Role of cardiovascular nuclear medicine in evaluating trauma and the postoperative patient

Role of Cardiovascular Nuclear Medicine in Evaluating Trauma and the Postoperative Patient Theodore R. Simon, Robert W. Parkey, and Samuel E. Lewis In the patient with cardiac trauma, radionuclide

imaging may provide important information about cardiac mechanical function, vascular anatomy and integrity, myocardial perfusion, and myocardial m e t a b o l i s m . Studies require only minimal patient cooperation, can be performed relatively rapidly and often at the bedside, and may be repeated at

A R D I A C I N J U R Y is common. It occurs in up to 76% 1-3 of patients with thoracoabdominal trauma and may represent the most common unsuspected visceral injury responsible for death in fatally injured accident victims? Despite the serious adverse effects of cardiac dysfunction in these patients, adequate diagnostic evaluation may be difficult/ Often cardiac injury is unsuspected at the initial evaluation because of attention directed toward more obvious injuries. Physical examination may be limited; auscultation and palpation, misleading. 6 ECG changes in myocardial contusion are often limited to ST-segment and T-wave alterations. 4'7'8 Such changes are common in patients with noncardiac trauma and do not offer the necessary specificity to diagnose myocardial contusion, z'3'9-jl In critically ill patients, ECG changes are not necessarily due to myocardial damage. ~2-14Dolara et al. 15studied ECG changes in 98 patients without open-chest injuries and found that 63% of those with severe trauma had ECG changes. Conversely, myocardial contusion documented by postmortem examination has been r e c o r d e d in patients without E C G changes. ~6 In experimental animal studies, induced chest trauma sufficient to produce mediastinal or pulmonary hemorrhage was associated with ECG changes even when cardiac findings at necropsy were normal. 3 Cardiac enzymes, including MB subunits of creatin kinase, are considered to be specific in diagnosing myocardial damage. However, enzyme studies are of limited value in patients with extensive musculoskeletal trauma or surgery. CK-MB elevations have been reported in tachyarrhythmias, trauma, crush injuries, muscle diseases, and gas gangrene. 16-~9A recent report by Potkin et al. 16 concluded that CK-MB is probably not a useful indicator of cardiac damage in the trauma

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Seminars in Nuclear Medicine, Vol. XIll, No. 2 (April), 1983

i n t e r v a l s f o r serial evaluations. These studies provide valuable adjunctive knowledge when selected and interpreted with knowledge of the mechanism of injury, timing of the examination r e l a t i v e to the time of injury, and most likely differential diagnoses. frequent

patient. Routine radiographic examination may underestimate cardiac trauma. Examination is often limited to portable AP films; but even upright PA and lateral films may not provide sufficient data to evaluate adequately the severity of cardiac mechanical dysfunction. 6 Even relatively invasive procedures such as pericardiocentesis may be inaccurate. Radionuclide studies have a definite place in the evaluation of the patient with suspected cardiac injury. Studies can be performed relatively rapidly, often at the bedside, and provide important information about cardiac mechanical function, intrathoracic vascular anatomy and integrity, myocardial perfusion, myocardial metabolism, and myocardial infarction. This review considers the relationships between cardiac pathology and the mechanisms of injury. Applicable radionuclide procedures are reviewed. Differential diagnoses are discussed with emphasis on the results of radionuclide studies. Finally, a strategy is suggested for radionuclide imaging in the trauma patient based upon the clinical setting, mechanism of injury, time of examination since injury, and differential diagnoses. METHOD OF INJURY

Cardiac injury may result from penetrating, impact, electrical, or perioperative trauma. Penetrating injuries are associated with an overall mortality of 65%-80%) o Such injuries may From the Department of Radiology, University of Texas Health Science Center, Dallas, TX. Address reprint requests to Samuel E. Lewis, MD, Director, Division of Nuclear Medicine, Department of Radiology, University of Texas Health Science Center, 5323 Harry Hines Blvd., Dallas, TX, 75235. 9 1983by Grune & Stratton, Inc. 0001-2998/83/1302-0005502.00/0

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cause hemodynamic crisis (rupture of the heart or major blood vessel, hemopericardium, cardiac tamponade, shock, traumatic shunt lesions, acute valvular insufficiency, life threatening dysrhythmias), ischemic injury (transection or obstruction of a coronary artery), or direct myocardial necrosis. The form and extent of injury depends upon the penetrating object and its path. For example, a knife wound to the anterior chest is most likely to rupture the right ventricle or transect the right coronary artery. Therefore, right ventricular dysfunction and right ventricular infarction may be expected. Direct myocardial necrosis is usually limited and clinically unimportant. 2' Low velocity or small caliber bullets are likely to disrupt vascular integrity and lead to hemodynamic instability. Ischemic injury may result from transection or obstruction of a coronary artery or from systemic hypotension. These entities are also unlikely to cause significant direct myocardial necrosis. 2' On the other hand, high velocity or large caliber bullets often cause direct myocardial necrosis (blast injury) in addition to their other effects. Mechanical injury to the heart may result from indirect force, unidirectional direct force, bidirectional direct force, acceleration-deceleration, blast or concussionY -24 Injuries are common in blunt thoracoabdominal trauma, especially those caused by motor vehicle accidents. Serious consequences include cardiovascular rupture, 25-26 myocardial contusion, 7'27-31 and lifethreatening dysrhythmias.32 Contusion injuries are especially subtle and may cause extensive alterations in coronary blood flow and mechanical function despite an absence of superficial signs. Electrical injuries are caused by either highvoltage contact accidents or direct current cardioversion. Both can cause fatal dysrhythmias or frank myocardial necrosis. Physical examination of the high-voltage accident victim, with careful localization of entrance and exit wounds, may help to predict the probability of myocardial injury. However, deep tissue necrosis may be present without superficial injury and "skip" injuries are not uncommon. 33 Cardioversion is most likely to cause myocardial necrosis 34 when multiple high-energy countershocks are necessary and when there is obvious superficial injury. 35

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Perioperative injuries include direct surgical trauma, vascular ruptures, dysrhythmia, ischemia, and mechanical dysfunction. Diagnosis of cardiac injury may be especially difficult because the usual signs and symptoms (chest pain, rales, electrocardiographic changes, enzyme alterations) are often unreliable. RADIONUCLIDE PROCEDURES IN CARDIAC TRAUMA

Radionuclide Angiography Radionuclide angiography may be performed using first-pass or equilibrium techniques. 36-4~A gamma camera, either multicrystal or single crystal, interfaced to a computer system is used to record either the initial passage or equilibrium distribution of a radioactive vascular tracer in the central circulation. First-pass techniques require both a rapid delivery of a tight bolus of radioactivity into an antecubital or jugular vein and a camera system with high count-rate capability. 36Any vascular tracer which emits photons of suitable energy may be employed. Classically, 99mTc-pertechnetate, diethylenetriaminepentaacetic acid (DTPA), gluconate, or sulfur colloid is used in doses of 370-925 MBq (10-25 mCi). Judicious tracer selection permits the acquisition of sequential studies in different projections. For example, an anterior study using 99mTc-sulfur colloid might be followed by a left anterior oblique examination using 99mTc-pertechnetate or DTPA. In the trauma patient, the initial study should be acquired in anterior projection. Data acquisition is begun simultaneously with tracer injection and continued for 60 sec. Data is acquired as sequential image frames at a rate greater than 20 frames/sec or in list mode. 41 List mode acquisition is more flexible and is preferred. In addition to permitting reformatting of data into frames with variable time intervals, list mode acquisition may be used to produce composite R-wave synchronized images of the right or left heart. Images are viewed in sequence using a cinematic video display. The anatomy and integrity of intrathoracic vascular structures are examined. Careful observation is made of global and segmental chamber contraction. Quantitative analysis includes at least determination of right and left ventricular ejection fractions and an analysis of the pulmonary time-

CARDIOVASCULAR NUCLEAR MEDICINE IN TRAUMA

activity curve. Additional parameters such as chamber volumes, ejection and filling rates, and cardiac output are measured as necessary. Compared to equilibrium imaging, first-pass methods tend to be limited statistically by detector sensitivity and injected dose. The use of ultrashort-lived tracers eliminates the latter. Iridium-191, 42~5 gold-195m, 46'47 and tantalum17848 have been reported to be superior first-pass markers. A second advantage of these agents is the ability to perform rapid sequential studies. Such tracers warrant further investigation. Equilibrium blood pool imaging requires the acquisition of composite R-wave synchronized images of the distribution of a tracer which remains confined to the vascular space. 49 The tracer of choice is 99mTc-red blood cells. Labeling in vivo39'50 is accomplished by intravenous injection of approximately 1 mg of stannous ion followed in 15-30 min by 99mTc-pertechnetate. Stannous ion is prepared by mixing a standard lypholized pyrophosphate kit with normal saline. Cells may also be labeled in vitro 51 using a kit supplied by Brookhaven National Laboratory. A third method combines features of in vivo and in vitro techniques. 52"53Some 20 min after the intravenous injection of stannous ion, 5-10 ml of

Fig. 1. Normal gated first-pass study. Normal appearance of the right heart on the gated first-pass study. Frame 1 is top left. Frame 16 is bottom right. The frames are in sequence from left-to-right across each row. There is good separation of right atrium and ventricle w i t h excellent delineation of the valve plane. The normal pattern of right ventricular contraction is nicely demonstrated. Contraction of the papillary muscles pulls the valve plane down toward the apex of the ventricle. Simultaneously, the free wall contracts upward toward the base of the ventricle. Contraction of the deep circular fibers of the left ventricle further augments right yentricular ejection by a bellows action.

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blood is withdrawn through a butterfly catheter (which contains 10-20 units of heparin) into a lead-shielded syringe (which contains 15-30 mCi of 99mTc-pertechnetate). The line is terminated with a 3-way stopcock. The syringe is inverted gently every 60 sec for 5-10 min and the contents reinjected. In our laboratory, this technique yields images which are superior to conventional labeling in vivo and which are comparable to labeling in vitro. A decision to perform equilibrium imaging does not preclude acquiring a first-transit study. Indeed, we recommend performing a first-pass study on every patient. A modification which we have found useful is the gated first-pass study 37'4~ (Fig. 1). The patient is outfitted with gating electrodes and connected to the computer system. The camera is placed in a 30 ~ right anterior oblique position. The computer is set to acquire a 16-frame per cycle gated study over 90% of an average R-R interval. R-wave tracking is disabled. Data acquisition is started immediately prior to the injection of tracer. The passage of tracer through the right heart is observed on the persistence oscilloscope. When activity is seen within the lungs, and before activity has entered the left heart, the study is terminated. If desired,

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a left heart study may be acquired as soon as the bolus has cleared the right heart. After allowing the tracer to equilibrate, multiple sets of gated blood pool images are acquired in various anatomic projections. It is important to acquire enough projections to view the entire intrathoracic vascular anatomy. We routinely acquire 30 ~ right anterior oblique (RAO), anterior, septal, and left lateral projections. Additional projections, such as left posterior oblique or slanthole collimator views, are obtained as necessary. The first step in data analysis is careful observation of the cinematic display. We prefer to look at 4 projections (16 frames/view) simultaneously. The study is evaluated for: (1) quality of the red cell label; (2) overall distribution of labeled red cells (this is an excellent means to identify intrathoracic and abdominal bleeding); (3) course and caliber of the aorta and major arteries; (4) course and caliber of the pulmonary arteries; (5) relative distribution of pulmonary blood flow; (6) abnormalities in the pericardial/ myocardial space (fluid, ventricular hypertrophy, blood); (7) shape and thickness of the interventricular septum; (8) clot or mass within the cardiac chambers; 54'58 (9) size and contraction of each of the chambers; and (10) relative time of contraction of the chambers. The examination should be tailored for each patient based upon the mechanism of injury and clinical suspicion. For instance, myocardial contusions often involve the right ventricle. Subtle wall motion abnormalities are easily missed if only anterior and septal projections are obtained. Quantitative analysis should include at least determination of right and left ventricular ejection fractions. 59 Stroke volume6~ and reverse stroke volume ("paradox") 6~ functional images should be generated in every patient. Additional quantitative analysis should be performed as necessary. Measurements of ventricular volumes and cardiac output directly assess the adequacy of cardiac mechanical function. Volumes may be calculated from chamber area-length 62-65 or radioactivity.66-7~ Area-length measurements assume that the ventricle has a simple geometric shape, an ellipsoid, and in most cases provide reasonable estimates of left ventricular volume. Right ventricular volume may also be estimated by geometric methods, 71-76 but the analysis is

SIMON, PARKEY, AND LEWIS

complex and probably less accurate. Scintigraphic dimensions (in pixels) must be converted to true area and length using a calibration source. Volume measurements based on chamber radioactivity make no assumptions about chamber shape. Detected ventricular activity must be corrected for detector efficiency and attenuation. Absolute ventricular volume is then derived from the corrected ventricular activity normalized for blood activity. Both left and right 77 ventricular volumes can be measured by this method. Accurate measurements of ventricular volume are possible only if the ventricles are isolated from the atria and other periventricular background activity. For the right ventricle, this usually requires a slanthole collimator rotated so that the holes look down the long axis of the heart, a right shoulder to left hip orientation. 77 Relative ventricular output may be used to assess the severity of acute valvular insufficiency. This subject has been reviewed by Nicod et al. 78 and by Alderson. 79 There are procedural differences between reported techniques for measuring the radionuclide regurgitant index. 8~ Stroke counts may be measured from fixed end-diastolic regions of interest or from separate end-diastolic and end-systolic areas or from the stroke volume image. Accuracy and reproducibility of the measurement is obviously influenced by these variations. However, adequate separation of the ventricles from each other and from the atria and other periventricular activity is paramount. We currently acquire two slanthole projections for calculation of the regurgitant index. Left ventricular output is measured from a view optimized for the left heart. Right ventricular output is measured from an optimized right heart view. 84 Fourier analysis and measurement of global and segmental contraction and relaxation parameters are additional analytic tools which may be helpful in patients with ischemia. Global contraction and relaxation rates are measured from the ventricular time-activity curve. 85-89Segmental changes may be characterized by analysis of activity changes, such as regional ejection fraction, or boundary movement. 9~ "Phase analysis" is also used to detect segmental ventricular dysfunction.92-97 The essence of temporal Fourier analysis of gated blood pool data is that each pixel describes a periodic time series. The first Fourier harmonic of a time series is a cosine

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function. Data points of the pixel time-activity curve are "fit" by a cosine function completely characterized by its amplitude and phase. Construction of a phase image has been used to highlight temporal differences in segmental function. This technique has also been used to investigate conduction abnormalities. Such analyses may be useful in selected patients. However, there are inherent inaccuracies in a firstharmonic approximation and the phase image must be interpreted with caution.% Some patients may benefit from prolonged hemodynamic monitoring. The nuclear probe is ideally suited to such measurement.98-1~176 Infarct-avid imaging in cardiac trauma permits visualization of ischemic or direct infarction. 2L'28-31'34"35The agent of choice remains 99mTcpyrophosphate (99mTc-PPi). The dose is 5501100 MBq (15-30 mCi) injected by direct venipuncture. Injection via an in-dwelling catheter may result in breakdown of the label and poor quality images. Imaging is begun no sooner than 3 hr after injection. Planar images should be acquired in at least four projections (anterior, 30~ LAO, 70~ LAO, and left lateral). The anterior image is acquired first and should contain at least 500,000 counts. Subsequent images are acquired for identical time. The key to interpreting the study is a careful search for abnormal activity in the expected location of the myocardium. A comparison chest radiograph is recommended. Myocardial localization may appear well-defined (focal) or pooly-localized. Welldefined myocardial uptake, unlike activity in overlying structures (cartilage, bone, chest wall), moves relative to the bony thorax in the routine views. Triangulation places the activity within the thorax. Poorly-localized myocardial uptake may be difficult to distinguish from blood pool or overlying structures. Observer experience is important. Relative intensity is not a useful criterion. Indeed, intensity grading should not be used as a test for abnormality, but rather as a measure of intraobserver variability. Myocardial uptake, of any intensity, is identified by anatomical position. Difficult cases require additional imaging. Planar images may be repeated 1-3 hr later. Residual blood pool activity should decrease with time. Blood pool activity can be a significant problem in patients with compromised circula-

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tion or chronic renal dysfunction. Problems may also be expected in elderly, obese, and poorly hydrated patients. Physiologic gating and tomography represent more aggressive solutions. On gated 99mTc-PPi studies, myocardial uptake is identified by a position just outside the blood pool. 1~ The uptake may show cardiosynchronous movement.1~ Temporal filtering helps to decrease high frequency noise. We recommend the acquisition of at least two gated projections--Anterior and one LAO. Studies are acquired for preset time. Gated blood pool images may be acquired immediately after the 99mTc-PPi images.5~176Exact registration of at least one projection can be obtained if neither patient nor detector are moved between examinations. Image sets are mapped into opposite ends of a linear bichromic color table and viewed as a cinematic overlay.1~ This technique is especially valuable in suspected right ventricular infarction. In patients with suspected contusion, we often perform gated blood pool imaging immediately following infarct-avid imaging. This is practical because blood radioactivity is much greater than osseous activity thereby effectively eliminating these structures (Fig. 2). Tomographic imaging with a rotating camera system provides even more sensitive detection of small infarcts. '~ Sixty-four to 128 projections are imaged over 360 ~ with each image containing 50-100,000 counts. Ungated blood pool projections are acquired immediately thereafter. Projections are corrected for field nonuniformity and center of rotation. Transverse section slices are reconstructed by filtered backprojection. Corresponding slices are color-coded and viewed as a cinematic display. Myocardial uptake is characterized by a position just outside of the cardiac blood pool. 1~ In experimental animals, infarctions as small as 1.0 g have been detected and accurately sized by tomography)~176 Preliminary studies have shown similar results in patients) ~176 Contusions may also be detected with greater sensitivity on tomographic studies (Fig. 3). Postinjury timing of infarct-avid imaging is critical. Tracer delivery to infarcts depends upon residual blood flow. In ischemic events, maximum myocardial uptake occurs 3-5 days after infarction, decreases in intensity thereafter, and often becomes normal by 10-14 days. Reperfu-

Fig. 2. Infarction and probable contusion. This 50-yr-old male was shot in t h e chest. Plan a r ~ " T c - p y r o p h o s p h a t e images are shown in panel A (anterior-top left, 35 ~ LAO-top right, 70 ~ LAO-bottom left, lateral-bottom right). There is a photophenic defect in t h e sternum. Tracer uptake to t h e right of t h e sternum corresponds to bone fragments and chest wall necrosis secondary to blast injury. The bullet penetrated the right h e a r t in t h e a t r i o v e n t r i c u l a r groove. Through and through injuries of t h e right venticle w e r e oversewn. A clot was found in t h e right coronary artery. The planar images s h o w an area of myocardial uptake of tracer along t h e inferior wall of the left ventricle. The activity is faint but is clearly outside t h e boundary of t h e blood pool. Similar findings are shown in t h e gated pyrophosphate scans shown in panels B and C. In panel D, four frames of a lateral v i e w ventriculogram are shown. This study was acquired immediately after t h e p y r o p h o s p h a t e s t u d y and showed focal akinesis of the basal posterior wall consistent w i t h acute infarction. This patient, therefore, had both direct and ischemic injuries.

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Fig. 3. Value of single photon emission t o m o g r a p h y of the heart. This 52-yr-old w h i t e male presented w i t h blunt trauma of t h e left chest as a result of a motor vehicle accident. Planar SemTc-PPi images (panel A) w e r e acquired in anterior (top left), 35 ~ LAO (top right), 70 ~ LAO (bottom left), and left lateral (bottom right) projections. On the anterior view, faint uptake is seen just medial to t h e costochondral junctions at the level of t h e xiphoid process. Transverse sections obtained w i t h a rotating camera tomograph are shown in panel B. Definite myocardial uptake is seen along t h e apical portion of the anterolateral wall of the left ventricle. Tomography may increase contrast between myocardial uptake of ~ T c - P P i and surrounding structures and t h e r e b y permit more accurate and confident diagnosis.

sion infarcts show earlier visualization and more rapid resolution. Indeed, the healing phase of myocardial contusion is characterized by new vessel formation, l~ The preservation of normal blood supply and rapid ingrowth of new vessels may explain enhanced early delivery of radiopharmaceutical to the injured cells and more rapid removal of dead cells by neutrophil and

macrophage activity. Thre is good evidence to suggest that patients with suspected contusion should be imaged with 99~Tc-PPi within 24 hr and restudied at 72 hr if negative. Indeed, Downey et al. ~~ found that contused myocardium sequestered 99mTc-PPi within 2 hr. In patients with suspected contusion, 99mTcPPi studies must be interpreted with knowledge

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of previous infarction. Some 30%-40% of patients with acute myocardial infarction retain a persistently abnormal scintigram for at least 6 mo) ~ This percentage may be even higher in diabetics. 1~2 The persistently abnormal scintigram is associated with a histologic appearance characterized by myocytolysis)13 Patients have a poorer prognosis than similar patients whose scintigrams become negative.H~ In the initial management of the trauma patient, an abnormal 99mTc-PPi scintigram identifies those at increased risk. Differentiating chronic from acute necrosis becomes more important in long-term management. Serial images demonstrating resolution of tracer uptake suggests acute rather than chronic infarction. There is considerable controversy regarding the accuracy of 99mTc-PPi scintigraphy for detecting myocardial contusion. 7"~6"27-3~Diagnostic criteria are not well-established. It seems clear, however, that most contusions will involve a relatively small amount of myocardium. Careful imaging, including gating and tomography may be required to visualize these lesions (Fig. 3). Radionuclide studies of myocardial perfusion are most commonly performed with TI-201 in the form of thallous chloride) ~4:15 TI-201 is a cyclotron-produced tracer that mimicks potassium. Imaging is performed immediately following the intravenous injection of 37-74 MBq (1-2 mCi). Planar images should be acquired in multiple projections (usually some combination of RAO, anterior, shallow LAO, steep LAO, and left lateral). Images may be acquired directly onto film, but digital acquisition is recommended. As with 99mTc-PPi imaging, tomography appears to improve diagnostic accuracy) ~ Perfusion studies are most likely to be of value in suspected ischemic infarction. Because the infarction of contusion is mostly epicardial and nontransmura|, perfusion studies are less likely to be useful than gated blood pool and pyrophosphate studies. Images should be obtained within 6-12 hr of injury and interpreted with knowledge of previous infarction. H8 Quantitative analysis of the relative radial distribution of thallium may be necessary to identify small areas of hypoperfusion) 19-~26Such analyses have considerable predictive value in patients with nontraumatic infarction and Killip class I or II congestive heart

SIMON, PARKEY, AND LEWIS

failure) 27 However, prognostic value in the trauma patient is not established. Images of metabolic markers are similar in appearance and diagnostic value to TI-201. Iodine-123 labeled fatty acids have been studied by several investigators.~28-~36However, routine clinical use has been hampered by the rapid appearance of free iodide in the blood concomittant with beta-oxidation by myocardium and liver. 128 A subtraction technique for blood iodide has been proposed and does improve image quality) 37 However, blood activity seriously limits the utility of straight chain radiolabeled fatty acids. Blood iodide can be chemically reduced by replacing the alkyl carbon-iodine bond with an aryl carbon-iodine bond so that metabolites retain the iodine label. 138Such agents are now in experimental animal and early clinical testing. Preliminary reports are encouraging. Other substrates have also demonstrated promise for myocardial imaging. These include radioiodinated norepipephrine storage analogs such as metaiodobenzylguanidine ~39'14~and cardioselective radiolabeled beta adrenergic antagonists. 14~ Images obtained with the recently developed tracers are impressive. As with perfusion imaging, however, metabolic studies probably have limited value in the trauma patient. DIAGNOSTIC STRATEGY

Improved transport of the critically injured and advances in on-the-scene resuscitative techniques have allowed more patients to arrive alive at the emergency room after severe blunt chest injuries or penetrating wounds of the heart. 142 Standard evaluation should include a chest radiograph, electrocardiogram, and complete physical examination with special emphasis on the structural integrity of the bony thorax, status of peripheral pulses, and adequacy of ventilation and circulatory hemodynamics. The initial evaluation should consider intrathoracic vascular rupture (hemopericardium, hemothorax, hemomediastinum, traumatic shunts), pericardial effusion and cardiac tamponade, myocardial ischemia secondary to transection or obstruction of a coronary artery, acute valvular regurgitation (aortic root dissection, direct trauma, papillary muscle dysfunction), pseudoaneurysm, pulmonary embolism (clot, fat, knife fragment, or

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Ventricular rupture and Fig. 4. hemopericardium. This 55-yr-old male presented w i t h acute chest pain and electrocardiographic evidance of acute anterior myocardial infarction. Four frames from a saptal view radionuclide ventriculogram performed shortly after hospital admission are s h o w n in the top row. The left ventricle is dilated and shows significant dysfunction. The myocardial/paricardial space is enlarged w i t h a pattern consistent w i t h pericardial fluid. Follow-up images w e r e acquired approximately 2 hr a f t e r the initial examination. Labeled red cells are now present in the pericardial space, Surgery confirmed the diagnosis of ventricular rupture and hemopericardium. We have seen similar findings in a patient who had undergone aortic valve replacement and who was found to be leaking at a suture line.

bullet), and systemic embolism (knife fragment or bullet). Diagnostic imaging may include echocardiography, contrast angiography, and radionuclide studies. In the initial evaluation of the patient with penetrating injury, radionuclide angiography is more likely to provide diagnostic information than infarct-avid or perfusion imaging. Active bleeding into the chest, mediastinum, pericardium, GI tract, and abdomen may be identified53'143-148 (Fig. 4). Acute pericardial effusions sufficient to cause tamponade are usually easily seen (Fig. 5). Traumatic shunt lesions may be localized and graded by first-pass analysis. 149-163 Severity of acute valvular regurgitation can also be estimated from right and left ventricular stroke volumes. ~64Determination of ventricular volumes and global ejection fractions can yield a direct assessment of hemodynamic impairment. Segmental ventricular dysfunction suggests localized ischemic or direct myocardial injury or pseudoaneurysm.16'21'87'165-174 At the very least, the study provides an important baseline. Infarct-avid imaging is performed 3-5 days following penetrating injury. Studies are of lim-

ited value in assessing direct myocardial necrosis from knife and low-velocity/small-caliber bullet wounds because the mass of necrotic myocardium is small.2~ 99mTc-PPi scintigraphy is more helpful in ischemic infarction or in high-velocity/ large-caliber bullet injury. Perfusion/metabolism imaging is probably best reserved for hemodynamically stable patients with suspected ischemia when imaging can be done within 6-12 hr. Blunt thoracicoabdominal trauma can also cause hemodynamic instability. The initial radionuclide study should be angiography. Myocardial contusion occurs with some frequency in such injuries ~69and may cause serious complications. Diagnosis may be difficult since the most frequent ECG changes are ST-segment and Twave alterations, and similar changes are often seen in patients without contusion. Conduction abnormalities are also nonspecific. Factors other than cardiac damage, such as vagal tone, sympathetic tone and electrolyte status (especially hypokalemia) can induce conduction disturbances in a normal heart. 12-14Infarct-avid imaging with 99mTc-PPi should be performed within the first 24 hr. Since contusions are often small

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Fig. 5. Pericardial effusion. The pulmonary arteries appear to draped over an enlarged myocardial/pericardial space. Motion of the entire heart is exagerated. Note the enhanced visualization of the inferior vena cava because of an absence of surrounding activity.

and nontransmural, care must be taken to search for myocardial uptake. Gated planar imaging with superimposition of gated blood pool images or tomographic imaging may be necessary. Perfusion or metabolic imaging is of lesser value. 17~ Blunt trauma may also produce coronary artery injury and ischemic infarction. The time-course of 99mTc-PPi scintigraphy in these patients closely resembles that of patients presenting with acute chest pain. Imaging schemes must be adjusted accordingly. Electrical injuries result from direct contact or direct current cardioversion. High-voltage injuries may cause life-threatening arrhythmia, ischemia, and direct myocardial necrosis. Infarct-avid imaging with 99mTc-PPi can detect, localize, and define the extent of myocardial necrosis, while total body imaging may demonstrate unsuspected deep skeletal muscle necrosis. Perfusion or metabolic imaging within the first 6-12 hr may identify ischemia and predict subsequent course. If thallium studies are performed, images should be obtained not only of the thorax but also of entry and exit sites. Cardioversion may also cause myocardial necrosis. The specific site of damage and whether it occurs at all will depend on the size and placement of the paddles, the interval between episodes of cardioversion, and the total amount of electric energy delivered. 21

Diagnosis of cardiac injury in the perioperative patient may be especially difficult. The choice of radionuclide procedure depends upon the differential diagnosis. Radionuclide angiography is most helpful in the unstable patient. Infarct-avid and perfusion or metabolic imaging should be used as dictated by clinical course. SCINTIGRAPHIC FINDINGS IN CARDIAC TRAUMA

The hemodynamically unstable patient is best examined by radionuclide angiography. Active bleeding is identified by extravasation and sequestration of labeled red cells. 171 Hemothorax, hemomediastinum, hemopericardium, and abdominal bleeding may be identified by this appearance (Fig. 4). Sites of previous bleeding may appear as well-defined photopenic areas. Since images may be obtained for at least 6 hr and often up to 18-24 hr after red cell labeling, serial imaging may be used to follow rebleeding. Rebleeding is seen as new activity at a previously photopenic site. We have noted extravasation of labeled red cells into the pericardial space at the second examination in two patients whose initial studies only showed pericardial fluid. Thoracic aortic aneurysm is often demonstrable by LAO first-pass or equilibrium studies. ]75J76Localized dilatation of the aorta exceeding its usual 3 cm diameter, is the characteristic

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finding. Aneurysm should be easily distinguished from unfolding of the aortic arch, which may also cause mediastinal widening. While aortic dissection may be difficult to diagnose by any technique, characteristic findings on radionuclide angiography include dilatation of the aortic root, abrupt and irregular narrowing of the aortic arch and tortuous descending aorta at the site of dissection. Activity is sometimes present in the dissection channel. Complementary findings on echocardiography help to establish the diagnosis. Interruption of the superior vena cava can be identified by first-pass examination. 177-179 Rupture causes extravasation. Acute obstruction presents as abrupt termination; collateralization may not be evident. 18~Traumatic obstruction of the carotid arteries may be evaluated by anterior and oblique gated blood pool images processed to generate a functional image where each pixel is replaced by the difference between its maximum and minimum activity during the cardiac cycle. Sites of absent or reduced pulsation thus show significant differences from normal. Aneurysm of the pulmonary artery presents as an increase in vessel caliber. It may be difficult to distinguish aneurysm from physiologic dilatation caused by aging or pulmonary hypertension. Enlargement of the hilar pulmonary arteries with or without rapid distal tapering, increased amplitude of pulsation in the main pulmonary artery, and complementary roentgenographic signs identify pulmonary hypertension. Displacement or abrupt changes in the caliber of the pulmonary arteries should suggest hematoma or other mass effect. Pulmonary capillary activity may be increased and show redistribution in left ventricular failure. Segmental defects would raise the suspicion of pulmonary emboli.

Fig. 6. Mural thrombos. Four frames of a septal view radionuclide ventriculogram are shown. The left ventricle is dilated and contracts poorly. A large photophenic region occupies the entire apex of the ventricle. On the cinematic display, the border of the photopenic area closest to the aortic valve plane could be seen to become more irregular during ventricular contraction. Echocardiography confirmed the presence of a large mural thrombus.

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Evaluation of the pericardial/myocardial space may identify fluid or ventricular hypertrophy. As previously noted, the appearance of labeled red cells in the pericardial space is diagnostic of cardiac rupture (Fig. 4). Pericardial effusion is most commonly characterized by a photopenic halo extending completely around the cardiac blood pool up to the level of the pericardial reflection (Fig. 5). Often the pulmonary arteries appear to drape over the halo. Loculated and small effusions may be difficult to establish by radionuclide techniques and are better evaluated by echocardiography. Care must be taken to distinguish pericardial fluid from left ventricular hypertrophy since both may increase the separation of ventricular blood pool and the lungs. Hypertrophy should not extend to the pericardial reflection and the outside border of the halo should demonstrate cardiosynchronous motion. Hypertrophy is also often concentric and symmetrical. Thus septal shape and thickness are valuable clues to the diagnosis. Traumatic shunt lesions are best identified on the first-pass study; visualization of the lesion depends upon its location and rate of flow. Gamma variate analysis of the pulmonary timeactivity curve provides an accurate assessment of the ratio of pulmonic to systemic flow. Clots (Fig. 6) or mass lesions (Fig. 7) within a cardiac chamber present as a filling defect.54-58 The key to this diagnosis is the acquisition of sufficient projections and care to note the expected notches in the left ventricular blood pool caused by the insertions of the papillary muscles and mitral annulus or valve leaflets. Analysis of chamber size and contraction is the cornerstone of the evaluation of cardiac mechanical function. Segmental ventricular dysfunction may be caused by direct trauma,

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Fig. 7. Right atrial myxoma. This 53-yr-old obese female presented w i t h a confusing constellation of symptoms following a motor vehicle accident. She also had a confirmed history of deep venous thrombosis. Four frames from a gated first-pass s t u d y are shown. The end-diastolic frame is t h e most informative. A large photopenic defect is seen along the diaphragmatic border of the right heart at the level of t h e tricuspid valve plane. This spherical object could be seen to move back and f o r t h across the valve plane on the cinematic display. Surgery confirmed the diagnosis of right atrial myxoma.

ischemia, or conduction abnormalities. Segmental wall motion should be graded as normal, mild hypokinesis, moderate hypokinesis, akinesis, or dyskinesis. Conduction abnormalities are visualized by alterations in the expected temporal relationships between contractions of the chambers. First-harmonic Fourier phase analysis may help to visualize both types of abnormalities. Acute tricuspid insufficiency is characterized by right atrial dilatation with distention during ventricular systole~81"182(Fig. 8). During the firstpass study, blood may be seen to reflux into the inferior vena cava and hepatic veins. 183 Phasic pulsations within th6 hepatic blood pool may be

identified by phase analysis or simple observation. Z84Reflux from the superior vena cava into the left brachiocephalic vein is an additional sign of elevated right atrial pressure. However, brachiocephalic and jugular reflux may be produced by a Valsalva maneuver. The right ventricle is dilated and the free wall is of normal thickness. Right ventricular ejection fraction is often normal. However, right ventricular ejection rate may be reduced, causing a prolonged ejection time. Remember to expect functional tricuspid insufficiency in patients with central venous or Swan-Ganz catheters. Catheter induced regurgitation is usually easily distinguished from the

Fig. 8. Acute tricuspid regurgitation. Summed images of t h e right heart phase of a first t r a n s i t s t u d y are s h o w n in panel A. There is definite reflux of tracer into the inferior vena cava. The right atrium and ventricle are enlarged. Right ventricular contraction is hyperdynamic, inferior vena cava reflux and abnormal hepatic pulsations w e r e seen on t h e equilibrium s t u d y (panel B). Auscultat o r y findings w e r e consistent w i t h a diagnosis of acute tricuspid regurgitation.

CARDIOVASCULAR NUCLEAR MEDICINE IN TRAUMA

gross hemodynamic derangements caused by a true valvular lesion. Acute pulmonic valvular insufficiency causes similar right ventricular findings, but right atrial abnormalities are usually absent. The pulmonary artery may show dilatation and increased pulsation. Acute mitral insufficiency causes left-sided abnormalities analogous to the right-sided lesions of acute tricuspid insufficiency.~85-~9~The left atrium will be dilated and distended during ventricular systole. The left atrial ejection time is prolonged. The left ventricle is dilated and may demonstrate both a decreased ejection rate and a prolonged emptying time. When regurgitation is secondary to papillary muscle dysfunction segmental wall motion abnormalities are often seen along the anterior and lateral wails. Examination of the pulmonary blood pool activity may reveal redistribution or congestion. Acute aortic regurgitation usually results in left ventricular dilatation, tgt-193 However, the enlargement may not be remarkable since weeks to months are required for the development of severe left ventricular dilatation. The ventricle may show early diastolic distention. Emptying time is usually prolonged. The left atrial size varies with the degree of left ventricular failure. Pulmonary vascular changes also depend upon the severity of left ventricular dysfunction. Pericardial tamponade 194-m~ is characterized by enlargement of the pericardial/myocardial space (Fig. 5). The amount of pericardial fluid necessary to induce tamponade depends upon the time course over which it accumulates, since the pericardial sac is not acutely distensible. The normal pericardial sac contains less than 50 ml of

Fig. 9. Pseuodoanourysm of left ventricle. This 65-yr-old male presented with presistent ST-segment elevation following coronary a r t e r y bypass g r a f t i n g . Four frames of a lateral view radionuclide ventriculogram are shown. A large, well-defined dyskinetic segment is seen at the base of the posterior wall. Psouodoaneurysm was confirmed at surgery.

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fluid. Rapid accumulation of as little as 150-200 ml may cause full-blown tamponade. In contrast, slowly developing pericardial effusions of a liter or more may be tolerated without difficulty if the pericardium is given sufficient time to distend. Acute accumulation of pericardial fluid causes an increase in pericardial pressure, which, in turn causes a progressive rise in right atrial and right ventricular distolic pressures. Venous return to the right heart is reduced. In some cases, the obstruction to venous return from the superior vena cava may be obvious on the first-pass study. With rapid fluid accumulation, the cardiac chambers appear small in size. During diastole, their filling is restricted. In contrast, when fluid accumulates slowly, the chambers appear nearly normal in size and there may be little if any restriction to filling. In such cases, the overall motion of the heart is greatly exaggerated, producing the so-called "swinging h e a r t . ''2~176 Myocardial infarction produces signs of mechanical dysfunction proportional to the size, transmural distribution, and location of the infarct. Global ejection fraction is often reduced, particularly in anterior infarcts. Inferior and nontransmural infarcts may not cause significant left ventricular dysfunction. Right ventricular ejection fraction may be reduced because of left ventricular dysfunction or right ventricular infarction. Segmental wall motion abnormalities are the most accurate scintigraphic sign of acute infarction. The apex of the left ventricle is difficult to evaluate. There is considerable variation in normal apical wall motion. Aneurysm is usually easily identified; but it may be difficult to distinguish true aneurysm from pseudoaneurysm (Fig. 9). The shape of the aneurysm, the aperture

SIMON, PARKEY, AND LEWIS

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o f e n t r y into t h e d y s k i n e t i c s e g m e n t , and its l o c a t i o n a r e i m p o r t a n t clues. M y o c a r d i a l i s c h e m i a a n d i n f a r c t i o n m a y also b e s t u d i e d b y i n f a r c t - a v i d or p e r f u s i o n / m e t a b o l i s m i m a g i n g . S c i n t i g r a p h i c findings in t h e s e c a s e s h a v e b e e n discussed. It is i m p o r t a n t to

e v a l u a t e all p o r t i o n s of t h e i m a g e w i t h a n y of t h e s e e x a m i n a t i o n s . 99mTc-PPi s t u d i e s m a y r e v e a l u n s u s p e c t e d c h e s t w a l l o r s k e l e t a l injury. S i m i l a r l y , t h e p u l m o n a r y a c t i v i t y on a p e r f u s i o n s t u d y h e l p s to i d e n t i f y left v e n t r i c u l a r failure.

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