**2. Historical developments**

The history of venous thrombosis and PE is intertwined with landmark developments in the disciplines of anatomy, pathology, hematology, and surgery [2]. While pathologic observa‐ tions of postmortem pulmonary thrombi were detailed by Morgagni [3], Laennec [4], and Cruveilhier [5] in the 18th and 19th centuries, it was not until the late 19th century that the concept of thromboembolism was by recognized by Virchow. Virchow wrote "A plug may extend into the vena cava as thick as the last phalanx of the thumb. These are the thrombi that constitute the source of real danger; it is in them that ensues the crumbling away which

© 2013 Hui and McFadden; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

leads to secondary occlusion in remote vessels" [6]. He was thus the first to ascribe a single pathophysiologic mechanism to these anatomically separate phenomena (Figures 1 and 2).

ies" [11]. This stimulated his work over the next twenty years to develop the heart-lung ma‐ chine, ultimately opening the doors to modern cardiac surgery and to the first successful pulmonary embolectomy on cardiopulmonary bypass (CPB) by Edward Sharp in 1962 [10].

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Other surgical developments benefited from Virchow's legacy by attacking the problem at its more proximate source. The American surgeon Alton Ochsner, who had been present at Kirschner's 1924 address, proposed with Michael DeBakey to ligate the IVC in 1932 [12, 13]. John Homans, a general surgeon focused on venous disease, performed prophylactic lower ex‐ tremity vein ligation [14]. Caval interruption commonly resulted in chronic lower extremity edema with the complications of varices, edema, and ulceration. As Spencer stated, "Because of the morbidity often following ligation of the vena cava, it is probably used too seldom and too late, being reserved as last resort..." [15]. Narrowing of the IVC via a right flank incision as an adjunct to pulmonary embolectomy has also been described, with the authors abandoning this technique due to impaired venous return [16]. Refinement of venous interruption came in the form of the Miles clip [17], partial caval plication, and finally percutaneous intraluminal oc‐ clusive devices (Figure 3). Early occlusive devices were hampered by complications of migra‐ tion, embolization, vena cava wall rupture, and the need for femoral cutdown. Current filters have evolved in ease of insertion, lower complication rates, and efficacy with long-term paten‐

cy rates of 98% and 3% recurrent embolism rates [18,19] (Figure 4).

**Figure 2.** The saddle embolism isolated

**Figure 1.** Autopsy photo demonstrating a sudden fatal saddle embolism which occurred six days following pulmonary lobectomy.

The surgical treatment of pulmonary embolism was first proposed by Friedrich Trendelen‐ burg, a German professor of surgery from Leipzig. Having studied the cases of nine patients who died from acute pulmonary embolism, he developed a technique of pulmonary embo‐ lectomy through animal experimentation. His first two human patients died at 15 hours and 37 hours, from heart failure and hemorrhage of the internal mammary artery respectively [7]. Trendelenburg's student Martin Kirschner reported the first successful pulmonary em‐ bolectomy to the German Surgical Conference in Berlin in 1924 [8]. In Europe this became a popular emergent bedside operation for patients in whom PE was strongly suspected. Surgi‐ cal residents were relegated to a bedside vigil and watched for sudden circulatory collapse and respiratory compromise in high-risk patients. Fewer than 10 patients survived the oper‐ ation in 300 cases over a decade [2]. Though popular in Europe, the first successful pulmo‐ nary embolectomy was not reported in the United States until 1958 [9]. Operative mortality was frequently due to myocardial ischemia resulting in ventricular fibrillation and death at anesthetic induction [10]. The development of extracorporeal circulation by John Gibbon was in fact stimulated by his reflections while keeping vigil over a patient who underwent an unsuccessful attempt at pulmonary embolectomy: "…During the hours that night, John watched the patient's distended veins and recorded the faltering pulse, respirations and blood pressure, the thought occurred to him and constantly recurred to him that her condi‐ tions could surely be improved if only there were some form of continuously withdrawing some of the blue blood from the swollen veins into an apparatus where the blood could pick up oxygen and discharge carbon dioxide, and then be pumped back into the patient's arter‐ ies" [11]. This stimulated his work over the next twenty years to develop the heart-lung ma‐ chine, ultimately opening the doors to modern cardiac surgery and to the first successful pulmonary embolectomy on cardiopulmonary bypass (CPB) by Edward Sharp in 1962 [10].

**Figure 2.** The saddle embolism isolated

leads to secondary occlusion in remote vessels" [6]. He was thus the first to ascribe a single pathophysiologic mechanism to these anatomically separate phenomena (Figures 1 and 2).

**Figure 1.** Autopsy photo demonstrating a sudden fatal saddle embolism which occurred six days following pulmonary

The surgical treatment of pulmonary embolism was first proposed by Friedrich Trendelen‐ burg, a German professor of surgery from Leipzig. Having studied the cases of nine patients who died from acute pulmonary embolism, he developed a technique of pulmonary embo‐ lectomy through animal experimentation. His first two human patients died at 15 hours and 37 hours, from heart failure and hemorrhage of the internal mammary artery respectively [7]. Trendelenburg's student Martin Kirschner reported the first successful pulmonary em‐ bolectomy to the German Surgical Conference in Berlin in 1924 [8]. In Europe this became a popular emergent bedside operation for patients in whom PE was strongly suspected. Surgi‐ cal residents were relegated to a bedside vigil and watched for sudden circulatory collapse and respiratory compromise in high-risk patients. Fewer than 10 patients survived the oper‐ ation in 300 cases over a decade [2]. Though popular in Europe, the first successful pulmo‐ nary embolectomy was not reported in the United States until 1958 [9]. Operative mortality was frequently due to myocardial ischemia resulting in ventricular fibrillation and death at anesthetic induction [10]. The development of extracorporeal circulation by John Gibbon was in fact stimulated by his reflections while keeping vigil over a patient who underwent an unsuccessful attempt at pulmonary embolectomy: "…During the hours that night, John watched the patient's distended veins and recorded the faltering pulse, respirations and blood pressure, the thought occurred to him and constantly recurred to him that her condi‐ tions could surely be improved if only there were some form of continuously withdrawing some of the blue blood from the swollen veins into an apparatus where the blood could pick up oxygen and discharge carbon dioxide, and then be pumped back into the patient's arter‐

lobectomy.

396 Principles and Practice of Cardiothoracic Surgery

Other surgical developments benefited from Virchow's legacy by attacking the problem at its more proximate source. The American surgeon Alton Ochsner, who had been present at Kirschner's 1924 address, proposed with Michael DeBakey to ligate the IVC in 1932 [12, 13]. John Homans, a general surgeon focused on venous disease, performed prophylactic lower ex‐ tremity vein ligation [14]. Caval interruption commonly resulted in chronic lower extremity edema with the complications of varices, edema, and ulceration. As Spencer stated, "Because of the morbidity often following ligation of the vena cava, it is probably used too seldom and too late, being reserved as last resort..." [15]. Narrowing of the IVC via a right flank incision as an adjunct to pulmonary embolectomy has also been described, with the authors abandoning this technique due to impaired venous return [16]. Refinement of venous interruption came in the form of the Miles clip [17], partial caval plication, and finally percutaneous intraluminal oc‐ clusive devices (Figure 3). Early occlusive devices were hampered by complications of migra‐ tion, embolization, vena cava wall rupture, and the need for femoral cutdown. Current filters have evolved in ease of insertion, lower complication rates, and efficacy with long-term paten‐ cy rates of 98% and 3% recurrent embolism rates [18,19] (Figure 4).

Concurrent with the developments in surgical techniques to treat PE were discoveries in an‐ ticoagulation. Heparin, discovered by McLean [20] and validated by Murray [21], has be‐ come the workhorse of initial therapy of PE. The discovery of oral dicumerol in the 1940s has led to the use of anticoagulation as the mainstay of both prevention of and therapy for venous thrombosis and PE. The efficacy of anticoagulants, thrombolytics, and vena caval fil‐ ters combined with the high mortality rate of pulmonary embolectomy, had led to a para‐

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Classification of PE was historically based on the angiographic burden, using the Miller In‐ dex [22]. Current classification by American Heart Association differentiates between mas‐ sive PE (sustained hypotension for at least 15 minutes or requiring inotropic support, pulselessness, or persistent profound bradycardia) from submassive (acute PE without sys‐ temic hypotension but with either RV dysfunction or myocardial necrosis) (Table 1) [23]. Early identification and risk stratification is mandatory at the time of diagnosis in order to coordinate multimodality treatment strategies. Prompt diagnosis and initiation of treatment can reverse RV failure and reduce mortality. Current tools for prognostication include clini‐

Acute PE with sustained hypotension (Systolic blood pressure <90 mm Hg for at least 15

Persistent profound bradycardia (heart rate<40 bpm with signs or symptoms of shock)

Acute PE without systemic hypotension (systolic blood pressure <90 mm Hg) but with

RV dilation (apical 4-chamber RV diameter divided by LV diameter > 0.9) or RV systolic

Electrocardiographic changes (new complete or incomplete right bundle-branch block,

RV dilation (4-chamber RV diameter divided by LV diameter > 0.9) on computed

anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)

either right ventricular (RV) dysfunction or myocardial necrosis *RV dysfunction means the presence of at least 1 of the following:*

Elevation of beta-natriuretic peptide (BNP >90 pg/mL) Elevation of N-terminal pro-BNP (> 500 pg/mL)

*Myocardial necrosis is defined as either of the following:*

Not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left

digm shift towards nonoperative management of acute massive PE.

cal parameters, radiographic findings, and laboratory markers.

**Massive PE**

**Submassive PE**

**3. Contemporary management: diagnosis and prognostication**

minutes or requiring inotropic support)

ventricular [LV] dysfunction

dysfunction on echocardiography

Elevation of troponin I (>0.4 ng/mL) or Elevation of troponin T (>0.1 ng/mL)

Pulselessness

tomography

**Table 1.** American Heart Association Classification of Pulmonary Embolism [23].

**Figure 3.** Vena Cava Filter.

**Figure 4.** Nitinol OptionTM Vena Cava Filter (Argon Medical Devices, Plano, TX). Features of contemporary filters in‐ clude retrievability, MRI compatibility, and percutaneous insertion.

Concurrent with the developments in surgical techniques to treat PE were discoveries in an‐ ticoagulation. Heparin, discovered by McLean [20] and validated by Murray [21], has be‐ come the workhorse of initial therapy of PE. The discovery of oral dicumerol in the 1940s has led to the use of anticoagulation as the mainstay of both prevention of and therapy for venous thrombosis and PE. The efficacy of anticoagulants, thrombolytics, and vena caval fil‐ ters combined with the high mortality rate of pulmonary embolectomy, had led to a para‐ digm shift towards nonoperative management of acute massive PE.
