High Risk Pulmonary Embolism

Tsuyoshi Mitarai

BACKGROUND

In an autopsy series of hospital deaths, pulmonary embolism (PE) was found in approximately 15% of the cases and—after excluding incidental PE—to be a primary or contributing cause of death in 3.4% to 8.9% of cases.^1–5 In only 30% of this group had there been an antemortem suspicion or diagnosis of PE, a statistic that fueled the argument that PE is an underdiagnosed disease.^3–6 Conversely, another study, done after the introduction of multidetector row computed tomographic pulmonary angiography (MDCTPA) in 1998, pointed to the possible overdiagnosis of PE.⁷ No significant change in the incidence of PE was reported between 1993 and 1998 (from 58.8 to 62.3 per 1,00,000; annual percentage change [APC] 0.5%). Between 1998 and 2006, when the use of MDCTPA increased 7- to 13-fold,^8–11 an 81% increase in incidence of PE was reported (from 62.1 to 112.3 per 1,00,000; APC 7.1%).⁷ Despite this improved detection of PE, reduction in PE-associated mortality has been modest,⁷ raising concern that we are diagnosing and treating (and sometimes overdiagnosing/overtreating) patients with low-risk PE and an intrinsically low mortality rate, while underdiagnosing and/or undertreating patients with high-risk PE. This hypothesis is supported by the findings in the Emergency Medicine Pulmonary Embolism in the Real World Registry (EMPEROR).¹² In the analysis of 1,880 emergency department (ED) patients with confirmed PE (88% diagnosed with CTPA), the all-cause mortality rate at 30 days was only 5.4%.¹² Although only 3% of the registry had a systolic blood pressure (SBP) <90 mm Hg at presentation, 30-day mortality of this subgroup was much higher than those with SBP >90 (14.0% vs. 1.8%).¹³ Furthermore, only 15.5% (9/58) of this high-risk subgroup received reperfusion therapy (systemic thrombolytic therapy or embolectomy).¹³ The review of data from the Nationwide Inpatient Sample also shows underutilization of reperfusion therapy among PE patients with shock or ventilator dependence (30%, 1.2%, and 0.3% for systemic thrombolytic therapy, surgical embolectomy, and catheter embolectomy, respectively). The review also reports higher case fatality rate attributable to PE not treated versus treated with systemic thrombolytic therapy (42% vs. 8.4%).¹⁴ To improve the mortality outcome of this disease, there needs to be an improvement in the care of patients in the high-risk PE subgroups. This chapter focuses on the diagnostic approach and management of unstable patients with suspected and confirmed PE in the ED. A discussion of the diagnosis and management of PE in stable patients may be found elsewhere.^15–18

CLASSIFICATION OF ACUTE PULMONARY EMBOLISM

One of the hallmarks of PE is its wide spectrum of clinical presentation. The mortality rate of PE ranges from approximately 1% for low-risk PE to 65% for massive PE with cardiac arrest.^19–22 Classification of PE into different risk subgroups is important for appropriate prognostication, treatment selection, and disposition. Classification of PE based solely on the degree of clot burden fails to account for the patient’s underlying cardiopulmonary reserve or physiologic response against the clot. In fact, anatomically massive PE—defined by an angiographic obstruction of >50% or obstruction of two lobar arteries—is rarely associated with shock and accounts for only 50% of fatal PE⁸; in patients with saddle emboli, only 8% to 14% are reported to have sustained hypotension.^23,24 Right ventricular (RV) failure and associated hemodynamic compromise, on the other hand, reflect both embolism size as well as underlying cardiopulmonary status and serve as a better indicator of clinical outcome.^6,25–27 In 2011, the American Heart Association (AHA) proposed classifying PE into three groups based on the patient’s physiologic response to the embolus: massive, submassive, and low-risk PE.²⁸ The European Society of Cardiology (ESC) guidelines use the terms high-risk, intermediate-risk, and low-risk PE.¹⁵

Massive PE is defined as an acute PE accompanied by any of the following:

• Systolic blood pressure < 90 mm Hg for at least 15 minutes or requiring inotropic support without alternative cause of hypotension, such as arrhythmia, hypovolemia, sepsis, or left ventricular dysfunction
  
• Pulselessness
  
• Persistent bradycardia with heart rate < 40 bpm with signs of shock

ESC guidelines include a drop of SBP > 40 mm Hg over 15 minutes in this category.^15,22

Submassive PE is defined as an acute PE without hypotension with any of the following:

• Myocardial necrosis
  
  
  
  • Troponin I > 0.4 ng/mL or troponin T > 0.1 ng/mL
  
  
• RV dysfunction
  
  
  
  • RV systolic dysfunction or dilation (apical four-chamber RV diameter divided by LV diameter > 0.9) on echocardiography
    
  • RV dilation on CT (four-chamber RV diameter divided by LV diameter > 0.9)
    
  • Brain natriuretic peptide (BNP) > 90 pg/mL
    
  • N-terminal pro-BNP > 500 pg/mL
    
  • Electrocardiographic (ECG) changes (new complete or incomplete right bundle branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)

Low-risk PE encompasses all other patients with PE not included in these first two categories.

In large registries, massive PE accounts for <5% of patients with acute PE,^12,29 but it is associated with a high mortality rate. The International Cooperative Pulmonary Embolism Registry (ICOPER) reported 90-day mortality rates of nonmassive and massive PE to be 15.1% and 58.3%, respectively.²⁹ The Management Strategy and Prognosis of Pulmonary Embolism Registry (MAPPET) reported an in-hospital mortality rate of 8.1% for submassive PE, 15% for massive PE meeting hypotension criteria without signs of shock or vasopressor use, 25% for massive PE with signs of shock or requiring use of vasopressors, and 65% in patients requiring cardiopulmonary resuscitation (CPR).²² A conceptual guide to the triage of PE patients by clinical severity subgroups is shown in Figure 11.1. The determination of which low-risk PE patients may be treated as an outpatient is outside the scope of this chapter.

MASSIVE PULMONARY EMBOLISM

Pathophysiology

The relative utility of various therapies for massive PE, including inotropic and vasopressor drugs, has yet to be assessed in a robust trial. However, a rational management strategy can be guided by an understanding of the pathophysiology of cardiovascular compromise in these patients (Fig. 11.2).

Acute PE produces an increase in pulmonary vascular resistance (PVR) through not only mechanical obstruction but also pulmonary artery vasoconstriction from hypoxia,³⁰ neural reflexes,³¹ and humoral factors.³² This sudden increase in PVR is poorly tolerated by the right ventricle (RV), which cannot generate mean pulmonary artery pressures (PAPs) of ≥40 mm Hg.³³ The increase in RV afterload results in a proportional decrease in RV stroke volume (RVSV) as well as RV dilation.^34,35 The decrease in RVSV compromises left ventricle (LV) preload and, thus, LV stroke volume (LVSV), which—once a patient’s compensatory sympathetic tachycardia and increased systemic vascular resistance (SVR) are no longer sufficient—eventually results in systemic arterial hypotension.

The accompanying RV dilation/increased RV end-diastolic volume (RVEDV) further complicates this process in several ways: (1) It produces significant tricuspid regurgitation (TR), which results in increased RV preload.³⁶ A volume-overloaded RV will eventually take residence on the descending portion of the Frank-Starling curve, further decreasing RVSV.³⁴ (2) It causes a shift of the interventricular septum toward the left ventricle, as well as an increase in pericardial constraint; both of these effects result in a drop of LV preload and thus a drop in LVSV.^36–39 (3) It causes an elevation in RV end-diastolic pressure (RVEDP), which results in an increase in RV wall stress (RV wall stress = RV radius × RVEDP) and an associated decrease in RV coronary perfusion pressure (RVCPP) (RVCPP = Mean arterial pressure − RVEDP).⁶ This increase in RV wall stress and decrease in RVCPP will produce higher RV oxygen demand and lower oxygen supply, respectively. These changes—particularly in the context of systemic hypotension—can easily precipitate RV ischemia or infarction.^40–43 Figure 11.2 demonstrates this vicious cycle, which explains how patients with massive PE can continue to deteriorate without a recurrent PE.

Considerations during Patient Stabilization

Untreated patients with massive PE can further decompensate through a loss of physiologic compensation, recurrent PE, and/or in response to interventions. Two-thirds of patients with a fatal PE die within the first hour of presentation.⁶ Careful stabilization, rapid diagnostic efforts, and appropriate treatment of suspected massive PE therefore need to take place simultaneously. The concept of a golden hour should be applied to these patients just as with patients with major trauma, ST elevation myocardial infarction (STEMI), and acute stroke.⁶ Understanding the physiology of massive PE as described above illuminates several key points that are important in stabilization of such patients in the ED:

• Excessive intravenous (IV) fluid in patients with massive PE suffering from RV dilation and failure can further compromise cardiac output by worsening of RV ischemia and increasing septal bowing toward the LV.^44–46 An initial 500-mL IV fluid bolus is reasonable, but if hemodynamic improvement is not observed, use of vasopressors should not be delayed. This is in stark contrast to the majority of hypotensive patients in the ED who typically require aggressive fluid resuscitation, including those with nonmassive PE but hemodynamic instability caused by sepsis and/or hypovolemia. Clinical impression and early bedside transthoracic echocardiogram (TTE) (see Diagnostic Approach to Suspected Massive PE) are therefore important determinants of the early resuscitative pathway.
  
• Vasopressor therapy should be considered early in massive PE in order to maintain RVCPP and minimize RV ischemia and infarction. There are no human trials data to establish superiority of one vasopressor over another in massive PE. In a canine PE model with relative hypotension, both norepinephrine and phenylephrine showed restoration of hemodynamics, but only the norepinephrine group showed improved RV function, presumably through its beta-1 properties.⁴⁷ Dopamine is known to have a higher tachyarrhythmia risk compared to norepinephrine for the treatment of patients with shock,⁴⁸ and such arrhythmia is poorly tolerated in patients with acute right ventricular failure.^35,49 Epinephrine has a theoretical benefit for its combined property of positive inotropy and vasoconstriction, but clinical evidence on its use is limited.⁵⁰ Therefore, norepinephrine seems to be a reasonable vasopressor of choice for massive PE, with epinephrine as a possible alternative. The risk of vasopressor infusion through a peripheral IV should be weighed against the risks of delay in blood pressure restoration and of increased bleeding from a central line insertion site (if thrombolytic agents are to be used).
  
• The inotropic agent dobutamine has been shown to improve cardiac output in PE patients with evidence of cardiogenic shock without profound hypotension in a small ICU study.⁵¹ However, in massive PE with significant hemodynamic compromise, dobutamine should be used cautiously, as it can worsen hypotension through systemic vasodilation and may necessitate the concurrent use of norepinephrine.³⁵
  
• Providing adequate oxygen promptly reduces PAP and improves cardiac output in patients with pulmonary hypertension.^35,52 Orotracheal intubation, however, poses a threat to patients with massive PE, as it removes the compensatory sympathetic tone and can exacerbate systemic hypotension.⁶ If intubation is necessary, vasopressor therapy should be titrated to maintain adequate mean arterial pressure (MAP) (i.e., ≥65 mm Hg), and induction agents known to cause systemic vasodilation, such as propofol, should be avoided. Care should be taken to minimize hypoxia, prolonged hypercarbia, and worsening of acidosis, all of which may increase PVR.^53–55 Unfortunately, despite these precautionary measures, a patient may still decompensate following intubation. A retrospective chart review of 52 normotensive and nonintubated patients requiring emergent pulmonary embolectomy showed 19% rate of hemodynamic collapse (refractory to fluid, inotrope, or vasopressor administration and requiring emergent cardiopulmonary bypass [CPB]) after receiving induction of general anesthesia for intubation.⁵⁶ The rate of hemodynamic collapse following emergency intubation for massive PE patients in the ED may be even higher. Although there are no data for the use of noninvasive positive-pressure ventilation (NIPPV) in massive PE, carefully selected patients may benefit from the use of short-term NIPPV as a bridge to definitive therapies, including administration of thrombolytic agents.
  
• Even after successful intubation, positive-pressure mechanical ventilation can produce substantial destabilizing cardiovascular effects, including a decrease in venous return and an increase in PVR, resulting in further RV decompensation and subsequent hypotension.⁶ It is thought that lung hyperinflation along with excessive positive end-expiratory pressure (PEEP) can significantly reduce RV systolic function and cardiac output.⁵⁷ A low tidal volume (6 mL/kg ideal body weight) with plateau pressure goal below 30 cm H₂O should be used in massive PE,¹⁵ since this strategy seems to provide both lung and RV protection in acute respiratory distress syndrome (ARDS)⁵⁸ with lower incidence of acute cor pulmonale.⁵⁹

Diagnostic Evaluation

Massive PE poses unique challenges for the emergency physician: time constraints, physiology that is unforgiving in response to common stabilizing measures, and diagnostic uncertainty where clinical instability may preclude or delay confirmatory diagnostic studies. A step-by-step diagnostic approach to suspected massive PE is proposed below:

Step 1. Suspecting massive PE among hypotensive patients:

Massive PE should be considered in all hypotensive patients, especially with suggestive symptoms. In the MAPPET study, which included both massive and submassive PE, acute onset of symptoms (<48 hours), dyspnea, and syncope were reported in 70%, 96%, and 35% of patients, respectively.²² In the subgroup analysis of massive PE patients in the ICOPER study, reported symptoms included dyspnea (81%), chest pain (40%), and syncope (39%).⁶⁰

Step 2: Transthoracic echocardiogram:

TTE is a noninvasive and easily repeatable bedside procedure that can be performed by the emergency physician without interfering with ongoing stabilizing interventions. In cases of massive PE, TTE may demonstrate RV dilation and hypokinesis, septal shift, and tricuspid regurgitation (TR). While the absence of these echocardiographic findings does not rule out PE (sensitivity 60% to 70%), it effectively eliminates PE as a cause of hemodynamic instability and encourages a search for alternative explanations of a patient’s hypotension.¹⁵ The presence of such TTE findings should change the urgency of a confirmatory PE study and justifies the initiation of stabilizing maneuvers discussed above. Finally, TTE will identify emboli in transit in 4% to 18% of patients with acute PE^61–64 and can help identify other causes of shock, including cardiac tamponade, aortic dissection, hypovolemia, LV dysfunction, and valvular insufficiency (see Chapter 6).¹⁵

Step 3: Confirmatory studies for massive PE:

Pending a confirmatory study, therapeutic anticoagulation with intravenous unfractionated heparin (UFH) should be started (in the absence of a drug contraindication) for all patients in whom there is high or intermediate suspicion of PE.²⁸ The standard dose of UFH for the treatment of PE is an 80 unit/kg IV bolus followed by 18 unit/kg/min.⁶⁵

Given its widespread availability, diagnostic accuracy, and short study time, MDCTPA is the study of choice for confirmation of massive PE. Because of the frequent finding of proximal or central pulmonary circulation clot in massive PE, MDCTPA is usually able to confirm the diagnosis.^15,66 Even in patients with renal insufficiency, the risk of contrast-induced nephropathy is likely outweighed by the risk of delay in the diagnosis and treatment.

Although its availability in the ED may be limited, transesophageal echocardiogram (TEE) should be considered in cases in which a patient has an IV contrast allergy or is hemodynamically too unstable to be transported to CT. In patients with suspected PE noted to have RV dysfunction on TTE, TEE has been shown to have a sensitivity of 80% to 96.7% and specificity of 84% to 100% for massive PE (by detection of proximal clots).^67–70

Ventilation/perfusion (V/Q) studies require a prolonged departure from the ED and have limited utility in a patient with massive PE. Similarly, lower extremity Doppler ultrasound, while increasing the likelihood of PE diagnosis if positive, neither confirms nor excludes a diagnosis of massive PE.

A confirmatory diagnosis of massive PE, while not required before initiating therapeutic anticoagulation, is preferred before initiating reperfusion therapy such as systemic thrombolytic therapy, surgical embolectomy, or catheter-directed therapy (CDT). However, if severe hemodynamic instability does not permit additional testing, aggressive measures may be warranted based on clinical suspicion and TTE findings alone.¹⁵ One study tested an institution-specific algorithm for suspected PE in ED patients with the goal of implementing appropriate treatment, including reperfusion therapy, in a timely manner. Twenty-one of the 204 patients had a shock index (SI) (SI = HR/SBP, normal range 0.5 to 0.7) of ≥1; of these, 14 demonstrated RV dysfunction on TTE. All 14 patients with RV dysfunction received reperfusion treatment without a confirmatory study (systemic thrombolysis, 7; catheter fragmentation, 4; and surgical embolectomy, 3) with an averaged time interval between ED admission and start of reperfusion therapy of 32 ± 12 minutes. In all 14 patients, PE was confirmed after initiation of reperfusion therapy.⁷¹

Management Guidelines

Systemic Thrombolytic Therapy

The Food and Drug Administration (FDA) has approved the following three drugs in the treatment of massive PE^15,28:

• Streptokinase: 250,000 IU IV bolus over 30 minutes followed by 100,000 IU/hour for 12 to 24 hours (or 1.5 million IU IV over 2 hours⁷²)
  
• Urokinase: 4,400 IU/kg IV bolus over 10 minutes followed by 4,400 IU/kg/h for 12 to 24 hours (or 1 million IU IV bolus over 10 minutes followed by 2 million IU IV over 110 minutes⁷³)
  
• Alteplase: 100-mg IV infusion over 2 hours (or 0.6 mg/kg IV over 15 minutes with maximum dose of 50 mg^74,75)

Systemic thrombolytic therapy is associated with more rapid clot lysis than heparin therapy alone.^76–81 In a study comparing a 2-hour infusion of 100 mg of alteplase (a recombinant tissue plasminogen activator [rt-PA]) combined with heparin versus heparin alone, at the 2-hour mark the alteplase group showed a 12% decrease in vascular obstruction, 30% reduction in mean PAP, and 15% increase in cardiac index. No changes were observed in the heparin group except for an 11% rise in mean PAP.⁷⁹ One week postintervention, however, the severity of vascular obstruction^79,82 and reversal of RV dysfunction⁸³ were similar in both groups.^6,15,28 Systemic thrombolytic therapy has been shown to have greatest benefit when started within 48 hours of symptom onset⁸⁰ but may still be useful for patients who have had symptoms for up to 14 days.^15,84

A mortality benefit of thrombolysis has not been found in patients with nonmassive PE and remains speculative in patients with massive PE, since there exists no large randomized controlled trial in this subgroup. One meta-analysis failed to demonstrate a superiority of thrombolysis compared with heparin alone with regard to recurrent pulmonary embolism or death as a composite outcome. However, when the study restricted analysis to trials that included massive PE patients, the composite outcome was 9.4% with the thrombolysis group versus 19.0% with heparin alone (odds ratio 0.45; NNT = 10).⁸⁵ In a large retrospective study that analyzed patients with a diagnosis of PE and shock or ventilator dependence, the case fatality rate attributable to PE was higher among patients not receiving systemic thrombolytic therapy (42% vs. 8.4%).¹⁴

The three drugs listed above appear to be comparable in efficacy and bleeding risk, provided doses are equivalent and given over the same time period.^72,73 Shorter infusion regimens (i.e., ≤2 hours) are preferred as they are associated with lower bleeding risk and more rapid clot lysis.⁸⁶ Drug delivery via peripheral IV is preferred, as pulmonary artery catheters are associated with an increased bleeding risk at the insertion site without an increase in efficacy.^86,87 IV UFH should be discontinued during systemic thrombolytic therapy.^15,28 Activated partial thromboplastin time (aPTT) should be checked after the completion of alteplase, and maintenance IV heparin should be restarted without a bolus if aPTT is <80 seconds (if not, it should be checked again in 4 hours).⁸⁸

An alteplase bolus regimen (0.6 mg/kg, maximum of 50 mg) given over 15 minutes appears to be comparable in both efficacy and bleeding risk to the more commonly used 100-mg infusion given over 2 hours.^74,75 Limited data exist for more rapid bolus infusions. In a study of a 2-minute alteplase infusion protocol (0.6 mg/kg ideal body weight, maximum dose not specified) versus heparin alone, a significant mean relative improvement in perfusion after 24 hours was reported (measured by perfusion lung scan, 37% vs. 18.8%, respectively) without an increase in major bleeding (minor bleeding was 45% vs. 4%).⁸¹ In patients in extremis, including cardiac arrest from massive PE, a bolus dose should be given.⁸⁶ However, thrombolysis for undifferentiated cardiac arrest is not recommended.²⁸

All thrombolytic drugs carry a risk of bleeding. The cumulative rate of major bleeding and intracranial/fatal hemorrhage in early trials was shown to be to be 13% and 1.8%, respectively.^{73,74,79,81,82,87,89–92} Life-threatening hemorrhage is less common in more recent trials.^78,91 Thrombolysis-related major bleeding is also less frequent when noninvasive imaging methods are used for PE diagnosis.⁹³ Of note, massive PE patients have higher bleeding rates when compared to patients with nonmassive PE, regardless of whether they are receiving thrombolysis plus heparin or heparin alone.^85,88 A retrospective chart review of patients who received IV alteplase 100 mg for PE between 1996 and 2004 showed a significant increase in bleeding risk among patients with hemodynamic instability requiring vasopressors prior to treatment (multivariate analysis: odds ratio 115).⁹⁴ Systemic thrombolytic therapy is nevertheless recommended for patients with massive PE considered to have acceptably low bleeding risk.^15,28,86 Absolute contraindications to systemic thrombolytic therapy for PE (listed after this paragraph) are extrapolated from guidelines for ST-segment elevation MI⁹⁵; clinicians are, however, encouraged to judge the relative merits of the therapy on a case-by-case basis.²⁸ Absolute contraindications to systemic thrombolytic therapy for MI might become relative in a patient with immediately life-threatening high-risk PE.¹⁵ Despite the recommendations of current guidelines and evidence in favor of systemic thrombolytic therapy in massive PE, this therapy continues to be grossly underutilized.^13,14

Absolute contraindications to systemic thrombolytic therapy in PE²⁸:

• Any prior intracranial hemorrhage
  
• Known structural intracranial malignant neoplasm or cerebrovascular disease (e.g., arteriovenous malformation)
  
• Ischemic stroke within 3 months
  
• Suspected aortic dissection
  
• Active bleeding or bleeding diathesis
  
• Recent (i.e., within preceding 3 weeks¹⁵) surgery encroaching on the spinal canal or brain
  
• Recent (i.e., within preceding 3 weeks¹⁵) significant closed-head or facial trauma with radiographic evidence of bony fracture or brain injury

Surgical Embolectomy

Historically, surgical embolectomy for PE was considered an option of last resort, reserved for patients in cardiogenic shock or requiring CPR.^15,96,97 However, as mortality rates have improved from 57% in the 1960s⁹⁸ to 26% (16% to 46%) in the late 1980s/early 1990s,⁹⁹ this procedure has reemerged as a viable treatment option for massive PE. Certain authors have attributed this change not to surgical technique, but rather to a more expeditious diagnostic approach and to advances in the perioperative management of these patients, specifically the preoperative application of CPB in moribund patients.⁹⁹ A more rigorous and discriminating patient selection process has likely also contributed to the improved outcomes. For example, instead of undergoing surgical embolectomy, patients with acute PE superimposed on chronic thromboembolic pulmonary hypertension are now transferred to centers that specialize in pulmonary endarterectomy.^15,100 The wide range of mortality rates reported in various case series reflects the importance of presurgical clinical status on postsurgical outcome; patients with no preoperative CPR, intermittent CPR with stable hemodynamics on arrival to the OR, and continuous CPR on arrival to the OR were reported to have mortality rate of 10%, 40%, and 80%, respectively.¹⁰¹

A recent study, extended inclusion criteria for surgical embolectomy to include hemodynamically stable patients with large clot and RV dysfunction, demonstrated an even lower mortality rate of 6%.⁹⁶ Although extending the indications to include submassive PE remains controversial, this and another recent series (0% perioperative mortality, 8% 30-day mortality)⁹⁷ suggest that surgical embolectomy is not as futile as once believed, provided there is appropriate patient selection and consideration of technical factors.

If surgical expertise and resources are available, indications for surgical embolectomy for massive PE are the presence of a contraindication to systemic thrombolytic therapy, failed systemic thrombolytic therapy, or hemodynamic instability that is likely to cause death before systemic thrombolytic therapy can take effect.⁸⁶ A surgical approach may also be appropriate in the case of impending paradoxical embolism (thrombus entrapped within a patent foramen ovale [PFO]).²⁸ Absolute contraindications to systemic thrombolytic therapy are present in approximately one-third of massive PE⁸⁸ (although this number varies depending on what is considered to be an absolute vs. relative contraindications). Failure of systemic thrombolytic therapy is defined as persistent clinical instability and residual echocardiographic RV dysfunction at 36 hours and is reported to occur in 8.2% of cases.¹⁰² In these cases, rescue embolectomy is recommended over repeat systemic thrombolytic therapy.¹⁰²

Catheter Embolectomy

The goal of the CDT is rapid central clot debulking to relieve life-threatening heart strain and improve pulmonary perfusion.¹⁰³ Modern CDT for massive PE is defined as the use of low-profile catheters and devices (<10 F) for the purpose of catheter-directed mechanical fragmentation and/or aspiration of emboli, as well as optional intraclot thrombolytic agent injection.¹⁰³ To avoid the risk of perforation, CDT is recommended only for use on major branches of the pulmonary artery and should be terminated as soon as hemodynamics improves, regardless of angiographic result.^15,104 However, because successful clot fragmentation increases the surface area of thrombus, some authors advocate giving an extended intraclot infusion of low-dose thrombolytics, especially to patients with residual elevation of PA pressure with right heart strain.^103,105,106

Large randomized controlled trials on CDT have been hindered by device variations, lack of well-established protocols, and feasibility issues. A meta-analysis of 35 studies conducted from January 1990 through September 2008 evaluated the safety and efficacy of CDT for massive PE.¹⁰⁷ Clinical success—defined as stabilization of hemodynamics, resolution of hypoxia, and survival to hospital discharge—was 86.5%.^103,107 In 96% of patients, systemic thrombolytic therapy was not given, and CDT was used as the first adjunct to heparin.¹⁰⁷ Approximately 30% of patients received mechanical fragmentation and/or aspiration of emboli only, and 60% of patients received an extended thrombolytic infusion through the catheter.¹⁰⁷ The pooled risk of major procedural complications (e.g., groin hematoma requiring transfusion) was 2.4%.¹⁰⁷

CDT shares the same indications as surgical embolectomy and is a relatively safe and highly effective treatment option for massive PE in an experienced center. Knowledge of local expertise should guide the emergency physician’s decision to pursue one or the other option,²⁸ and establishing a transfer protocol is encouraged in facilities that lack either option. A management algorithm for suspected massive PE in the ED is shown in Figure 11.3.

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