Surgical intervention in patients with necrotizing pancreatitis

BACKGROUND: This study evaluated the various surgical strategies for treatment of (suspected) infected necrotizing pancreatitis (INP) and patient referrals for this condition in the Netherlands. METHODS: This retrospective study included all 106 consecutive patients who had surgical treatment for INP in the period 2000-2003 in one of eight Dutch university medical centres including three teaching hospitals. Surgical approaches included an open abdomen strategy, laparotomy with continuous postoperative lavage, minimally invasive procedures or laparotomy with primary abdominal closure. The National Hospital Registration System was searched to identify patients with acute pancreatitis who were admitted to the 90 Dutch hospitals that did not participate in the present study. RESULTS: The overall mortality rate was 34.0 per cent, 70 per cent (16 of 23) for the open abdomen strategy, 25 per cent (13 of 53) for continuous peritoneal lavage, 11 per cent (two of 18) for minimally invasive procedures and 42 per cent (five of 12) for primary abdominal closure (P < 0.001). During the study interval, 44 (12.2 per cent) of 362 patients with acute pancreatitis who were likely to require surgical intervention had been referred to university medical centres. CONCLUSION: Laparotomy with continuous postoperative lavage is the surgical strategy most often used in the Netherlands. The results of the open abdomen strategy are poor whereas a minimally invasive approach seems promising.     

Randomized clinical trial of standard laparoscopic versus robot-assisted laparoscopic Nissen fundoplication for gastro-oesophageal reflux disease

BACKGROUND: Robotic systems for minimally invasive surgery may be of added value during extensive dissection and suturing in confined spaces, such as laparoscopic Nissen fundoplication (LNF). The purpose of this trial was to compare standard LNF with robot-assisted Nissen fundoplication (RNF). METHODS: Between 2003 and 2005, 50 patients with confirmed refractory gastro-oesophageal reflux disease were assigned to LNF (25) or RNF (25). Patients who had undergone previous antireflux surgery were excluded. Independent assessment of dysphagia, regurgitation, heartburn and general well-being was performed before and 6 months after surgery using questionnaires. Objective outcome was studied 6 months after surgery by oesophageal manometry, 24-h pH monitoring, barium oesophagram series and upper endoscopy. RESULTS: Operating time, blood loss, postoperative pain scores, hospital stay and complication rates did not differ significantly between the two groups. Reoperation rates were the same (one incisional hernia after LNF and one patient with repeat Nissen after RNF because of persistent dysphagia). Postoperative self-rated change in reflux symptoms and quality of life improved equally in both groups. The reduction in oesophageal acid exposure, increase in lower oesophageal sphincter tone and mucosal healing were comparable in both groups at follow-up. CONCLUSION: RNF yielded similar subjective and objective results to LNF in this study. Therefore no additive value of robotic systems for this procedure was detected up to 6 months after surgery.     

Impaired bolus transit across the esophagogastric junction in postfundoplication dysphagia

OBJECTIVES: This study assessed the effect of fundoplication on liquid and solid bolus transit across the esophagogastric junction (EGJ) in relation to EGJ dynamics and dysphagia. METHODS: Twelve patients with gastro-esophageal reflux disease (GERD) were studied before and after fundoplication. Concurrent high-resolution EGJ manometry and fluoroscopy were performed whilst swallowing liquid barium and a solid bolus. The EGJ transit time, EGJ opening duration, transit efficacy, and EGJ relaxation were measured. During the test symptoms of dysphagia were scored using a visual analog scale. RESULTS: The minimal opening aperture at fluoroscopy was located at the manometric EGJ in all subjects. Fundoplication markedly reduced the EGJ opening diameter from 1.0 +/- 0.1 to 0.6 +/- 0.1 cm (p < 0.01) and rendered deglutative EGJ relaxation incomplete. After fundoplication, a higher intrabolus pressure was found (p < 0.05) associated with a reduced axial bolus length (p < 0.001). EGJ transit time increased from 6.9 +/- 0.9 to 9.8 +/- 1.0 s for liquids (p < 0.01) and from 2.8 +/- 0.5 to 5.8 +/- 0.8 s (p < 0.01) for solids after fundoplication. No relation between EGJ transit and dysphagia scores was observed before fundoplication. In contrast, EGJ transit time significantly correlated with dysphagia scores both during liquid (r = 0.84; p < 0.01) and solid (r = 0.69; p < 0.05) bolus transit following fundoplication. CONCLUSIONS: Fundoplication patients exhibit a restricted hiatal opening and an incomplete deglutative EGJ relaxation. To facilitate EGJ transit despite these altered EGJ dynamics a higher intrabolus pressure is created by augmented bolus compression. Fundoplication increases EGJ transit time, the degree of which is associated with postoperative dysphagia.     

Interrelationship between TP53 gene deletion, protein expression and chromosome 17 aneusomy in gastric adenocarcinoma

Background  

This study evaluates the existence of numerical alterations of chromosome 17 and TP53 gene deletion in gastric adenocarcinoma. The p53 protein expression was also evaluated, as well as, possible associations with clinicopathological characteristics.     

Systematic mechanism-orientated approach to chronic pancreatitis pain

Pain in chronic pancreatitis(CP) shows similarities with other visceral pain syndromes(i.e.,inflammatory bowel disease and esophagitis),which should thus be managed in a similar fashion.Typical causes of CP pain include increased intrapancreatic pressure,pancreatic inflammation and pancreatic/extrapancreatic complications.Unfortunately,CP pain continues to be a major clinical challenge.It is recognized that ongoing pain may induce altered central pain processing,e.g.,central sensitization or pro-nociceptive pain modulation.When this is present conventional pain treatment targeting the nociceptive focus,e.g.,opioid analgesia or surgical/endoscopic intervention,often fails even if technically successful.If central nervous system pain processing is altered,specific treatment targeting these changes should be instituted(e.g.,gabapentinoids,ketamine or tricyclic antidepressants).Suitable tools are now available to make altered central processing visible,including quantitative sensory testing,electroencephalograpy and(functional) magnetic resonance imaging.These techniques are potentially clinically useful diagnostic tools to analyze central pain processing and thus define optimum management approaches for pain in CP and other visceral pain syndromes.The present review proposes a systematic mechanism-orientated approach to pain management in CP based on a holistic view of the mechanisms involved.Future research should address the circumstances under which central nervous system pain processing changes in CP,and how this is influenced by ongoing nociceptive input and therapies.Thus we hope to predict which patients are at risk for developing chronic pain or not responding to therapy,leading to improved treatment of chronic pain in CP and other visceral pain disorders.     

The effect of donor red cell sedimentation rate on efficiency of granulocyte collection by centrifugal leukapheresis

BACKGROUND: Granulocyte collection relies on the use of a red cell- sedimenting agent and is influenced by poorly defined intrinsic donor characteristics. The donor's baseline red cell (erythrocyte) sedimentation rate (ESR), a readily measurable intrinsic donor variable, may influence the effectiveness of red cell-sedimenting agents and affect the granulocyte yield. STUDY DESIGN AND METHODS: The in vitro and in vivo effects of 6-percent hydroxyethyl starch on the donor ESR were prospectively studied in 67 granulocytapheresis procedures with a blood cell separator, and the findings were correlated with granulocyte collection efficiency (GCE). A relationship that predicts the GCE on the basis of the donor ESR was then derived and tested. RESULTS: The 3.7-fold mean increase in the donor ESR measured after in vitro addition of hydroxyethyl starch approximated the 3.3-fold increase measured when it was administered to the donors. Higher baseline ESR correlated with larger in vitro and in vivo hydroxyethyl starch-induced increases in ESR and predicted more efficient cell collections and greater cell yields. Furthermore, both ESR and GCE, which varied significantly among donors, remained constant for a given donor undergoing repeat procedures. The results could be summarized by a simple predictive formula that relates the GCE (%) to the ESR (mm/hour): GCE = 1.3ESR + 45. The GCE and yield as predicted by the formula were accurate within 10 percent of the observed values in six subsequent procedures. CONCLUSION: In granulocyte harvests using a blood cell separator with hydroxyethyl starch as the sedimenting agent, 1) both ESR and GCE vary widely among donors yet may remain relatively constant for a given donor; 2) the baseline ESR correlates with hydroxyethyl starch-modified ESR and with GCE; and 3) it may be possible to predict GCE and yield from the donor's baseline ESR.     

Inhibition of prostaglandin E2 restores defective lymphocyte proliferation and cell-mediated lympholysis in recipients after allogeneic marrow grafting

Prostaglandins are said to influence T and B cell function by inhibiting the generation of interleukin 2 (IL 2) and the formation of suppressor lymphocytes. After bone marrow transplantation, patients usually have a profound immunodeficiency that persists in recipients with chronic graft-v-host disease (GVHD) and generally resolves in long- term survivors without GVHD. In vitro tests of lymphocyte function such as allogeneic mixed lymphocyte culture (MLC) and cell-mediated lympholysis (CML) have been shown to be impaired in many patients. We postulated that prostaglandin E2 (PGE2) plays a role in the impaired in vitro tests. To test this hypothesis, we studied in vitro tests in the presence of PGE2 antagonists, indomethacin, and anti-PGE2 antiserum with cells from 22 short-term patients (less than 100 days postgrafting) and 32 long-term survivors with or without GVHD. Results show that blockade of PGE2 release by indomethacin and anti-PGE2 significantly (P less than .01) enhanced the MLC (+67%) and the CML responses (+10.5%) of cells from long-term survivors with chronic GVHD but not from those of long-term, stable recipients. No enhancement of MLC and CML activity was observed with cells from donors of long-term recipients. In patients shortly after marrow grafting, enhancement in the MLC was not significant. However, CML activity in this patient group was significantly increased (+12.5% in recipients with no GVHD, 8.5% in those with acute GVHD, P less than .01). Indomethacin also suppressed the activity of nonspecific suppressor cells in patients with chronic GVHD. When cells from patients with chronic GVHD were treated with recombinant IL 2 and IL 2 combined with indomethacin, it was possible to get an additional augmentation of lymphocyte proliferation after the addition of indomethacin to IL 2-treated cultures. Thus it is very likely that PGE2 inhibits T lymphocyte proliferation, not exclusively by inhibition of IL2 production or activity. We conclude that PGE2, among other factors, may play a role in the pathogenesis of the immunodeficiency after transplantation. PGE2 does not act primarily by interfering with IL2 but presumably by inducing a suppressorlike activity.