Introductory Chapter: Pulmonary Embolism

*Cynthia Sadera, Sharon Halliburton, Ladan Panahi and George Udeani*

### **1. Introduction**

Pulmonary embolism (PE) is typically caused by emboli, originating from venous thrombi traveling to and occluding the lung's arteries. These emboli characteristically arise in the leg, referred to as deep vein thrombosis (DVT), which may detach and travel to the pulmonary arteries, halting blood flow, and resulting in tissue ischemia. While there are a variety of etiologies, associated with pulmonary embolism, the most prevalent is DVT. Patients with specific disease states, including blood coagulation disorders, cancer, stroke, paralysis, coronary artery disease, and hypertension, have an increased risk of developing a pulmonary embolism. Surgical procedures and skeletal fractures also threaten the occurrence of coagulation, where the risk of pulmonary embolism tends to increase weeks after either event. Other risk factors include prolonged inactivity, obesity, cigarette use, recent endothelial injury, old age, and hypercoagulable states (cancer). Patients who are pregnant or within 6 weeks of giving birth also carry an increased risk of pulmonary infarction. Certain medications such as oral contraceptives, hormone replacement therapy, and chemotherapeutic agents can also correlate with higher incidences of pulmonary embolism [1]. Virchow triad (stasis, vascular wall injury, and hypercoagulable state) may be employed in the assessment of the risk of thrombi formation [2]. Pulmonary embolism is one of the most dangerous categories of venous thromboembolism, with high fatality rates if undiagnosed or untreated [3]. Furthermore, the post-PE syndrome may occur in individuals who survive PE. This is characterized by chronic thrombotic remains in the pulmonary arteries, tenacious right ventricular dysfunction, decreased quality of life, or chronic functional limitations [4]. Right ventricular dysfunction associated with acute PE can lead to complications such as arrhythmia, hemodynamic collapse, and shock [5].

Acute PE is a major global health concern. Approximately 10 million DVT cases are diagnosed globally annually, with one million cases occurring in the United States and approximately 700,000 in France, Italy, Germany, Spain, Sweden, and the United Kingdom combined annually [6–8]. In the United States, an estimated 100,000 to 200,000 individuals die annually from pulmonary embolism [9]. The incidence of acute PE in China tripled from 3.9 per 100,000 in 2000–2001 to 11.7 per 100,000 in 2010–2011 and is projected to increase, given the expected increase in China's population [10, 11].

Despite its devastating mortality, pulmonary embolism can be prevented, particularly by implementing certain safeguard measures. Such safeguards include lower extremities mobility, particularly during periods of prolonged inactivity, routine exercise, a healthy diet, decreased alcohol, nicotine, and caffeine intake,

and early post-surgical ambulation after a recent surgery or medical illness to reduce risks. Prevention of deep vein thrombosis further reduces the risk of pulmonary embolism. Employing compression stockings, sequential compression devices, lifestyle modification to include exercise, and therapeutic agents as prophylactic measures have long-term implications in reducing fatal pulmonary embolism [12]. Pulmonary embolism response teams (PERTs), similar to Code Blue teams employed during emergency cardiopulmonary arrests in hospitals, are emerging globally to mitigate this international PE crisis [13].

Clinical presentation of pulmonary embolism frequently overlaps with other disease states; thus, it is not unusual for pulmonary embolism to be misdiagnosed. Symptoms such as shortness of breath, chest pain, coughing with or without bloody sputum, cardiac arrhythmias, anxiety, cyanosis, lightheadedness, tachypnea, sweating, or tachycardia are symptoms of a pulmonary embolism and a variety of other cardiopulmonary conditions [14]. Other signs such as edema, erythema, pain, or tenderness of the leg may indicate DVT, with a direct risk of pulmonary embolism. Therefore, it is imperative that clinicians pay close attention to the latter in making an accurate diagnosis and thus employing appropriate therapeutic interventions that will yield positive outcomes in these patient populations. The medical history, physical exam, and certain test results are employed for the differential diagnosis of pulmonary embolism from other conditions. Accurate history and physical examination, pertinent lab values such as D-Dimer, employment of leg ultrasound, computed tomography (CT) scan, lung ventilation-perfusion scan, blood tests, echocardiography, chest X-ray, or chest MRI are all avenues employed in the timely and accurate diagnosis, and thus intervention in pulmonary embolism to reduce mortality and improve patient outcomes [15].

Once the diagnosis of a pulmonary embolism is confirmed, it is critical to initiate treatment immediately. Such treatment typically occurs in emergency medicine, or inpatient environments, with the emergent goal of halting the blood clot transit progression and preventing new clot development. A myriad of anticoagulation therapies is currently available to manage pulmonary embolism, ranging from parenteral to oral treatments. Anticoagulation therapy inhibits certain aspects of the clotting cascade to prevent the growth of the clot infarction and avoid additional thrombogenesis. Common anticoagulants employed include heparin, warfarin, and direct-acting oral anticoagulants. It is critical to monitor for signs and symptoms of bleeding, food, and drug interactions, as well as efficacy associated with these treatment modalities, for optimal outcomes. Adverse events to these agents may occur; these include bright red or coffee grounds emesis, black tarry stool, and abdominal pain without attributable cause are all signs of gastrointestinal bleeding. Additionally, patients on such therapies may experience severe headaches, sudden vision changes, sudden loss of movement or feeling in any extremities, memory loss, or disorientation, which are all signs of intracranial bleeding [16].

Other forms of therapy include fibrinolytics, catheter-directed therapies, and surgical embolectomy [17]. Fibrinolytic therapy is indicated in a select group of hemodynamically unstable patients. Surgical therapy in these patients is employed as a last resort. These procedures include inferior vena cava (IVC) filter placement, pulmonary embolectomy, and percutaneous thrombectomy. IVC filter insertion is indicated in patients with medical contraindications to anticoagulation, anticoagulant-induced hypercoagulation, or patients with excessive bleeding risks [18].

Pulmonary embolism is a preventable manifestation of venous thromboembolism which may be misdiagnosed, due to its non-specific symptoms. Pulmonary embolism prevention via lifestyle modification, increased physical exercise, and

*Introductory Chapter: Pulmonary Embolism DOI: http://dx.doi.org/10.5772/intechopen.105018*

early employment of prophylactic therapy in at-risk populations are the best approaches. Rapid detection, diagnosis, and early employment of therapeutic or surgical interventions are vital to improving outcomes and decreasing morbidity and mortality.
