Small Arterially Enhancing Hepatic Lesion in Cirrhotic Patients

Axial T1WI post contrast images in arterial and portovenous phase demonstrates a tiny enhancing nodule in hepatic segment V, which becomes isosignal to the liver on the portovenous phase. This nodule is occult on unenhanced T1WI and T2WI.

Hepatic Arterial Phase Detection of Small HCC

• Hepatic arterial phase imaging very important to detect small HCCs, which may be occult with other pulse sequences, at unenhanced or portovenous phase MR imaging
• Most HCCs demonstrate arterial enhancement and moderate T2 hyperintensity
• Some small HCCs, however, are seen only during the hepatic arterial phase

Differential Diagnosis of Small Arterially Enhancing Lesion in Cirrhotic Liver

• Hepatocellular carcinoma
• High-grade dysplastic nodule
• Focal nodular hyperplasia (FNH)
• Hemangioma
• Pseudolesions: arterial-portal venous shunt, aberrant venous drainage

Hepatic Pseudolesions

• Arterial enhancement but occult on portovenous and/or equilibrium phases, and at unenhanced T1- and T2-weighted MR imaging
• A retrospective study of 16 patients with 45 lesions showed that the majority (93%) of them were benign without any correlative pathologic findings. The remaining 7% that lesions were HCC, did have other concomitant HCC.
• It seems reasonable to follow these lesions closely with imaging to ensure they do not grow (if they grow, they are likely to represent HCC)

Our case - hepatic pseudolesion, the nodule has disappeared on follow-up MRI performed 3 months later.

Reference:

Holland AE, Hecht EM, Hahn WY, et al. Importance of small (equal or less than 20 mm) enhancing lesions seen only during the hepatic arterial phase at MR imaging of the cirrhotic liver: evaluation and comparison with whole explanted liver. Radiology 2005; 237:938-944.

Soft Tissue Evaluation on Wrist Radiography

Two images demonstrate five fat planes on the PA wrist radiograph, and four fat planes on the lateral wrist radiograph that should be scrutinized on any wrist radiography interpretation.

Facts:

• Soft tissue swelling is almost always seen in one or more compartments in cases of acute fracture or dislocation
• When swelling is observed on a trauma wrist radiograph, all soft tissue areas should be examined thoroughly and the assumption is that they may be a fracture or dislocation associated with swelling
• Abnormal fat planes = fat plane is convex out of the underlying bone, or loss of its distinct plane

What Do They Suggest?

• Dorsal hand swelling -> 2nd through 5th metacarpal injury
• Dorsal wrist swelling -> carpal fractures or wrist dislocation
• Dorsal radial swelling -> forearm fractures
• Pronator fat pad swelling -> forearm fractures
• Thenar swelling -> thumb fractures
• Hypothenar swelling -> 2nd through 5th metacarpal injury
• Scaphoid swelling -> carpal fractures
• Pararadial swelling -> forearm injury
• Paraulnar swelling -> forearm fracture

Reference:

Curtis DJ, Downey, Jr., EF, Brower AC, et al. Importance of soft-tissue evaluation in hand and wrist trauma: statistical evaluation. AJR 1984; 142:781-788.

Bladder Stones

Transverse ultrasound image of the urinary bladder shows a 5-cm mobile hyperechoic lesion (between arrows) with posterior acoustic shadowing within the bladder lumen.

Facts:

• Risk factors: urinary stasis (voiding dysfunction i.e., urethral stricture, benign prostatic hyperplasia, bladder neck contracture, neurogenic bladder), infection, bladder diverticula, foreign body (Foley catheter balloon, suture material, etc)
• Common compositions: uric acid, ammonium urate, calcium oxalate
• Uric acid stones predominate in a setting of bladder outlet obstruction
• Magnesium ammonium phosphate and apatite stones predominate in a setting of urinary tract infection (UTI)
• Patient presentation: hematuria, suprapubic pain, interruption of urine stream

Imaging

• If sufficiently calcified, bladder stones may be visible on radiography
• Tends to locate in the midline when the patient is supine
• If calcification is located laterally, think of a stone in the diverticulum or ureterocele
• Key to confirm that the abnormality is a stone = mobility (either on radiography or ultrasound)

Reference:

1. Zagoria RJ. Genitourinary Radiology: the Requisites, 2004.

2. Tanagho EA, McAninch JW. Smith's General Urology, 2004.

Lumbosacral Agenesis

Authors: Sanjay B. Nathani, M.D. (Radiodiagnosis), J.P. Agarwal, M.D. (Paediatrics).

Editor: Rathachai Kaewlai, M.D.

Fig. 1: There is poor development of the lower extremities with popliteal webbing, deformed hip, ankles and calcaneus.

Fig. 2: AP and lateral spinal radiographs demonstrate absence of normal vertebra distal to T12, with L1 and L2 hemi- and butterfly vertebra. The sacrum is absent. Both iliac bones articulate with each other resulting in decreased transverse pelvic diameter.

Fig. 3: T1W and T2W sagittal MR images of the spine shows complete agenesis of L3, L4, L5 and sacrum. Conus medullaris ends at the level of T8 with a blunted tip. The distal thecal sac tapers to a narrow channel at T12.

Brief Facts

• Caudal regression syndrome is characterized by absence of segment(s) of the lumbosacral spine
• Unknown etiology but associated with maternal insulin-dependent diabetes
• Associated with multiple congenital anomalies
• On radiography, absence of segment(s) of lumbosacral spine is characteristic. There may be fusion of the iliac bones resulting in small pelvis.
• MR imaging provides information about the position and appearance of conus medullaris, which defines two distinct groups of this disease. In group I the conus ends cephalad to the lower border of L1. In group II the conus terminates below L1 known as tethered cord.

Facts

Caudal regression syndrome is a rare congenital malformation characterized by absence of variable segments of lumbosacral spine. The etiology of the syndrome is unknown. It is possibly associated with maternal insulin-dependent diabetes (16% - 50% of cases). A dominant inheritant form of lumbosacral agenesis has been shown to result from defects in the HLXB9 homeobox gene mapping to chromosome 7q36. This gene is also expressed in pancreas perhaps accounting for the association of lumbosacral agenesis with insulin and diabetes.

Motor deficits are present and correspond to the level of vertebral agenesis. Associated conditions are OEIS complex (omphalocele, cloacal extrosphy, imperforate anus, spinal deformities), VATER syndrome, congenital heart defects, genitourinary complaints with unilateral renal agenesis, hydronephrosis, pelvic and horseshoe kidneys, epispadias and hypospadias, orthopedic deformities such as hip dislocation, flexion contractures, genu recurvatum, posterior compartment atrophy, talipes deformities and scoliosis, progressive neurological deficits and back and leg pain, uterine anomalies or rectovaginal fistulas.

Renshaw reviewed 22 patients over 18 years and proposed a classification as follows:

Type I - total or partial unilateral sacral agenesis

Type II - partial sacral agenesis but bilaterally symmetrical defect

Type III - variable lumbar and total sacral agenesis with the ilia articulating with the sides of the lowest vertebra present

Type IV - variable lumbar and total sacral agenesis with the caudal endplate of the lowest vertebra resting above either fused ilia or an iliac amphiarthrosis.

As seen on MR imaging, the position of the conus defines two distinct groups of patients with sacral agenesis. In group I, the conus ends cephalic to the lower border of L1. The conus typically deforms and terminates abruptly at T11 or T12 as if the normal distal tip was absent. The distal central canal may be slightly dilated as a terminal hydromyelia. In this group, the sacrum usually ends at or above S1. Coronal T1WI will show Christmas tree configuration formed by the distal thecal sac, root sleeves and nerve roots within the epidural fat of the spinal canal.

In group II, the conus ends lower, below L1, and is elongated, tethered by a thick filum. There can be associated terminal myelocystocele, transitional lipoma, or elongated cord with terminal hydromyelia. Neurological deficit is more in patients with low tethered cords.

About Authors: Drs. Nathani and Agarwal work for Goyal Hospital and Research Center in Jodhpur, Rajasthan, India. Their work does not have any support for the work in the form of grants, equipments or drugs.

References:

1 . Renshaw T.S. Sacral Agenesis. The Pediatric Spine -Principles and Practice. 1:2214,1994, Raven Press, NewYork

2. Phillips W.A. Sacral Agenesis. Spine - Principles andPractice. 1:2214,1994, Raven Press, New York

3. A.James Barkovich, Congenital Anomalies of the spine.In: Paediatric Neuroimaging ,Vol 2 ,3rd edition, Lippincott Williams & Wilkins,2000 (650-651),

4. Phyllis Glanc et al, The Fetal Musculoskeletal System. In : Carol M. Rumack's Diagnostic Ultrasound;Vol 2, 2nd edition, Mosby. (1224).

5. Beryl R. Benacerraf,Caudal Regression Syndrome and Sirenomelia; in Ultrasound of Fetal Syndromes,edition 1998, (page 250-254); Churchill Livingstone,Philadelphia.

6. Thomas.P.Naidich,Susan I.Blaser,Bradley M.Delman,Congenital Anomalies of Spine and Spinal Cord. In:Scott W. Atlas, Magnetic Resonance Imaging of the Brain and Spine(vol 1) 3rd edition. Philadelphia: Lippincott Williams & Wilkins,2002;( 1589-1593)

7. Renshaw, T. S., 1978. Sacral agenesis: a classification and review of twenty-two cases. Journal of Bone and Joint Surgery, 60A, 373-383.

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