The measurement of competence. Current plans and future initiatives of the American Board of Surgery.

In summary, the ABS is committed to the competence initiative. Not to do so would be to risk irrelevance. In order for the initiative to succeed, it is clear that the board must partner with specialty societies and most particularly with the American College of Surgeons. That partnership should take the form of collaboration to "teach and test" core information in general surgery and in the surgical specialties and to adjudicate appropriate risk-adjusted outcomes. The aim of the initiative is practice improvement and practice improvement only. It is the hope of the board that diplomates and Fellows will see value in the exercise and will endorse it because of pride in their profession and pride in themselves.

Work loads and practice patterns of general surgeons in the United States, 1995-1997: a report from the American Board of Surgery.

OBJECTIVE: To characterize the work loads and practice patterns of general surgeons in the United States over a 3-year period (1995 to 1997). METHODS: The surgical operative logs of 2434 "generalist" general surgeons recertifying in surgery form the basis of this report. Selected demographics of the group are as follows: location: 50% Northeast and Southeast, 21 % Midwest, 29% West and Southwest; practice type: 45% solo, 40% group, 9% academics; size of practice community: 46% highly urban, 19% rural. Parameters evaluated were the average number of procedures and their distribution by category related to geographic area, practice type, community size, and other parameters. Statistical analysis was accomplished using analysis of variance. RESULTS: No significant year-to-year differences were observed between cohorts. The average numbers of procedures per surgeon per year was 398, distributed as follows: abdomen 102, alimentary tract 63, breast 54, endoscopic 51, vascular 39, trauma 6, endocrine 4, and head and neck, 3. Eleven percent of the 398 procedures were performed laparoscopically. Major index cases were largely concentrated with small groups of surgeons representing 5% to 10% of the total. Significant differences were as follows: surgeons in the Northeast and West performed far fewer procedures than those elsewhere. Urban surgeons performed a few more tertiary-type procedures than did rural ones; however, rural surgeons performed many more total procedures, especially in endoscopy, laparoscopy, gynecology, genitourinary, and orthopedics. Academic surgeons performed substantially fewer total procedures as a group than did nonacademic ones and in all categories except liver, transplant, and pancreas. Male surgeons performed more procedures than did female surgeons, except those involving the breast. More procedures were done by surgeons in group practice than by those in solo practice. U.S. medical graduates and international medical graduates had similar work loads but with a different distribution. CONCLUSIONS: This unique database will be useful in tracking trends over time. More importantly, it demonstrates that general surgery practice in the United States is extremely heterogeneous, a fact that must be acknowledged in any future workforce deliberations.

Effects of polyunsaturated fatty acids on bile acid-induced gastric mucosal injury.

Arachidonic acid is a polyunsaturated fatty acid precursor to prostaglandin formation in the stomach. When applied topically to gastric mucosa it prevents injury from a variety of damaging agents, similar to the effects observed with exogenous prostaglandins. Alternatively, fatty acids could act as mild irritants and protect the gastric mucosa in an adaptive cytoprotective process. This study was undertaken to ascertain whether arachidonic acid attenuates gastric injury from bile acid by acting as a mild irritant to the gastric epithelium or by increasing biosynthesis of cytoprotective prostaglandins. Accordingly, adult anesthetized rat stomachs were pretreated for 30 min with either topical 1 mM arachidonic acid, docusahexaenoic acid or eicosatrienoic acid prior to injury with topical 5 mM acidified taurocholate. In a second set of experiments using a similar protocol, the role of prostaglandins was evaluated by giving indomethacin (5 mg/kg/sc) 30 min prior to fatty acid pretreatment. Mucosal injury was assessed by measuring net transmucosal ion fluxes, the appearance of DNA into the gastric lumen, and histology. Gastric luminal PGE2 content was determined by radioimmunoassay. Pretreatment with topical arachidonic acid, but not docusahexaenoic acid or eicosatrienoic acid, significantly (P < 0.05) decreased bile acid induced net luminal ion fluxes, DNA accumulation and histologic injury scores, an effect negated by indomethacin. Further, pretreatment with arachidonic acid was associated with increased luminal PGE2 content, an effect also abolished by indomethacin. Thus, arachidonic acid does not act as a mild irritant, but protects the gastric mucosa from bile acid injury through a mechanism involving increased bio-availability of substrate for prostaglandin formation.

Isoproterenol-induced gastric mucosal protection from bile acid. Role of endogenous prostaglandins.

Topical isoproterenol is a potent protective agent against bile acid-induced gastric mucosal injury in hypotensive and normotensive rats. This study was undertaken to ascertain what role endogenous prostaglandins and gastric mucosal blood flow play in isoproterenol-induced protection. Accordingly, anesthetized, fasted rats were given the cyclooxygenase inhibitor, indomethacin (5 mg/kg subcutaneously), 30 min prior to topical pretreatment with 3 ml of intragastric saline, isoproterenol (3 microM), or 16,16-dimethyl prostaglandin E2 (3 microM) for 15 min. Gastric injury was induced with topical 5 mM acidified taurocholate and damage assessed by measuring net transmucosal ion fluxes, the appearance of DNA into the gastric lumen, and histology of the gastric epithelium. In a separate set of experiments, the effects of topical isoproterenol on gastric mucosal blood flow (laser Doppler flowmetry) and luminal PGE2 concentrations (125I radioimmunoassay) were examined. Pretreatment with topical isoproterenol or 16,16-dimethyl prostaglandin E2 significantly decreased bile acid-induced net luminal ion fluxes and DNA accumulation, suggesting mucosal protection. The protective effect of isoproterenol, but not 16,16-dimethyl prostaglandin E2, was negated by indomethacin (corroborated by histology). Further, isoproterenol did not significantly alter gastric mucosal blood flow, but did augment luminal PGE2 concentrations, an effect also abolished by indomethacin. Thus, isoproterenol appears to protect the gastric mucosa from the damaging effects of bile acid through a mechanism that requires the synthesis and release of cytoprotective endogenous prostaglandins.

The role of calcitonin gene-related peptide and nitric oxide in gastric mucosal hyperemia and protection.

It has been suggested that capsaicin-induced hyperemia and mucosal protection occurs via calcitonin-gene-related peptide (CGRP) release from gastric afferent sensory neurons and nitric oxide (NO)-mediated vasodilation. The purpose of this study was to determine whether capsaicin and/or bile acid induced hyperemia is mediated by CGRP and/or NO. Male Sprague-Dawley rats (280-350 g) were anesthetized, and the glandular stomach (blood supply intact) was chambered between two plastic rings. Animals were divided into six groups. Normal saline (groups 1 and 4), the NO inhibitor N-nitro-L-arginine methyl ester (L-NAME; 3.75 mg/ml, groups 2 and 5), or the CGRP antagonist hCGRP8-37 (0.047 mg/ml, groups 3 and 6) was continuously infused intraarterially (ia) close to the stomach at a rate of 0.034 ml/min for 1 hr via a catheter inserted retrogradely into the splenic artery. Fifteen minutes after the onset of this infusion, the gastric mucosa was topically exposed to neutral saline solution for 15 min, followed by 160 microM capsaicin for 15 min. The mucosa was then injured by a 15-min exposure to either 5 mM acidified taurocholate (ATC, pH 1.2) in groups 1-3 or 10 mM ATC in groups 4-6. Gastric mucosal blood flow (ml/min/100 g) was continuously measured (laser doppler), and injury was assessed by measuring net transmucosal H+ flux, luminal accumulation of DNA, and histologic grading (0 = no injury to 3 = severe) by an independent observer. Intraarterial infusion of L-NAME significantly blocked the hyperemic response of topical capsaicin while having minimal effect on bile acid-induced hyperemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Capsaicin-induced gastric hyperemia and protection are NO- dependent.

Topical treatment of gastric mucosa with capsaicin (cap) increases gastric mucosal blood flow (GMBF) and protects the mucosa from injury by acidified bile salts. The purpose of this study was to test the hypothesis that this hyperemia related "cytoprotection" is mediated by nitric oxide. Male Sprague-Dawley rats were anesthetized and the glandular stomach (blood supply intact) was chambered between two plastic rings. Animals were divided into four groups. All groups received a 5-min topical saline exposure. Groups 1 and 2 received iv saline or nitro-L-arginine methyl ester (L-NAME, 25 mg/kg iv), a specific nitric oxide inhibitor, 5 min prior to baseline treatment, followed by a 15-min preinjury period of saline and a 15-min injury period of 10 mM acidified taurocholate (ATC, pH 1.2). Groups 3 and 4 were treated as above except topical cap (160 microM) was used during the preinjury period. GMBF was measured with a laser Doppler flowmeter (ml/min/100 g tissue). Injury was assessed grossly (grade 0-3), histologically (grade 0-3), and by measuring DNA content of a 5-min N-acetylcysteine wash (DNAE). Baseline GMBF of 30 +/- 1.5 significantly decreased to 15 +/- 1.2 in group 1 versus group 2 (P < 0.05). When topical ATC was used GMBF increased to 59 +/- 4.9 and 25 +/- 2.8, respectively. Injury by grade and DNAE was not significantly different between these groups. GMBF during cap exposure was 42 +/- 4 and 22 +/- 2 in groups 3 and 4, respectively. Graded histologic and gross injuries were significantly worse in group 4 compared to group 3 (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Capsaicin-induced gastric mucosal hyperemia and protection: the role of calcitonin gene-related peptide.

BACKGROUND: Topical capsaicin augments gastric mucosal blood flow and is cytoprotective. This phenomenon is blocked by nitric oxide (NO) synthase and cyclooxygenase inhibition. Capsaicin-sensitive neurons store and release calcitonin gene-related peptide (CGRP). The purpose of this investigation was to study the effects of a CGRP antagonist on capsaicin-induced hyperemia and protection and to determine the role of NO and the cytoprotective prostaglandin PGE2 in this process. METHODS: The glandular stomachs in male Sprague-Dawley rats (280 to 350 gm) were chambered with the blood supply intact. Animals were divided into four groups. Normal saline solution (group 1) or the CGRP antagonists hCGRP8-37 (groups 2 through 4, 0.047 mg/ml) were continuously infused intraarterially via a retrograde splenic artery catheter at a rate of 0.034 ml/min after rats were given an intravenous bolus of either NSS (groups 1 and 2), L-arginine (group 3), or D-arginine (group 4) (200 mg/kg). The gastric mucosa was then topically exposed to normal saline solution (pH 7.4), followed by 160 mumol/L capsaicin and then 100 mmol/L acidified taurocholate (pH 1.2), each for 15 minutes. Gastric mucosal blood flow (ml/min/100 gm tissue) was continuously measured (laser Doppler) and mucosal injury was assessed. Luminal PGE2 production was measured during the bile acid injury period by radioimmunoassay. RESULTS: The CGRP antagonist hCGRP8-37 significantly inhibits capsaicin-induced hyperemia and its associated mucosal cytoprotection and also significantly decreases luminal mucosal PGE2 production. Pretreatment with L-arginine, but not D-arginine, reverses these effects of CGRP antagonism. CONCLUSIONS: CGRP is a mediator of capsaicin-induced hyperemia and protection. This effect may be dependent on both NO and PGE2 production.

Alkaline reflux gastritis.

Alkaline reflux gastritis is a putative postgastrectomy syndrome presumably caused by excessive reflux of upper gastrointestinal content into the residual stomach after operations for peptic ulcer. In this article, the theoretic basis for the existence of such a syndrome is critically examined and found to be wanting in several respects. The diagnosis is therefore one of exclusion. Most nonoperative therapies are only modestly effective, with the possible exception of feeding patients ursodeoxycholic acid. When operation is indicated, the creation of a long-limb (45-cm) Roux-en-Y eliminates reflux. Unfortunately, symptoms are not invariably alleviated. Complications of operation include marginal ulceration and the Roux stasis syndrome.

Topical prostaglandin E2 and isoproterenol reduce bile acid-induced gastric mucosal injury in shocked rats.

In shocked animals, topical application of bile acids at low pH to gastric mucosa results in gross mucosal injury. Both systemic prostaglandins and isoproterenol reduce this injury, but side effects may limit their clinical usefulness. The purpose of this study was to determine the effect of topical pretreatment with isoproterenol and prostaglandin E2 on gastric mucosal injury induced by low concentrations of bile acid in shocked and normotensive rats. Mucosal injury was assessed by measuring net transmucosal ion fluxes (H+,K+) and luminal accumulation of DNA (DNAE), a sensitive and specific indicator of gastric mucosal cell exfoliation. In this model of mucosal injury, pretreatment with prostaglandin E2 or isoproterenol significantly and dose dependently decreased luminal hydrogen loss, potassium gain, and DNA accumulation in both shocked and normotensive animals. Thus, both topical prostaglandin E2 and isoproterenol reduce gastric mucosal injury caused by low concentrations of bile acid in shocked and normotensive rats, findings corroborated by histology. These findings provide a physiologic basis for the possible use of these agents as prophylaxis or treatment of stress gastritis and gastroduodenal ulcer in the critically ill patient.

Sensory neuron-mediated gastric mucosal protection is blocked by cyclooxygenase inhibition.

BACKGROUND: Sensory neurons have been proposed to play a critical role in the protection of the gastric mucosa from a variety of necrotizing agents. The purposes of this study were (1) to investigate the effect of topical capsaicin, a sensory neuron stimulant, on the gastric mucosal injury caused by the topical application of low concentrations of bile acid and (2) to determine whether local neuronal blockade with topical lidocaine or cyclooxygenase blockade with systemic indomethacin has any effect during pretreatment with capsaicin. METHODS: Before injury with topical 5 mmol/L acidified taurocholate (pH 1.2) rat stomachs were pretreated with either vehicle or capsaicin (160 mmol/L), both with and without prior administration of either lidocaine (1%) or indomethacin (5 mg/kg subcutaneously). Injury was assessed by measuring net transmucosal ion fluxes, the appearance of deoxyribonucleic acid into the gastric lumen, and gross and histologic injury scores. RESULTS: Pretreatment with topical capsaicin significantly (p < 0.05) decreased bile acid-induced net luminal ion fluxes and luminal deoxyribonucleic acid accumulation, an effect blocked by both lidocaine and indomethacin. CONCLUSIONS: Thus both local neuronal blockade and cyclooxygenase inhibition block the protective effect of capsaicin, findings corroborated by gross and histologic injury analysis. This study suggests that sensory neurons may mediate gastric mucosal protection from bile acid injury by increasing synthesis of endogenous prostaglandins.

Effect of local acid-base status on gastric mucosal blood flow and surface cell injury by bile acid.

Topical application of 5 mM sodium taurocholate (5 TC, pH 1.2) to canine gastric mucosa results in luminal hydrogen ion (H+) loss and surface epithelial cell (SEC) injury. However, gross mucosal injury does not occur because of a protective increase in gastric mucosal blood flow (GMBF). The mechanism of this blood flow response is unknown. To test the hypothesis that mucosal acid-base status influences mucosal blood flow and surface cell injury, three groups of dogs with vascularized chambered gastric mucosae were studied during two sequential 30-min periods. Mucosae were exposed during period I to topical acidified isotonic saline (ATS, pH 1.2), and during period II to topical 5 TC. During both periods, group A (n = 5) received close intraarterial (ia) NaCl (0.15 M), group B (n = 5) close ia HCO3 (0.32 M), and group C (n = 4) close ia HCl (0.2 N). Parameters evaluated during both ATS and 5 TC periods included the luminal accumulation of DNA (DNAE, a sensitive marker of SEC exfoliation), luminal H+ loss, and GMBF measured using radiolabeled microspheres. Gastric venous pH was also measured. It was found that, compared to the NaCl group, the HCO3 group had no increase in GMBF after 5 TC exposure. Simultaneously, however, SEC loss was reduced by 48%, 604 +/- 72 with NaCl versus 314 +/- 59 micrograms/30 min DNA with HCO3, P < 0.025. Infusion of ia HCl generated a large increase in GMBF without an increase in SEC injury compared to ia NaCl. Thus, mucosal acid-base status is an important modulator of mucosal blood flow which is itself critically important to gastric mucosal protection during bile acid induced injury.

Effects of topical isoproterenol on bile acid-induced gastric mucosal injury.

Topical isoproterenol protects the gastric mucosa from the severe necrosis induced by 100 per cent ethanol. Its effect on gastric mucosal blood flow is unknown. The purpose of this study was to determine the effect of topical isoproterenol on gastric mucosal blood flow and on the less severe gastric mucosal injury caused by dilute bile acid. Prior to injury with topical 5 mM acidified taurocholate (pH 1.2), stomachs were pretreated with either saline or isoproterenol (low dose = 50 micrograms/kg; high dose = 500 micrograms/kg). Mucosal injury was assessed by measuring net transmucosal ion fluxes (H, K) and the appearance of DNA into the gastric lumen (DNAE). Gastric mucosal blood flow was determined by using laser doppler. Pretreatment with isoproterenol significantly decreased bile acid-induced net transmucosal ion fluxes and luminal accumulation of DNA, suggesting mucosal protection. Furthermore, this effect was dose-dependent on H and DNAE but not K. Pretreatment with topical high dose isoproterenol had no significant effect on gastric mucosal blood flow. Thus, topical pretreatment with isoproterenol dose dependently protects the gastric mucosa from the superficial injury caused by the application of dilute bile acid. This protective effect appears to be mediated by a mechanism other than augmentation of gastric mucosal blood flow.

Selective lipoxygenase inhibitor reduces bile acid-induced gastric mucosal injury.

Leukotriene receptor blockade attenuates topical bile acid-induced gastric mucosal injury, suggesting that peptidyl-leukotrienes may be mediators of this injury. The purpose of this study was to test the hypothesis that a selective 5-lipoxygenase inhibitor protects against bile acid-induced gastric epithelial injury in the rat. Prior to injury with 10 and 20 mM acidified taurocholate (pH 1.2), rat stomachs were pretreated with either vehicle or WY50295K (selective 5-lipoxygenase inhibitor, 20 mg/kg). Injury was assessed by measuring net transmucosal hydrogen ion flux, luminal appearance of DNA, and gross mucosal injury. Topical 5-lipoxygenase inhibitor significantly reduced luminal H+ ion loss, surface epithelial cell loss (as measured by luminal accumulation of DNA), and gross mucosal injury in bile acid-injured stomachs compared to controls. This study lends further support to the hypothesis that leukotrienes may be mediators of bile acid-induced gastric mucosal injury.

Do leukotrienes mediate bile acid-induced gastric mucosal injury?

Leukotrienes C4 and D4 are potent vasoconstrictors and have been proposed as mediators of the severe gastric mucosal injury caused by a variety of necrotizing agents. The purpose of this study was to investigate the role of leukotrienes on the less severe gastric mucosal injury caused by low concentrations of bile acid. Prior to injury with 5 mM acidified taurocholate (pH 1.2), rat stomachs were pretreated with either normal saline, leukotrienes C4 or D4 (10(-6), 10(-8), and 10(-9) M), or SKF-104353 (a leukotriene D4 receptor antagonist 10(-7) M). Injury was assessed by measuring net transmucosal hydrogen ion flux, luminal appearance of DNA, and histologic injury. Topical pretreatment with LTC4 and LTD4 significantly increased bile acid-induced luminal hydrogen ion loss and DNA accumulation in a dose-dependent manner. Leukotriene receptor blockade with SKF-104353 significantly decreased these parameters. Thus, both LTC4 and LTD4 exacerbate the gastric mucosal injury caused by the application of low concentrations of bile acid while leukotriene receptor blockade reduces this injury (corroborated by histologic injury analysis). This study suggests that leukotrienes may be mediators of bile acid-induced gastric mucosal injury.

Effect of capsaicin on gastric mucosal injury and blood flow following bile acid exposure.

Topical bile acid at low pH stimulates gastric mucosal blood flow (GMBF), thereby limiting injury to surface epithelial cells (SEC). Capsaicin-sensitive afferent neurons (ASN) are possible mediators of the GMBF response and, therefore, of mucosal protection. In order to investigate the effect of topical capsaicin (ASN stimulant) and topical lidocaine (ASN inhibitor) on SEC exfoliation and GMBF, vascularized wedges of canine gastric corpus were mounted in lucite chambers. Mucosae were pretreated for 15 min with saline (NSS), 160 microM capsaicin (CAP), 4% lidocaine (LIDO), or CAP and LIDO, followed by a 30-min exposure to acid test solution (ATS; pH 1.2). The same mucosae were then pretreated in an identical fashion followed by a second 30-min exposure to 5 mM taurocholate (5 TC; pH 1.2). Parameters evaluated during both ATS and 5 TC periods were the luminal accumulation of DNA (DNAE, a sensitive marker of SEC exfoliation) and GMBF measured using radiolabeled microspheres. It was found that, relative to NSS pretreatment, CAP pretreatment increased GMBF and decreased DNAE during exposure to both ATS and 5 TC. LIDO blocked the CAP effect on GMBF but not on DNAE. Thus, ASN stimulation by CAP enhances GMBF and is protective. ANS inhibition blocks CAP's GMBF increase but not its protective capabilities. Therefore, augmentation of GMBF is not the only mechanism by which ASNs blunt SEC exfoliation.

Do sensory neurons mediate adaptive cytoprotection of gastric mucosa against bile acid injury?

Pretreatment with the mild irritant 1 mmol acidified taurocholate protects the gastric mucosa from the injury induced by the subsequent application of 5 mmol acidified taurocholate, a phenomenon referred to as "adaptive cytoprotection." How this occurs remains an enigma. The purpose of this study was to investigate the role of sensory neurons and mucus secretion in this phenomenon. Prior to injury with 5 mmol acidified taurocholate (pH 1.2), the stomachs of six groups of rats were subjected to the following protocol. Two groups were topically pretreated with either saline or the mild irritant 1 mmol acidified taurocholate. Two other groups received the topical anesthetic 1% lidocaine prior to pretreatment with either saline or 1 mmol acidified taurocholate. The last two groups got the mucolytic agent 10% N-acetylcysteine (NAC) after pretreatment with either saline or 1 mmol acidified taurocholate. Injury was assessed by measuring net transmucosal ion fluxes, luminal appearance of deoxyribonucleic acid (DNA), and gross and histologic injury. Pretreatment with the mild irritant 1 mmol acidified taurocholate significantly decreased bile acid-induced luminal ion fluxes and DNA accumulation, suggesting mucosal protection (corroborated by gross and histologic injury analysis). This effect was negated by lidocaine but not by NAC. Thus, it appears that sensory neurons, and not increased mucus secretion, play a critical role in adaptive cytoprotection.