Lidocaine attenuates acute lung injury induced by a combination of phospholipase A2 and trypsin

OBJECTIVE: Acute severe pancreatitis is often associated with acute lung injury, including acute respiratory distress syndrome. Acute lung injury induced by phospholipase A2 (PLA2) or trypsin, a pancreatic enzyme, is an experimental model resembling acute respiratory distress syndrome. Neutrophils and platelets are thought to play a pivotal role in the pathogenesis of acute respiratory failure. Lidocaine inhibits some aspects of neutrophil and platelet functions. We conducted the current study to assess the effects of pretreatment with lidocaine on acute lung injury induced by a combination of PLA2 and trypsin. DESIGN: Prospective, randomized animal study. SETTING: University research laboratory. SUBJECTS: Twenty-one adult male Japanese White rabbits (weight range, 2.0-2.4 kg). INTERVENTIONS: The animals were mechanically ventilated with a tidal volume of 10 mL/kg and an Fio2 of 0.4, and thereafter, they were randomly assigned to three groups. Acute lung injury was induced by a combination of PLA2 (1000 units/kg/hr) and trypsin (5000 units/kg/hr) infused intravenously for 4 hrs. Immediately before induction of the acute lung injury, the lidocaine treatment group received intravenous lidocaine (2 mg/kg bolus followed by 2 mg/kg/hr) until they were killed. In the nontreatment group, saline was given instead of lidocaine. Rabbits in the nonlung-injury group received saline infusion instead of the pancreatic enzymes. MEASUREMENTS AND MAIN RESULTS: During the experimental period (4 hrs), arterial blood gases, lung mechanics, and peripheral neutrophil and platelet counts were measured. Immediately after killing, the wet weight/dry weight ratio of the lung was recorded. Light microscopic findings (lung injury score and number of neutrophils) were compared between the three groups. The combination of PLA2 and trypsin decreased Pao2, lung compliance, and peripheral counts of neutrophils and platelets and increased alveolar/arterial oxygen tension difference, lung resistance, wet weight/dry weight ratio, and the number of neutrophils in the lung. Lidocaine treatment attenuated these changes. The two pancreatic enzymes caused extensive morphologic lung damage, which was lessened by lidocaine. CONCLUSIONS: We conclude that pretreatment with intravenous lidocaine attenuated the lung injury induced by the pancreatic enzymes. However, further studies are required to determine whether this drug has a therapeutic effect once the lung injury has developed.     

Intravenous Chlorhexidine Gluconate Causing Acute Respiratory Distress Syndrome

Case Report: A 67-year-old man undergoing a colectomy for colon cancer was unintentionally administered 0.8 mg of chlorhexidine gluconate intravenously and subsequently developed acute respiratory distress syndrome. The operation was discontinued immediately. Respiratory failure progressed despite three cycles of plasma exchange beginning on day 1. Extracorporeal membrane oxygenation for 72 h beginning on day 3 was associated with dramatic improvement. The patient showed complete recovery of intellectual function and subsequently underwent a colectomy with lymph node dissection for colon cancer. Conclusion: For acute respiratory distress syndrome secondary to chlorhexidine gluconate intoxication, consideration should be given to the treatment of initial respiratory distress and subsequent pneumonia. The benefit of extracorporeal membrane oxygenation and plasma exchange may merit further investigation.     

Exogenous surfactant therapy in a patient with adult respiratory distress syndrome after near drowning

A 24-year-old woman developed adult respiratory distress syndrome (ARDS) after near-drowning due to attempted suicide. Conventional mechanical ventilation together with prone positioning and inhaled nitric oxide could not provide sufficient oxygenation. Surface tension data (gamma min=27 dyn/cm, stability index=0.341) from a lavage sample supported the hypothesis that the surfactant function of this patient was drastically reduced due to a washout effect by aspiration of fresh water. Porcine surfactant (Curosurf®, 50 mg/kg for each lung) was instilled via fibreoptic bronchoscope. The partial arterial carbon dioxide pressure (paCO₂) and fraction of inspired oxygen (FiO₂) ratio as well as shunt fraction (Qs/Qt) improved impressively. When respiratory situation deteriorated again, surfactant application was repeated. Altogether, six bolus instillations of surfactant (total dose 300 mg/kg=18 000 mg) were administered until the respiratory situation had stabilized and oxygenation could be maintained by conventional mechanical ventilation. The radiological findings did not show substantial amelioration. The patient developed septic shock and died 12 days after admission. Surfactant application apparently led to a significant improvement of the respiratory function. However, the outcome could not be influenced positively. The high cost of surfactant therapy prevents the more widespread early administration in patients at risk.     

Incidence,clinical course,and outcome in 217 patients with acute respiratory distress syndrome

OBJECTIVE: To assess prospectively acute respiratory distress syndrome incidence, etiologies, physiologic and clinical features, and mortality and its predictors in four intensive care units in Argentina. DESIGN: Prospective inception cohort. SETTING: Four general intensive care units in teaching hospitals. PATIENTS: All consecutive adult patients admitted between January 3, 1999, and January 6, 2000, that met the criteria of the American-European Consensus Conference for acute respiratory distress syndrome. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: A total of 235 patients developed acute respiratory distress syndrome, and 217 survived for >24 hrs; these were further analyzed. Main risk factors were: sepsis (44%, including 65 pneumonia cases), shock (15%), trauma (11%), gastric aspiration (10%), and other (34%). At admission, nonsurvivors had significantly higher Acute Physiology and Chronic Health Evaluation II, Sequential Organ Failure Assessment and McCabe scores, and lower oxygenation and pH. During the first week, Pao2/Fio2, Sequential Organ Failure Assessment, pH, base excess, and driving pressure consistently discriminated between survivors and nonsurvivors. Hospital mortality was 58%. One third of patients died early. Main causes of death were multiple organ dysfunction syndrome, sepsis, and septic shock; refractory hypoxemia was uncommon. Factors independently associated with mortality were organ dysfunctions on day 3, Pao2/Fio2 on day 3, and McCabe score. CONCLUSIONS: Acute respiratory distress syndrome was a frequent syndrome in this cohort. Sepsis was its leading cause, and pneumonia was the most common single diagnosis. Mortality was high but similar to most recent series that included serious comorbidities. Independent predictors of death 72 hrs after admission emphasize the importance of both extrapulmonary and pulmonary factors together with preexisting severe illnesses.     

丙泊酚复合利多卡因或芬太尼用于人工流产术的临床观察

目的观察丙泊酚复合芬太尼或利多卡因用于人工流产术镇痛的效果。方法选择早孕病例80例,随机分为两组,每组40例。A组（丙泊酚复合芬太尼组）先静脉推注芬太尼1μg/kg,后再静脉推注丙泊酚1.5～2.5 mg/kg;B组（丙泊酚复合利多卡因组）。先缓慢静脉注射利多卡因30～40 mg,然后静脉推注丙泊酚1.5～2.5 mg/kg。比较两组诱导时间、诱导量、用药总量、苏醒时间及不良反应。结果两组镇痛效果均满意,但A组呼吸抑制发生率为25%,B组仅有2例发生呼吸抑制;A组苏醒时间长于B组。结论丙泊酚复合利多卡因用于无痛人工流产麻醉效果理想,对呼吸影响轻微,苏醒快,镇痛效果理想,不良反应少,适合临床广泛运用。     

Nonventilatory interventions in the acute respiratory distress syndrome

Acute respiratory distress syndrome was first described in 1967. Acute respiratory distress syndrome and acute lung injury are diseases the busy intensivist treats almost daily. The etiologies of acute respiratory distress syndrome are many. A significant distinction is based on whether the insult to the lung was direct, such as in pneumonia, or indirect, such as trauma or sepsis. Strategies for managing patients with acute respiratory distress syndrome/acute lung injury can be subdivided into 2 large groups, those based in manipulation of mechanical ventilation and those based in nonventilatory modalities. This review focuses on the nonventlilatory strategies and includes fluid restriction, exogenous surfactant, inhaled nitric oxide, manipulation of production, or administration of eicosanoids, neuromuscular blocking agents, prone position ventilation, glucocorticoids, extracorporeal membrane oxygenation, and administration of beta-agonists. Most of these therapies either have not been studied in large trials or have failed to show a benefit in terms of long-term patient mortality. Many of these therapies have shown promise in terms of improved oxygenation and may therefore be beneficial as rescue therapy for severely hypoxic patients. Recommendations regarding the use of each of these strategies are made, and an algorithm for implementing these strategies is suggested.     

Turning points: implementing kinetic therapy in the ICU

Kinetic therapy improves oxygenation, thus decreasing length of stay for patients with pulmonary disorders, such as nosocomial pneumonia, atelectasis, acute respiratory distress syndrome, and acute lung injury.     

氯氮平中毒继发急性肺损伤/急性呼吸窘迫综合征的抢救体会

目的:探讨氯氮平中毒继发急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)有效的治疗方法。方法:总结分析16例氯氮平中毒继发ALI/ARDS患者的临床表现和治疗方法。患者在中毒后6～144h出现ALI/ARDS表现,予气管插管、机械通气,抗胆碱药物治疗及血液灌流等综合治疗。结果:本组患者均治愈,平均住院时间(14±1.6)d;机械通气时间平均(134±12)h,中毒后(48～96)h意识转清。结论:氯氮平中毒继发的急性肺损伤/急性呼吸窘迫综合征主要与肺水肿、吸入性肺炎及氯氮平对肺组织的直接损伤作用有关。早期进行机械通气联合血液灌流和合理抗胆碱药物的,是治疗重度氯氮平重度并发急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)的有效方法。     

Surfactant replacement therapy in acute respiratory distress syndrome from viral pneumonia

A modified natural surfactant was administered to a patient with life-threatening adult respiratory distress sydrome caused by viral pneumonia. Subsequently, there was a marked improvement in gas exchange. In order to assess the mechanism for improved oxygenation, computed tomography of the lungs was done. Quantitative analysis of the scans taken before and after surfactant administration indicates that improvement in gas exchange was largely due to the expansion of underinflated and collapsed lung areas. Although this is a single case report, it provides insight into the possible beneficial effect of instilled surfactant in severe respiratory distress from viral pneumonia.     

Airway pressure release ventilation with a short release time in a child with acute respiratory distress syndrome

Airway pressure release ventilation (APRV) allows ventilation and oxygenation to occur at lower peak and mean airway pressures than conventional positive pressure ventilation. The use of APRV in adults is an effective method of ventilation for patients with acute lung injury and acute respiratory distress syndrome. However, the use of APRV in children is less established. We report the use of APRV with a short release time of 0.2 s in a child with acute respiratory distress syndrome secondary to respiratory syncytial virus pneumonia.     

Respiratory distress in the newborn

The most common etiology of neonatal respiratory distress is transient tachypnea of the newborn; this is triggered by excessive lung fluid, and symptoms usually resolve spontaneously. Respiratory distress syndrome can occur in premature infants as a result of surfactant deficiency and underdeveloped lung anatomy. Intervention with oxygenation, ventilation, and surfactant replacement is often necessary. Prenatal administration of corticosteroids between 24 and 34 weeks' gestation reduces the risk of respiratory distress syndrome of the newborn when the risk of preterm delivery is high. Meconium aspiration syndrome is thought to occur in utero as a result of fetal distress by hypoxia. The incidence is not reduced by use of amnio-infusion before delivery nor by suctioning of the infant during delivery. Treatment options are resuscitation, oxygenation, surfactant replacement, and ventilation. Other etiologies of respiratory distress include pneumonia, sepsis, pneumothorax, persistent pulmonary hypertension, and congenital malformations; treatment is disease specific. Initial evaluation for persistent or severe respiratory distress may include complete blood count with differential, chest radiography, and pulse oximetry.     

51例不明原因重症肺炎导致急性肺损伤的临床分析

目的提高对不明原因重症肺炎导致急性肺损伤的认识。方法回顾性分析甲型H1N1流感暴发流行期间同济大学医学院附属上海市肺科医院急诊科收治的51例伴有急性肺损伤的不明原因重症肺炎病例。结果51例患者临床表现为咳嗽51例，咳痰31例，发热45例，气急51例，肌肉酸痛13例；入院时氧合指数（PaO2／FiO2）200～300者22例，〈200者29例。影像学表现以双肺渗出性改变为主，有斑片状、毛玻璃状、网状和结节样改变，病灶迅速进展或融合。本组双侧肺病变占94．1%（48／51）。15例死亡，病死率29．4％（15／51），死亡病例均为急性呼吸窘迫综合征（ARDS）病例，占ARDS病例数51．7％（15／29），10例有基础肺病，占死亡病例66．7％。51例患者中，41例使用甲泼尼龙静脉给药治疗，28例患者存活。明确诊断6例，为侵袭性肺曲霉病3例，甲型H1N1流感3例。51例血清支原体、衣原体、军团菌抗体均阴性。痰真菌培养肺曲霉阳性6例中，G试验阳性2例，GM试验均阴性。人类免疫缺陷病毒（HIV）抗体阳性6例。32例进行血清病毒（巨细胞病毒、腺病毒和呼吸道合胞病毒）抗体检测，巨细胞病毒IgG阳性9例。结论重症肺炎导致急性肺损伤的病因学诊断是临床难题，存在基础肺部疾病可能与重症肺炎的预后相关。激素的早期应用对急性肺损伤的预后有一定的积极作用。     

Pneumonia and seizures due to hypereosinophilic syndrome—organ damage and eosinophilia without synchronisation: A case report

BACKGROUNDHypereosinophilic syndrome (HES) is a condition characterized by increased eosinophil proliferation in the bone marrow, as well as tissue eosinophilia, often causing organ damage. The cause of the disease is unknown. Initial symptoms include fatigue, cough, shortness of breath, myalgia, angioedema, fever, and pneumonia. In addition to the respiratory symptoms, damage to the central nervous system can lead to severe seizures. Here, we report a case with pneumonia and complex partial seizures secondary to HES.CASE SUMMARYA 94-year-old woman was admitted to our hospital for heart failure and bloody stools. After admission, she also showed symptoms of pneumonia. Non-contrast computed tomography of the chest showed pleural effusion and infiltrative shadows. Lower gastrointestinal endoscopy showed multiple ulcers in the sigmoid colon. Blood analyses showed marked eosinophilia (eosinophils 1760/mm³, total leukocytes 6850/mm³). Initial treatment with furosemide 20 mg/d and prednisolone 25 mg/d relieved these symptoms. However, the patient subsequently experienced localised epileptic seizures characterized by bilateral eyelid twitching and eyes rolling upwards, without generalized convulsions, and respiratory arrest occurred. Electroencephalography showed spikes and waves. Non-contrast magnetic resonance imaging of the brain showed extensive periventricular hyperintensity. With administration of levetiracetam 1000 mg/d the epileptic seizures disappeared. However, the patient’s consciousness remained impaired, and her pneumonia worsened again. Two weeks later, she died of pneumonia. CONCLUSIONHES symptoms are variable and atypical, and the level and timing of eosinophilia and organ damage are often discordant.     

Extracorporeal membrane oxygenation as a bridge to liver transplantation for acute respiratory distress syndrome-induced life-threatening hypoxaemia aggravated by hepatopulmonary syndrome

Introduction

Combined with massive lung aeration loss resulting from acute respiratory distress syndrome, hepatopulmonary syndrome, a liver-induced vascular lung disorder characterized by diffuse or localized dilated pulmonary capillaries, may induce hypoxaemia and death in patients with end-stage liver disease.

Methods

The case of such a patient presenting with both disorders and in whom an extracorporeal membrane oxygenation was used is described.

Results

A 51-year-old man with a five-year history of alcoholic cirrhosis was admitted for acute respiratory failure, platypnoea and severe hypoxaemia requiring emergency tracheal intubation. Following mechanical ventilation, hypoxaemia remained refractory to positive end-expiratory pressure, 100% of inspired oxygen and inhaled nitric oxide. Two-dimensional contrast-enhanced (agitated saline) transthoracic echocardiography disclosed a massive right-to-left extracardiac shunt, without patent foramen ovale. Contrast computed tomography (CT) of the thorax using quantitative analysis and colour encoding system established the diagnosis of acute respiratory distress syndrome aggravated by hepatopulmonary syndrome. According to the severity of the respiratory condition, a veno-venous extracorporeal membrane oxygenation was implemented and the patient was listed for emergency liver transplantation. Orthotopic liver transplantation was performed at Day 13. At the end of the surgical procedure, the improvement in oxygenation allowed removal of extracorporeal membrane oxygenation (Day 5). The patient was discharged from hospital at Day 48. Three months after hospital discharge, the patient recovered a correct physical autonomy status without supplemental O₂.

Conclusions

In a cirrhotic patient, acute respiratory distress syndrome was aggravated by hepatopulmonary syndrome causing life-threatening hypoxaemia not controlled by standard supportive measures. The use of extracorporeal membrane oxygenation, by controlling gas exchange, allowed the performing of a successful liver transplantation and final recovery.     

Intravenous immunoglobulin in adult varicella pneumonia complicated by acute respiratory distress syndrome

Pneumonia is a rare but serious complication of varicella in adults. We report a case of a previously healthy 32-year-old man with varicella pneumonia that was complicated by acute respiratory distress syndrome. He was treated successfully with acyclovir and intravenous immunoglobulin in addition to mechanical ventilation. We conclude that intravenous immunoglobulin, in combination with acyclovir, is a safe and probably effective therapy for adult varicella pneumonia that is complicated by acute respiratory distress syndrome.     

肺泡表面活性物质联合鼻塞持续气道正压通气治疗早产儿呼吸窘迫综合征的疗效及护理

目的:观察肺泡表面活性物质治疗早产儿呼吸窘迫综合征的疗效。方法:将156例呼吸窘迫综合征患儿随机分为治疗组(78例)及对照组(78例)。治疗组于出生后30min～2h从气管插管内滴入肺泡表面活性物质(固尔苏),每次100～200mg/kg,用药后应用鼻塞持续气道正压(NCPAP)装置辅助呼吸;对照组单纯应用NCPAP装置辅助呼吸。两组其他治疗及护理措施相同。结果:治疗组辅助呼吸、机械通气、住院时间明显缩短,与对照组比较,差异有显著性(均P0.05);治疗组72h胸部X线摄片正常率高于对照组(P0.05)。结论:保持呼吸道通畅,采取正确的氧疗和加强机械通气的管理,配合早期足量的应用肺泡表面活性物质,可提高呼吸窘迫综合征患儿的疗效和缩短病程。     

高频振荡通气在新生儿呼吸窘迫综合征治疗中的应用

目的 探讨高频振荡通气(HFOV)治疗新生儿呼吸窘迫综合征(NRDS)的疗效及安全性.方法 对NRDS 64例,随机分为常频机械通气(CMV)30例和高频振荡通气(HFOV)34例,比较两组患儿治疗前后的血气分析、吸入氧浓度(FiO2)、氧合指数(OI)及并发症等.结果 HFOV组患儿吸入氧分数明显低于CMV组,PaCO2及氧合指数迅速下降,pH及PaO2明显上升,HFOV组发生肺气漏及慢性肺部疾病(CLD)等并发症低于CMV组(P<0.05).结论 HFOV用于治疗新生儿呼吸窘迫综合征,是一种疗效肯定、安全性好的新型机械通气方法.     

社区获得性鲍曼不动杆菌肺炎一例并文献回顾

本文报道1例社区获得性鲍曼不动杆菌肺炎患者,并发急性呼吸窘迫综合征（ARDS）,先后采取小潮气量肺保护性通气、滴定式液体复苏、俯卧位通气、连续性肾替代治疗（CRRT）稳定内环境、调整抗生素剂量、升级抗生素、体外膜肺氧合（ECMO）等治疗,但病情还是进展加重,最终死亡。回顾治疗过程,感染未能完全控制是患者死亡的主要原因。因此,本文将患者的病情发展、治疗过程加以总结,以期为类似患者改善预后提供经验。     

In vivo evaluation of the inhibitory capacity of human plasma on exogenous surfactant function

Objective The adult respiratory distress syndrome (ARDS) and neonatal respiratory distress syndrome (RDS) are characterized by high permeability pulmonary edema which contains plasma-derived proteins inhibiting pulmonary surfactant function. Currently, discussion continues as to what dose of surfactant is required for treatment of these syndromes. Design The purpose of this study was to investigate the amount of exogenous surfactant needed to overcome the inhibitory components in human plasma. Male adult rats suffering from respiratory failure due to surfactant depletion after whole-lung lavage received human plasma (4 ml/kg body weight) mixed with surfactant at different concentrations, intratracheally. Rats receiving surfactant only at different concentrations served as controls. Blood gas analysis was performed. Measurements and results It was demonstrated that plasma (4 ml/kg≈273 mg, plasma proteins/kg) mixed with surfactant at 300 mg/kg was able to increase and maintain PaO₂ at normal values. Plasma mixed with surfactant at 100 mg/kg, after initial restoration of blood gases, showed deterioration of PaO₂ values. Plasma mixed with surfactant at a dose of 50 mg/kg did not improve PaO₂ whereas surfactant at 50 mg/kg, without plasma, restored blood gases to pre-lavage values. Conclusion It is concluded that approximately 1 mg surfactant phospholipids is required to overcome the inhibitory effect of approximately 1 mg plasma proteins. For clinical practice this means that an excess of surfactant should be given, or repeatedly be substituted (“titrated”) at low concentrations, until blood gases improve. This work was financially supported by the Dutch Foundation for Medical Research     

Pulse methylprednisolone therapy in type 3 adenovirus pneumonia with hypercytokinemia

Adenovirus pneumonia is uncommon but its severe infection has a mortality as high as 10%, and survivors may have residual airway damages, manifested by bronchiectasis, bronchiolitis obliterans, or pulmonary fibrosis. We report a case of adenovirus pneumonia demonstrating fatal respiratory distress. Adenovirus was isolated from pharyngeal specimens using cell culture and typed as serotype 3 by a combination of polymerase chain reaction (PCR) and restriction fragment length polymorphism analysis. The patient characteristically showed hypercytokinemia, characterized by increased levels of lactate dehydrogenase, ferritin, and several cytokines including interferon-gamma and interleukin-6. We treated the patient with pulse methylprednisolne therapy (25 mg/kg/day, for 3 days), resulting in the rapid amelioration of respiratory distress. This is the first report describing the treatment of pulse methylprednisolone therapy in fatal adenovirus pneumonia. During the clinical course, serum Krebs von den Lungen-6 (KL-6), which is a marker for the activity of diffuse interstitial lung disease, was elevated, suggesting that serum KL-6 could be available as a marker of pulmonary prognosis in viral pneumonia.