Splanchnic Ischemia Research Articles

Treatment of mild acute pancreatitis during pregnancy using retrograde cholangiography and endoscopic sphincterotomy

normalization occurred within next 36 to 48 h. During endoscopy, the first case was identified as a gallstone-induced AP, the second one as idiopathic and suspected of occult microlithiasis, the third one was due to microvascular abnormalities-induced splanchnic ischemia, and the fourth one was a stenotic papillitis. No early recurrence of pancreatitis or fetal loss occurred. Results suggest that emergency papillotomy may have both diagnostic and therapeutic significance, with the minimal risk of post-sphincterotomy AP, and without an increase in the risk of fetal loss. Prevailing guidelines on AP management state that only patients with the severe type of disease should undergo urgent papillotomy [2,3] (the gold standard in the definitive treatment of the biliary AP), however consideration should be given to extending the therapeutic indications for emergency papillotomy to mild and idiopathic types of gestational AP. The risk of AP recurrence is 3-fold higher if previous AP was treated without papillotomy and next 10% of patients are suspected of having chronic pancreatitis in the future [4].

Splanchnic ischemia and gut permeability after acute brain injury secondary to intracranial hemorrhage

Splanchnic ischemia (SI) and increased gut permeability (GP) have been described in acute brain injury (ABI), although their incidence and relation to the type and severity of injury are uncertain. The aim of this study was to evaluate the incidence of both abnormalities in a series of patients with severe ABI secondary to intracranial hemorrhage (ICH) managed with a resuscitation protocol pursuing adequate cerebral and systemic hemodynamics. Eight patients with severe ABI secondary to ICH were admitted to the ICU and were mechanically ventilated and monitored with intracranial pressure measurement, jugular bulb venous oxygen saturation, arterial lactate concentration and gastric tonometry. All patients were managed actively to maintain adequate blood and cerebral perfusion pressures with a protocol based on aggressive fluid resuscitation prior to vasoactive drugs administration. GP was assessed using the lactulose/mannitol test (LMT). Values were recorded during the first 7 days of hospital stay. Arterial lactate concentration was within the normal range (1.9 +/- 0.5 mmol/l) in all patients. Upon admission, the mean pCO(2) gap was 8.2 +/- 4.3 mmHg (1.09 +/- 0.57 kPa) with an intramucosal pH of 7.4 +/- 0.1. All patients had an abnormal LMT (0.066 +/- 0.055) compared with 19 healthy volunteers (0.025 +/- 0.004) (p < 0.05, Mann Whitney test). Splanchnic ischemia is uncommon among patients with acute brain injury secondary to intracranial hemorrhage, provided they are adequately resuscitated with a protocol based mainly on fluids to achieve an adequate CPP. Gut hyperpermeability is commonly present, despite the absence of splanchnic ischemia.

Splanchnic ischemia and reperfusion injury is reduced by genetic or pharmacological inhibition of TNF-α

In the present study, we used TNF-alpha receptor 1 knockout (TNF-alphaR1KO) mice to evaluate a possible role of TNF-alpha on the pathogenesis of ischemia and reperfusion injury of the multivisceral organs. Ischemia and reperfusion injury was induced in mice by clamping the superior mesenteric artery and the celiac artery for 30 min, followed thereafter by reperfusion. Sixty minutes after reperfusion, animals were killed for histological examination and biochemical studies. Injured wild-type (WT) mice developed a significant increase of ileum TNF-alpha levels, myeloperoxidase activity, and marked histological injury and apoptosis. Ischemia and reperfusion injury of the multivisceral organs was also associated with a significant mortality. Reperfused ileum sections from injured WT mice showed positive staining for P-selectin, VCAM, ICAM-1, and E-selectin. The intensity and degree of P-selectin, E-selectin, VCAM, and ICAM-1 were reduced markedly in tissue sections from injured TNF-alphaR1KO mice. Ischemia and reperfusion-injured TNF-alphaR1KO mice also showed a significant reduction of neutrophil infiltration into the intestine, a reduction of apoptosis, an improved histological status of the intestine, and survival. In addition, we investigated the effect of Etanercept, a TNF-alpha soluble receptor construct, on ischemia and reperfusion injury of the multivisceral organs. Etanercept (5 mg/kg administered i.p. 5 min prior to reperfusion) significantly reduced the inflammatory response and the ileum injury. Taken together, our results clearly demonstrate that TNF-alpha plays an important role in the ischemia and reperfusion injury and put forward the hypothesis that modulation of TNF-alpha expression may represent a novel and possible strategy.

Transient Profound Mesenteric Ischemia Strongly Affects the Strength of Intestinal Anastomoses in the Rat

Experimental data suggest that transient preoperative ischemia and reperfusion may compromise anastomotic strength. However, data on this subject are equivocal, in particular as to the onset and duration of this effect. This study was designed to comprehensively characterize the effects of profound transient intestinal ischemia on anastomotic healing during the first postoperative week. Ischemia was induced in rats by clamping both the superior mesenteric artery and ileal branches for 30 minutes. Immediately after declamping, anastomoses were constructed in both terminal ileum and descending colon. After three, five, or seven days, both bursting pressure and breaking strength were measured. Anastomotic collagen content, gelatinase activity, and histology were analyzed. Anastomotic leakage rate was 13 percent in ischemia-reperfusion group and 0 percent (P=0.02) in controls. The breaking strength in ileum remained significantly (P<0.05) lower in the ischemic groups than in the control groups at all time points. Bursting pressure in the ileum was not significantly different between ischemic and control groups at either of the time points measured. However, at Day 7 the bursting site was significantly more frequent within the suture line in the ischemic groups. In the colon, at Day 3 the bursting pressure was 35 percent lower in the ischemic group than in the control group (P<0.05). Anastomotic collagen content and gelatinase activity were similar in ischemic and control groups. Transient profound splanchnic ischemia compromises anastomotic strength throughout the entire first postoperative week. This effect does not seem to be caused by impaired accumulation of wound collagen.

Membrane microdialysis: Evaluation of a new method to assess splanchnic tissue metabolism*

Measuring peritoneal lactate concentrations could be useful for detecting splanchnic hypoperfusion. The aims of this study were to evaluate the properties of a new membrane-based microdialyzer in vitro and to assess the ability of the dialyzer to detect a clinically relevant decrease in splanchnic blood flow in vivo. A membrane-based microdialyzer was first validated in vitro. The same device was tested afterward in a randomized, controlled animal experiment. University experimental research laboratory. Twenty-four Landrace pigs of both genders. In vitro: Membrane microdialyzers were kept in warmed sodium lactate baths with lactate concentrations between 2 and 8 mmol/L for 10-120 mins, and microdialysis lactate concentrations were measured repeatedly (210 measurements). In vivo: An extracorporeal shunt with blood reservoir and roller pump was inserted between the proximal and distal abdominal aorta, and a microdialyzer was inserted intraperitoneally. In 12 animals, total splanchnic blood flow (measured by transit time ultrasound) was reduced by a median 43% (range, 13% to 72%) by activating the shunt; 12 animals served as controls. In vitro: The fractional lactate recovery was 0.59 (0.32-0.83) after 60 mins and 0.82 (0.71-0.87) after 90 mins, with no further increase thereafter. At 60 and 90 mins, the fractional recovery was independent of the lactate concentration. In vivo: Abdominal blood flow reduction resulted in an increase in peritoneal microdialysis lactate concentration from 1.7 (0.3-3.8) mmol/L to 2.8 (1.3-6.2) mmol/L (p = .006). At the same time, mesenteric venous-arterial lactate gradient increased from 0.1 (-0.2-0.8) mmol/L to 0.3 (-0.3 -1.8) mmol/L (p = .032), and mesenteric venous-arterial Pco2 gradients increased from 12 (8-19) torr to 21 (11-54) torr (p = .005). Peritoneal membrane microdialysis provides a method for the assessment of splanchnic ischemia, with potential for clinical application.

Intraperitoneal microdialysis: Postoperative monitoring of splanchnic ischemia by measurements of the lactate pyruvate ratio*

Department of Intensive Care and Anaesthesiology, University Hospital of Örebro, Örebro, Sweden (Jansson) Department of Surgery, University Hospital of Örebro, Örebro, Sweden (Strand) Department of Surgery, University Hospital of Örebro, Örebro, Sweden (Jansson) Drs. Jansson, Strand, and Jansson were supported in part by a grant from CMA Microdialysis AB.

Barrera intestinal del paciente crítico: realidades y tendencias

The disturbances of gut barrier in critically ill patients may influence their outcome and prognosis. Experiments in animals show that fasting and stress collaborate to produce intestinal atrophy and translocation of microorganisms and toxins. This fact is one of the main arguments to promote the use of early enteral feeding in critically ill patients. However, the intestinal barrier behaves differently in humans than in animals. The human enteral cells have a good tolerance to fasting and stress, mucosal atrophy is mild and it is not always associated with changes in intestinal permeability. Moreover, the relationship between intestinal permeability with sepsis and bacterial translocation is controversial. This last phenomenon also happens in normal subjects and may be a mechanism to build immunological memory. One of the most important factors that influence bacterial translocation is the microorganism, that under stress conditions can adhere to the intestinal cell and penetrate the intestinal barrier. Splanchnic ischemia and reperfusion is one of the main pathogenic factors in the failure of intestinal barrier. Finally, the fact that the small bowel is an inflammatory target of extra intestinal injuries, explains several clinical situations. The pathophysiology of the intestinal barrier definitely requires more research.

Electro-optical techniques for the investigation of photoplethysmographic signals in human abdominal organs

There is a need for reliable continuous monitoring of abdominal organ oxygen saturation (SpO2). Splanchnic ischaemia may ultimately lead to cellular hypoxia and necrosis and may well contribute to the development of multiple organ failures and increased mortality. A new reflectance electro-optical photoplethysmographic (PPG) probe and signal processing system were developed. PPG signals from abdominal organs (bowel, liver, and kidney) and the finger were obtained from 12 anaesthetised patients. The amplitudes of the abdominal organ PPGs were, on average, approximately the same as those obtained simultaneously from the finger. These observations suggest that pulse oximetry may be a valid monitoring technique for abdominal organs such as the bowel liver and kidney.

Rapid decrease in plasma D-lactate as an early potential predictor of diminished 28-day mortality in critically ill septic shock patients

Splanchnic ischemia plays a major role in the development of organ failure during septic shock. Plasma D-lactate has been proposed as a better marker of splanchnic hypoperfusion than L-lactate. We studied the prognostic ability of plasma D- and L-lactate levels. A prospective study was performed in an intensive care unit and included patients with septic shock. Two samples for plasma D- and L-lactate determination were collected: the first within 6 h after the patient met the criteria for septic shock (day 1) and the second 24 h later (day 2). In univariate analysis, day 1 plasma D- and L-lactate values were associated with 28-day mortality. For plasma D- and L- lactate, the area under the receiver operating characteristic curve was 0.68+/-0.09 and 0.84+/-0.07 on day 1 (p=0.09), and 0.74+/-0.10 and 0.90+/-0.07 on day 2 (p=0.06), respectively. In survivors, D-lactate levels decreased between day 1 and day 2 (p=0.03), but L-lactate did not (p=0.29). In septic shock patients, plasma D- and L-lactate levels reliably discriminate between survivors and non-survivors. The prognostic ability of plasma L-lactate was better than that of plasma D-lactate. A rapid decrease in plasma D-lactate during the course of septic shock could indicate reduced 28-day mortality.

Alterations In Liver Function Tests Following Laparoscopic Cholecystectomy

Background: The pneumoperitoneum and the resulting high intraabdominal pressure may have several systemic effects including splanchnic ischemia. Disturbances of liver function tests following laparoscopic cholecystectomy have been previously reported although their etiology still remains uncertain. This prospective study was planned to explore further the incidence and significance of this alteration. Materials and Methods: Over a two-year period, laparoscopic cholecystectomy was performed in 262 consecutive patients with symptomatic cholelithiasis. Total and indirect bilirubin (TB and IB), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and a-glutamyl-transpeptidase (γ-GT) were tested preoperatively as well as 24 hours following surgery. Strict exclusion criteria were adopted in order to eliminate any known cause of possible liver function disturbances. Results: Totally 198 patients fulfilled the criteria and were included in the study. A statistically significant increase of TB, IB, ASP, ALT and a significant decrease of ALP were noted postoperatively, whereas γ-GT showed slight not significant elevation. A 48.4% mean increase of TB value, duplication of IB in 16% of cases, and an up to 100% mean increase of both ASP and ALT values were seen. Conclusion: Transient alterations of hepatic enzymes are frequently observed after uneventful laparoscopic cholecystectomy, presumably attributed to the elevated intraabdominal pressure of the pneumoperitoneum. Further studies could enlighten the exact pathogenetic mechanism.

Oxygen Consumption, pCO 2 Gradients and Regional Blood Flow Distribution in an Alternative Model of Intestinal Autotransplantation 1

Postoperative complications after intestinal transplantation can be attributed to hypothermic storage and reperfusion injury. Our objective was to evaluate, in an alternative model of intestinal autotransplantation, the initial effects of isolated intestinal hypothermic perfusion (at 4 degrees C, IHP) on mucosal and serosal blood flow distribution and correlate these findings with other systemic and regional markers of mesenteric ischemia. In addition, we sought to obtain evidence that intestinal pCO2 measurement can be a useful method for monitoring graft perfusion and early histological changes after small bowel transplantation. Eight dogs (23.3+/-1.1 kg) were submitted to a in situ IHP for 30 min, followed by a 180-min reperfusion period. Cardiac output, mesenteric vein, and intestinal serosal blood flows (SMVBF and SBF, ultrasonic flowprobe); intestinal mucosal-arterial pCO2 gradient (Dt-apCO2, tonometry); and O2-derived variables were evaluated. IHP induced a reduction in SMVBF (579+/-53 to 321+/-10 mL/min) and SBF, (44.7+/-3.2 to 29.1+/-5.3 mL/min), and an increase in Dt-apCO2 (2+/-2.8 to 20.5+/-4.5 mm Hg). No alterations on systemic metabolic or O2-derived variables were observed. The increase of the Dt-apCO2 correlated with the grade of mucosal injury. IHP induces a proportional reduction on blood flow in all layers of the intestine, and none of the systemic markers of splanchnic ischemia predict the intestinal blood flow disturbances during the early phase of intestinal transplantation. In addition, intestinal pCO2 measurement seems to be a useful way for monitoring graft perfusion and histological changes after hypothermic ischemia and reperfusion.

Postoperative changes in liver function tests: randomized comparison of low- and high-pressure laparoscopiccholecystectomy

Pneumporeitoneum at 14 mmHg causes dangerous hemodynamic disturbances in some patients, leading to splanchnic ischemia. Laparoscopic cholecystectomy (LC) using low-pressure pneumoperitoneum (7 mmHg) minimizes adverse hemodynamic effects on hepatic portal blood flow and hepatic function. This study evaluated the changes in liver function tests after high-pressure LC (HPLC; 14 mmHg) and low-pressure LC (LPLC; 7 mmHg). For this study, 50 patients were randomly assigned to undergo either HPLC (n = 25) or LPLC (n = 25) Liver function tests including total bilirubin, gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were obtained preoperatively, then 24 and 48 h postoperatively. All patients had normal values on the preoperative liver function tests. The anesthesiologic protocol was uniform. The findings showed that ALT after 24 h (LPLC: 1473.72 +/- 654.85; HPLC: 2233.74 +/- 1247.33; p = 0.0096) and 48 h (LPLC: 1322.99 +/- 601.51; HPLC 2007.80 +/- 747.55; p = 0.0008) and AST after 24 h (LPLC: 1189.96 +/- 404.79 i.j.; HPLC: 1679.40 +/- 766.13; p = 0.0069) were increased in the patients who underwent HPLC. The AST levels after 48 h were statistically unchanged from baseline in both groups. Total bilirubin, ALP, and GGT levels remained unchanged from baseline in both groups, without a significant difference between the two groups. Because LPLC minimizes adverse hemodynamic effects on hepatic function, a low-pressure pneumoperitoneum should be considered for patients with compromised liver function, particularly those undergoing prolonged laparoscopic surgery.

Oxidative Stress Markers After Laparoscopic and Open Cholecystectomy

Surgical injury is associated with oxidative stress, often due to ischemia/reperfusion injury. During laparoscopy, increased intra-abdominal pressure caused by pneumoperitoneum may cause splanchnic ischemia followed by reperfusion due to deflation. We measured several markers of oxidative stress in patients undergoing laparoscopic cholecystectomy (LC) versus open cholecystectomy (OC) to find if these surgical procedures result in different patterns of oxidative stress. This prospective study enrolled 43 patients with symptomatic cholelithiasis, of whom 21 underwent open, and 22 laparoscopic, cholecystectomy. Twenty healthy adults comprised the control group. Total antioxidant status (TAS), superoxide dismutase (SOD), endogenous peroxide level (POX), oxidized low density lipoprotein (oLDL) autoantibodies (oLAb), and neopterin were measured preoperatively and on postoperative days 1, 3, and 7. POX values decreased significantly on postoperative day 1 in the OC (P<0.01), but not in the LC, group. On postoperative day 7, POX values were higher than preoperatively in both groups (P<0.01) with no difference between the LC and OC groups. Significant postoperative elevations of oLAb and neopterin levels were observed only on postoperative day 7 in the OC group. There were no changes of oLAb and neopterin levels in the LC group. TAS and SOD levels did not change after either LC or OC. Cholecystectomy, either open or laparoscopic, caused only moderate oxidative stress. Open cholecystectomy caused changes of oLAb and neopterin, suggesting more severe oxidative stress, and a possible role of reactive oxygen species in the healing of the laparotomic wound.

Increased Intra-Abdominal Pressure Causes Bacterial Translocation in Rabbits

Abdominal compartment syndrome (ACS) is defined as intra-abdominal hypertension associated with organ dysfunction. Subsequently, increased intra-abdominal pressure (IAP) adversely affects the pulmonary, cardiovascular, renal, musculoskeletal/integumentary and central nervous systems. Bacterial translocation (BT), which is defined as the movement of viable enteric bacteria to the mesenteric lymph nodes, liver and spleen, occurs after various types of stress and results in splanchnic ischemia. In this experimental study, we aimed to investigate the effects of various levels of increased IAP on BT in rabbits; IAP was increased by the intra-abdominal balloon-insufflation method, thus simulating noncompliant abdominal-wall closure under tension. Fifty rabbits were randomly assigned to 1 of 5 groups, with each group comprising 10 animals. In group I (control group), an intra-abdominal balloon was placed without inflation. In groups II, III, IV and V, IAPs of 10, 15, 20 and 25 mmHg, respectively, were established via inflation of the intra-abdominal balloon. All groups underwent laparotomy after 12 hours. Multiple biopsies were taken from ileocecal lymph nodes, the spleen and liver. BT was observed to some degree in all 4 experimental groups. A gradual increase in the phenomenon was noted as IAP increased from 10 to 15 mmHg; and BT was overt at 20 mmHg, and significant at 25 mmHg. Klebsiella pneumoniae, Serratia marcescens, and Escherichia coil were the predominant pathogens identified by culture. We propose that an intravesical pressure (IVP) of 15 mmHg is the critical point for BT in patients with increased IAP. In this experimental study, BT occurred when IVP reached 20 mmHg. We suggest that IVP monitoring is desirable in the management of patients with ACS, and that decompressive laparotomy should be performed in patients with IVP >20 mmHg.

PARG activity mediates intestinal injury induced by splanchnic artery occlusion and reperfusion

Poly (ADP-ribosyl)ation, an early post-translational modification in response to DNA damage, is catalyzed by poly (ADP-ribose) polymerase (PARP-1) and catabolized by poly(ADP-ribose) glycohydrolase (PARG). The aim of this study was to investigate the role of PARG on the modulation of the inflammatory response caused by splanchnic ischemia and reperfusion. SAO shock in rats and wild-type (WT) mice was associated with a significant neutrophil infiltration in the ileum and production of tumor necrosis factor-alpha (TNF-alpha). Reperfused ileum tissue sections from SAO-shocked WT mice and rats showed positive staining for P-selectin and ICAM-1 localized mainly in the vascular endothelial cells. Genetic disruption of the PARG gene in mice or pharmacological inhibition of PARG by PARG inhibitors significantly improved the histological status of the reperfused tissues associated with reduced expression of P-selectin and ICAM-1, neutrophil infiltration into the reperfused intestine, and TNF-alpha production. These results suggest that PARG activity modulates the inflammatory response in ischemia/reperfusion and participates in end (target) organ damage under these conditions.

Levosimendan is superior to milrinone and dobutamine in selectively increasing microvascular gastric mucosal oxygenation in dogs*

The effect of levosimendan, a novel inotropic vasodilator (inodilator), on the microvascular gastric mucosal hemoglobin oxygenation (muHbo(2)) is unknown. A possible effect could thereby be selective for the splanchnic region or could primarily reflect changes in systemic oxygen transport (Do(2)) and/or oxygen consumption (Vo(2). We compared systemic and regional effects of levosimendan with those of established inotropes, milrinone and dobutamine. Laboratory experiment. University animal research laboratory of experimental anesthesiology. Chronically instrumented dogs with flow probes for cardiac output measurement. Anesthetized, mechanically ventilated dogs (each group n = 6) on different days randomly received levosimendan (10 microg.kg, followed by four infusion steps: 0.125-1.0 microg.kg.min), milrinone (5.0 microg.kg, followed by 1.25-10 microg.kg.min), or dobutamine (2.5-10.0 microg.kg.min). Since these drugs may modify regional or systemic responses to fluid load, an additional predefined volume challenge was subsequently performed with hydroxyethyl starch 6% (10 mL.kg). We measured muHbo(2) (reflectance spectrophotometry), Do(2), Vo(2), and systemic hemodynamics. Levosimendan significantly increased muHbo(2) from baseline (approximately 55% for all groups) to 64 +/- 4% and further to 69 +/- 2% with volume challenge (mean +/- sem). At the systemic level, levosimendan alone only slightly increased Do(2) at a Vo(2). Milrinone elicited similar systemic effects (Do(2), Vo(2), hemodynamics) but failed to increase muHbo(2). Dobutamine, conversely, increased muHbo(2) to a similar extent as levosimendan; however, this was accompanied by marked increases in Do(2) and Vo(2). The gastric mucosa selectivity of these interventions, expressed as slope of the muHbo(2)/Do2 relation, was highest for levosimendan (+1.89 and +1.14, without and with volume challenge), compared with milrinone (+0.45 and + 0.47) and dobutamine (+0.48 and + 0.33). Levosimendan is superior to milrinone (no significant regional effects) and dobutamine (marked systemic effects) in increasing gastric mucosal oxygenation selectively (i.e., at only moderately increased Do(2) and stable Vo(2). If our experimental data apply to the clinical setting, levosimendan may serve as an option to selectively increase gastrointestinal mucosa oxygenation in patients at risk to develop splanchnic ischemia.

Abdominal organ injury after cardiac surgery.

Gastrointestinal complications occur in about 2.5% of patients undergoing cardiac surgery, are associated with a high mortality (about 33%), and account for nearly 15% (and perhaps increasing) of all postoperative deaths. The various complications and risk factors are reviewed. Splanchnic ischemia prior to, during, and especially postoperatively appears to be an important cause of these complications. In addition, splanchnic ischemia is hypothesized to be one cause of the systemic inflammatory response syndrome and multiorgan failure that may follow cardiac surgery. The physiology of splanchic perfusion and the effects of cardiac surgery, including cardiopulmonary bypass, on it are reviewed. Finally, possible methods to minimize splanchnic ischemia and reduce the incidence of abdominal complications are discussed.

Early enteral feedings in adults receiving venovenous extracorporeal membrane oxygenation.

For over 20 years extracorporeal membrane oxygenation (ECMO) has been an advanced treatment for adults, children and neonates with severe respiratory failure that has failed to respond or improve with conventional therapy. Withholding enteral feeding in patients on ECMO is common practice in many centers, based partly on the risk of splanchnic ischemia resulting in loss of intestinal integrity, predisposing to bacterial translocation and sepsis. We report one center's experience with early enteral nutrition in adult patients receiving venovenous (VV) ECMO for severe respiratory failure. Adult patients that received VV ECMO at LSUHSC-Shreveport over the last 8 years were eligible for inclusion. A total of 27 patients met these criteria and their charts and nutrition therapy reviewed. Average duration of ECMO support was 8.7 +/- 3.6 days. Twenty-six of 27 (96%) received enteral nutrition via gastric tube alone or in combination with total parenteral nutrition (TPN). Eighteen patients received enteral nutrition as their only source of nutritional supplementation, with the remainder receiving partial nutrition support via the parenteral route. Seventy-five percent of the patients received prokinetic medication within the first 24 hours, with 95% receiving prokinetic therapy by 48 hours. No patients developed intestinal ischemia, gastrointestinal bleeding, or other complications related to early enteral feeding. Enteral nutrition started within the first 24 to 36 hours of initiating venovenous ECMO support is safe and well-tolerated in adults. No serious adverse events were attributable to enteral nutrition in these patients.

Unspecific clinical presentation of bowel ischemia in the very old. Digitalis treatment - a reason for higher mortality?

Ischemic bowel disease predominantly affects the elderly (>65 years). Early diagnosis and treatment are of vital importance for the outcome. The vague symptoms of ischemic bowel disease entail a risk of delayed diagnosis, with a subsequent risk of increased mortality. The aims of this retrospective study were to identify symptoms and prodromes, to study factors associated with mortality in ischemic bowel disease, and to describe the influence of age, by comparing patients <80 and > or = 80 years. The subjects of the study were 135 patients, mean age 77 years, admitted to Malmö University Hospital, Sweden, between 1987 and 1996, with a ICD-9 diagnosis of acute or chronic splanchnic ischemia. Patients aged 80 years or more presented with a significantly higher prevalence of confusion (29% vs 12%), hematemesis (57% vs 14%), vomiting (82% vs 65%) and dehydration (58% vs 36%) at admission compared with patients aged under 80 years, and presented a higher mortality (87% compared with 65%, p=0.003). The prevalence of digitalis treatment was 34%, which was high compared with other Swedish cohort studies. Digitalis, adjusted for age, congestive heart failure and atrial fibrillation, was associated with increased mortality (odds ratio 4.6, 95% CI 1.3-16.1). Prodromal signs predicted poor outcome, and were found in one out of 4 patients, without any age differences. Bowel ischemia in the very old is associated with a different clinical presentation and a higher mortality compared with younger patients. Digitalis treatment seems to be associated with increased mortality in ischemic bowel disease. Prodromal signs are prognostically unfavorable.

Splanchnic metabolism during gut ischemia and short-term endotoxin and hemorrhagic shock as evaluated by intravasal microdialysis.

The splanchnic area is of considerable interest in different types of shock. To characterize the metabolic changes in the splanchnic region in response to different types of shock we used a model where shock-induced metabolic changes in the splanchnic region were studied by the use of intravasal microdialysis. 23 anesthetized domestic pigs were randomized into four groups: Group I, serving as controls (n = 5); Group II, mesenteric ischemia for 180 followed by 120 min of reperfusion (n = 5); Group III, endotoxin shock for 5 h (n = 5); and Group IV, hemorrhagic shock for 180 min followed by re-transfusion of shed blood (n = 8). Microdialysis catheters were placed in the left femoral artery, portal vein and a small ileal mesenteric vein. Samples of the perfusate were continuously collected in micro-vials and analyzed for glucose, lactate, pyruvate and glycerol. In gut ischemia and endotoxin shock the outflow-pattern of lactate, lactate/pyruvate ratio and glucose in the mesenteric vein differed significantly from controls and hemorrhage whereas an increase in glycerol was only noted in the ischemic group. The most prominent differences were detected in lactate/pyruvate ratio, a marker of tissue ischemia with the most pronounced changes during mesenteric ischemia/reperfusion. During endotoxin shock increases in microdialysate metabolites were only noted in the splanchnic region suggesting a specific vulnerability in the region. Studying the lactate/pyruvate ratio may provide additional information when interpreting increased blood lactate levels. In addition glycerol may prove to be a useful marker of splanchnic ischemia. Intravasal microdialysis represents a potentially useful method for monitoring regional metabolic events.