高原小儿外科感染性休克探讨

本文对105例高原小儿外科感染性休克进行了总结.临床观察和实验室资料表明,高原地区健康小儿的血液流态具有粘、浓、聚三大特点,微血管在缺氧环境下处于痉挛代偿状态.感染性休克时血管痉挛明显加重,持续时间长,代偿机能差,休克早期就会出现微循环障碍,因而高原小儿感染性休克具有发病急、进展快,病情重、病死率高等临床特点.早期诊断、早期治疗对于提高抢救成功率,降低病死率有重要意义.

开窗引流治疗小儿急性化脓性心包炎(附49例报告)

我院自1966～1985年采用心包开窗引流术治疗小儿急性化脓性心包炎49例,取得较好效果,现报告如下.临床资料一、一般资料年龄60天～13岁,病程5～50天.其中伴多发性脓肿22例、骨髓炎11例、肺炎5例、脓胸及肺脓疡各1例.全部病例均作了心包穿刺确诊.心包液培养:金黄色葡萄球菌24例、溶血性链球菌6例、大肠杆菌4例、枯草杆菌及绿脓杆菌各1例.

Sepsis and septic shock have continued to produce significant morbidity and mortality, in recent times, in acutely injured patients as well as patients in the intensive care units despite advances in antibiotic therapy and in the cardi ovascular and pulmonary support for these patients. This emphasizes the need to gain a better understanding of the fundamental mechanisms of the pathogenesis of sepsis syndrome in the critically ill or injured patients. The present knowled ge of the mechanisms of septic pathogenesis clearly indicates involvement of mod ulations in the functions of the cells of body's immune defense system, namely, monocytes/macrophages, polymorphonuclear leukocytes, and lymphocytes. Most of su ch knowledge has been derived from laboratory experiments in animal models of se ptic injury, or from studies of immune-system cells, in vitro. Clinical stud ies have also supported the role of immune perturbations. Yet, to date, very few the rapeutic approaches are available to effectively counter the sepsis-related immu ne disturbances. Functional modulations in the immune system cells, in the injured/septic hos ts, can exert not only adaptive/beneficial effects but also profoundly adverse effects on the non-immune-system cells such as endothelial, epithelial, neurona l, endocrine, neuro-endocrine, smooth muscle, skeletal muscle, and cardiac muscl e cells. The primary functional modulation in the immune-system cells after inju ry or with critical illness is activation of such cells via molecules from pat hogens, for example, lipopolysaccharide from gram negative organisms, lipoteic hoic acid/peptidoglycan from gram positive organisms, or zymosan from fungi. Suc h pathogenic molecules activate monocytes and tissue macrophages to result in th e expression and release of cytokine mediators (TNFα, IL-1, IL-6, IL-8, and IL- 10), as well as certain lipid mediators (PGE2, LTB4, PAF). While these media tors could play a host-defense role in support of the host via containment/destr uctio n of the pathogens, they could also exert detrimental effects in the host and co ntribute to host morbidity and mortality. Some of these mediators (TNFα, IL-1, IL-6, IL-8, LTB4, PAF) have been shown to be “pro-inflammatory”,and to potenti al ly exert a harmful effect on non-immune cell systems such as endothelial cells, epithelial cells, and muscle cells. Among the pro-inflammatory mediators, TNFα a nd IL-1 could play major harmful roles, and thus contribute to the injured host morbidity and mortality. Mediators, IL-10 and PGE2 have been shown to be “an ti-inflammatory” and to potentially contribute to a dreadful state of immuno-s uppression in the injured hosts, which can also lead to morbidity and mortality. Whi ch is worse, a harmful pro-inflammatory phase or harmful immuno-suppression ? Or Which occurs first, a harmful pro-inflammatory condition or a harmful immuno-su ppression? These are questions which can not be definitively answered for the g eneral population of critically ill/injured patients. It is reasonable to assum e that the answers to these question would vary from one patient subset to anot her patient subset. Thus, whether to treat the patient with a putative anti-pro- inflammatory agent or with a putative anti-anti-inflammatory agent remai ns unresolved for the general sepsis patient population. Paradoxically, TNFα, IL-1, and other pro-inflammatory mediators under certa in circumstances may serve as natural “blockers” of immuno-suppression or “pr omoters” of immune stimulation. This may be true in the case of some of the se ptic patients. Understandably, these patients should not be treated with anti-pro-inf lammatory agents. On the other hand, the anti-inflammatory mediators such as PGE 2, IL-10, and certain other naturally occurring antagonists of TNFα and IL-10 a ctions (TNFα, and IL-1 receptor antagonists) could not only be producing a cert ai n level of immune-suppression but also serving as important feed back controller of the pro-inflammatory mediators. Thus some of the naturally occurring anti-I nflammatory agents could indeed serve as adaptive/beneficial “anti-pro-inflamma tory”, therapeutic agents in certain subset of sepsis patients. Although there is little doubt that effective therapeutic control of the sep sis syndrome could be achieved via appropriate modulation of the cells of the I mmune system, at the present time we do not have an immune therapeutic regimen w hich can singly be efficacious for the general population of patients with the s eptic complication. This implies that before an effective treatment of sepsis p atients, the patients must be identified, by some diagnostic procedure, as to wh ether they need an anti-pro-inflammatory therapy or an anti-anti-inflammatory th erapy. Thus, although immuno-therapy of sepsis remains promising, its efficacy a waits further investigative work particularly through clinical studies in sepsis patients.

严重脓毒症的治疗进展

美国和欧洲重病医学会(Society of Inten-live Care Medicine)自2002年开始发起"拯救脓毒症运动(Surviving Sepsis Campaign)",并于近年再版了脓毒症生存运动:《治疗严重脓毒症和感染性休克国际指南》(Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock:2012)[1].定义脓毒症(sepsis)为感染(可能的或确定性)引起的全身表现.严重脓毒症(severe sepsis)为脓毒症伴有脓毒症引起的器官功能异常(organ dysfunction)或组织灌注压降低(tissue hypoperfusion).严重脓毒症极易引起多脏器功能障碍综合症,是患者死亡的主要原因.本文就这一新的治疗指南和近来发表的有关严重脓毒症治疗进展作一综述.

连续性静脉-静脉血液滤过治疗肺炎支原体感染致横纹肌溶解综合征并发感染性休克一例

肺炎支原体(MP)感染并发横纹肌溶解综合征(RM)国内外罕见.现将我院使用连续性静脉-静脉血液滤过(CVVH)成功救治1例MP感染致RM及感染性休克报道如下.

赵淳中西医结合救治感染性休克经验浅探--附32例临床观察

感染性休克是由病原微生物及其毒素所产生的生物活性物质的作用引起的微循环障碍,导致以组织血流灌注不足、细胞缺氧及重要脏器损害为特征的综合征,与祖国医学热毒内陷所致“厥脱证”相符合.

去甲肾上腺素治疗感染性休克时对肺静脉血管阻力的影响

感染性休克致体循环阻力血管功能瘫痪,严重的低血压引起多脏器灌注不足,终导致患者死亡.而肺脏是易受累的器官[1].肺循环阻力包括肺动脉阻力和肺静脉阻力,两者阻力大致相等.近几年来,去甲肾上腺素(NE)已经成为治疗感染性休克的首选药物,它可直接收缩血管达到升血压作用.但NE治疗感染性休克时对肺循环的作用是加重肺高压还是改善肺高压有待进一步澄清.

血管升压药物在感染性休克中的应用

"拯救脓毒症运动"提出通过液体复苏和应用血管升压药物等手段尽早恢复中心静脉压、平均动脉压及中心静脉血氧饱和度等指标,以此改善重症感染与感染性休克患者氧供应与氧需求的失衡状态,并终达到降低病死率的目的[1].

Lipopolysaccharide (LPS), or endotoxin, is the major component of the outer surface of gram-negative bacteria. LPS is a potent activator of the cells of the immune and inflammation systems, including macrophages, monocytes and endothelial cells, and contributes to systemic changes seen in septic shock.1,2 It has long been believed that LPS is responsible for several fatal consequences of gram-negative infection. Cell activation by LPS constitutes the first step in the cascade of events believed to lead to the manifestation of gram-negative sepsis, which results in approximately 20 000 annual deaths in the United States3 and 30% mortality rate of known cases in China.Therefore, the action mechanism of LPS is one of the most important problems in the research field of immunity, inflammation and surgery. Researchers have investigated the mechanism of cell activity and injury of LPS for a long time. In 1990, CD14，the glycosyl-phosphatidylinositol (GPI)-linked plasma membrane protein, was identified as a proximal LPS receptor on the cell surface of macrophages, and it was suggested that CD14 and LBP (lipopolysaccharide binding protein) played an important role in the effect mechanism of LPS. CD14 seemed to receive LPS via transfer from the plasma protein LBP. Then, two action patterns were recognized. CD14 positive cells, such as macrophages and leukocytes, were activated after LPS combined with LBP and interacted with CD14. But, CD14 negative cells (for example, endothelial cells), were activated through other receptors that we did not know of in the cell surface after LPS, LBP and soluble CD14 (sCD14) combined with the compounds. However, there are some questions to be answered. Firstly, because CD14 lacks cytoplasmic doman, it is unlikely to act as the transducer. Secondly, the action pattern of LPS through CD14 and LBP may be in dose-dependent mode, but, in conditions of high dosage and long exposure to LPS action, CD14 and LBP do not play an important role in LPS activation effect. Finally, for CD14 negative cells, the receptor combined LPS-LBP-sCD14 compound has not yet been identified. Some details indicated that a “co-receptor” for LPS signal transduction must exist. Although standard biochemical approaches, transfection assay, and immunologic tacties were all employed to search for this co-receptor, it has not yet been found. The find of Toll-like receptor 4 (TLR4) provides a new opportunity to study the mechanism of LPS action.