term engraftment of cardiac and small bowel allografts across strong multiple major histocompatibility barriers. The possibility that tolerance might render the host susceptible to graft-versus-host disease (GVHD) has not been investigated in this or other models of tolerance. To test this possibility chimeras were created by transplantation of T-cell depleted ACI and Lewis bone marrow into lethally irradiated Lewis rats. Chimerism was determined post bone marrow transplant (BMTx) by flow cytometry of lymphocytes from reconstituted animals. ACI/Lew chimeras (ALC), Lewis/ACI F1 (LACF1), and Lewis (LEW) rats all received heterotopic ACI vascularized small bowel grafts. A second group of chimeras received small bowel grafts from ACI rats pretreated with low dose irradiation to eliminate T-cells from the graft. LEW-->LEW small bowel isografts were also performed. Animals were examined for evidence of GVHD by clinical signs and histologic examination of biopsied tissues. GVHD was quantified using the popliteal lymph node enlargement assay. All LACF1 rats developed severe lethal GVHD following ACI small bowel transplant. Bone marrow chimeras, ALC (n = 6), developed fatal GVHD in a similar fashion after receiving a small bowel transplant. LEW-->LEW isografts and chimeras receiving bowel from irradiated ACI rats survived long term without GVHD while ACI-->LEW allogeneic transplants all underwent acute rejection. GVHD or its absence was confirmed histologically. Popliteal lymph node enlargement indices reflected the presence of GVHD in the chimeras (1.87) and LACF1 (5.4) receiving allografts, but not in isografts or chimeras receiving irradiated allogeneic transplants. Analysis of cytokines in the tongues of rats undergoing GVHD showed elaboration of Th1 type proinflammatory cytokines which was not seen in isografted rats or rats receiving preirradiated small bowel. These results demonstrate that tolerance induction through mixed chimerism results in susceptibility to small bowel induced GVHD. Preirradiating the donor bowel prior to SBTx can prevent GVHD.

Glucocorticoids upregulate intestinal nutrient transport in a time-dependent and substrate-specific fashion.

Glucocorticoids mediate skeletal muscle proteolysis during critical illness to provide substrates for hepatic acute-phase protein synthesis and gluconeogenesis. The effects of hypercortisolemia on splanchnic substrate uptake are not well defined. This study characterizes intestinal nutrient transport in response to acute elevations of plasma glucocorticoid levels. New Zealand White rabbits were randomized to receive either dexamethasone (2 mg/kg intramuscularly) or vehicle and were killed 8, 16, or 24 hours after steroid treatment. Brush-border membrane vesicles were prepared from pooled small intestinal mucosa and the uptake of tritiated substrates was quantified. Serum insulin-like growth factor 1 (IGF-1) levels, mucosal DNA content, and mucosal morphology were determined. Glucocorticoids increased glucose and leucine uptake at 8 hours (80% and 24%, respectively) and 24 hours (147% and 50%, respectively). Glutanmine, alanine, and arginine transport increased by 42%, 96%, and 236%, respectively, at 24 hours. Sodium-independent transport (diffusion) of all substrates was increased by 240% by dexamethasone treatment at 24 hours. Mucosal DNA content increased by 32%, whereas microvillus heights decreased by 27% at 24 hours. No effects were noted on IGF-1 levels or gross villus heights. Glucocorticoids acutely accelerate intestinal nutrient transport in a time-related and substrate-specific fashion. Although the mechanism of glucocorticoid action remains unclear, both genomic and plasma membrane effects are implicated.

Enterocyte nutrient transport is preserved in a rabbit model of acute intestinal ischemia.

BACKGROUND: The use of enteral nutrition in patients with nonocclusive splanchnic hypoperfusion is controversial. This study aims to quantitate enterocyte nutrient transport and correlate function with morphology during intestinal ischemia. METHODS: New Zealand White rabbits were randomized to control (celiotomy only) 60-minute infrarenal aortic clamp (IRC) or 60-minute supraceliac aortic clamp (SCC). Small intestinal brush border membrane vesicles (BBMVs) were prepared by magnesium precipitation and serial differential centrifugation. Sodium-dependent uptake of glucose, glutamine, alanine, leucine, and arginine into BBMVs was quantitated by rapid mixing and filtration. Histologic examination of the intestine was performed by a pathologist blinded to groups. Data are reported as mean values+/-SEM, with significance determined by analysis of variance at p < .05. RESULTS: Villus heights in the IRC and SCC groups were 20% and 48% less than control, respectively. SCC histology was characterized by extensive epithelial denudation and necrosis, whereas IRC had mild focal villus edema only. Sodium-dependent glucose and leucine transport each exhibited nonsignificant increases of 20% to 25% in the IRC group and 30% to 55% in the SCC group. No changes were noted in sodium-dependent glutamine, alanine, and arginine uptake or sodium-independent transport. CONCLUSIONS: Enteral nutrient transport does not correlate with mucosal architecture, is maintained during splanchnic hypoperfusion states, and likely occurs via intact crypt cells.

Epidermal growth factor and human growth hormone accelerate adaptation after massive enterectomy in an additive, nutrient-dependent, and site-specific fashion.

BACKGROUND: After massive enterectomy (ME), remnant intestine undergoes compensatory adaptation. Epidermal growth factor (EGF) and human growth hormone (hGH) have each been shown to enhance total length small intestine nutrient transport after ME. This study aims to determine the differential effects of EGF and hGH on proximal and distal small intestinal remnants after ME. METHODS: New Zealand white rabbits underwent 70% mid-jejunoileal resection. After 1 week, animals received hGH (0.2 mg/kg/day), EGF (1.5 micrograms/kg/hr), hGH + EGF, or vehicle (equal volume) for 7 days. Sodium-dependent uptake of glucose, glutamine, alanine, leucine, and arginine into brush border membrane vesicles was quantitated. Serum insulin-like growth factor-I concentrations as well as proximal and distal villus and microvillus heights were measured. IGF binding protein-3 and -4 mRNA expression was determined in full-thickness proximal and distal gut remnants. RESULTS: Concomitant hGH and EGF treatment up-regulates glucose (100%), glutamine (80%), and leucine (60%) transport in the proximal remnant; alanine (150%) and arginine (400%) transport in the distal remnant; and microvillus height (25% to 35%) both proximally and distally. Serum IGF-I levels and gross villus heights were not different among groups. CONCLUSIONS: Co-infusion of hGH and EGF accelerates intestinal adaptation after ME in an additive, nutrient-dependent, and site-specific fashion via enhanced nutrient transport as well as microvillus hypertrophy.

Gastric adenocarcinoma and dysplasia in fundic gland polyps of a patient with attenuated adenomatous polyposis coli.

Gastric adenocarcinoma has been previously recognized as a potential complication of familial adenomatous polyposis coli (APC) and attenuated forms of APC (AAPC). This tumor has only been reported to originate from adenomatous polyps of the gastric mucosa in these clinical conditions. There have been no previous case reports of gastric adenocarcinoma arising from the more commonly found fundic gland polyps associated with AAPC or APC. We report the first definitive case of gastric adenocarcinoma arising from a hyperplastic polyp of the fundis of a patient with AAPC.

Human growth hormone induces system B transport in short bowel syndrome.

BACKGROUND: After massive enterectomy, remnant intestine undergoes compensatory adaptation. A combination of human growth hormone (hGH) and a glutamine-enriched modified diet induces further adaptation in patients with short bowel syndrome (SBS) on long-term total parenteral nutrition. The specific actions of each component, however, are not well-defined. METHODS: New Zealand White rabbits were randomized to control, sham operation, or SBS (70% midjejunoileal resection) groups and treated with either hGH or saline. Sodium-dependent uptake of glucose, glutamine, alanine, leucine, and arginine into brush border membrane vesicles was quantitated. Serum insulin-like growth factor-I (IGF-I) levels were determined by immunoradiometric assay. Mucosal mRNA expression of IGF-I and IGF binding protein 4 (IGFBP-4) was evaluated by northern blot analysis using rat cDNA probes. RESULTS: Glutamine and leucine transports were 33 and 39% greater, respectively, in the hGH-treated versus saline-treated SBS group (P < 0.05), supporting induction of system B amino acid transport. This upregulation was due, in part, to an 88% increase in glutamine carrier capacity (Vmax) with no change in carrier affinity (Km). Both hGH treatment and SBS increased serum IGF-I levels without direct correlation with increased nutrient transport. IGFBP-4 mRNA expression in small bowel mucosa of saline-treated SBS animals was significantly greater than saline-treated unoperated control values. Mucosal IGFBP-4 mRNA was not significantly altered from control in the other study groups. IGF-I mRNA expression was not detected in mucosa, but weak hybridization was noted in rabbit liver. CONCLUSIONS: Human growth hormone accelerates early adaptation in SBS by upregulation of system B carrier capacity. Serum IGF-I levels and mucosal IGF-I and IGFBP-4 mRNA expression did not directly correlate with this enhanced nutrient transport, suggesting that hGH might exert its adaptive effects by mechanisms that are independent from the IGF system in this model.

Epidermal growth factor and neurotensin induce microvillus hypertrophy following massive enterectomy.

The compensatory hypertrophy that develops after massive enterectomy is rarely adequate to prevent the development of short bowel syndrome. Trophic hormones such as epidermal growth factor (EGF) and neurotensin (NT) may be useful in improving and accelerating this adaptive response. This study delineates the effects of NT and EGF on remnant small bowel at the microvillus cellular level, which is the prime determinant of surface area. New Zealand white rabbits (2 kg) underwent midgut transection (sham) or 70% jejunoileal resection. Alzet pumps containing saline solution (control), EGF (1.5 microg /kg/hr), or NT (900 microg/kg/day) were implanted in resected animals after which they underwent 1 week of infusion. A second group of EGF animals was killed 2 weeks after infusion completion to assess delayed effects (EGF-delayed). Proximal jejunum was fixed for light and electron microscopy; villus and microvillus parameters were read in a blinded fashion. EGF (2.17+/-0.05 microm), EGF-delayed (2.26+/-1.5 microm, and NT (1.96+/-0.02 microm) animals had significantly increased microvillus heights compared to the control group (1.49+/-0.04 microm). Calculated brush-border surface areas were increased in a similar fashion. EGF and NT failed to elicit increases in jejunal gross villus heights. EGF and NT induce enterocyte microvillus hypertrophy and increase absorptive surface area in remnant bowel after massive enterectomy. In addition, the trophic effects of EGF persist after cessation of infusion. These peptides may be useful in accelerating small bowel adaption and preventing the development of short gut syndrome.

Octreotide diminishes luminal nutrient transport activity, which is reversed by epidermal growth factor.

BACKGROUND: Octreotide (SMS) is a somatostatin analogue utilized in patients with short bowel syndrome (SBS) to decrease output. It may inhibit small bowel adaptation by blocking the secretion of trophic hormones such as epidermal growth factor (EGF). This study delineates the effects of SMS and EGF on nutrient transport in SBS. METHODS: One week after 70% jejunoileal resection, 20 New Zealand White rabbits (2 kg) received subcutaneous infusions of saline or EGF (1.5 micrograms/kg/hr) and injections of saline or SMS s.q.b.i.d. The study groups were EGF/saline, saline/saline, saline/SMS, and EGF/SMS. After 7 days of infusion, intestinal brush border membrane vesicles were prepared and nutrient transport measured. RESULTS: SMS reduced active nutrient transport. Kinetics confirmed this was secondary to a reduction in functional carriers in the brush border membrane, without a change in carrier affinity. The coinfusion of EGF ameliorated this effect. On an individual basis, EGF alone did not significantly increase nutrient transport, but when taken as a group, nutrients transport was upregulated 26%. CONCLUSIONS: SMS is detrimental to small bowel adaptation. EGF reverses this effect and may benefit patients with SBS who require SMS to control high intestinal output.

Sequential alterations in gut mucosal amino acid and glucose transport after 70% small bowel resection.

BACKGROUND: Studies in animals with short bowel syndrome (SBS) suggest that up-regulation of nutrient transporter activity occurs as an adaptive response to the loss of absorptive area. It is unclear, however, whether nutrient transport is altered at the cell membrane in SBS. The purpose of this study is to clarify amino acid and glucose transport in small intestinal luminal mucosa after 70% small bowel resection in rabbits. METHODS: New Zealand white rabbits underwent 70% jejunoileal resection (n = 27) or a sham operation (n = 19). Brush border membrane vesicles were prepared from small intestinal mucosa at 1 week, 1 month, and 3 months by magnesium aggregation-differential centrifugation. Transport of L-glutamine, L-alanine, L-leucine, L-arginine, and D-glucose was assayed by a rapid mixing-filtration technique. RESULTS: We observed no difference in uptake of all amino acids and glucose at 1 week. The uptake of amino acids and glucose was decreased by 20% to 80% in animals with SBS at 1 month. By 3 months all uptake values except that of glucose returned to normal. Kinetic studies of the system B transporter for glutamine indicate that the decrease in uptake at 1 month was caused by a reduction in the Vmax (1575 +/- 146 versus 2366 +/- 235, p < 0.05) consistent with a decrease in the number of functional carriers on the brush border membrane. CONCLUSIONS: In addition to the anatomic loss of absorptive area after massive bowel resection, alterations in enterocyte transport function may be responsible for malabsorption in patients with SBS.

Low-dose enteral feeding is beneficial during total parenteral nutrition.

BACKGROUND: Enteral support is the preferred feeding route for stressed patients due in part to the provision of gut-specific fuels. In those patients who must be maintained parenterally, small amounts of enteral stimulation might blunt gut atrophy and lead to improvement in host defense mechanisms decreasing macromolecular and/or bacterial translocation (BT). METHODS: Forty-eight rats were infused with TPN for 9 days, and were randomized to receive 0%, 6%, 12%, or 25% of their calories as partial enteral nutrition (PEN) in an isocaloric, isonitrogenous fashion. Twenty-four hours before harvest animals were gavaged with lactulose and urinary excretion quantified. At harvest, mesenteric lymph nodes were cultured to assess BT and intestinal histology determined. RESULTS: Provision of as little as 25% of total calories PEN improved nitrogen balance and reduced BT, in a dose dependent fashion. It did not alter TPN-associated increased macromolecular lactulose permeability (4.4% +/- 1.0%). CONCLUSION: Concurrent small amounts of PEN, aimed to support the gut's metabolic needs, are beneficial during periods of prolonged TPN.

Disinfectant colitis. Rinse as well as you wash.

Commercially available endoscope disinfecting solutions readily cause colonic damage if allowed to contact mucosa. The two most common cleaning solutions differ in their initial toxic effect (glutaraldehyde directly injuries crypt epithelium, and hydrogen peroxide compromises mucosal stroma), but both ultimately result in tissue necrosis over time. Within 12-48 h after colonoscopy, patients show signs of bloody diarrhea, cramping, and fever--symptoms that may be confused with an infectious process. Based on a literature review and our own experimental studies, we conclude that hydrogen peroxide alone is responsible for a unique form of colitis commonly referred to as pseudolipomatosis by pathologists. This controversial lesion becomes visible as opaque plaques or pseudomembranes even while colonoscopy is in progress and is almost assuredly due to the effervescent release of molecular oxygen. Diligent rinsing is necessary to minimize patients' exposure to residual disinfecting chemicals in the endoscope. When an automatic disinfecting machine is employed, it may require strict adherence to proper maintenance and volume adjustments in the rinse cycle. Forced air drying and an additional preprocedure rinse of channels and the exterior of the scope should ensure a chemical-free examination.