DOI:10.2214/AJR.04.1850
AJR 2006; 186:1116-1119
© American Roentgen Ray Society
Dependent Venous Contrast Pooling and Layering: A Sign of Imminent Cardiogenic Shock
Chris Roth1,
Michael Sneider1,
Naama Bogot1,
Michael Todd1 and
Paul Cronin1
1 All authors: Department of Radiology, University of Michigan Health Systems
and University of Michigan Hospitals, B1 132F Taubman Center, 1500 E Medical
Center Dr., TC 2910, Ann Arbor, MI 48109.
Received December 4, 2004;
accepted after revision February 21, 2005.
Address correspondence to P. Cronin.
Keywords: cardiogenic shock • cardiovascular imaging • contrast material
Introduction
Contrast-enhanced CT is widely used for assessment of a broad spectrum of
thoracic and abdominal conditions. Findings of sudden cardiac arrest during CT
examination have been reported
[1]. Lack of flow during a
fully arrested state causes pooling and layering of contrast material in the
major dependent areas of the venous system, such as the inferior vena cava
(IVC) and the major tributaries of the hepatic veins. We describe two cases of
dependent venous contrast pooling shown on CT as early indicators of imminent
circulatory failure and death.
Case Reports
The first patient, a 63-year-old man, underwent successful aortic root,
ascending aorta, and partial aortic arch replacement for an acute Stanford
type A aortic dissection. He presented to clinic 3 months postoperatively with
symptoms of weight loss, feeling increasingly ill, and dyspnea at rest and on
exertion. He had clinical signs of heart failure, including peripheral edema,
ascites, and bilateral pleural effusions.
CT aortography was performed. The aortic repair exhibited no evidence of a
contrast leak on arterial phase imaging. At this point, the aortic dissection
extended into the left common carotid artery origin and extended distally to
the level of the left common iliac artery. CT showed thickening of the
pericardium up to 10 mm, a tubular-appearing right ventricle, and a
straightened interventricular septum. There were marked abdominal ascites and
moderate bilateral pleural effusions. These findings were consistent with
constrictive pericarditis with elevated right heart pressure to the point of
near right heart failure (Figs.
1A,
1B,
1C, and
1D). Interestingly, this
chronic decompensation manifested as IV contrast layering dependently in the
superior vena cava (SVC) and right atrium. CT also showed a contrast-blood
interface and pooling in the multiple abdominal and pelvic veins, including
the IVC, dependent hepatic veins, right renal vein, lumbar veins, and iliac
veins.
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Fig. 1A —63-year-old man after type A aortic dissection repair. CT image at
level of left main pulmonary artery shows type A aortic dissection repair
(black asterisk), pericardial thickening and fluid (arrow),
a blood-contrast level within superior vena cava (arrowhead), and
bilateral pleural effusions (white asterisks).
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Fig. 1B —63-year-old man after type A aortic dissection repair. Note presence
of pericardial thickening (arrow), straightened interventricular
septum (arrowhead), and small right ventricle (black
asterisk).
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Fig. 1C —63-year-old man after type A aortic dissection repair. Dependent
venous pooling of contrast material in dependent hepatic veins
(arrows) and intrahepatic inferior vena cava (IVC) (black
asterisk).
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The patient was admitted to the general surgical floor that afternoon. Over
the evening, because of increasing respiratory distress, the patient was
intubated and transferred to the ICU. Emergent transesophageal
echocardiography revealed a dilated and noncontractile right atrium; a small,
poorly filled, and akinetic right ventricle; right ventricular pressure
overload; and a hypokinetic left ventricle. There was also thrombus beneath
the pericardium on the transesophageal echocardiogram. An ECG at that time did
not show ST segment changes, and troponin levels were normal. Because the
patient grew increasingly hypotensive and hypoxemic, he was taken to surgery
the following morning for an urgent pericardectomy. Very dense pericardial
tissue was evident on opening the chest cavity. Even after thick adhesions
were dissected from the epicardium, there was minimal right ventricular
function despite maximal inotropic support, and the patient died.
The second patient, an 87-year-old woman with a medical history significant
for hypertension, coronary artery disease, congestive heart failure, and
chronic obstructive pulmonary disease, presented to the emergency department
with acute onset of dyspnea and hypoxemia. Bedside chest radiography showed a
wide mediastinum, and subsequent emergent CT was performed to evaluate for
possible acute aortic dissection. Although CT showed a normal aorta, there was
striking reflux of contrast material into the IVC, hepatic and iliac veins,
and the dependently positioned right renal vein (Figs.
2A and
2B). In addition, findings
included dependent ground-glass opacities as a manifestation of pulmonary
congestion and left heart failure (not shown). ECG T wave changes were
compatible with anterolateral and inferior ischemia. An echocardiogram showed
severe left ventricular systolic dysfunction, an ejection fraction of 15%, and
an akinetic apex. Cardiac enzymes indicated acute myocardial infarction. The
patient died later that day.
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Fig. 2B —87-year-old woman with acute myocardial infarction and congestive
heart failure. Composite image of two CT series shows venous pooling and
layering of contrast material within superior vena cava, right atrium of
heart, inferior vena cava, and other dependent venous structures.
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Discussion
Contrast-enhanced CT findings of dependent venous contrast pooling and
hypostasis have been described in cases of patients having acute cardiac
arrest while undergoing CT [2]
and in postmortem scans [3].
The patients presented here are unique in that both patients were alive at the
time of scan, the dependent contrast pooling in the abdominal venous system
was a sign of cardiac failure, and dependent contrast layering was a sign of
imminent cardiogenic shock. Both patients died within 48 hr of the CT.
Reflux to the IVC and dilated hepatic veins are common manifestations of
right heart failure and tricuspid regurgitation. Even more so, passive hepatic
congestion with reticulated mosaic patterns on contrast-enhanced abdominal CT
has been well documented and is commonly seen as a sign of right heart failure
[4]. When cardiac function is
so poor, in cases with dependent venous pooling, blood cannot be propelled
against gravity.
In our series, contrast material refluxing retrogradely from an upper
extremity injection into the IVC and resulting in a dependent contrast-blood
level indicates even greater circulatory dysfunction than that of heart
failure and hepatic venous opacification typical of hepatic congestion and
indicates the development of cardiogenic shock.
Cardiogenic shock is a disorder of tissue hypoxia caused by decreased
systemic cardiac output despite adequate intravascular volume. The incidence
of cardiogenic shock has remained relatively constant during the last 20 years
at approximately 7% [5]. The
hospital mortality rate for patients with cardiogenic shock is between 55% and
70% [5]. Our cases illustrate
that very different conditions—severe right heart dysfunction and severe
left heart dysfunction—can manifest similarly as dependent venous
contrast pooling in cases of grossly insufficient cardiac output. Treatments
of such compromised cardiac output are largely dependent on the mechanism
causing heart failure and must be instituted quickly to restore adequate
cardiac output.
Constrictive pericarditis and ischemic cardiomyopathy are two common causes
of diminished cardiac output
[6]. Constrictive pericarditis
is an infrequent complication of cardiac surgery
[7] and is notoriously
difficult to diagnose because of its largely nonspecific signs and symptoms of
fatigue, dyspnea, sensation of abdominal fullness, and increased abdominal
girth [7,
8]. Thickened pericardium on CT
is a sensitive indicator of constrictive pericarditis, with the upper limit of
normal pericardial thickness being 2 mm
[7]. Dense adhesions and
stiffness of the pericardium limit diastolic compliance, which manifests as
diminished cardiac output with venous engorgement and stasis.
Ischemic cardiomyopathy and myocardial infarction distort the proper
myocardial contraction sequence and motion, resulting in dangerously low
cardiac output [5]. Cardiogenic
shock after myocardial infarction occurs in approximately 7% of infarct
patients [5]. Because
revascularization is associated with better outcomes than intensive medical
therapy in patients with shock, early angioplasty or coronary bypass graft
surgery may be lifesaving in patients presenting with dependent venous
contrast pooling [5].
In summary, the findings of dependent venous pooling of contrast material
and contrast-blood levels seen on contrast-enhanced CT carry a grave prognosis
for the patient. This condition can be seen after serious myocardial
infarction and in cases of severe diastolic dysfunction secondary to
constrictive pericarditis. The managing physicians should be notified quickly
to institute quick definitive therapy when these CT findings are present
because they indicate cardiac failure and imminent severe cardiogenic
shock.
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Introduction
Case Reports
