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文献 JAMA ヘリコプター広域搬送の有効性について

2012年04月27日 07時19分22秒 | 論文紹介 臨床研究
Association between helicopter vs ground emergency medical services and survival for adults with major trauma.
Galvagno SM Jr, Haut ER, Zafar SN, Millin MG, Efron DT, Koenig GJ Jr, Baker SP, Bowman SM, Pronovost PJ, Haider AH.
JAMA. 2012 Apr 18;307(15):1602-10.

Abstract
CONTEXT:
Helicopter emergency medical services and their possible effect on outcomes for traumatically injured patients remain a subject of debate. Because helicopter services are a limited and expensive resource, a methodologically rigorous investigation of its effectiveness compared with ground emergency medical services is warranted.
OBJECTIVE:
To assess the association between the use of helicopter vs ground services and survival among adults with serious traumatic injuries.
DESIGN, SETTING, AND PARTICIPANTS:
Retrospective cohort study involving 223,475 patients older than 15 years, having an injury severity score higher than 15, and sustaining blunt or penetrating trauma that required transport to US level I or II trauma centers and whose data were recorded in the 2007-2009 versions of the American College of Surgeons National Trauma Data Bank.
INTERVENTIONS:
Transport by helicopter or ground emergency services to level I or level II trauma centers.
MAIN OUTCOME MEASURES:
Survival to hospital discharge and discharge disposition.
RESULTS:
A total of 61,909 patients were transported by helicopter and 161,566 patients were transported by ground. Overall, 7813 patients (12.6%) transported by helicopter died compared with 17,775 patients (11%) transported by ground services. Before propensity score matching, patients transported by helicopter to level I and level II trauma centers had higher Injury Severity Scores. In the propensity score-matched multivariable regression model, for patients transported to level I trauma centers, helicopter transport was associated with an improved odds of survival compared with ground transport (odds ratio [OR], 1.16; 95% CI, 1.14-1.17; P

 

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細胞内情報伝達 Glucocorticoid-induced Myopathy

2012年04月24日 07時05分51秒 | 論文紹介 細胞内情報伝達
Horm Res. 2009 Nov;72 Suppl 1:36-41.

Mechanisms of muscle atrophy induced by glucocorticoids.
Schakman O, Gilson H, Kalista S, Thissen JP.

Source
Unité de Diabétologie et Nutrition, Université Catholique de Louvain, Brussels, Belgium.

Abstract
BACKGROUND: Many pathological states characterized by muscle atrophy (e.g., sepsis, cachexia, starvation, metabolic acidosis and severe insulinopenia) are associated with an increase in circulating glucocorticoid (GC) levels, suggesting that GC could trigger the muscle atrophy observed in these conditions. GC-induced muscle atrophy results from decreased protein synthesis and increased protein degradation. The inhibitory effect of GCs on protein synthesis is thought to result mainly from the inhibition of the p70 ribosomal S6 protein kinase. The stimulatory effect of GCs on muscle proteolysis results from the activation of two major cellular proteolytic systems: ubiquitin proteasome and lysosomal systems. The decrease in muscle production of insulin-like growth factor I (IGF-I), a muscle anabolic growth factor, could contribute to GC-induced muscle atrophy. By activating the phosphatidylinositol-3-kinase/Akt pathway, IGF-I overrides GC action to stunt muscle atrophy. Evidence also indicates that increased production of myostatin, a catabolic growth factor, could play a critical role in GC-induced muscle atrophy. CONCLUSIONS: Recent progress in understanding the role of growth factors in GC-induced muscle atrophy allows investigation into new therapies to minimize this myopathy.


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症例報告 MRSHによる重症敗血症

2012年04月22日 18時57分35秒 |  ひまわり日記
2011年 Meticillin-Resistant Staphylococcus haemolyticusにリネゾリドが奏功した一例
名古屋大学大学院医学系研究科 救急・集中治療医学分野
● 東 倫子,久保寺 敏,靍谷悠大,山本尚範,武田真輔,稲葉正人,村田哲哉,松島 暁,沼口 敦,鈴木秀一,都築通孝,角 三和子,村瀬吉郎,足立裕史,高橋英夫,松田直之

 コアグラーゼ陰性ブドウ球菌には,メチシリン耐性黄色ブドウ球菌をはじめとするいくつかの多剤耐性株の存在が知られており,治療に難渋することが多い。今回,早期からのリネゾリド選択が効果的であった高度肥満症例を経験した。
【症例】35歳の女性,身長154 cm,体重95 kg,BMI 40.1。13歳頃から若年性周期性精神病の診断を受けて精神科でフォローされていた。統合失調症と診断された後は,病勢に応じて精神科への入退院を繰り返していたが,精神科入院中に肺血栓塞栓症によって心肺停止状態となった。直ちに経皮的心肺補助装置を用いて蘇生に成功し,同日深夜には心肺補助循環から離脱したが,以後,肺血栓塞栓症による低酸素血症,高度の肥満に伴う活動性低下と低換気に対して集中治療を継続した。その後,続発した発熱に対して悪性高熱症などを想定した管理を施行していたが,血液および喀痰培養検査でコアグラーゼ陰性ブドウ球菌属が検出され,ACME-arcA,native arcA,SCCmec遺伝子を持つMeticillin-Resistant Staphylococcus haemolyticus(MRSH)と同定した。40℃以上の発熱,140回/分以上の頻脈,意識混濁,ショックを特徴とし,PIPC,IPM resistant,MINO,VCM,TEIC,LZD sensitiveのため,リネゾリド1,200 mg/dayを選択した。リネゾリド投与時には80,000 /μLレベルの血小板減少症を認めたが,投与開始後にはさらに血小板数が50,000/μLレベルに低下し,解熱傾向の認められた5日間で,リネゾリドの投与を中止とした。しかし,その後,再び 40℃以上の発熱と上室性頻拍が出現し,Staphylococcus haemolyticusによる敗血症が疑われたため,リネゾリド1,200 mg/dayの投与を再開した。翌日より直ちに解熱傾向を認め,29.9 mg/dLまで上昇したCRP値が,翌日には18.9 mg/dL,4日後には4.34 mg/dLまで低下し,血小板数の漸減を認めず,約9日間でリネゾリドの投与を終了できた。以後,発熱や炎症活性の上昇を認めず,引き続く監視血液培養の結果も陰性だった。この発熱の経過過程において,気管切開術を施行して人工呼吸管理を継続したが,感染症の改善と共に人工呼吸器から離脱でき,さらに第45病日には意識と呼吸の改善により,精神科病棟へ転棟管理とした。
【結語】本症例は,高度肥満患者であり,肺血栓塞栓症により心停止をきたした患者である。蘇生後管理において全身状態を改善させる過程で,MRSH肺炎および敗血症性ショックに至った。このようなMRSHに対して,リネゾリドを早期から使用することで,敗血症から速やかに離脱できた一例である。


Journal of Medical Microbiology 2009;58,:731–736

Distribution of the ACME-arcA gene among meticillin-resistant Staphylococcus haemolyticus and identification of a novel ccr allotype in ACME-arcA-positive isolates
Borui Pi, Meihong Yu, Yagang Chen, Yunsong Yu and Lanjuan Li
State Key Laboratory for Diagnosis and Treatment of Infectious Disease, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, PR China

Abstract

The aim of this study was to investigate the prevalence and characteristics of ACME (arginine catabolic mobile element)-arcA-positive isolates among meticillin-resistant Staphylococcus haemolyticus (MRSH). ACME-arcA, native arcA and SCCmec elements were detected by PCR. Susceptibilities to 10 antimicrobial agents were compared between ACME-arcA-positive and -negative isolates by chi-square test. PFGE was used to investigate the clonal relatedness of ACME-arcA-positive isolates. The phylogenetic relationships of ACME-arcA and native arcA were analysed using the neighbour-joining methods of MEGA software. A total of 42 (47.7 %) of 88 isolates distributed in 13 PFGE types were positive for the ACME-arcA gene. There were no significant differences in antimicrobial susceptibility between ACME-arcA-positive and -negative isolates. A novel ccr allotype (ccrABSHP) was identified in ACME-arcA-positive isolates. Among 42 ACME-arcA-positive isolates: 8 isolates harboured SCCmec V, 8 isolates harboured class C1 mec complex and ccrABSHP; 22 isolates harbouring class C1 mec complex and 4 isolates harbouring class C2 mec complex were negative for all known ccr allotypes. The ACME-arcA-positive isolates were first found in MRSH with high prevalence and clonal diversity, which suggests a mobility of ACME within MRSH. The results from this study revealed that MRSH is likely to be one of the potential reservoirs of ACME for Staphylococcus aureus.



JOURNAL OF CLINICAL MICROBIOLOGY 2009; 47:1172–1180

Biofilm Formation by Staphylococcus haemolyticus

Elizabeth Gladys Aarag Fredheim1, Claus Klingenberg1,2, Holger Rohde3, Stephanie Frankenberger3, Peter Gaustad4, Trond Flægstad1,2 and Johanna Ericson Sollid5

1Department of Pediatrics, Institute of Clinical Medicine, University of Tromsø, Tromsø, Norway
2Department of Pediatrics, University Hospital of North Norway, Tromsø, Norway
3Institut für Medizinische Mikrobiologie, Virologie und Hygiene, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany
4Institute of Microbiology, Rikshospitalet, and University of Oslo, Oslo, Norway
5Department of Microbiology and Virology, Institute of Medical Biology, University of Tromsø, Tromsø, Norway


ABSTRACT

Infections due to coagulase-negative staphylococci (CoNS) most frequently occur after the implantation of medical devices and are attributed to the biofilm-forming potential of CoNS. Staphylococcus haemolyticus is the second most frequently isolated CoNS from patients with hospital-acquired infections. There is only limited knowledge of the nature of S. haemolyticus biofilms. The aim of this study was to characterize S. haemolyticus biofilm formation. We analyzed the biofilm-forming capacities of 72 clinical S. haemolyticus isolates. A detachment assay with NaIO4, proteinase K, or DNase was used to determine the main biofilm components. Biofilm-associated genes, including the ica operon, were analyzed by PCR, and the gene products were sequenced. Confocal laser scanning microscopy (CLSM) was used to elucidate the biofilm structure. Fifty-three isolates (74%) produced biofilms after growth in Trypticase soy broth (TSB) with glucose, but only 22 (31%) produced biofilms after growth in TSB with NaCl. It was necessary to dissolve the biofilm in ethanol-acetone to measure the optical density of the full biofilm mass. DNase, proteinase K, and NaIO4 caused biofilm detachment for 100%, 98%, and 38% of the isolates, respectively. icaRADBC and polysaccharide intercellular adhesin (PIA) production were found in only two isolates. CLSM indicated that the biofilm structure of S. haemolyticus clearly differs from that of S. epidermidis. We conclude that biofilm formation is a common phenotype in clinical S. haemolyticus isolates. In contrast to S. epidermidis, proteins and extracellular DNA are of functional relevance for biofilm accumulation, whereas PIA plays only a minor role. The induction of biofilm formation and determination of the biofilm mass also needed to be optimized for S. haemolyticus.

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文献 腹腔内膿瘍 外科的ドレナージ vs 経皮的ドレナージ

2012年04月17日 07時01分42秒 | 論文紹介 感染症管理
Am Surg 2011 Jul;77(7):862-7.

Differences in morbidity and mortality with percutaneous versus open surgical drainage of postoperative intra-abdominal infections: a review of 686 cases.
Politano AD, Hranjec T, Rosenberger LH, Sawyer RG, Tache Leon CA.

Abstract
Intra-abdominal infections following surgical procedures result from organ-space surgical site infections, visceral perforations, or anastomotic leaks. We hypothesized that open surgical drainage is associated with increased patient morbidity and mortality compared with percutaneous drainage. A single-institution, prospectively collected database over a 13-year period revealed 2776 intra-abdominal infections, 686 of which required an intervention after the index operation. Percutaneous procedures (simple aspiration or catheter placement) were compared with all other open procedures by univariate and multivariate analyses. Analysis revealed 327 infections in 240 patients undergoing open surgical drainage and 359 infections in 260 patients receiving percutaneous drainage. Those undergoing open drainage had significantly higher Acute Physiology Score (APS) and Acute Physiology and Chronic Health Evaluation (APACHE) II scores and were more likely to be immunosuppressed, require intensive care unit treatment, and have longer hospital stays. Mortality was higher in the open group: 14.6 versus 4.2 per cent (P = 0.0001). Variables independently associated with death by multivariate analysis were APACHE II, dialysis, intensive care unit (ICU) care, age, immunosuppression, and drainage method. Open intervention for postsurgical intra-abdominal infections is associated with increased mortality compared with percutaneous drainage even after controlling for severity of illness by multivariate analysis. Although some patients are not candidates for percutaneous drainage, it should be considered the preferential treatment in eligible patients.

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アニメーション Toll like受容体を介したNF-kB活性化と免疫活性化シグナル

2012年04月15日 02時19分41秒 | その他のお知らせ
Toll like受容体を介したNF-kB活性化と免疫活性化シグナル
短絡化していますが,初心者には理解しやすいアニメーションと思います。
NF-κB 2量体が,なかなかやんちゃな表情をしています。


mRNAについても,昼食時のお味噌汁のようなレベルで参考として下さい。

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EM-ICU内Pro&Con 肝性脳症に対する栄養や分枝鎖アミノ酸の位置付け

2012年04月13日 01時51分32秒 | 論文紹介 臨床研究
名大ICUでも急性肝不全の治療が増えてきておりますが,
より良き急性期治療を目指して,討論を交えたカンファレンスを行っております。
木曜日の全症例カンファレンスの後にPro & Cons討論(演者選定)も行われます。
分枝鎖アミノ酸? 経腸栄養推進松田の観点など,参考として下さい。

参考文献

Three targets of branched-chain amino acid supplementation in the treatment of liver disease.
Holecek M.
Nutrition. 2010 May;26(5):482-90. Epub 2010 Jan 13. Review.

Protein intake in renal and hepatic disease.
Ambühl PM.
Int J Vitam Nutr Res. 2011 Mar;81(2-3):162-72. Review.

Branched-chain amino acids in liver disease: new aspects of long known phenomena.
Plauth M, Schütz T.
Curr Opin Clin Nutr Metab Care. 2011 Jan;14(1):61-6. Review.

Branched-chain amino acid metabolism in heart disease: an epiphenomenon or a real culprit?
Huang Y, Zhou M, Sun H, Wang Y.
Cardiovasc Res. 2011 May 1;90(2):220-3. Review.

Nutraceutical approach for preventing obesity-related colorectal and liver carcinogenesis.
Shimizu M, Kubota M, Tanaka T, Moriwaki H.
Int J Mol Sci. 2012;13(1):579-95. Epub 2012 Jan 5.

Nutrition in hepatic encephalopathy.
Chadalavada R, Sappati Biyyani RS, Maxwell J, Mullen K.
Nutr Clin Pract. 2010 Jun;25(3):257-64. Review.

Branched chain amino acids supplemented with L-acetylcarnitine versus BCAA treatment in hepatic coma: a randomized and controlled double blind study.
Malaguarnera M, Risino C, Cammalleri L, Malaguarnera L, Astuto M, Vecchio I, Rampello L.
Eur J Gastroenterol Hepatol. 2009 Jul;21(7):762-70.

Aromatic amino acid metabolism during liver failure.
Dejong CH, van de Poll MC, Soeters PB, Jalan R, Olde Damink SW.
J Nutr. 2007 Jun;137(6 Suppl 1):1579S-1585S; discussion 1597S-1598S. Review.

など



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JC文献 Syndecan-4の血管系における役割

2012年04月12日 12時23分37秒 | 論文紹介 全身性炎症反応
2012年4月12日 救急・ICU Journal Clubの1つの討議内容 杤久保順平先生担当

Xiahui Tan, Najwa Khalil, Candice Tesarik, Karunasri Vanapalli, Viki Yaputra, Hatem Alkhouri, Brian G. G. Oliver, Carol L. Armour, and J. Margaret Hughes
Th1 cytokine-induced syndecan-4 shedding by airway smooth muscle cells is dependent on mitogen-activated protein kinases
Am J Physiol Lung Cell Mol Physiol April 1, 2012 302:L700-L710; published ahead of print January 20, 2012


In asthma, airway smooth muscle (ASM) chemokine secretion can induce mast cell recruitment into the airways. The functions of the mast cell chemoattractant CXCL10, and other chemokines, are regulated by binding to heparan sulphates such as syndecan-4. This study is the first demonstration that airway smooth muscle cells (ASMC) from people with and without asthma express and shed syndecan-4 under basal conditions. Syndecan-4 shedding was enhanced by stimulation for 24 h with the Th1 cytokines interleukin-1β (IL-1β) or tumor necrosis factor-α (TNF-α), but not interferon-γ (IFNγ), nor the Th2 cytokines IL-4 and IL-13. ASMC stimulation with IL-1β, TNF-α, and IFNγ (cytomix) induced the highest level of syndecan-4 shedding. Nonasthmatic and asthmatic ASM cell-associated syndecan-4 protein expression was also increased by TNF-α or cytomix at 4–8 h, with the highest levels detected in cytomix-stimulated asthmatic cells. Cell-associated syndecan-4 levels were decreased by 24 h, whereas shedding remained elevated at 24 h, consistent with newly synthesized syndecan-4 being shed. Inhibition of ASMC matrix metalloproteinase-2 did not prevent syndecan-4 shedding, whereas inhibition of ERK MAPK activation reduced shedding from cytomix-stimulated ASMC. Although ERK inhibition had no effect on syndecan-4 mRNA levels stimulated by cytomix, it did cause an increase in cell-associated syndecan-4 levels, consistent with the shedding being inhibited. In conclusion, ASMC produce and shed syndecan-4 and although this is increased by the Th1 cytokines, the MAPK ERK only regulates shedding. ASMC syndecan-4 production during Th1 inflammatory conditions may regulate chemokine activity and mast cell recruitment to the ASM in asthma.


さらにこれを評価しておくこと

Role of vessel wall and bone marrow syndecan-4 in neointimal hyperplasia: the plot thickens.
Caplice NM.
Arterioscler Thromb Vasc Biol. 2011 May;31(5):952-3.

CXCR7 and syndecan-4 are potential receptors for CXCL12 in human cytotrophoblasts.
Schanz A, Baston-Bust D, Krussel JS, Heiss C, Janni W, Hess AP.
J Reprod Immunol. 2011 Apr;89(1):18-25.

Synectin/syndecan-4 regulate coronary arteriolar growth during development.
Dedkov EI, Thomas MT, Sonka M, Yang F, Chittenden TW, Rhodes JM, Simons M, Ritman EL, Tomanek RJ.
Dev Dyn. 2007 Jul;236(7):2004-10.

Mechanical strain regulates syndecan-4 expression and shedding in smooth muscle cells through differential activation of MAP kinase signaling pathways.
Julien MA, Wang P, Haller CA, Wen J, Chaikof EL.
Am J Physiol Cell Physiol. 2007 Jan;292(1):C517-25.

Effects of L-arginine on fibroblast growth factor 2-induced angiogenesis in a model of endothelial dysfunction.
Voisine P, Li J, Bianchi C, Khan TA, Ruel M, Xu SH, Feng J, Rosinberg A, Malik T, Nakai Y, Sellke FW.
Circulation. 2005 Aug 30;112(9 Suppl):I202-7.

Beta1 and beta3 integrins cooperate to induce syndecan-4-containing cross-linked actin networks in human trabecular meshwork cells.
Filla MS, Woods A, Kaufman PL, Peters DM.
Invest Ophthalmol Vis Sci. 2006 May;47(5):1956-67.

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JC文献 肺細動脈細胞におけるオートファジーとアポトーシスのROSを介した相互関係

2012年04月12日 12時13分22秒 | 論文紹介 全身性炎症反応
2012年4月12日 救急・ICU Journal Clubの1つの討議内容 杤久保順平先生担当

Ru-Jeng Teng, Jianhai Du, Scott Welak, Tongju Guan, Annie Eis, Yang Shi, and Girija G. Konduri
Cross talk between NADPH oxidase and autophagy in pulmonary artery endothelial cells with intrauterine persistent pulmonary hypertension
Am J Physiol Lung Cell Mol Physiol April 1, 2012 302:L651-L663

Autophagy is a process for cells to degrade proteins or entire organelles to maintain a balance in the synthesis, degradation, and subsequent recycling of cellular products. Increased reactive oxygen species formation is known to induce autophagy. We previously reported that increased NADPH oxidase (NOX) activity in pulmonary artery endothelial cells (PAEC) from fetal lambs with persistent pulmonary hypertension (PPHN) contributes to impaired angiogenesis in PPHN-PAEC compared with normal PAEC. We hypothesized that increased NOX activity in PPHN-PAEC is associated with increased autophagy, which, in turn, contributes to impaired angiogenesis in PPHN-PAEC. In the present study, we detected increased autophagy in PPHN-PAEC as shown by increased ratio of the microtubule-associated protein 1 light chain (LC3)-II to LC3-I and increased percentage of green fluorescent protein-LC3 punctate positive cells. Inhibiting autophagy by 3-methyladenine, chloroquine, and beclin-1 knockdown in PPHN-PAEC has led to decreased autophagy and increased in vitro angiogenesis. Inhibition of autophagy also decreased the association between gp91phox and p47phox, NOX activity, and superoxide generation. A nonspecific antioxidant N-acetylcysteine and a NOX inhibitor apocynin decreased autophagy in PPHN-PAEC. In conclusion, autophagy may contribute to impaired angiogenesis in PPHN-PAEC through increasing NOX activity. Our results suggest that, in PPHN-PAEC, a positive feedback relationship

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JC文献 ARDSにおける治療薬

2012年04月12日 11時46分07秒 | 論文紹介 臨床研究
2012年4月12日 救急・ICU Journal Clubの1つの討議内容 杤久保順平先生担当

Cochrane Database Syst Rev. 2004 Oct 18;(4):CD004477.
Pharmacologic therapies for adults with acute lung injury and acute respiratory distress syndrome.
Adhikari N, Burns KE, Meade MO.
Source
Critical Care Medicine and Medicine, Sunnybrook and Women's College Health Centre, 2075 Bayview Avenue, B7.04a, Toronto, M4N 3M5, Ontario, Canada. neill.adhikari@sw.ca
Abstract
BACKGROUND:
Multiple pharmacologic treatments have been studied for acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).
OBJECTIVES:
Our objective was to determine the effects of pharmacologic treatments on clinical outcomes in adults with ALI or ARDS.
SEARCH STRATEGY:
We searched OVID versions of CENTRAL (The Cochrane Library Issue 3, 2003), MEDLINE (1966 to week 2, January 2004), EMBASE (1980 to week 4, 2004), CINAHL (1982 to week 2, January 2004), and HEALTHSTAR (1995 to December 2003); proceedings from four conferences (1994 to 2003); and bibliographies of review articles and included studies.
SELECTION CRITERIA:
Randomized controlled trials of pharmacologic treatments compared to no therapy or placebo for established ALI or ARDS in adults admitted to an intensive care unit, with measurement of early mortality (primary outcome), late mortality, duration of mechanical ventilation, ventilator-free days to day 28, or adverse events. We excluded trials of nitric oxide, partial liquid ventilation, fluid and nutritional interventions, oxygen, and trials in other populations reporting outcomes in subgroups of patients with ALI or ARDS.
DATA COLLECTION AND ANALYSIS:
Two reviewers independently screened titles and abstracts, rated studies for inclusion, extracted data and assessed methodologic quality of included studies. Disagreements were resolved by consensus in consultation with a third reviewer. For each pharmacologic therapy, we quantitatively pooled the results of studies using random effects models where permitted by the available data. We contacted study authors when clarification of the primary outcome was required.
MAIN RESULTS:
Thirty three trials randomizing 3272 patients met our inclusion criteria. Pooling of results showed no effect on early mortality of prostaglandin E1 (seven trials randomizing 697 patients; relative risk [RR] 0.95, 95% confidence interval [CI] 0.77 to 1.17), N-acetylcysteine (five trials randomizing 239 patients; RR 0.89, 95% CI 0.65 to 1.21), early high-dose corticosteroids (two trials randomizing 187 patients; RR 1.12, 95% CI 0.72 to 1.74), or surfactant (nine trials randomizing 1441 patients; RR 0.93, 95% CI 0.77 to 1.12). Two interventions were beneficial in single small trials; corticosteroids given for late phase ARDS reduced hospital mortality (24 patients; RR 0.20, 95% CI 0.05 to 0.81), and pentoxifylline reduced one-month mortality (RR 0.67, 95% CI 0.47 to 0.95) in 30 patients with metastatic cancer and ARDS. Individual trials of nine additional interventions failed to show a beneficial effect on prespecified outcomes.
REVIEWERS' CONCLUSIONS:
Effective pharmacotherapy for ALI and ARDS is extremely limited, with insufficient evidence to support any specific intervention.


グルタチオン前駆体としてのNACについて
1.
[N-acetylcysteine (NAC) inhibited pulmonary fibrosis in acute respiratory distress syndrome (ARDS)].
Li XF, Ouyang B, Wu JF, Chen J, Guan XD.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2011 Oct;23(10):599-601. Chinese.
PMID: 22242225 [PubMed - in process]
Related citations

2.
From neurogenic pulmonary edema to fat embolism syndrome: a brief review of experimental and clinical investigations of acute lung injury and acute respiratory distress syndrome.
Chen HI.
Chin J Physiol. 2009 Nov 30;52(5 Suppl):339-44. Review.
PMID: 20359124 [PubMed - indexed for MEDLINE]
Related citations

3.
N-acetylcysteine improves group B streptococcus clearance in a rat model of chronic ethanol ingestion.
Tang SM, Gabelaia L, Gauthier TW, Brown LA.
Alcohol Clin Exp Res. 2009 Jul;33(7):1197-201. Epub 2009 Apr 9.
PMID: 19389194 [PubMed - indexed for MEDLINE] Free PMC Article
Related citations

4.
Attenuation of pulmonary inflammation after exposure to blast overpressure by N-acetylcysteine amide.
Chavko M, Adeeb S, Ahlers ST, McCarron RM.
Shock. 2009 Sep;32(3):325-31.

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救急医療/集中治療 胃管が入らないときの注意事項

2012年04月08日 22時54分13秒 | 救急医療

胃管挿入では無理は禁物

〜胃管が入らないときの注意事項〜

名古屋大学大学院医学系研究科 救急・集中治療医学分野

教授 松田直之

 

【はじめに】 

 経鼻胃管の挿入により,重症患者さんにおいてもできるだけ早く早期経腸栄養を開始できます。これは,1)消化管免疫を維持できること(人工呼吸器関連肺炎阻止策),2)薬剤や炎症性分子などの脂溶性分子の胆汁排泄の正常化,3)消化管血流維持を主な目的としています。しかし,胃管を胃内に留置できないときがあります。例えば,喉元で跳ね返ってくる場合,鼻腔から40cm程度で先に進まない場合などです。心肺停止蘇生後の胃内の脱気と胃内圧減少を目的とした場合や,集中治療開始において,早く胃管を挿入したいのですが,胃管が挿入できない。胃管を挿入できない場合があるのです。しかし,それで良いのです。胃管挿入には,いくつかのリスクがありますので,十分に注意していただき,診断の上で丁寧に挿入することをお勧めしています。もちろん,緊急の場合でない限り,胃がんや食道がんなどの術後であるとか,胃管挿入のリスクとなる内容について情報を得ておくことも必要となります。

【胃管留置における3つの注意事項】

 経鼻胃管挿入における障害ポイントとして,3つの狭窄部位(1.頚部:食道入口部,2.大動脈弓部による狭窄の胸部中部食道部,3.横隔膜下の腹部食道部)に注意して対応して下さい。

1.食道入口部:食道入口部を胃管が通過できるとよいのですが,重症患者さんでは頭頸部にダメージがある場合や救急でよく言うところのAのトラブル(Airway)では要注意です。このトラブルとしては,反転してきて食道へ進まないだけではなく,声門を通過してしまい気管内に誤入してしまう危険性です。気管内挿入は,気管挿管していても注意が必要です。胃管が40cmレベルから進まない??この確認として挿入したチューブから呼吸音が聞こえてこないか,スーハースーハー,人工呼吸の吸気/呼気に合わせて,胃管からの空気が漏れでてくるくるかどうかを必ず確認するようにしましょう。

2.胸部中部食道部:胸部大動脈解離がある患者さんでは特に注意が必要です。ここに炎症や損傷を起こすことで,吐血,大動脈食道瘻などの合併に注意が必要となります。

3.横隔膜下の腹部食道部:高齢者,胃食道逆流症(Gastro Esophageal Reflux Disease:GERD),横隔膜裂肛ヘルニアなどで注意をしています。また,心肺蘇生後などでは下部食道に食物残渣が残存している場合などもあります。私の経験では,ここに鶏肉が詰まっており,胃管が40cmから進まない。腹部食道部のトラブルとして,胃管が40cm〜45cmから進まないことに注意します。

【診断の重要性:胃管を留意できない場合】

 救急医療や集中治療などの全身管理では,集中治療室入室前に胸部から骨盤までの単純CT像を評価しておくことをお勧めしています。例えば,ショックや心肺蘇生後の全身管理において,蘇生による障害の評価が必須となります。多発外傷では,集中治療管理前にかならず頭頸部および胸部〜骨盤までのCT評価を行います。ここで,食道および胃を確認します。胸部大動脈解離の否定,胸下部食道や腹部食道の狭窄や食物残渣の沈着などがないことをCTで評価します。私からのアドバイスとしては,胃管挿入が難しい場合は,「必ず理由がある」,「挿入できない原因を評価して下さい」ということとなります。

【胃管挿入方法】

1.食道入口部:気管挿管下で食道内へ入っていかない場合は,喉頭鏡を使用したり,マギール鉗子を用います。気管挿管チューブのカフ圧については人工呼吸管理における最大気道内圧レベルの適切なカフ圧とし,食道入口部通過後に胃管が進みにくいなどのことがないように注意します。

2.胸部中部食道部:食道がんなどがない場合は,胸部大動脈解離でも通過してしまうと思いますが,胸部大動脈解離の有無には十分に注意し,胃管留置が食道・大動脈瘻孔(吐血)の原因となる危険性を皆で共有し,ご家族を含めて審議しておくことになります。

3.下部食道に食物残渣が確認された場合:気管挿管下での全身管理での胃管挿入では,経鼻胃管を鼻腔から挿入し,気管内挿入でないこと(胃管呼吸のないことの確認)とし,胃管に20 mLの水を出したり入れたりして愛護的に洗う方法があります。とにかく,気管内挿入でないことに注意しますが,慎重に20 mL程度の水の出し入れで洗っていると,すっと胃内に挿入できる場合があります。

【おわりに】

 胃管を挿入できない場合には,原因がありますので,その原因がどのようなことであるのかを評価するようにして下さい。このため,胃管を挿入できない場合には,CTなどで胃と食道を確認するように私はしています。これは,もちろん救急医療や集中治療の超急性期管理のためとなります。看護師さんに胃管挿入をお願いすることも多いですので,途中で止まってしまって挿入できない場合には,遠慮なく医師を呼ぶことをお勧めしています。


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ジャーナルクラブ British Journal of Pharmacology 2012年3月号

2012年04月05日 12時04分19秒 | ジャーナルクラブ 松田直之指導
私が指導する名大Journal Club 4月5日編です。
4月よりランチタイム前に1時間~1時間半基礎研究を雑誌1冊報告して頂き,
私が補則解説をし,最終的なレビューをしています。
これを2年間続けると,かなり基本ができます。

2012年3月号のBritish Journal of Pharmacologyを足立裕史先生に担当して頂きましたが,
この号を読むだけで,Gタンパク共役型受容体についてかなり詳細に整理できます。
Gタンパク共役型受容体: molecular pharmacology of GPCRs

総説 Molecular Pharmacology of GPCRs

GPCR expression in tissues and cells: Are the optimal receptors being used as drug targets?
PA Insel, A Snead, F Murray, L Zhang, H Yokouchi, T Katakia, O Kwon, D Dimucci and A Wilderman
British Journal of Pharmacology
Special Issue: Themed Section: Molecular Pharmacology of GPCRs. Guest Editor: Roger J Summers
Volume 165, Issue 6, pages 1613–1616, March 2012

ケモカイン受容体についても非常によくまとめられています
British Journal of Pharmacology 2012;165:1617-1643
DJ Scholten, M Canals, D Maussang, L Roumen, MJ Smit, M Wijtmans, C de Graaf, HF Vischer and R Leurs
Pharmacological modulation of chemokine receptor function

オピオイドの急性耐性についてもまとめられています
British Journal of Pharmacology 2012;165:1704-1716
Vu C Dang and MacDonald J Christie
Mechanisms of rapid opioid receptor desensitization, resensitization and tolerance in brain neurons

clathrin coated vesicle-mediated endocytosisなど
Gタンパク共役型受容体の細胞膜移動トラフィッキングに関与するタンパクが楽しくまとめられています
British Journal of Pharmacology 2012;165:1717-1736
Ana C Magalhaes, Henry Dunn and Stephen SG Ferguson
Regulation of GPCR activity, trafficking and localization by GPCR-interacting proteins

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