Injuries in women's professional soccer.

OBJECTIVE: The injury data from the first two seasons of the Women's United Soccer Association (WUSA) were analysed to determine the injury incidence, anatomic location of injuries, and relation of player position. METHODS: Injury data on 202 players from eight teams during the first two seasons of the WUSA were prospectively collected and analysed. RESULTS: A total of 173 injuries occurred in 110 players with an overall injury incidence rate of 1.93 injuries per 1000 player hours. The incidence of injury during practice and games was 1.17 and 12.63 per 1000 player hours, respectively. Of the injuries 82% were acute and 16% were chronic. Most of the injuries (60%) were located in the lower extremities. Strains (30.7%), sprains (19.1%), contusions (16.2%), and fractures (11.6%) were the most common diagnoses and the knee (31.8%) and head (10.9%) were the most common sites of injury. Anterior cruciate ligament (ACL) injuries accounted for 4.6% of all injuries and the incidence of ACL tears was 0.09 per 1000 player hours (practice 0.04, game 0.90). Midfielders suffered the most injuries (p<0.007). CONCLUSION: We conclude that the injury incidence in the WUSA is lower than the 6.2 injuries per 1000 player hours found in the corresponding male professional league (Major League Soccer); however, knee injuries predominate even in these elite female athletes.

Hip fracture-dislocation in football: a report of two cases and review of the literature.

Soccer is the world's most popular sport, with over 200 million participants world wide. Fractures account for only 4-9% of acute injuries, and hip fracture-dislocation is extremely uncommon. The potentially serious long term sequelae require that team physicians have an awareness of this injury. Two cases of traumatic hip fracture-dislocation are here reported in recreational soccer players sustained by low energy mechanisms. Prompt reduction and fixation are important to produce a stable and congruent joint.

Pseudarthrosis of the first rib in the overhead athlete.

Fractures of the first rib are uncommon in athletes and present a different clinical entity from traumatic first rib fracture associated with high energy thoracic trauma. These fractures are stress induced and precipitated by chronic muscular forces acting on the first rib. Typically they heal with conservative treatment. This report describes a fracture of the first rib in a tennis player that developed into a symptomatic pseudarthrosis as a result of persistent overhead activities. Symptoms mimicked ipsilateral shoulder injury. Pseudarthrosis of the first rib should be included in the differential diagnosis of chronic persistent shoulder pain in the overhead athlete.

Subcellular kinetics of early trypsinogen activation in acute rodent pancreatitis.

To investigate the debated role of intracellular trypsinogen activation and its relation to lysosomal enzyme redistribution in the pathogenesis of acute pancreatitis, rats were infused with the cholecystokinin analog caerulein at 5 micrograms.kg-1.h-1 for intervals up to 3 h, and the changes were contrasted with those in animals receiving saline or 0.25 microgram.kg-1.h-1 caerulein. Saline or 0.25 microgram.kg-1.h-1 caerulein did not induce significant changes. In contrast, 5 micrograms.kg-1.h-1 caerulein caused significant hyperamylasemia and pancreatic edema within 30 min. Pancreatic content of trypsinogen activation peptide (TAP) increased continuously (significant within 15 min). TAP generation was predominantly located in the zymogen fraction during the first hour but expanded to other intracellular compartments thereafter. Cathepsin B activity in the zymogen compartment increased continuously throughout the experiments and correlated significantly with TAP generation in the same compartment. Total trypsinogen content increased to 143% with marked interstitial trypsinogen accumulation after 3 h. Supramaximal caerulein stimulation causes trypsinogen activation by 15 min that originates in the zymogen compartment and is associated with increasing cathepsin B activity in this subcellular compartment. However, a much larger pool of trypsinogen survives and accumulates in the extracellular space and may become critical in the evolution of necrotizing pancreatitis.

Interventional and surgical treatment of pancreatic abscess.

Pancreatic abscess is one of the infectious complications of acute pancreatitis. It is a collection principally containing pus, but it may also contain variable amounts of semisolid necrotic debris. Most of these abscesses evolve from the progressive liquefaction of necrotic pancreatic and peripancreatic tissues, but some arise from infection of peripancreatic fluid or collections elsewhere in the peritoneal cavity. Included also are abscesses found after surgical débridement and drainage of pancreatic necrosis. Although open surgical treatment of infected necrosis is the established treatment of choice, percutaneous drainage of abscesses is successful in some circumstances. We used percutaneous catheter drainage in 39 patients during 1987-1995. Only 9 of 29 (31%) attempts at primary therapy were successful; 2 patients died, and 18 required subsequent surgical drainage. On the other hand, 14 of 14 patients with recurrent or residual abscesses after surgical drainage were successfully drained percutaneously. Percutaneous catheter drainage of pancreatic abscesses may be useful for initial stabilization of septic patients, drainage of further abscesses after surgical intervention (especially when access for reoperation will be difficult), associated abscesses remote from the pancreas, and selected unilocular collections at a sufficient interval after necrotizing pancreatitis to have allowed essentially complete liquefaction.

Benefits of various dextrans after delayed therapy in necrotizing pancreatitis of the rat.

OBJECTIVE: Ultrahigh-molecular dextran (500,000 Da) has been shown to prevent pancreatic necrosis when given 30 min after induction of pancreatitis. This study should clarify the following: (a) are dextrans still effective after prolongation of the therapy-free interval? (b) what is the impact of the molecular weight of the dextrans? and (c) is their effect influenced by the dextran concentration or by the addition of hypertonic saline? ANIMALS AND INTERVENTIONS: Acute pancreatitis was induced in 70 male dextran-tolerant Wistar rats using intraductal bile-salt infusion and intravenous hyperstimulation. After 3 h, animals were assigned to one of seven groups (n = 10 per group) receiving either Ringer solution or different dextrans (10%) including 70,000 Da (DEX-70), 160,000 Da (DEX-160), 300,000 Da (DEX-300) or 500,000 Da (DEX-500). Additional groups included DEX-70 (6%) and DEX-70 (10%) in combination with hypertonic NaCl (7.5%) (HHS-70). Ringer solution was given at 24 ml/kg and all dextrans at 8 ml/kg. MEASUREMENTS AND RESULTS: Trypsinogen activation peptides (TAP) were quantified in ascites and acinar necrosis after death or sacrifice at 9 h. As an index of less pathological trypsinogen activation, the mean TAP levels in ascites were significantly lower in DEX-70 and DEX-160 compared to Ringer controls (p < 0.05, t-test). Furthermore, the amount of acinar necrosis was significantly lower in all dextran groups except the HHS-70 in comparison with Ringer controls (p < 0.01, t-test). Finally, mortality was significantly reduced from 60% in Ringer controls to 10 and 0%, respectively, in the groups treated with DEX-70 and DEX-160 (p < 0.03, Fisher's Exact test). There was a similar trend in all other groups except the HHS-70. CONCLUSIONS: Despite a therapy-free interval of 3 h, dextrans reduce trypsinogen activation, prevent acinar necrosis, and improve survival in necrotizing rodent pancreatitis. The molecular weight and concentration of dextran are of secondary importance for these beneficial effects.

Recurrent acute pancreatitis caused by afferent loop stricture after gastrectomy.

Afferent loop obstruction after gastrectomy and Billroth II gastrojejunostomy is only rarely diagnosed as the cause of recurrent acute pancreatitis. Three patients are described in whom afferent loop stricture after gastrectomy and Billroth II reconstruction manifested as recurrent pancreatitis 13 to 24 years after the initial procedure. Late onset, nonspecific symptoms, and other simultaneous gastrointestinal pathologic features promoted a chronic clinical course in all patients. Symptoms included acute abdominal pain, vomiting, jaundice, hyperamylasemia, weight loss, and anemia. A thorough history, barium examination, cholescintigraphy, and endoscopy were central in establishing the diagnosis. The pathogenesis of stricture formation is thought to be ischemic mucosal damage from intestinal crossclamping. Surgical decompression provided lasting relief of the symptoms. Afferent loop stricture should be considered in the different diagnosis in patients with recurrent acute pancreatitis and previous gastrectomy with Billroth II reconstruction.

Antibiotic treatment improves survival in experimental acute necrotizing pancreatitis.

BACKGROUND & AIMS: It is still unproven whether prophylactic antibiotics can reduce mortality from acute necrotizing pancreatitis (ANP). The aim of this study was to investigate whether antibiotic therapy can influence long-term outcome in ANP and how appropriate this therapy is. METHODS: ANP was induced in rats by standardized intraductal bile acid infusion and cerulein hyperstimulation. Serum trypsinogen activation peptide levels were used to verify comparable disease severity. Starting 6 hours after induction, animals randomly received saline (n = 60), 20 mg/kg imipenem (n = 62), or 10 mg/kg ciprofloxacin (n = 60) every 8 hours for 7 days. On day 7, half of each group was killed so a quantitative pancreatic bacteriology could be conducted. The other half was analyzed at 21 days for long-term mortality, late bacteriologic changes, abscesses, and pseudocysts. RESULTS: Comparable trypsinogen activation peptide increases confirmed equally severe ANP in each group before treatment. Imipenem and ciprofloxacin significantly reduced the number of infected pancreatic specimens, bacterial counts, and identified species at 1 week. At 3 weeks, pancreatic infection prevalence was lower in animals treated with antibiotics; abscess formation was reduced and pseudocysts were smaller and less frequently infected. Survival was significantly improved by imipenem and ciprofloxacin. CONCLUSIONS: Antibiotic treatment reduces early and late septic pancreatic complications and improves survival from experimental ANP.

Calcium administration augments pancreatic injury and ectopic trypsinogen activation after temporary systemic hypotension in rats.

BACKGROUND: Calcium infusion and hypotension have been described as the most important risk factors for pancreatic injury after cardiopulmonary bypass. METHODS: Rats were randomly allocated to three experimental groups undergoing either sham operation and saline infusion (Control, n = 30), hemorrhagic reduction of mean arterial pressure to 30 mmHg for 30 min alone (hypotension, n = 51), or hypovolemic hypotension followed by bolus infusion of CaCl2 (200 mg.kg-1; hypercalcemia, n = 85). Serum ionized calcium, amylase activity, trypsinogen activation peptide in pancreatic tissue homogenates, pancreatic wet/dry weight ratio, histologic changes, and mortality were assessed for 24 h. RESULTS: Control rats showed no significant changes of any parameter throughout the experiments. In contrast, hypotension significantly increased serum amylase (P < 0.001), tissue trypsinogen activation peptide (P < 0.01), wet/dry weight ratio (P < 0.001), and histologic scores for edema (P < 0.001) and pancreatic necrosis (P < 0.05). Subsequent CaCl2 administration transiently increased [Ca2+] (P < 0.001) with the concentration rapidly returning to baseline within 3 h. That infusion of CaCl2 further increased amylase (P < 0.05), tissue trypsinogen activation peptide (P < 0.05), wet/dry weight ratio (P < 0.001), and histologic evidence of pancreatic edema (P < 0.05) and acinar necrosis (P < 0.05) when compared with hypotension alone. Whereas all Control animals survived the experiments, 22% (P < 0.05) and 47% (P < 0.05 vs. hypotension) of animals died in the hypotension and hypercalcemia groups, respectively. CONCLUSIONS: Temporary hypotension alone causes ectopic trypsinogen activation and lethal acute pancreatitis. Super-imposed hypercalcemia significantly aggravates hypotension-induced pancreatic injury and mortality in rats.

Quantitative assay of trypsinogen by measurement of cleaved activation peptide after activation with enterokinase.

Measurement of trypsinogen by quantitative immunosorbent assay of the highly specific and inert trypsinogen activation peptide following complete activation of trypsinogen by enterokinase offers a simple and sensitive method that provides reliable results over a wide range of trypsinogen concentrations. This method offers a significant advantage in being applicable to complex biological tissues.

Pathogenesis and prevention of early pancreatic infection in experimental acute necrotizing pancreatitis.

OBJECTIVE: The authors test antibiotic strategies aimed at either mitigating bacterial translocation from the gut or delivering antibiotics specifically concentrated by the pancreas for prevention of early secondary infection after acute necrotizing pancreatitis. BACKGROUND: Infection currently is the principal cause of death after severe pancreatitis. The authors have shown that the risk of bacterial infection correlates directly with the degree of tissue injury in a rodent model of pancreatitis. Bacteria most likely arrive by translocation from the colon. METHODS: Severe acute necrotizing pancreatitis was induced in rats by a combination of low-dose controlled intraductal infusion of glycodeoxycholic acid superimposed on intravenous cerulein hyperstimulation. At 6 hours, animals were randomly allocated to five treatment groups: controls, selective gut decontamination (oral antibiotics and cefotaxime), oral antibiotics alone, cefotaxime alone, or imipenem. At 96 hours, surviving animals were killed for quantitative bacterial study of the cecum, pancreas, and kidney. RESULTS: The 96-hour mortality (35%) was unaffected by any treatment regimen. Cecal gram-negative bacteria were significantly reduced only by the oral antibiotics. Pancreatic infection was significantly reduced by full-gut decontamination and by imipenem, but not by oral antibiotics or by cefotaxime alone. Renal infection was reduced by both intravenous antibiotics. CONCLUSIONS: Early pancreatic infection after acute necrotizing pancreatitis can be reduced with a full-gut decontamination regimen or with an antibiotic concentrated by the pancreas (imipenem) but not by unconcentrated antibiotics of similar spectrum (cefotaxime) or by oral antibiotics alone. These findings suggest that 1) both direct bacterial translocation from the gut and hematogenous seeding interplay in pancreatic infection while hematogenous seeding is dominant at extrapancreatic sites and 2) imipenem may be useful in clinical pancreatitis.

Acute hypercalcemia causes acute pancreatitis and ectopic trypsinogen activation in the rat.

BACKGROUND & AIMS: Clinical and experimental observations have associated acute and chronic hypercalcemia with pancreatitis. The aim of this study was to determine whether acute hypercalcemia can induce acute pancreatitis and, if so, whether the pathogenesis involves premature protease activation. METHODS: Rats given bolus infusions of CaCl2 (200 mg/kg; n = 76) were compared with saline-treated controls (n = 40). Serum [Ca2+], serum amylase activity, trypsinogen activation peptide (TAP) concentration in serum and pancreatic tissue, pancreatic wet/dry weight ratio, and histology were assessed for 24 hours. For dose-response analysis, CaCl2 was injected at a dose of 50-200 mg/kg, and the aforementioned indices were assayed for 1 hour (n = 5 each). RESULTS: There were no significant changes in the controls. Calcium infusion increased serum [Ca2+] 3-fold after 5 minutes (P < 0.001). Within 1 hour, serum amylase (2.5-fold) and tissue TAP (3-fold) levels increased along with macroscopic and microscopic edema formation and leukocytic infiltration. The extent of the changes at 1 hour correlated with the calcium dose. Amylase and tissue TAP concentrations remained elevated until 24 hours when serum TAP concentration had increased (P < 0.001) and focal acinar necrosis became evident. CONCLUSIONS: Acute experimental hypercalcemia induces dose-dependent morphological alterations characteristic of acute pancreatitis, acute hyperamylasemia, and early ectopic trypsinogen activation. This supports the pathophysiological relevance of excess calcium and offers a possible pathogenetic mechanism for its association with clinical pancreatitis.

Increased intrapancreatic trypsinogen activation in ischemia-induced experimental pancreatitis.

OBJECTIVE: The potential of pancreatic ischemia to cause acute pancreatitis as indicated by morphologic changes and ectopic trypsinogen activation was investigated. BACKGROUND: Experimental evidence has shown that pancreatic ischemia is important in the evolution of severe pancreatitis, but whether ischemia can initiate pancreatitis has been disputed. METHODS: Pancreatic ischemia was induced in rats by hemorrhagic hypotension (30 mm Hg for 30 min; n = 64). Changes of pancreatic microcirculatory perfusion were studied using diffuse reflectance spectroscopy. Serum amylase, trypsinogen activation peptide (TAP) in serum and pancreatic tissue, wet/dry weight ratio, and histology were determined over 24 hours and compared with sham-operated control subjects (n = 35). RESULTS: In control animals, serum amylase (47.9 +/- 2.1 units/L), serum (7.9 +/- 0.7 nmol/L) and tissue TAP (63.0 +/- 5.4 nmol/L x g), wet/dry weight ratio (2.8 +/- 0.1), and histology remained unchanged. Temporary hypotension markedly decreased pancreatic perfusion with incomplete recovery after reperfusion. Pancreatic isoamylase activity increased within 1 hour (110 +/- 5 units/L, p < 0.05) and further to 151 +/- 18 units/L at 24 hours. Tissue TAP was elevated at 1 hour (134 +/- 16 nmol/L x g, p < 0.05) and increased to 341 +/- 43 nmol/L x g (p < 0.001) after 24 hours, whereas serum TAP remained unchanged (8.3 +/- 0.5 nmol/L). Morphologic alterations included elevated wet/dry weight ratio (4.1 +/- 0.3, p < 0.01) and increased histologic scores for edema (p < 0.05) and acinar necrosis (p < 0.05) at 24 hours. Trypsinogen activation preceded the development of pancreatic necrosis. CONCLUSIONS: In addition to its potentiating role, severe pancreatic ischemia can play a pathogenetic role in the initiation of acute pancreatitis.

Hypercalcemia causes acute pancreatitis by pancreatic secretory block, intracellular zymogen accumulation, and acinar cell injury.

BACKGROUND: Because hypercalcemia is a known etiologic factor for human acute pancreatitis, studies of the pancreatic pathophysiology and pathomorphology of experimental hypercalcemia have potential clinical significance. MATERIALS AND METHODS: Rats received central venous infusion of either 0.6 mmol/kg per hour CaCl2 or 0.9% NaCl infusion for 12 hours. Pancreatic tissue samples were obtained and prepared for electron microscopy. Tissue homogenates were examined for DNA, lactate dehydrogenase (LDH), protein, amylase, and calcium contents. Basal or stimulated (cerulein 0.25 microL/kg per hour) pancreatic secretions were analyzed for volume, protein, and amylase output, as well as protein composition on sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). RESULTS: The tissue calcium content and the ratio of LDH to DNA was unchanged after calcium infusion, but the ratios of total protein to DNA and of amylase to DNA were significantly larger. Basal output of pancreatic juice volume, protein, and amylase were significantly lower. SDS-PAGE of pancreatic juice revealed weakening of a 70,000-d band and appearance of lower molecular weight bands in two samples. Ultrastructural examination demonstrated accumulation of zymogen granules in the acinar cell, large autophagic vacuoles containing remnants of condensing vacuoles. CONCLUSIONS: These findings suggest that hypercalcemia induces pancreatic injury via a secretory block, accumulation of secretory proteins, and possibly activation of proteases.

Measurement of blood flow in pancreatic exchange capillaries with FITC-labeled erythrocytes.

Characterization of pancreatic capillary blood flow by in vivo microscopy has been limited by technical shortcomings associated with the use of plasma tracers and the lack of quantitative data. Therefore, fluorescent-labeled erythrocytes were evaluated for quantitation of pancreatic capillary blood flow in rats in physiological state and under defined conditions of increased and impaired pancreatic blood flow. Physiological blood flow was 1.21 +/- 0.06 nl/min per capillary with stable capillary perfusion pattern. Reduction of pancreatic blood flow by decreasing systemic arterial pressure to 60 mmHg through controlled hemorrhage produced a profound decrease of volumetric flow to 0.21 +/- 0.05 nl/min (P < 0.05). The number of perfused capillaries was reduced to 52 +/- 8% of baseline (P < 0.001) and the intermittent perfusion pattern was altered in 26 +/- 5% (P < 0.001) of observed capillaries. Stimulation of pancreatic perfusion with intravenous secretin (5 CU/kg/hr) induced a transient decline to 0.94 nl/min (P < 0.05) followed by a continuous increase to 2.39 nl/min (P < 0.001). The intermittent flow pattern was modified in 15 +/- 3% of capillaries (P < 0.05). Fluorescent-labeled erythrocytes provide unique and reliable qualitative and quantitative data about pancreatic microcirculatory changes. Confinement of the fluorescent tracer to erythrocytes prevents extravasation and minimizes phototoxicity, thereby improving intravital analysis of blood flow in pancreatic exchange capillaries.

Time course of bacterial infection of the pancreas and its relation to disease severity in a rodent model of acute necrotizing pancreatitis.

BACKGROUND: Bacterial infection of pancreatic necrosis is thought to be a major determinant of outcome in acute necrotizing pancreatitis. The determinants and possibilities for prophylaxis are unknown and difficult to study in humans. OBJECTIVE: The time course of bacterial infection of the pancreas in a rodent model of acute necrotizing pancreatitis was characterized. The authors ascertained if there is a correlation with the degree of necrosis. METHODS: Acute pancreatitis (AP) of graded severity was induced under sterile conditions by an intravenous infusion of cerulein (5 micrograms/kg/hr) for 6 hours (mild AP), or a combination of intravenous cerulein with an intraductal infusion of 10-mM glycodeoxycholic acid (0.2 mL for 2 min for moderate AP, 0.5 mL for 10 min for severe AP). Sham-operated animals (intravenous and intraductal NaCl 0.9%) served as controls. Ninety-six hours after induction, animals were killed for quantitative bacterial examination and histologic scoring of necrosis. In addition, groups of animals with severe AP were investigated at 12, 24, 48, 96, and 144 hours. RESULTS: No significant pancreatic necrosis was found in control animals (0.3 +/- 0.1) or animals with mild AP (0.6 +/- 0.1) killed at 96 hours. Necrosis scores were 1.1 +/- 0.2 for animals with moderate AP and 1.9 +/- 0.2 for animals with severe AP. Control animals did not develop significant bacterial infection of the pancreas (> or = 10(3) CFU/g). At 96 hours, the prevalence of infection was 37.5% in animals with mild AP and 50% in animals with moderate AP. In animals with severe AP, infection of the pancreas increased from 33% in the first 24 hours to 75% between 48 and 96 hours (p < 0.05). The bacterial counts and the number of different species increased with time and was maximal (> 10(11) CFU/g) at 96 hours. CONCLUSION: Bacterial infection of the pancreas in rodent AP increases during the first several days, and its likelihood correlates with the severity of the disease. This model, which closely mimics the features of human acute pancreatitis, provides a unique opportunity to study the pathogenesis of infected necrosis and test therapeutic strategies.

Mitochondrial poisons cause depletion of reduced glutathione in isolated hepatocytes.

Antimycin A, KCN, and 1-methyl-4-phenylpyridinium ion (MPP+) all produced a marked depletion of cellular GSH levels in freshly isolated hepatocytes. This effect was consistently observed before the onset of cytotoxicity and seemed to be correlated with the loss of cellular ATP induced by these mitochondrial poisons. Concentrations of GSSG remained unchanged both intracellularly and extracellularly, indicating that oxidation was not involved in the events leading to GSH depletion. Approximately 40% of the decrease of intracellular GSH was accounted for by efflux of this tripeptide, assessed by increased formation of cysteinyl-glutathione when hepatocytes were incubated in the presence of 0.2 mM cystine. Therefore, an overall loss of glutathione was observed during incubations with all three inhibitors of mitochondrial function. Addition of 10 mM fructose to the incubation media substantially protected against GSH depletion caused by antimycin A, KCN, and MPP+. These results indicate that energy-dependent mechanisms are involved in the maintenance of intracellular GSH levels, and suggest that GSH depletion may be a general phenomenon associated with impairment of mitochondrial function.