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1、Adult Respiratory distress syndrom(ARDS)成人呼吸窘迫综合征急救部 秦宇红1.Difinition-定义vALI and its more severe sub-set, ARDS, is a common clinical disorder characterized by injury to the alveolar epithelial and endothelial barriers of the lung, acute inflammation, and protein-rich pulmonary oedema leading to acute
2、 respiratory failure. Often occurs in the setting of MOF. 急性肺损伤及其更加严重的情况ARDS是一种常见的临床异常状况，以肺泡上皮细胞及肺内皮细胞屏障损害、急性炎症反应、富含蛋白的肺水肿导致的急性呼吸衰竭为特点。经常发生于多器管衰竭的情况下。Diagnostic criteriavAcute onset of respiratory failure with one or more risk factors (table, opposite)vHypoxaemiaALI: Ratio PaO2 (kPa) : FiO2 40ARDS:
3、Ratio PaO2 (kPa) : FiO2 27vBilateral infiltrates on CXRvPulmonary capillary wedge pressure 19mmHg, with normal colloid oncotic pressure (in patients with hypoalbuminaemia, the critical PCWP is approx. serum albumin (g/l) 0.57, see P282) or clinical exclusion of cardiac failure. 诊断标准v发生急性呼吸衰竭，伴有1或多个危
4、险因素（见对侧表）v低氧血症 ALI : PaO2 (kPa) : FiO2 40 FiO2 为吸氧浓度之意 ARDS: PaO2 (kPa) : FiO2 27v胸部X线检查示双肺浸润v肺动脉嵌压（PCWP）小于19mmHg，胶体渗透压正常（在低蛋白血症患者，PCWP大约为血清白蛋白(g/l) 0.57）或临床排除心力衰竭。 Disorders associated with the development of ARDSDirect lung injury 直接肺损伤 vAspiration 误吸Gastric contents 胃内容物Near drowning 淹溺vInhalatio
5、n injury 吸入性损伤Noxious gases 有毒气体Smoke 烟Disorders associated with the development of ARDSvPneumonia 肺炎Any organism 任何病原菌PCP（Pneumocystis pneumonia）卡氏肺囊虫性肺炎vPulmonary vasculitides 肺血管炎vPulmonary contusion 肺挫伤vDrug toxicity or overdose 药物中毒或过量Oxygen 氧中毒Opiate overdose 阿片剂过量Bleomycin 博来霉素Salicylates 水杨酸
6、盐Indirect (non-pulmonary) injuryvShock 休克 vSepticaemia 脓毒血症vAmniotic or fat embolism 羊水或脂肪栓塞vAcute pancreatitis 急性胰腺炎vMassive haemorrhage 大出血vMultiple transfusions 大量输血vDIC（diffusion intravascular coagulation）Indirect (non-pulmonary) injuryvMassive burns 大面积烧伤vMajor trauma 严重创伤vHead injury 头外伤Raised
7、 ICP 颅内压升高Intracranial bleed 颅内出血vCardio-pulmonary bypass 心肺旁路术vAcute liver failure 急性肝衰减InvestigationsvCXRvABG (consider arterial line as regular samples may be required)vTake blood for FBC, U&Es, LFTs and albumin, coagulation, X-match, and CRPvSeptic screen (culture blood, urine, sputum)vECGvConsi
8、der drug screen, amylase if history suggestivevPulmonary artery catheter to measure PCWP, cardiac output, mixed venous oxygen saturation and to allow calculation of haemodynamic parameters检查v胸部X线检查v动脉血气分析v采血查全血细胞、肾功、电解质、肝功和白蛋白、凝血功能、X-match和 CRPv感染筛查（血、尿、痰培养）v心电图v如有相关病史行药物筛查及淀粉酶检测v肺动脉导管测量PCWP，心输出、混合静
9、脉氧浓度并计算血流动力学参数。Other investigations if appropriate其它可用检查CT chestBroncho-alveolar lavage for microbiology and cell count (?eosinophils)Carboxy-haemoglobin estimation. 胸部CT检查支气管-肺泡灌洗查微生物及细胞计数（嗜酸性粒细胞？）碳-氧血红蛋白测定ManagementvAlmost all cases of ALI alone will require HDU/ICU care: liaise earlyvThe main aim
10、 is to identify and treat the underlying cause whilst providing support for organ failure:Respiratory support to improve gas exchange and correct hypoxiaCardiovascular support to optimize oxygen delivery to tissuesReverse or treat the underlying cause.治疗v几乎所有的ALI患者需要重症监护v主要目的是明确诊断，治疗原发病并对衰竭器管提供支持。 呼
11、吸支持以改善通气、纠正缺氧。 心血管系统支持以改善组织供氧 逆转和治疗原发病Respiratory support -Spontaneously breathing patientvIn very mild ALI, hypoxia can be corrected with increased inspired oxygen concentrations (FiO2 40-60%). However, such patients are rarely recognized as having ALI as a cause of their respiratory failure.v对于非常轻
12、症的ALI患者,增加吸入氧浓度(FiO2 40-60%)即可纠正缺氧。然而，这样的轻症患者很少被诊断出ALI作为其呼吸衰竭的原因。自主呼吸患者的呼吸支持vPatients invariably require higher oxygen concentrations (non-rebreather masks with reservoir FiO2 60-80%) or CPAP (see P904). Consider transfer to HDU/ICUv如果患者总是需要高浓度给氧（带贮气器的非再呼吸面罩，给氧浓度60%80%）或持续正压通气支持，考虑转入ICU。Mechanical v
13、entilationvIndications for mechanical ventilationInadequate oxygenation (PaO2 0.6)Rising or elevated PaCO2 (6kPa)Clinical signs of incipient respiratory/cardiovascular failure.v机械通气适应症. 氧合不足（当 FiO2 0.6时PaO2 45mmHg) 临床出现呼吸或循环衰竭 Mechanical ventilationvThis is the realm of the ICU physician. Main aim i
14、s to improve oxygenation/ ventilation while minimizing the risk of further ventilator-induced lung injury; termed lung protective ventilation.v机械通气属于ICU医师的工作范围。主要目的是改善氧合/通气同时最小化通气诱发的肺损伤，也就是肺保护性通气策略。Mechanical ventilation -General principles（一般原则）vControlled mechanical ventilation with sedation ( neu
15、romuscular blockade).v用镇静剂(神经肌肉阻滞剂)实现可控机械通气vAim for tidal volume 6ml/kg. Recent evidence has confirmed that ventilation with smaller tidal volumes is associated with improved outcome compared to the traditional approach (10-12ml/kg).v目标潮气量6ml/kg。最近的证据表明小潮气量通气与传统的方法（ 10-12ml/kg ）比可明显改善愈后。Mechanical v
16、entilation -General principlesvStart with FiO2 = 1.0. Subsequent adjustments are made to achieve oxygen saturation 90% with FiO2 0.6.v开始用纯氧，继而调整使得在给氧浓度小于0.6时氧饱和度达到90%以上。vPositive end expiratory pressure (PEEP) improves oxygenation in most patients and allows reduction in FiO2. Usual starting level,
17、5-10cm H2O, with optimal levels in the range 10-15cm H2O. Beware hypotension due to reduction in venous return.v在大多数患者，PEEP可以改善氧合从而可降低给氧浓度。通常从5-10cm H2O开始，理想水平为10-15cm H2O。需小心因静脉回流减少而导致的低血压。Mechanical ventilation -General principlesvThe use of smaller tidal volumes may impair CO2 clearance with resu
18、lting acidosis despite high ventilatory rates (20-25 breaths/minute). Further increases in rate or tidal volume risk worsening ventilator-induced lung injury. Gradual increases in pCO2 (up to 13kPa) are well tolerated in most patients and acidosis (pH 7.25) can be treated with intravenous bicarbonat
19、e, so-called permissive hypercapnia.v尽管通气频率高（20-25次/分） ，应用小潮气量通气模式可能降低CO2清除率导致酸中毒。进一步增加呼吸频率或潮气量则增加通气诱发的肺损伤的风险。大多患者可以耐受缓慢增加的pCO2（最高可达13kPa/97.7mmHg ，酸中毒时(pH 48 hours, or multi-organ failure.v治疗肾衰：肾衰常见，可能需要肾脏替代治疗以控制液体平衡和血生化。v经肠道饮食:有助于保持消化道内膜的完整性，与全胃肠外营养比较落，可以减少全身脓毒症的风险。 胃排空延迟、肠蠕动减弱在ICU患者中常见，对促胃肠动力药物（胃
20、复安、红霉素）有反应，或需要经鼻导管空肠饮食。如果机械通气超过48小时或有多脏器衰竭，应考虑应激性溃疡的预防（ H2-blockers ）On-going managementvCoagulopathy. Common and if mild does not require therapy. If severe/DIC, expert advice should be sought.v凝血障碍：常见，如果轻微则不需治疗。如出现严重凝血障碍如DIC，则需寻求专家的指导。vSteroid therapy 激素治疗ALI/ARDS: no benefit in the acute stage. T
21、reatment (2mg/kg/day of methylprednisolone) later in the course of the disease (7-10 days) may improve prognosis but further studies are awaited.ALI/ARDS：在急性期使用无益处。在疾病晚期（7-10天）治疗可以改善预后，但需待进一步的研究结果。On-going managementoSepsis: evidence suggests that some patients with refractory septic shock (ongoing/
22、increasing vasopressor requirements) may have relative or functional adrenal insufficiency and may benefit from supraphysiological steroid replacement (200-300mg/day hydrocortisone). Identification of patients likely to benefit unclear at present, but ACTH stimulation test may help discriminate.o脓毒症
23、：证据表明，一些难治性脓毒症性休克（正在使用或需增加血管活性药物用量）患者有相对的功能性肾上腺功能不全，可能从超生理剂量的激素（200-300mg氢化可的松）替代治疗获益。目前如何识别这些可能获得益的患者尚不清楚，但ACTH刺激试验可能有助于区分他们。Causes of sudden deterioration in ARDSARDS患者病情突然恶化的原因Respiratory 呼吸系统vPneumothorax 气胸vBronchial plugging 支气管堵塞vDisplaced ET tube 气管内导管移位vPleural effusion (haemothorax) 胸膜渗出（血
24、胸）vAspiration (e.g. NG feed) 误吸（如经鼻-胃管饮食）Cardiovascular 心血管系统vArrhythmia 心律失常vCardiac tamponade 心包添塞vMyocardial infarction 心肌梗死vGI bleed (stress ulcer) 消化道出血（应激性溃疡）vSepticaemia 脓毒血症Outcome-愈后vThe outcome for ALI/ARDS has improved in recent years, with overall mortality rates of 40%.v近年来，ALI/ARDS的愈后已
25、大大改善，总死亡率40%。vPatients with ALI/ARDS and sepsis, liver disease, non-pulmonary organ dysfunction, or advanced age have higher mortality rates.v对于有脓毒症的ALI/ARDS患者合并肝脏疾病、非肺器管功能不全、高龄等死亡率较高。vIn survivors, although formal lung function tests are abnormal, respiratory compromise at 1-2 years is unusual.v在存活
26、患者，尽管正规的肺功能检测异常，但呼吸功能损害在1-2年内是罕见的。vThere is increasing evidence that survivors suffer considerable neuromuscular and psychological disability. This may reflect the period of prolonged critical illness rather than be specific for ALI/ARDS.v越来越多的证据表明，存活者存在相当严重的神经肌肉残疾和心理障碍。这可能是长期严重疾病的结果，而不是因为ALI/ARDS有什么特殊。
