Imaging Pulmonary Embolism
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Pulmonary embolism remains one of the most important life-threatening disorders of the pulmonary circulatory system. This article will give the technologist the tools needed to understand and properly image pulmonary emboli. This article emphasizes CT, nuclear V/Q scan, interventional radiology evaluation and treatments of PE, and briefly discusses ultrasound of deep vein thrombosis.
Author: Joseph, Nicholas RT(R) (CT)
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Pulmonary embolism (PE) is a highly lethal condition. We now know that it occurs quite frequently, and more often than was previously thought. Surprisingly, it is the third most common cause of death in hospitalized patients in the United States. Pulmonary embolism is like a two edged sword, on the one hand when diagnosed the condition is highly treatable with good overall results; however, undiagnosed it contributes to significant numbers of morbidity and mortality for many of its victims. Pulmonary embolism is a major health concern in the United States with more than 650,000 deaths occurring annually. It is estimated annually that upwards to 2 million cases may actually occur, though many go undiagnosed until autopsy. Consider this; pulmonary embolism is second only to sudden cardiac death, and is the number one cause of unexpected death in most age groups! The sarcastic expression, “drop dead” comes from historical observations of sudden death in seeming healthy young adults from pulmonary embolus.
The basis of PE is the formation of a blood clot inside a blood vessel, which is called a thrombosis. The term thrombus distinguishes abnormal intravascular clot from the normal extravascular clotting mechanism that is a healing process, for example, clot formation after laceration or abrasion. Thrombosis formation is a major medical problem because it causes loss of life, sometimes loss of an affected limb, or a multitude of other complications. Thrombus is more likely to form in areas where sluggish blood flow occurs. Usually there are underlying pathological conditions that are favorable to clotting, e.g., post-surgical changes in the deep veins of the leg, or post partum. Basically, sluggish blood flow allows clotting factors to accumulate and cascade, whereas normal blood flow moves them along in the blood decreasing their interactions. Another stimulus for thrombus formation is torn or diseased localized areas of a blood vessel. These changes generally occur in the intima layer of a vein. An example of a diseased intima would be plaque build-up in a vein or artery.
Pulmonary embolus and thromboembolism are often complications of underlying venous thrombosis that occurs most commonly in the deep veins of the legs, and also in deep veins of the upper extremities. Statistically, the occurrence of leg thrombosis is most often caused by a combination of three factors: 1) venostasis, 2) hypercoagulability, and 3) venous wall inflammation. These three underlying causes of pulmonary thromboembolus are collectively known as Virchow’s triad. Anyone with one or more elements of Virchow triad is at risk for pulmonary embolus.
Massive pulmonary embolism, such as a saddle embolus is problematic and is led only by coronary artery disease as a cause of unexpected sudden death. Although PE can be a fatal condition it remains greatly unappreciated clinically as it is more often missed than diagnosed. Current estimate is that over 400, 000 cases each year are missed; yet autopsy confirms PE in approximately 80% of unsuspected deaths. The seriousness of undiagnosed pulmonary embolism hits home when one considers that approximately 10% of acute PE patients die within the first 60 minutes of the event. This disorder is so serious that about 30% of those diagnosed with PE and treated will still die of a subsequent PE in their lifetime. This is because medical understanding and options for treating PE is relative poor when measuring long-term outcomes. Anticoagulant treatment does decrease the mortality rate to less than 5% overall, however, this is not outstandingly encouraging for those who do not survive.
The clinical presentations of pulmonary embolus have shortcomings for definitive diagnose even when retrospectively the patient proves positive after diagnostic testing. A study tracking patients 60 minutes post presentation at emergency rooms showed that only about one-third of positive PE patients are diagnosed. The other two-thirds of positive presenters are in the group of those 400,000 patients each year in the United States that go undiagnosed. A significant number of both diagnosed and undiagnosed positive pulmonary embolus cases will die. So you can see why physicians must evaluate chest pain for pulmonary embolus in all cases suspicious for PE. A quick very accurate diagnosis of PE can be made from a computed tomography (CT) scan in most cases. When properly performed, the overall negative predictive value of multi detector row CT is greater than 99%. This makes CT the gold standard for diagnosing acute pulmonary embolus. Other modalities that are useful in evaluating pulmonary embolus or its primary cause include: interventional direct angiography, nuclear medicine imaging, magnetic resonance imaging (MRI), and ultrasound imaging modalities.
These two photographs taken at autopsy show a large saddle embolus in the pulmonary trunk extending into the pulmonary arteries. The photograph on the left shows the pulmonary trunk removed exposing the clots in both pulmonary arteries. The pulmonary trunk is dissected in the photo on the right to show the large saddle embolus involving the trunk (purple arrow) and pulmonary branching of the clot (yellow arrow). The pulmonary embolus seen here was first diagnosed by computerized tomography and confirmed at autopsy. Pulmonary embolism is discovered as the cause of approximately 80% of unexpected sudden deaths at autopsies.
Pathophysiology of Thrombus Formation
Although this article will focus on pulmonary embolus, you should be aware that physicians are concerned with several broader related terms: venous thromboembolism (VTE), which refers to deep vein thrombus (DVT), pulmonary embolism (PE), or a combination of both. Health care practitioners should have a working knowledge of these terms. A thrombus can be defined as a blood clot or mass formed within a blood vessel but remain attached at its place of origin. An embolus is an abnormal particle (such as an air bubble, blood clot, foreign body) circulating in the blood. For example, if a thrombus breaks away from its site of origin becoming free circulating in the blood, it is called an embolus. A thromboembolism is the term for the blocking of a remote blood vessel by a clot that has broken away from its site of formation. Venous thromboembolism describes a thromboembolism in the venous system such as a pulmonary artery or other peripheral venous vessel.
In the United States VTE is a common health problem that poses risk to as many as 250,000 to 2 million persons each year. We now know that most victims plagued with VTE are predisposed to it either by inherited disorders or by an acquired condition. There are also some physical states can induce VTE, for example, being bedridden because this promotes venous stasis. This places those patients who suffer major fractures, such as pelvic and femoral fractures at risk. Some surgical procedures, hospitalization, and being elderly can promote varying degrees of immobilization that increases risk. An injury that damages veins can also provoke venous thrombus formation during the normal healing process, which involves clot formation, and can occasionally produce a pulmonary embolus. Medical observations supported by scientific evidence show that in the absence of trauma the main cause of DVT and PE is related to an underlying hypercoagulable state in the individual. In recent years it has been discovered that there are inheritable genetic factors that make many individuals susceptible to VTE.
These three radiographic images show complex fractures involving the lower extremity. Some types of fractures, like the ones seen here, can cause damage to blood vessels leading to thrombus formation in them. For example, external pressure causing bulging in the lumen of a blood vessels or intima damage can create coagulation conditions. Being bedridden, surgery, extreme blood loss, and underlying hypercoagulable state also predispose to thrombus formation. However, complex fractures like the ones seen above along with postoperative bedridden can greatly increase the risk of thrombus formation in some individuals.
Research has discovered a genetic basis for hypercoagulative state in some individuals with VTE. The two main genetic causes of hypercoagulation are Factor V Leiden and prothrobin 20210 gene mutations. Fortunately, genetic testing to detect these genetic factors can be quickly performed in most cases. The physician can test for factor V Leiden (a.k.a. factor V Leyden), or prothrobin 20210 (PT 20210) gene mutations in suspected individuals. Basically factor V Leiden mutation and prothrobin 20210-gene mutation tests are used to help diagnose the cause for venous thromboembolism, not the thrombus itself. Other types of deficiencies related to DVT or PE include protein C, protein S, or antithrombin III deficiencies. Those who do not know they have a gene mutation may suffer PE or VTE leading to discovery of this underlying genetic condition. Family members of those who present with symptoms of PE may at some time need to be screened for genetic based hypercoagulative state.
Screening for activated protein C (APC) resistance is an indirect test for factor V Leiden. Active protein C is a blood-clotting factor that helps regulate coagulation by inactivating other blood clotting factors. Thus, the role of active protein C is to slow clotting. This is a normal process that helps normal individuals repair injury such a laceration. So a person who is resistant to activated protein C may poorly regulate clotting, which puts them at risk for thrombosis. The importance of a positive APC resistance is that 95% of these individuals have factor V Leiden mutation. If a person test positive for factor V Leiden mutation they are further tested to determine if they are heterozygous, or homozygous (more severe) for the mutation. As you may recall from sickle cell disease, the Mendalian genetic status of the individual will also determine the likelihood of passing the mutation on to off spring. Fortunately, only about 10% of those with factor V Leiden mutation will actually have a thrombolic episode. The low incidence of factor V Leiden causing VTE raises many questions of the possibility of other unknown gene mutations playing a role in clotting. As for the PT 20210 gene, it can only be diagnosed with genetic testing because an elevated prothrombin level seen with this mutation is clinically unreliable.
Genetics alone is not the only cause for VTE. It is possible to acquired risk factors for VTE and pulmonary embolism. Perhaps the most widely known is the association of venous stasis and long air flight time. The relationship of sitting too long on transatlantic or transpacific flights as a cause of venous stasis is well documented. Other risk factors include: obesity, pregnancy, cancer, smoking, oral contraceptives and others have been documented. The important thing to know is that risk factors for a disease are considered cumulative. For example, a person with known factor V Leiden mutation will have a 2 to 3 times greater risk for PE; however, if the same person uses oral contraceptives the risk increases to 25 times that of factor V Leiden alone. The most important acquired risk factors for PE are prior history of deep vein thrombosis (DVT), recent surgery, pregnancy, prolonged immobilization, and cancer. Maintaining good blood circulation through the legs in these individuals helps reduce the risk of venous stasis in bedridden or post-operative patients. This is why respiratory changes in a hospitalized patient always raise concern for pulmonary embolus.
A thrombosis is defined as the formation in the circulation of a solid mass from constituents in the streaming blood. The mass formed is termed a thrombus because it is stationary, attached to the vessels inner wall. The thrombus mass or clot is usually composed of aggregated platelets and fibrin with trapped red and white blood cells. Three classical causes of thrombus formation were described in 1846 as Virchow’s triad. The elements of Virchow’s triad again are: 1) changes in the vessel wall, 2) changes in blood flow, and 3) changes in the composition of the blood.
A change in the vessel wall is an important finding in some types of thrombus formations. This is more often seen in the right atrial wall or in the walls of veins in conditions like thrombophlebitis. Inflammation in the vessel wall is the primary cause of thrombus formation in thrombophlebitis. Damage to the intima layer by atheroma is also a common cause of thrombus formation. Anatomic lesions that predispose to thrombosis include bulging of the vessel caused by external pressure or spasm, aneurysm and sclerotic rigid valves. Phlebothrombosis is a term referring to blood stasis in veins that have no inflammation. Thrombophlevitis refers to stasis in which the vein wall is inflamed. Stasis or slowing of blood flow is a know cause of thrombus formation in veins and arteries. Thrombus is also seen the wall of some types of aneurismal sacs. Turbulence in blood flow, called eddying is also an important factor. Eddying is seen in fast moving blood such as the arterial flow or in the heart proper. Turbulence is thought to damage endothelial cells that line blood vessels leading to platelet deposition and aggregation.
Changes in blood composition that increases platelets or clotting factors may contribute to thrombosis. In many circumstances this is transient such as parturition, surgery, trauma, or severe hemorrhaging. Chronic conditions like polycythemia vera and hyperlipidemia cause persistent blood changes that risk thrombus formation. Hyperlipidemia shortens clotting time and inhibits clot breakdown (fibrinolysis).
A thrombosis can start in any vein due to a number of causes that include trauma, gynecological surgery, or long term indwelling intravenous catheter to name a few. What is observed is that in most symptomatic patients for deep vein thrombosis (DVT) the initial event occurs in the calf veins. Many factors can precipitate deep vein thrombosis, like immobilization, pregnancy, trauma, stroke, venous stasis, oral contraceptives, estrogen replacement, varicose veins, long bone fracture, and many other causes listed in the table above. The development of VTE due to some of these causes is explained below:
These two radiographs are from a venogram study that demonstrates the larger veins of the lower leg. These radiographs show the deep veins such as the popliteal vein (at the knee joint), and veins of the lower leg. Some superficial veins of the calf are also seen; however, most thrombus begins in the deep veins. These are all tributaries that drain the lower leg into vessels that form the inferior vena cava. Deep vein thrombus can form in any of these vessels; however, the deep veins such as the greater saphenous, femoral, and popliteal are more likely to form a thrombus that can embolize and travel to the pulmonary vessels.
Histology of a Vein
The main functions of the cardiovascular system are to distribute metabolites and oxygen to all cells of the body and collect waste products and carbon dioxide from the body�s cells for excretion. It also distributes hormones to target cells and participates in thermoregulation. The driving force of the system is the heart; arteries distribute to the cells, veins collect blood and serve as a blood reservoir; and the capillaries are the functional exchange sites for the system. At any given time 65-75 percent of the body�s blood volume is in the venous system. Blood returned to the heart is distributed to the lungs for oxygenation. Any mechanism that diminishes the supply of oxygenated blood to the body�s tissues, such as a pulmonary embolus can be life threatening.
The central mechanism for VTE and PE is venous stasis. To answer the question of why venous stasis causes VTE we must investigate the structure veins and the mechanism of venous blood return to the heart. The walls of arteries and veins are composed of three-tissue layer called tunics. The outermost layer is the tunica externa, the middle layer is called the tunica media, and the innermost layer over which blood flows is called the tunica intima. The tunica externa is composed of mostly loose connective tissue, which anchors the blood vessel to tissues through which it passes. The tunica media is composed of circular layers of smooth muscle in various amounts. Smooth muscle allows the blood vessel to contract and dilate which decreases and increases the diameter of the vessel. The tunica intima is the innermost layer of a blood vessel and lines the vessel lumen. Although the intima is a very thin tissue layer is composed of three distinct layers. Its innermost layer consists of squamous cells called the endothelium. The endothelium lines the lumen of all blood vessels in the body. The endothelium rests on a basement membrane that has some connective tissue fibers in its structure. The third outer layer of the intima is called the internal elastic lamina because it is composed of elastin, a name for elastic stretchable type fibers.
Arteries have thicker walls than veins, which are contributed mostly to having a thicker middle layer (the tunica media). Having a stronger muscle layer is what allows arteries to transmit blood under high pressure, e.g. ejection of blood from the heart to the aorta. In order to perform its function an artery must be able to stretch and recoil with the blood pressure when it receives blood volume. Elastic recoil of large arteries is due to a large amount of elastin. Elastin allows arteries to recoil following expansion due to blood volume received and transmitted away from the heart. You can feel this pressure wave as its proprogated from the heart through arteries in the upper and lower extremities as a carotid, radial, or femoral pulse.
These two light micrographs show both a vein (left) and an artery (right). Notice that the main difference in these two structures is the thickness of their smooth muscle layers, or tunica media layer. The yellow arrow (left) points to the circular muscle of the vein and a blue arrow (right) show the same muscle layer of the artery. Veins carry deoxygenated blood back to the heart, whereas arteries carry oxygenated blood back to the body.
The microcirculation, which is composed of arterioles, venules, and capillary beds, is where the work of the circulatory system takes place. At the capillary bed oxygen, nutritive materials, and hormones are distributed to tissues. Carbon dioxide and metabolic byproducts are received and carried to excretory organs. In the lung alveoli the microcirculation exchanges gases removing carbon dioxide and collecting oxygen for the body’s use. Capillaries are so small that red blood cells must pass in single file through them. In the lungs this anatomical arrangement allows carbon dioxide to be exchanged for oxygen achieving 100% saturation of hemoglobin. This is usually measured using a pulse oximeter placed over the fingernail of any finger.
This electron micrograph shows a venule (large white arrow), arteriole (yellow arrow), and capillary beds between them (smaller arrows). The same parts of the microcirculation are shown, but unlabeled on its negative electron micrograph on the right.
This electron micrograph images show a magnified viewing of the venule (white arrow) and capillary (yellow arrow). Notice the red blood cell (pink arrow) within the capillary travels in single file because the diameter of the vessel is very small. The micrograph on the right shows these structures without labeling.
The venous system is a low-pressure collecting network for returning deoxygenated blood and cellular waste from the body’s capillary beds back to the heart. Blood flow in the venous system is passive in that is it does not move with the beating of the heart. The heart and arterial branches are the high-pressure part of the cardiovascular system. Blood flow from the aorta to the most distal small arterioles follows a decreasing pressure gradient. Arterial blood flow is dependent on four major parameters: elasticity of the arterial system, mean arterial blood volume, pulse pressure, and systemic uptake of blood by the arteries. These four parameters are contained in what is known as Hook’s law.
The venous segment of the vascular system is characterized as being a highly distensible blood reservoir. Venous system functions are dependent on gravity (peripheral pooling and hydrostatic effects), venous valves, skeletal muscle pumps, ventilation, and positive end-expiratory pressure (PEEP). We will only be concerned with the role of venous valves, skeletal muscle pumps, and ventilation. When blood reaches the venules, which is the first part of the collecting system the blood pressure is diminished and is not capable of returning blood to the heart. Contraction of skeletal muscle aids venous return by compressing veins as they course between contracting muscles. The action of skeletal muscle propels blood towards the heart passively in this low pressure system. This is a relatively slow moving system that depends on venous valves to stay the movement of blood and prevent backflow. Large muscles like those in the legs surround large veins to move blood. However, in the abdomen and thorax muscle does not surround large veins such as the inferior vena cava. Therefore, blood movement in the chest and abdomen requires the body to create a negative pressure gradient. Inspiratory breathing creates this negative pressure propelling blood towards the heart. During expiratory breathing blood does not move towards the heart and may flow backwards. Valves within veins prevent backflow of blood during expiration. The competency of veins is therefore necessary for good venous health.
Sometimes valves become incompetent or even destroyed when overstretched by prolonged excessive venous blood pressure. Those who apend a great amount of time standing, lack exercise, and pregnancy are common conditions that may produce weakened valves of the legs. Chronic increased blood volume causes veins to stretch pathologically increasing their cross-sectional area. Because valves do not stretch, they do not close completely across the cross-sectional area of a stretched vein. This allows reverse blood flow, which further increases venous pressure and engorgement of the vein. When it reaches a pathological state the condition is called varicose veins.
These two venogram images show deep veins in the upper arm region. The blue arrow in the radiograph on the right points to a valve within the brachial vein of the arm. Blood flow in the venous system is passive depending on a number of factors including skeletal muscle pumps. Good muscle tone helps propel blood towards the heart in muscular areas such as upper and lower extremities.
This drawing demonstrates the function of skeletal muscle pumps that propel blood towards the heart. Muscle in the relaxed state (left drawing) creates no pressure on the vein so that backflow is prevented by closure of the valves. During contraction, veins are squeezed allowing blood to flow towards the heart through one-way valves. Incompetent valves, venous stasis, and hypercoagulative states promote thrombus formation.
Pulmonary Blood Flow
Proper imaging of the pulmonary arteries and lung parenchyma to diagnose PE requires a thorough understanding of blood circulation through the right heart to the lungs. Equally important is how the lungs saturate deoxygenated blood with oxygen as it traverse the alveoli, and how blood is returned to the left heart to be distributed to the body. Deoxygenated blood is received into the right atrium from three sources: the superior vena cava (SVC), inferior vena cava (IVC), and coronary sinus. The upper extremities, head, and neck returns deoxygenated blood to the right atrium through the superior vena cava (SVC). The superior vena cava is formed by the right and left brachiocephalic veins that receive blood from their respective upper extremities. The heart also receives deoxygenated blood from the lower body by way of the inferior vena cava, and from the heart through the coronary sinus. Thus the superior vena cava receives blood from the neck, head, and upper extremities. The inferior vena cava receives blood from the lower extremities, chest, and abdomen and pelvis. The coronary sinus returns blood from the heart veins. Blood in the right atrium is pumped pass the tricuspid valve into the right ventricle. The tricuspid valve is an atria-ventricular valve that lies between the right atrium and right ventricle. Contraction of the right ventricle pushes blood through the pulmonary valve into the pulmonary trunk to be distributed to the right and left pulmonary arteries, then to the lungs. The pulmonary valve lies in the root of the pulmonary trunk. Branches of the pulmonary arteries get smaller becoming secondary, tertiary, and segmental branches as they deliver blood to capillary beds. When blood reaches the capillary beds of the lungs oxygenation of hemoglobin within red blood cells take place. This is also where carbon dioxide crosses the membranes of the lungs to enter the bronchial channel.
Understanding the pathway of blood flow from the right side of the heart to the pulmonary circulation is important for CT angiogram (CTA) imaging for PE. Two main reasons to know this anatomy well are that the pulmonary circulation is where an embolus lodges to cause the symptoms of a pulmonary embolus. Secondly, to image this area the technologist must be able to identify certain parts of the pulmonary arterial circulation when performing the pulmonary CTA. A true pulmonary CTA study will demonstrate the pulmonary arteries with little to no contrast filling the pulmonary veins.
This drawing shows an open thorax view of the lungs and heart. The superior vena cave (SVC) receives deoxygenated blood from the brachiocephalic veins, which are formed from their respective subclavian veins (C &F;). . Tributaries to the subclavian veins are the right internal jugular (D) and left internal jugular (E) veins. Blood flows from the superior vena cava to the right atrium (RA) through the bicuspid valve into the right ventricle (RV). From the right ventricle deoxygenated blood is pumped into the pulmonary trunk (P) and distributed to the right and left lung (G). Also labeled are the lung pleura (H), diaphragm (I), and left ventricle (LV).
(Left) is a picture of a heart model that displays the right atrium (RA) that receives deoxygenated blood from the superior vena cava (SVC). The blood then flows to the right ventricle (RV)) and to the pulmonary trunk (PT). These structures are also seen on the coronal CT image on the right. Also labeled are the aorta (A) and left ventricle (LV).
Heart model on the left profiles the right ventricle (RV), pulmonary trunk (PT), and left pulmonary artery (LPA). The anatomy of blood flow from the lungs to the left heart is shown. On the model, the Left atrium (LA) is labeled; the left ventricle is just below it. Blood flows from the left ventricle to the ascending aorta (AA) to the aortic arch (AOA) and to the descending aorta to be distributed to the body. The coronal CT image on the right shows iodinated contrast media in the right ventricle (RV) being pumped into the pulmonary trunk (PT). Notice the left ventricle (LV) and ascending aorta (AA) are not contrast filled. This is because contrast media has not gone through the lungs to return to the heart.
The process of delivering blood to the capillary beds is called perfusion (Q). The process of delivering oxygen to the capillary beds is called ventilation (V). Ventilation and perfusion (V/Q) should be matched, that is blood and oxygen should arrive at the capillary beds continuously so that red blood cells are 100% saturated with oxygen during passage through the lungs. By definition, capillaries are the smallest blood vessels in the body. It is also where the work of the circulatory system is performed. Capillaries are so small that red blood cells (RBC) pass through their length single file. This assures that the gases have adequate time to diffuse across the red blood cell membrane during passage through the lungs. Gases such as oxygen and carbon dioxide pass freely across cellular membranes from high concentration to low concentration by a process called diffusion. In the body’s tissues carbon dioxide is high so it moves into the red blood cell. Likewise oxygen is high in the red blood cell as it passes through tissue allowing oxygen to flow into the tissues. In the lungs carbon dioxide is low and oxygen high causing oxygen to flow freely into the red blood cell and carbon dioxide out of the red blood cell. Blockage of either ventilation or perfusion can be life threatening because it alters homeostasis of gas exchange. If a significant number of red blood cells do not flow through the capillaries due to partial or complete blockage by a pulmonary embolus there will be decreased oxygen delivered to the body. Likewise, if the ventilation pathway is diminished, for example, inhaling a foreign object, so that little oxygen is available to saturate red blood cells in the lungs, the body�s oxygen supply is proportionately diminished.
This electron micrograph shows a portion of the microcirculation venule (white arrow) and a red blood cell (pink arrow) passing through a pulmonary capillary (yellow arrow) in single file. This allows the hemoglobin within the RBC to be 100% saturated. Capillary blood saturation can be measured from the skin surface using a pulse oximeter, which is generally placed on a finger for monitoring. The RBC is saturated with oxygen as its hemoglobin release carbon dioxide in the lungs. Carbon dioxide passively crosses the membrane of the RBC into the bronchial tree in exchange for oxygen.
The primary function of the respiratory system is to aid in exchanging carbon dioxide from the blood for oxygen inhaled from the atmosphere. Gases diffuse freely through biological membranes moving from high concentration to an area of low concentration. Therefore, oxygen, which is more concentrated in the atmosphere, is inhaled through the bronchial passages where it crosses the respiratory airway into the blood. Carbon dioxide, which is more concentrated in the blood moves into the airways of the lungs to be expired into the atmosphere. The respiratory system is conveniently divided into four parts: pharynx, trachea, bronchi, and lungs. We will just briefly look at the pharynx and trachea since these structures are not of concern for PE. Then we will discuss the anatomy of the airway from the bronchi to the alveoli.
This reformatted sagittal CT image demonstrates the upper airway. An orange arrow points to the pharynx, and a green arrow points to the trachea. These areas are not of concern to us when doing a CTA pulmonary angiogram.
These two 3D CT volume rendered images show the vast distribution of the bronchial-pulmonary airway. The image on the left shows the bronchial pathways in relation to the whole lungs, and on the right the lungs are diminished to amplify the bronchial tree. Notice the distribution of the airways closely follows the vascular distribution of the lungs.
These two CT images show the pulmonary-bronchial distribution throughout the lungs. The vast airway reaches down to the alveoli where oxygen is exchanged for carbon dioxide. The airway is studied mainly with the nuclear ventilation scan; however, CT can also be used to demonstrate lung parenchyma and the bronchi.
This picture shows the distal branches of the conducting pathway and the blood supply to the alveoli. Notice that small capillaries and arterioles surround each alveolus to participate in gas exchange. Within the acinus each capillary (A) releases carbon dioxide into the open space of the alveolus (C) and oxygen diffuses into the vessel (B). The movement of gas is passive as gasses flow freely across membranes of the capillaries. Since oxygen is in high concentration in the lungs it moves down its concentration gradient into the capillaries. Likewise, carbon dioxide, which is more concentrated in the blood capillaries, is released down its concentration gradient into the alveoulus. This is a dynamic process that yields 100 percent saturation of red blood cells as they leave the lungs in normal individuals.
CT Pulmonary Anatomy
When imaging the pulmonary arteries and their distribution to evaluate for PE it is important that the CT technologist have a good working knowledge of CT anatomy. A good starting place for discussing pertinent anatomy of the pulmonary system is at the pulmonary trunk. The pulmonary trunk arises from the right ventricle to serve as a conduit for deoxygenated blood to the pulmonary capillary-alveolar interface. The pulmonary trunk is about 5 cm long and 3 cm in diameter. It is located immediately below the aortic arch at about the level of the fifth thoracic vertebrae, where it divides into right and left pulmonary arteries. The bifurcation of the pulmonary trunk is anterior, inferior, and to the left of the tracheal bifurcation. The bifurcation occurs anatomically near the tracheobronchial lymph nodes, which are between it and the esophagus. The bifurcation of the trachea at the carina is a good radiological CT landmark for localizing the pulmonary trunk. The pulmonary trunk lies below the aortic notch seen on the PA/AP chest x-ray, which is the aortic arch.
Ideally, intravenous contrast agent is administered via the right brachial vein in the antecubital fossa of the arm. Contrast enters the right atrium via the superior vena cava from the subclavian veins. It then flows from the right atrium through the tricuspid valve into the right ventricle. The tricuspid valve is an atrioventricular valve lying between the atrium and ventricle. From the right ventricle blood is pumped into the pulmonary trunk and distributed to the right and left pulmonary arteries. The pulmonary arteries carry deoxygenated blood to the lungs to be oxygenated. Carbon dioxide from the tissues is released from hemoglobin in the red blood cells in exchange for oxygen in the lungs. The red blood cells are saturated with oxygen in the alveolar beds of the lungs and returned to the left atrium by four pulmonary veins. The pulmonary veins carry oxygen rich blood back to the left heart to be pumped to the body. Blood is received into the left ventricle as it passes through the bicuspid valve, which is between the left atrium and left ventricle. The left ventricle pumps oxygenated blood into the aorta past the aortic valve, which lies between it and the root of the root of the aorta. Once blood enters the ascending aorta it is propelled to all parts of the body.
This 3-D volume rendered CT image shows the relative position of the pulmonary trunk to the aorta (left). The pulmonary trunk (PT) lies immediately below the aortic arch. The axial CT image (right) shows the pulmonary trunk (PT) and right pulmonary artery (RPA). Notice the relationship of the pulmonary trunk and right pulmonary artery to the ascending aorta (AA) and descending aorta (DA). This relationship can be fully appreciated by observing the 3D image on the left.
These three CT images show the relationships of the aortic arch (AA) with the pulmonary trunk (PT) The pulmonary trunk lies just below the aortic arch and posterior to the ascending aorta. The relationship of the left pulmonary artery (yellow arrow) to the pulmonary trunk and aorta is seen on the parasagittal CT image on the right.
These two reconstructed coronal CT images show the flow of contrast through the right heart to the lungs. Left image shows contrast in the right ventricle (RV) being pumped into the pulmonary trunk (PT). The image on the right shows contrast distribution to the right pulmonary artery (yellow arrow) and left pulmonary artery (green arrow). The right pulmonary artery runs just posterior to the ascending aorta and in front of the tracheal bifurcation. The left pulmonary artery is shorter and smaller and runs anteroinferior to the descending aorta. Notice the left ventricle (LV) and aortic arch (AA) are not filled with contrast. Contrast seen in these images represents the normal flow of blood through the heart to the pulmonary circulation.
Blood in the pulmonary arteries reach the distal parts of the lungs to the capillary beds of the alveoli. These two coronal CT images demonstrate contrast in the distal branches of the pulmonary arteries in normal lungs (left-blue arrows) and in abnormal lungs (right-yellow arrows). The importance of these images is that the distal branches of the pulmonary arteries must be demonstrated on the CTA pulmonary study since a pulmonary embolus can lodge in these distal segments.
The left pulmonary artery is connected to the descending aorta by the ligamentum arteriosum. The ligamentum arteriosum is a remnant of the ductus arteriosus, which is a fetal vessel that connects the left pulmonary artery with the descending aorta. The fetal ductus arteriosum shunts oxygenated blood from the right fetal heart to the aorta bypassing the deflated nonfunctional fetal lungs. This arterial shunt closes off at birth becoming a ligamentous attachment. It is important to note that this attachment can cause rupture of the aorta when stretched. This frequently occurs with high impact trauma to the chest, as in a motor vehicle accident.
Knowing the anatomy of the pulmonary trunk and pulmonary arteries is important because this allows the technologist to locate them in different body habitus types. When we discuss imaging protocol for the CT PE angiogram it will be important to have a good working knowledge of the cardiopulmonary anatomy.
Occurrences of PE Correlated to Clinical History
The presentation of pulmonary embolism (PE) varies from dyspnea that gradually progresses to dramatic sudden onset respiratory collapse. Therefore, any emergent patient who presents with unexplained respiratory symptoms must be evaluated understanding PE is in the differential. This is because the symptoms of PE are most often not specific enough to make the initial diagnosis. Therefore the index for suspicion is high in patients who have had recent surgery, present in a hypercoagulable state, or whose status includes decreased physical activity or immobility.
It is important for the CT technologist to understand that clinically presentation can have a predictive value to a possible diagnosis of PE. Clinical presentations are generally categorized into 4 broad classes based on expected severity of pulmonary artery occlusion. These categories are 1) massive PE, 2) acute pulmonary infarction, or 3) embolus without infarction, and 4) multiple PE. The general characteristics of patient presentation for these categories are:
These two CT images show a large pulmonary embolus in the left main branch of the pulmonary artery. On the left is a lateral view of the artery and on the right is the anterior view of the same artery. This patient presented to a local emergency room with chest pain, hypotensive, oliguria, and a high D-Dimer.
These coronal CT images show large occluding pulmonary emboli in branches of the left pulmonary artery and distal peripheral branches (orange arrows). This patient presented to a local emergency with pleuritic chest pain, short of breath, and hemoptysis. The ECG was normal and there was no pain relief with two doses of nitroglycerine.
These two coronal CT images are of the same patient who presented with dyspnea, chest pain, and mild core pulmonale. The chest CT angiogram reveals multiple PE (arrows) as was suspected by clinical observations. Pulmonary emboli were found in several secondary, tertiary, and distal branches of the pulmonary arteries.
The accuracy of clinical determination of venous thromboembolic disease and pulmonary embolus without diagnostic testing is less than 50%. Therefore, diagnostic testing including laboratory and diagnostic imaging is needed to confirm or disprove VTE or PE. A specific blood test, the D-dimer level in a suspected patient can be used in many cases to guide clinical decisions. D-dimer test measures clotting activity in the body. Appropriate use of negative D-dimer measurements in clinical trials was able to guide physicians in withholding anticoagulant therapy in suspect VTE patients. When used as part of the diagnostic strategy D-dimer can also decrease need for serial radiological testing. Normal D-dimer level alone does not specifically exclude PE or VTE, neither does a high or low D-dimer give a specific diagnosis of PE or VTE.
D-dimers are fibrinolytic (anticloting) products formed when the fibrin within a clot is proteolyzed by plasmin products. D-dimers are produced in many disease states such as severe infection, malignancy, renal failure, sickle cell crisis, pregnancy, recent hemorrhaging to mention a few (see table below). The point here is that they are highly nonspecific, but are highly associated with thrombosis and thrombolysis. What can be said about D-dimers is that they are specific for indicating degradation of clots (lysis of crossed-linked fibrin), but are not specific for diagnosis of VTE or PE. Therefore, the use of D-dimer assay alone to confirm or refute PE is highly inaccurate, even when lab values fall within the normal range. So the question becomes what good is the D-Dimer test and how can it be useful in guiding test for PE?
Compounding the reliability problems of D-dimer assay is its low sensitivity. This means its ability to rule out VTE or PE based on a negative test is low. In an ideal world it would be great to know that a negative or normal value D-dimer excludes VTE or PE; however, D-dimer does not do this. We can understand the reason by looking at the statistical evaluation of the likelihood ratio (LR), or LR of a negative (normal) D-dimer. The likelihood ratio evaluates the probability of finding a negative D-dimer measurement among those without VTE or PE, compared to negative finding in those with the disease. In evaluating LR keep in mind that a LR of 1 means the likelihood of finding a normal value in those without PE or VTE is the same as in those with the condition. This would mean the test has no diagnostic value because the results are the same in both populations.
Likelihood ratio is one of the best ways to measure diagnostic accuracy since it includes sensitivity and specificity of the test. By sensitivity we mean how well the test measures the probability of a positive test among patients with disease. In other words, sensitivity in a D-dimer test would indicate a high D-dimer in those with VTE or PE. By specificity we mean the probability of a negative test among patients without VTE or PE is high. So, we would get no diagnostic value out of the D-dimer if the sensitivity for thrombosis is 90%, but the sensitivity for VTE or PE is only 10%. This is often the case because many conditions can cause an elevated d-dimer. For example, D-dimer in the elderly it is reported to be only 9% specific for VTE. Therefore, in this population the LR is equal to 1 and D-dimer has no diagnostic value. You will often notice that physicians order imaging studies on this population even when D-dimer is normal.
Now consider what the value of D-dimer testing would be if its specificity for PE were high. If the D-dimer assay had a high specificity, then it would be a diagnostic tool in exclusion of VTE or PE when a negative (normal) measurement is reported. Not all D-dimer laboratory tests are highly specific. Only those types used in clinical research trials should be used to determine patient outcome strategies. Recommended clinical trials test to determine D-dimer that are highly specific are enzyme-linked immunosorbent assay (ELISA) and whole-blood assays such as Simpli-RED commercially available tests. Latex agglutination test is not reliable since it depends on the qualitative visual reading by the lab technician. These reading varied significantly within the Bounameaux study, and between institutions. Statistically, 1 in 1000 patients could die of missed PE for every 2% decrease in sensitivity of D-dimer measurement. So it is important that the physician knows what type of D-dimer assay is used in their laboratory when relying on its measurement.
Of the several clinical assessments for the role of D-dimer in determining VTE or PE none concluded an independent role for negative dimer measurement in ruling out VTE or PE. Therefore, no clinical decision based on negative D-dimer alone is definitive. But when used in combination with noninvasive testing such as normal compression ultrasound (CUS), normal impedance plethysmography (IPG), or negative/indeterminate V/Q scan is highly accurate for clinical decision-making. This criterion of using a noninvasive test is called “low pretest clinical probability”. Studies following patients 3 months or more who had negative D-dimer assay and a qualifying low pretest clinical probability and did not receive anticoagulant therapy showed excellent predictive results. The incidence of VTE in this population was from 0% to 1.75%, which is an acceptable clinical threshold. This is why PE studies such as CTA and V/Q scanning is performed on some patients with negative D-dimer.
The lung V/Q scan is still currently used to evaluate some cases of suspected PE. A V/Q can give a highly sensitive and highly specific evaluation for PE when the probability for PE is low, or very high. It is also very beneficial for patients who have allergy to iodinated contrast agents and acutely cannot be premedicated. Otherwise, helical CT angiography is the modality of choice for evaluating PE. The Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) and PIOPED II studies have sufficiently evaluated effectiveness of Lung scintigraphy and CT angiography for diagnosing PE. The purpose of the PIOPED study was to evaluate the sensitivity and specificity of two major, widely used technologies, radionuclear imaging (ventilation-perfusion scanning) and pulmonary angiography, for the diagnosis of pulmonary embolism. The purpose of PIOPED II was to evaluate the role of spiral CT scan in the diagnosis of PE by comparison with reference tests, including pulmonary angiography and V/Q lung scan in patients without prior PE. It also evaluated compression ultrasound of the lower extremities in patients with no prior deep venous thrombosis (DVT).
PIOPED study found that a normal V/Q scan excluded any significant clinical PE. The study also showed that a high probability for PE V/Q scan was highly specific and sensitive. But the most important disadvantage of the V/Q scan is that a rather large gray area of scans, called indeterminate does exist. Therefore, when evaluating PE using nuclear lung scintigraphy, a clear chest x-ray is prerequisite. The study also concluded that lung scintigraphy to evaluate PE must involve both perfusion-lung imaging and ventilation-lung imaging. Perfusion imaging is a noninvasive method of evaluating pulmonary arterial blood flow. Ventilation imaging uses radioactive gases to evaluate lung pathology quantitatively and qualitatively.
Several pathologies can cause an indeterminate finding for the V/Q scan. This does not mean that the scan cannot be performed when known pathology exists. The lung V/Q scan is performed for reasons other than to evaluate PE. For example, bronchogenic carcinoma, which characteristically causes a decrease blood flow to the affected segment, is evaluated by V/Q scan. This allows for determination of how much blood flow to the remaining portions of the lungs should the segment(s) be surgically removed. It is recommended that the chest x-ray be compared with the V/Q scan. But for evaluation of PE it is recommended that a clear chest x-ray be prerequisite, otherwise a CT angiogram should be considered.
The PA chest x-ray on the left is clear of obvious lung pathology. In this case evaluation for PE using the nuclear V/Q scan can give definitive results of either high or low probability for PE. The PA chest x-ray on the right has distinct lung pathology (arrow) that could compromise the scan. If a nuclear V/Q scan is performed, the result may yield an indeterminate diagnosis for PE. The Nuclear Medicine Society has established that frontal and lateral radiographs be taken prior to the V/Q scan.
The perfusion scan is made after administering radiopharmaceutical macroaggregated albumin. The radiopharmaceutical Technetium 99m macroaggregated albumin (Tc-99m MMA) is used as the perfusion agent. This is a noninvasive approach to evaluating pulmonary blood flow. Radiopharmaceutical is injected intravenously and works by lodging in the pulmonary arterioles mapping pulmonary circulation. Radiopharmaceutical particle size and number is important for several reasons. The study mechanism requires the particles be physically trapped in the pulmonary system in sufficient numbers to be recorded by scintigraphy. Ideally, the particles should be lodged in the pulmonary arterioles. A particle size of less than 7 micrometers (7 U) will pass through the pulmonary capillaries and are not counted in the pulmonary data. Particles larger than 150 U lodge higher in the pulmonary artery circulation either mimicking or causing a PE. Therefore, all MMA particles must have a size ranging from 10 to 90 U. Homogeneity of the scintigraphic images depends on the number of particles. Between 200,000 and 700,000 particles are needed to produce a diagnostic perfusion scan. The energy of Tc-99m is 140 keV. The half-life of TC-99m MMA is 5 hours. Elimination of MMA is through the urinary system. Approximately 20% is eliminated within 24 hours of administration.
Eight views should be obtained, the views should each be labeled in the sequence: anterior, posterior, right lateral, left lateral, right posterior oblique (RPO) 45 degrees, left posterior oblique (LPO) 45 degrees, right anterior oblique (RAO) 45 degrees, and left anterior oblique (LAO) 45 degrees. These are labeled and shown on the images below:
Eight views of the lungs are commonly taken for the nuclear perfusion scan: these are the anterior, posterior, right anterior oblique (RAO), left anterior oblique (LAO), right lateral, left lateral, right posterior oblique (RPO), and left posterior oblique (LPO) views.
The lungs are normally cone-shaped with a near horizontal cutoff at their bases. Because of this the lung bases at the diaphragm are not seen on the anterior view (left). A photophenic area is seen centrally, which is the cardiac shadow and aorta. The posterior view (right) shows most of the lung and the bases better than the anterior view. From the posterior view the spine is seen as an area absent of perfusion. Some segments of the lungs are superimposed on the anterior and posterior views so additional views like the obliques are needed to separate these segments.
The lateral views demonstrate the lungs within the contour of the diaphragm and spine. These views demonstrate defects in some of the lobes of the lungs. When these are positioned correctly and the spine and diaphragm are normal in position, and absence of perfusion is considered abnormal. Occasionally because the lungs are superimposed on the lateral view, �shine through� from the opposite lung can occur. This phenomenon can hide small subtle defects.
The anterior and posterior oblique views demonstrate peripheral lung segments better than the other views. The lung projected closer to the scintillation camera will demonstrate perfusion defects better that the lung further away.
Some conditions are indistinguishable from PE on the perfusion scan, for example, emphysema, pneumonia, carcinoma, etc. So to increase the specificity of the lung scan the ventilation scan is performed along with the perfusion scan. The perfusion scan is correlated with the ventilation scan and chest x-rays. When a pulmonary embolus is present, the ventilation scan is normal in areas of non-perfusion identified on the perfusion scan. Likewise, a normal perfusion scan eliminates the diagnosis of PE. The ventilation scan is usually performed first because perfusion radioisotope can contaminate the ventilation scan causing false readings.
Ventilation/inhalation studies (Q) use inert radioactive gas to quantitatively and qualitatively evaluate lung pathology. Inert gases are chemically unreactive and so make a good contrast agent in airways of the lungs. Gases currently used for ventilation nuclear imaging include: Xenon 127 (Xe127), Xenon133 (Xe133), Krypton 81m (Kr81m), and Technetium 99m (Tc99m) pentetate a.k.a. DTPA. Krypton gas is least used because of its short half-life of 13 seconds. The other radioactive gases have half-lives of hours to days, which increase bio effectiveness. Almost all radioactive gases must be collected to prevent high room concentrations of these gases with the exception of krypton. These gases must be collected by aerosol filter or passed through an activated charcoal column.
The routine view for the ventilation scan is the posterior view. The procedure begins with when the patient is instructed to breathe xenon gas with the facemask firmly in place covering the nose and mouth. The patient takes a deep breath and holds it for 15 seconds. This image is recorded and labeled 15-second inspiration. The patient returns to normal breathing for 60 seconds. At 60 seconds the image is recorded and labeled 60-second equilibrium. Then the patient breathes room air through the mask and three to six images are taken at 60-second intervals until the xenon has been completely exhaled. These are labeled washout images. Xenon gas is not absorbed by the lung and is completely exhaled during the washout phase. The ventilation scan is usually performed first since it does not contribute background radiation to the perfusion scan, but the perfusion scan can contribute background radiation to the ventilation scan. The collected gas is stored in a shielded environment until it returns to background levels.
These 10 image spots represent a normal ventilation portion of a V/Q scan. The images normally taken vary from institution to institution based on radiologist preference. The top row from left to right represents the first breath (15-second image), equilibrium (60-second image), and RPO and LPO views during washout. The remaining images were taken during washout with complete clearance seen beyond 180 seconds.
You may notice that anatomy is not as clearly defined on the ventilation scan as it is on the perfusion scan. This is because many pathologies and even normal lung anatomy appears to cross segmental boundaries, which may distort the image. Several pathologies can be determined on the ventilation scan, such as chronic obstructive pulmonary disease (COPD), bronchogenic carcinoma, pulmonary fibrosis, pneumonia, and space-occupying lesions to name a few. But our topic is diagnosing pulmonary embolus using the V/Q scan. As we stated earlier, the ventilation scan is generally normal in patients having a pulmonary embolus. Accordingly, finding two or more segmental perfusion defect and a normal ventilation scan shows a high probability for pulmonary embolus (greater than 85%). In the absence of a clear chest x-ray the diagnosis may be indeterminate. Likewise, an indeterminate ventilation scan may require a CT angiogram or direct angiography to determine the presence or absence of PE. The basic patterns of diagnosis are covered by PIOPED criteria.
This ventilation scan was performed after administering inhaled Xenon-133 (24.6 mCi) with subsequent washout images. The study was compared to the chest radiographs taken the same day. The ventilation scan is unremarkable with no significant air trapping. The chest radiograph was also clear. The perfusion scan is seen below.
Intravenous dose of 5.9 mCi TC 99m MMA was given and the perfusion phase of the V/Q scan taken. The perfusion scan shows a large mismatch in the right middle lobe and a moderate sized mismatch in the right upper lobe. These are well seen on the RAO and right lateral images. The LPO image shows a large mismatch in the superior segment of the left lobe. The left lateral also shows moderate mismatch in the left upper lobe, and is seen on the LAO image as well. Because the ventilation scan was unremarkable and the chest x-ray was clear of infiltrates, this is a high probability for PE scan.
RAO (left) and right lateral (right) taken from the study below are magnified to show the areas of perfusion mismatch. When two or more segments are mismatches along with a normal ventilation scan, a diagnosis of pulmonary emboli is highly probable.
LPO (left), left lateral (middle) and LAO (right) are magnified images from the full scan seen above. Again, The LPO image shows a large mismatch in the superior segment of the left lobe. The left lateral also shows moderate mismatch in the left upper lobe, and is seen on the LAO image as well. Findings on the right lateral and RAO show there are more than two areas of mismatch. This along with a normal ventilation scan indicates a high probability for pulmonary emboli.
In conclusion, we see that the nuclear ventilation and perfusion scans are very accurate in diagnosing pulmonary embolus. Distinct criteria must be followed in order to achieve reliable results, for example, a clear chest x-ray is prerequisite to the scan. The V/Q scan is also useful when the patient has difficulty holding their breath for the pulmonary angiogram, or is useful when the patient is allergic to iodinated contrast agents. Although the nuclear V/Q scan does not demonstrate the pulmonary embolus, it does show the lung segment involved when an embolus is present. Readings are described as low probability, indeterminate, and high probability. In either the low or high probability case there is a high degree of confidence in the diagnostic prediction of the V/Q scan.
CT Pulmonary Angiogram (CTA)
Fast helical CT scanning of the pulmonary vasculature during a timed intravenous injection of contrast media allows for evaluation for pulmonary emboli. CT offers a method of direct visualization of the pulmonary vessels and lung parenchyma using diagnostic x-ray images. The key to achieving a highly diagnostic study of the pulmonary vessels is rapid data acquisition during accurately timed intravenous delivered contrast agent to the vessels. Multidetector row helical CT scanning offers the most sensitive and accurate diagnosis of pulmonary embolus. Modern 16, 64, 128, and 256 slice and faster scanners make nearly motion free images of the pulmonary vasculature and lung parenchyma. Axial acquired images can then be reconstructed using various techniques in coronal and sagittal planes if needed.Historically, there are three imaging procedures used in radiography to determine if a patient has a pulmonary embolism. These are the nuclear ventilation/perfusion (VQ) scan, helical CT pulmonary angiography (CTA), and direct catheter pulmonary angiography. While all three of these methods of diagnosis are in current use, of these, the preferred method for PE evaluation is the CT angiogram. In some cases, as we have already discussed, the nuclear V/Q scan may be performed rather than CTA. Alternatively and rarely, chest angiogram, which is performed in the interventional radiology suite, can also provide definitive diagnosis of pulmonary embolism. In this section we will look at how the CT pulmonary angiogram is performed and discuss what a good diagnostic scan should look like. Also we will discuss scan parameters that produce an optimal scan of the pulmonary vessels.
Clinical indications for CT pulmonary angiography have and continue to evolve based on research and new imaging procedures. Currently pulmonary CTA is the gold standard for diagnosing pulmonary embolus. Some indications for CTA are: 1) primary diagnosis of PE when clinical, laboratory, or radiologic finding are suggestive, 2) suspected PE in those with extensive heart disease or lung disease that reduce the probability of an accurate nuclear V/Q scan. Often a clear chest x-ray is required to determine if a nuclear V/Q scan can be performed in place of the pulmonary CTA scan. Pulmonary CTA is indicated when an immediate diagnosis of PE is needed, for example, respiratory distress in an emergency room patient, respiratory dysfunction in an unresponsive patient, etc.
One major advantage of performing pulmonary CTA is its ability to provide differential diagnosis in 50-60% of cases negative for pulmonary embolus. Some of these alternate diagnoses include: pneumothorax, dissection of the aorta, pericarditis, lung cancer, pleural effusion and others. Unlike the V/Q scan the pulmonary CTA gives good contrast and detail imaging of the lung parenchyma. Even when the test proves negative for pulmonary embolus, pathologies within the differential diagnosis can be confirmed or refuted.
A major concern when performing pulmonary CTA is the diagnostic qualities of scan images. A recent study reported in the American Journal of Radiology, November 2009 issue reported that approximately 19% of scans were below the diagnostic standard. Patient motion, morbid obesity, image noise, or improper contrast bolus timing can reduce the diagnostic quality of a scan. A good diagnostic CT scan will show the pulmonary trunk and pulmonary arteries, and their large secondary, subsegmental, and tertiary branches down to small distal branches distributing to the lung bases. Optimal radiocontrast distribution should be limited to the pulmonary arteries and their branches with little to no filling of the pulmonary veins. Ideally, there should be no contrast in the pulmonary veins or their tributaries, bronchial arteries, aorta, or superior vena cava. An optimal study limits contrast perfusion to the distribution of the pulmonary arteries, including subsegmental and distal branches. In some cases, such as a double rule out scan in which PE and aortic dissection is evaluated, a longer scan time is optimal. This is because contrast must fill the pulmonary vasculature and the proximal aorta.
A scan performed on 16-slice multi-detector row CT scanner or 64-slice CT machine can reduce the exposure time to roughly 7 seconds or less. Newer CT scanners offering 256 detector rows or more can reduce exposure time to 1-2 seconds. This vastly improves the quality of the scan by eliminating involuntary patient motion. However, the faster the scan time the more difficult it is to catch optimally timed contrast distribution. All scans require the timing of the contrast bolus be accurate and that the scanner is capable of completing the scan when the contrast is optimally distributed. A single slice CT scanner, 4-slice, or 8-slice CT scanners are not capable of completing the scan within ideal parameters. However, these low slice scanners do offer a highly accurate scan with mild to moderate pulmonary vein and aorta filling. Likewise fast scanners like a 64 or 256 slice scanners pose the risk of outrunning the contrast if not optimally timed. When this happens there is contrast in the proximal pulmonary artery segments, but none in the distal branches. One can also be late timing contrast moving through the pulmonary arteries. When this happens there is slight opacification of the pulmonary trunk and bright opacification of the aorta. In either case the patient may need to be rescanned, which raises the total radiation dose to the patient. Rescanning a patient is very concerning, especially young female patients because the radiation dose to the breast greatly exceeds mammography dose. Therefore, technologist skill does play a major role in the quality of the scan.
The time it takes for contrast to get from the site of the intravenous injection to the pulmonary trunk and pulmonary arteries determines the start time for the scan. The timing will be different for each individual based on his or her own unique physiology or pathological state. There are two ways in which the timing is calculated: 1) using multiple image region of interest (MIROI) technique, or 2) using a “smart prep” technique. MIROI function gives a graphic of CT number change over time. Multiple scans are taken at the same anatomical location. Measurement scale is the Hounsfield unit (HU) in relative or absolute scale. The relative scale displays the first reading as zero and the difference in CT numbers from one scan to the next. The absolute scale displays the actual HU number and the difference from one scan to the next. The region of interest (ROI) is selected using an elliptical, box, or trace function in the location to be measured. The goal of the timing bolus using MIROI or “Smart-prep” is to calculate the scan parameters needed to optimize contrast brightness of the pulmonary arteries.
A scanogram, or scout image is taken to localize the pulmonary trunk. Then, an elliptical or box ROI is selected to measure the density change as contrast enters the region of interest. Successive images are taken at 1 or 2 seconds apart. The time it takes the injected contrast to reach 100 percent saturation in the region of interest is the timing parameter for the start of the scan. Let’s consider the graph below and the multiple CT images taken using the MIROI function to demonstrate these principles.
The radiograph on the left is a scout taken to localize the pulmonary trunk, which is just at or below the level of the bifurcation of the trachea (white lines). The resulting axial CT localization image is shown on the right. An elliptical ROI is placed in the right pulmonary artery to measure the time for contrast to reach this area from the injection site. The pulmonary artery will become bright as radiocontrast infuses the artery. The time it takes to reach 100% saturation will be calculated and displayed in a graph.
Once the timing bolus is administered the correct exposure factors are selected and the scan commences. Keep in mind that there is a narrow window of time for completing the scan if only the pulmonary arteries are studied. Likewise, there is a narrow window of time to include the pulmonary trunk, pulmonary arteries, and the proximal aorta when a double-rule out scan is performed. A double-rule out scan evaluates the pulmonary arteries for PE and the proximal aorta for dissection using a single contrast bolus injection.
This MIROI graph shows that the contrast injected into the right anticubital fossa vein reached the pulmonary trunk in 8 seconds. The superimposed graph showing aortic perfusion of contrast agent takes about 14 seconds. While most CT technologists� only monitor the pulmonary phase in which contrast flows from the pulmonary arteries to the capillary beds, it is also observed that venous return to the pulmonary veins has occurred when contrast enhancement is seen in the proximal aorta.
These two axial CT images demonstrate how the timing bolus is used to determine scan parameters. The image on the left demonstrates filling of the pulmonary trunk (yellow arrow) and pulmonary arteries. Notice the aorta is not filled with contrast media as this represents narrow timing for the PE bolus. On the right is the same image showing poor filling of the pulmonary trunk and bright opacification of the ascending (pink arrow) and descending (blue arrow) aorta.
Once the timing of the contrast bolus is determined the scan of the pulmonary vessels is made. The scan should include from the top of the lungs through the lung bases. Axial and coronal images are the standard image formats for interpretation. Thin slice mages are acquired in the axial plane. It is desired that the images presented for reading are 1.25 X 1.25 mm (thickness and interval). However, to reduce patient radiation exposure the scan may be performed at 5.0 X 5.0 mm and reconstructed to thinner slices. Keep in mind that the scan time, that is the time it takes to acquire scan data through the lung field, is shorter for a 5 mm scan and longer for a 1.25 mm scan. So, while it is important to get a good scan through the main pulmonary artery tree, it is also important to see contrast in the distal portions of the arteries at the lung bases.
The axial CT image (left) shows large pulmonary emboli bilaterally. The pulmonary arteries from this image are magnified on the right to show these emboli better (yellow arrows). Although the initial CT scan is acquired in the axial plane, these are reformatted into coronal and sometimes sagittal images. Coronal images allow the radiologist to see distal branches of the pulmonary artery better as a whole vessel rather than in thin slice images.
These two axial CT images show profound pulmonary emboli. On the left the embolus almost completely blocks the right pulmonary artery (yellow arrow). Right image show an extensive saddle embolus forming in both pulmonary arteries and becoming extensive. Both of these types of pulmonary emboli are life threatening and require immediate medical attention.
This reformatted coronal image shows a large pulmonary embolus in the several segments of the right pulmonary artery. The pulmonary trunk and right pulmonary artery is magnified on the right to show a portion of the pulmonary embolus (yellow arrow). The superior segment of the right pulmonary artery also shows a blunting of its tip caused by pulmonary embolus. Coronal images give a better view of the whole vessel making smaller vessels easier to trace to their origin.
This coronal image shows a large pulmonary embolus in a branch of the left pulmonary artery and scattered emboli in both lung fields. A magnified view of the chest is seen on the right with arrows pointing to several pulmonary emboli. Coronal images help show extensive emboli with present that can be correlated with axial images.
Sagittal images are not routinely made for the chest CTA; however, it is shown here (right) to show the extensive distribution of the pulmonary embolus seen on the coronal image (left). These images show why the CTA pulmonary study is the gold standard for diagnosing PE.
The distal branches of the pulmonary tree should also be seen on the axial and coronal images because pulmonary emboli can occur in these areas of the lung too. Consider the CT images above that demonstrate the distal branches of the pulmonary arteries (yellow arrows). Thick slab coronal CT images also help distinguish pulmonary branches from pulmonary veins (blue arrows). Filling defects in the pulmonary veins can mimic a pulmonary embolus in a distal pulmonary artery branch.
This sagittal CT image shows small subsegmental branches of the pulmonary artery. Radiocontrast outlines pulmonary emboli in some of these small branches (yellow arrows). This shows why it is important to calculate the timing of the contrast bolus so that distal branches down to the lung bases are opacified.
Computerized tomography angiography of the pulmonary arteries is considered the gold standard for diagnosing pulmonary embolus. Unlike the nuclear medicine ventilation/perfusion scan a clear chest x-ray is not required. However, the patient must have normal renal function and not be allergic to iodinated contrast agents. The CTA scan offers the capability of a quick diagnosis in just a few minutes, yet it still has its drawbacks. For example, its use must be held to risk vs. benefit standards because the radiation dose to the breast is considered high. The American College of Radiology recommends a radiation dose not to exceed 0.3 rad (rad is a unit of radiation absorbed dose) for 2-view screening mammography images. The estimated breast dose for CTA pulmonary scan is 2.0 rad to each breast. Therefore, the CT technologist should employ every measure acceptable to the radiologist staff to reduce dose. Dose can be reduced by eliminating repeat scans, decreasing tube current and voltage, reducing table increment, increasing exposure time, increasing acquired scan slice thickness, and properly explaining the procedure to the patient. The patient should be instructed on proper breathing protocols, and informed of sensations caused by intravenous contrast agent. Bismuth and tungsten breast shield that do not affect image quality, but do reduce breast dose nearly 57% should also be used. Overall, CT angiography of the chest is considered safe and is often necessary for diagnosing acute cases of suspected pulmonary embolus.
Pulmonary angiography is a procedure in which a flexible catheter is placed in the pulmonary trunk and iodinated contrast media is injected into the pulmonary arteries to demonstrate the presence of a pulmonary embolus. This is an invasive procedure that at one time was considered the gold standard for diagnosing pulmonary embolus. This being an invasive procedure poses some risks and has limitations as to what patients are candidates for the procedure. Pulmonary arteriography is more accurate compared to radioisotope scanning. Pulmonary angiography did not replace the nuclear scan because a positive V/Q scan and chest x-ray template was needed to guide the procedure.
Pulmonary angiography can provide hemodynamic evaluation in addition to radiographic imaging of the pulmonary vasculature. Several conditions such as left ventricular disease, cardiac tamponade, cor pulmonale, and definitive prove of the presence or absence of PE can be obtained by direct angiography. Pressure values in the pulmonary arteries can be quite beneficial. A patient with no cardiopulmonary disease and pulmonary hypertension can be indicative of PE. An acute mean pulmonary arterial pressure greater than 25 mm Hg is often an indicator of an obstructing pulmonary embolus. Normal pressure in the pulmonary arteries is 7 mm Hg. As the mean arterial pressure approaches 40 mm Hg pulmonary obstruction when caused by PE approaches 60-70%.
Direct angiography requires a flexible catheter be placed in the pulmonary vessels so that radiographic contrast agent can be administered. The approach options include percutaneous venous puncture of the upper extremity, cut-down puncture of the anticubital vein, transjugular, and percutaneous venipuncture of the femoral vein. Which option is used is up to the radiologist performing the procedure. Each route has its rationale based on patient presentation. For example, in cases of high suspicion of pulmonary embolus the upper extremity route is most often preferred. Likewise, the femoral vein approach is sometimes contraindicated because most emboli occur in the legs or deep pelvic veins causing this approach to complicate the patient�s condition. Catheter manipulation is somewhat easier from the upper extremity approach since the catheter must be routed up the inferior vena cava through the right atrium and ventricle to reach the pulmonary vessels from below.
To perform the pulmonary angiogram a site for percutaneous puncture and catheter insertion is selected. The Seldinger technique is the most commonly used entry technique for inserting the guidewire, which is followed by the catheter insertion. The most common types of catheters in use are the closed-end, multiple-side-hole, and pigtail. The pigtail catheter has multiple side ports and an end hole for dispensing radiographic contrast agent. The most common type of pigtail in use is the Grollman catheter. The Seldinger technique is the most commonly used entry technique for inserting a guidewire into the pulmonary trunk. Using the Seldinger technique, the pigtail is slid over the guidewire into the selected pulmonary artery and the guidewire removed. If the site of entry is the femoral artery, then an ultrasound of the area is recommended to rule out a thrombus at of distal to the site.
This radiograph taken in the angio suite shows a Grollman catheter within the pulmonary trunk of a patient undergoing a pulmonary angiogram. The catheter was introduced transjugular (entry not shown). The left radiograph shows the catheter in a positive image format and on the right is the same radiograph in a negative image format. Radiographs can be viewed in either format during the procedure because the images are digital.
The primary site of injection of contrast media is the pulmonary trunk or pulmonary arteries. Alternative sites are the right atrium or selective vessel catheterizations. If the patient exhibits pulmonary hypertension such that the pulmonary artery pressure is near equal to arterial systemic pressure, or greater than 60 mm Hg, injection of contrast media directly into the pulmonary trunk or pulmonary arteries is contraindicated. In such case injection into the right atrium is the preferred alternate site. Injection of radiographic contrast agent into the pulmonary artery when there is severe pulmonary hypertension can cause cardiac arrhythmia and even pulmonary edema to occur. Before injecting contrast media the site of catheter placement is verified by taking the pressure in the right atrium, right ventricle, and pulmonary arteries. The standard unit for pressure is mm Hg (millimeters mercury).
Left- axial CT image demonstrate the anatomical presentations of the pulmonary trunk when normal in size, caliber, and pressure (yellow arrow), and on the right an example of a large widened pulmonary trunk (pink arrow) due to pulmonary hypertension.
Pulmonary and cardiac pressures of importance to the angiographer are the systolic, diastolic, end-diastolic, right atrium mean, right ventricular, left ventricular systolic, pulmonary arterial, and aortic systolic and diastolic. The systolic pressure is the pressure during ventricle contraction and ejection of blood. Diastolic pressure is the pressure during dilatation of the ventricles to receive blood from the atria. Just as there is a slight contraction of the ventricle, but before systolic ejection of blood is when the end-diastolic pressure is measured. The mean pressure is the average pressure in the vessel or heart chamber. The mean pressure in the right atrium is less than 8 mm Hg, and in the right ventricle 15 to 30 mm Hg systole and less than 7 mm end-diastolic. Several conditions can cause an increase in these systolic pressures including pulmonary hypertension and pulmonary vessel stenosis. End-diastolic pressure rises as the ventricles undergo hypertrophy, fibrosis, or ventricular failure. Pulmonary artery pressure ranges from 10 to 20 mm Hg with mean pressure of 15 mm Hg. End diastolic pressure in the pulmonary arteries is 5 to 14 mm Hg. A rise in pulmonary artery pressure can be an indicator of pulmonary embolus or other conditions like pulmonary vascular disease or obstruction of pulmonary venous return.
The right side of the heart and pulmonary artery flow is a low-pressure system. The left heart and aorta is a high-pressure system. The left ventricular systolic pressure normally ranges from 90 to 150 mm Hg as with aortic systolic pressure. Low cardiac output and cardiogenic shock are examples of conditions that lower systolic pressure. Aortic stenosis is a condition that can cause an increase in left ventricular systolic pressure. Normal aortic systolic pressure is 90 to 150 mm Hg, and aortic diastolic pressure range is 90 to 120 mm Hg.
Nonionic radiographic contrast media is used to opacify the pulmonary vessels during pulmonary angiography. Iso-osmolar media has been shown to reduce effect of contrast media on pulmonary arterial pressure, patient discomfort related to injection of contrast, blood pressure, and heart rate. The amount administered depends on the site of interest based on the V/Q scan. In general, 50 to 60 ml is needed when the injection is made in the pulmonary trunk at a rate of 25-30 ml/sec. If selective right or left pulmonary artery is the injection site, only 30 to 40 ml is needed at a rate of 15 ml/sec. Since the total time of pressure injection of contrast media last 1 to 3 seconds, rapid serial radiographs are taken. At least 27 frames per second or faster is recommended. The patient is positioned 10 to 15 degrees left posterior oblique to demonstrate the right pulmonary artery. A 30 to 45 degree right posterior oblique demonstrates the left main pulmonary artery. Initial imaging in the AP supine position is used to assess symmetric flow and vessel size.
This angiograph is a localization image that shows placement of the pigtail catheter in the pulmonary artery for selective angiography. The radiograph on the left is the positive image and on the right the negative image. Using digital imaging the angiographer is able to evaluate radiographs using both presentations.
These three angiographs show opacification of the pulmonary vessels by selective catherization of the left pulmonary artery. These images were taken after administering 40 ml of nonionic contrast media. On the right is a magnified portion of the radiograph showing a large filling defect in a branch of the pulmonary artery, which is a pulmonary embolus (arrows). This patient presented with ah clinical history of chest pain, advanced peripheral vascular disease, diabetic, smoker, and hypertension.
These three high-resolution serial angiographs were taken following injection of non-ionic contrast media. Multi-frame radiographs at more than 30 images per second can be made so that progressive filling of vessels can be recorded. Notice that these images are displayed using digital subtraction of bone and lung tissue to enhance resolution of the pulmonary vessels.
Although the direct puncture angiogram is no longer the gold standard for diagnosing pulmonary embolus, it is still used in selective cases. The pulmonary angiogram is still a highly diagnostic study that yields anatomical and physiological evaluation of the cardio-pulmonary system.
Ultrasound Deep Vein Thrombosus (DVT) Study
Compression ultrasound of the deep veins of the leg or upper extremity is performed to confirm the primary cause of suspected pulmonary embolus. There are two diagnostic strategies involving the use of real-time venous compression ultrasound for diagnosing deep vein thrombosis. In the past, phlebography (a.k.a. venography) was the gold standard for evaluating the lower extremity for venous thrombosus. Currently venous compression ultrasonography, which is a non-invasive diagnostic tool, is standard. Compression ultrasonography has a sensitivity of 97%[95% confidence interval (CI) 96�98%] and a specificity of 98% for symptomatic proximal deep vein thrombosis (DVT). Because of its high sensitivity for DVT, CUS along with color Doppler enhancement has become the gold-standard for DVT diagnosis in clinically suspected individuals. It is well validated in many clinical research studies have validated a main diagnostic criterion on CUS, absence of full compressibility of deep veins with gentle ultrasound probe pressure, confirms deep vein thrombosis on CUS.
The emphasis of continuing ultrasound research is to determine whether or not an extensive exam of the lower extremity to include the calf, or serial CUS studies decrease PE morbidity and mortality. Since the early 1990�s when CUS began replacing phlebography this issue has been debated among experts. Studies examining thromboembolic risk in patients with a negative CUS in proximal leg veins with negative CUS is proven to be low. The 3-month thromboembolic risk is 1-2% for negative CUS compared to 1.9% for those with a negative venogram. Studies show that a complete CUS (CCUS) to include the posterior tibial, peroneal, and calf muscle veins have a higher than acceptable risk for false-positive results. The 3-month risk when these veins are not included is exceptionally low, while positive findings may falsely add to the risk of over diagnosis and over treatment. Imaging the distal veins require the sonographer be especially skilled as this is a very cumbersome area. Clearly, a diagnostic strategy should include clinical evaluation for PE, pulmonary CTA or V/Q scan, and evaluation for DVT to significantly decrease the number of patients requiring pulmonary angiography, or to significantly decrease thromboembolitic risk. CCUS protocol offers a low technical failure rate, safely excludes or confirms DVT, and reduces the diagnostic workup for DVT to a single ultrasound examination.
The study below is of a patient who presented with chest pain and shortness of breath. The results of the CT pulmonary angiogram showed pulmonary emboli in both pulmonary arteries and subsegmental branches bilaterally. Presented is the right lower extremity duplex venous Doppler and right lower extremity arterial duplex Doppler scans. Indications for the ultrasound exam were a cold extremity, leg pain, and edema on physical examination. The ultrasound images revealed occlusive thrombus within the left common femoral vein with extension into the profunda femoris and greater saphenous vein. A duplicated superficial femoral vein had nonocclusive thrombus extending to just above the level of the popliteal veins. Popliteal and posterior tibial veins are patent. With this overview in mind, let�s look at some of the ultrasound images, which should give us an appreciation for the value of ultrasound imaging.
These two crossection ultrasound images through the right common femoral vein (CFV) show a large nonocclusive thrombus in the vessel lumen (yellow arrow). The image on the left shows the common femoral vein prior to compression being applied with a large clot within it. The ultrasound image on the right demonstrates noncompression of the vein when the sonographer applied gentle probe pressure. Noncompression of a vein containing a clot is a diagnostic sign for deep vein thrombosis.
These three views of the proximal femoral vein show the diameter of an occluding thrombus within the vessel. The middle image shows no compression of the vessel; the longitudinal image on the right shows the length of the thrombus. This clot extends into the profunda femoris and greater saphenous veins, as we shall see shortly. A clot this large can break away from the vessel wall becoming an embolus that may lodge in the pulmonary veins or go upward to occlude blood supply to the brain.
Color flow Doppler measuring within the right proximal femoral vein for 6.6 seconds shows no waveform. This indicates no blood flow due to occlusion by the large thrombus. It is important when a patient presents with pulmonary embolus that the source of the embolus is found, which is why this ultrasound study was performed. The clot was followed distally to determine its extent within the femoral vein.
These three images through the mid portion of the femoral vein show no compression (middle) of the vein. The longitudinal (right) and transverse (left) images show the clot within the vein. The entire length of a vessel must be demonstrated when a thrombus is found. Color Doppler was also taken at this location and is presented below. Notice there is no waveform seen in the mid femoral vein (images below).
The ultrasound image left) shows the distal femoral vein, which is duplicated. The wave form in both branches is also shown.
There is duplication of the superficial femoral vein (V1 and V2) with nonocclusive thrombus extending to just above the level of the popliteal vein. Therefore the waveform in both of these vessels is also measured. The waveform images are seen below.
These three ultrasound images show that the clot seen in the femoral vein does not extend into the popliteal vein. On the left is an axial view of the popliteal vein with no thrombus seen. The middle image shows compression of the popliteal vein, and the Doppler waveform (right image) shows biphasic pattern of blood flow.
In rare cases deep vein thrombosis occurs in the upper extremity, usually around the axilla and near the clavicle. These types of clots are called axillary-subclavian vein thrombosis. Upper-extremity deep vein thrombosis (UEDVT) is clinically important having about 33% of cases presenting with pulmonary embolus. UEDVT present a host of clinical complications including painful extremity, edema, superior vena cava syndrome, and compromised medical venous access. The incidence of UEDVT is about 2 per 100,000 persons per year. There appears to be a statistically significant increase in cases of UEDVT in recent years. The increase is due to central venous catheter use for chemotherapy, dialysis, bone marrow transplantation, parenteral nutritional support and the like. Primary upper extremity thrombosis occurs in two forms, Paget-Schroetter Syndrome (also called effort thrombosis), or idiopathic UEDVT. Paget-Schroetter syndrome occurs spontaneously following strenuous activity such as weight lifting, wrestling, rowing, baseball pitching, and the like in otherwise healthy young athletes. The cause is damage to the intima lining of a major vein or from compression of the vessel causing activation of the coagulation cascade. Patients with idiopathic UEDVT have no obvious underlying cause; however, about one-fourth of these patients have occult cancer.
The ultrasound image on the left shows a small clot formed within the mid portion of the right subclavian vein. The waveform (right image) confirms the clot only partially obstructs the lumen. Central intravenous lines, pacemakers, port-a-cath devices and the like are responsible for the rise in UEDVT.
The upper portion of the cephalic vein (left) is clear of clot and compresses well (right image). Large clots that include large portions of the upper extremity are problematic and may require a subclavian venous filter.
These two ultrasound images through the right cephalic vein mid humerus show no compression of the vein (right). This indicates that a clot is present in the vein, which partially obstructs flow. Though not common, there is a rise in the incidence of upper extremity deep vein thrombosis.
Deep vein thrombus as a primary cause of pulmonary embolus is the leading cause of PE. Compression ultrasound is the primary method used to diagnose DVT/VTE. The importance of ultrasound imaging is that pulmonary emboli are caused by a thrombus that breaks away from a vessel wall and travels to the lungs via the bloodstream. Ultrasound imaging is able to detect a thrombus, which guides the physician in choosing a treatment regime that not only dissolves clots, but to prevent future clots from reaching the lungs.
Treatment of DVT and Pulmonary Embolus
Deep vein thrombosis and pulmonary embolism (PE) are two pinnacles of a single disease process. The disease is a major heath care concern in the United States having annual incidence of 250,000 to 20,000,000 cases, making it the third leading cause of cardiovascular death. The core treatment for acute DVT and PE is systemic anticoagulation with intravenous heparin. Ongoing therapeutic treatment for prevention of DVT often includes oral warfarin (Coumadin). This treatment alone has been shown to reduce the risk of fatal PE by 75%. The recurrence risk for PE and DVT without anticoagulation therapy is 25 and 47 percent, respectively. However, anticoagulation therapy reduces the risk of recurrent PE and DVT to 2 percent. Other treatments include thrombolysis and IVC filter placement to prevent migratory emboli from reaching the pulmonary circulation.
During the acute stage of pulmonary embolus thrombolysis may be helpful for some types of clots. Thrombolysis is a procedure in which a thrombus is destroyed by applying a solution directly to the clot to dissolve it. This procedure involves directly applying a clot-dissolving agent through a catheter into the clot. Urokinase, which is a naturally occurring enzyme that dissolves blood clots, was once the most commonly used dissolving agent; however it was removed from the marketplace in 1988. In the years that followed most clots were dissolved using mechanical devices to physically break the clot; however, this carries the risk of vascular puncture, heart puncture, arrhythmias and other potentially adverse outcomes. When necessary, a clot can be reduced using direct catheter insertion to apply an anticlotting agent. The most commonly used clot-busting agent is tissue plasminogen activator (t-PA). Generally, thrombolytics are not given if the person has bleeding problems, bleeding ulcers, recent surgery, trauma, recent head injury, or uncontrolled high blood pressure.
Several arrays of catheters are commercially available for thrombolysis of various pathological presentations. For example, different catheters are selected depending on whether the clot is short and focal or occludes a long segment of a vessel. During the procedure a guide wire is positioned through the soft clot. Then a catheter having side holes is advanced over the guide wire deep into the clot. A slow infusion of the clot-dissolving agent is administered over hours or days. During the procedure heparin, which is also an anticlotting agent may be used to prevent clot formation in the catheter.
For those who do not need thrombolysis anticoagulation is the preferred method of dissolving clots. Several types of blood thinners (anticoagulants) are available such as warfan (Coumadin), Hirudin, Danaparoid and Fondaparinux (Arixtra), heparin, and others. These all function is various capacities to inhibit substances that help in the formation of clots. Heparin is the most commonly used anticoagulant in a hospital setting for acutely diagnosed VTE or PE. However, for ongoing anticoagulation therapy following hospitalization Coumadin is most prescribed. Anticoagulation therapy may not be enough to prevent recurrent PE in some patients. Recent studies show that nearly 33% of PE victims develop a second PE while receiving adequate anticoagulation therapy. Another concern is that some patients are unable to receive anticoagulants because they are at high-risk for hemorrhage, stroke, bleeding diathesis, falls, or pregnancy. Also, Coumadin crosses the placenta and may have a profound adverse effect on a developing fetus. About 1-3% of patients who get heparin acquire an immune-mediated heparin-induced thrombocytopenia (HIT). Thrombocytes are blood cells that produce platelets needed for normal clotting. For those who anticoagulation strategy fails or is not an option, strategies for interrupting the flow of blood clots through the inferior vena cava (IVC) to the lungs has been devised.
When anticoagulation therapy fails or is not an option, other alternatives such as ligation of the IVC, caval plication, and caval clips have been used. In 1967 the Food and Drug Administration (FDA) approved a revolutionary filter for use in the IVC called the Mobin-Uddin umbrella. Today, the standard treatment for recurring clots in some patients is to use a filter to partially interrupt the IVC, effectively �catching� emboli before they reach the pulmonary arteries. There are some contraindications for placing an IVC filter such as acute multiple traumatic injuries, hemorrhagic stroke, major surgery, internal bleeding, or bleeding diathesis such as hemophilia. Because these are metal filter and are permanent in most cases, those to undergo magnetic resonance procedure may not be a candidate.
Some indications for placing an IVC filter include: prior to orthopedic surgery in a patient with DVT, chronic pulmonary hypertension/low cardiopulmonary reserve, severe pelvic fractures, severe head injury and lower extremity fractures, spinal cord injury (with or without paralysis), to name a few. Likewise, a filter may not be placed if thrombus lies between the venous access site and filter deployment site. Also, a non-ferromagnetic filter should not be place in a patient who may need to undergo magnetic resonance imaging. There are many types of FDA and European filters available. Some of them by name are: stainless steel Greenfield filter (SGF), (Kimray-Greenfield filter), titanium Greenfield filter (TGF), Vena Tech-LGM filter, Vena Tech LP filter, Simon nitinol filter, Bird’s nest filter (BNF), TrapEase filter, G2 Recovery Filter, Gunther Tulip filter, OptEase filter, and Celest Filter. Titanium filters allow the patient to remain a candidate for magnetic resonance imaging because they are nonferromagnetic. With all filter placements the patient is carefully assessed for type of filter to be deployed, and filter placement is weighed against other types of test that may need to be performed for contraindications.
Inferior vena cava filters are most often placed in the angiographic suite by an interventional radiologist. The technologist�s role is to prepare and manage the sterile environment and instruments and operate fluoroscopy. The radiologist, based on patient presentation and manufacturers� recommendations decides the IVC filter type and approach. This is to insure the filter is placed in the correct orientation and the approach does not dislodge a thrombus into the circulation. The general approach is percutaneous puncture of the right jugular or femoral vein. The femoral route to the IVC is more common because the catheter does not need to be manipulated through the heart as with the right jugular vein approach. Most filters are placed infrarenal (below the lowest renal vein) at minimal distance from the distal most renal vein. Suprarenal placement is also an option especially when a clot in the IVC extends above the renal veins, or when there is renal or ovarian vein thrombosis, or pregnancy. It may be necessary to place the filter in the superior vena cava due to upper extremity thrombus; however, this is a rare occurrence.
The Seldinger technique is used to puncture the skin and access the inferior vena cava. The Seldinger technique uses an entry needle to puncture the IVC. Then a guide wire is passed into the lumen of the needle to the desired location in the IVC. A catheter is passed over the guide wire to a position below the renal veins. Once the catheter is in place an IVC angiogram is performed to check for clots in the IVC, determine placement below the IVC, and to check for anatomical variations such as a duplicated vena cava. The size of the IVC is also approximated because a filter may not be placed in a vessel greater than 28 mm. This is because the function of a caval filter may be compromised if the caval diameter exceeds 28 mm. IVC filters are available in sizes ranging from 29-40 mm. Intravenous contrast media is administered to perform the IVC angiogram. The catheter is then removed and a catheter loaded with the filter is passed over the guide wire. Once in place the filter is released and the guide wire and catheter are removed. Anchoring hooks in the filter anchor it to the vessel wall. The filter traps clots and its lytic system dissolves them while allowing partial blood flow through it.
These anteroposterior images are selections from an inferior venacavographic examination. The left and middle radiographs show a catheter in the inferior vena cava with entry from the right femoral vein. The femoral vein approach is preferred since a jugular approach requires manipulation of the filter through the heart. Filling of the IVC with iodinated contrast media permits its evaluation for thrombus. The diameter is also measured and a location for filter placement below the distal renal vein is selected. Inflow from the renal veins can be seen at the level of the L1 vertebral body (yellow arrow). When there is a clot between a femoral insertion point and the renal vein the right jugular vein approach is preferred to bypass it. The radiograph on the right shows catheter entry from the right jugular vein.
This radiograph shows the deployment of a Celect IVC filter. This conical type filter has a remarkable track record for catching emboli. The design of the filter made it possible for thrombi to fill and occlude 70% of the filter cone. If the cone is filled to 80% of total volume, the reduction of cross-sectional area is 64%. Greenfield type filters have been on the market longer than any other type of IVC filter.
Once the filter is placed in the IVC (left radiograph) contrast media is injected to check its placement, and verify flow through the filter (right radiograph). Making sure the filter is well anchored to the vessel wall is also verified on the post insertion radiographs.
There are few complications of filter placement, yet a major concern is that many of these filters are permanent or require complicated removal techniques. Complications include filter migration, post insertion thrombosis, infection, and occlusion of the IVC. Filters have migrated into the heart and lungs, therefore, the patient is observed for 2-3 days post filter insertion. A CT or ultrasound scan can be made to assess the penetration of the hooks into the wall in case of suspected migration. Extension of the filter struts beyond the vessel wall indicates perforation. The most serious complication associated with the IVC filter is caval occlusion. The design of the Greenfield filter, for example, when at 70% occlusion, reduces the cross-sectional area by 50%. At 80 % filling of the filter the cross-section of the IVC is reduced by 64%.
This patient with a known TrapEase type IVC filter presented with symptoms of IVC occlusion. The fluorospot radiograph on the left shows the filter in good placement within the IVC. A major concern was that the filter may have migrated slightly to obstruct the IVC. A venacavogram was performed (left radiograph), which demonstrates a large clot below the filter with minimal contrast flow through it.
This venacavogram radiograph shows a large clot in the filter (white arrow) and partial obstruction of the inferior vena cava (blue arrow). Because there is only a partial obstruction some blood flow is seen in the IVC above the filter (yellow arrow). Long term complications of IVC filters include migration, perforation, and most seriously obstruction of the filter or IVC.
This radiograph shows the insertion of a secondary filter (yellow arrow) above the clotted filter (blue arrow) to catch any new clots that may escape. There are few options in this scenario; however, insertion of a second filter has good prognosis.
Pulmonary embolus is a major health problem that is highly treatable when diagnosed, but carries high risk for morbidity and mortality is undiagnosed. Radiography is a major diagnostic tool in finding pulmonary embolus. There are several diagnostic studies like CT, nuclear V/Q scan and angiographic procedures that diagnose pulmonary embolus. The main cause of PE is venous thromboembolus that is diagnosed with ultrasound. Treatment for both PE and VTE can reduce the risk of recurring disease to below 2%, which is medically acceptable.
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