Maternal mood disorders and lithium exposure in utero were not associated with poor cognitive development during childhood.

AIM: This study evaluated whether maternal mood disorders (MMD), particularly bipolar disorder, and lithium treatment during pregnancy influenced the neonatal health and cognition of children born from 2006 to 2010. METHODS: Our study at Karolinska University Hospital, Stockholm, Sweden, focused on women with and without mood disorders and their children. Information on pharmacotherapy, mental health, delivery and neonatal complications was retrospectively collected from electronic patient records. Children were tested in a blinded manner at four to five years of age with the Wechsler Preschool and Primary Scale of Intelligence, 3rd edition. Maternal health, child health and social situations were evaluated. RESULTS: Of the 39 children, 20 were exposed to lithium and MMD during pregnancy, eight were exposed to MMD but not lithium and 11 were not exposed to MMD or lithium. The children's full scale intelligence quotient (IQ), performance IQ and verbal IQ results did not differ significantly between the groups. The processing speed quotient was significantly lower in children exposed to mood disorders, but there was a high level of missing data for this subtest. CONCLUSION: This small, clinical cohort showed no significant association between mothers' prenatal exposure to lithium or mood disorders and their offspring's IQ.

Host species-specific translocation of Escherichia coli.

The purpose of this paper is to investigate the rate of translocation of Escherichia coli strains in different experimental/animal models. Four proficient translocating E. coli strains isolated from mesenteric lymph nodes (MLNs) and/or the blood of rats (strains KIC-1 and KIC-2), from a fatal case of pancreatitis (HMLN-1) and from pigs (PC-1 isolated in this study) were tested for their ability to translocate across two host species and the Caco-2 cell line as a model of the human gut epithelium. HMLN-1 was found in the MLNs of all 15 pigs tested. This strain, however, did not translocate in any rats and only colonised the caecum of four rats in small numbers. HMLN-1 and PC-1 were the dominant translocating strains in Caco-2 cells compared to KIC-1 and KIC-2, which were found to translocate at a lower rate in pigs and in Caco-2 cells. The rate of translocation of PC-1 in rats was also very low compared to KIC-1 and KIC-2. We suggest that, in studies aiming to investigate the mechanism of translocation of E. coli strains isolated from humans, rats may not be an appropriate animal model and that the Caco-2 cells or pigs are more suitable in vitro and in vivo models, respectively.

Complication rate lower after percutaneous endoscopic gastrostomy than after surgical gastrostomy: a prospective, randomized trial.

BACKGROUND: Percutaneous endoscopic gastrostomy (PEG) has increasingly replaced surgical gastrostomy (SG) as the primary procedure for the long-term nutrition of patients with swallowing disorders. This prospective randomized study compares PEG with SG in terms of effectiveness and safety. METHODS: This study enrolled 70 patients with swallowing disorders, mainly attributable to neurologic impairment. All the patients, eligible for both techniques, were randomized to PEG (pull method) or SG. The groups were comparable in terms of age, body mass index, and underlying diseases. Complications were reported 7 and 30 days after the operative procedure. RESULTS: The procedures were successfully completed for all the patients. The median operative time was 15 min for PEG and 35 min for SG (p < 0.001). The rate of complications was lower for PEG (42.9%) than for SG (74.3%; p < 0.01). The 30-day mortality rates were 5.7% for PEG and 14.3% for SG (nonsignificant difference). CONCLUSION: The findings show PEG to be an efficient method for gastrostomy tube placement with a lower complication rate than SG. In addition, PEG is faster to perform and requires fewer medical resources. The authors consider PEG to be the primary procedure for gastrostomy tube placement.

Microbial translocation and inflammatory response in patients with acute peritonitis.

BACKGROUND: In peritonitis, increased production of cytokines and changes in the splanchnic cellular immune system may cause translocation of bacteria and endotoxins. The aims of this study were to assess the frequency of translocation and relate translocation to the immune response in patients with acute peritonitis. METHODS: Patients with local (LP, n=20) or general peritonitis (GP, n=15) were compared with controls (C, n=12). Blood was obtained preoperatively for cultures, and analyses of endotoxin and cytokines (tumour necrosis factor-alpha, interleukins 6 and 10). Mesenteric lymph nodes (MLNs) were excised for culturing and immunohistochemistry using antibodies CD4, CD8 and CD68. RESULTS: Positive blood and MLN cultures were not obtained in controls. DNA typing proved bacterial translocation in one patient with local and one patient with general peritonitis. Thus translocation was proven to occur in 6% of patients with peritonitis. Endotoxaemia was predominantly found in the GP group. Cytokines increased during peritonitis and more so in patients with GP than in those with LP. More CD8 and CD68 cells were found in MLNs from LP patients than in C patients and more CD4 and CD8 cells in LP patients than in GP patients. There was no significant difference in this regard between the GP and C groups. CONCLUSIONS: Bacterial translocation occurs during acute peritonitis but seems to be fairly infrequent. Peritonitis causes significant inflammatory cellular reactions.

Intramucosal pH and pCO(2) do not strictly correlate with intestinal energy metabolism in experimental peritonitis.

This study aimed to investigate tissue hypoxia on the cellular level in sepsis. Eighteen pigs weighing 18-27 kg were studied. Intramucosal-arterial PCO(2) gradient (PCO(2)-gap) and intramucosal pH (pH(i)) were calculated using tonometry. A blind loop of the small intestine was constructed for repeated tissue biopsies to measure intestinal energy-related metabolites and lactate concentration. Six animals served as controls. In 12 animals, faecal peritonitis was induced. Six of these animals were studied without further interventions, while the others were resuscitated with dextran to maintain cardiac index at baseline level. Untreated peritonitis caused an increase in PCO(2)-gap and a drop in pH(i). The intestinal energy metabolism was not disturbed until the end of the experimental period, with a decreased energy charge value and a moderately increased lactate concentration. In peritonitis-dextran animals, PCO(2)-gap and pH(i) remained at baseline level and the energy metabolism was not disturbed. We conclude that in peritonitis, PCO(2)-gap - like pH(i) - can be influenced by other factors than strictly anaerobic tissue metabolism.

Bacterial translocation in experimental shock is dependent on the strains in the intestinal flora.

BACKGROUND: Enteric microorganisms are responsible for a significant proportion of post-surgical infections. Intestinal mucosal injury may permit translocation of bacteria and endotoxin. This study investigates translocation in peritonitis and ischemia/reperfusion by inoculating different bacterial species into the small intestine. METHODS: Twenty-five pigs were monitored hemodynamically and divided into three groups: controls (C), ischemia/reperfusion (I/R), and peritonitis (P). Intramucosal pH (pHi) was calculated tonometrically. A perfusion tube was positioned in the ileum for inoculation of the bacterial strains. In a first study period a non-pathogenic bacterium was used, whereas Escherichia coli strains with known ability to translocate were used in a second. Blood and mesenteric lymph nodes (MLNs) were obtained for bacterial culture and endotoxin analyses. RESULTS: Mesenteric arterial blood flow and pHi decreased in groups I/R and P. Endotoxin levels increased in these groups in period 1, whereas in period 2 an increase over time was only observed in group P. No bacterial translocation to blood or MLNs occurred in period 1. In period 2 bacteria translocated to MLNs in all animals, including controls. Translocation to central and/or mesenteric venous blood was found in all groups, but mainly in I/R and P. The incidence of mucosal injury was similar in the two periods. CONCLUSIONS: Since positive blood and MLN samples were only found in period 2, we conclude that translocation of bacteria seems to be more dependent on the presence of translocating strains in the intestinal bacterial flora than on the mucosal insult.

Immune cell distribution in gut-associated lymphoid tissue and synthesis of IL-6 in experimental porcine peritonitis.

This study aimed to evaluate the possibility to detect early changes in gut-associated lymphoid tissue related to an inflammatory response. Anaesthetised pigs were subjected to faecal peritonitis (n = 9) or to a sham procedure (n = 8). Blood from the vena cava and the superior mesenteric vein was repeatedly sampled, and the levels of interleukin-6 (IL-6) were analysed. Biopsies of the small intestine and mesenteric lymph nodes (MLNs), harvested at 300 min, were incubated with monoclonal antibodies specific for CD2 (T lymphocytes), IgM (B lymphocytes) and CD11a/CD18 (leucocyte adhesion molecule). The number of positive (+) cells was scored. During peritonitis, IL-6 increased significantly. Compared to controls, the number of CD2+ cells decreased, IgM+ cells tended to increase and CD11a/CD18+ cells increased in the mucosa during peritonitis. In MLNs, the number of cells positive for all studied markers increased during peritonitis. We conclude that peritonitis causes an inflammatory response in the gut reflected by changes in the distribution of immune cells in gut-associated lymphoid tissue and release of IL-6 to venous blood.

Intestinal blood flow and intramucosal pH in experimental peritonitis.

BACKGROUND AND AIMS: Experimental peritonitis causes gut intramucosal acidosis indicating intramucosal ischemia. However, tissue acidosis may reflect other conditions than ischemia. An increased mucosal-arterial Pco2 difference ( Pco2-gap) is suggested to be a more adequate measure of tissue ischemia than intramucosal pH (pHi). This study was performed to elucidate whether keeping cardiac index (CI) and splanchnic blood flow normal or supranormal by administration of colloids and an inotropic drug could prevent the acidosis as well as reduce the Pco2-gap. A secondary aim was to study to what degree the low pHi in peritonitis really reflects ischemia. SUBJECTS: 24 anesthetized pigs (18-27 kg) divided into four groups. MODELS: A Swan-Ganz catheter, transonic flow meters and catheters for blood sampling were applied. pHi was calculated using tonometry. Standardized fecal peritonitis was induced, except in controls. One peritonitis group was given dextran (Group P(DEX)) and another in addition dobutamine (Group PDOB) to keep CI normal or supranormal, respectively. RESULTS: After 4 h, a significant drop in pHi was found in all peritonitis groups, most pronounced in untreated peritonitis (to 7.09+/-.02). Corresponding values in Group P(DEX) and Group P(DOB) were 7.22+/-.03 and 7.22+/-.01, respectively, and in controls 7.30+/-.02. The Pco2-gap and the mucosal-arterial [H+] difference ([H+]-gap) increased significantly in untreated peritonitis but did not increase in groups given dextran and dextran + dobutamine. CONCLUSION: Maintaining CI in peritonitis attenuated the reduction in pHi and prevented the increased Pco2- and [H+]-gap. It seems justified from these data to conclude that the somewhat reduced pHi in treated peritonitis groups did not reflect tissue ischemia.

Small intestinal mucosal pH and lactate production during experimental ischemia-reperfusion and fecal peritonitis in pigs.

The aim of this study was to investigate mucosal pH and lactate production in a porcine model of ischemia/reperfusion and sepsis using both tonometry and a technique for segmental intestinal perfusion. Eighteen pigs (17-23 kg) were anesthetized and mechanically ventilated. They were divided into three groups and followed for 4 h. Group C (n = 6) served as controls. In the ischemia/reperfusion group (I/R; n = 6), the superior mesenteric artery was totally occluded for 60 min. In group P (n = 6), sepsis was induced by fecal peritonitis. Cardiac index (CI) was determined by thermodilution and blood flow in the superior mesenteric artery (QSMA), using a Transonic flow probe. Intramucosal pH (pHi) was calculated using tonometry. A special balloon tube for segmental perfusion was introduced in the midileum for lactate measurement. Lactate and oxygen saturation were measured in arterial blood and in the superior mesenteric vein. CI, QSMA, pHi, and lactate in blood and perfusate remained unchanged in controls. Occlusion of intestinal blood flow induced a fall in pHi from 7.28 +/- .02 to 6.76 +/- .04, a marked rise in lactate in the perfusate, and an increased arteriovenous lactate difference. During reperfusion, pHi tended to return to baseline values. Lactate in the perfusate and the arteriovenous lactate difference decreased. In sepsis there was a continuous reduction in CI and QSMA to 45 +/- 13% and 40 +/- 20% of baseline, respectively. pHi decreased moderately from 7.22 +/- .09 to 6.98 +/- .25. Lactate remained unchanged in blood and perfusate. Microscopic mucosal injury was observed in all animals subjected to ischemia/reperfusion and in three of six pigs in group P. A good association between pHi and lactate production was seen in ischemia/reperfusion. However, in sepsis, lactate in superior mesenteric venous blood or in intestinal perfusate did not increase, despite the fall in pHi. The mechanism causing ischemic mucosal injury has different characteristics in sepsis and in ischemia caused by arterial occlusion.

Effects of pneumoperitoneum on splanchnic hemodynamics: an experimental study in pigs.

OBJECTIVE: To study the effects on splanchnic haemodynamics of pneumoperitoneum induced by carbon dioxide insufflation. DESIGN: Controlled experimental study. ANIMALS: 11 Pigs weighing 19-30 kg. INTERVENTION: The animals were divided into a control group (n = 4) and a experimental group (n = 7). Experimental animals were subjected to stepwise increasing intra-abdominal pressure from 0 mm Hg to 25 mm Hg by carbon dioxide insufflation. MAIN OUTCOME MEASURES: Portal venous blood flow, portal venous blood pressure, portal/hepatic vascular resistance, and gastrointestinal vascular resistance. RESULTS: At 25 mm Hg portal venous blood flow was reduced (66% of baseline), and portal venous blood pressure and portal/hepatic vascular resistance were increased (360% and 650% of baseline, respectively). The increase in gastrointestinal vascular resistance was less pronounced. CONCLUSIONS: Increased intra-abdominal pressure caused significant changes in the splanchnic haemodynamics. The risk was greater if the intra-abdominal pressure exceeded 15 mm Hg.

Acute cholecystitis in the elderly.

After a controlled randomized trial, the management of patients with acute cholecystitis was changed from delayed to early cholecystectomy. The results obtained in 125 consecutive patients some years before the trial and in 144 consecutive patients after the trial were compared. All patients were 70 years or older. The comparison confirmed that early cholecystectomy reduces morbidity and mortality. Early cholecystectomy for acute cholecystitis in the elderly is strongly recommended.