Increased circulating D-lactate levels predict risk of mortality after hemorrhage and surgical trauma in baboons.

Patients with hemorrhagic shock and/or trauma are at risk of developing colonic ischemia associated with bacterial translocation that may lead to multiple organ failure and death. Intestinal ischemia is difficult to diagnose noninvasively. The present retrospective study was designed to determine whether circulating plasma D-lactate is associated with mortality in a clinically relevant two-hit model in baboons. Hemorrhagic shock was induced in anesthetized baboons (n = 24) by controlled bleeding (mean arterial pressure, 40 mmHg), base excess (maximum -5 mmol/L), and time (maximum 3 h). To mimic clinical setting more closely, all animals underwent a surgical trauma after resuscitation including midshaft osteotomy stabilized with reamed femoral interlocking nailing and were followed for 7 days. Hemorrhagic shock/surgical trauma resulted in 66% mortality by day 7. In nonsurvivor (n = 16) hemorrhagic shock/surgical trauma baboons, circulating D-lactate levels were significantly increased (2-fold) at 24 h compared with survivors (n = 8), whereas the early increase during hemorrhage and resuscitation declined during the early postresuscitation phase with no difference between survivors and nonsurvivors. Moreover, D-lactate levels remained elevated in the nonsurvival group until death, whereas it decreased to baseline in survivors. Prediction of death (receiver operating characteristic test) by D-lactate was accurate with an area under the curve (days 1-3 after trauma) of 0.85 (95% confidence interval, 0.72-0.93). The optimal D-lactate cutoff value of 25.34 µg/mL produced sensitivity of 73% to 99% and specificity of 50% to 83%. Our data suggest that elevation of plasma D-lactate after 24 h predicts an increased risk of mortality after hemorrhage and trauma.

Nitric oxide-supplemented resuscitation improves early gastrointestinal blood flow in rats subjected to hemorrhagic shock without late consequences.

BACKGROUND: we have shown that hemorrhage/resuscitation altered gastrointestinal blood flow (GI-BF) and that gastric perfusion did not recover after resuscitation. This study aimed to determine the effect of nitric oxide (NO) supplemented resuscitation on the mean arterial blood pressure (MAP), GI-BF, and outcome after hemorrhagic shock. METHODS: rats were subjected to hemorrhage and resuscitation with/without the NO-donor S-nitroso human serum albumin (S-NO-HSA). GI-BF was determined using colored microspheres. RESULTS: NO supplementation significantly decreased MAP at the end of resuscitation. At the same time point, the GI-BF has significantly increased in the stomach, duodenum, and colon. Two hours after treatment discontinuation, there was no difference in either MAP or GI-BF between NO-supplemented and control groups. The survival times indicated that S-NO-HSA treatment was noninferior compared with control. CONCLUSIONS: NO-supplemented resuscitation improves the GI-BF during the early stage of resuscitation without a negative impact on short-/long-term survival despite a transient MAP decrease.

Intermittent hepatic portal vein gas complicating diverticulitis--a case report and literature review.

CASE REPORT: This report describes a case of intermittent hepatic portal venous gas (HPVG) because of colonic diverticulitis in a 48-year-old man, who was successfully treated by surgery. CONCLUSION: Based on an extensive literature search, which produced 21 observations, the etiology, symptoms, imaging features, clinical significance, treatment strategy, and outcome of HPVG because of colonic diverticulitis are evaluated: While observations with an underlying intramesocolic abscess carry a favorable prognosis, the prognosis of observations because of septic thrombophlebitis with gas forming germs is poor.

[Appendix vermiformis duplex--a rare surprise]. / Appendix vermiformis duplex -- Eine seltene Uberraschung.

Duplication of the vermiform appendix is extremely rare. It is found in only 1/25.000 patients (0.004%) operated on for acute appendicitis. A 60-year-old male patient was hospitalized for a peridiverticular sigmoid abscess without signs of a free abdominal perforation and an abscess cavity in the small pelvis. A Hartmann's resection and an appendectomy (the vermiform appendix was part of the abscess wall) were performed. The pathology report described an external appendicitis. After 3 months, the intestine was successfully reanastomosed. During mobilisation of the coecum, a second retrocoecal vermiform appendix was surprisingly found. Because of signs of a chronic appendicitis a second resection was performed. Although the diagnosis of an appendix duplex is a rarity, surgeons should be aware of the possibility, especially when clinical signs and symptoms point to appendicitis, although at laparotomy the appendix looks normal. A routine exploration for a second appendix is definitely not indicated because of the rarity and the increased complication rate.

Mechanisms of vasodilatation induced by nitrite instillation in intestinal lumen: possible role of hemoglobin.

It has been shown that nitrite can be reduced to nitric oxide (NO) in intestine and a number of other tissues and released into the blood to form nitrosylhemoglobin (NO-Hb), existing in an equilibrium with S-nitrosohemoglobin. The latter has been suggested to be an NO transporter to distant organs. The aim of this study was to define the pathway of nitrite reduction to form NO in intestinal wall and to estimate whether this pathway has an effect on peripheral circulation. We have shown that in rat intestine at pH 7.0 70% of nitrite is converted to NO in mitochondria. At pH 6.0, nonenzymatic nitrite reduction becomes as efficient as the mitochondrial pathway. To prove whether the NO formed from nitrite in intestine can induce vasodilatation, sodium nitrite was instilled into intestinal lumen and the concentration of NO formed and diffused into the blood was followed by measuring of NO-Hb complex formation. We found that the concentration of NO-Hb gradually increases with the increase of nitrite concentration in intestinal lumen. However, it was not always accompanied by a decrease in systemic blood pressure. Blood pressure dropped down only after NO-Hb reached a threshold concentration of approximately 10 microM. These data show that NO-Hb cannot provide enough NO for vasodilatation if the concentration of NO bound to Hb is < 10 microM. The exact mechanism underlying vasodilatation observed when the concentration of NO-bound Hb was > 10 microM is, however, not clear yet and requires further studies.

Hemorrhage- and resuscitation-related alterations in gastrointestinal circulation: effect of a low dose of L-NMMA.

The gastrointestinal tract, including its mucosal barrier, is most sensitive to ischemic insults. The present study was conducted to evaluate hemorrhage- and resuscitation-related regional alterations in gastrointestinal circulation in presence or absence of a low dose of N(G)-monomethyl-L-arginine (L-NMMA), a nonspecific nitric oxide synthase inhibitor. Organ-specific circulation was studied using the colored microsphere technique in rats subjected to prolonged hemorrhagic shock (180 min) followed by resuscitation with or without L-NMMA (2 mg/kg body weight) treatment at the end of resuscitation. We found an initial distal gradient in the intestinal blood flow with the highest rate in duodenum followed by jejunum, ileum, and colon. Hemorrhage resulted in the highest decrease in gastric blood flow. Resuscitation restored circulation in the intestinal tract to baseline levels except for gastric blood flow. L-NMMA treatment after completion of resuscitation did not deteriorate gastrointestinal blood flow. Our data show (a) a distal gradient in the intestinal blood flow from duodenum to colon, (b) that hemorrhage and resuscitation cause different degrees of alteration in gastric and intestinal blood flow, (c) that gastric perfusion does not recover after resuscitation, predisposing to further organ damage, and (d) that a low dose of L-NMMA does not deteriorate intestinal circulation in rats subjected to hemorrhage and resuscitation.

Nitric oxide synthase inhibitors affect nitric oxide synthesis in normoxic but not in ischemic organs during intestinal ischemia and early reperfusion.

Inhibition of endogenous nitric oxide (NO) synthesis during early intestinal ischemia/reperfusion (I/R(i)) enhances remote organ damage related to I/R(i). However, the effects of NO synthase (NOS) inhibitors on NO formation in various organs have not yet been specified. We therefore investigated the effects of N-G-monomethyl-L-arginine (L-NMMA), a nonspecific NOS inhibitor, and L-arginine, the NOS substrate, on NO formed in ischemic intestine versus normoxic remote organs (lung and liver). We used electron paramagnetic resonance spectroscopy and a specific NO trap to assay NO in blood, intestine, lung, and liver of rats subjected to local I/R(i), with and without L-NMMA and L-arginine supplementation. We found that I/R(i) increased NO levels in the intestine and blood, but not in the remote organs lung and liver. Administration of L-NMMA before I/R(i) decreased I/R(i)-independent basal NO levels in normoxic lung and liver without influencing I/R(i)-induced increase in NO levels in intestinal tissue or in blood. L-arginine supplementation increased circulating levels of NO, with sensitivity to L-NMMA, without affecting NO levels in normoxic or ischemic tissue. Our data suggest that NOS activity controls the NO generated in normally perfused remote organs during early I/R(i). Hence NOS inhibitors, when administered during I/R(i), decrease physiological NO levels in normoxic remote organs without affecting increased NO levels originating from ischemic intestine. This may explain the harmful effect of nonspecific NOS inhibitors during early I/R(i). In addition, the generation of NO in remote organs is not limited by tissue L-arginine concentrations and, therefore, not influenced by exogenous L-arginine. The protective effect of L-arginine supplementation during I/R(i) is probably related to increasing intravascular NO formation.