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H J Sugerman

Publications and source records attributed to H J Sugerman.

At least 55 records · Page 3Linked to original sources
PubMed1998

Adjustable laparoscopic gastric band for the treatment of morbid obesity: radiologic evaluation.

OBJECTIVE: This article describes the radiographic appearance of a recently developed laparoscopically placed adjustable gastric band for the treatment of morbid obesity. The optimal technique for contrast evaluation of the device, complications associated with its use, and the technique for stoma adjustments are also discussed. SUBJECTS AND METHODS: Between May and December 1996, 23 patients at our institution underwent laparoscopic placement of adjustable silicone gastric bands for treatment of morbid obesity. All patients underwent a barium upper gastrointestinal series before surgery, 1 day after band placement, at variable intervals when each patient returned for band adjustment, and at 1 year. RESULTS: Unlike the case in other gastric weight loss procedures, the optimal patient position for contrast evaluation of gastric bands was anteroposterior or slightly right posterior oblique. Twenty-one of 23 patients had no complications shown on the postoperative upper gastrointestinal series. Stoma size was approximately 3-8 mm, and most patients showed delayed esophageal emptying without obstruction. Two patients had herniation of the stomach through the gastric band with pouch enlargement, resulting in obstruction and the need for additional surgery. We saw no leaks or band erosions. Nineteen stoma adjustments were performed in 13 patients. One patient had an inverted port that could not be accessed for adjustment. CONCLUSION: As adjustable gastric bands become more widely used, radiologists need to be familiar with the radiographic appearance of the devices, the complications associated with their use, and the optimal patient positioning for contrast evaluation. Radiologists may also be involved with band adjustment to decrease or increase the stoma size and therefore need to understand the technique and potential difficulties of adjusting the stoma.

Adult↗
PubMed1997

Delayed administration of inhaled nitric oxide preserves alveolar-capillary membrane integrity in porcine gram-negative sepsis.

OBJECTIVE: To determine the effect of delayed administration of inhaled nitric oxide (NO) on acute lung injury after the onset of gram-negative sepsis. DESIGN: Nonrandomized controlled study. SETTING: University medical center laboratory. SUBJECTS: Yorkshire swine. INTERVENTIONS: Five groups of swine were anesthetized, mechanically ventilated, and studied for 5 hours. After surgical preparation, control (n = 10) and NO-treated control (n = 6) animals received a 1-hour infusion of sterile saline solution. Sepsis was induced with a 1-hour intravenous infusion of live Pseudomonas aeruginosa. Untreated animals with sepsis (n = 10) received no treatment. Inhaled NO at 20 ppm was administered to NO30-treated animals with sepsis (n = 7) and NO60-treated animals with sepsis (n = 8) beginning at 30 and 60 minutes after bacterial infusion was begun, respectively. MAIN OUTCOME MEASURES: Systemic and pulmonary hemodynamics, arterial blood gas determination, bronchoalveolar lavage protein and neutrophil content, neutrophil oxidant burst, lung myeloperoxidase content, and scanning electron micrographic studies. RESULTS: A progressive, significant (P < .05) decline in PaO2 developed in untreated animals with sepsis, which was prevented in NO30- and NO60-treated animals with sepsis. A significant (P < .05) increase in bronchoalveolar lavage protein and neutrophil counts compared with baseline values was observed in untreated animals with sepsis, indicating acute lung injury. These variables exhibited no notable increase in NO30- and NO60-treated animals with sepsis and were significantly (P < .05) reduced compared with untreated animals with sepsis. The lung myeloperoxidase content was significantly (P < .05) elevated at 5 hours in all groups with sepsis compared with baseline values and the control and NO-treated control groups. The total phorbol myristate acetate-induced polymorphonuclear leukocyte oxidant burst at 5 hours was significantly (P < .05) decreased in the NO30- and NO60-treated animals with sepsis compared with untreated animals with sepsis. Untreated and NO30- and NO60-treated animals with sepsis showed a significant (P < .05) increase in pulmonary artery pressure at 30 minutes, followed by a progressive decline. These changes were significant (P < .05) compared with baseline values and the control groups. No significant (P < .05) difference in pulmonary artery pressure or systemic arterial pressure was found at any time between untreated and NO30- and NO60-treated animals with sepsis. CONCLUSIONS: The delayed administration of inhaled NO preserves alveolar-capillary membrane integrity in this porcine model of gram-negative sepsis. The inhibition of neutrophil transendothelial migration, rather than neutrophil rolling or tight adhesion, may be a critical mechanism by which inhaled NO produces this effect. Decreased oxidant production by activated neutrophils may be a secondary mechanism by which inhaled NO reduces acute lung injury.

Animals↗
PubMed1997

OPC-6535, a superoxide anion production inhibitor, attenuates acute lung injury.

A large body of evidence has demonstrated that inhibition of the neutrophil's oxidant burst attenuates sepsis-induced acute lung injury. The present study sought to evaluate the ability of OPC-6535, a superoxide anion production inhibitor, to attenuate sepsis-induced acute lung injury. Four groups of swine were anesthetized, ventilated, and studied for 5 hr. Following surgical preparation, control (n = 10) and OPC-control (n = 2) animals received a 1-hr infusion of sterile saline. Sepsis was induced with a 1-hr intravenous infusion of live Pseudomonas aeruginosa. Untreated septic animals (n = 10) received no treatment. Animals treated with OPC-6535 (n = 6) received a 1 mg/kg bolus of OPC-6535 15 min prior to initiation of the bacterial infusion. Changes in systemic and pulmonary hemodynamics, arterial oxygen tension, bronchoalveolar lavage protein and neutrophil content, neutrophil integrin expression, neutrophil oxidant burst, and lung myeloperoxidase content were used as outcome measures. Treatment with OPC-6535 significantly reduced acute lung injury, as indicated by improved bronchoalveolar lavage protein and neutrophil content, resulting in a significant improvement in arterial oxygenation. Treatment with OPC-6535 failed to prevent the development of pulmonary hypertension and systemic hypotension. Neutrophils from animals with both treated and untreated sepsis exhibited significant up-regulation of CD18 and production of increased levels of oxidants, indicating significant activation when compared to neutrophils from control animals. Although animals treated with OPC-6535 produced 25% less superoxide anion than untreated septic animals, this decrease was not statistically significant. Treatment of animals with OPC-6535 prior to the onset of sepsis produced significant protection against acute lung injury but failed to attenuate hemodynamic derangements associated with sepsis.

Administration, Inhalation↗
PubMed1997

Corticosteroids repress the interleukin 1 beta-induced secretion of collagenase in human intestinal smooth muscle cells.

BACKGROUND & AIMS: The cytokine interleukin (IL)-1 beta induces collagenase expression and inhibits collagen expression in human intestinal smooth muscle (HISM) cells. Corticosteroids cause transrepression of certain genes, including the collagenase gene. The aim of this study was to determine if corticosteroids repress the induction of collagenase expression and the inhibition of collagen secretion by IL-1 beta in HISM cells. METHODS: HISM cells were exposed to IL-1 beta (1-100 pmol/L) for 24 hours in the presence or absence of dexamethasone (10(-6) mol/L). Collagenase messenger RNA (mRNA) levels were determined by ribonuclease protection assay. Collagenase and tissue inhibitor of metalloproteinase protein secretion were determined by enzyme-linked immunosorbent assay of culture medium. Procollagen and collagen secretion were determined by polyacrylamide slab gel analysis of radiolabeled proteins in culture medium. RESULTS: A 30-fold induction of collagenase mRNA and collagenase protein secretion by IL-1 beta was completely abrogated by dexamethasone. Dexamethasone at 10(-6) mol/L also reduced basal levels of collagenase mRNA by 50% and blocked the IL-1 beta-induced inhibition of collagen secretion. CONCLUSIONS: Corticosteroids repress the collagenolytic action of IL-1 beta on HISM cells in vitro and therefore should promote healing in the inflamed intestine.

Collagen↗
PubMed1997

A proposed relationship between increased intra-abdominal, intrathoracic, and intracranial pressure.

OBJECTIVES: To determine the effect of acutely increased intra-abdominal pressure on pleural pressure, intracranial pressure, and cerebral perfusion pressure, and to clarify the relationship between these parameters. DESIGN: Nonrandomized, controlled study. SETTING: Laboratory at a university medical center. SUBJECTS: Yorkshire swine, weighing 15 to 20 kg. INTERVENTIONS: Anesthetized, ventilated swine had a balloon inserted into the peritoneal cavity and catheters placed for measurement of intracranial pressure, pleural pressure, central venous pressure, pulmonary artery occlusion pressure, and mean arterial pressure. Following baseline measurements, intra-abdominal pressure was increased by incrementally inflating the intraperitoneal balloon. All parameters were remeasured 30 mins after each increase in intra-abdominal pressure. Two groups were studied: a) group 1 (n = 9) animals had intra-abdominal pressure increased to 25 mm Hg above baseline, then released; b) group 2 (n = 3) animals underwent sternotomy and pleuropericardotomy to prevent an increase in pleural pressure with increasing intra-abdominal pressure. MEASUREMENTS AND MAIN RESULTS: Increase of intra-abdominal pressure to 25 mm Hg above baseline caused significant (p < .05) increases in intracranial pressure (7.3 +/- 0.6 [SEM] to 16.4 +/- 1.9 mm Hg), pleural pressure (4.3 +/- 1.3 to 11.8 +/- 1.9 mm Hg), pulmonary artery occlusion pressure (9.0 +/- 0.6 to 14.3 +/- 0.8 mm Hg), and central venous pressure (6.6 +/- 0.7 to 10.7 +/- 0.9 mm Hg). The cardiac index (3.4 +/- 0.3 to 1.6 +/- 0.1 L/min/m2) and cerebral perfusion pressure (75.6 +/- 3.6 to 62.0 +/- 6.8 mm Hg) deceased significantly (p < .05), whereas mean arterial pressure (82.8 +/- 3.2 to 78.4 +/- 6.6 mm Hg) remained essentially constant. Sternotomy and pleuro-pericardotomy negated all effects of increased intra-abdominal pressure except the decreased cardiac index (1.6 +/- 0.1 to 2.5 +/- 0.2 L/min/m2). CONCLUSIONS: Acutely increased intra-abdominal pressure causes a significant increase in intracranial pressure and a decrease in cerebral perfusion pressure. Increased intra-abdominal pressure appears to produce this effect by augmenting pleural and other intrathoracic pressures and causing a functional obstruction to cerebral venous outflow via the jugular venous system. It is possible that the same phenomenon may be why persons with chronically increased intra-abdominal pressure, such as the morbidly obese, suffer from a high frequency rate of idiopathic intracranial hypertension.

Abdomen, Acute↗
PubMed1997

Pretreatment with inhaled nitric oxide inhibits neutrophil migration and oxidative activity resulting in attenuated sepsis-induced acute lung injury.

OBJECTIVE: To determine if, and by what mechanisms, inhaled nitric oxide attenuates acute lung injury in a porcine model of adult respiratory distress syndrome induced by Gram-negative sepsis. DESIGN: Nonrandomized, controlled study. SETTING: Laboratory at a university medical center. SUBJECTS: Thirty pathogen-free Yorkshire swine (15 to 20 kg). INTERVENTIONS: Four groups of swine were anesthetized, mechanically ventilated, and studied for 5 hrs. Both control-nitric oxide and septic-nitric oxide animals received inhaled nitric oxide at 20 parts per million throughout the study. Control (n = 10) and control-nitric oxide (n = 5) animals received a 1-hr infusion of sterile saline. Sepsis was induced in septic (n = 10) and septic-nitric oxide (n = 5) animals with a 1-hr intravenous infusion of live Pseudomonas aeruginosa. MEASUREMENTS AND MAIN RESULTS: Untreated septic animals developed a progressive decrease in Pao2 that was prevented in septic-nitric oxide animals (73 +/- 4 vs. 214 +/- 23 torr [9.7 +/- 0.5 vs. 28.5 +/- 3.1 kPa], respectively, at 5 hrs, p < .05). Untreated septic animals showed a significant increase in bronchoalveolar lavage protein and neutrophil count at 5 hrs, compared with the baseline value, indicating acute lung injury. Septic-nitric oxide animals showed no significant increase in these parameters. Peripheral blood neutrophils from untreated septic animals and septic-nitric oxide animals exhibited significant (p < .05) up-regulation of CD18 receptor expression and oxidant activity (10.5 +/- 0.9 and 5.0 +/- 0.9 nmol of superoxide anion/10(6) neutrophils/10 mins, respectively) compared with both control and control-nitric oxide animals (3.0 +/- 0.6 and 2.6 +/- 0.2 nmol of superoxide anion/10(6) neutrophils/10 mins, respectively). Also, priming for the oxidant burst at 5 hrs was decreased by 50% in septic-nitric oxide animals compared with untreated septic animals. Both untreated septic and septic-nitric oxide animals showed a significant increase in pulmonary arterial pressure at 30 mins (47.5 +/- 2.4 and 51.0 +/- 3.0 mm Hg, respectively), followed by a progressive decrease (32.8 +/- 2.6 and 31.3 +/- 5.4 mm Hg, respectively, at 5 hrs). Both of these changes were significant (p < .05) compared with baseline values and compared with the control groups. There was no significant difference in pulmonary arterial pressure or systemic arterial pressure at any time between untreated septic and septic-nitric oxide animals. CONCLUSIONS: These results demonstrate that inhaled nitric oxide attenuates alveolar-capillary membrane injury in this porcine model of Gram-negative sepsis but does not adversely affect systemic hemodynamics. The data suggest that inhaled nitric oxide preserves alveolar-capillary membrane integrity by the following means: a) inhibiting transendothelial migration of activated, tightly adherent neutrophils; and b) possibly by attenuating the neutrophil oxidant burst.

Administration, Inhalation↗
PubMed1997

Elevated intra-abdominal pressure increases plasma renin activity and aldosterone levels.

OBJECTIVE: To study the effects of elevated intra-abdominal pressure upon renal function and the renin-angiotensin-aldosterone system. MATERIALS AND METHODS: Two groups of anesthetized, ventilated swine were studied. Intra-abdominal pressure was increased in experimental animals (n = 6) by incrementally instilling an isosmotic ethylene glycol solution into the peritoneal cavity until intra-abdominal pressure was 25 mm Hg above baseline. The intravascular volume was then expanded until cardiac index returned to baseline. Lastly, the solution was drained to decompress the abdomen. Control animals underwent surgical preparation but did not have their intra-abdominal pressure raised. Changes in systemic and pulmonary hemodynamic parameters, renal venous pressure, and urine output were recorded. Venous samples for plasma renin activity, aldosterone, and atrial natriuretic factor were drawn after each change in either intra-abdominal pressure or intravascular volume in experimental animals, and at the same time points in control animals. MEASUREMENTS AND MAIN RESULTS: Elevated intra-abdominal pressure significantly (p < 0.05, analysis of variance) increased renal venous pressure, pleural pressure, wedge pressure, and pulmonary artery pressure compared to both baseline and control animals; whereas cardiac index and urine output decreased significantly. Both plasma renin and aldosterone levels increased significantly compared with baseline and controls. Intravascular volume expansion significantly increased urine output and decreased significantly both plasma renin activity and aldosterone levels. Abdominal decompression further significantly decreased both plasma renin activity and aldosterone levels. There were no significant changes in atrial natriuretic factor at any time point. CONCLUSIONS: Elevated intra-abdominal pressure decreases urine output and significantly up-regulates the hormonal output of the renin-angiotensin-aldosterone system. Intravascular volume expansion in combination with abdominal decompression reverses the effects of acutely elevated intra-abdominal pressure upon renal function and the renin-angiotensin-aldosterone system.

Abdomen↗
PubMed1997

Multicenter, randomized, prospective trial of early tracheostomy.

OBJECTIVES: Determine the effect of early (days 3-5) or late (days 10-14) tracheostomy on intensive care unit length of stay (ICU LOS), frequency of pneumonia, and mortality, and evidence of short-term or long-term pharyngeal, laryngeal, or tracheal injury in head trauma, non-head trauma, and critically ill nontrauma patients. STUDY DESIGN: Randomized, prospective. SETTING: Five Level I trauma centers. METHODS: Data were obtained prospectively and included Acute Physiology and Chronic Health Evaluation III score (AIII), Glasgow Coma Scale score, Emergency Room Trauma Score, Injury Severity Score, Acute Injury Score, type of endotracheal tube or tracheostomy, level of positive end-expiratory pressure, and peak inspiratory pressure. Patients were to undergo laryngoscopy for detection of injury according to the Lindholm criteria at the time of endotracheal tube or tracheostomy removal and be reevaluated at 3 to 5 months after discharge. RESULTS: One hundred fifty-seven patients were entered, 127 to early randomization (3-5 days) and 28 to late randomization (10-14 days); however, only 112 patients with early and 14 with late randomization had completed data forms for the primary study goals. An additional 22 patients from the early entry groups were rerandomized late. Early randomization data: the AIII score was higher (p < 0.05) in the head trauma tracheostomy (65 +/- 4) than in the nontracheostomy group (51 +/- 4) and in the nontrauma tracheostomy (92 +/- 6) than in the nontracheostomy group (68 +/- 7), but was equivalent in the non-head trauma group. Glasgow Coma Scale score, Emergency Room Trauma Score, Injury Severity Score, Acute Injury Score, positive end-expiratory pressure, and peak inspiratory pressure were not significantly different in any of the groups. There were no significant differences in ICU LOS, frequency of pneumonia, or death in any of the groups after either early or late tracheostomy compared with continued endotracheal intubation. Only 83 patients underwent postextubation laryngoscopy. There were no significant differences between the groups; however, there were trends to more vocal cord ulceration and subglottic inflammation in the continued intubation group. No patient was seen in this study with late vocal cord or laryngeal stenosis; there were no tracheal-innominate artery fistulae. Seven of the patients with abnormal findings at extubation had normal 3- to 5-month postextubation laryngoscopy. CONCLUSION: Physician bias limited patient entry into the study. Although there were higher AIII scores in the head trauma early tracheostomy patients, there were no differences in the primary end points of ICU LOS, pneumonia, or death in any of the groups studied. Long-term endoscopic follow-up was poor, but no known late tracheal stenosis was seen.

APACHE↗
PubMed1997

Protective role of synthetic sialylated oligosaccharide in sepsis-induced acute lung injury.

Proper engagement of leukocyte and endothelial cell selectins with their counterreceptors is an initial step in neutrophil trafficking to sites of inflammation. Certain fucosylated carbohydrate determinants such as sialyl Lewis-x are proposed to act as these counterreceptors. We studied the effects of a synthetic sialyl Lewis-x analog, CY-1503, on the course of hemodynamic derangements and acute lung injury during experimental gram-negative sepsis. Anesthetized ventilated swine were made septic with an infusion of live Pseudomonas aeruginosa. A treatment group received an initial bolus of CY-1503 (60 mg/kg) before sepsis, followed by continuous infusion of CY-1503 (15 mg.kg-1.h-1). Treatment with CY-1503 did not prevent the development of pulmonary hypertension, systemic hypotension, decline in cardiac output, or severe neutropenia. However, CY-1503 significantly attenuated lung injury, demonstrated by decreased bronchoalveolar lavage protein content and neutrophil influx, lowered lung myeloperoxidase activity, and improved arterial oxygenation. Neutrophils from septic and CY-1503 animals showed significant activation, reflected by upregulated CD18 expression and priming for oxidant burst compared with control animals. This study suggests blockade of selectin interactions as a potential therapeutic intervention in sepsis-induced lung injury.

Animals↗
PubMed1997

Increased intra-abdominal pressure and cardiac filling pressures in obesity-associated pseudotumor cerebri.

OBJECTIVES: To determine whether intra-abdominal pressure (as estimated from urinary bladder pressure) is elevated in patients with central obesity (as measured by sagittal abdominal diameter) and pseudotumor cerebri and whether this increased intra-abdominal pressure is associated with increased pleural pressure and cardiac filling pressure, implying a resistance to venous return from the brain. DESIGN: Nonrandomized, prospective. SETTING: University hospital, operating room. MAIN OUTCOME MEASUREMENTS: Intracranial pressure, urinary bladder pressure, sagittal abdominal diameter, transesophageal pleural pressure, central venous pressure, pulmonary artery pressure, and pulmonary artery occlusion pressure. SUBJECTS: Six women with pseudotumor cerebri (one with CSF leak, one with lumboperitoneal shunt). RESULTS: Urinary bladder pressure (22 +/- 3 cm H2O) and sagittal abdominal diameter (29 +/- 3 cm) were significantly elevated in these patients with elevated intracranial pressure (293 +/- 80 mm H2O) compared with a previously reported group of nonobese control patients. The transesophageal pleural pressure (15 +/- 10 mm Hg), central venous pressure (20 +/- 6 mm Hg), mean pulmonary artery pressure (31 +/- 6 mm Hg), and pulmonary artery occlusion pressure (21 +/- 7 mm Hg) were all markedly elevated compared with published normal values and with previous data from obese patients without pseudotumor cerebri. CONCLUSIONS: These data support the hypothesis that central obesity raises intra-abdominal pressure, which increases pleural pressure and cardiac filling pressure, which impede venous return from the brain, leading to increased intracranial venous pressure and increased intracranial pressure associated with pseudotumor cerebri.

Abdomen↗
PubMed1996

Pulmonary artery endothelial cell function in swine pseudomonas sepsis.

A substantial increase in pulmonary vascular resistance is associated with sepsis and its sequelae (sepsis syndrome and septic shock). It is postulated that increased resistance may result from sepsis-induced endothelial cell injury or altered vasoreactivity secondary to pulmonary hypertension. We, therefore, tested the hypothesis that sepsis causes endothelial cell injury and that increased pulmonary pressure alters vascular reactivity. Young swine (15-25 kg) were anesthetized and ventilated. Septic animals received a 1-hr infusion of live Pseudomonas aeruginosa (n = 11), and the control cohort received 0.9% NaCl (n = 7). All animals were studied for 300 min following the infusion. Postmortem branches of peripheral pulmonary arteries were prepared and tested in a vessel myograph. Ring segments were set to 90% of the circumference the vessels would have at pressures of 20, 30, 40, or 50 mmHg (L90), corresponding to varying pulmonary pressures observed in sepsis. A high dose of potassium was used to obtain maximum possible contraction. Prostaglandin was used to precontract the vessels before testing endothelial cell responses to acetylcholine or bradykinin. Sodium nitroprusside was added at the end of each experiment to obtain maximum possible smooth muscle relaxation. No differences in contraction or relaxation were observed when vessels were set to different pressures (i.e., 20 vs 50 mmHg). Maximum possible contraction to KCl was significantly decreased after 300 min of sepsis compared to control. No differences between groups were found in contractility to prostaglandin. Bradykinin-induced EDRF/NO production, mediated by BK2 receptors, was not altered in Pseudomonas sepsis (97-98% of total relaxation control and 91-95% septic cohort). Response to acetylcholine was significantly decreased after sepsis (89-95% of total relaxation control and 51-61% of septic cohort relaxation). Decreased response to acetylcholine could not be attributed to decreased smooth muscle sensitivity to nitric oxide because the response to bradykinin plus sodium nitroprusside was not altered following sepsis. Vessel reactivity was not altered by increasing pressure settings reflective of changing pulmonary pressure in vivo. These results strongly suggest a sepsis-induced alteration in pulmonary artery endothelial cell receptor sensitivity to acetylcholine, independent of changing pulmonary arterial pressures. This is the first time this decrease has been shown in pseudomonas sepsis.

Animals↗
PubMed1996

Conversion of failed or complicated vertical banded gastroplasty to gastric bypass in morbid obesity.

BACKGROUND: Previous studies have documented a significantly better we weight loss for gastric bypass (GBP) than for vertical banded gastroplasty (VGB). Additional problems associated with VBG include intractable vomiting or gastroesophageal (GE) reflux, intragastric migration of the polypropylene band, staple line disruption, or inadequate weight loss due to excessive ingestion of high-calorie liquid or soft carbohydrates. PATIENTS AND METHODS: Fifty-eight morbidly obese patients underwent conversion from VBG to GBP for either weight-loss failure (15) or complications of VBG (43), including 2 who where referred with anastomotic leaks and peritonitis, 3 with band erosion, 15 with staple line disruption, and 23 with stomal stenosis, of whom 6 had severe GE reflux, with a Barrett's esophagus in 1. RESULTS: Percentage of excess weight loss in the 53 patients followed up for at least 1 year after conversion increased from 36% +/- 24% to 67% +/- 18%, and in the 15 "sweets eaters" from 20% +/- 19% to 70% +/- 19% (both P <0.001), was equal to weight loss after primary GBP, and was reasonably constant over 8 years in those patients who could be contacted for follow-up, although average follow-up after 5 years was only 45% All patients had resolution of GE reflux symptoms immediately after surgery and for at least 1 year or at last contact. Complications of conversion included 2 anastomotic leaks with major wound infections (1 in a referred patient requiring emergency subtotal gastrectomy following a VBG leak), 3 staple line disruptions (2 subclinical), 3 small-bowel obstructions, and 20 marginal ulcers or stomal stenoses (all responded to endoscopic balloon dilation or acid reduction therapy). Hemoglobin, calcium, and vitamin B12 levels remained within normal levels with prophylactic supplementation in patients who returned for follow-up evaluation. CONCLUSIONS: These data support the efficacy of conversion to GBP in morbidly obese patients with a failed or complicated VBG.

Gastric Bypass↗
PubMed1996

Greater risk of incisional hernia with morbidly obese than steroid-dependent patients and low recurrence with prefascial polypropylene mesh.

BACKGROUND: Incisional hernia is a serious complication of abdominal surgery. We compared incisional hernia frequency following gastric bypass (GBP) for morbid obesity versus total abdominal colectomy and ileal pouch-anal anastomosis (IPAA) for ulcerative colitis. A prefascial polypropylene mesh repair was also evaluated. PATIENTS AND METHODS: All patients had midline incisions, xiphoid to umbilicus in GBP patients and midepigastrium to pubis in IPAA patients. Fascia were closed with running No. 2 polyglycolic acid suture. Ninety-eight patients underwent prefascial polypropylene mesh repair; 80 were GBP patients, 46 had 1 previous repair, and 17 had 2 to 9 previous repairs (6 with properitoneal mesh). RESULTS: Incisional hernia occurred in 20% (198/968) of GBP patients (19% without versus 41% with a previous hernia, P < 0.001) versus 4% (7/171) of the IPAA patients (P < 0.001), of whom 102 (60%) were taking prednisone (32 +/- 2 mg/d) and 5 were quite obese (body mass index > or = 30 kg/m2). Additional risk factors for hernia in GBP patients included wound infection, diabetes, sleep apnea, and obesity hypoventilation. For the 98 patients who underwent prefascial polypropylene mesh repair, the mean follow-up was 20 +/- 2 months (range 6 to 104), and complications occurred in 35% of patients, including minor wound infection (12%), major wound infection (5%), seroma (5%), hematoma (3%), chronic pain (6%), and recurrent hernia (4%). CONCLUSIONS: Severe obesity is a greater risk factor for incisional hernia and hernia recurrence than chronic steroid use in nonobese colitis patients. A prefascial polypropylene mesh repair minimizes recurrence.

Abdomen↗
PubMed1996

Effects of increased intra-abdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion.

OBJECTIVE: To study the effects of elevated intra-abdominal pressure (IAP) upon intracranial (ICP) and cerebral perfusion pressure (CPP) before and after intravascular volume resuscitation. MATERIALS AND METHODS: Intra-abdominal pressure was increased in five anesthetized swine by inflating an intraperitoneal balloon until the IAP was 25 mm Hg above baseline. Intravascular volume was then expanded and finally abdominal decompression was performed. Changes in ICP and systemic and pulmonary hemodynamic parameters secondary to increasing IAP were measured. The effect upon CPP was derived from these measurements. PaO2 and PaCO2 were maintained relatively constant by increasing ventilatory rate. MEASUREMENTS AND MAIN RESULTS: Elevated IAP significantly increased ICP (7.6 +/- 1.2 vs. 21.4 +/- 1.0), pleural pressure and central venous pressure; whereas cardiac index and CPP (82.2 +/- 6.3 vs. 62.0 +/- 10.0) decreased significantly. Intravascular volume expansion further significantly increased ICP (27.8 +/- 1.0), and significantly increased both mean arterial pressure (83.4 +/- 14.0 versus 103.4 +/- 8.9) and CPP (75.6 +/- 9.0). Abdominal decompression returned ICP (11.2 +/- 1.8) toward baseline and further increased CPP (79.8 +/- 9.7). CONCLUSIONS: Elevated IAP increases ICP and decreases CPP and cardiac index. Volume expansion further increases ICP yet improves CPP via its greater positive effect upon mean arterial pressure (*p < 0.05, analysis of variance. All measurements are mean +/- SEM in mm Hg).

Abdomen↗
PubMed1995

Sepsis-induced acute lung injury is attenuated by selectin blockade following the onset of sepsis.

OBJECTIVE: To determine the effect of infusion with a dual-binding antibody to E- and L-selectin, EL-246, in a postonset model of sepsis. DESIGN: Nonrandomized controlled study. STUDY SUBJECTS: Young Yorkshire swine. INTERVENTIONS: Three groups were studied. Controls (n = 8) received saline solution only. Untreated animals with sepsis (n = 8) received a 1-hour intravenous infusion of live Pseudomonas aeruginosa. Animals treated with EL-246 (n = 6) received the same bacterial infusion and a 2-mg/kg bolus of EL-246 at 30 minutes. OUTCOME MEASURES: Systemic and pulmonary hemodynamics, arterial blood gas determination, bronchoalveolar lavage protein and neutrophil content, neutrophil integrin and selectin expression, neutrophil oxidant burst, and organ myeloperoxidase content. RESULTS: Treatment with EL-246 significantly reduced lung injury, as indicated by improved bronchoalveolar lavage protein and neutrophil content, resulting in a significant improvement in arterial oxygenation. This reduction in lung injury was produced by a reduction in lung myeloperoxidase content. Treatment with EL-246 failed to prevent the development of pulmonary hypertension and systemic hypotension. Neutrophils from animals with sepsis exhibited significant activation and upregulation of CD18, shedding of L-selectin, and production of increased levels of oxidants compared with controls. CONCLUSION: Treatment of animals with EL-246 soon the onset of sepsis produced significant protection against acute lung injury but failed to attenuate hemodynamic derangements associated with sepsis.

Animals↗
PubMed1995

Tumor necrosis factor-alpha and interleukin-6 selectively regulate neutrophil function in vitro.

The neutrophil is an important effector cell of the host response to sepsis. Tumor necrosis factor-alpha (TNF-alpha), a cytokine mediator of the septic response, is rapidly released following endotoxemia or gram-negative bacteremia. Interleukin-6 (IL-6) is another cytokine mediator of the host response to sepsis whose role is less well understood than that of TNF-alpha. It is known to be elevated in gram-negative sepsis, where peak levels have been correlated with mortality. This study examined the effect of IL-6 alone and in combination with TNF-alpha on three neutrophil functions--CD18 adhesion receptor expression, phagocytosis, and superoxide anion generation. Neutrophils from human volunteers were incubated with amounts of IL-6 ranging from 10 to 1000 ng/ml. At a concentration of 1000 ng/ml, IL-6 increased neutrophil phagocytosis of opsonized bacteria (826 +/- 255 x 10(3) MESF vs 552 +/- 103 MESF, P < 0.05) and also increased neutrophil superoxide anion generation (18.41 +/- 1.86 vs 12.6 nmol O2-/10(6) PMN/10 min, P < 0.05). Lesser amounts of IL-6 had no effect on phagocytosis or superoxide generation. IL-6 did not increase neutrophil CD18 adhesion receptor expression. Combining IL-6 with TNF-alpha at doses of 100 ng/ml and 100 U/ml, respectively, neutrophil phagocytosis (221 +/- 455 MESF vs 552 +/- 103 MESF) and superoxide generation (23.18 +/- 1.86 vs 12.6 nmol O2-/10(6) PMN/10 min) were significantly (P < 0.05) increased above control by an amount similar to that seen with 1000 U/ml TNF-alpha alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗