Nihon Kyukyu Igakukai Zasshi
Online ISSN : 1883-3772
Print ISSN : 0915-924X
ISSN-L : 0915-924X
Volume 23, Issue 8
Displaying 1-6 of 6 articles from this issue
Review Article
  • Norifumi Ninomiya, Kayo Nemoto, Masamune Kuno
    2012Volume 23Issue 8 Pages 333-341
    Published: August 15, 2012
    Released on J-STAGE: September 17, 2012
    JOURNAL FREE ACCESS
    We have been conducting basic experiments on sepsis to gain further understanding of its pathophysiology and treatment. Guinea pig endotoxaemia models were used due to their LPS induced biological response and simple experimental procedure. We particularly focused on bowel movement paralysis after administration of LPS. We found that the peak reaction of intestinal tract relaxation was observed at 2-3 hours after administration of LPS in the guinea pig endotoxaemia model. During this period, there was a variety of ongoing inflammatory responses. We investigated bowel movement by using agonists and antagonists assumed to affect intestinal tract movement within the signal cascade. We carried out experiments using anandamide and 2-arachidonoilglycerol, which are endocannabinoids, as agonists; and used the following antagonists: polymyxin B immobilized fiber, which absorbs LPS; TAK-242, a TLR4 inhibitor; AM281 and rimonabant, which are CB1 receptor inhibitors; and meloxicam, a COX-2 inhibitor. It was observed that administration of cannabinoids induced bowel movement paralysis, as did LPS administration. LPS-induced bowel movement paralysis was significantly inhibited with pretreatment with each inhibitor. Based on these examinations, it is anticipated that endocannabinoids and arachidonate metabolites mediate bowel movement paralysis. It was also found that since PMX and TAK-242 had larger effects in the regulation of the paralysis, it is effective to eliminate causative substances within the early phase of sepsis. When treating sepsis patients, it is necessary to take into consideration the above mentioned mediators acting in the background to sepsis. Previous studies showed that treatments such as single mediator inhibition did not obtain good results, and inhibition of multiple mediators seems to be required.
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Original Article
  • Fumiaki Iwase, Tatsuho Kobayashi, Yoshibumi Miyazaki, Masahiko Maki, K ...
    2012Volume 23Issue 8 Pages 342-348
    Published: August 15, 2012
    Released on J-STAGE: September 17, 2012
    JOURNAL FREE ACCESS
    Objective: For coagulopathy in severe trauma patients requiring massive blood transfusion, we examined whether administration of fresh frozen plasma (FFP) would improve their outcome.
    Materials and Methods: We retrospectively evaluated trauma patients who were transported to our emergency department between January 2006 and December 2010 and received 8 units or more of red blood cell concentrates (RCC) within 24 h. Patients were divided on the basis of the ratio of FFP to RCC administered within 24 h into the low FFP/RCC group (n=51) and the high FFP/RCC group (n=54).
    Results: A total of 105 patients (average age, 56.3 ± 20.6 years old; 75 males (71.4%); injury severity score (ISS), 30.7 ± 11.3) met inclusion criteria. Age, sex, mechanism of injury, blood pressure, body temperature, ISS, revised trauma score, probability of survival, hemoglobin, prothrombin time, base excess, APACHE II, SOFA score, and RCC and platelet transfusion within 24 h were similar between the groups. The 24-h survival rate was significantly higher in the high FFP/RCC group (83.3%) than in the low FFP/RCC group (64.7%) (p<0.05). Survival to hospital discharge was also significantly higher in the high FFP/RCC group (74.1%) than in the low FFP/RCC group (54.9%) (p<0.05).
    Conclusion: For severe trauma patients requiring massive transfusion, aggressive administration of FFP has the potential to improve their outcome.
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Case Report
  • Norihisa Ninomiya, Tatsuya Sugino, Masanobu Kono, Kazuo Noguchi, Takes ...
    2012Volume 23Issue 8 Pages 349-356
    Published: August 15, 2012
    Released on J-STAGE: September 17, 2012
    JOURNAL FREE ACCESS
    We report two cases of dysphagia with different pathophysiologies. In Case 1, dysphagia occurred after anterior cervical spine surgery for a C5-level spinal cord injury. The symptom of difficulty in swallowing saliva was recognized ∼40 days postoperatively at the time of ventilator weaning. Dysphagia persisted even after weaning from ventilator (hospital day 56) and oxygen (hospital day 67). In Case 2, cervical necrotizing fasciitis and descending necrotizing mediastinitis were treated by transcutaneous catheter drainage. After drainage for ∼50 days, tracheostomy was performed. Dysphagia was found at the time of ventilator weaning. In both cases, dysphagia remained despite changing the tracheal tube. VFs were performed in a time series to assess the mechanism and degree of dysphagia. Bedside swallowing training was continued daily and the tracheal tube selection was considered. The dysphagia duration was ∼125 days in Case 1 and ∼150 days in Case 2. The dysphagia recovery period after changing to a cuffless tube was ∼45 days and ∼17 days, respectively. Dysphagia is not an urgent symptom, and may not be taken into consideration during emergency and critical care. In tracheostomy patients, appropriate tube selection should be carefully considered to shorten the placement duration, and swallowing function should be evaluated without delay by VFs if dysphagia persists.
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  • Kenya Kawakita, Yuko Abe, Kazutaka Kirizume, Natsuyo Shinohara, Nobuyu ...
    2012Volume 23Issue 8 Pages 357-363
    Published: August 15, 2012
    Released on J-STAGE: September 17, 2012
    JOURNAL FREE ACCESS
    Posterior reversible encephalopathy syndrome (PRES) is characterized by clinical symptoms of headache, disturbance of consciousness, seizures and visual disturbances. Neuroimaging shows brain edema, mainly in the occipital, parietal and temporal lobes and basal ganglia, and the clinical signs and abnormalities visible on imaging are always reversible. The most common causes of PRES are hypertensive encephalopathy, eclampsia, renal failure, and use of immunosuppressive agents and steroids. Pathologically, PRES is thought to be caused by disruption of the blood-brain barrier. We describe 5 patients with PRES. All patients were female (mean age, 33 years). At onset, the clinical manifestations were headache, seizure, visual disturbance and hypertension. On magnetic resonance imaging (MRI), most patients had brain edema in the occipital lobe, temporal lobe and basal ganglia, while 1 patient had brain stem and cerebellar edema, and another had a caudate nucleus hemorrhage. Most lesions revealed high signal intensities on apparent diffusion coefficient (ADC) maps and represented vasogenic edema pathologically. Receiving MRI examination at an early stage, patients were treated with antihypertensive and antiepileptic medications, and those who were pregnant immediately underwent a cesarean section. All patients made a complete recovery. In general, PRES has a benign course; however, delayed diagnosis and treatment may lead to increased morbidity. We need to consider PRES for patients with characteristic symptoms and causes. Prompt imaging examinations using mainly MRI and following appropriate therapy including removal of the causative factors, are critically important.
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  • Wataru Ishii, Ryoji Iiduka, Ken Shinoduka, Satoshi Higaki, Naoki Kakih ...
    2012Volume 23Issue 8 Pages 364-368
    Published: August 15, 2012
    Released on J-STAGE: September 17, 2012
    JOURNAL FREE ACCESS
    A 65-year old man was consulted to the emergency department of our hospital with a chief complaint of sudden abdominal pain. He was alert, had diffuse abdominal pain, and showed slight peritoneal signs. He had undergone total gastrectomy with Roux-Y reconstruction. The liver function was slightly impaired and the serum amylase level was markedly increased. Abdominal CT with contrast showed dilatation of the intestine and wall thickening of the intestine in the left abdomen, but blood flow in the intestinal wall was maintained. A long tube was inserted. Abdominal pain was still present five hours after admission, and abdominl CT was performed, whic revealed the dilatation of duodenum to anastomosis site of the small intestine. Intraoperative findings showed that the small intestine on the anal side was tucked inward to the space between the mesenterys at the afferent small bowel anastomosis site, and it had caused the internal hernia. As bowel necrosis was not observed, the intestine was restored, hernial orifice was closed, and surgery was completed. There are few reported cases of internal hernia after total gastrectomy, and so we report this case, along with a literature review.
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