气腹性肺损伤的机制与防治策略

背景 腹腔镜手术具有创伤小、恢复快等特点.但手术过程中建立CO2气腹会造成腹腔内高压和酸碱平衡失调,引起不同程度的肺组织损伤,导致术后肺功能不全,严重者甚至可以发展为急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS). 目的 阐述气腹性肺损伤的机制和防治研究新进展. 内容 气腹性肺损伤的发生机制很复杂,可由通气/血流比例失调、氧化和抗氧化系统失衡、缺血/缺氧、缺血/再灌注损伤、促炎和抗炎反应失衡等因素引起.通过小潮气量联合呼气末正压通气的肺通气模式,允许性高碳酸血症,气腹前预处理和药物的应用可以减轻气腹引起的肺损伤. 趋向 通过对CO2气腹引起肺损伤的发生机制及防治策略进行综述,期望为气腹性肺损伤的预防及治疗提供新的思路.     

Concomitant administration of mannitol and N-acetylcysteine for the prevention of lung reperfusion injury

BACKGROUND: Mannitol (MN) and N- acetylcysteine (NAC) are partially successful in preventing lung reperfusion injury after liver ischemia reperfusion (IR). Their concomitant administration might enhance the individual effects of each. METHODS: Rat isolated livers were perfused with Krebs-Henseleit solution (controls) or made globally ischemic (IR) for 2 hours. Separately isolated lungs were paired with livers and each pair was reperfused in-series for 15 minutes. During reperfusion, eight groups were treated with Krebs containing two low and two high doses of MN and/or NAC; one group received no treatment. RESULTS: The tested lung parameters were unchanged in all control groups. Pulmonary perfusion or ventilatory pressures, weight gain and bronchoalveolar lavage volume increased by 30 to 70% of baseline in the nontreated IR-paired lungs and in the only IR-MN 0.44- and the IR-NAC 0.25 mmol (weight/body weight) treated lungs but remained preserved by the two higher monotherapies (MN 0.55 mmol and NAC 0.37 mmol) and by the four bitherapies. The reduced glutathione content in all lung tissue subgroups treated by the bitherapies was higher by 63 to 124% of the corresponding monotherapy values. Xanthine oxidase activity in the bitherapies-treated IR-lungs decreased 1.5 to twofold compared with the corresponding monotherapies. CONCLUSIONS: Co-administration of MN and NAC augments the amount of lung protection afforded by each drug individually and enhances their antioxidant potentials.     

Playground injury prevention

Playground safety recently has received increasing attention from parents and municipalities. Orthopaedic surgeons treat a large number of the more than 350,000 injuries per year sustained on the play areas of this country's school, home, and community play areas. A parent brings a child to the playground for fun, healthy exercise, and imaginative play. Unfortunately, most parents may not be aware of recommended injury prevention methods. Data from the Consumer Product Safety Commission and other epidemiologic studies document frequency, identify at-risk activities and equipment, give direction for additional research, and guide regulations. It is appropriate for the medical community to lead in this safety effort and to contribute to additional research and advocacy efforts.     

Acute lung injury

Acute lung injury (ALI) and its extreme manifestation the acute respiratory distress syndrome (ARDS) are characterized by acute refractory hypoxaemia, decreased pulmonary compliance and diffuse alveolar infiltrates on chest radiography. The incidence of ALI and ARDS is thought to be 17.9 and 13.5/100,000, respectively. The development of management strategies has led to improvements in its associated mortality. This article describes the epidemiology, the pathogenesis and the management of ALI with emphasis on strategies aimed at reducing the ventilator-associated injury that has been shown to affect outcome adversely. Existing interventions and those in the experimental phase are discussed in the context of existing evidence.     

Acute lung injury

Acute lung injury is a clinically and radiologically defined syndrome which is commonly diagnosed in intensive care. This article describes the epidemiology, pathology and pathophysiology as well as current management strategies with supporting evidence where available.     

Perioperative lung injury

Patients are at risk for several types of lung injury in the perioperative period. These injuries include atelectasis, pneumonia, pneumothorax, bronchopleural fistula, acute lung injury and acute respiratory distress syndrome. Anesthetic management can cause, exacerbate or ameliorate most of these injuries. Clinical research trends show that traditional protocols for perioperative mechanical ventilation, using large tidal volumes without positive end-expiratory pressure (PEEP) can cause a sub-clinical lung injury and this injury becomes clinically important when any additional lung injury is added. Lung-protective ventilation strategies using more physiologic tidal volumes and appropriate levels of PEEP can decrease the extent of this injury.     

Acute lung injury

Acute lung injury and acute respiratory distress syndrome are serious and devastating conditions affecting very ill patients and usually necessitate mechanical ventilation and prolonged stay in the ICU. This article describes the basic pathology and pathogenesis of their development and subsequent progression, followed by a review of the strategies used in the management of these patients in the critical care setting.     

The prevention of burning injury

Say not ‘I have found the path of the soul’.

Say rather 'I have met the soul walking upon my path'. For the soul walks upon all paths.

The soul walks not upon a line, neither does it grow like a reed.

The soul unfolds itself, like a lotus of countless petals.

Kahlil Gibran, The Prophet     

Enhancement of lung preservation by prevention of lung collapse

Previous investigations of important factors in lung preservation have stressed the importance of denervation and ischemia as deterimental factors. We believe that lung collapse below the level of functional residual capacity during preservation also decreases the ability of the transplanted lung to provide total pulmonary function.To validate this assumption, four groups of five dogs each were studied utilizing the in vivo isolated lung preparation. This preparation simulates autotransplantation but avoids the attendant time-consuming anastomoses which markedly increase collapse time. In Group I, the isolated ischemic lungs were ventilated for 3 hr with the chest open, thus allowing total collapse of the lung with each respiratory cycle. Subsequently, circulation was restored, the contralateral pulmonary artery was ligated, and the chest was closed for chronic survival. Groups II, III, and IV differed only in that the chest was closed during ischemic periods of 3, 4, and 5 hr, respectively, thus preventing lung collapse below FRC. No dogs survived in Group I. Chronic survivors in Groups II, III, and IV numbered three, two, and one, respectively, supporting the contention that prevention of lung collapse below FRC enhances the ability of lung grafts to assume total respiratory function after implantation.We believe that the prevention of collapse is a much more critical factor in lung preservation than is lung ischemia. So long as collapse time during harvesting, implantation, and the so-called preservation period is less than 30–60 min, one may be able consistently to preserve a lung, under conditions of normothermic ischemia with ventilation above FRC, for 3 hr, with occasional satisfactory preservation up to 5 hr.Failure to minimize lung collapse during the preservation period and during harvesting and implantation may mean the difference between survival and death in lung allograft recipients.     

Effect of thermal injury on endotoxin-induced lung injury

We studied the effects of a burn injury on the response of the lung to endotoxin. Seventeen unanesthetized sheep with lung lymph fistulas were studied. Eight were given Escherichia coli endotoxin (1.5 micrograms/kg) alone and nine were given the same dose 72 hours after a 25% total body surface burn injury. At this time after burn, all physiologic parameters were at baseline levels. A characteristic two-phase lung injury was seen after administration of endotoxin with an initial hypertension phase, characterized by pulmonary artery hypertension, and a second or permeability phase, characterized by an increase in protein-rich lymph flow. all eight animals that underwent only endotoxin administration survived, whereas four of the nine burned animals died during the permeability phase in pulmonary edema. Major physiologic differences between the groups were noted during the permeability phase, including a more severe hypoxia, pulmonary hypertension, and increased postburn lymph flow. Major biochemical changes included significant increases in lymph thromboxane, thromboxane B2, and beta-glucuronidase activity in the burn group. We conclude that the lung is more sensitive to endotoxin after burn, probably as a result of an increased release of products of arachidonic acid metabolism and products of leukocyte activation caused by the body burn.     

Ventilator-associated lung injury.

There is injury caused in numerous animal species when overdistending airway pressure and volume are delivered. The extent of this injury is attenuated by the application of PEEP. Patient case series point to the benefit of LPVS. In randomized controlled trials, the data may appear confusing. However, based on the data from the Amato and colleagues' trial, it seems prudent to employ an LPVS based on the individual patient's lung mechanics. Based on the trials discussed it appears that many have been convinced of the detrimental effects of high peak alveolar pressure. It remains to convince clinicians of the beneficial effects of the use of higher PEEP early in ARDS based on respiratory system mechanics of the individual patient and to use recruitment maneuvers. In conclusion, I concur with Dreyfuss and Saumon and Slutsky and Tremblay that the use of an LPVS may not only attenuate the severity of ARDS by preventing VALI, but may also prevent MODS or attenuate its severity.     

Morphine-induced acute lung injury

A 38-year-old woman who had familial adenomatous polyposis was admitted to the intensive care unit with an episode of severe sepsis 5 days after undergoing a pancreas-preserving duodenectomy. Laparotomy with removal of an intra-abdominal abscess, followed by closed postoperative continuous lavage for 10 days, was performed. During two courses of planned tracheal extubation, the patient developed an acute lung injury, making a reintubation necessary. In both events, the patient received small doses of continuous morphine before the extubation. Morphine may induce the development of an acute lung injury in patients, whereas the exact pathophysiologic and pharmacologic mechanisms remain unclear.     

Transfusion-related acute lung injury

Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related mortality. It is characterized by injury to the alveolar-capillary membrane precipitated by transfusion factors, antibodies, and/or inflammatory mediators, in a susceptible host. In the absence of a specific test, TRALI is defined clinically as a syndrome of acute lung injury that develops during or within 6 h of transfusion. The absence of left atrial hypertension and large protein content of edema fluid may help differentiate TRALI from hydrostatic pulmonary edema. The treatment is supportive. The blood bank needs to be notified promptly so that an appropriate workup and prevention are initiated in a timely manner.