Thursday, September 30, 2010

Axillary Segment of the Right Upper Lobe

In some patients, an extra bronchus (the axillary bronchus) supplies the lateral aspect of the right upper lobe. The axillary bronchus may be subsegmental (most common) or segmental. A segmental axillary bronchus most commonly arises adjacent to the posterior bronchus.

Aspirtation in the right lateral decubitus position can preferentially involve the axillary segment.

An axillary segment can also be present on the left.


  • Ribaudo CA, Grace WJ. Pulmonary aspiration. Am J Med. 1971 Apr;50(4):510-20.
  • Slowinski J, Bloom S, Oates E. The diseased axillary segment of the lung: characteristic radiographic and scintigraphic appearance. AJR Am J Roentgenol. 1992 Oct;159(4):899-900.
  • Wu JW, White CS, Meyer CA, Haramati LB, Mason AC. Variant bronchial anatomy: CT appearance and classification. AJR Am J Roentgenol. 1999 Mar;172(3):741-4.

Wednesday, September 29, 2010

Perilunate Dislocation

A perilunate dislocation is the second stage of ligamentous injury around the lunate. It occurs at the midcarpal row, with dorsal dislocation of the capitate from the lunate and concordant dorsal translation of the rest of the carpus. The lunate stays where it is, articulating with radius.

Perilunate dislocations are the most frequent carpal dislocation and represent the least severe of the ligamentous injuries around the lunate. When purely ligamentous, they are referred to as lesser arc injuries. When associated with a fracture of one or more bones around the lunate, they are referred to as greater arc injuries (twice as common as lesser arc injuries).

Greater arc injuries have a special naming convention. The bone with the fracture gets a "trans-" prefix, followed by "perilunate dislocation." For example, a perilunate dislocation associated with a scaphoid fracture (the most common associated fracture) is referred to as a transscaphoid perilunate dislocation.

Fractures of the other perilunate carpal bones (trapezium, capitate, hamate, or triquetrum) are less common. Combination fractures can also occur. One such combination fracture is the scaphocapitate fracture, a transverse fracture through the scaphoid waist and capitate, where the proximal capitate fragment ends up perpendicular to the distal fragment and the long axis of the radius with its articular surface towards the palm.

On radiographs, look for disruption of the carpal arcs; triangular or pie-slice appearance of the lunate (indicating volar rotation of the lunate); fractures of the carpal bones around the lunate; and the David Letterman sign, indicating widening of the scapholunate interval.

The lateral projection is the most helpful when positive and may show dorsal translocation of the capitate and the rest of the carpus in relation to the lunate. The lunate should keep its articulation with the radius.

The images show lateral, oblique, and frontal radiographs of a perilunate dislocation. The green arrow shows the David Letterman sign. A small avulsion fragment seen on CT in the lunotriquetral space (blue arrow) was not appreciated on the radiographs.


Tuesday, September 28, 2010

Partial Anomalous Pulmonary Venous Return

Partial anomalous pulmonary venous return (PAPVR) has an overall incidence of less than 1% and occurs more frequently on the right. On the right, drainage can be into the superior or inferior vena cava, azygos vein, right atrium, or coronary sinus. The most common pattern on the right is a clinically insignificant anomalous drainage of the right upper lobe into the superior vena cava. If you see this type of drainage, however, it is important to look for a sinus venosus type of atrial septal defect, which is commonly associated with partial anomalous pulmonary venous return.

The scimitar syndrome is a special case of PAPVR, where there is right-sided drainage into veins below the diaphragm (e.g., inferior vena cava or portal or hepatic veins) associated with right lung hypoplasia. Other associated anomalies include an atrial septal defect, systemic blood supply to the lung, extralobar sequestration, horseshoe lung, pulmonary arteriovenous malformation, and various forms of congenital heart disease. The appearance has been described ad nauseum in multiple sources and will not be repeated here.

The pseudoscimitar syndrome has a similar radiographic appearance, but has anomalous drainage into the left atrium rather than the inferior vena cava.

On the left, anomalous drainage is also most frequent in the upper lobe, where drainage is into a vertical vein lateral to the aortic arch that joins the left brachiocephalic vein. The main differential consideration on CT for this pattern is a left-sided superior vena cava, which can mimic the vertical vein on slices above the aortic arch. The two can be differentiated below the left main bronchus, where a single vessel (left superior pulmonary vein) is normally found anterior to the left main bronchus. In patients with the anomalous left upper lobe drainage, the left superior pulmonary vein is absent, so no vessel is seen anterior to the left main bronchus. In patients with a left-sided superior vena cava, both the left superior pulmonary vein and the left superior vena cava are found anterior to the left main bronchus.

The case shown here reveals anomalous venous drainage (red) of the medial basal segment of the right lower lobe into the azygos vein (blue). As shown here, all PAPVRs are left-to-right shunts, but most are not hemodynamically significant.


Demos TC, Posniak HV, Pierce KL, Olson MC, Muscato M. Venous anomalies of the thorax. AJR Am J Roentgenol. 2004 May;182(5):1139-50.

Monday, September 27, 2010

Exogenous and Endogenous Lipoid Pneumonia

Lipoid pneumonia can be classified as either exogenous or endogenous based on the source of the lipid.

Exogenous lipoid pneumonia occurs with aspiration or inhalation of oils. The classic clinical scenario is one of prolonged laxative ingestion or use of oil-based nose drops. Less common causes include accidental aspiration in children, ingestion in fire eaters, and chronic use of lubricants such as vaporub and lip gloss. Chronic inhalation of oils can also occur in certain occupations, such as those involved in the lubrication and cleaning of machinery and the spraying of pesticides or paints.

Endogenous lipoid pneumonia (cholesterol pneumonia, golden pneumonia), is classically caused by obstruction, resulting in consolidation with accumulation of lipid-filled macrophages and eosinophilic proteinaceous material (e.g., surfactant) from degenerating cells.

Non-obstructive processes may also result in endogenous lipoid pneumonia. These include fungal infections, pulmonary alveolar proteinosis, and lipid-storage disorders (e.g., Niemann-Pick disease).


Betancourt SL, Martinez-Jimenez S, Rossi SE, Truong MT, Carrillo J, Erasmus JJ. Lipoid pneumonia: spectrum of clinical and radiologic manifestations. AJR Am J Roentgenol. 2010 Jan;194(1):103-9.

Sunday, September 26, 2010

Normal Limits for Thoracic Lymph Nodes

Upper paratracheal
7 mm
7 mm
Lower paratracheal
10 mm
10 mm
10 mm
7 mm
AP window
9 mm
7 mm
All numbers are short-axis dimensions.


Glazer GM, Gross BH, Quint LE, Francis IR, Bookstein FL, Orringer MB. Normal mediastinal lymph nodes: number and size according to American Thoracic Society mapping. AJR Am J Roentgenol. 1985 Feb;144(2):261-5.

Saturday, September 25, 2010

Echogenic Renal Cortex in Children

In neonates and infants, the renal parenchyma may have increased echogenicity as a normal finding. In older children and adults, the normal renal cortex should be less echogenic than the liver. Causes of abnormally increased renal cortical echogenicity include:
  • Renal dysplasia: Small kidneys
  • Chronic renal failure: Small kidneys

  • AIDS: Normal-sized kidneys

  • Nephrotic syndrome: Normal to large kidneys
  • Acute glomerulonephritis: Normal to large kidneys (case shown above in a 7-year-old patient with enlarged hyperechoic kidneys).
  • Hemolytic uremic syndrome: Normal to large kidneys
  • Lymphoma: Normal to large kidneys
  • Acute pyelonephritis: Normal to large kidneys
  • Sickle cell anemia: Normal to large kidneys

  • Glycogen storage disease: Large kidneys
  • Polycystic kidney disease: Large kidneys


Friday, September 24, 2010

Aberrant vs. Lateralized Internal Carotid Artery

An aberrant internal carotid artery (ICA) is thought to be caused by regression of the cervical (C1) ICA during embryogenesis resulting in an absent vertical petrous (C2) segment and aplasia of the ascending carotid canal.

Blood then takes an aberrant course to get from the common carotid artery to the horizontal petrous (C2) segment of the ICA. The inferior tympanic artery and the hyoid/caroticotympanic arteries are involved in this process (see Lo et al below for a great diagram). The inferior tympanic artery normally arises from the ascending pharyngeal artery (branch of the proximal external carotid artery), travels through the inferior tympanic canaliculus, and anastomoses with the caroticotympanic artery (a remnant of the embryologic hyoid artery). In patients with an aberrant ICA, the inferior tympanic artery and inferior tympanic canaliculus enlarge. Blood is redirected through the hyoid artery into the horizontal petrous segment of the ICA. This aberrant course gives rise to the "7" or reversed "7" appearance seen on angiography.

A lateralized (also known as laterally displaced and dehiscent) ICA, on the other hand, has a normal course but a focally dehiscent lateral wall of the carotid canal (pink arrows compared to the normal side indicated by the blue arrow), usually near the basal turn of the cochlea. In contrast to patients with an aberrant ICA, the vertical carotid canal is present and the inferior tympanic canaliculus is not enlarged. The genu of the petrous segment lies more laterally and posteriorly.


Thursday, September 23, 2010

Peripheral Distribution of Pulmonary Opacities

The reverse bat wing or reverse butterfly pattern of pulmonary opacities can be seen with:
  • Acute respiratory distress syndrome:
  • Lung contusion:
  • Cryptogenic organizing pneumonia:
  • Simple pulmonary eosinophilia: Loeffler syndrome. Migratory peripheral ground-glass opacity or airspace consolidation involving mainly the middle and upper lung zones. Single or multiple airspace nodules with surrounding ground-glass opacity can also be seen.
  • Chronic eosinophilic pneumonia (shown above): Classic radiographic finding is nonsegmental peripheral airspace consolidation involving mainly the upper lobes.
  • Pneumonia:
  • Pulmonary infarction:
  • Sarcoidosis: Pulmonary nodules and masses when seen in sarcoidosis (15%–25% of patients with parenchymal opacities) are ill-defined and irregular and represent coalescent interstitial granulomas. They may be located in perihilar or peripheral regions. Small satellite nodules can be seen around them ("galaxy sign", nonspecific).
  • Vasculitides:


Wednesday, September 22, 2010

Glenolabral Articular Disruption (GLAD)

A glenolabral articular disruption (GLAD) lesion is a nondisplaced superficial tear of the anterior-inferior labrum that is accompanied by injury to the adjacent articular cartilage. The articular cartilage injury may range from fibrillation to a depressed osteochondral defect.

A GLAD lesion is thought to result from a forced adduction of the shoulder with the arm in abduction and external rotation.


  • Steinbach LS. Chapter 5. In Chung CB and Steinbach LS. MRI of the Upper Extremity: Shoulder, Elbow, Wrist, and Hand. Lippincott Williams & Wilkins. 2010. p 293.
  • Sanders TG, Tirman PF, Linares R, Feller JF, Richardson R. The glenolabral articular disruption lesion: MR arthrography with arthroscopic correlation. AJR Am J Roentgenol. 1999 Jan;172(1):171-5.

Tuesday, September 21, 2010

Pectoralis Major Tear

The pectoralis major is a fan-shaped muscle with two heads. The clavicular head originates at the medial two thirds of the clavicle, while the larger stenral head originates at the anterior manubrium, sternum, and the cartilage of the first 6 ribs. The two heads insert at the lateral lip of the bicipital groove of the humerus.

Tears of the pectoralis major muscle can occur in the muscle (usually due to direct trauma), at the myotendinous junction (most common), or at the tendinous insertion. Tears are classically seen in weightlifters.

Partial tears are more common and tend to occur at the myotendinous junction. Complete tears, on the other hand, tend to occur at the tendon-bone interface. Sternal head tears are more common, but clavicular head tears occur as frequently as sternal head tears in elderly patients.

Here we see a large partial tear of the myotendinous junction of the sternal head of the pectoralis major muscle on fluid-sensitive sequences (from top to bottom: axial, sagittal, and coronal).


Connell DA, Potter HG, Sherman MF, Wickiewicz TL. Injuries of the pectoralis major muscle: evaluation with MR imaging. Radiology. 1999 Mar;210(3):785-91.

Monday, September 20, 2010

Achilles Tendon Rupture: Radiography

Radiographic findings in achilles tendon rupture include:
  • Obscuration of the tendon: Bleeding, edema and loss of the tendon cause obscuration of the anterior margin on the Achilles tendon on the lateral view.
  • Posterior encroachment on the Kager fat pad: Blood and edema encroach on the Kager fat pad. The fat pad is narrowed by edema,
  • Skin indentation at the rupture site: Not a great example here, but a small dimple (white arrow) can be seen at the rupture site. Usually obscured by swelling and hemorrhage.
  • Soft-tissue mass at the tendon ends: The ends of the ruptured tendon retract and coil, resulting in swelling at the tendon ends. Look for the tendon rupture site in the zone of relative avascularity 2–6 cm from the calcaneal insertion.
  • Identification of the severed ends: When widely separated, the tendon ends may be visualized. The proximal end is usually obscured by swelling and hemorrhage, but the distal end can be separated from the surrounding fat in 50% of cases.


Reveno PM, Kittleson AC. Spontaneous Achilles' tendon rupture. Radiology. 1969 Dec;93(6):1341-4.

Sunday, September 19, 2010

Myocardial Uptake on Bone Scan

Myocardial uptake on nuclear medicine bone scan can be seen in the following conditions:
  • Long-standing congestive heart failure:
  • Myocardial infarction: Focal localization to calcium hydroxyapatite from local tissue necrosis or damage.
  • Unstable angina: Patchy uptake is seen.
  • Pericarditis:
  • Amyloidosis: Abnormal extracellular deposition of protein. Important to note because cardiac involvement indicates a worse prognosis. 99mTc phosphate binds to calcium-binding sites of amyloid.
  • Hyperparathyroidism:
  • Postresuscitation/cardiac contusion:
  • Post defibrillation:
  • Cardiomyopathy: Diffuse uptake.
  • Pericardial tumor: Diffuse uptake.


  • Fard-Esfehani A, Assadi M. Myocardial Tc-99m MDP Uptake on the Bone Scintigraphy in the Hemodialysis-Associated Amyliodosis (an incidental finding). Alasbimn Journal. 2005; 8(30): AJ30-7.
  • Gentili A, Miron SD, Bellon EM. Nonosseous accumulation of bone-seeking radiopharmaceuticals. Radiographics. 1990 Sep;10(5):871-81.
  • Janowitz WR, Serafini AD. Intense myocardial uptake of 99mTc-diphosphonate in a uremic patient with secondary hyperparathyroidism and pericarditis: case report. J Nucl Med. 1976 Oct;17(10):896-8.
  • Kida T, Hujita Y, Sasaki M, Inoue J. Myocardial and vascular uptake of a bone tracer associated with secondary hyperparathyroidism. Eur J Nucl Med. 1986;12(3):151-4.
  • Love C, Din AS, Tomas MB, Kalapparambath TP, Palestro CJ. Radionuclide bone imaging: an illustrative review. Radiographics. 2003 Mar-Apr;23(2):341-58.

Saturday, September 18, 2010

Acute Disseminated Encephalomyelitis

Acute disseminated encephalomyelitis (ADEM) is an uncommon demyelinating disease of the central nervous system. It is an immune-mediated inflammatory process that may occur after a viral infection or vaccination, in association with rheumatic fever, or without a recognized trigger.

CT and MR findings are nonspecific and the differential should include infectious and other demyelinating conditions. There are multiple lesions in the white matter and basal ganglia with or without spinal cord involvement. The gray matter may also be involved.

MRI will show bilateral, asymmetric foci of increased signal on T2 and FLAIR sequences, predominantly involving the gray-white interface and sparing of the periventricular white matter (in contrast to multiple sclerosis). The lesions demonstrate variable restricted diffusion in acute lesions. ADC maps will reveal increased signal. However, unlike multiple sclerosis, the normal-appearing white matter will demonstrate normal ADC values. The lesions may have punctate, ring/incomplete ring, or peripheral enhancement. There may also be enhancement of the cranial nerves.

Differential considerations, as alluded to above, include:
  • Infection: Ring enhancement may be similar.
  • Multiple sclerosis: May have identical imaging features, so repeat MR is needed to differentiate ADEM (monophasic) from multiple scelrosis. Multiple scelrosis does have a tendency to involve the periventricular white matter and has lesions that are often more symmetric in distribution.
  • Autoimmune-mediated vasculitis
  • Fabry disease: Scattered non-enhancing white matter lesions in patients with renal failure or heart disease.
  • Behçet: Tendency to involve the midbrain. Lesions show nodular enhancement in acute phase.


Friday, September 17, 2010

Posterior Fossa Ependymoma

The differential diagnosis of posterior fossa masses in children essentially comes down to medulloblastoma, astrocytoma (e.g., brainstem "glioma" and pilocytic astrocytoma), and ependymoma. Posterior fossa ependymomas are most commonly associated with the fourth ventricle and may extend out of the foramina of Luschka and Magendie.

CT may show an iso or hypoatyenuating mass. Compared to other posterior fossa masses in children, ependymomas have a greater tendency for calcification, which is usually punctate. Cysts are present in a minority of cases and are usually small. There is mild contrast enhancement

On MRI, ependymomas are T1-hypointense (upper left image) and intermediate intensity on T2 (upper right image) with foci of hypointensity due to calcifications or hemorrhage (GRE: bottom left image). There may be extension of the lesion out of the foramina of Luschka (post-contrast axial: bottom right image) and Magendie.


Neuroradiology Requisites (2nd ed). pp 127-128.

Thursday, September 16, 2010

Perisylvian Polymicrogyria Syndrome

Perisylvian polymicrogyria syndrome is the most commonly described polymicrogyria syndrome. Like other forms of polymicrogyria, it is characterized histologically by an abnormal 4-layer cortex. On the gross level, there are multiple small, partly fused gyri separated by shallow sulci in a perisylvian and perirolandic distribution with exposure of the insula. These findings are symmetric in 80% of cases. In addition, there is increased cortical thickness and irregularity of the gray-white matter junction.

Inheritance may be autosomal dominant, autosomal recessive, or X-linked. Patients may have pseudobulbar signs, cognitive impairment, epilepsy, arthrogryposis and/or lower motor neuron disease.


  • Chang B, Walsh CA, Apse K, Bodell A. Polymicrogyria Overview. In: Pagon RA, Bird TC, Dolan CR, Stephens K, editors. GeneReviews [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2005 Apr 18 [updated 2007 Aug 6].
  • Kuzniecky R, Andermann F. The congenital bilateral perisylvian syndrome: imaging findings in a multicenter study. CBPS Study Group. AJNR Am J Neuroradiol. 1994 Jan;15(1):139-44.
  • Sztriha L, Guerrini R, Harding B, Stewart F, Chelloug N, Johansen JG. Clinical, MRI, and pathological features of polymicrogyria in chromosome 22q11 deletion syndrome. Am J Med Genet A. 2004 Jun 15;127A(3):313-7.

Wednesday, September 15, 2010

Celiac Disease

Celiac disease is a helper T cell-mediated enteropathy that is triggered by dietary gluten in susceptible individuals (1% of the population). Gluten is the alcohol-soluble protein component of cereals, such as wheat, rye, and barley. Pathologically, there is villous atrophy and crypt hyperplasia in the small bowel.

Most patients respond to a gluten-free diet; however, some patients may be classified as having refractory celiac disease if they continue to have severe symptomatic enteritis that does not respond to at least 6 months of a strict gluten-free diet. Patients with refractory celiac disease are at a higher risk of developing complications (see below).

Refractory celiac disease can be classified as type 1 and type 2. Patients with type 1 refractory celiac disease have a normal intraepithelial lymphocyte phenotype, while those with type 2 have clonal expansion of aberrant intraepithelial lymphocyte populations and are at increased risk for developing lymphoma (enteropathy-associated T-cell lymphoma). Because of this risk of neoplasm (both lymphoma and carcinoma), abdominal pain in patients with celiac disease should increase suspicion of malignancy.

Small bowel series and CT enteroclysis may reveal:
  • Reversed jejunoileal fold pattern: Loss of jejunal folds with a compensatory increase in ileal folds (the reverse of the normal pattern). This is the single most reliable sign for the diagnosis of celiac disease.
  • Early flocculation: Barium droplets falling out of suspension due to increased secretions. Seen in other malabsorption syndromes. May obscure more specific features of celiac disease.
  • Malabsorption: Dilution of contrast in the small bowel.
  • Bowel dilatation: Jejunal dilatation > 4 cm; ileal dilatation gt; >3 cm.
  • Delayed transit: Small bowel transit time is normally between 45 minutes and 90 minutes, but is significantly delayed in patients with celiac disease.
  • Transient intussusception: Non obstructive and transient.
Conventional CT may reveal engorgement of mesenteric vessels and mesenteric adenopathy, the latter of which is more frequently seen in patients with refractory type 2 celiac disease and in patients with enteropathy-associated T-cell lymphoma. Conventional CT is also better at defining dilated loops of bowel than CT enteroclysis. Another suggestive finding is intramural fat deposition in the submucosal layers of the duodenum and jejunum.

Imaging is invaluable in defining the complications of this systemic disease, including:
  • Small bowel intussusception: Rarely symptomatic
  • Ulcerative jejunoileitis: Multiple benign ulcers of variable depth, predominantly involving the jejunum, but can also involve the colon. Occurs most commonly in patients with type 2 refractory celiac disease. On small-bowel series we may see focal constrictions, a spiculated pattern, or alternating areas of narrowing and dilatation. The clinical presentation may be similar to those of celiac disease complicated by a malignant neoplasm.
  • Pneumatosis intestinalis: May reflect dissection of intraluminal gas into the inflamed small-bowel wall without accompanying intraabdominal abnormalities such as ischemic bowel or perforation. Pneumoperitoneum due to subserosal rupture of bubbles may also be seen and should not cause additional concern for rupture or ischemic bowel in isolation from clinical findings.
  • Lymphoma: The most common malignant disease complicating celiac disease. This is mostly of T-cell in origin, but B-cell lymphoma of the gastrointestinal tract and extraintestinal lymphoma can also be seen. Typical imaging features include circumferential ulcers with short strictures in the proximal small bowel. Other imaging findings may include a nodular appearance to the bowel, an exophytic mass, or an aneurysmal pattern (cavitary dilatation of the small-bowel lumen and annular wall thickening). Clinically patients may present with abdominal pain and diarrhea despite strict adherence to a gluten-free diet; or bowel perforation, obstruction, and hemorrhage. Lymphoma may also predate clinical recognition of celiac disease.
  • Cavitating lymphadenopathy syndrome: Rare complication of celiac disease characterized by cystic changes in mesenteric lymph nodes. On CT, there are cystic mesenteric masses with central low attenuation (fluid or fat) and thin, enhancing rims. Fat-fluid levels, if present, are unique to cavitating lymphadenopathy syndrome. Otherwise, differential considerations for low-attenuation mesenteric masses includes: Mycobacterial infection, Whipple disease, lymphoma, and necrotic metastases (e.g., germ cell tumors).
  • Carcinoma: Patients with celiac disease are more susceptible to developing carcinoma of the pharynx, esophagus, duodenum, jejunum, and rectum.
  • Hyposplenism: Splenic atrophy is found in up to 50% of adult patients with celiac disease and correlates with the severity of disease.
  • Thrombocytosis:
  • Thrombocytopenia:
  • Venous thromboembolism: Characteristically involving the portal or hepatic veins.
  • Leukopenia:
  • Immunoglobulin A deficiency:
  • Lane-Hamilton syndrome: Idiopathic pulmonary hemosiderosis in association with celiac disease.
  • Hepatic disease: Most commonly steatosis, causing laboratory abnormalities. Nodular regenerative hyperplasia may also be seen.
  • Biliary disease: Possible association with primary biliary cirrhosis.


Tuesday, September 14, 2010

Prominent Calcaneal Trabeculation

A prominent calcaneal trabeculation can appear as a sclerotic line along the inferior aspect of the calcaneus on the lateral view. It is a common normal variant that may simulate a stress fracture.


Keats TE and Anderson MW. Atlas of Normal Roentgen Variants That May Simulate Disease. 8th edition, page 886; Mosby (2004).

Monday, September 13, 2010

Subperiosteal Orbital Hemorrhage

Subperiosteal orbital hemorrhage is an uncommon condition that may be caused by direct trauma or various behaviors that result in increased venous pressure, such as the Valsalva maneuver. Its name describes the pathology and suggests the imaging findings.

CT and MRI will show a well-defined blood collection in the orbit, usually superiorly, that displaces the conal fat and extra-ocular muscles. Differential considerations include metastasis, lymphoma, or orbital pseudotumor.


Crawford SD, Patel MR. Bilateral supraorbital masses after prolonged headlock injury: an unusual manifestation of orbital subperiosteal hematomas. AJR Am J Roentgenol. 2005 Mar;184(3 Suppl):S2-3.

Sunday, September 12, 2010

Endocardial Fibroelastosis

Endocardial fibroelastosis is a rare condition that results in diffuse thickening of the ventricular endocardium and presents as unexplained heart failure in infants and children.

It can be divided into primary and secondary forms. Primary endocardial fibroelastosis is not associated with any significant structural cardiac abnormality, while secondary endocardial fibroelastosis is associated with congenital cardiac abnormalities, most commonly hypoplastic left heart syndrome and aortic stenosis.

Echocardiography may show echogenic endocardial surface and a spherical shape to the left ventricle, but this appearance has a weak correlation with endocardial fibroelastosis on histology. Perfusion MRI shows a hypointense layer at the endocardial surface that corresponds to an area of delayed enhancement.


  • Stranzinger E, Ensing GJ, Hernandez RJ. MR findings of endocardial fibroelastosis in children. Pediatr Radiol. 2008 Mar;38(3):292-6.
  • Tworetzky W, del Nido PJ, Powell AJ, Marshall AC, Lock JE, Geva T. Usefulness of magnetic resonance imaging of left ventricular endocardial fibroelastosis in infants after fetal intervention for aortic valve stenosis. Am J Cardiol. 2005 Dec 1;96(11):1568-70.

Saturday, September 11, 2010

Mesenteric Calcifications

  • Calcified lymph nodes: Treated lymphoma, infection (tuberculosis, fungal), sarcoidosis
  • Pancreatic saponification:
  • Mucinous metastases: From ovarian or gastrointestinal neoplasms
  • Carcinoid tumor: Single mass with significant desmoplastic reaction causing tethering of adjacent loops of small bowel toward the mass
  • Calcified metastatic implants: Ovarian carcinoma, mucinous colon carcinoma, or gastric carcinoma.
  • Chronic sclerosing mesenteritis:
  • Peritoneal echinococcosis:


  • Macari M, Balthazar EJ. CT of bowel wall thickening: significance and pitfalls of interpretation. AJR Am J Roentgenol. 2001 May;176(5):1105-16.
  • Pickhardt PJ, Bhalla S. Unusual nonneoplastic peritoneal and subperitoneal conditions: CT findings. Radiographics. 2005 May-Jun;25(3):719-30.
  • Sheth S, Horton KM, Garland MR, Fishman EK. Mesenteric neoplasms: CT appearances of primary and secondary tumors and differential diagnosis. Radiographics. 2003 Mar-Apr;23(2):457-73.

Friday, September 10, 2010

Congenital Pulmonary Airway Malformation

Congenital pulmonary airway malformation (CPAM), formerly congenital cystic adenomatoid malformation (CCAM), is the most commonly diagnosed prenatal lung malformation. There is abnormal branching of the immature bronchioles and abnormal alveolar development. The immature airways usually communicate with the normal tracheobronchial tree, resulting in both cystic and solid areas.

The expanded classification of CPAM includes the original types 1, 2, and 3, and two new types: 0 and 4.
  • Type 0: Represents an abnormality of the trachea and mainstem bronchi. Incompatible with life.
  • Type 1: Represents an abnormality of the bronchial/proximal bronchiolar region. The most common type (60%). Single or multiple large cysts (2–10 cm in diameter) surrounded by smaller cysts and a compressed normal parenchyma. CT shows one or more large, air-filled cysts with or without gas-fluid levels. MR shows T2-hyperintense uni- or multilocular lesions with discrete walls.
  • Type 2: Represents an abnormality of the bronchiolar region. Small cysts (0.5 cm - 2 cm). Second most common type (20%). Frequently associated with other congenital anomalies. CT may show a gas-filled multicystic mass or a focal area of consolidation (our case). The MR appearance depends on the composition of the malformation and is variable.
  • Type 3: Represents an abnormality of the terminal bronchiolar/alveolar duct region. Third most common type (10%). Tiny cysts (< 0.2 cm in diameter). Frequently associated with other congenital anomalies. Associated with maternal polyhydramnios in ~80% of cases. Can involve an entire lobe or the whole lung. The tiny cysts are too small to resolve by CT; therefore, the lesion appears as a solid mass. MR shows a homogeneously T2-hyperintense solid mass with normal adjacent parenchyma.
  • Type 4: Represents an abnormality of the distal acinus or alveolar saccular/alveolus region. May or may not be the same thing as pleuropulmonary blastoma. Presents before 4 years of age. Sudden respiratory distress due to tension pneumothorax is a unique feature of this subtype. Imaging reveals a large lesion, usually localized to one lobe, with large air-filled cysts. Mediastinal shift may be out of proportion to the mild/absent symptoms.
It is important to remember that CPAM and sequestration can coexist and manifest as a mixed lesion, so a search for systemic arterial supply is helpful. Internal gas-fluid levels may be seen in any of the subtypes if there is superimposed infection.

The images shown here are from a neonate with a lung mass identified at prenatal ultrasound. The radiograph shows an oval lesion in the left lung base medially, which was confirmed by CT. Biopsy showed a type 2 CPAM.


Thursday, September 9, 2010

Splenic Abscess after Infarction

Emboli (septic or sterile) are the most common cause of splenic infarctions, followed by local thrombosis (e.g., myelofibrosis, sickle cell disease, leukemia, and lymphoma), vasculitiides, pancreatic disease, splenic artery aneurysm, and splenic torsion.

In the acute phase, splenic infarctions are characterized peripheral low-attenuation lesions that may be wedge-shaped (classic), round or irregular (more common). In some cases, they may present as heterogeneous and poorly marginated lesions that are similar to abscesses and tumors. Later on, there is progressive volume loss and possibly calcification with hypertrophy of the surrounding normal spleen. Liquefaction and necrosis may also occur, with the risk of outward expansion, subcapsular hemorrhage, peritoneal hemorrhage.

Splenic infarctions may be complicated by abscess. The presence of gas in an intrasplenic collection suggests an abscess, but the majority of splenic abscesses do not contain gas. When gas is seen in an infarcted spleen, however, the issue is a bit more complicated. This is because gas in an organ following infarction does not always point to an infectious etiology. Gas formation has been reported in the kidney, liver, and spleen after transcatheter embolization, and is thought to be due to liberation of oxygen from oxyhemoglobin.

Therefore, it is important to differentiate gas in an abscess from gas following infarction. Multiple small gas bubbles throughout the organ, with most of the gas in the more central portions suggests a nonsuppurative origin.


  • Levy JM, Wasserman PI, Weiland DE. Nonsuppurative gas formation in the spleen after transcatheter splenic infarction. Radiology. 1981 May;139(2):375-6.
  • Rabushka LS, Kawashima A, Fishman EK. Imaging of the spleen: CT with supplemental MR examination. Radiographics. 1994 Mar;14(2):307-32.

Wednesday, September 8, 2010

Polypoid Lesions of the Small Bowel

Polypoid lesions of the small bowel can be mucosal or submucosal, which are differentiated by the angle they form with the small bowel wall. Mucosal lesions tend to form acute angles, while submucosal lesions form right or slightly obtuse angles. This distinction gets hard with small (< 2cm) lesions, however.

Almost 50% of submucosal lesions undergo necrosis and cavitation, giving us a submucosal "bull's-eye" or "target" appearance.

Muscosal lesions
  • Polyps: May be pedunculated or sessile. Most commonly adenomas or hamartomas. When multiple, consider familial adenomatous polyposis syndrome (small bowel involved in 95% of patients) or Peutz-Jeghers syndrome (hamartomas). Coexistence of multiple duodenal polyps should steer you towards familial adenomatous polyposis syndrome, while a few large polyps in the distal duodenum and jejunum should steer you towards Peutz-Jeghers syndrome. Obviously if you could look at the patient and saw pigmented skin and mucosal lesions, you'd go with Peutz-Jeghers.
  • Carcinoid: Can appear as mucosal lesions as one or more small sessile polyps in the distal ileum. By far the most common neoplasm in the distal small bowel.
  • Adenocarcinomas: Usually in the duodenum, at or distal to the papilla of Vater, or in the proximal jejunum within 30 cm of the ligament of Treitz. Can ulcerate.
Submucosal Lesions
  • Multiple submucosal masses: Think of hematogenous metastases (melanoma, breast or lung), lymphoma, multiple carcinoid tumors (will be mostly in the ileum), multiple neurofibromas (rarely ulcerate), and Kaposi sarcoma
  • Solitary submucosal mass: Think benign lesions like lipoma, gastrointestinal stromal tumor, hemangioma, or neurofibroma.
  • Pedunculated lesions: Large pedunculated lesions in the ileum are most commonly lipomas, inflammatory fibroid polyps, and inverted Meckel diverticula.


Levine MS, Rubesin SE, Laufer I. Pattern approach for diseases of mesenteric small bowel on barium studies. Radiology. 2008 Nov;249(2):445-60.

Tuesday, September 7, 2010

Ductus Arteriosus and its Remnants in Adults

The ductus arteriosus involutes during infancy, sometimes leaving a small remnant called the ductus bump or diverticulum. It can also remain patent into adulthood or form into an aneurysm.

A ductus bump or diverticulum is a focal outpouching of the proximal descending aorta and is a normal variant, not to be confused with either a patent ductus arteriosus, aneurysm, or pseudoaneurysm.

Aneurysm of the ductus diverticulum is rarely seen in adults . Patients may present with hoarseness, dyspnea, hemoptysis, and/or cough. The aneurysm can erode into a bronchus, the esophagus, pericardium, or pleural cavity, with disastrous consequences. Risk of rupture increases when the aneurysm is larger than 3 cm. The main differential consideration for a ductus aneurysm is just a regular aortic arch aneurysm. Three dimensional reconstructions help by showing ductus aneurysms pointing toward the left pulmonary artery.

A traumatic pseudoaneurysm is also a consideration. They tend to occur in the region of the isthmus and usually form an acute angle with the aorta, unlike the more gentle obtuse angle of the ductus bump.

On the axial images, we see a rounded structure (pink arrow) arising from the aortic arch (blue arrow) and heading toward the left pulmonary artery. At this point, we could be dealing with a patent ductus arteriosus or a diverticulum. The fact that the study was done without intravenous contrast limits our evaluation of this incidental finding in a 70-year-old woman, but coronal and sagittal oblique maximum intensity projections help a bit. In the case of a diverticulum, we'd expect to see a plane between the structure and the left pulmonary artery, but we don't see one here.


  • Goitein O, Fuhrman CR, Lacomis JM. Incidental finding on MDCT of patent ductus arteriosus: use of CT and MRI to assess clinical importance. AJR Am J Roentgenol. 2005 Jun;184(6):1924-31.
  • Lee EY, Boiselle PM, Cleveland RH. Multidetector CT evaluation of congenital lung anomalies. Radiology. 2008 Jun;247(3):632-48
  • Sugimoto T, Takahashi T, Inui K, Minowa T, Watanabe T, Shimazaki Y. Aneurysm of the ductus diverticulum in adults: the diagnostic value of three-dimensional computed tomographic scanning. Jpn J Thorac Cardiovasc Surg. 2003 Oct;51(10):524-7.

Monday, September 6, 2010

Left Aortic Arch with an Aberrant Right Subclavian Artery

Left aortic arch and aberrant right subclavian artery (ARSCA) is commonly referred to as the most common congenital arch anomaly, affecting 1% of the population. Sometimes the statement is qualified by noting that the so-called bovine arch, which occurs in ~15% of the population, is actually more common.

An aberrant right subclavian artery refers is a right subclavian artery that arises from the aortic arch distal to the left subclavian artery origin. The ARSCA then may travel posterior to esophagus (most common course), between the trachea and esopahgus (~20% of cases), or anterior to the traches (~5% of cases).

While dysphagis lusoria, described in 1794 by David Bayford as a lusus naturae (freak or jest of nature), was in reference to dysphagia due to an aberrant right subclavian artery, most people with left aortic arch and ARSCA are asymptomatic. About a third do experience symptoms, with dysphagia being the complaint in about 90% of cases. Airway symptoms may also occur, but are much less common.

The diagnosis is easy on cross sectional imaging. Chest radiographs do not demonstrate the anomaly directly, but in the rare case of coarctation of the aorta proximal to an ARSCA, unilateral left rib notching may be seen.

An aberrant right subclavian artery is more than just an incidental finding or a trivia question about unilateral left rib notching. It's important to make note of it for many reasons:
  • Head and neck surgeons will want to know about this because of the association of ARSCA with a nonrecurrent laryngeal nerve (NRLN). A NRLN is a laryngeal nerve that leaves the vagus nerve in the neck to directly innervate the larynx, instead of swinging down below the arch. The nerve can be inadvertently injured in carotid artery or thyroid procedures if this anomalous course is not suspected.
  • Thoracic surgeons will want to know about this because of the association with an aberrant course of the thoracic duct. In addition, clamping the aorta proximal to the left subclavian artery during surgery will occlude both vertebral arteries, which will lead to brainstem infarction.
  • Pediatric cardiologists will want to know about an ARSCA, because it is found in 35% of children with Down syndrome who have other cardiac anomalies. An ARSCA in a child with Down syndrome should prompt further investigation.
  • Trauma surgeons will care because an aortic dissection may extend into the ARSCA, which may perforate into the esophagus and lead to exsanguination.
Here we see an aberrant right subclavian artery (pink arrow) arising from a diverticulum of Kommerell (blue arrow) and traveling posterior to the esophagus.


Sunday, September 5, 2010

Intrapulmonary Lymph Nodes

One of the main reasons people go into radiology is the promise that one day, if they play their cards right, they can spend half their day doing nothing but hunting nodules on chest CTs ordered for "cough." Not uncommonly, we come across peripheral nodules that may or may not be intrapulmonary lymph nodes.

At least two papers (one from our institution back in 1996, and a recent one from NYC) have described the CT appearance of these intrapulmonary lymph nodes. They tend to be predominantly in the lower lobes and in the right middle lobe, all below the carina.

They can range in size from a few mm to 9 mm and are located within 20 mm of the chest wall, with the ones farthest away from the chest wall abutting fissures. The nodules are sharply defined and uncalcified. They may have a discrete thin tag or thickened interlobular septum extending to the pleural surface.


  • Bankoff MS, McEniff NJ, Bhadelia RA, Garcia-Moliner M, Daly BD. Prevalence of pathologically proven intrapulmonary lymph nodes and their appearance on CT. AJR Am J Roentgenol. 1996 Sep;167(3):629-30.
  • Shaham D, Vazquez M, Bogot NR, Henschke CI, Yankelevitz DF. CT features of intrapulmonary lymph nodes confirmed by cytology. Clin Imaging. 2010 May-Jun;34(3):185-90.

Saturday, September 4, 2010

Radiographic Findings in Aortic Trauma

The most reliable signs of mediastinal hemorrhage on supine radiographs are an abnormality of the aortic contour or the presence of one or more of the following:
  • Transverse mediastinal width > 8 cm just above the aortic knob
  • Apical cap sign
  • Widening (> 5 mm) of the right paratracheal stripe
  • Deviation of the nasogastnic tube to the right of the T4 spinous process
We can achieve a sensitivity of 93% and specificity of 60% for ruptured aorta in a trauma patient with evidence of mediastinal hemorrhage if at least one of these two signs is present:
  • Deviation of the nasogastnic tube to the right of the T4 spinous process
  • Widening (> 5 mm) of the right paratracheal stripe
When both the nasogastric tube and trachea are deviated to the right, we have a 96% chance of having an aortic rupture, and some feel that this is a very specific sign for aortic rupture.

Displacement of the left mainstem bronchus inferiorly and to the right can be seen with mediastinal hemorrhage and has been advocated as a specific sign of aortic isthmus rupture

Signs such as an increased (> 0.25) mediastinal width to chest width ratio, tracheal deviation to the right of midline, left hemothorax without associated rib fracture, widening of the paraspinal lines, and aortopulmonary window opacification do not reliably separate patients with mediastinal hemorrhage from normal.


Woodring JH, Loh FK, Kryscio RJ. Mediastinal hemorrhage: an evaluation of radiographic manifestations. Radiology. 1984 Apr;151(1):15-21.

Friday, September 3, 2010

Reversed Halo Sign

The reversed halo sign, also known as the atoll sign, refers to a round area of ground-glass attenuation surrounded by a crescent (> 3/4 of a circle) or ring of airspace consolidation that is greater than 2 mm in thickness.

The reversed halo sign has been classically described in cryptogenic organizing pneumonia, but can be seen in a number of conditions. Recently it has been suggested that nodularity of the ring can be used to differentiate granulomatous infections and active sarcoidosis from cryptogenic organizing pneumonia, which has a smoother ring.

Differential considerations include:
  • Cryptogenic organizing pneumonia (COP): Classical description of the reversed halo sign. Seen in up to 20% of patients with COP and thought to be fairly specific, although it can be seen in other conditions.
  • Infections: Cryptococcosis, South American blastomycosis (paracoccidioidomycosis), schistosomiasis, pneumonococcal pneumonia, tuberculosis.
  • Vasculitides: Wegener granulomatosis, dermatomyositis.
  • Sarcoidosis:
  • Lymphomatoid granulomatosis: Rare Epstein-Barr virus–associated lymphoproliferative disease, characterized by vascular destruction, classically in the lungs.


  • Agarwal R, Aggarwal AN, Gupta D. Another cause of reverse halo sign: Wegener's granulomatosis. Br J Radiol. 2007 Oct;80(958):849-50.
  • Algin O, Gokalp G, Topal U. Signs in chest imaging. Diagn Interv Radiol. 2010 Jul 28.
  • Benamore RE, Weisbrod GL, Hwang DM, Bailey DJ, Pierre AF, Lazar NM, Maimon N. Reversed halo sign in lymphomatoid granulomatosis. Br J Radiol. 2007 Aug;80(956):e162-6.
  • Gasparetto EL, Escuissato DL, Davaus T, de Cerqueira EM, Souza AS Jr, Marchiori E, Müller NL. Reversed halo sign in pulmonary paracoccidioidomycosis. AJR Am J Roentgenol. 2005 Jun;184(6):1932-4.
  • Kim SJ, Lee KS, Ryu YH, Yoon YC, Choe KO, Kim TS, Sung KJ. Reversed halo sign on high-resolution CT of cryptogenic organizing pneumonia: diagnostic implications. AJR Am J Roentgenol. 2003 May;180(5):1251-4.
  • Kumazoe H, Matsunaga K, Nagata N, Komori M, Wakamatsu K, Kajiki A, Nakazono T, Kudo S. "Reversed halo sign" of high-resolution computed tomography in pulmonary sarcoidosis. J Thorac Imaging. 2009 Feb;24(1):66-8.
  • Marchiori E, Grando RD, Simões Dos Santos CE, Maffazzioli Santos Balzan L, Zanetti G, Mano CM, Gutierrez RS. Pulmonary tuberculosis associated with the reversed halo sign on high-resolution CT. Br J Radiol. 2010 Mar;83(987):e58-60.
  • Marchiori E, Zanetti G, Hochhegger B, Irion KL. Re: Reversed halo sign: nodular wall as criterion for differentiation between cryptogenic organizing pneumonia and active granulomatous diseases. Clin Radiol. 2010 Sep;65(9):770-1.
  • Tokuyasu H, Isowa N, Shimizu E, Yamadori I. Reversed halo sign associated with dermatomyositis. Intern Med. 2010;49(15):1677-8.
  • Tzilas V, Bastas A, Provata A, Koti A, Tzouda V, Tsoukalas G. The "reversed halo" sign in pneumonococcal pneumonia: a review with a case report. Eur Rev Med Pharmacol Sci. 2010 May;14(5):481-6.
  • Voloudaki AE, Bouros DE, Froudarakis ME, Datseris GE, Apostolaki EG, Gourtsoyiannis NC. Crescentic and ring-shaped opacities. CT features in two cases of bronchiolitis obliterans organizing pneumonia (BOOP). Acta Radiol. 1996 Nov;37(6):889-92.

Thursday, September 2, 2010

Nuclear Medicine and Liver Lesions

Remembering which lesions do what with which radiotracers can be more difficult than understanding this sentence. Some (perhaps over-simplified) points:
  • Tc-99m sulfur colloid: Shows Kupffer cell activity.
  • Tc-99m HIDA: Shows hepatocyte function.
  • Tc-99m red blood cell: Shows tumor vascularity.
Focal nodular hyperplasia (FNH) has hepatocytes but disorganized biliary canaliculi. As a result, it will take up HIDA rapidly, but because of the disorganized biliary canaliculi, will keep the tracer around longer than the rest of the liver. FNH also has Kupffer cells of varying function; therefore, most are indistinguishable from the rest of the liver on sulfur colloid, but they may infrequently be cold or hot. FNH is a vascular tumor, so tagged red blood cell scans will show early uptake with or without persistent uptake on delayed images.

Adenomas are derived from hepatocytes, but and may show uptake on HIDA. They don't have that many Kuppfer cells, however, so the majority will be cold on sulfur colloid, but about 20% will be warm. Adenomas are vascular tumors, so tagged red blood cell scans will show early uptake with or without persistent uptake on delayed images.

Hepatocellular carcinoma (HCC) is also derived from hepatocytes, but these mutated hepatocytes may or may not function that well, so about 50% of HCCs will show uptake on HIDA and may be associated with a better prognosis. Whatever Kuppfer cells there may have been in the beginning are overrun by the cancer, so HCC is usually cold on sulfur colloid imaging in cirrhotic livers. HCC is a vascular tumor, so tagged red blood cell scans will show early uptake with or without persistent uptake on delayed images.

Hemangiomas are a tangle of vessels that takes up space amidst normal hepatocytes and Kuppfer cells, so they will be cold on sulfur colloid and HIDA scans. Tagged red blood cell scans will show a focal cold spot on early images and persistent filling on delayed images. This is the same as its behavior on dynamic CT, since we're basically following blood in both modalities.

Finally, liver metastases are alien to the liver, so they will not pick up hepatocyte or Kuppfer cell agents, appearing cold on sulfur colloid and HIDA scans.


  • Mettler FA and Guiberteau MJ. Chapter 8. In Essentials of Nuclear Medicine Imaging. Fifth Edition. Saunders, Philadelphia. 2006. pp 203-242.
  • Schulze PJ, Stritzke P, Stolzenbach G. Liver imaging and detection of liver metastases with 99mTc-HIDA. Nuklearmedizin. 1981 Oct;20(5):214-9.

Wednesday, September 1, 2010

Duplex Evaluation of the Carotid Arteries

Degree of stenosis ICA PSV
Plaque ICA/CCA PSV ratio ICA EDV
Normal <125 None < 2.0 <40
< 50% <125 <50% < 2.0 <40
50%-69% 125-230 ≥50% 2.0-4.0 40-100
≥70<near occlusion >230 ≥50% > 4.0 > 100
Near-occlusion Anything goes Visible Anything goes Anything goes
Total occlusion Undetectable No detectable lumen NA NA

A tight stenosis in an internal carotid artery (ICA) can cause falsely elevated peak systolic and end diastolic velocities in the contralateral ICA evaluated by duplex ultrasound. This artifactually increased velocity can lead to a false positive diagnosis of a stenosis. One explanation put forward is that the increased flow is caused by cross filling via the circle of Willis to the cerebral hemisphere on the same side as the tight stenosis. Unfortunately, this has not been confirmed by angiography. In any case, if you see a velocity increase out of proportion to real-time vessel characteristics (i.e., large plaque), you should do a careful evaluation for high-grade stenosis of the contralateral ICA.

Aortic regurgitation can present with different findings on carotid duplex. Aortic regurgitation results in reflux of blood from the aorta back into the left ventricle, and causes a widened pulse pressure and increased stroke volume. Ejection fraction may be normal or high early on, but as left ventricular decompensation occurs with longstanding aortic regurgitation, the ejection fraction normalizes and then drops.

A bisferious pulse, also known as pulsus bisferiens, is the presence of two systolic peaks that can be seen in pressure tracings of the the ascending aorta, the aortic arch, and the carotid artery in patients with aortic regurgitation with or without concurrent aortic stenosis. It can also be seen in patients with severe obstructive hypertrophic cardiomyopathy.

Reversal of diastolic flow direction can also be seen in the carotid arteries of patients with aortic regurgitation

Aortic stenosis can cause a characteristic tardus-parvus waveform: prolonged systolic acceleration time (tardus) with low peak systolic velocity (parvus). Bilateral tardus-parvus waveforms in the carotids can be seen with aortic stenosis. In general a tardus-parvus waveform is indicative of a severe stenosis proximal to the point of measurement. For example when sampling distal renal artery branches in a patient with renal artery stenosis.

Right subclavian steal can be reflected in the carotids as a tardus-parvus waveform of the right common and internal carotid arteries.

Cardiac dynamic factors can also affect the carotid waveform. Hypertension can result in high flow (> 135 cm/s) in both common carotid arteries, whereas poor cardiac output can lead to low flow (< 45 cm/s) in both common carotid arteries.

Bradycardia, by allowing longer diastolic filling of the left ventricle, produces increased stroke volume and increased systolic velocities in the carotids. The prolonged diastolic time also leads to a longer diastolic runoff and spuriously decreased end diastolic values.