Marshall Peter S, Mathews Kusum S, Siegel Mark D
Pulmonary & Critical Care Section, Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
J Intensive Care Med. 2011 Sep-Oct;26(5):275-94. doi: 10.1177/0885066610392658. Epub 2011 May 23.
Pulmonary embolus (PE) is estimated to cause 200 000 to 300 000 deaths annually. Many deaths occur in hemodynamically unstable patients and the estimated mortality for inpatients with hemodynamic instability is between 15% and 25%. The diagnosis of PE in the critically ill is often challenging because the presentation is nonspecific. Computed tomographic pulmonary angiography appears to be the most useful study for diagnosis of PE in the critically ill. For patients with renal insufficiency and contrast allergy, the ventilation perfusion scan provides an alternative. For patients too unstable to travel, echocardiography (especially transesophageal echocardiography) is another option. A positive result on lower extremity Doppler ultrasound can also aid in the decision to treat. The choice of treatment in PE depends on the estimated risk of poor outcome. The presence of hypotension is the most significant predictor of poor outcome and defines those with massive PE. Normotensive patients with evidence of right ventricular (RV) dysfunction, as assessed by echocardiography, comprise the sub-massive category and are at intermediate risk of poor outcomes. Clinically, those with sub-massive PE are difficult to distinguish from those with low-risk PE. Cardiac troponin, brain natriuretic peptide, and computed tomographic pulmonary angiography can raise the suspicion that a patient has sub-massive PE, but the echocardiogram remains the primary means of identifying RV dysfunction. The initial therapy for patients with PE is anticoagulation. Use of vasopressors, inotropes, pulmonary artery (PA) vasodilators and mechanical ventilation can stabilize critically ill patients. The recommended definitive treatment for patients with massive PE is thrombolysis (in addition to anticoagulation). In massive PE, thrombolytics reduce the risk of recurrent PE, cause rapid improvement in hemodynamics, and probably reduce mortality compared with anticoagulation alone. For patients with a contraindication to anticoagulation and thrombolytic therapy, surgical embolectomy and catheter-based therapies are options. Thrombolytic therapy in sub-massive PE results in improved pulmonary perfusion, reduced PA pressures, and a less complicated hospital course. No survival benefit has been documented, however. If one is considering the use of thrombolytic therapy in sub-massive PE, the limited documented benefit must be weighed against the increased risk of life-threatening hemorrhage. The role of surgical embolectomy and catheter-based therapies in this population is unclear. Evidence suggests that sub-massive PE is a heterogeneous group with respect to risk. It is possible that those at highest risk may benefit from thrombolysis, but existing studies do not identify subgroups within the sub-massive category. The role of inferior vena cava (IVC) filters, catheter-based interventions, and surgical embolectomy in life-threatening PE has yet to be completely defined.
据估计,肺栓塞(PE)每年导致20万至30万人死亡。许多死亡发生在血流动力学不稳定的患者中,血流动力学不稳定的住院患者估计死亡率在15%至25%之间。危重症患者的PE诊断往往具有挑战性,因为其临床表现不具有特异性。计算机断层扫描肺动脉造影似乎是危重症患者PE诊断最有用的检查。对于肾功能不全和对比剂过敏的患者,通气灌注扫描提供了一种替代方法。对于病情过于不稳定无法转运的患者,超声心动图(尤其是经食管超声心动图)是另一种选择。下肢多普勒超声检查结果呈阳性也有助于治疗决策。PE的治疗选择取决于估计的不良结局风险。低血压的存在是不良结局最显著的预测因素,并定义了大面积PE患者。经超声心动图评估,有右心室(RV)功能障碍证据的血压正常患者属于次大面积类别,不良结局风险中等。临床上,次大面积PE患者很难与低风险PE患者区分开来。心肌肌钙蛋白、脑钠肽和计算机断层扫描肺动脉造影可增加对患者患有次大面积PE的怀疑,但超声心动图仍然是识别RV功能障碍的主要手段。PE患者的初始治疗是抗凝。使用血管加压药、正性肌力药、肺动脉(PA)血管扩张剂和机械通气可使危重症患者病情稳定。大面积PE患者推荐的确定性治疗是溶栓(除抗凝外)。在大面积PE中,与单独抗凝相比,溶栓可降低复发性PE的风险,使血流动力学迅速改善,并可能降低死亡率。对于有抗凝和溶栓治疗禁忌证的患者,手术取栓和基于导管的治疗是选择。次大面积PE的溶栓治疗可改善肺灌注,降低PA压力,并使住院过程并发症减少。然而,尚未证明有生存获益。如果考虑在次大面积PE中使用溶栓治疗,必须将有限的已记录获益与危及生命出血风险增加进行权衡。手术取栓和基于导管的治疗在该人群中的作用尚不清楚。有证据表明,次大面积PE在风险方面是一个异质性群体。最高风险的患者可能从溶栓中获益,但现有研究未识别出次大面积类别中的亚组。下腔静脉(IVC)滤器、基于导管的干预措施和手术取栓在危及生命的PE中的作用尚未完全明确。