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Biomedical subjects

R J Joehl

Publications and source records attributed to R J Joehl.

At least 19 recordsLinked to original sources
PubMed1999

A learning curve for laparoscopic splenectomy at an academic institution.

BACKGROUND: Laparoscopic splenectomy is emerging as the standard for treatment of benign splenic disorders. Since splenectomy is indicated relatively infrequently, issues arise concerning training of surgeons to perform laparoscopic splenectomy. Our experience with 50 laparoscopic splenic procedures is reported with emphasis on the learning curve at an academic institution. MATERIALS AND METHODS: Data were prospectively collected on 50 consecutive patients undergoing attempted or successful laparoscopic surgical procedures on the spleen at Northwestern Memorial Hospital or The Chicago Health Care System, Lakeside Division, from April 1993 to April 1998, and on 5 patients undergoing open splenectomy from April 1993 to October 1995. Outcomes including conversion rate, operative time, day feedings were tolerated, and length of hospital stay was examined and correlated with the number of attempted cases. RESULTS: Laparoscopic splenectomy progressed from an operation requiring two advanced laparoscopic surgeons to one performed by carefully supervised senior residents. Success rates increased from 60% initially to greater than 95% recently. Likewise, operative time decreased significantly from 195 to 97 min, while length of stay declined from 2.5 to 1.5 days. High success rates, low operative times, and short length of stays were achieved during the last 20 patients while surgical residents were taught to perform the procedures. The reasons for improvement are multifactorial including use of the harmonic scalpel, a change to the lateral position, and increasing experience with the procedure. CONCLUSIONS: Laparoscopic splenectomy is a safe and effective procedure that reduces postoperative length of hospital stay. It can be performed successfully in most patients with operative times comparable to those of open splenectomy. Moreover, the procedure can (and should) be taught to residents once they master basic and advanced laparoscopic skills.

Adult↗
PubMed1999

Altered gallbladder bile acidification with long-term total parenteral nutrition.

BACKGROUND: An important function of the gallbladder is to acidify and concentrate bile. Acidification helps protect against the precipitation of calcium salts, which promote gallstone formation. Altered acidification may result in pigment gallstones. We investigated gallbladder composition in a model of TPN-associated pigment gallstones to test whether changes in acidification may be important in this gallstone model. MATERIALS AND METHODS: Ten miniswine were intravenously fed for 21 to 27 days (mean 23 days). Ten fed pig chow with intravenous infusion of saline served as controls. Gallbladder and hepatic bile electrolytes, lipids, pH, and pCO2 were measured. RESULTS: All animals remained healthy and gained weight. Hepatic bile electrolytes and pH were similar among all animals. Pigs on TPN had a higher gallbladder pH and the [H+] was half the value of controls [8.1 +/- 1.6 x 10(-8) meq/liter (control) versus 3.9 +/- 0.7 x 10(-8) meq/liter (TPN)]. Gallbladder bile pCO2, sodium (Na), and potassium were higher in controls. Biliary lipids [bile salts (BS), phospholipids, and cholesterol] with TPN were decreased in both hepatic and gallbladder bile. CONCLUSIONS: Unlike short-term TPN where gallbladder pH and [BS] are similar, with long-term TPN pH is higher with lower [H+], [Na], and [BS]. Despite a presumed longer residence time in the gallbladder, intravenous feeding without oral intake results in gallbladder bile that is less concentrated and acidified. Enteral stimulation may be an important stimulus for gallbladder acidification and periods without feeding may promote gallstone formation by increasing the pH of gallbladder bile.

Animals↗
PubMed1998

Bilateral adrenal cortical adenomas in primary hyperaldosteronism.

Bilateral adrenal cortical adenomas in the presence of primary hyperaldosteronism is an extremely rare condition. We present a case of primary hyperaldosteronism in which a unilateral hypersecreting aldosterone-producing adenoma coexisted with a large, contralateral adrenal mass ultimately found to be consistent with cortical adenoma. Management consisted of total adrenalectomy and enucleation of adenoma from the opposite adrenal. The patient is normotensive 3 years after surgery. Enucleation as a successful approach to hyperfunctioning cortical adenomas is proposed.

Adrenal Cortex Neoplasms↗
PubMed1998

Impact of fundoplication on bolus transit across esophagogastric junction.

This study analyzed the effect of fundoplication on the mechanics of liquid and solid bolus transit across the esophagogastric junction (EGJ). The squamocolumnar junction was endoscopically clipped in seven controls, seven hiatal hernia patients, and seven patients after laparoscopic Nissen fundoplication. Concurrent manometry and fluoroscopy were done during swallows of liquid barium and a 13-mm-diameter marshmallow. The EGJ opening, pressure gradients, transit efficacy, and axial motion were measured. The axial motion of the EGJ was reduced in the fundoplication and hiatal hernia patients. The opening dimensions at the squamocolumnar junction were similar among groups, but in each case the constriction limiting flow to the stomach was at the hiatus and this was substantially narrowed with fundoplication. As a result, liquid intrabolus pressure was increased and marshmallow transit frequently required multiple swallows. We conclude that fundoplication limits the axial mobility of the EGJ and leads to a restricted hiatal opening. These alterations decrease the efficacy of solid and liquid transit into the stomach and are potential causes of dysphagia in this population.

Adult↗
PubMed1997

Complement component C5 deficiency reduces edema formation in murine ligation-induced acute pancreatitis.

The complement cascade is activated in humans and animals with acute pancreatitis. Activation of complement component C5 liberates C5a, C5a-desarg, and terminal complement complexes (TCCs) that increase capillary permeability, edema, and leukocyte chemotaxis at injured sites. Complement activation plays a major role in pathogenesis of capillary leak and edema formation in severe acute pancreatitis; however, the contribution of C5 (C5a/C5a-desarg, TCCs) has not been defined. Using He gene mutant mice lacking circulating C5, the role of C5 in ligation-induced acute pancreatitis was evaluated. We performed the following experiments: C5-sufficient (Hc1/Hc1) and C5-deficient (Hc0/Hc0) mice had bile and pancreatic ducts ligated. Sham-operated mice had ducts dissected but not ligated. Mice were killed at 4, 8, and 24 hr after bilepancreatic duct ligation. Serologic and morphologic evidences of acute pancreatitis were evaluated. Pancreatic edema was assessed using analysis of pancreatic water content, histologic edema score, and determination of wet weight ratio. After 4, 8, and 24 hr of bile-pancreatic duct ligation, hyperamylasemia and histologic changes of acute pancreatitis were observed in both C5-deficient and C5-sufficient mice. Edema developed in all mice with acute pancreatitis. However, when compared to C5-sufficient mice, mice deficient in C5 developed significantly less pancreatic edema at both 8 and 24 hr of bile-pancreatic duct ligation. This difference was not observed 4 hr after induction of acute pancreatitis. We conclude that C5 contributes to edema formation in murine ligation-induced acute pancreatitis. The presence of an early C5-independent phase, in conjunction with the observation of significant edema in mice deficient in C5, suggests there are other mediators of edema formation in this acute pancreatitis model.

Amylases↗
PubMed1996

Ligation-induced acute pancreatitis increases pancreatic circulating trypsinogen activation peptides.

Ligation of the common bile-pancreatic duct induces hyperamylasemia and acute pancreatitis in rats. Pancreatic morphologic changes include edema, acinar cell damage, and mild inflammation. The pathogenesis of acute pancreatitis in this model is not understood, but may involve altered secretion and intrapancreatic activation of acinar proteases. We hypothesized that trypsinogen activation, measured by the production of plasma and pancreatic trypsinogen activation peptides (TAP), occurs early in this model. We performed the following experiments: rats were prepared with (1) bile-pancreatic ducts ligated and (2) ducts dissected but not ligated (sham). Rats were killed after 6, 24, and 48 hr. Serum amylase was measured and histologic sections were analyzed for morphologic changes. TAP was measured in both serum and pancreatic tissue homogenates using a specific polyclonal. anti-TAP antibody in an enzyme-linked immunosorbant assay. After 6, 24, and 48 hr of bile-pancreatic duct ligation, hyperamylasemia and acute morphologic changes of acute pancreatitis were observed. Evidence of acinar cell destruction was not evident until 48 hr after ligation. Levels of serum and pancreatic tissue TAP were significantly elevated at both 24 and 48 hr after ligation compared to those of sham. We conclude that increased intrapancreatic trypsinogen activation occurs early in this form of experimental acute pancreatitis and that it occurs prior to evidence of acinar cell destruction. These data and observations support the possibility that intrapancreatic protease activation contributes to the pathogenesis of ligation-induced acute pancreatitis.

Acute Disease↗
PubMed1996

Bile-pancreatic juice replacement not cholinergic- and cholecystokinin-receptor blockade reverses acinar cell hyperstimulation after bile-pancreatic duct ligation.

BACKGROUND: Acinar cell inhibitors (eg, atropine) fail to ameliorate clinical and experimental acute pancreatitis. We hypothesized that amelioration of pancreatic acinar cell hyperstimulation after bile and pancreatic duct ligation is better with gut replacement of bile and pancreatic juice than with cholinergic- and cholecystokinin (CCK)-receptor blockade. METHODS: Using acinar cell amylase activity as an index of hyperstimulation, we studied 63 rats in two sets of experiments. Bile-pancreatic juice exclusion from gut--without (set one) and with (set two) bile and pancreatic duct obstruction--was treated with atropine and CCK-receptor antagonist L-364,718, or with enteral replacement of bile-pancreatic juice. RESULTS: In the set one experiment, acinar cell hyperstimulation after bile-pancreatic juice exclusion was reversed by combined L-364,718 and atropine pretreatment. In set two, acinar cell hyperstimulation after bile and pancreatic duct ligation was reversed by enteral bile and pancreatic juice replacement, but not by combined L-364,718 and atropine pretreatment. CONCLUSIONS: According to this experimental corollary of early gallstone impaction, prevention of acinar cell hyperstimulation after duct occlusion should be aimed at the source of the response to bile-pancreatic juice exclusion, namely, the gut, rather than at the target of the response, the pancreatic acinar cell.

Amylases↗
PubMed1996

Laparoscopic splenectomy.

Dramatic decreases in length of hospital stay and time to complete recovery with laparoscopic cholecystectomy have led to the development of more advanced laparoscopic procedures. The rationale, technique, and early results with laparoscopic splenectomy are described in this article. Laparoscopic splenectomy is a complex procedure with a real potential for significant operative bleeding, but it can be accomplished successfully in greater than 80% of selected patients with minimal blood loss. If successful, length of stay is reduced in most patients to 1 to 3 days, but this benefit is not always seen in patients with complicated medical problems or with massive splenomegaly. The effects of increased blood loss in patients whose operations are converted to open operations are also not yet clear. Laparoscopic splenectomy is a procedure with great potential, but it is still in evolution.

Blood Loss, Surgical↗
PubMed1995

Gastrointestinal tract complications after acute spine injury.

OBJECTIVES: To determine the incidence, risk factors, and mortality rate of gastrointestinal complications in patients with acute spine injury and to derive methods by which mortality can be reduced. DESIGN: Case series. SETTING: Regional tertiary care center. PATIENTS: Consecutive sample of 1952 patients with acute spine injury with complete medical records who were admitted from 1981 through 1990. MAIN OUTCOME MEASURES: Gastrointestinal tract complications, age, sex, time from injury to admission, cause of injury, level of spine injury, neurologic deficit, head injury, injury to other organ systems, incidence of surgical intervention for spine injury, length of hospital stay, and mortality rate. RESULTS: The incidence of gastrointestinal complications was 1.9%. Gastrointestinal hemorrhage was the most frequent complication. Risk factors for gastrointestinal complications were increasing age (P < .02), male sex (P < .01), injury to other organ systems (P < .02), head injury (P < .02), cervical spine injury (P < .02), and neurologic deficit (P < .005). The mortality rate was 19% in patients with gastrointestinal complications, significantly greater (P < .005) than the 2.9% rate in patients without gastrointestinal complications. CONCLUSIONS: Gastrointestinal complications after acute spine injury are uncommon but frequently lethal. Prophylaxis against hemorrhage and earlier diagnosis and surgical intervention are recommended.

Adolescent↗
PubMed1995

Cystic neoplasms of the pancreas. A clinicopathologic study, including DNA flow cytometry.

OBJECTIVE: To review the classification, clinical behavior, and appropriate therapy for cystic neoplasms of the pancreas. We examined patient demographics, clinical parameters, preoperative imaging modalities, histologic findings, and tumor DNA content to determine which best predict outcome. DESIGN: Case series and survey of pathologic specimens. SETTING: Tertiary care center. PATIENTS: Twenty-two patients with cystic neoplasms of the pancreas treated at affiliates of Northwestern University Medical School, Chicago, Ill. MAIN OUTCOME MEASURES: Predictive value of preoperative testing, tumor DNA content, patient survival. RESULTS: In 20 patients undergoing computed tomographic scan, the tumor was visualized in every case. All other imaging studies evaluated were less likely to demonstrate the lesion. Eight of 10 patients with serous cystadenomas were alive with no evidence of disease at the time of this report; one patient was alive with local recurrence, and a second patient had died of unrelated causes. All patients with mucinous cystadenomas were alive with no evidence of disease. Three of seven patients with cystadenocarcinomas had aneuploid, high S-phase tumors, and one had a diploid, high S-phase tumor; all four died (mean survival, 4.8 months). Two patients with cystadenocarcinomas had diploid, low S-phase tumors; both were long-term survivors but died of their disease at 8.6 and 9.3 years. CONCLUSIONS: (1) Computed tomographic scan is the most valuable diagnostic imaging study for preoperative evaluation of these patients. (2) Precise preoperative determination of tumor type is not possible. (3) DNA flow cytometry may help identify patients with aggressive tumors who may benefit from adjuvant chemoradiation.

Actuarial Analysis↗
PubMed1995

Ligation-induced acute pancreatitis in opossums: acinar cell necrosis in the absence of colocalization.

Acute necrotizing pancreatitis in opossums after bile and pancreatic duct ligation (BPDL) is a useful experimental corollary of gallstone-induced acute pancreatitis in humans. In experimental and human acute pancreatitis, a loss of segregation of the lysosomal enzyme cathepsin B and the zymogen proenzyme trypsinogen (colocalization) is implicated as the triggering event of disease pathogenesis, as cathepsin B can activate trypsinogen. The object of this study was to quantitate acinar cell necrosis and to study subcellular distribution of cathepsin B in BPDL-induced acute necrotizing pancreatitis in opossums. Bile and pancreatic ducts were ligated separately (no bile reflux) in four opossums while ducts were dissected in four sham controls. Opossums were killed 24 hr after operation. Three equidistant cross-sectional portions of each opossum pancreas were submitted to histologic examination. In blinded fashion, each focus of acinar cell necrosis was photographed and quantitated with digitizing morphometry. Numerical density (foci/cm2) and areal density (x10(3) micron 2/cm2) of focal acinar cell necrosis were determined. Differentially centrifuged pancreatic homogenates were assayed for cathepsin B, the lysosomal marker enzyme N-acetylglucosaminidase, and amylase. Morphometric quantitation of acinar cell necrosis confirmed development of acute necrotizing pancreatitis after 24 hr of BPDL in opossums. However, colocalization was not observed after BPDL, as evidenced by an absence of subcellular shift of cathepsin B activity (and N-acetyl-glucosaminidase activity) from the lysosome-enriched to the zymogen-enriched subcellular fraction. Amylase activity was increased in subcellular fractions after BPDL.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1995

Bile and pancreatic juice replacement ameliorates early ligation-induced acute pancreatitis in rats.

BACKGROUND: In healthy rats, combined bile and pancreatic juice diversion from gut has a synergistic rather than additive effect on stimulation of exocrine pancreatic protein secretion. We hypothesized that exclusion of combined bile and pancreatic juice from gut exacerbates bile and pancreatic-duct ligation-induced acute pancreatitis in rats to a greater extent than exclusion of either bile or pancreatic juice alone. METHODS: Bile and pancreatic juice (obtained fresh from donor rats) were replaced, separately or together, via a duodenal fistula beginning immediately before 6 hours of duct ligation. Pancreatic morphologic changes were evaluated with an acute pancreatitis histology score and morphometric quantitation of acinar-cell necrosis. Plasma amylase and cholecystokinin concentrations and pancreatic subcellular distribution of cathepsin B activity were determined. Characteristics of bile and pancreatic juice obtained from donor rats were also studied. RESULTS: Combined bile and pancreatic juice replacement limited the increase in acute pancreatitis histology score by 77%, acinar cell necrosis by 95%, hyperamylasemia by 77%, and hypercholecystokininemia by 99%, while preventing subcellular redistribution of cathepsin B. Amelioration of pancreatic morphologic changes was significantly greater with combined bile and pancreatic juice replacement than with replacement of either bile or pancreatic juice alone. CONCLUSION: In this experimental corollary of early gallstone-induced acute pancreatitis, combined bile and pancreatic juice exclusion from gut contributes to disease pathogenesis to a greater extent than exclusion of either bile or pancreatic juice alone.

Acute Disease↗
PubMed1994

Ligation-induced acute pancreatitis in rats and opossums: a comparative morphologic study of the early phase.

Bile and pancreatic duct ligation (BPDL) in rats does not induce severe acute pancreatitis but only mild inflammation, which is self-limiting and eventually leads to pancreatic atrophy. However, BPDL in opossums induces severe acute necrotizing pancreatitis which uniformly leads to death within 14 days. We compared pancreatic morphologic changes after 24 hr of BPDL in rats and opossums. Pancreatitis histology score and acinar cell ultrastructural changes were evaluated. In both species, BPDL was associated with significant increases in histology score compared to sham controls (5.0 +/- 0.3 vs 1.5 +/- 0.3 in rats, 5.3 +/- 0.4 vs 1.1 +/- 0.1 in opossums; mean +/- SEM, ANOVA, P < 0.05). However, there was no significant difference in histology score between rats and opossums following BPDL; histologic changes, such as white blood cell infiltration, acinar cell vacuolation, and focal acinar cell necrosis, were similar. Acinar cell ultrastructural changes after BPDL in both species included dilated endoplasmic reticulum and autophagic vacuole formation. These findings indicate that the early morphologic changes after BPDL in rats are quite similar to those seen early in the course of BPDL-induced acute necrotizing pancreatitis in opossums. As the rat is a more economical and convenient model to study than the opossum, this study supports the use of the rat model to conduct pilot studies of early events in the development of BPDL-induced acute pancreatitis. This study also suggests the potential for investigating mechanisms that may be present in the rat which protect against progressive and fatal acute necrotizing pancreatitis as observed in opossums after longer periods of BPDL.

Acute Disease↗
PubMed1994

A new model for study of pancreatic exocrine secretion: the tethered pancreatic fistula rat.

Diversion and recirculation of bile and pancreatic juice in rats are done in studies of pancreatic exocrine secretion. Previously, the modified Bollman cage was used to restrain rats with bile and pancreatic fistulas. To mimic physiologic conditions as closely as possible and to develop a more humane model, we designed a partial-restraint tethering system to study pancreatic exocrine secretion. Eight rats were prepared with biliary pancreatic, and duodenal fistulas, of which five were given enteral supplements via a gastric fistula and three were given saline supplements via a jugular venous line. Catheters exited at the nape of the neck and passed through the hollow of a cable coil that tethered the rat. On the fourth postoperative day pancreatic juice flow and protein output were studied. The tethering system allowed grooming, feeding, and ample mobility. This model of the tethered pancreatic fistula rat is a more human model for studies of pancreatic exocrine secretion in conscious rats, compared with the Bollman cage system of near total restraint.

Animals↗
PubMed1993

Laparoscopic inguinal hernia repair. A preliminary experience.

OBJECTIVE: To evaluate the safety and efficacy of laparoscopic inguinal hernia repair. DESIGN: Nonrandomized trial. SETTING: Veterans Affairs hospital and a large university hospital. PATIENTS: The study included 38 patients (36 male and two female) who had an acceptable risk for general anesthesia, presented electively, and gave informed consent; patients were excluded for whom general anesthesia had a high risk or who had incarcerated or strangulated hernias. INTERVENTION: Laparoscopic inguinal hernia repair was performed with general anesthesia through bilateral, lower-abdominal, 12-mm lateral rectus sheath ports with an umbilical 30 degrees viewing laparoscope. After the peritoneum was incised and flaps were raised, an onlay patch of polypropylene mesh, secured with staples, covered both indirect and direct hernia regions in each patient. Small hernia sacs were usually reduced or excised. RESULTS: From December 1991 through October 1992, 40 inguinal hernias were repaired; two patients had bilateral hernias. There were 22 indirect and 17 direct inguinal hernias and one femoral hernia. Nine of the hernias repaired were recurrent, and five were sliding hernias. Complications occurred in nine patients, but there were no recurrences during a median follow-up of 26 weeks. All but one patient resumed preoperative activities by 7 days after the operation. CONCLUSIONS: Laparoscopic inguinal hernia repair is an effective operation with low morbidity. Long-term follow-up is needed to determine the durability of the repair.

Adolescent↗
PubMed1993

Increased circulating cholecystokinin in obstruction-induced acute pancreatitis. I. Bile duct obstruction with and without pancreatic duct obstruction.

Bile exclusion from the gut exacerbates pancreatic duct obstruction-induced acute pancreatitis. We hypothesized that obstruction-induced acute pancreatitis involves an increase in circulating cholecystokinin (CCK), as bile and pancreatic juice exclusion from the gut stimulates duodenal CCK release. We studied 54 rats after the following operations: (1) sham operation (n = 18), (2) hepatic bile duct obstruction alone (n = 18), (3) hepatic bile duct and common bile-pancreatic duct obstruction (n = 18). Rats recovered and were killed in subgroups of six rats each at 3, 6, and 18 hr after operation; blood was collected for measurement of plasma CCK and amylase concentrations. Each pancreas was excised, weighed, and processed for histological examination; an acute pancreatitis score was determined. Combined bile and pancreatic duct obstruction induced acute pancreatitis and was associated with a marked increase of circulating CCK concentration. Bile duct obstruction alone did not induce acute pancreatitis but was associated with an increase of circulating CCK of lower magnitude. The time course of circulating CCK increase showed an early peak. These findings support our hypothesis and suggest that CCK plays a role in the pathogenesis of obstruction-induced acute pancreatitis.

Amylases↗
PubMed1993

Increased circulating cholecystokinin in obstruction-induced acute pancreatitis. II. Pancreatic duct obstruction with and without bile duct obstruction.

Pancreatic exocrine stimulation by cholecystokinin (CCK) has been implicated in the pathogenesis of experimental acute pancreatitis. Bile exclusion from the gut stimulates duodenal CCK release and exacerbates obstruction-induced acute pancreatitis. Pancreatic and bile duct obstruction increases circulating CCK concentration. We hypothesized that acute pancreatitis induced by pancreatic and bile duct obstruction would be ameliorated when bile was returned to the duodenum. As many small pancreatic ducts drain into the bile duct in rats, preservation of bile flow required the use of a bile shunt. We studied acute pancreatitis and the time course of circulating CCK increase in three groups of rats after: (1) sham operation (dissection, no obstruction), (2) bile and pancreatic duct obstruction, and (3) bile and pancreatic duct obstruction with bile shunt. The rats were killed at 3-, 6-, and 18-hr intervals after operation. Their blood was collected for measurement of CCK, amylase, and bilirubin concentrations. The pancreata were excised, weighed, and processed for histological examination. The shunting of bile back to the duodenum ameliorated the acute pancreatitis along with a simultaneous limitation of the rise in CCK concentration. This suggests that bile duct obstruction, another form of bile exclusion, exacerbates pancreatic duct obstruction-induced acute pancreatitis. The elevation in CCK concentration showed an early peak indicating that the potential role of CCK in the pathogenesis of obstruction-induced acute pancreatitis is predominantly in the early phase of its development.

Acute Disease↗