Welcome to the Hitachi Medical Systems America, Inc. MRI Anatomy and Positioning Series. We are offering teaching modules to allow users of Hitachi MRI scanners to review the anatomy and pathology they will be seeing on various MRI exams, as well as to advance their positioning skills. Proper positioning is one of the most important components that is required to ensure the best possible image quality for your MR studies.
In this fourth module, we will discuss MRA, or Magnetic Resonance Angiography. We will review the anatomy of the various areas of the body where MRA is used. We will discuss the additional imaging techniques used in conjunction with MRA, such as gating and post- processing. We will examine the most common contrast-enhanced and non-contrast examinations currently being performed on Hitachi MRI systems, including the sequences used as the basis for each exam, and related slice or slab positioning.
Within our modules, we will offer suggestions as to the RF coils to be used for various MRI exams. Regardless of the RF coil that is being used, every attempt should be made to route the coil cable(s) in a manner that will avoid contact with the patient.
We will also discuss uses for the various pads that are furnished with our MRI systems (trough pads, table pads, accessory pads, coil cable pads, etc.). It is important to use the pads that are provided to assist in eliminating, or at least minimizing, the amount of each patient’s skin-to-skin, skin-to-bore, or skin-to-cable contact. Reducing the amount of each of the aforementioned contacts reduces the patient’s chances of thermal injury. Please refer to the MR Patient Warming Prevention Plan published by Hitachi Medical Systems America, Inc. for more information concerning the prevention of patient warming.
Magnetic Resonance Angiography involves the use of magnetic resonance imaging to examine blood vessels in key areas of the body. This may include vessels in the brain, neck, heart, chest, abdomen, pelvis, as well as the upper and lower extremities. MRA can be performed with or without the use of intravenous contrast material to provide high-quality images of many blood vessels. We will be discussing and reviewing contrast-enhanced MRA methods, to include FLUTE (FLUoro Triggered Examination), TRAQ (Time Resolved AcQuisition), and timed CE-MRA (Contrast-Enhanced MRA). The non-contrast MRA methods we will investigate include TOF (Time Of Flight), VASC-ASL (Veins and Arteries Sans Contrast-Arterial Spin Labeling), and VASC-FSE (Veins and Arteries Sans Contrast- Fast Spin Echo).
CE-MRA, or Contrast-Enhanced MRA methods use a contrast agent to enhance the signal intensity of the blood flow. The Timed Bolus CE-MRA method involves the use of a test injection to determine a precise travel time for the bolus contrast injection. A mask scan with no contrast is performed first, which is a 3D RSSG sequence. A 2D RSSG sequence is then performed for the test injection. Through the use of the Stopwatch tool, a time can be selected when maximum contrast is seen in the target vessel. This time is considered the “travel time”- the amount of time it will take for the bolus of contrast to travel to the target vessel. Another 3D RSSG sequence is performed after the contrast injection. The mask sequence and the post-contrast sequence are then subtracted from each other, resulting in images of the contrast-filled target vessel.
FLUTE, or FLUoro Triggered Examination, is a contrast-enhanced MRA method that uses MR fluoro to observe the arrival of the contrast bolus. There is no need for a test injection with FLUTE. The mask, or pre-contrast scan, and the live, or post-contrast scan, have the same scan parameters. Both the mask and live scans are 3D RSSG sequences (RF Spoiled SARGE, which is a Steady state Acquisition with Rewound Gradient Echo). The fluoro scan, which is performed in between the mask and live scans, is a 2D RSSG sequence. Once the contrast is observed nearing the anatomy of interest on the fluoro scan, the 3D live scan is started. Use of the echo allocation TPEAKS (Triggered PEak Artery enhancing K-space filling Sequence)ensures consistent capture of the critical arterial phase.
TRAQ, or Time Resolved AcQuisition, is another contrast-enhanced MRA method that involves the use of multiple dynamic scans to capture not only the anatomy of the blood vessels, but also the dynamics of the blood flow. TRAQ does not involve precise timing for the injection of the contrast bolus. Once the contrast is injected, multiple 2D or 3D RSSG sequences are performed to acquire arterial, venous and equilibrium phases of blood flow. TRAQ also incorporates PAPE (PArtial Phase Encode), a segmented method of K-space filling that allows for a reduction in scan time.
TOF angiography is based on the phenomenon of flow-related enhancement of spins that are entering into an imaging slice. Gradient echo sequences with very short TR periods are used, as they saturate the signal from stationary tissue. The blood flowing into the slice group or slab has not been saturated, so its signal is stronger than that of the stationary tissues. TOF can be performed in 2D or 3D, and can be performed with multiple stacks or slabs. It can be combined with presaturation bands to suppress either arterial or venous flow. MIP (Maximum Intensity Projection) Post Processing is typically performed on the source images from a TOF sequence to enable the technologist to isolate the vessels from surrounding soft tissue, as well as to manipulate the vessels for better viewing (Circle of Willis and carotids).
VASC (Veins and Arteries Sans Contrast) is a non-contrast angiography method in which both veins and arteries can be visualized. VASC is commonly used for the renal arteries and the hepatic portal veins. The sequence used for VASC is a 3D BASG (Balanced Sarge) with fatsat, and the examination is performed using respiratory gating.
Variations on the VASC sequence include VASC-ASL and VASC-FSE. VASC-ASL (VASC Arterial Spin Labeling) uses an IR (Inversion Recovery) pulse with the 3D BASG sequence to view the flow of blood in the body. The IR pulse is spatially applied over an anatomic region, with the desired end result being bright signal in the selected target blood vessels. Imaging can be performed with or without the use of subtraction. When using the subtraction method, images are acquired with the selective IR pulse both off and ON. Arterial and venous blood both have bright signal when the IR pulse is off. When the IR pulse is turned ON, it is positioned to suppress the target vessels, so they will be dark on these images. Subtraction of these two sets of images yields high signal from the blood flow in the target vessels only. Imaging performed with the Selective IR pulse in the ON position only does not require subtraction. The IR pulse is applied to the anatomy that the target vessels will be flowing into. Fresh inflowing blood retains its high signal, while the signal from all other blood is suppressed.
VASC-FSE is a non-contrast angiography method that involves scanning the same region at diastole and systole, then subtracting the images to view only the arteries. Both arteries and veins have high signal intensity during diastole. During systole, fast-flowing arteries have low signal, while veins are emphasized and visualized. After the subtraction process, only the arteries remain, visualized with high signal. The VASC-FSE method incorporates a Phase Contrast (PC) scan to determine the Delay time and velocity of a target vessel. The main scan is a 3D primeFSE with ECG gating.
The benefits of MRA become very apparent when it is compared to other methods of angiography, namely CT angiography and catheter angiography. Magnetic resonance angiography can be performed with or without the use of IV contrast materials. This concept is quite beneficial to those patients with severe contrast allergies, as well as those with poor kidney function. When contrast is used, MRA contrast is based on gadolinium, rather than iodine, resulting in a decrease in allergic reactions. Smaller amounts of contrast can be used for MRA, based on the fact that MRI measures the effects of the contrast agent, rather than the concentration of the contrast agent itself. MRA is non-invasive, and does not use ionizing radiation. When comparing MRA to catheter angiography, MRA involves a much shorter procedure time, no recovery time, and usually a lower cost. In general, MRI is often considered to be superior to other imaging modalities due to its excellent differentiation of diseased tissue versus normal tissue.
The majority of the risks or limitations associated with MRA also apply to routine examinations that are performed in MRI. The inherent risks that are present in and around an MRI system require strict safety guidelines that must be followed for all MRI procedures. Limiting factors for both MRA and MRI are often more patient-related, rather than procedure-related. Can the patient fit into the MRI machine? Is the patient claustrophobic? Can the patient remain still during the examination? Can the patient participate in performing breath-holds, if required? Does the patient have any implanted medical devices or other issues that are contraindications for MRI? Does the patient have contrast allergies or kidney function issues? The use of contrast is preferred for some MRA procedures, as well as in specific instances in routine MRI procedures (history of cancer, post-op, etc.). With the improvements that have been made to non-contrast MRA methods, patients can now benefit from an MRA examination with good image quality and important angiographic information, without the risks that contrast injections posed in the past. Technological advances in both hardware and imaging techniques are allowing MRA to rapidly expand in the area of clinical applications. With higher field strength systems and optimized pulse sequences, one can acquire high quality images with excellent spatial resolution in shorter scan times, with lesser amounts of contrast, or no contrast at all.
The use of respiratory gating is often necessary, and sometimes required, when performing MRA examinations. VASC-ASL sequences are all performed with respiratory gating. The various MRA examinations that are performed in the abdomen necessitate some control over respiratory motion.
When respiratory gating is used, the patient’s expirations trigger the sequence acquisitions. The respiratory bellows must be positioned and secured on the patient before scanning begins. The respiratory waveform is monitored to acquire the average respiratory rate. The average number of respirations is then input in the Beat Rate field under the Gating section of parameters, or on the Gating tab. Numerous additional Gating parameters can be manipulated.
Respiratory gating equipment for the Oasis and Echelon systems consists of respiratory bellows, a respiratory belt, and a respiratory hose, as seen in Figure 1. Briefly observe the patient’s breathing to determine proper placement of the respiratory bellows and belt. The belt must be tight enough so the bellows can react to the patient’s breathing, but not too tight as to constrict the patient’s breathing. The respiratory hose is plugged into the monitoring module on the MRI system. The Waveform window should be open to monitor the respiratory waveform before scanning begins (Figure 2). This is done to ensure proper placement of the respiratory gating equipment on the patient, as well as to ensure proper working order of the equipment, resulting in a strong, steady signal.
Respiratory gating equipment for the Echelon OVAL system consists of respiratory bellows, respiratory sensor tubing, and a wPPU Wireless Module. A battery from the Wireless Module Battery Charger should be inserted into the back of the wPPU Wireless Module (Figure 3), and the battery and communication statuses confirmed on the front of the Module. The respiratory sensor tubing should be attached to the respiration connector of the wPPU Wireless Module (Figure 4). Briefly observe the patient’s breathing to determine proper placement of the respiratory bellows. A belly band can be used to hold the respiratory bellows in place. The band must be tight enough so the bellows can react to the patient’s breathing, but not too tight as to constrict the patient’s breathing (Figure 5). The respiration sensor tubing should lie along the body axis, and the wPPU Wireless Module should be placed in a secure position outside the FOV. The Waveform can be monitored on the WIT Monitor on the gantry (Figure 6), or on the Waveform window on the console before scanning begins (Figure 7). This is done to ensure proper placement of the respiratory gating equipment on the patient, as well as to ensure proper working order of the equipment, resulting in a strong, steady signal.
When imaging the abdominal organs, the use of breath-holds or respiratory gating is necessary, due to the constant motion of the abdomen from patient respirations. Faster imaging techniques typically allow for scan performance in a single breath-hold. Expiration is preferred, as the position of the organs (at least the kidneys) remains more constant on expiration, as compared to inspiration. On the Oasis, Echelon, and Echelon OVAL systems, breath-holds can be acquired by setting the Wait mode field to ON. This field is found under the Scan Control section of parameters. Breath-hold instructions can be given manually, by speaking to the patient over the microphone each time, or Auto Voice may be used. The Auto Voice Setting window can be found under the System Settings launcher button (Figure 8). Breathing instructions and timing settings can be selected and saved with specific names. Saved selections are displayed in a dropdown listing for the Auto Voice field, which is also found in the Scan Control section.
Certain post-processing tasks are incorporated with MRA scanning, and may be performed during or after the actual scan. The Oasis, Echelon, and Echelon OVAL systems can be set up to automatically perform subtracted images. This is often done with VASC-FSE sequences. The choice can be made as to whether or not the Selective IR pulse images are displayed (Org. Image), or if only subtracted images are displayed (Calc Image), as seen in Figure 9.
MIP post processing is performed on a variety of MRA images, whether they are scanned with or without contrast. Bright signal intensities are extracted from the source images (such as the vessels in MRA). The source data is compressed and displayed in the MIP viewports in the three orthogonal planes, and an output viewport (Figure 12). By tracing around the vessels in the viewport for each plane, excess tissue and extraneous vessels can be eliminated. Various MIP projections offering various results are available, including Radial, Expanding, Sliding, and Rotating (recommended for COW). The projection that is selected is typically based on the type of imaging that was performed. Additional “Setting Parameters” that correlate with the selected projection must be input (Figure 10). Setting parameter fields may include start and end angles and increments for radial projections; thickness, angle and intervals for sliding projections; thickness, angle, and increase for expanding projections; rotate, tilt, start angle and increment for rotating projections. Clipping or “cutting” selections must also be indicated, which can range from free hand drawing, to the creation of rectangles and ellipses (Figure 11). Once the MIP process is performed, the resultant post-processed images can be added to the patient’s folder, along with the other completed MRA images.
When dynamic CE-MRA examinations are performed, individual dynamic runs in the series can be selected for the MIP function. In the Acquisition area of the MIP parameters, the Acquisition No. (or dynamic run number) can be selected. The Acquisition Scope should be set to Current, as only the currently selected dynamic run is to be put through the MIP process (Figure 13).
With the advent of Nephrogenic Systemic Fibrosis (NSF), the field of MRI has been driven to explore the development of additional non-contrast and/or reduced contrast MRA examinations. The early observations of NSF were made after injections of Omniscan in 1997 in patients with severely impaired renal function. The incidences of NSF appeared to increase with a history of repeated contrast administrations, as well as with higher contrast doses. The FDA alert for all gadolinium-based contrast agents first went out in 2006. A determination could not be made as to whether the risk of NSF was higher with any specific contrast type. Prior to 2007, the literature does not record any NSF reports for patients with normal renal function, or mild to moderate renal insufficiency, after gadolinium-based contrast injections. Current recommendations state that patients in Stage 1 or 2 of chronic kidney disease should not receive Omniscan contrast for MRI exams. Glomerular Filtration Rate (GFR) for Stage 1 is greater than 90 ml/min, while Stage 2 is 60-89 ml/min. Patients in Stages 3-5, which are moderate, severe, and end-stage chronic kidney disease respectively, should have a risk/benefit assessment performed before contrast administration for an MRI. This would include informed consent from the patient, as well as radiologist-ordered contrast brand, dose, rate, and route of injection. Hemodialysis can be considered for patients in Stages 4 and 5 within 2 hours after a contrast injection, and again in 24 hours post-injection. MRI technologists should be sure to update their comprehensive screening forms to identify patients with renal disease. The results of any lab tests required by the radiologist prior to contrast injections should be included on these screening forms.
The circle of Willis (COW) is an anastomotic system of arteries that sits at the base of the brain. It was named after Thomas Willis, the author of a book entitled Cerebri Anatome, which depicted and described this vascular ring. The circle of Willis provides important communications between the blood supply of the forebrain and hindbrain. A complete circle of Willis is present in most individuals; however, less than half of the population has well-developed communications between each of the parts of this circle.
This circle of communicating arteries begins with the internal carotid and vertebrobasilar arteries (Figure 14). From this circle, numerous arteries branch off and travel to all parts of the brain. If one of the main arteries is occluded, collateral circulation allows the distal smaller arteries to receive blood from other arteries involved in this circular configuration.
The anterior circulation of the circle of Willis is formed when the internal carotid arteries (ICA) divide into the anterior cerebral artery (ACA) and middle cerebral artery (MCA) bilaterally (Figure 15). The internal carotid arteries supply blood to the anterior three-fifths of the cerebrum, except for parts of the temporal and occipital lobes. Any decrease in blood flow through one of the internal carotid arteries brings about some impairment in the function of the frontal lobes. This impairment may result in numbness, weakness, or paralysis on the opposite side of the body from the obstructed artery.
The anterior cerebral arteries (ACA) extend upward and forward from the internal carotid arteries (Figure 16). They are united by an anterior communicating (ACOM) artery. The anterior cerebral arteries supply the frontal lobes, which are the parts of the brain that control logical thought, personality, and voluntary movement, especially movement of the legs. A stroke in the anterior cerebral artery results in weakness of the opposite leg.
The middle cerebral arteries (MCA) are the largest branches of the internal carotid arteries (Figure 19). They supply a portion of the frontal lobe, as well as the lateral surfaces of the temporal and parietal lobes, including the primary motor and sensory areas of the face, throat, hands and arms. Damage to the middle cerebral artery in the dominant hemisphere can affect the area of speech. The middle cerebrals are the arteries most often occluded in strokes. The lenticulostriate arteries, which are small, deep penetrating arteries, branch from the middle cerebral arteries.
The posterior circulation of the circle of Willis is formed by the left and right posterior cerebral arteries (PCA), as seen in Figure 20. The posterior cerebrals are branches of the basilar artery, which is formed from the union of the left and right vertebral arteries (Figure 18). Left and right posterior communicating arteries (PCOM) connect the posterior cerebrals to the internal carotid arteries to complete the circle of Willis.
The posterior cerebral arteries (PCA) typically stem from the singular basilar artery (Figure 17). The posterior cerebrals supply the temporal and occipital lobes of the left and right cerebral hemispheres. When infarction occurs in the region of the posterior cerebral arteries, it is usually secondary to embolism from lower segments of the vertebral basilar system or the heart. Occlusion of a posterior cerebral artery can cause varying clinical symptoms, depending on the location of the occlusion. Symptoms may include thalamic syndrome, contralateral hemiplegia, hemianopsia, color blindness, verbal dyslexia, and hallucinations. The most common finding is occipital lobe infarction, leading to an opposite visual field defect.
Asymmetry of the circle of Willis results in asymmetry of flow, which is an important factor in the development of intracranial aneurysms and ischemic stroke (Figure 21). Patients with aneurysms are more likely to have asymmetry or an anomaly of the circle of Willis. Patients with internal carotid artery occlusive disease, and a nonfunctional anterior collateral pathway in the circle of Willis, are associated with an increased incidence of ischemic stroke.
Occlusions of the penetrating artery branches that arise from the circle of Willis, the cerebellar arteries, the basilar artery, as well as the previously mentioned lenticulostriate arteries, are referred to as lacunar strokes (Figure 22). In these strokes, cells that are distal to the occlusion will die. If the occlusion occurs in a small area, only minor deficits may be seen. However, if the occlusion leads to an infarction (tissue death due to an inadequate blood supply) in a critical location, more severe manifestations may develop, such as paralysis and sensory loss. Within a few months of the occlusion, necrotic brain cells will be reabsorbed by macrophage activity, leaving a very small cavity that is referred to as a lacuna. While lacunar strokes account for only approximately 20 percent of all strokes, the use of MRI has increased the probability that these infarctions can be appreciated on imaging. The penetrating arteries where the occlusions associated with lacunar strokes occur typically branch from larger, high-pressure main arteries. Patients suffering from hypertension add a pounding pulse to these high pressure arteries, thereby increasing their chances of suffering from lacunar strokes.
A small clot, or occlusion, that causes a lacunar stroke may interfere with blood flow for only a few minutes. The clot may dissolve before it causes damage, and the patient’s symptoms may improve in a very brief time. If treatment is not necessary, and the patient has a full recovery in less than 24 hours, the episode is called a TIA, or transient ischemic attack.
The right and left common carotid arteries are the arteries that supply the neck and head with oxygenated blood. These two arteries have different sites of origin (Figure 23). The left common carotid originates from the arch of the aorta. The right common carotid originates from the brachiocephalic trunk, which is the largest branch of the arch of the aorta. (The brachiocephalic trunk is also referred to as the brachiocephalic artery, or the innominate artery). The right and left common carotid arteries both branch into external and internal carotid arteries on their respective sides of the neck.
The external carotid arteries ascend through the upper part of the side of the neck and behind the lower jaw, entering the parotid glands. Here they divide into various branches that nourish the face, scalp, skull, and meninges. The internal carotids, together with the vertebral arteries, are the primary arterial supplies for the brain (Figure 24). The internal carotids and vertebrals have additional characteristics in common: they all lie at some depth from the surface in their course to the brain, they all have curves or twists in their paths to the brain, and none of them have larger collateral branches. Our discussion will concentrate on the internal carotid arteries, as these vessels are usually of greater importance when performing MRA.
The right and left internal carotids arise from the common carotid arteries in the neck, and enter the head at the base of the skull via the carotid canal. The internal carotids terminate at their bifurcations into the anterior cerebral arteries and the middle cerebral arteries (Figure 25). These bifurcations are referred to as the “carotid T”, due to their shape, or as the “top-of-the-carotids”, due to their location. While discussing their anatomy, we will refer to the internal carotid arteries in singular form, as these vessels are usually similar on the right and left sides of the neck.
The internal carotid artery is further classified into seven segments with alphanumeric identifiers (C1 through C7, see Figure 26), or as four portions, with additional divisions. We will attempt to combine the classifications to gain a better understanding of the course and branches of this vessel. The literature is quite variable in terms of the definitions of the various segments and portions, as well as the origins of the arterial branches. This may be due to the high degree of variations found between individuals when examining this vessel. The internal carotid artery begins in the area called the cervical portion, also known as the C1 cervical segment (Figure 27). This portion begins at the carotid bifurcation (usually at the level of the third cervical vertebrae), and ends at the skull base. This is the only extracranial portion or segment, and it has no branches. It receives approximately eighty percent of the flow of the common carotid arteries. This portion has two further divisions, which are the carotid bulb and the ascending cervical segment. The carotid bulb, or carotid sinus, is a focal dilation of the internal carotid artery at its origin. It contains sensors that help regulate blood pressure. At this point of dilation, the internal carotid artery measures approximately 7.4 mm in diameter, while the common carotid artery measures only 7.0 mm. The ascending cervical segment of the internal carotid is distal to the carotid bulb, and measures approximately 4.7 mm in diameter. This lesser diameter is maintained through the remainder of the course of the internal carotid artery. The ascending cervical segment runs vertically upward in the carotid sheath, which is the dense, fibrous tissue that envelopes the carotid artery, the internal jugular vein, and the vagus nerve. This segment runs anterior to the transverse processes of the upper three cervical vertebrae, but behind and lateral to the external carotid. It is more superficial at its start, where it is bounded by muscles in the carotid triangle of the neck. As the internal carotid moves superiorly, it is separated to a greater degree from the external carotid, due to muscles, ligaments and nerves.
The second portion of the internal carotid artery is the petrous portion, which includes the C2 petrous segment, and the C3 lacerum segment (Figure 28). The petrous portion extends from the opening of the carotid canal in the base of the skull to the posterior edge of the foramen lacerum. The C2 petrous segment is located inside the petrous part of the temporal bone, and extends to the foramen lacerum. This segment is further divided into three sections. The ascending or vertical section is found where the internal carotid enters the petrous portion and ascends a short distance (this section is approximately 10mm in length). As the internal carotid curves anteriorly and medially it is referred to as the genu section, meaning there is a bend in the vessel of ninety degrees. The final section of the petrous segment is the horizontal section, which is approximately 20mm long, and courses anteromedially toward the petrous area. The petrous segment includes two named branches of the internal carotid artery, which are the vidian artery, and the caroticotympanic artery. The C3 lacerum segment is a very short segment that begins above the foramen lacerum and ends at the petrolingual ligament.
The cavernous portion is the third portion of the internal carotid artery, and is almost identical to the C4 cavernous segment (Figure 29). It averages 39mm in length. The artery is situated between layers of dura mater and is surrounded by the cavernous sinus. This is the only place in the human body where an artery moves entirely through a venous structure; here, the internal carotid artery is moving blood from the brain and face back to the heart to be oxygenated. In this S-shaped cavernous portion, the internal carotid artery winds anteriorly and superomedially. It ascends toward the posterior clinoid process, passing forward against the lateral surface of the body of the sphenoid bone in a groove called the carotid sulcus. The artery curves upward again on the medial side of the anterior clinoid process to perforate the dura mater that forms the roof of the sinus. Due to its S-shaped curve, as well as for more precise identification purposes, the cavernous portion is further divided into five sub segments- posterior vertical, posterior bend, horizontal, anterior bend, and anterior vertical. The curving area that begins at the posterior bend of the cavernous portion, and ends at the internal carotid bifurcation (in the supraclinoid portion) is referred to as the carotid siphon. This area has complex and variable anatomy, and is often a site for aneurysms. Arterial branches from the cavernous portion of the internal carotid artery include the meningohypophyseal artery and the inferolateral trunk.
The fourth and final portion of the internal carotid artery is the supraclinoid portion, which includes the C5 clinoid segment, the C6 ophthalmic segment, and the C7 communicating segment (Figure 30). This portion bends posteriorly and laterally between the oculomotor and optic nerves. The supraclinoid portion ends at the point where the internal carotid artery bifurcates into the anterior and middle cerebral arteries. The C5 clinoid segment is a short segment which begins after the internal carotid exits the cavernous sinus. It extends distally to the distal dural ring, after which it is considered to be intra-dural, as it has entered the subarachnoid space. It normally has no named branches. The C6 ophthalmic segment extends from the distal dural ring to the origin of the posterior communicating artery. This segment is fairly horizontal, running parallel to the optic nerve. The ophthalmic artery and the superior hypophyseal artery are the named branches typically found in this segment (Figure 31). The ophthalmic artery offers the potential for collateral flow in case of proximal occlusion of the carotid artery. The terminal segment of the internal carotid artery is the C7 communicating segment. This segment begins just proximal to the origin of the posterior communicating artery, which is the artery that connects the anterior circulation (carotid system) with the posterior circulation (vertebrobasilar system). The posterior communicating artery is also a common site for aneurysms (Figure 32). The last named branch that originates from the internal carotid is the anterior choroidal artery (Figure 33). The internal carotid then divides to form its terminal branches, which are the anterior and middle cerebral arteries. These arteries form a part of the cerebral arterial circle known as the Circle of Willis, which is an important collateral pathway for blood flow to the internal carotid artery.
The internal carotid arteries supply the oxygen-rich blood to the brain. Restriction or occlusion of this blood flow can result in a stroke or “brain attack”. Carotid artery disease causes more than half of the strokes that occur in the United States. The carotid arteries may be severely narrowed or blocked before they cause signs or symptoms, so a TIA (transient ischemic attack) or stroke may be the first sign that someone has carotid artery disease. Under age 75, men are at a higher risk of developing carotid artery disease than women. Over age 75, women are at greater risk than men. Anyone with coronary artery disease is at an increased risk for carotid artery disease as well.
This disease seems to start when damage occurs to the inner layers of the carotid arteries. Factors that contribute to this damage include smoking, high levels of certain fats and cholesterol in the blood, high blood pressure, or high levels of sugar in the blood due to insulin resistance or diabetes. The body’s response is to start a “healing process”, which may cause a buildup of plaque in the area where the artery has been damaged (Figure 34). Plaque is a waxy material that is created from an accumulation of fatty substances and cholesterol deposits on the artery walls, resulting in a condition called atherosclerosis. Over time, this plaque can harden and cause narrowing of the arteries, which is called carotid artery stenosis. This narrowing of the arteries leads to a decrease in blood flow to the brain, which then increases the risk of stroke (Figure 35). Plaque in an artery can also crack or rupture. The body perceives this as an injury, and tries to heal it by sending blood cell fragments called platelets to the injury site. The platelets may clump together and form blood clots, which can partially or completely block a carotid artery. In addition, a blood clot or a piece of plaque can break away from the wall of the carotid artery and travel through the bloodstream. If the clot or plaque becomes lodged in one of the brain’s smaller arteries, blood flow can be blocked, resulting in a stroke.
Any form of carotid artery disease that results in low or no blood flow to the brain increases one’s risk of suffering from a TIA or stroke. Although their symptoms may be similar, the treatments and outcomes from TIA’s and strokes are quite different. Both require emergency medical intervention, as no one can predict if or when a TIA might progress into a major stroke. Signs and symptoms of a TIA or stroke include vision difficulties, sudden dizziness or confusion, difficulty swallowing, sudden severe headache, memory problems, difficulty speaking (aphasia), loss of balance or coordination, and weakness, tingling, or numbness on one side of the face, in one arm or leg, or on one side of the body.
TIA’s are referred to as “mini-strokes”, occurring when there is low blood flow, or a clot briefly blocking an artery that supplies blood to the brain. The major difference between TIA’s and strokes is that TIA symptoms typically resolve within 24 hours, sometimes disappearing within minutes or a few hours. However, estimates are that one-third of those people that have a TIA will have a stroke at some point, usually within a year of their TIA occurrence.
Strokes that result from carotid artery disease are typically of the ischemic type, meaning that a blood clot blocks the normal blood flow. Ischemic strokes can be caused by a clot that forms in an artery that is already very narrow, as from plaque buildup (thrombotic stroke), or by a clot that breaks off in another part of the body and moves to this area (embolic stroke). The best chance for full recovery occurs if treatment to dissolve or break up the clot is given within three to six hours of the onset of symptoms. Thrombolytic, or “clot-busting” drugs are not given in cases of hemorrhagic stroke, or when patients have additional medical issues that involve bleeding problems. If the patient does not or cannot receive thrombolytic therapy, more permanent disabilities may result, such as the inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or an inability to see one side of the visual field.
Since there may be no signs or symptoms of carotid artery disease before a TIA or stroke, it is important that those persons with risk factors for this condition maintain regular visits with their family doctors. By listening to the carotid arteries with a stethoscope, a doctor may be able to diagnose a bruit, which is an audible vascular sound associated with turbulent blood flow. This sound may be indicative of atherosclerotic stenosis in the carotid artery. A variety of imaging examinations can be used to diagnose the presence of carotid artery disease (Figure 36). Carotid ultrasound can be used to view the structure of the arteries, while Doppler ultrasound will show how the blood moves through the carotid arteries. Magnetic Resonance Angiography (MRA) can be used (with or without contrast) to view disease in the arteries, as well as to detect stroke damage in the brain. Computerized Tomography Angiography (CTA) produces cross-sectional images of the carotid arteries (and brain) but does involve radiation. Carotid angiography is a more invasive procedure, but it allows the radiologist a “real-time” view of the blood flow through the carotid arteries.
Treatment of carotid artery disease can begin with lifestyle changes and medications. Lifestyle changes include maintaining a healthy weight, exercising, cessation of smoking, a diet low in saturated fats, trans fats, cholesterol, and salt, and control of hypertension and diabetes. Medications may be necessary to reduce high blood pressure and cholesterol. Some patients require antiplatelet medications that reduce the chances of blood clot formation, thereby reducing the risk of stroke. For patients with severe narrowing or blockage of the carotid artery, invasive medical procedures may need to be performed. Carotid endarterectomy may be performed in cases where artery blockage is fifty percent or greater. This procedure involves the surgical removal of both plaque and the diseased portion of the carotid artery (Figure 37). Carotid angioplasty uses a balloon catheter to push plaque outward against the wall of the artery. A stent, which is a small mesh tube, is then placed in the artery to support the artery wall, thus preventing the artery from narrowing or becoming blocked again (Figure 38). The goal of both procedures is to increase blood flow to the brain and reduce the risk of future strokes (Figure 39).
An understanding of pulmonary circulation, especially the pulmonary arteries and veins, is important for contrast-enhanced MRI examinations. Proper timing of image acquisitions depends on awareness of how the pulmonary circulation functions, as well as the patient-related factors that can influence the cardiovascular circulation time. The technologist’s knowledge of the vessels that are to be imaged with contrast enhancement, and the location of these vessels relative to the pulmonary arteries and veins can greatly impact the success of the patient’s MRI examination.
The path that contrast takes in the blood vessels to the anatomical area that is to be imaged begins with a peripheral venous injection, typically in the antecubital fossa. It is recommended that the right arm be used for this injection, as it offers the most direct venous path to the pulmonary circulation. Use of the left arm means that the contrast must cross the brachiocephalic vein in order to reach the superior vena cava, which empties blood into the heart. This could cause a delay and a dilution of the contrast bolus in older patients if they have atherosclerotic, ectatic aortas that press against the sternum and pinch the left brachiocephalic vein. It is especially important to use the right arm for injections when performing imaging of the aortic arch, so as to avoid overlapping enhancement in the brachiocephalic vein.
From the site of the injection, the contrast travels in the venous system to the superior vena cava, then into the right atrium and right ventricle of the heart (Figure 40). The deoxygenated blood (and contrast), is then pumped out of the right ventricle into the pulmonary trunk. The pulmonary trunk divides into the right and left pulmonary arteries, which take the deoxygenated blood to the lungs. Re-oxygenated blood from the lungs is returned to the left atrium via the pulmonary veins. The re-oxygenated blood (and contrast) is pumped out of the left ventricle into the aorta. The blood flows into the ascending aorta, through the aortic arch (with its branches to the head and neck), into the descending thoracic aorta, and finally to the abdominal aorta. There are numerous arterial branches from each of these regions of the aorta that help to deliver the arterial blood (and contrast) to the head and body.
The pulmonary circulation runs contrary to the theory that arteries always carry oxygen-rich blood, and veins always carry de-oxygenated blood. It is more accurate to categorize arteries as the vessels that carry blood away from the heart, and veins as the vessels that carry blood back towards the heart.
The circulatory system forms a large closed loop. The heart pumps oxygenated blood to the arteries, which divide into smaller vessels, called arterioles, as they travel away from the heart. The arterioles divide further into tiny, thin-walled vessels called capillaries (Figure 41). The exchange of nutrients and gases occurs across the thin capillary walls. As the blood travels through the complex network of capillaries throughout the body, it releases oxygen to the tissues. The blood becomes progressively deoxygenated, although it is picking up carbon dioxide (Figure 42). In most cases, blood flows through only one capillary, then enters a systemic venule. Venules carry the deoxygenated blood away from the tissues and merge to form larger systemic veins. The systemic veins return the deoxygenated blood to the right side of the heart, which pumps it to the lungs through the pulmonary arteries. The blood is re-oxygenated in the lungs and returns to the left side of the heart through the pulmonary veins. After passing through the left atrium and ventricle, the oxygenated blood enters the aorta and begins its journey again.
The four-chambered design of the heart is important for keeping the blood moving in the proper direction (Figure 43). The deoxygenated blood is pumped through the right side of the heart, while the re-oxygenated blood is pumped through the left. Although the pulmonary arteries and veins that transport blood to and from your lungs are continuous with the remainder of the circulatory system, they are classified as part of the pulmonary circuit. The pulmonary circuit includes the heart, the pulmonary arteries, the lungs, and the pulmonary veins. The systemic circuit is that portion of the circulatory system that serves the remainder of the body.
The right and left pulmonary arteries are the terminal branches of the pulmonary trunk, which arises from the right ventricle of the heart. When the right ventricle contracts, the blood that is inside it is put under pressure. The tricuspid valve between the right atrium and ventricle closes, leaving the pulmonary trunk as the blood’s only exit route. The pulmonary valve (between the right ventricle and the pulmonary trunk) opens, allowing the de-oxygenated blood in the right ventricle to flow into the pulmonary trunk. The pulmonary trunk extends upward, then divides into the right and left pulmonary arteries, which convey the deoxygenated blood to the lungs. When this blood reaches the pulmonary capillaries, it unloads carbon dioxide, which is exhaled, and picks up inhaled oxygen. The freshly oxygenated blood returns to the heart via the pulmonary veins (Figure 44).
The two pulmonary arteries differ in length and anatomy. The right pulmonary artery is the longer of the two, as it must pass transversely across the midline in the upper chest. It passes below the aortic arch and enters the hilum of the right lung as part of its root. The left pulmonary artery is shorter, and pierces the pericardium to enter the hilum of the left lung.
A condition that may affect the pulmonary arteries is pulmonary artery stenosis. This is a narrowing of the artery which can occur in the pulmonary trunk, as well as in the right and/or left branches. This narrowing makes it difficult for the blood to reach the lungs for re-oxygenation, which can affect the heart, as well as the rest of the body. In order to overcome the narrowing and slowdown of blood flow, the pressure in the right ventricle may increase, eventually rising to levels that can be damaging to the heart muscle. Pulmonary artery stenosis is considered a congenital heart defect, not a disease. It is often found in combination with other congenital heart defects, such as Tetralogy of Fallot, pulmonary atresia, pulmonary valve stenosis, etc. Pulmonary artery stenosis can also be caused by other syndromes that affect the heart, or it can be the result of surgical procedures that have been used to correct other heart defects. Depending on the severity of the narrowing, this defect may be found in children when they are quite young, or it may not be discovered until adulthood. If the narrowing of the artery is more than fifty percent, children may experience symptoms such as shortness of breath, fatigue, heavy or rapid breathing, rapid heart rate, swelling in the feet, ankles, face, etc. This condition may be diagnosed during a routine examination by a doctor, based on abnormal heart sounds. A variety of additional tests, including imaging tests, may be ordered to verify a diagnosis of pulmonary artery stenosis. This testing should include an EKG, which would show abnormal heart rhythms and heart muscle stress. An echocardiogram uses sound waves to create a moving picture of the heart’s internal structures. It is often combined with a Doppler ultrasound, which measures blood flow across the heart’s valves and vessels. Cardiac MRI can offer great detail about blood flow through the heart and vessels (Figure 47). Cardiac CT, used with IV contrast, can visualize cardiac anatomy and the great vessels. Pulmonary angiography also uses IV contrast to visualize the pulmonary arteries and veins. Treatment of pulmonary artery stenosis varies with the amount of narrowing that has occurred. Mild to moderate narrowing in one or more branches may not require any treatment. More severe cases may require some form of therapy or surgery. Balloon dilation treatment involves the use of a balloon dilation catheter that is placed in the narrowed area and inflated under increasing amounts of pressure until the narrowed area is widened (Figure 45). In approximately fifteen to twenty percent of cases, the artery narrows again over time, and the procedure must be repeated. Another type of balloon dilation has been developed with a “Cutting Balloon” (Figure 46). This balloon has small blades running up and down its length. When the balloon is inflated, the blades are activated, and they cut through the narrowed area. The cutting action makes the vessel easier to dilate, resulting in a larger opening. Researchers have also developed a stainless steel balloon-expandable stent, which may improve on the results from standard balloon dilation treatment. The stent is mounted on a balloon angioplasty catheter and covered with a sheath as it is moved into position. The sheath is then withdrawn from the stent-balloon assembly, and the balloon is inflated to its recommended pressure. The balloon inflation expands the stent and anchors it in place. Surgical repair of pulmonary artery stenosis may be required for more severe cases. The method used depends on the characteristics of the stenosis, as well as the surrounding vessels and structures (Figures 48, 49).
Pulmonary hypertension is another condition that affects the pulmonary arteries. This condition involves increased pressure in the pulmonary arteries as they transport the blood from the heart to the lungs for re-oxygenation. Pulmonary hypertension may develop if the arterial walls tighten, if the arterial walls are stiff at birth or become stiff from an overgrowth of cells, or if blood clots form in the arteries. The cells lining the pulmonary arteries become changed and inflamed, making it hard for the heart to push the blood through the pulmonary arteries to the lungs. Pressure in the pulmonary arteries rises. The heart is forced to work harder than normal, which results in straining and weakness of the right ventricle (Figure 50). The heart can become so weak that it can no longer pump enough blood to the lungs, resulting in heart failure, which is the most common cause of death for people suffering from pulmonary hypertension. Symptoms of pulmonary hypertension include shortness of breath during routine activities, tiredness, chest pain, and a racing heartbeat. As the condition worsens, its symptoms may limit all physical activity. Pulmonary hypertension most commonly occurs along with another disease or condition, and usually develops between the ages of 20 and 60. Those considered to be at risk for pulmonary hypertension include those with a family history of this condition, those with heart, lung, or liver disease, those with HIV infection, those with blood clots in the pulmonary arteries, those who use street drugs or certain diet medicines, and those who live at high altitudes.
Pulmonary hypertension is divided into five groups, based on the cause of this condition. In all of these groups, pulmonary arterial pressure is higher than 25 mmHg (millimeters of mercury) at rest or 30 mmHg during physical activity. Normal pulmonary arterial pressure is 8-20 mmHg at rest. Only group 1 is called pulmonary arterial hypertension (PAH), while groups 2-5 are called pulmonary hypertension, or secondary pulmonary hypertension. Group 1 pulmonary arterial hypertension includes those with this condition with no known cause, also referred to as primary or idiopathic pulmonary arterial hypertension. Group 1 also includes those that have inherited this condition, those that have this condition due to other problems that affect the veins and small blood vessels of the lungs, those that have this condition due to drugs, toxins, or certain diet medicines, or those that have this condition due to other diseases (connective tissue diseases, HIV infection, liver disease, congenital heart disease, sickle cell). In many parts of the world, group 1 PAH is caused by schistosomiasis, which is an infection caused by a parasite. Pulmonary arterial hypertension that occurs with a known cause is often referred to as “associated” PAH. Treatments for group 1 include medicines that may be taken orally, inhaled, or injected. The main objectives of the medicines are to relax the blood vessels in the lungs, and to reduce excess cell growth in the blood vessels. As the blood vessels relax, more blood can flow through them. To determine which medicines work best, patients may undergo an acute vasoreactivity test, which is performed during right heart catheterization. The test shows how the pressure in the pulmonary arteries reacts to certain medicines.
Group 2 pulmonary hypertension includes those with left heart disease. Conditions that affect the left side of the heart, such as mitral valve disease or long-term high blood pressure, can cause left heart disease, which is likely the most common cause of pulmonary hypertension. Treating the underlying conditions will help treat group 2 pulmonary hypertension. Treatments may include medicines, surgery, and/or lifestyle changes.
Group 3 pulmonary hypertension is associated with lung diseases, such as COPD (chronic obstructive pulmonary disease) and interstitial lung diseases. The latter can cause scarring of the lung tissue. This group also includes pulmonary hypertension associated with sleep-related disorders, such as sleep apnea. Treatment for this group may include oxygen therapy to raise the level of oxygen in the blood. Additional treatments may be necessary if the patient has an underlying lung disease.
Those with blood clots in the lungs or blood clotting disorders make up group 4. Treatment may include blood-thinning medicines, which prevent clots from forming or increasing in size. Surgery may be necessary to remove scarring in the pulmonary arteries from old blood clots.
Group 5 involves pulmonary hypertension that is caused by a variety of other diseases or conditions. Examples of these include blood disorders (polycythemia vera, thrombocythemia), systemic disorders (sarcoidosis, vasculitis), metabolic disorders (thyroid disease, glycogen storage disease), as well as other conditions, such as kidney disease, or tumors that press on the pulmonary arteries. Treatment for group 5 pulmonary hypertension involves treating its cause.
There are additional medications and treatments that may benefit those in groups 2-5 of pulmonary hypertension. Diuretics may be used to help reduce fluid buildup in the body, especially swelling in the ankles and feet. Blood-thinning medicines help prevent blood clots from forming, or from getting larger. Digoxin may be prescribed to help the heart beat stronger and pump more blood. This medication is also used to control the heart rate if abnormal heart rhythms, such as atrial fibrillation, occur. Oxygen therapy can be used to raise the level of oxygen in the blood. Regular physical activity may be recommended to decrease future chances of limitations on activity due to this disease.
The basic function of the pulmonary veins is similar to other veins in the body- to transport blood back to the heart. However, as part of the pulmonary circulation, pulmonary veins carry oxygenated blood, while the veins of the systemic circulation are carrying deoxygenated blood. The pulmonary veins arise in the lungs from a network of capillaries that are different from capillaries elsewhere in the body (Figure 51). Pulmonary capillaries surround and embrace millions of alveoli, which are the tiny air sacs in the lungs. Oxygen in the air that is inhaled into the lungs is drawn from the alveoli by the pulmonary capillaries (Figure 52). As these capillaries leave the alveoli and travel toward the heart, they unite to form progressively larger venules and veins, gathering in the fissures that divide the lungs into segments or lobes. Eventually, all of the veins within one lung segment unite to form a single or segmental vein. These segmental veins typically travel alongside the bronchus that serves the same lung segment. Just prior to exiting the lungs, the segmental veins from each lung join to form the superior and inferior pulmonary veins. The pulmonary veins enter the heart through the posterior aspect of the left atrium.
There are three lobes (upper, middle, and lower) in the right lung, but only two lobes (superior and inferior) in the left lung, as the left lung must allow room for the heart. Generally, the vein from the middle lobe of the right lung unites with the vein from the right upper lobe, so each lung sends two pulmonary veins back to the heart, one superior vein and one inferior vein. Occasionally, the three veins on the right side remain separate, and frequently the two left pulmonary veins end by a common opening into the left atrium. Consequently, in the healthy population, the number of pulmonary veins opening into the left atrium can vary between three and five (Figure 53). At the root of the lung, the superior pulmonary vein lies in front of and slightly inferior to the pulmonary artery. The inferior pulmonary vein lies at the lowest part of the hilus of the lung, and on a plane posterior to the superior pulmonary vein. As the veins travel towards the left atrium of the heart, the right pulmonary veins pass posterior to the right atrium and the superior vena cava. The left pulmonary veins pass anterior to the descending aorta. The right and left superior and inferior pulmonary veins open separately into the superior and posterior aspects of the left atrium (Figure 54).Similar to the pulmonary arteries, the pulmonary veins can be affected by stenosis. This is a rare and serious condition in which there is a blockage in these blood vessels that are bringing the oxygen-rich blood from the lungs back to the heart. The blockage is typically an abnormal thickening and narrowing of the venous walls (Figure 55). This condition may be isolated to one vein, but often affects multiple veins (typically, there are a total of four pulmonary veins). Pulmonary vein stenosis is a progressive condition, and may lead to total obstruction of the blood vessel(s). The most common occurrence is that all of the pulmonary veins of one lung are affected, leading to pulmonary hypertension and pulmonary arterial hypertension. Surgery and catheterization to widen the narrowed veins are usually short-term solutions, as the obstruction typically recurs (Figure 56).
The pulmonary veins play a major role in treatment for atrial fibrillation. When this condition exists, the heart’s electrical rate and rhythm are not being controlled. The atria experience a fast, chaotic rhythm, and cannot contract or squeeze blood effectively into the ventricles. The goal of treatment for “atrial fib” is to slow the heart rate, return the heart rhythm to normal, and reduce the risk of blood clots and stroke. For those patients with severe symptoms, prior treatments, or medical conditions that may affect the risk of treatment, pulmonary vein ablation may be the treatment answer. Research has shown that atrial fibrillation usually begins in the pulmonary veins or at their attachment to the left atrium. There are typically four major pulmonary veins, and they may all be involved in triggering atrial fibrillation. In the ablation procedure, a catheter is guided into the atrium, and energy is delivered through the catheter tip into the targeted tissue (Figure 57). The energy is applied around the connections of the pulmonary veins to the left atrium. Other areas that may be involved in triggering or maintaining the atrial fibrillation will also be targeted. Small circular scars form in these targeted areas, preventing the abnormal signals that cause atrial fibrillation from reaching the rest of the atrium. It may take two to three months for these scars to form, but the scars will then block any impulses that are firing from within the pulmonary veins. These errant impulses are electrically disconnected or isolated from the heart. This is the basis for another name for the pulmonary vein ablation procedure, which is pulmonary vein antrum isolation, or PVAI. The success rate of a single ablation procedure is highly dependent on the type of atrial fibrillation that the patient has, the amount of time that the patient has had this condition, as well as the effects of any additional heart disease. Secondary ablation procedures are not uncommon, with the ultimate goal of eliminating the need for patient medication for the atrial fibrillation condition (Figure 58).
As the oxygenated blood flows from the left ventricle into the aorta, the systemic circulation begins. The aorta is the main delivery system of oxygenated blood. When tracking a contrast bolus in contrast-enhanced MR imaging, it is important to understand the anatomy of the aortic arch and its branches in order to achieve correct timing for the image acquisition (Figure 59). The ascending aorta is the first portion of the aorta, originating at the orifice of the aortic valve, which separates the aorta from the left ventricle of the heart. The ascending aorta has some twists with the pulmonary trunk, as the aorta starts out posterior to the pulmonary trunk, then twists to its right and anterior side. The ascending aorta transitions to the aortic arch, which loops over the right pulmonary artery and posterior to the bifurcation of the pulmonary trunk. The aortic arch has three major branches, which include (from right to left) the brachiocephalic trunk, the left common carotid artery, and the left subclavian artery. The brachiocephalic artery branches into the right subclavian artery and the right common carotid artery. The left common carotid artery and left subclavian artery both normally branch directly from the aortic arch. This difference is important to note when performing contrast-enhanced imaging of the carotid arteries. Technologists must be aware of any aortic abnormalities, as they can affect the flow and timing of contrast injections during examinations (Figures 60, 61).
The abdominal arteries and veins that are most frequently examined using various sequences in MRI include the superior mesenteric artery, the renal arteries, the inferior vena cava, the hepatic portal vein, and the hepatic veins. We will review the anatomy and interrelationships of these vessels, the various diseases that affect them, the use of MRI and other imaging modalities in disease diagnosis, as well as recommended treatments.
The superior mesenteric artery (SMA) arises from the anterior surface of the aorta, just inferior to the origin of the celiac trunk (which gives off the common hepatic, splenic and left gastric arteries). It is typically located anterior to the lower border of the first lumbar vertebra in an adult, and approximately one cm. inferior to the celiac trunk. The superior mesenteric artery initially travels in an anterior/inferior direction, passing behind/under the splenic vein and the neck of the pancreas, where it begins giving off its branches (Figure 63). It supplies the intestine from the duodenum and pancreas to the left colic flexure. Branches of the superior mesenteric artery include the inferior pancreaticoduodenal artery, the middle colic artery (which supplies the superior ascending colon and a portion of the transverse colon), the right colic artery (which supplies the middle of the ascending colon), the ileocolic artery (which supplies the last portion of the ileum, the cecum, and the appendix), as well as various branches to the jejunum and ileum. The middle, right and ileocolic branches anastomose with each other to form a “marginal” artery along the inner border of the colon (Figure 62). This marginal artery is completed by branches of the left colic artery, which is a branch of the inferior mesenteric artery.
The superior mesenteric artery is largely spared from the effects of atherosclerosis, at least when compared to other vessels of similar size. This may be due to some protective hemodynamic conditions. The SMA does play a large part in other “syndromes” that can have devastating effects on the left renal vein and the intestines.
The superior mesenteric artery plays a part in nutcracker phenomenon, which can lead to nutcracker syndrome, or renal vein entrapment syndrome. This phenomenon most commonly results from compression of the left renal vein between the abdominal aorta and the superior mesenteric artery (Figure64). The venous compression causes impaired blood outflow into the inferior vena cava, often accompanied by dilatation of the hilum of the renal vein. The name was derived from the imaginative thought that the aorta and SMA, in the sagittal and/or transverse plane, look like the legs of a nutcracker that is crushing a nut, which is the left renal vein. Diagnostic criteria for this phenomenon/syndrome are not well defined, and there appears to be a wide range of clinical presentations. Normal anatomical variations that could present with symptoms similar to the nutcracker phenomenon must also be ruled out. Symptoms may include hematuria, abdominal or flank pain, fatigue, orthostatic proteinuria, varicocele formation, nausea and vomiting, etc. A number of imaging modalities have been used to aid in the diagnosis of this condition, including CT venography, MR angiography, and Doppler ultrasonography (Figure 65). Treatment for nutcracker phenomenon/syndrome ranges from observation to nephrectomy, depending on the severity of symptoms. The patient’s age and “stage” of the syndrome are additional concerns. Interventions should only be considered when symptoms are severe or persistent. Most interventions aim to decrease left renal vein hypertension. Surgical approaches have included superior mesenteric artery transposition, left renal vein bypass, renal-to-IVC shunt, intravascular stenting, and even nephrectomy.
Superior mesenteric artery syndrome (or Wilkie’s syndrome) is an uncommon, but well recognized clinical situation characterized by compression of the transverse portion of the duodenum between the superior mesenteric artery anteriorly and the aorta posteriorly. This results in chronic, intermittent or acute complete or partial duodenal obstruction. This syndrome is usually associated with conditions that cause significant weight loss, such as anorexia nervosa, malabsorption, or hypercatabolic states, such as burns, major surgery, severe injuries, or malignancies. SMA syndrome can also be precipitated by conditions such as increased spinal lordosis, a short ligament of Treitz, or an unusually low origin of the SMA. Under normal conditions, fat and lymphatic tissues around the SMA provide protection to the duodenum against compression. Under conditions of severe weight loss, the cushion around the SMA is diminished, causing angulation and reduction in the distance between the aorta and the superior mesenteric artery. The normal aortomesenteric distance and aortomesenteric angle are 10 to 20 mm and 38 to 56 degrees, respectively. In SMA syndrome, these values are reduced to ranges of 2 to 8 mm and 6 to 25 degrees (Figures 66, 67). The reduced aortomesenteric distance and angle can lead to entrapment and compression of the third part of the duodenum as it passes between the superior mesenteric artery and the aorta. Patients affected by this syndrome typically present with a bloating sensation, epigastric pain, nausea and vomiting. They tend to find relief from these symptoms when they lay prone, in the left lateral decubitus position, or in a knee-to-chest position.
Contrast-enhanced CT or MRA enable visualization of vascular compression of the duodenum, and allow for precise measurement of the aortomesenteric distance (Figure 68). Both procedures are noninvasive, and roughly equivalent to the reported “reference standard” of angiography for establishing a diagnosis of SMA syndrome. Abdominal ultrasound with Doppler can also provide aortomesenteric angle and distance readings. Treatment of this syndrome involves correcting the electrolyte imbalance, decompressing the obstruction (usually via a nasogastric tube), and offering nutritional support. Symptoms should improve once the patient begins to gain weight. If that is not the case, surgical mobilization of the duodenum can be performed, which moves the duodenum to the right of the SMA so it does not lie in the acute angle between the SMA and the aorta.
A rare but potentially life-threatening disease is mesenteric artery ischemia. Causes of this disease include acute thrombotic and acute embolic mesenteric artery ischemia, visceral venous thrombosis, chronic mesenteric ischemia, and nonocclusive mesenteric ischemia. Mesenteric emboli account for 50 percent of all cases of mesenteric ischemia, but usually cause less ischemic disease and have better survival rates, as they typically lodge in the SMA, distal to the origin of the middle colic artery. Thrombosis typically occurs at the origin of the artery, where an occlusion affects more structures. Regardless of the cause, the disease results in a decreased blood supply to the small and/or large bowel, resulting in ischemia, bowel infarction, necrosis, sepsis, and ultimately death. Risk factors for this disease include atherosclerosis, arrhythmias, hypovolemia, congestive heart failure, recent myocardial infarction (MI), valvular disease, advanced age, and intra-abdominal malignancy. Mesenteric artery stenosis is found in approximately 17 percent of independent elderly adults, leaving them open to the development of chronic mesenteric ischemia.
The consequences of vascular occlusion and ischemia depend on the vessels involved. The celiac axis, the superior mesenteric artery and the inferior mesenteric artery supply the foregut, midgut and hindgut, respectively. A patient with chronic mesenteric ischemia with an embolism to a branch of the SMA may experience minimal symptoms due to adequate collateral flow. A patient with an acute thrombosis may lose perfusion from the origin of the SMA, resulting in a greater amount of dead bowel. Mucosal villi become necrotic within four hours after ischemia begins. Full-thickness infarction can be observed as early as 6 hours. Fortunately, the mesenteric system offers multiple areas with the potential for collateral flow, so at least two of the three vessels mentioned above must be occluded to produce chronic ischemia.
The renal arteries carry the blood supply to the kidneys. The kidneys remove waste substances from the blood, and aid in fluid conservation and in stabilization of the chemical composition of the blood. The renal arteries enter the kidneys through an opening at the inner concavity of each kidney called the hilum. They typically divide into two large branches, with each branch continuing to divide into smaller arteries that take blood to the nephrons, the functioning units of the kidney. Blood that has been processed by the nephrons then moves to the renal veins, which carry it back to the inferior vena cava and ultimately to the right side of the heart. The renal arteries deliver about 1.2 liters of blood per minute to the kidneys, which is approximately one-quarter of the heart’s output. Therefore, once every four to five minutes, the kidneys process a volume of blood equal to the total amount found in the adult body. The renal arteries also contain self-regulatory mechanisms that allow for some adaptation to stress. Sensory receptors in the renal artery walls are affected by increases and decreases in total body blood pressure. These receptors cause the renal arteries to expand or contract to maintain a constant volume of blood flow.
The renal arteries arise from the sides of the aorta, just below the anterior origin of the superior mesenteric artery (Figure 69). The right renal artery is typically longer than the left, coursing behind the inferior vena cava to reach the right kidney. The left renal artery may lie superior to the right artery, and is crossed by the inferior mesenteric vein. Renal artery variations, including their number, source, and course are very common (Figures 70, 71). References state that irregularities are found in approximately 35 percent of cases studied, with the most common being the presence of an additional vessel (28 percent). Supernumerary vessels are more frequent on the left side as opposed to the right, and may total as high as six end arteries supplying one kidney.
Many renal artery diseases may have their beginnings with a blockage or obstruction of the renal artery. A blockage in the artery leads to a decrease in blood flow to the kidney (Figure 72). Because the kidney is good at sensing any blood pressure changes, it reacts as if the body’s overall blood pressure is low, rather than simply responding to the low pressure in the affected kidney. To combat low blood volume (or low sodium), the kidney releases a protein (enzyme) called renin, which raises the pressure outside the kidney. Renin can cause constriction (spasm) of smaller vessels, and cause the body to retain sodium that is normally lost through excretion of urine. These events cause the blood pressure to rise, resulting in a condition called renovascular hypertension. As these blockages worsen, the kidney may have difficulty in clearing the body’s waste products, and kidney failure can occur. Common conditions that can cause renal artery blockages include atherosclerosis, fibromuscular dysplasia, and renal artery aneurysms. Atherosclerosis occurs due to cholesterol and plaque build-up in the renal arteries, similar to what occurs in the coronary and carotid arteries (Figure 73). This is the most common cause of renovascular hypertension (95 percent). Men are affected twice as often as women, with the most common age for diagnosis being 55 years. Fibromuscular dysplasia (FMD) is an abnormal tissue build-up on the interior of the renal artery, which causes a “string of beads” appearance (Figure 74). FMD typically affects women under the age of 45, and is the cause of approximately 5 percent of renovascular hypertension. A rather uncommon cause of renovascular hypertension would be a renal artery aneurysm (Figure 75). This is an abnormal bulging of a part of the renal artery, which can then twist or compress a nearby renal artery, causing it to become narrowed. Renal artery aneurysms rarely rupture.
Signs and symptoms of renovascular hypertension are often minimal or non-existent. The most common symptoms, if any occur, are lethargy and extreme fatigue. Hypertension that does not respond to medication, especially in women under the age of 45, may be another sign. Renovascular hypertension should be considered in patients whose kidney functions for clearing the body’s waste products are decreasing, especially for those patients already on anti-hypertensive medications. Those with severe renovascular hypertension may report unusual nose bleeds, ringing in the ears, and headaches involving the back of the head. If left untreated, this disease may lead to serious cardiovascular and kidney problems, including stroke, cardiac hypertrophy leading to cardiac failure, worsening of arteriosclerosis throughout the body, or renal failure that requires dialysis.
Renovascular disease can be diagnosed using various imaging modalities, including ultrasound, CT, MRA, and conventional arteriography. The goal of treatment of renovascular hypertension is to restore normal blood flow to the kidney. Dilation of renal arteries can be accomplished through balloon angioplasty. In cases where arteriosclerosis is causing the blockage, a stent may be required to keep the vessel open (Figure 76). Treatment of fibromuscular dysplasia rarely requires the use of stents. Surgical interventions include endarterectomy to remove the material that is obstructing an artery in cases of arteriosclerosis. A blocked artery can be “bypassed” using an artificial graft or a vein from the patient’s leg (Figure 77). Aneurysm treatment involves the removal of the aneurysmal vessel and repair of the affected artery (Figure 78). In rare cases, the artery cannot be repaired and the kidney must be removed. Beneficial treatment outcomes that either cure the problem or result in marked improvement in the control of hypertension range from 60 to 95 percent. Results are dependent on the type of obstructing disease, the age of the patient, and the type of treatment that is undertaken.
Renal artery stenosis is another condition that can cause generalized hypertension as well as long term detrimental effects on the kidneys. This condition involves a narrowing of the renal arteries, most commonly caused by atherosclerosis, the same build-up of cholesterol plaques that can cause coronary heart disease and stroke (Figure 80). Due to their involvement in the renin-angiotensin-aldosterone hormone system, the kidneys play a large role in the regulation of blood volume and blood pressure throughout the body. Stenosis of a renal artery causes a decrease in blood flow to a kidney. Specialized kidney cells may incorrectly interpret this low blood flow as a low blood pressure situation that is affecting the entire body. The kidneys then release hormones that increase blood pressure as well as the amount of fluid within the blood vessels, resulting in hypertension. Patient risk factors for renal artery stenosis include smoking, diabetes, and hypertension. Additional causes of renal artery stenosis include fibromuscular dysplasia (an abnormal thickening of the muscles of the arterial wall), inflammation of the artery, aneurysm of the artery, or compression of the artery by an outside mass (Figure 79). Hypertension resulting from renal artery stenosis may present with minimal or no symptoms. Renal artery stenosis should be considered in patients with presentation of initial hypertension under age 30 or over age 50. The long term effects of decreased blood flow to the kidneys can result in an overall decrease in kidney function (azotemia), which carries its own symptoms. These may include fatigue, malaise, and slight confusion due to a gradual buildup of waste products in the body. On physical examination, a physician may hear a bruit, which is a “rustling sound in the artery, similar to rapids in a river. This sound can be attributed to the turbulence of blood flowing through a narrowed artery.
The diagnosis of renal artery stenosis can be accomplished using a variety of imaging modalities. Ultrasound, arteriography, CTA and MRA can all be performed, but the risks and benefits of each test must be considered on an individual basis (Figures 81-84). The patient’s kidney function must be evaluated, especially if the imaging procedure involves the use of intravenous contrast. MRA offers the highest accuracy rates in middle aged and elderly individuals, due to its excellent demonstration of proximal vessels. Ninety percent of renal artery stenosis is caused by atherosclerotic stenosis, which usually affects the proximal vessels in the aforementioned age groups. Treatment of renal artery stenosis ranges from the administration of medication to invasive surgery. If the stenosis causes less than a 50 percent narrowing of the artery, and kidney function is maintained, medications that block the actions of angiotensin may be used. (Angiotensin is a hormone that causes vasoconstriction and a subsequent increase in blood pressure). Balloon angioplasty can be used to compress cholesterol plaques into the artery walls, if they are the cause of the stenosis. A stent can then be placed in the affected area to maintain the unrestricted artery. If angioplasty fails or is not feasible, bypass surgery can be performed. A piece of normal vein, or a synthetic tube, can be used to connect the aorta and kidney, bypassing the stenotic renal artery. The return of blood flow to the kidney does not guarantee the return of kidney function if the renal artery stenosis is longstanding, and kidney function has been compromised for a prolonged period of time. By minimizing the risk factors of stenosis, patients can decrease the likelihood that this condition will start or reoccur. The patient should control hypertension, cholesterol levels, lipid levels, diabetes, and they cannot smoke. The more severe the stenosis is at the time of diagnosis, the higher the chances are of restenosis or complete occlusion of the renal artery in the future.
The inferior vena cava (IVC) is the largest vein in the body, and one of the great vessels of the body. It is a large, valveless, venous trunk that ascends through the abdomen in the retroperitoneum, to the right of the aorta, draining into the heart at the lower right posterior area of the right atrium (Figures 85, 86). Its function is to carry deoxygenated blood back to the heart from smaller veins in the lower half of the body.
The inferior vena cava is formed by the union of the right and left common iliac veins, which are the two major veins from the legs. This occurs at approximately the L5 level. Unlike the superior vena cava, the inferior vena cava has numerous tributaries between its point of origin and its terminus at the heart (Figure 87). The abdominal wall tributaries include the inferior phrenic vein (T8 level) and four lumbar veins (L1-L5 levels). The lateral visceral tributaries include the right suprarenal vein (L1 level), the right testicular or ovarian vein (L2 level), and the renal veins (L1 level). The anterior visceral tributaries are the hepatic veins (T8 level). The inferior vena cava is not centrally located, so there are some asymmetries in its tributary drainage patterns. The right suprarenal and testicular/ovarian veins drain into the IVC, but the left suprarenal and testicular/ovarian veins drain into the left renal vein, which in turn drains into the IVC.
Conditions that might affect the inferior vena cava include trauma, congenital heart defects, cancer, occlusion, abdominal aortic aneurysm, and transposition of the great vessels (Figures 88-90). Afflictions attributed to the inferior vena cava are often the result of compression of this vessel. Sources of external pressure can include an enlarged aorta (abdominal aortic aneurysm), gravid uterus (aortocaval compression syndrome), and various abdominal malignancies (colorectal cancer, ovarian cancer). Rupture of the IVC is rare, as this vessel has a low intraluminal pressure. Occlusion of the inferior vena cava is also rare, but is considered a life-threatening emergency. Occlusion can be associated with deep vein thrombosis (DVT), IVC filters, liver transplantation, or instrumentation (i.e. a catheter in the femoral vein). Dilation of the IVC can be an indication of right-sided heart failure. Clinical presentation may include dyspnea, leg edema, and, in acute cases, pulsatile flow in the hepatic veins.
Inferior vena caval thrombosis (IVCT) is a condition that may be accompanied by a wide range of signs and symptoms (Figure 91). Patients may be asymptomatic, or they may present only after complications have arisen. Their symptoms may be thrombotic or embolic in nature. Pulmonary embolism may be the first sign of IVCT. Thrombotic findings depend on the degree of occlusion of the vena cava, as well as the location, between the iliac confluence and the right atrium. Classic presentation of inferior vena caval thrombosis includes bilateral lower extremity edema with dilated, visible superficial abdominal veins. If the thrombus is confined to the vena cava, and does not involve the iliac or femoral system, the collateral pathways form along the posterior abdominal wall. Occlusive thrombus of the IVC at the juxtarenal level can affect renal function by altering renal perfusion. Even with adequate collaterals, it is hypothesized that blood return with an absent inferior vena cava is inadequate. This condition can result in chronic venous hypertension in the lower extremities, and can cause venous stasis that precipitates thrombosis.
Inferior vena cava syndrome (IVCS) results from obstruction of the inferior vena cava. The obstruction can be caused by invasion, compression due to a pathological process, or by thrombosis in the vein itself (IVCT) (Figure 92). IVCS can occur during pregnancy, especially in the later months. Pregnancy can be accompanied by problems with venous blood return due to high venous pressure in the lower limbs, the failure of blood to return all the way to the heart, decreased cardiac output due to obstructions in the inferior vena cava, a decrease in renal function, and sudden rises in venous pressure that can lead to placental separation. Symptoms of late pregnancy IVCS include intense pain in the right side, muscle twitching, fluid retention, and a drop in blood pressure. Pregnant women should be encouraged to lie on their left sides, especially during the third trimester, as lying supine in late pregnancy can cause compression of the inferior vena cava (Figure 93). IVCS may be difficult to diagnose clinically, due to its wide variety of signs and symptoms. Edema of the lower extremities may be present, due to an increase in the blood pressure in the veins in that area. Tachycardia (abnormally fast resting heart rate) may occur due to decreased preload, meaning a decrease in venous blood pressure. The heart increases its frequency to compensate for lower blood pressure, but then pumps less efficiently. Additional symptoms include supine hypotensive syndrome, and signs of fetal hypoxia and distress in pregnant women caused by decreased perfusion of the uterus.
There are a variety of imaging modalities and interventions for the diagnosis and treatment of inferior vena caval thrombosis and/or inferior vena cava syndrome. The most reliable, non-invasive diagnostic methods include CT with contrast, MRI with contrast, and contrast venography, which is the criterion standard for diagnosis of DVT. Abdominal CT in blunt trauma patients is valuable for the diagnosis of serious cardiovascular situations. A flattened IVC at multiple levels is a strong indicator of hypovolemia or hypotension, and may signify impending cardiovascular collapse. A flat IVC coupled with a decreased caliber of the aorta, marked diffuse bowel distention, moderate to extensive hemoperitoneum, and hyperenhancement of the bowel wall, kidneys, and pancreas constitutes the “hypoperfusion complex” (Figures 94, 95). A quick diagnosis can be life-saving for these trauma patients.
MRI allows for multi-planar examinations, accurate estimation of the thrombus age, and is helpful in determining the proximal extent of thrombosis. Both contrast enhanced CT and contrast-enhanced MR can suffer from a partial volume averaging artifact and flow-related phenomenon that displays on images of the IVC as a pseudo filling defect (Figures 96, 97). This is commonly seen at the level of the renal veins in the portal venous phase, as enhanced blood in the renal veins flows parallel to the unenhanced venous return from the lower part of the body. This pseudo filling defect usually resolves on the delayed post-contrast image, which is more reliable for distinguishing true thrombus from pseudothrombus. Contrast venography, which involves x-rays of the veins with contrast injection, offers the advantages of limited false-positive studies, as well as access for therapy, thrombolytic agents, a caval interrupting device, or even pulmonary angiography. Disadvantages are that it is more invasive than other imaging modalities, more than one access site may be required to document the extent of a thrombus if the IVC is occluded by clot, and the possibility exists for a post-procedure DVT.
Medical and surgical options are available for treatment of IVCT. Thrombolytic agents can be used, but the merits of thrombolytic therapy must be weighed against the risks of hemorrhagic complications. Treatments that fall under the category of caval interruption include filters and ligation. Filters are relatively non-invasive and allow central flow. They appear as baskets that are made of numerous wires. When inserted into the IVC, these filters trap blood clots that can break loose from the veins in the legs or pelvis (Figure 98). They can prevent a large blood clot from reaching the lungs, which can be a life-threatening situation. IVC filters can be removed within several months of placement, which is possible for approximately 80 percent of patients that receive them (Figures 99, 100). Filters may be placed at several different anatomic levels, as indicated by the clinical situation. However, thrombosis may occur at the insertion site or at the site of the filter itself. Ligation involves a permanent, complete occlusion of the IVC, so the proper level must be chosen. In addition, this method does not eliminate the risk of recurrent pulmonary embolism. Additional interventional procedures used to treat IVCT include balloon angioplasty and stent placement.
The hepatic portal vein drains deoxygenated, but nutrient rich blood from various organs to the liver. It is not a “true” vein, in that it does not return the deoxygenated blood to the heart. It drains blood from the abdominal part of the gastrointestinal tract, which includes the lower third of the esophagus, the stomach, all three parts of the small intestine, all parts of the large intestine, and the upper half of the anal canal. The hepatic portal vein also drains blood from the accessory organs of the digestive system, including the spleen, pancreas, and gall bladder (Figure 101). It is approximately three inches in length, and is formed by the union of the superior mesenteric vein and the splenic vein. Each of these major veins receives numerous tributaries from throughout the abdomen. One of the larger tributaries is the inferior mesenteric vein, which joins the splenic vein just before its unification with the superior mesenteric vein. The hepatic portal vein is joined by the hepatic artery and the common bile duct at the porta hepatis, where the vein and artery are bringing blood into the liver, and the bile duct is carrying bile out of the liver. Approximately 75 percent of the blood entering the liver is venous blood from the portal vein, with the remaining 25 percent being arterial blood from the hepatic artery. The hepatic portal vein and the hepatic artery have multiple branches in the liver (Figure 102). These vessels meet up again with the bile ducts to form triads at the corners of the liver lobules, which are the divisions of the liver tissue. Within the lobules are vascular channels called sinusoids that receive blood from both the portal vein and the hepatic artery (Figure 103). The sinusoids are lined with hepatocytes that process the blood (detoxify it, metabolize it, store iron and vitamins) then deliver the blood into central veins. The central veins coalesce into the three hepatic veins, which leave the superior aspect of the liver and empty into the inferior vena cava.
The hepatic portal vein has an influence in pharmacology in a process called “first pass metabolism”. Drugs that are orally administered become part of the stomach contents. The stomach contents diffuse into the blood to be carried to the heart, but they get to the heart by way of the liver and the hepatic portal vein. Subjecting a drug to the metabolic enzymes of the liver may alter it to a point where it is no longer active, before it even reaches the systemic circulation. This “first pass metabolism” can cause a decrease in the bioavailability of a drug if a portion of the drug is rendered inactive during liver metabolism. Exceptions to this situation are “prodrugs”, which take advantage of first pass metabolism by being converted into an active form while in the liver, rather than being inactivated.
A dangerous condition that affects the portal system is portal vein thrombosis (PVT). This refers to a complete or partial obstruction of blood flow in the portal vein due to the presence of a thrombus in the vessel lumen. This condition is responsible for 5 to 10 percent of overall cases of portal venous hypertension, and is a common complication of liver cirrhosis. Clinical presentations differ between acute and chronic portal vein thrombosis, and also depend on the development and extent of collateral circulation. Acute PVT may present as intestinal congestion and ischemia with abdominal pain, diarrhea, rectal bleeding, abdominal distention, vomiting, anorexia, fever, etc. Chronic PVT can be asymptomatic, or these patients may have splenomegaly and pancytopenia. Esophageal varices are found in the majority of patients with chronic PVT. Patients should be investigated for PVT if portal venous hypertension is present, especially in patients with cirrhosis of the liver. Early diagnosis and appropriate management of secondary portal venous hypertension could be life-saving.
If portal blood flow ceases due to a thrombus, the liver loses two thirds of its blood supply. The body has two compensatory mechanisms for this situation. The hepatic artery may dilate, which can preserve liver function in acute stages of PVT. The venous system’s rescue is to rapidly develop collateral veins to bypass the obstruction. This vascular neo-formation can begin in a few days after portal vein obstruction, and finalize within three to five weeks. The thrombosed portal vein is replaced by a network of collateral vessels called cavernoma, which connect the two patent portions that are proximal and distal to the thrombus (Figure 104). The original portal vein may become thin and fibrotic, and may be difficult to visualize. The development of cavernoma does affect the liver tissue, as it involves increased mitotic activity in the normally perfused liver lobe. This is an important observation if liver surgery is performed.
Factors that may lead to an increased chance of PVT include inflammatory processes in the abdomen- appendicitis, diverticulitis, inflammatory bowel disease, pancreatitis, cholecystitis, and cirrhosis. Malignancies that are hepatic or pancreatic in origin may account for 21 to 24 percent of the overall cases of portal vein thrombosis. A neoplastic PVT can develop from direct vascular invasion, compression by a tumor mass, or a hypercoagulable state. Thirty percent of liver transplant candidates are found to have PVT, as are 10 to 40 percent of those patients with hepatocellular cancer. Additional systemic risk factors include the presence of myeloproliferative diseases (excess cell production in bone marrow, as in chronic myelogenous leukemia) and prothrombotic conditions (tendency for occurrence of thrombosis). In cases of chronic portal vein hypertension, patients with cirrhosis of the liver have a risk of variceal bleeding that is 80-120 times higher than the risk in patients with no liver disease. In twenty to forty percent of cases of chronic PVT, the first presenting symptom is an episode of GI bleeding. More than eighty percent of those with chronic PVT have an extrahepatic biliary tree.
The diagnosis of portal vein thrombosis can be made from the presence of solid material within the vessel lumen. Suspicion of PVT should be high for patients with hypersplenism and portal hypertension. Imaging procedures may begin with ultrasound, with the inclusion of Doppler to confirm the absence of flow in all or part of the vessel lumen. Endoscopic ultrasound is recommended for PVT diagnosis, as it can find small and non-occluding thrombi. CT and MRI excel in determining the extension of a thrombus into the mesenteric circulation, as well as estimating the impairment of the bowel or adjacent organs (Figure 105). MRI may be able to confirm a vascular occlusion. In T1-weighted spin echo sequences, a clot will appear isointense, or hyperintense if more recent. Clots usually have more intense signal on T2-weighted spin echo images. CE-MRA is useful in assessing the patency and flow direction in the portal venous system, as well as in identifying cavernomatous transformation, determining the presence of varices, and in verifying the correct function of surgical shunts. MRA has high accuracy when used to follow the portal venous system both before and after liver transplantation surgery.
Prevention is the first aim of portal vein thrombosis management in patients with advanced liver disease. PVT that accompanies liver cirrhosis includes serious complications, as well as high morbidity and mortality. Portal flow velocity below 15 cm/s on Doppler ultrasound can be a significant predictor of PVT development. In patients with advanced liver disease, the risk of portal vein thrombosis is increased in males, those who have had previous surgery or interventional treatment for portal hypertension, previous variceal bleeding, low platelet count, or those with advanced liver failure. PVT can be an indication for a liver transplant, as well as for other surgical options. If more than half of the portal vein is obstructed, there are typically more peri-operative complications, a higher mortality rate, and a decrease in long-term survival. Surgical thrombectomy is not typically recommended, as it carries high morbidity and mortality rates. The treatment goal for both acute and chronic PVT is the same- correct the causal factors, prevent the extension of the thrombosis, and achieve portal vein patency. Anticoagulation therapy may be needed to obtain portal vein recanalization. Although acute portal vein thrombosis typically has a good prognosis, outcomes are highly dependent on the amount and type of underlying liver disease.
As mentioned above, portal vein thrombosis is one of the causes of portal hypertension. This condition involves elevated pressure within the portal system, including the portal vein, and the tributary veins that drain into it. Pressure within the portal system is not usually measured, and is not an issue until an illness or disease occurs that makes it difficult for the blood to flow through the liver tissue. The effect of having a “dam” in the portal system increases the pressure within the portal venous system, causing potential problems with liver function. Portal hypertension may be present with the onset of other symptoms that are associated with liver disease. The obstruction of blood flow through the liver can be intrahepatic, pre-hepatic, or post-hepatic. Intrahepatic causes include cirrhosis, hepatic fibrosis or scarring, and a wide variety of illnesses, such as alcohol abuse, fatty liver, hepatitis B and C, hemochromatosis, etc. Pre-hepatic causes might include portal vein thrombosis, or congenital portal vein atresia. Post-hepatic causes include a hepatic vein or inferior vena cava thrombosis, or a disease such as restrictive pericarditis, where the heart lining stiffens, and does not allow the heart to relax and expand fully when blood returns to it. This condition can be brought on by TB, fungal infections, tumors, or complications from radiation therapy.
If blood cannot easily get through the liver architecture, it attempts to bypass the portal system by using the systemic venous system to return to the heart. Symptoms of portal hypertension are a result of both the complications of decreased blood flow through the liver, and increased pressure within the veins where blood is shunted (Figure 106). Varices (enlarged veins) may occur when blood that was meant for the portal system is diverted to and gathers in other veins that are making their way to the heart. Varices typically occur in the esophagus, stomach, around the umbilicus, and in the anus or rectum (Figure 107). Esophageal and gastric varices can put patients at risk for life-threatening bleeding. Vomiting blood or blood in the stool are signs and symptoms of varices. Black, tarry stools indicate the possibility of upper GI bleeding. Ascites can be another symptom of portal hypertension. This abnormal fluid collection can occur when there is decreased protein in the body. Since the liver produces the body’s protein, and portal hypertension and underlying liver disease decrease the liver’s ability to function, decreased protein and ascites result. A buildup of waste products in the body can occur due to the liver’s inability to adequately filter the waste during portal hypertension, resulting in hepatic encephalopathy. Symptoms of this condition include confusion and lethargy. Splenomegaly can also be caused by portal hypertension. A back-up of blood traps the various blood components (red and white cells, and platelets) in the spleen, causing anemia and thrombocytopenia (low platelet count in the bloodstream). A decrease in white cell counts also increases the risk of general infection. Spontaneous bacterial peritonitis (an infection in the peritoneal sac) can be a consequence of long-standing portal hypertension.
Diagnosis of portal hypertension is often times not made until well after the process has begun, when complications begin to occur. Pressures within the portal vein are not usually measured, but diagnosis can be confirmed through blood test, x-ray, CT, MRI, or endoscopy. Treatment of portal hypertension is centered on preventing complications. Some underlying causes, such as alcohol abuse, can be limited by the patient. Over the counter medications that contain acetaminophen (Tylenol) should be avoided to decrease the risk of further liver damage. Dietary restrictions include the limitation of salt, to prevent further ascites fluid, and protein restriction. Protein overload can overwhelm the liver’s ability to synthesize it, and may lead to hepatic encephalopathy. Medications can be prescribed to decrease the pressure within the portal system. These may include nitroglycerin, and/or beta blockers. More invasive procedures include endoscopy, which is performed to band or tie off varices in the esophagus. This may prevent catastrophic and life-threatening bleeding. An interventional radiologist can perform a TIPS procedure- Transjugular Intrahepatic Portosystemic Shunt. This procedure involves the catheterization of a hepatic vein by the transjugular approach (through the jugular vein), followed by the puncturing of an intrahepatic portal vein, and the placement and expansion of a stent to connect the liver tissue at this juncture (Figures 108, 109). This type of connection of the portal vein with the hepatic vein decreases the pressure within the liver, and reduces the pressure within the veins of the stomach and esophagus (Figures 110, 111). The TIPS procedure would also decrease the risk of bleeding. Prevention of portal hypertension is possible when this condition occurs due to alcohol or drug abuse. Chronic alcoholism can lead to cirrhosis and portal hypertension. IV drug abuse can lead to hepatitis B or C, which can result in cirrhosis. Congenital anatomy issues or congenital metabolism errors are examples of instances where portal hypertension cannot be prevented. The worse the patient’s liver function is, the worse their prognosis will be. This dangerous condition can be controlled if patients are compliant with dietary restrictions, and they abstain from alcohol and drugs.
The hepatic veins transport the liver’s deoxygenated blood and blood which has been filtered by the liver (blood from the pancreas, colon, small intestine, and stomach) to the inferior vena cava. The hepatic veins originate in the central veins of the liver lobules, where they receive blood from branches of both the hepatic arteries and the hepatic portal vein (Figure 112). The hepatic vein branches terminate in three large veins, designated right, middle, and left. They transport blood to the inferior vena cava, which passes along a groove in the posterior aspect of the liver (Figure 113). The inferior vena cava then carries the blood to the right atrium of the heart. A unique characteristic of the hepatic veins is that, unlike most veins, they do not have valves.
Hepatic vein obstruction prevents blood from flowing out of the liver and back to the heart. The obstruction may be in the intrahepatic or extrahepatic vessels, but often occurs in both. Hepatic vein obstruction can result in congestion of the sinusoids in the liver, hepatomegaly, portal hypertension, reduced portal blood flow, ascites, and splenomegaly. The “clinical picture” caused by this obstruction is termed Budd-Chiari syndrome.
The primary cause (75 percent) of Budd-Chiari syndrome is thrombosis of the hepatic vein. Conditions that may make a thrombus more likely to form in the hepatic veins include myeloproliferative disorders (cause abnormal cell growth in bone marrow), cancers, chronic inflammatory or autoimmune diseases, hereditary or acquired clotting disorders, infections, oral contraceptives, and pregnancy. At least two of the three hepatic veins must be occluded for the syndrome to develop. The secondary cause (25 percent) of this syndrome is compression of the hepatic vein by an outside structure, such as a tumor. Signs and symptoms of this disorder can vary, depending on whether the obstruction occurs acutely or over time. Acute obstruction, which occurs in approximately 20 percent of cases, causes fatigue, right upper quadrant pain, nausea, vomiting, mild jaundice, tender hepatomegaly, and ascites. This typically occurs during pregnancy. Chronic obstruction, which occurs over weeks or months, may be asymptomatic until it progresses, or may cause fatigue, abdominal pain, and hepatomegaly as it develops. Lower extremity edema and ascites may result from hepatic venous obstruction. Cirrhosis may develop, leading to variceal bleeding, massive ascites, splenomegaly, and hepatopulmonary syndrome, or a combination of these symptoms. Budd-Chiari syndrome may lead to complete obstruction of the inferior vena cava, which causes edema of the abdominal wall and the legs, and visibly tortuous superficial veins from the pelvis to the costal margin.
Budd-Chiari syndrome should be suspected in patients presenting with hepatomegaly, ascites, liver failure, or cirrhosis with no obvious cause or explanation. Diagnosis should include clinical evaluation, liver function tests, and vascular imaging. Patient history should be reviewed for risk factors for thrombosis. Liver function tests are usually abnormal. Imaging may begin with abdominal Doppler ultrasonography, as it can show the direction of blood flow, as well as the site of obstruction. CT and MR are quite useful, often displaying large regenerative nodules in patients with Budd-Chiari syndrome. These nodules are benign hypervascular liver lesions, commonly seen when there are vascular disorders of the liver. They are typically bright on T1-weighted MR images, displaying marked enhancement after gadolinium contrast injection (Figure 114). They remain hyperintense during the post-contrast portal venous phase. The regenerative nodules are predominantly isointense or hypointense relative to the liver on T2-weighted images (Figure 115). Additional imaging features that may be seen in cases of Budd-Chiari syndrome include heterogeneous hepatic parenchyma with patchy enhancement, direct findings of hepatic venous occlusion, hypertrophy of the caudate lobe, and other hepatic morphologic changes. Intrahepatic collateral vessels are often seen in chronic Budd-Chiari syndrome patients. Extrahepatic findings may include ascites, splenomegaly and portosystemic collateral vessels (varices). These findings are typically due to portal hypertension, which can occur when the numerous, large regenerative nodules trap the portal triads (branches of hepatic artery, portal vein, and bile ducts in liver lobules). CT can demonstrate thrombosed hepatic veins, but they are usually more evident on MRI or ultrasonography. It is important for the radiologist to understand the imaging appearance of the regenerative nodules associated with Budd-Chiari syndrome in order to prevent their misdiagnosis as a different hypervascular mass. This could have an impact on therapies or surgeries recommended for the patient. If therapeutic or surgical interventions are planned, conventional angiography should be added, including venography with pressure measurements and arteriography. Liver biopsies are done occasionally to diagnose the acute stages of obstruction, and to determine if cirrhosis has developed.
Treatment of this syndrome varies according to its onset and severity. The main goals in management of this syndrome are to give supportive therapy directed at the possibility of complications, to decompress the congested liver (maintain venous outflow), and to prevent propagation of the clot. A minority of patients can be treated medically with sodium restriction, diuretics to control ascites, anticoagulants such as heparin and warfarin, and general symptomatic management. Aggressive interventions, such as thrombolysis and stenting, may be performed when the disease is acute (within 4 weeks of development) and there is no cirrhosis present. Thrombolysis can dissolve acute clots, which allows for recanalization, and relief of hepatic congestion. Radiologic procedures play a major role, offering angioplasty, stenting, and portosystemic shunts for treatment (Figure 116). In cases of hepatic stenosis, decompression with balloon angioplasty and intraluminal stents can maintain hepatic outflow (Figures 117, 118). If the hepatic outflow narrowing cannot be dilated, transjugular intrahepatic portosystemic shunting (TIPS) and various surgical shunts can provide decompression by diverting blood into the systemic circulation. This procedure can be successful in maintaining long-term patency and prevent or halt the progression of cirrhosis in patients with Budd-Chiari syndrome. These shunts are not used in cases of hepatic encephalopathy, as they worsen liver function. In addition, shunts tend to thrombose, especially when associated with hematologic disorders. Long-term anticoagulation is often necessary to prevent recurrence of hepatic vein obstruction. Liver transplantation may be necessary as liver failure can be life-threatening.
The hepatic veins can also be the site of hepatic veno-occlusive disease, or sinusoidal obstruction syndrome. This syndrome is usually caused by endothelial injury, leading to nonthrombotic occlusion of the terminal venules and hepatic sinusoids, instead of affecting the hepatic veins (as in Budd-Chiari syndrome). Venous congestion can cause portal hypertension and ischemic necrosis, which can lead to cirrhosis. Common causes of veno-occlusive disease include irradiation, graft-vs.-host disease (from bone marrow transplantation), alkaloids in certain herbs and plants, and other hepatotoxins. Initial signs and symptoms include sudden jaundice, ascites, and tender, smooth hepatomegaly. If this syndrome occurs after a bone marrow transplant, it is usually within the first three weeks after transplantation. Other patients have reported recurrent ascites, portal hypertension, splenomegaly, and eventually, cirrhosis. Diagnosis of this disease is made from clinical evaluation, liver function tests, and ultrasonography. Veno-occlusive disease should be suspected in patients with unexplained clinical or laboratory evidence of liver disease, particularly those with known risk factors, such as bone marrow transplantation. Laboratory results may be non-specific, but PT/INR usually becomes abnormal when this disease is severe. Ultrasonography may show retrograde flow in the portal vein. If the diagnosis is unclear, invasive tests may become necessary. This might involve a liver biopsy, or measurement of the portal-hepatic venous pressure gradient. To measure the pressure across the liver, a catheter is inserted percutaneously into a hepatic vein, then wedged into the liver. This “wedged” pressure reflects portal vein pressure, with a pressure gradient greater than 10mmHg suggestive of veno-occlusive disease. Treatment involves supportive care, treatment of specific causes, and the TIPS (Transjugular Intrahepatic Portosystemic Shunt) procedure to relieve portal hypertension in cases of progressive disease (Figure 119). Veno-occlusive disease is severe in approximately 25 percent of cases, and may require liver transplant as a last resort.
The acronym FLUTE stands for FLUoro Triggered Examination. FLUTE is a contrast-enhanced method that allows the technologist to monitor the dynamics of the contrast agent in “semi real-time” using MR fluoroscopy. The imaging acquisition can be triggered when there is peak arterial enhancement, allowing for the consistent capture of vessels in the critical arterial phase. Contrast-enhanced imaging can be greatly influenced by patient-specific circulatory properties, such as heart rate, heart volume, and the various disease processes that affect the patient’s circulation. The ability to view the contrast as it enters the anatomical region of interest minimizes any “guesswork” involved in contrast-enhanced imaging. Selection of the RF coil that is used for a FLUTE exam is determined by the anatomical region that is to be examined (Figures 120, 121).
MR fluoroscopy is a continuous and repetitive imaging mode with specific imaging parameters. The progression of normal imaging is pre-scan, scan, and reconstruction. With fluoroscopy, the scan and reconstruction processes overlap. (A pre-scan is performed once at the beginning of the sequence). Only specific sequences can be performed using fluoro. The scan interval should be set at the shortest time available, which will depend on the other scan parameters that have been selected.
Hitachi’s FLUTE sequences are typically set up as an Acquisition Plan which includes:
The initial setup of a FLUTE scan occurs in the Acquisiton Plan Properties area. The Group scan field is set to Dynamic, and the Repeat mode field is set to Yoyo. The two sequences are listed in the Acquisition Plan area as Pre/Post FLUTE first, with the Fluoro Scan listed below it. The Yoyo selection enables the examination to proceed by starting with the pre-contrast scan, moving down to the fluoro scan, then moving back up to the post-contrast scan, which follows the same movement pattern as a yoyo. Scanograms, a shim sequence, and additional routine sequences will be performed prior to the FLUTE sequences for optimal positioning of the vessels of interest. Once the FLUTE acquisition plan is selected, positioning of the slice slab must be performed for both the Pre/Post FLUTE sequence, as well as the Fluoro sequence. The Fluoro sequence should be the “selected” sequence when the FLUTE acquisition plan is started in order to display the two fluoro viewports (Figure 122). The fluoro viewport in the lower left of the screen displays the fluoro images, while the fluoro viewport in the middle displays the subtracted fluoro images (Figure 123).
The initial selection of the Start button begins the prescan for all of the FLUTE sequences. When the prescan is finished, the system will move on to the Pre FLUTE (mask) sequence. These images must reconstruct before scanning can resume, and should be reviewed for proper positioning and good image quality. At this point, selection of the Continue button initiates the Fluoro scan. Fluoroscopic views of the scan in progress will display in the fluoro viewports, as previously mentioned. The contrast injection is performed, and the fluoro viewports are monitored for signs of the approaching contrast. As the contrast nears the target vessels, the Next button is selected, which ends the Fluoro scan and initiates the Post FLUTE (live) sequence. The goal is to capture the vessels at the point of peak arterial filling. Post-processing typically involves the MIP (Maximum Intensity Projection) process.
FLUTE sequences are most commonly used for CE-MRA examinations of the carotid and renal arteries (Figures 124, 125). FLUTE is available on the Oasis, Echelon, and Echelon Oval MR systems. Refer to the “How-To” Manual available for each MR system listed above for step-by-step instructions for the performance of FLUTE examinations.
The acronym TRAQ stands for Time Resolved AcQuisition. TRAQ is a contrast-enhanced method that eliminates the need for precise timing and synchronization of the contrast injection with imaging of the vessels of interest. This method reduces the overall data acquisition time, and still acquires multiple dynamic runs that supply information about the anatomy of the blood vessels, as well as the dynamics of blood flow. Selection of the RF coil that is used for a TRAQ exam is determined by the anatomical region that is to be examined (Figures 126, 127).
The improved time resolution available with the TRAQ method occurs through the use of PAPE, which stands for PArtial Phase Encode. This method reduces the number of phase encoding steps by sharing portions of the image data that has been acquired. Phase encodes are part of the scan time formula, so if they decrease, overall scan time decreases as well. When PAPE is used, K-space is divided into an odd number of segments in the phase encoding direction (segment range is 3-9). This number is specified in the Segment field of the PAPE parameters (Figure 128). As the segment number increases, the scan time per cycle decreases. All of K-space is filled during the first scan, which becomes the mask image. The scan time for the mask image is displayed in the Scan Time field in the PAPE parameters. In the second run, the center of K-space and the top segment will receive new data that is to be measured, while the remaining segments will be filled with previously acquired data. In the third run, the center of K-space and the second segment from the top will receive new data, while the remaining segments are filled with previously acquired data. This method continues in this manner, filling the center portion of K-space and one segment above or below the center, dependent on the number of scans entered in the Scan Control parameter section. Each of these subsequent scans will take less time than the scan time for the first (or mask) scan, in which all segments of K-space were filled with new data, as only two segments of K-space are being filled with new data. PAPE parameters also include a Data Rate[%] field, which determines the percentage of the total amount of K-space that will be included in the central segment.
Scanograms, a shim sequence, and additional routine sequences will be performed prior to the TRAQ sequence for optimal positioning of the vessels of interest. The actual TRAQ sequence is a 3D RSSG sequence, with the imaging volume positioned based on previous scans. After the prescan is completed, the first “run” acquires the mask data. This will be the longest sequence, as it fills all the segments of K-space. When the mask scan is completed, the contrast should be injected. Multiple short consecutive acquisitions are then acquired, providing dynamic images of all phases of arterial and venous circulation. The mask series is subtracted from the live series to produce images with the vessels of interest enhanced with contrast. The subtraction process can be set up to perform automatically in the Scan Control area of the parameters. Post-processing typically involves the MIP process. Specific acquisition numbers can be selected for the MIP process, usually those where the arteries and veins display maximum filling.
TRAQ sequences are most commonly used for CE-MRA examinations of the chest, as well as the renal vessels (Figure 129). Due to the speed of the multiple dynamic acquisitions, the use of TRAQ for chest anatomy enables superb visualization of both the pulmonary arteries and pulmonary veins in the same sequence (Figure 130). TRAQ is available on the Oasis, Echelon, and Echelon Oval MR systems. Refer to the “How-To” Manual available for each MR system listed above for step-by-step instructions for the performance of TRAQ examinations.
The test injection method used for CE-MRA examinations involves the injection of a small amount of contrast (a test injection dose), and the calculation of the time it takes that contrast to reach the vessel of interest. This “travel time” calculation is added to the parameters of the main scan. When the bolus contrast injection is performed during the main scan, the travel time and an additional delay time calculated by the system enable the data acquisition to be performed at the time when the contrast arrival in the vessel and the filling of the central portion of K-space coincide. Selection of the RF coil that is used for a Test Injection exam is determined by the anatomical region that is to be examined (Figure 131).
Scanograms, a shim sequence, and additional routine sequences will be performed prior to the test injection sequence for optimal positioning of the vessels of interest. The test injection imaging procedure typically includes a 2D RSSG test injection sequence, and a 3D RSSG main dynamic scan. During the 2D RSSG test injection sequence, the Multi scan mode field in the Scan Control area is set to Fluoro (on Oasis, Echelon, and Echelon Oval systems). A small amount of gadolinium contrast is injected, followed by a saline flush (in the same amount as the test injection). Fluoro images are acquired and displayed in the lower left viewport. The sequence can be stopped after the contrast has passed through the vessels of interest. If the Sync StopWatch field is set to ON, the StopWatch begins to run when the Start button is selected, and a time stamp will appear on the fluoro images. Travel time can be determined from the time that is displayed on the fluoro image that best displays contrast in the vessel of interest (Figure 132). A more accurate determination of travel time can be achieved through the use of the Dynamic Analysis task on the Oasis, Echelon, and Echelon Oval systems. The images produced in the test injection sequence are loaded into a Dynamic Analysis task. An ROI is drawn in the vessel of interest, being careful not to touch the vessel walls. The “Apply to Same Slice Position” button is selected, and the Start button is selected. The results showing the time at which the ROI intensity is greatest can be interpreted from the graph or from the Dynamic Analysis Table (Figure 133). Using the Dynamic Analysis Table, the highest number in the ROI (ratio) column represents the area of greatest intensity, and can be matched with the number from the Acquisition Time column, which is the travel time. This value is then input in the Travel Time field in the Scan Control parameter area (on Oasis, Echelon, and Echelon Oval systems) for the contrast enhanced sequence.
The contrast enhanced sequence is a 3D RSSG sequence. It is typically set up to run the precontrast scan, which is the mask, when the Start button is selected. The system then pauses and displays the Continue button in place of the Start button. The mask images should be reviewed for proper positioning and good image quality. When the Continue button is selected, the dynamic contrast- enhanced scan starts. The bolus of contrast is injected at this point. The Oasis, Echelon, and Echelon Oval systems can be set up to automatically run the subtraction scans. A MIP post processing sequence may be performed on the final images.
The Test injection method is most commonly used for renal CE-MRA examinations. Use of this method with fluoro is available on the Oasis, Echelon, and Echelon Oval systems (Figure 134). Refer to the “How-To” Manual available for each MR system listed above for step-by-step instructions for the performance of test injection examinations.
Time of flight (TOF) angiography is a non-contrast method that is used to visualize blood vessels. It is also referred to as flow-dependent angiography or inflow angiography. Bright vascular images are created without the use of contrast media due to differences in flow effects between unsaturated and saturated spins.
TOF angiography is based on the phenomenon of flow-related enhancement of spins that are entering into an imaging slice. Gradient echo sequences with very short TR periods are used, as they saturate the signal from stationary tissue. The blood flowing into the slice group or slab has not been saturated, so its signal is stronger than that of the stationary tissues. The strength of the vascular signal depends on the flow velocity and type, the sequence parameters (TR, TE, flip angle, and slice thickness), and the length and orientation of the vessel being examined. Vascular signal is better if the slice is perpendicular to the axis of the vessel. TOF images can be acquired with either 2D or 3D methods. With 2D TOF, multiple thin imaging slices are acquired with a flow-compensated gradient echo sequence. The images can be combined by using a post processing technique such as Maximum Intensity Projection (MIP) to obtain a pseudo-volume image of the vessels similar to conventional angiography. The thin slices used in 2D offer better sensitivity to slow flow, which does not remain in the slice for long and will therefore not be saturated. One of the drawbacks of 2D acquisitions is poor spatial resolution along the axis of the slice stack. In 3D TOF, a volume of images is obtained simultaneously, offering good spatial resolution and a better signal to noise ratio than 2D. However, each repetition excites the entire volume, and can produce a progressive saturation of the flows. The combination of thicker volumes and slow flowing blood can result in a loss of signal in 3D TOF. Vessels with the slowest flow may disappear entirely. Flow saturation in 3D can be reduced by dividing the imaging volume into multiple slabs, or by using the Sloped Slab Profile (SSP) parameter. SSP uses a smaller flip angle as flow enters the volume, and a larger flip angle as flow leaves the volume. The increase in flip angle across the imaging volume compensates for the signal decay resulting from saturation of the blood flow. 3D TOF images are commonly put through the MIP post processing procedure, resulting in images of vessels with a three dimensional appearance.
Time of Flight angiography is sensitive to flow-related artifacts, as well as artifacts related to the imaging of multiple slabs. Turbulent flow in vessels can cause intra-voxel dephasing and a loss of signal. Saturation artifacts can be caused by laminar flow, where the blood flow is slower near the vessel walls than in the center of the vessel. The blood near the vessel walls can become saturated, leading to an apparent reduction in the caliber of the vessel. Venetian blind artifact or slab boundary artifact occurs in 3D TOF imaging when multiple slabs are used. Although the use of multiple slabs decreases the problem of flow saturation, loss of flow-related enhancement may become evident as vessels approach the “exit” side of each slab. This artifactual signal loss can be reduced by “adding” vascular signal at the exit side of the slab. Since vascular signal increases with an increase in flip angle, the Sloped Slab Profile parameter can be incorporated to increase the flip angle across the imaging volume. By correcting for this vascular signal loss, the vasculature takes on a more seamless appearance across the multiple slabs.
Time of Flight sequences are “flow dependent”, but optimization of parameters, and awareness of the type of flow that might be encountered in the vessels being examined can improve imaging results. Very short TR times can lead to poor signal suppression of the stationary tissues that have short T1 relaxation times (fat, hematoma, thrombus). This can result in less contrast between the blood signal and the static tissue signal. Addition of an MTC pulse, water excitation or fat saturation may improve the vascular contrast by further suppressing the static tissue signal. The selections for TR and slice thickness should be appropriate for the expected flow velocity. Signal loss can be linked to the spin dephasing that occurs when flows are complex or turbulent, when flows are oriented parallel to the slice plane, or when flows are too slow (which is the case with aneurysms). The use of 2D or 3D sequences, and single slab or multiple slab coverage will depend on the requirements for coverage of the vessel, and the range of flow velocities that may be encountered in the vessel. TOF sequences are also “flow direction sensitive”. The direction of the flow to be visualized can be selected by placing a presaturation band above or below the vessels of interest to suppress unwanted arterial or venous flows.
Time of flight sequences are typically performed when imaging the vessels of the head and neck, especially the carotid arteries and the Circle of Willis (Figures 135,136). They offer a non-invasive method to visualize and evaluate these vessels. TOF sequences are available on all Hitachi MRI systems.
The acronym VASC-ASL stands for Veins and Arteries Sans Contrast- Arterial Spin Labeling. VASC-ASL is a non-contrast MRA method that allows the viewing of blood flow in both the veins and the arteries. It incorporates a 3D BASG sequence and a selective IR pulse that is positioned to affect only a “select” area of the anatomy. Images can be acquired with the selective IR pulse turned ON only, or with the selective IR pulse set to both OFF and ON. In the latter case, subtraction is performed, resulting in high signal only in the blood that is labeled by the IR pulse. VASC-ASL examinations are performed using respiratory gating as well as the MIP and/or sliding MIP post processing tasks. VASC-ASL is primarily used for imaging of pulmonary vessels, as well as a variety of abdominal vessels, especially the renal arteries and the hepatic portal vein.
VASC-ASL performed without subtraction utilizes the Selective IR pulse set in the ON position only. The Selective IR pulse should cover the slice slab, as well as the vessels that are distal to the slice slab (“downstream” from the target vessels, as in Figure 137). When set in this manner, the images will display high signal from the fresh blood that is flowing in to the slice slab. The Selective IR pulse will suppress any other blood signal (Figure 138).
VASC-ASL performed with subtraction involves imaging with the Selective IR pulse in both the OFF and ON positions, so actual scanning time is doubled. The Selective IR pulse is positioned “upstream” from the target blood vessels, resulting in suppression of the inflowing blood when the Selective IR pulse is set to ON (Figure 139). The inflowing or fresh blood has a low signal in the imaging area, so the target vessels will be darker. When the Selective IR pulse is turned OFF, the inflowing blood has a high signal in the imaging area, so the target vessels will be brighter. After the Subtraction process is performed, the blood flow in the imaging area has high signal, resulting in bright target vessels on the subtracted images (Figure 140). This process may be easier to understand by exploring veins and arteries separately:
When veins are the target vessels, they are suppressed when the Selective IR pulse is ON; subtraction results are:
Bright veins and arteries (Sel. IR OFF) – Bright arteries (Sel. IR ON) = Bright veins
When arteries are the target vessels, they are suppressed when the Selective IR pulse is ON: subtraction results are:
Bright veins and arteries (Sel. IR OFF) – Bright veins (Sel. IR ON) = Bright arteries
VASC-ASL is available for the Oasis, Echelon, and Echelon Oval MR systems. Refer to the “How-To” Manual available for each MR system listed above for step-by-step instructions for the performance of VASC-ASL examinations for a variety of vessels.
The acronym VASC-FSE stands for Veins and Arteries Sans Contrast- Fast Spin Echo. This sequence is currently primarily used for non-contrast PVA (Peripheral Vascular Angiography) examinations of the arteries. Each anatomical region is scanned in both diastole and systole. Diastole occurs when the heart is in a state of relaxation and dilatation, while the ventricles are filling with blood. Both veins and arteries appear bright or have high signal intensity on images acquired during the diastolic phase (Figure 141). Systole occurs when the left ventricle of the heart contracts and drives the blood to the aorta and the pulmonary arteries. Due to the fast blood flow during this phase, the arteries typically display low signal, while the veins have brighter signal and are well visualized (Figure 142). Subtraction of the systolic phase images from the diastolic phase images results in images with high signal in the arteries only (Figure 143). VASC-FSE provides images of the peripheral vessels with excellent image quality without the use, and inherent risks, of intravenous contrast.
PVA examinations typically cover the vessels in the anatomic region from the aortic bifurcation, down through the lower extremities to the pedal vessels. The examination is divided into multiple stations in order to include all the pertinent vessels, and involves the use of the table move function to achieve the correct table position for each station. PVA exams using VASC-FSE consist of a phase contrast scan, a velocity analysis, and the VASC-FSE scan, all of which are performed at each station (Figure 144). The VASC-FSE scan is a 3D primeFSE sequence that is performed with ECG gating. Post processing typically includes the MIP function, to eliminate background tissue, and the Stitching function, which uses the MIP results to create one image that includes all of the peripheral arteries.
The phase contrast scan and the velocity analysis that are performed at each station are used to determine the velocity of the target vessel, and to determine the Delay time that will be input in the Gating area of the VASC-FSE scan parameters. Velocity data from the phase contrast scan is loaded into the velocity analysis scan task. The images are reviewed, and an image is selected in which the arteries appear dark. An ROI is placed over the dark artery or arteries. The velocity analysis displays a graph of the velocity vs. delay time for the ROI, from which the peak systolic velocity can be determined. The phase contrast image that displays the same peak velocity value associated with the ROI is located. The systolic delay time displayed on the next phase contrast image is the information that is used in the VASC-FSE scan. This value is entered in the Delay Sys. (delay time of systole) field in the Gating parameters. The system can be set up to automatically perform subtraction on the VASC-FSE images (Diastolic images – systolic images). The subtracted images (displaying bright arteries only) can then be put through the MIP process to eliminate background tissues and other vessels (Figure 145). When all stations have been scanned, subtracted, and MIPPED, the final results can be Stitched together to display the peripheral arteries, from the aortic bifurcation to the pedal vessels, in one large image (Figure 146).
Refer to the “How-To” Manual for the Echelon, Echelon OVAL, and Oasis MR systems for step-by-step instructions for the performance of VASC-FSE examinations.