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Findings in this case: 1) There is calcification in the pericardium. 2) The entire inferior vena cava is not demonstrated however there is dilatation of the visualized portions of the inferior vena cava which is definitely significantly larger than the visualized descending aorta. 3) Apical LEFT ventricular aneurysm. 4) Minimal ascites visualized around the anterior margin of the liver. Visualized portions of the LEFT lobe of the liver are enlarged.
Diagnosis: Calcified pericarditis in this case secondary to histoplasmosis. Evidence suggesting constrictive pericarditis with enlarged inferior vena cava. Apical LEFT ventricular aneurysm. Enlarged liver of uncertain etiology.
File: 1 B.
Organ system: 1. Cardiovascular system.
Organ: B. Pericardium.
Information:
Etiology and incidence: 1) The causes of pericardial calcification include; a) Infectious and/or inflammatory processes, postsurgical changes, previous trauma, prior myocardial infarction and nonspecific/idiopathic cases. 2) Infectious causes of pericardial calcification include tuberculosis, fungal, viral and bacterial etiologies.
Diagnosis: 1) Clinical; a) Pericardial calcification by itself is asymptomatic; b) Symptoms are secondary to any associated processes including constrictive pericarditis; c) More than half of patients with calcified pericardium will have evidence of constrictive pericarditis; d) Clinical differential diagnosis includes restrictive cardiomyopathy. 2) Radiology; a) Pericardial thickness is normally less than 2 mm. Calcification is not considered a normal finding; b) The inferior vena cava: Aortic ratio is typically <2 with a normal range of 0.5 – 1.3; c) Small degrees of pericardial effusion are difficult to differentiate from pericardial thickening. Pericardial thickening/effusion of greater than 4 mm is considered potentially significant; d) CT without contrast is sensitive for evaluating the pericardial thickness and for calcification. Contrast enhanced CT may demonstrate enhancement of the pericardium encases of inflammation/infection; d) MRI without contrast may be helpful in determining effusion versus hemorrhage. MRI with contrast is more sensitive than CT for evaluating inflammatory changes.
Prognosis/treatment: 1) As noted above, more than half of patients with pericardial calcification will have constrictive pericarditis. 2) Treatment; a) Surgical removal/trapping of the pericardium may be necessary. There is no effective medical therapy. Mortality rate is between 5 and 10%.
Figure 1. This patient has constrictive pericarditis. The open arrow is the inferior vena cava, the solid arrow is the aorta. There is a significantly increased IVC/aortic ratio. The differential diagnosis includes inflow obstruction (including constrictive pericarditis and cardiac tamponade). An abnormal ratio can also be seen in patients secondary to volume status – hypervolemia. In young patients with enthusiastic breath holding during a CT scan, there can be artifactual significant increases in the inferior vena caval size.
References:
Sonographic inferior vena cava/aorta diameter index, a new approach to the body fluid status assessment in children and young adults in emergency ultrasound–preliminary study.
Am J Emerg Med. 2008 Mar;26(3):320-5.
Kosiak W, Swieton D, Piskunowicz M.
Pediatric Nephrology Department, Medical University of Gdansk, 80-952 Gdansk, Poland.
Abstract
Body fluid status is one of the most important parameters estimated during every clinical examination. In many disorders, the therapy and its effectiveness depend on appropriate evaluation of body water status. There are some useful methods of evaluating body fluid incontinence; however, all of them are burdened with some limitations, especially when used in the emergency department. We introduce a new sonographic parameter, the “inferior vena cava (IVC)/aorta (Ao) diameter (IVC/Ao) index,” as a convenient, quick, and effective way of evaluating body fluid status. The usefulness of the sonographic assessment of IVC diameter has already been proven in children with nephrotic syndrome, in hemodialysis patients, and in patients hospitalized in intensive care units. However, this method is limited by the necessity of comparing IVC diameter to body surface, measuring IVC diameter during maximal inspiration and expiration, or lack of reference values for the pediatric population, which can be eliminated in our new method of body fluid status assessment.
Imaging of the Inferior Vena Cava with MDCT
Sheila Sheth1 and Elliot K. Fishman
http://www.ajronline.org/cgi/content/full/189/5/1243
Abstract
OBJECTIVE. The purpose of this pictorial essay is to illustrate the role of MDCT in the diagnosis of disease processes affecting the inferior vena cava (IVC).
CONCLUSION. High-speed MDCT has the potential to replace traditional imaging techniques in the evaluation of pathologic processes involving the IVC. The ability to acquire near-isotropic data allows high-quality reconstructions in the sagittal and coronal planes and thus overcomes one of the major limitations of CT in evaluating the IVC.
Pseudopancreatitis in Trauma Patients
http://www.ajronline.org/cgi/content/full/193/3/W193
Abstract
OBJECTIVE. The purpose of our study was to review the significance of intra- and peripancreatic fluid in trauma patients who have no other signs of pancreatic injury.
CONCLUSION. We propose that intra- and peripancreatic fluid may be the consequence of hypovolemic shock treated with hyperhydration when there is significant delay between injury and imaging.
IVC/Aorta ratio for normal nontrauma patients of 0.5–1.3 (mean, 0.86).
Periportal low density on CT in patients with blunt trauma: association with elevated venous pressure
K Shanmuganathan, SE Mirvis and M Amoroso
http://www.ajronline.org/cgi/content/abstract/160/2/279?ijkey=ab60182688d7f9063959cd5ecb7291a61ab4cbd7&keytype2=tf_ipsecsha
OBJECTIVE. We postulated that the CT finding of periportal low density after acute blunt trauma of the abdomen or pelvis results from elevated central venous pressure caused by rapid expansion of intravascular volume during IV resuscitation or by other trauma-related pathologic changes.
MATERIALS AND METHODS. CT scans and medical records of 58 patients, including 42 with CT evidence of hepatic injury and 16 with periportal low density without CT evidence of hepatic injury, were reviewed retrospectively to determine the extent of liver injury, the extent of periportal low density, and the ratio of the transverse diameter of the inferior vena cava to the transverse diameter of the aorta at the level of the right adrenal gland. The ratio, which served as an indirect measure of central venous pressure, was also measured in 20 randomly selected nontrauma patients with normal findings on abdominal CT scans.
RESULTS. The ratios in 29 patients with CT evidence of liver injury without periportal low density were 0.6-2.0 (mean, 1.22), the ratios in 13 patients with diffuse (six) or focal (seven) periportal low density were 0.8-1.6 (mean, 1.31), and the ratios in 16 patients with periportal low density but no evidence of liver injury were 1.1-2.5 (mean, 1.36). The ratios were not statistically different among these three groups of patients. The ratios were 0.5-1.3 (mean, 0.86) for the 20 nontrauma control patients and were significantly lower than those in the trauma patients (p < or = .05). In all patients with periportal low density, the inferior vena cava remained distended at multiple levels through the abdomen without the variation in size expected from respiration, whereas a change in diameter was always observed on sequential CT sections in the nontrauma group. Among the 16 patients with periportal low density but no hepatic injury, a likely cause for elevated central venous pressure, excluding IV volume expansion, was observed in three.
CONCLUSION. The CT finding of periportal low density after blunt abdominal trauma indicates acute elevation of central venous pressure and does not by itself signify hepatic parenchymal injury, as has been previously reported.
Imaging Findings in Cardiac Tamponade with Emphasis on CT1
http://radiographics.rsna.org/content/27/6/1595.full
C. Santiago Restrepo, MD,Diego F. Lemos, MD,Julio A. Lemos, MD,Enrique Velasquez, MD,Lisa Diethelm, MD,Ty A. Ovella, MD,Santiago Martinez, MD,Jorge Carrillo, MD,Rogelio Moncada, MD andJeffrey S. Klein, MD
Abstract
Cardiac tamponade is a life-threatening condition that results from slow or rapid heart compression secondary to accumulation of fluid, pus, blood, gas, or tissue within the pericardial cavity. This condition can be associated with multiple causes including trauma, inflammation, scarring, or neoplastic involvement of the pericardial space among others. The main pathophysiologic event leading to tamponade is an increase in intrapericardial pressure sufficient to compress the heart with resultant hemodynamic impairment, which leads to limited cardiac inflow, decreased stroke volume, and reduced blood pressure. These events result in diminished cardiac output, which manifests clinically as a distinctive form of cardiogenic shock. Although cardiac tamponade is a clinical diagnosis, imaging studies play an important role in assessment and possible therapeutic intervention. Computed tomographic (CT) findings associated with cardiac tamponade include pericardial effusion, usually large, with distention of the superior and inferior venae cavae; reflux of contrast material into the azygos vein and inferior vena cava; deformity and compression of the cardiac chambers and other intrapericardial structures; and angulation or bowing of the interventricular septum. Familiarity with the clinical and pathophysiologic features of cardiac tamponade and correlation with the associated CT findings are essential for early and accurate diagnosis.
