Design and benchtop validation of a handheld integrated dynamic breast imaging system for noninvasive characterization of suspicious breast lesions.

We have developed a portable, handheld, integrated, dynamic breast imaging system that integrates a near infrared tissue oximeter, clinical ultrasound, and two pressure sensors for noninvasive detection of pressure-induced structural and functional dynamics of suspicious breast lesions. A series of benchtop tests were conducted to validate multiple performance characteristics of the integrated dynamic near infrared/ultrasound breast imaging system (idNIRUS), including the reconstruction of the absorptive heterogeneities and the generation of the dynamic compression stimuli. In absorptive heterogeneity testing, we reconstructed the absorption coefficients of transparent polypropylene tubing circulated with a skim milk-India ink mixture and embedded in a gel wax tissue simulating phantom. High linear correlations (R(2) greater than 0.989) were observed between the reconstructed and the measured absorption coefficients of the embedded tubing. In dynamic compression testing, five volunteer operators generated ten successive compression sessions by compressing the idNIRUS imager on a breast self examination wearable model following the computer simulated pressure profile. The manually generated pressure profiles demonstrated an accuracy of 95.7% and operator-dependent variation of less than 5%. The results of the current benchtop tests will help to optimize the most appropriate testing conditions for our future planned clinical trial.

Novel expression of gastrin (cholecystokinin-B) receptors in azaserine-induced rat pancreatic carcinoma: receptor determination and characterization.

Many reports have emphasized the role of gastrin as a growth factor for normal gastrointestinal mucosa and gastrointestinal cancers. Recent studies have pointed out that this peptide acts also as a growth factor for the pancreatic cancer cell line AR42J. This effect is mediated by gastrin [cholecystokinin (CCK)-B] receptors. In the present study, we investigated gastrin (CCK-B) receptor expression in the azaserine-induced rat pancreatic carcinoma DSL-6, comparing it to normal rat pancreas, and we also characterized CCK receptor subtypes in this tumor. The results showed that there is extensive gastrin binding to the DSL-6 pancreatic carcinoma. No evidence of specific gastrin binding to normal pancreas was found. Analysis of the ability of gastrin-17-I to inhibit 125I-gastrin-I binding demonstrated that gastrin bound to a single class of receptors with a Kd of 0.21 +/- 0.04 nM and a binding capacity of 184 +/- 29 fmol/mg protein. 125I-Gastrin-I binding was inhibited by the specific CCK-B receptor antagonist L365,260 approximately 40 times more effectively than by the specific CCK-A receptor antagonist L364,718. Analysis of the ability of cholecystokinin octapeptide (CCK-8) to inhibit 125I-Bolton-Hunter-CCK-8 binding revealed two CCK binding sites, i.e., a high affinity site and a low affinity site. The observed binding affinities of CCK-8 were then introduced into the computer analysis of the dose-inhibition curve of the ability of gastrin-17-I to inhibit binding of 125I-Bolton-Hunter-CCK-8, which was significantly better fit by a three-site model than by a two-site model. The three sites meet the criteria for CCK-B, high affinity CCK-A, and low affinity CCK-A receptors. The binding capacity of CCK-B receptors constitutes 34% of the total high affinity CCK binding sites. This study demonstrated that DSL-6 pancreatic carcinoma expresses three subtypes of CCK receptors. Gastrin (CCK-B) receptors, which were not detected in normal rat pancreas, constitute about one third of the total high affinity CCK receptors. We suggest that novel expression of gastrin (CCK-B) receptors may be generated by gene mutation or amplification during carcinogenesis and may play an important role in promoting tumor growth.

Stimulation of growth of azaserine-induced putative preneoplastic lesions in rat pancreas is mediated specifically by way of cholecystokinin-A receptors.

Cholecystokinin (CCK) has been shown to stimulate the growth of both normal pancreas and azaserine-induced putative preneoplastic pancreatic lesions in the rat. The present study was performed to determine whether these effects are mediated by way of CCK-A receptors, CCK-B receptors, or both. Sixteen-day-old male Lewis rats were given i.p. injections of azaserine at 30 mg/kg body weight. Starting on day 21, rats were given s.c. injections, 5 days/week for 16 consecutive weeks, of either (a) CCK octapeptide (nonselective CCK agonist) (2.50 micrograms/kg body weight, n = 17), (b) tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2-methylphenylaminocarbonyl++ +)-Asp- (N-methyl)-Phe-NH2 (highly selective CCK-A agonist) (1.84 micrograms/kg body weight, n = 18), (c) [(2R,3S)-beta-MePhe28,N-MeNle31]CCK26-33 (highly selective CCK-B agonist) (2.40 micrograms/kg body weight, n = 18), or (d) normal saline solution (control, n = 17). Rats were subsequently sacrificed, pancreatic weights were determined, and quantitative morphometric analysis of atypical acinar cell foci and nodules was performed. Both CCK octapeptide and the selective CCK-A agonist tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2- methylphenylaminocarbonyl)-Asp-(N-methyl)-Phe-NH2 stimulated pancreatic growth and the development of acidophilic atypical acinar cell foci and nodules. Furthermore, the effect produced by the selective CCK-A agonist tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2- methylphenylaminocarbonyl)-Asp-(N-methyl)-Phe-NH2 was greater than that produced by CCK octapeptide. In contrast, the selective CCK-B agonist [(2R,3S)-beta-MePhe28,N-MeNle31]CCK26-33 had no effect. These findings suggest that the growth of putative preneoplastic lesions (acidophilic atypical acinar cell foci and nodules) in the rat pancreas during the early stages of azaserine-induced pancreatic carcinogenesis is mediated specifically by way of CCK-A receptors.

Ex vivo electrical impedance measurements on excised hepatic tissue from human patients with metastatic colorectal cancer.

Point-wise ex vivo electrical impedance spectroscopy measurements were conducted on excised hepatic tissue from human patients with metastatic colorectal cancer using a linear four-electrode impedance probe. This study of 132 measurements from 10 colorectal cancer patients, the largest to date, reports that the equivalent electrical conductivity for tumor tissue is significantly higher than normal tissue (p < 0.01), ranging from 2-5 times greater over the measured frequency range of 100 Hz-1 MHz. Difference in tissue electrical permittivity is also found to be statistically significant across most frequencies. Furthermore, the complex impedance is also reported for both normal and tumor tissue. Consistent with trends for tissue electrical conductivity, normal tissue has a significantly higher impedance than tumor tissue (p < 0.01), as well as a higher net capacitive phase shift (33° for normal liver tissue in contrast to 10° for tumor tissue).

Gastric schwannoma found incidentally 19 years after a horizontal gastroplasty for morbid obesity.

This report represents the first known case of a gastric schwannoma in a patient subsequent to a gastric stapling and partitioning procedure for morbid obesity. The submucosal tumor found in the collapsed distal portion of the stomach was merely an incidental finding and it appeared that all of the patient's ongoing symptomatology (nausea and vomiting after meals) was a reflection of the chronic obstruction that was present at the gastric partitioning staple-line. No correlation between gastric stapling and partitioning and the development of gastric schwannoma is known or is suggested in this report.

Efficacy of drug regimen exceeds electrostimulation in treatment of avian muscular dystrophy.

Autosomal-recessive dystrophic chickens were treated in three experimental groups with an intraperitoneal multicomponent drug mixture (50 mg/kg Ep475, 20 mg/kg Cinanserin, 10 mg/kg stanazolol, 100 mg/kg leucine, 0.1 mg/kg insulin, 100 mg/kg glucose, and 50 mg/kg carnitine), percutaneous high-frequency electrostimulation of the pectoralis muscle, or a combination of both drug and electrostimulation treatments. Therapeutic efficacy was determined in each group by measurements of strength, righting ability, and histomorphometric analyses of the pectoralis musculature. Drug treatment alone was found to significantly improve muscular strength, function, and relative myofiber necrosis compared with sham-injected controls. The efficacy of drug treatment was found to be equal to or better than singular electrostimulation treatment; there was no apparent additive effect of electrostimulation. As a result, these findings support the use of drug treatment as a useful nongenetic approach to the management of human muscular dystrophy where there is the potential risk of injury from exercise usage.

Evaluation of percutaneous penetration of natural rubber latex proteins.

Latex allergy is recognized worldwide as a serious health risk. To date, exposure assessment and intervention strategies have focused primarily on respiratory protection; this work evaluates the potential role of dermal protein penetration in the development of latex allergy. In vitro penetration models using flow-through diffusion cells and both human surgical specimens and hairless guinea pig skin (CrL: IAF/HA) demonstrated iodinated latex proteins (ammoniated and non-ammoniated) penetrating into and through both intact and abraded skin. Although less than 1% penetration was observed with intact skin, up to 23% of latex proteins applied to abraded skin were recovered from receptor fluid within 24 h of exposure. Phosphoimaging of the concentrated effluent revealed proteins ranging in size from 3 to 26 kDa. Using a (3)H(2)O penetration assay to evaluate barrier integrity, the amount of latex protein penetration was found to positively correlate with the degree of dermabrasion. Immunohistochemistry of the skin localized latex proteins in the Langerhans cell-rich epidermis and in the dermis. Both in vitro penetration studies and immunohistochemistry supported the use of hairless guinea pig skin as a surrogate for human skin in evaluating latex protein penetration. In studies performed in vivo, 35% of hairless guinea pigs topically exposed to latex proteins (100 microg) 5 days per week for 3 months demonstrated elevations in latex-specific IgG1. The implication for these data is that the skin is not only a plausible route for latex sensitization but can be a major exposure route when the integument has been compromised.

Temporal expression of the gastrin (CCK-B) receptor during azaserine-induced pancreatic carcinogenesis.

Cholecystokinin (CCK-A) and gastrin (CCK-B) receptors have been demonstrated in the azaserine-induced rat pancreatic carcinoma DSL-6. In order to determine at what stage in azaserine-induced pancreatic carcinogenesis gastrin (CCK-B) receptors are first expressed, we examined the binding of [125I]gastrin-I to normal rat pancreas, azaserine-induced premalignant pancreatic nodules, grossly normal internodular pancreas, and DSL-6 carcinoma. We observed that specific gastrin binding was absent in normal pancreas, premalignant nodules, and internodular pancreas, and also reconfirmed our previous report of marked overexpression of gastrin (CCK-B) receptors in the DSL-6 carcinoma. Specific cholecystokinin (CCK) binding was present in all pancreatic tissue types tested. Therefore, we conclude that the presence of gastrin (CCK-B) receptors in the azaserine-induced pancreatic carcinoma DSL-6, in contrast to their absence in premalignant nodules, suggests that the expression of the gastrin (CCK-B) receptor may be important in the transformation from premalignant nodules to pancreatic cancer.

Autoradiographic localization of cholecystokinin (CCK) receptor expression during the development of azaserine-induced rat pancreatic carcinoma.

The peptide hormone cholecystokinin (CCK) has been shown to stimulate the growth of azaserine-induced preneoplastic nodules in the rat pancreas. Previously, our labortory demonstrated by classical binding studies that CCK receptors are overexpressed in azaserine-induced rat pancreatic neoplasms. In the present study, we utilized autoradiography to determine the temporal course of this increased receptor binding. Male Lewis rats were given azaserine or saline injections and sacrificed at 2, 4, 8, 12, and 18 months of age. Pancreatic tissue was harvested and autoradiography using 125l-labeled. CCK-8 was performed. Densitometry measurements of azaserine-induced pancreatic nodules, internodular pancreas, and normal pancreatic tissue (from saline-treated controls) of each age group were taken with an image analyzer. There was no statistically significant difference in CCK binding to internodular pancreas and normal pancreas at any age. At 2 months of age, there was no significant increase in CCK binding to azaserine-induced pancreatic nodules. However, at 4, 8, 12, and 18 months of age there was significantly greater CCK binding to azaserine-induced pancreatic nodules than to both internodular pancreas and normal pancreas (p < 0.001 for all groups). At 18 months of age, one azaserine-treated animal developed a pancreatic acinar cell carcinoma, which likewise exhibited significantly greater CCK binding than internodular pancreas or normal pancreas (p < 0.001 for both). These findings demonstrate increased CCK binding in azaserine-induced preneoplastic pancreatic nodules and pancreatic acinar cell carcinoma, compatible with our previous demonstration of receptor overexpression in these tissues. Increased CCK binding first becomes apparent by 4 months following exposure to azaserine. These result suggest that overexpression of CCK receptors, located specifically on preneoplastic and neoplastic pancreatic lesions, results in increased CCK binding and is involved in the mediation of CCK-stimulated growth during azaserine-induced pancreatic carcinogenesis.

Ki-ras and p53 mutations in pancreatic ductal adenocarcinoma.

Pancreatic adenocarcinoma involves activation of the Ki-ras oncogene, inactivation of the p53 tumor suppressor gene, and dysregulation of growth factors and perhaps metastasis genes. Ki-ras oncogene point mutations are known to be involved in pancreatic oncogenesis. The p53 tumor suppressor gene product plays a critical role in cell cycle regulation and also functions as a nuclear transcription factor. Point mutations in the p53 gene have been observed in a variety of malignancies. We determined the frequency of p53 protein overexpression and p53 point mutations in the conserved and nonconserved domains in pancreatic cancers as well as the coincidence of Ki-ras mutation in pancreatic ductal adenocarcinoma. Genomic DNA was isolated from 20 frozen pancreatic adenocarcinomas (14 primary, six metastases) along with six specimens of control pancreatic tissue and screened by single-strand conformation polymorphism (SSCP) analysis followed by direct genomic sequencing of SSCP variants. SSCP analysis was accomplished by incorporating 32P-dCTP in 12 separate polymerase chain (PCR) amplifications covering the p53 coding exons 2-11. All mobility shifts on SSCP were subjected to direct genomic sequencing by the modified dideoxy method. Immunoperoxidase (IP) staining was also done with a p53 monoclonal antibody. Ki-ras codon 12 mutational analysis was accomplished by incorporating 32P-dCTP by polymerase chain reaction amplification utilizing mismatched primers, which create a BstN1 restriction endonuclease site spanning codon 12; the products were digested by BstN1. Polyacrylamide gel electrophoresis allowed distinction between wild-type and mutant Ki-ras. p53 mutations were found in 5 of 20 pancreatic cancers (three of 14 primary tumors, two of six metastatic tumors). Point mutations were observed in three of 14 primary tumors, and one of six metastases, while a 2-base pair duplication resulting in a premature stop codon in exon 5 was found in one metastatic tumor. Point mutations were noted in conserved domains (exons 4, 5, 8) and in the nonconserved domain (exon 10). IP staining revealed that eight of 14 of the primary tumors and two of six metastases exhibited moderate to strong nuclear staining (> 30%), while no nuclear staining was evident in the controls. Ki-ras codon 12 mutations were found in 14 of 20 (70%) pancreatic cancers (nine of 14 primary tumors, five of six metastatic tumors) and none of the six controls. Fifty percent of the primary pancreatic tumors demonstrated moderate to strong nuclear staining. Extensive genetic analysis demonstrated mutations in 30% of the pancreatic cancers. One cancer had a nonsense mutation not detected by IP. Seven of 19 (37%) pancreatic cancers exhibited both Ki-ras point mutation and p53 protein overexpression or mutation. Both genetic analysis and IP are required to characterize all p53 mutations in pancreatic cancer. Ki-ras codon 12 mutations and p53 protein overexpression are important steps in pancreatic oncogenesis.

Preoperative biliary drainage: impact on intraoperative bile cultures and infectious morbidity and mortality after pancreaticoduodenectomy.

Whether it is necessary to perform biliary drainage for obstructive jaundice before performing pancreaticoduodenectomy remains controversial. Our aim was to determine the impact of preoperative biliary drainage on intraoperative bile cultures and postoperative infectious morbidity and mortality following pancreaticoduodenectomy. We retrospectively analyzed 161 consecutive patients undergoing pancreaticoduodenectomy in whom intraoperative bile cultures were performed. Microorganisms were isolated from 58% of these intraoperative bile cultures, with 70% of them being polymicrobial. Postoperative morbidity was 47% and mortality was 5%. Postoperative infectious complications occurred in 29%, most commonly wound infection (14%) and intra-abdominal abscess (12%). Eighty-nine percent of patients with intra-abdominal abscess (P = 0.003) and 87% with wound infection (P = 0.003) had positive intraoperative bile cultures. Microorganisms in the bile were predictive of microorganisms in intraabdominal abscess (100%) and wound infection (69%). Multivariate analysis of preoperative and intraoperative variables demonstrated that preoperative biliary drainage was associated with positive intraoperative bile cultures (P <0.001), postoperative infectious complications (P = 0.022), intra-abdominal abscess (P = 0.061), wound infection (P = 0.045), and death (P = 0. 021). Preoperative biliary drainage increases the risk of positive intraoperative bile cultures, postoperative infectious morbidity, and death. Positive intraoperative bile cultures are associated with postoperative infectious complications and have similar microorganism profiles. These data suggest that preoperative biliary drainage should be avoided in candidates for pancreaticoduodenectomy.

Cholecystokinin receptor characterization and cholecystokinin-A receptor messenger RNA expression in transgenic mouse pancreatic carcinomas and dysplastic pancreas.

Transgenic mice bearing the rat elastase I promoter - SV40 T-antigen (ELSV) fusion gene develop pancreatic acinar cell carcinomas by 3-6 months of age. In other animal models of pancreatic cancer, cholecystokinin (CCK) has been shown to be a tumor promoter. Therefore, we characterized CCK binding properties and CCK-A receptor mRNA expression in pancreatic carcinomas and dysplastic pancreata from the Tg(Ela-1, SV40E+Ela-1, neo)Bri19 strain of ELSV transgenic mice. To accomplish this, we utilized 125I-Bolton-Hunter-labeled-cholecystokinin octapeptide (125I-BH-CCK-8) binding studies, reverse transcription-polymerase chain reaction (RT-PCR), and Southern blot analysis to examine pancreatic carcinomas from 26-week-old male ELSV transgenic mice, dysplastic pancreata from 8-week-old male ELSV transgenic mice, and normal pancreas from 30-week-old nontransgenic male mice (SJL/J) and 8-week-old nontransgenic male mice (B6SJLF1/J). Optimal saturable CCK-8 binding was detected at pH 6.5, 22 degrees C. Competitive inhibition 125I-BH-CCK-8 binding assays performed on all four mouse pancreatic tissues showed that CCK-8 bound to two classes of CCK binding sites: a high affinity, lower capacity CCK binding site and a low affinity, higher capacity CCK binding site. RT-PCR and Southern blot analysis confirmed the 125I-BH-CCK-8 binding studies by demonstrating CCK-A receptor mRNA expression in the ELSV transgenic pancreatic carcinomas and dysplastic pancreas, as well as in normal nontransgenic mouse pancreas. In conclusion, pancreatic carcinomas and dysplastic pancreas from ELSV transgenic mice and normal nontransgenic mouse pancreas all bind 125I-BH-CCK-8 and express mRNA for the CCK-A receptor. In contrast to chemically-induced pancreatic tumors in the rat, ELSV transgenic mouse pancreatic tumors do not appear to significantly overexpress CCK-A receptors.

Mechanism of prevention of development of N-nitrosobis(2-oxopropyl)amine induced pancreatic carcinoma by a protein-free diet in hamsters.

It has been shown that feeding a protein-free diet prior to injection of N-nitrosobis(2-oxopropyl)amine (BOP) can inhibit the development of pancreatic carcinoma in the hamster. The purpose of this study was to determine whether this inhibition is due to a direct effect on the pancreas or to a systemic mechanism. Pancreas transplantation was used to create four groups of two-pancreas hamsters (Group 1: protein-containing diet donor/protein-containing diet host; Group 2: protein-containing diet donor/protein-free diet host; Group 3: protein-free diet donor/protein-containing diet host; Group 4: protein-free diet donor/protein-free diet host). Animals were fed either a protein-containing diet or a protein-free diet for four weeks preoperatively. One day after transplantation, the two-pancreas animals received a 40 mg/kg body weight, subcutaneous, single dose of BOP. Animals in all groups were maintained on a regular protein-containing diet postoperatively, and were then sacrificed 42 weeks after BOP injection. The results showed that a) the incidence of carcinoma in groups 2, 3, and 4 was significantly lower than that in group 1; b) there was no significant difference in group 2 between donor and host pancreas; c) the incidence of carcinoma in the donor pancreas was lower than that in the host pancreas in groups 3 and 4. These results confirm that the protein-free diet significantly inhibits the development of BOP induced pancreatic carcinoma in the hamster. The inhibitory effect appears to act both directly on the pancreas and through an indirect systemic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Novel applications of Endo GIA linear staplers during pancreaticoduodenectomy and total pancreatectomy.

Pancreaticoduodenectomy and total pancreatectomy remain a formidable challenge to many surgeons. This report describes the utilization of Endo GIA linear staplers for division of the proximal jejunal mesentery and division of the uncinate process during pancreatic surgery. Their use may help to reduce undue bleeding during surgery, reduce total operative time, and ultimately reduce postoperative morbidity and mortality.

Novel expression of gastrin (CCK-B) receptors in pancreatic carcinomas and dysplastic pancreas from transgenic mice.

Transgenic mice bearing the elastase I promoter--SV40 T-antigen fusion gene (ELSV) develop pancreatic acinar cell carcinomas by 3 to 6 months of age. The purpose of the study was to determine if pancreatic carcinomas and dysplastic pancreas from the Tg (Ela-1, SV40E + Ela-1, neo) Bri19 strain of ELSV transgenic mice express gastrin (CCK-B) receptors. To accomplish this, we utilized iodine 125 (125I)-gastrin binding studies, reverse transcription-polymerase chain reaction (RT-PCR), and Southern blot analysis to examine pancreatic carcinomas from 26-week-old male ELSV transgenic mice, dysplastic pancreas from 8-week-old male ELSV transgenic mice, and normal pancreas from 30-week-old nontransgenic male mice (SJL/J) and from 8-week-old nontransgenic male mice (B6SJLF1/J). No saturable gastrin binding to normal nontransgenic mouse pancreas was found. In contrast, saturable gastrin binding was detected at pH 6.5, 22 degrees C, in 9 of 13 pancreatic carcinomas and all 5 dysplastic pancreata. Competitive inhibition 125I-gastrin binding assays showed gastrin bound to a single class of high-affinity receptors (receptor binding affinity [Kd] 0.11 +/- 0.02 nM, binding capacities ranging from 1 to 60 fmol/mg protein for pancreatic carcinomas; Kd: 0.15 +/- 0.04 nM, binding capacities ranging from 1 to 9 fmol/mg protein for dysplastic pancreas). RT-PCR and Southern blot analysis confirmed 125I-gastrin binding studies by demonstrating gastrin (CCK-B) receptor mRNA expression in pancreatic carcinomas and dysplastic pancreas but an absence of mRNA expression in normal nontransgenic mouse pancreas. In conclusion, pancreatic carcinomas and dysplastic pancreas in ELSV transgenic mice novelly express gastrin (CCK-B) receptors. This expression may provide a growth advantage to acinar cells as part of the multistage process of carcinogenesis.

Risk factors for catheter-related thrombosis (CRT) in cancer patients: a patient-level data (IPD) meta-analysis of clinical trials and prospective studies.

BACKGROUND: Knowledge of independent, baseline risk factors for catheter-related thrombosis (CRT) may help select adult cancer patients who are at high risk to receive thromboprophylaxis. OBJECTIVES: We conducted a meta-analysis of individual patient-level data to identify these baseline risk factors. PATIENTS/METHODS: MEDLINE, EMBASE, CINAHL, CENTRAL, DARE and the Grey literature databases were searched in all languages from 1995 to 2008. Prospective studies and randomized controlled trials (RCTs) were eligible. Studies were included if original patient-level data were provided by the investigators and if CRT was objectively confirmed with valid imaging. Multivariate logistic regression analysis of 17 prespecified baseline characteristics was conducted. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated. RESULTS: A total sample of 5636 subjects from five RCTs and seven prospective studies was included in the analysis. Among these subjects, 425 CRT events were observed. In multivariate logistic regression, the use of implanted ports as compared with peripherally implanted central venous catheters (PICCs), decreased CRT risk (OR, 0.43; 95% CI, 0.23-0.80), whereas past history of deep vein thrombosis (DVT) (OR, 2.03; 95% CI, 1.05-3.92), subclavian venipuncture insertion technique (OR, 2.16; 95% CI, 1.07-4.34) and improper catheter tip location (OR, 1.92; 95% CI, 1.22-3.02), increased CRT risk. CONCLUSIONS: CRT risk is increased with use of PICCs, previous history of DVT, subclavian venipuncture insertion technique and improper positioning of the catheter tip. These factors may be useful for risk stratifying patients to select those for thromboprophylaxis. Prospective studies are needed to validate these findings.

A prospective analysis of the cephalic vein cutdown approach for chronic indwelling central venous access in 100 consecutive cancer patients.

BACKGROUND: Chronic indwelling central venous access devices (CICVAD) generally are placed by the percutaneous subclavian vein approach. The cephalic vein cutdown approach is used only infrequently. Although the technique has been well described, few prospective data are available on the cephalic vein cutdown approach. METHODS: From September 9, 1998, to July 20, 1999, the cephalic vein cutdown approach was attempted in 100 consecutive cancer patients taken to the operating room with the intention of placing CICVAD. Median patient age was 54.5 years (range 18-88), with 46 men and 54 women. Twenty-five patients had gastrointestinal malignancies, 17 had breast cancer, 15 had lymphoma, 13 had lung cancer, 12 had leukemia, 5 had multiple myeloma, and 13 had other malignancies. Patients were followed prospectively for immediate and long-term outcome. RESULTS: CICVAD placement via the cephalic vein cutdown approach was successful in 82 patients; the remaining 18 patients required conversion to a percutaneous subclavian vein approach. The reasons for inability to place CICVAD via cephalic vein cutdown approach were a cephalic vein that was too small (10 patients), an absent cephalic vein (7 patients), and inability to traverse the angle of insertion of the cephalic vein into the subclavian vein (1 patient). There were 56 subcutaneous ports and 26 tunneled catheters. Median operating time was 44 minutes (range, 26-79 minutes). No postoperative pneumothorax occurred. Median catheter duration was 198 days (range, 0-513 days). Long-term complications included catheter-related bacteremia (6%), site infection (2%), deep venous thrombosis (5%), port pocket hematoma (1%), and superior vena cava stricture (1%). Thirty-seven percent of patients have died since CICVAD placement. Twenty-nine percent of the CICVADs have been removed. CONCLUSIONS: The cephalic vein cutdown approach was successful in 82% of patients. This approach is a safe and useful alternative to the percutaneous subclavian vein approach.