The gut is the natural habitat for a large and dynamic bacterial community, and is considered an important target organ of injury following severe insult such as sepsis, trauma, and shock. Previous reports have shown that critically ill patients are susceptible to injury of the intestinal mucosa, changes in gut permeability, and failure of intestinal defense mechanisms. The impact of bacterial translocation and inflammatory mesenteric lymph on systemic inflammatory responses and multiple organ damage has been investigated in animals, but dynamic changes in the gut flora and environment have not been com-pletely elucidated in critically ill patients. We quantitatively evaluated changes in the gut microflora and environment in patients with SIRS and examined the effects of synbiotic treatment on clinical course. We show the following results with reviews on gut function in critically ill patients. 1) The gut flora and environment are significantly altered in patients with SIRS. Analysis of fecal flora confirmed that patients with SIRS showed significantly lower total anaerobic bacterial counts, in particular, 2-4log units fewer beneficial Bifidobacterium and Lactobacillus and 2log units more pathogenic Staphylococcus and Pseudomonas group counts than did healthy volunteers. Concentrations of total fecal organic acids, in particular, beneficial short-chain fatty acids such as acetic acid, propionic acid, and butyric acid, were significantly decreased in the patients, whereas pH was markedly increased. 2) Synbiotics maintain the gut flora and environment in patients with SIRS and significantly reduce the incidence of septic complications. The incidences of infectious complications in patients with SIRS were significantly lower in the synbiotics group than in the control group (enteritis, 7% vs. 46%, pneumonia, 20% vs. 52%, and bacteremia, 10% vs. 33%, respectively). These beneficial effects of synbiotics in the present study may be due to improved gut flora, increased short-chain fatty acids, and decreased pH. 3) Synbiotics may be used as a novel strategy to protect the critically ill patients from infectious complications. Further study is needed to clarify the mechanisms by which synbiotics decrease septic complications in patients with SIRS.

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Sivelestat sodium hydrate (sivelestat), a neutrophil elastase inhibitor, is used to treat acute lung injury (ALI) associated with systemic inflammatory response syndrome (SIRS). Effects of the agent on the intestine have not been elucidated. In the present study, the effects of sivelestat were investigated in LPS-induced intestinal paralysis in conscious guinea pigs, about which we reported previously. Intestinal movement and body temperature of guinea pigs were measured successively. Intestinal movement was observed by telemetry using a force transducer installed on the taenia caecum. Simultaneously, body temperature was measured using a plate-type thermometer attached to the dorsum of the animal. On the 4th post-operative day, when intestinal movement was stabilized, lipopolysaccharide (LPS, E. coli, 0111: B4) was administered intraperitoneally. In guinea pigs that received sivelestat 10min before and 1h after LPS administration, the intestinal relaxation and lowering of body temperature 2h after LPS administration were suppressed by sivelestat dose-dependently. Guinea pig plasma elastase activity increased significantly 2h after LPS administration. The increase was suppressed significantly by sivelestat. On histopathological examination, there was no neutrophil accumulation in the taenia caecum 2h after LPS administration at the dose used in the study. The above findings suggest that the neutrophil elastase inhibitor sivelestat is effective for LPS-induced intestinal paralysis.

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Superior mesenteric artery occlusion (SMAO) remains a challenge to those involved in its diagnosis and treatment. We report a case of SMAO improved by percutaneous transluminal angioplasty (PTA) without laparotomy. A 77-year-old man with hypertension, atrial fibrillation, angina pectoris and arteriosclerotic obliteration was admitted for epigastralgia and vomiting. Abdominal CT revealed complete occlusion of the SMA. Six hours after onset of this complaint, abdominal angiography was conducted to dilate the occlusive artery with balloon catheter. Immediately after the treatment, the embolic occlusion and symptoms resolved. The patient recovered well without laparotomy and was discharged 2 weeks later. The present case and a review of literature suggest that this treatment will be useful for achieving rapid and sufficient revascularization in SMAO if instituted within early times after the onset of embolic occlusion.

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We report a case of axonal Guillain-Barré syndrome (GBS) in which differential diagnosis from critical illness polyneuropathy (CIP) was difficult. A 64-year-old male patient was admitted to the ICU because of sepsis complicated with acute lung injury and acute renal failure after two weeks of oral medication for common cold-like symptoms. On the 7th ICU day, functions of impaired organs had improved, but weaning from mechanical ventilation was impossible because of insufficient volume of spontaneous breathing. On the 15th ICU day, the tracheal tube was extubated, but lack of spontaneous movement of the extremities and an absence of deep tendon reflex were found. On the 21st ICU day, since anti-mycoplasma antibody titer was found to be extremely high (×2, 560) on the 4th ICU day. Electrophysiological studies showed remarkable reduction in muscle action potentials combined with mild reduction of motor nerve conduction velocities (NCV) and normal sensory NCV. He was diagnosed as having acute motor axonal neuropathy type of GBS based on the results of these electrophysiological examinations. When preceding infection develops to sepsis, differential diagnosis of GBS from CIP may be difficult by clinical features. Therefore, differential diagnosis of CIP from GBS should be considered using electrophysiological examination when prolonged neuropathy occurs after sepsis treatment.

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