Parthasarathy Ganesan, MD

A 20-year-old male was admitted with three-day history of central, colicky abdominal pain, distension, vomiting and constipation. The abdomen was distended, and resonant, with no signs suggestive of peritonitis. There was no palpable lump. Routine lab investigations were normal.The abdominal plain film showed dilated small bowel loops, with air-fluid levels. A diagnosis of small bowel obstruction was made, and CT was done.

 A: Axial CECT shows dilated jejunal loops with air-fluid levels (white arrow). Large bowel is collapsed. B: Proximal ileal loops are dilated (blue arrow), while distal ileum is collapsed (yellow arrow), suggesting zone of transition at ileal level.

 Serial axial sections (craniocaudal) demonstrate a blind-ending loop, filled with fluid and air, seen in relation to the umbilicus distally, and proximally merging into a distal ileal loop, consistent with Meckel diverticulum.

 Serial coronal MPR images show the Meckel diverticulum, amongst the dilated jejunal and ileal loops.

 Serial sagittal MPR images show the Meckel diverticulum, in relation to the anterior abdominal wall and the distal ileal loops.

CECT confirmed the presence of small bowel obstruction, with zone of transition at the ileal level. There was a blind ending loop, which was in relation to the umbilicus at its distal end, while proximally terminating into a distal ileal loop. Minimal interbowel loop fluid was seen. Meckel diverticulum was suggested as the probable cause of small bowel obstruction.

At laparotomy, the Meckel diverticulum was found to arise about 50 cm proximal to the ileocecal valve from the distal ileum, and attached to the abdominal wall by a very short thin fibrous cord. It had trapped and engaged a distal ileal segment across it, leading to obstruction. The diverticulum was resected, and end-to-end anastomosis of the bowel was performed. The post-operative period was uneventful.

Discussion: Meckel diverticulum is the most common congenital anomaly of the gastrointestinal tract, and is due to the persistence of vitello-intestinal duct, which normally obliterates by the 5th embryonic week. The rule of 2s : it occurs in 2 percent of population, symptomatic usually before age 2, located within two feet of ileocecal valve, and has a length of 2 inches.

Children usually present with painless GI bleeding secondary to ulceration (in 95 percent due to heterotopic gastric mucosa). Older patients are more likely to present with intussusception or small bowel obstruction than with GI bleeding. Plain abdominal radiographs may show obstruction, which - if it has led to volvulus and infarction - may be associated with air in the bowel wall or portal vein or even with free intraperitoneal air. Contrast studies are of little use.

Parthasarathy Ganesan, MD, GTB Hospital, Delhi, India

Articles

Case History: A 20-year-old male was admitted with three-day history of central, colicky abdominal pain, distension, vomiting and constipation.

Meckel Diverticulum 

A 4-week-old male neonate was brought with the complaints of vomiting after feeds for the past two weeks. It was projectile, nonbilious vomiting, progressively increasing in severity. On examination, no lump (‘olive’) was palpable. Transabdominal ultrasound was performed.

 Axial oblique ultrasound shows thickened, hypoechoic muscular wall (5.4 mm) and elongated pyloric canal (17.2 mm approximately).

 Congenital hypertrophic pyloric stenosis. Pyloric canal length was greater than 16 mm, and single wall thickness greater than 3 mm.

Ultrasound shows the fluid filled, distended stomach, due to delayed gastric emptying.

The distended stomach displaces the hypertrophied pyloric canal posteriorly, which resembles the uterine cervix (cervix sign). To the experienced radiologist and surgeon, the hypertrophied pylorus often looks obvious at first glance: “the hot dog in a bun” appearance.

 Hypertrophic pyloric stenosis is idiopathic thickening of pyloric muscle in infancy which creates progressive gastric outlet obstruction. It is typically seen in 2- to 12-week-old infants with worsening projectile vomiting. Dehydration, hypochloremic alkalosis, and jaundice may develop. Boys outnumber girls, 4:1. On physical examination, 10 percent to 40 percent of patients have either hyperperistaltic waves or a palpable pyloric “olive.” The latter finding is rarely felt except by experienced observers, wherein imaging may not be indicated. Otherwise, ultrasound is the procedure of choice. The cut-off values for muscle thickening, and elongated pyloric channel vary by author. Commonly accepted threshold values for HPS

• Single wall thickness of pylorus> 3 mm
• Pyloric channel length > 16 mm
• Pyloric diameter> 15 mm

On cross-section, the hypoechoic ring of hypertrophied pyloric muscle around the central echogenic mucosa, gives the appearance of bull’s eye/ dough-nut (target sign). Echogenic mucosal lining also tends to hypertrophy, and becomes redundant. Gastric hyperperistalsis and obliterated pyloric lumen are seen on dynamic exam. When duodenal bulb is easily identified, distended with fluid, diagnosis of HPS is unlikely.

Color Doppler shows increased flow in both the muscle and mucosa of infants with HPS. Barium studies may be used if the history is atypical, the emesis is bilious, and to evaluate for other causes of vomiting.

 Sonographic image resembling few of the UGI study findings. White arrow: Teat sign, Yellow arrow: Beak sign; Blue arrow: Shoulder sign.

The characteristic findings on UGI study are:
• Pyloric wall thickness >10 mm
• Elongation and narrowing of pyloric canal (2-4 cm in length)
• "Double / triple track sign" - Crowding of mucosal folds in pyloric channel
• "String sign" - Passing of small barium streak through pyloric channel
• Twining recess = "diamond sign"- Transient triangular tentlike cleft/niche in midportion of pyloric canal with apex pointing inferiorly secondary to mucosal bulging between two separated hypertrophied muscle bundles on the greater curvature side within pyloric channel
• "Pyloric teat" - Outpouching along lesser curvature due to disruption of antral peristalsis
• "Antral beaking" - Mass impression upon antrum with streak of barium pointing toward pyloric channel
• Kirklin sign = "mushroom sign"- Indentation of base of bulb (in 50%)
• Gastric distension with fluid
• Active gastric hyperperistalsis- "Caterpillar sign" (hyperperistaltic waves)


Pylorospasm (muscle thickness between 1.5-2 mm), can best be regarded as delayed gastric emptying. After a variable period (days to weeks), the symptoms of pylorospasm disappear. Whether or not pylorospasm represents a forme fruste of pyloric stenosis is not certain because adrenogenital syndrome, dehydration, and sepsis have also been implicated as causes. Finally, gastroenteritis, pyloric channel (stress) ulcer, and congenital abnormalities such as antral web and gastric duplication may cause symptoms similar to those of HPS. However, USG is usually successful in excluding HPS when one of these other conditions is present.


1. Radiology review manual, 6th edition, Dahnert.
2. Diagnostic imaging – Pediatrics, 1st edition, Donnelly.
3. Pediatric radiology, the requisites, 3rd edition.

Case history: A 4-week-old male neonate was brought with the complaints of vomiting after feeds for the past two weeks. It was projectile, nonbilious vomiting, progressively increasing in severity. 

Congenital Hypertrophic Pyloric Stenosis

 A 16-year-old boy presents with right-sided nasal obstruction and intermittent, spontaneous epistaxis. There were no otologic complaints. On examination, he had a large fleshy mass completely filling the nasopharynx. Other physical examination and laboratory investigations were normal. CECT was done.

Homogenously enhancing mass lesion centered at sphenopalatine foramen (widened by the mass, shown by black arrows), extending into nasopharynx (yellow arrow) and pterygopalatine fossa (red arrow). The mass also fills ipsilateral nasal cavity, pushing the septum to left.
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Coronal bone CT revealing the widened right sphenopalatine foramen (arrows) due to the juvenile angiofibroma.

Coronal CT image showing superior extension into right sphenoid sinus through erosion of its floor and extension into infratemporal fossa (infrazygomatic masticator space)

Axial CECT image showing extension of the lesion into right buccal space (obliterating the retromaxillary fat pad which is normally present- denoted by asterisk on left side) and into right masticator space (infratemporal fossa, M- Masseter muscle) through pterygomaxillary fissure. The arrow indicates the characteristic anterior bowing of the posterior wall of maxillary sinus due to juvenile angiofibroma.

Arrow indicates the anterior displacement of the posterior wall of the right maxillary sinus by the mass lesion (bow sign), in a sagittal reconstruction image. This is also known as the Holman - Miller sign, which was initially described on plain X-ray films. The contralateral normal posterior wall is shown for comparison.

Coronal bone CT showing the widening of gap between ramus of mandible and maxillary body on the right side compared to left, suggestive of infratemporal fossa involvement by juvenile angiofibroma. This is the Hondousa sign initially described on X-ray.

CT scan shows a large, lobular, well-circumscribed soft tissue mass lesion centered in the posterior part of nasal cavity at the margin of sphenopalatine foramen on right side with multiple surrounding extensions. The mass lesion shows diffuse avid enhancement on administering contrast, findings consistent with juvenile angiofibroma. The lesion widens the sphenopalatine foramen and extends into the pterygopalatine fossa and also extends into nasal cavity anteriorly. The lesion further extends into buccal space and masticator space (infratemporal fossa). Superiorly, it extends into the right sphenoid sinus through roof of nasopharynx. However, there is no extension into the orbit or middle cranial fossa.

The patient underwent surgical resection of the lesion and histopathology confirmed juvenile angiofibroma.

 Juvenile angiofibroma (JAF) is a benign, vascular, non-encapsulated locally invasive nasal cavity mass found exclusively in adolescent males. It extends from posterior nasal cavity into nasal cavity, nasopharynx and pterygopalatine fossa.

On NCCT, it is seen as a soft tissue mass originating at the sphenopalatine foramen margin with multiple surrounding extensions and shows intense enhancement on CECT. On MR, it displays intermediate signal on T1W and bright signal intensities on T2W images with avid enhancement on post-gadolinium images. Punctuate and serpentine flow voids may be seen within the tumor.
Internal maxillary and ascending pharyngeal arteries from the ECA are the most common feeding vessels.

Different staging systems have been in use, most commonly those of Chandler, Sessions and Fisch.The radiologist should look for the extensions into surrounding structures, particularly orbit via inferior orbital fissure and cranial cavity through foramen rotundum/ vidian canal. Failure to identify them may result in incomplete surgical resection.

Differential diagnoses include encephalocele, antrochoanal polyp, hemangioma and rhabdomyosarcoma.
 

Parthasarathy Ganesan, MD
GTB Hospital, Delhi, India

Diagnostic Imaging- Head and Neck, Harnsberger, 1st edition, 2004.

Yadav SP et al, Nasopharyngeal Angiofibroma; J Otolaryngol, 31(6): 346-50, 2002.

Juvenile Angiofibroma

Axial CECT showing CCA proximal to its bifurcation.

A 24-year-old female presented with painless, slowly enlarging mass lesion at the angle of mandible on right side of 14 months duration. There was no history of dysphagia/ hoarseness/ headache. She did not have symptoms or signs of Horner’s syndrome or catecholamine excess. Her past medical history was insignificant and there was no family history of similar complaints.

The patient was moderately built and her general physical examination was unremarkable except for pallor. Her vitals were within normal limits. On local examination, there was an ovoid, firm, non-tender, pulsatile mass lesion, 3 x 1.8 cm size, located along the anterior border of sternomastoid at the level of hyoid bone on right side. The swelling was freely movable laterally than vertically (Fontaine’s sign positive). There was no audible bruit or palpable lymph nodes.
Routine lab investigations were normal.

Axial CECT showing CCA proximal to its bifurcation Axial CECT revealing the paraganglioma sitting at carotid bifurcation

Axial CECT showing completely encased ECA and partially encased ICA. Two intersecting lines are drawn between the centre of ICA and the points of contact of the circumference of the vessel with the edges of the tumor to obtain the angle.

Oblique sagittal MPR image showing the tumor at Y of carotid bifurcation Sagittal MIP image demonstrating the relation of tumor to vessels.

CECT was done which showed a lobulated soft tissue mass located at carotid bifurcation extending cephalad and measuring 3.9(craniocaudal) x 1.9(transverse) x 2.2(anteroposterior) cm. There was intense blush on administering iv contrast and splaying of internal and external carotid arteries (Lyre sign) was noted which suggested carotid body paraganglioma. The lesion was seen to completely encase ECA and had 1690 circumferential contact with ICA classifying it as Shamblin type I tumor.

She underwent surgery and histopathology confirmed the lesion as paraganglioma. Her post-operative period was uneventful.

Discussion: Paragangliomas are slow growing hypervascular tumors arising from neural crest derivatives. They occur at multiple levels in the head and neck including the carotid bifurcation, along the nodose ganglia of vagus nerve (glomus vagale tumors), in the jugular bulb region (glomus jugulare) and in middle ear cavity (glomus tympanicum).

Carotid body paraganglioma is the most common location for head and neck paragangliomas (60 percent to 67 percent) typically occurring in the fourth and fifth decade with female predilection. They usually present as painless pulsatile mass in the angle of mandible, with about 20 percent having symptoms of vagal or hypoglossal neuropathy. They rarely secrete catecholamines. A small number are familial and multicentric. So, the radiologist must always look for the 2nd lesion in jugular foramen or nasopharyngeal carotid space.

CT and MRI are usually required to assess the extent of lesion and to rule out other masses mimicking these tumors. On Non-contrast CT, the density is similar to neck muscles. On CECT, the characteristic location at carotid bifurcation and the splaying of vessels and its avid enhancement aid in diagnosis. On MR, they have intermediate signal intensity on all sequences. Large tumors (>2 cm) give the ‘salt and pepper appearance’ due to serpentine flow void of small vessels and subacute hemorrhages.

Angiography is the most specific diagnostic technique and features include moderate enlargement of feeding arteries (ascending pharyngeal artery is the main feeder), early intense parenchymal blush, and rapid venous filling.

The addition of diffusion weighted MRI and calculation of ADC values to routine MR protocols is valuable as it has been observed that depending on the tumor size, the DWI and ADC show a high signal in paragangliomas.

The preferred treatment for carotid body tumors is surgery. Shamblin classified them into three types based on operative notes and gross specimen examination depending on the relationship of the tumor with carotid vessels. Because the relation of the tumor to the ICA is most critical for surgical planning, the circumferential degree of contact of the tumor with the ICA is used to classify the tumor radiologically into 3 types in an attempt to predict the Shamblin group of the tumors: type I- less than or equal to 180°; type II- greater than 180° and less than 270°; and type III- greater than or equal to 270°.

Differential diagnosis: Neurogenic tumors are the most common carotid space lesions. A tumor arising from vagus nerve displaces ICA/CCA anteromedially and IJV posterolaterally and does not splay ICA – ECA at carotid bifurcation. Vagal schwannoma present as a fusiform enhancing carotid space mass in CT/MR without flow voids on MR. Intramural cystic changes may be present. Vagal neurofibromas have characteristic low density (near water) on CT due to lipid rich Schwann and fat cells scattered in the tumor and there is no appreciable contrast enhancement. On MRI, an area of relatively hypointense central signal with peripheral hyperintense signal – ‘target sign’ might be seen on T2W sequences.

Glomus jugular tumor are centered more rostrally than carotid body tumors, approximately 2 cm below the skull base.

Vascular nodal metastases from RCC, papillary thyroid carcinoma show flow voids on MR but do not cause displacement of vessels.

Parthasarathy Ganesan, MD, GTB Hospital, Delhi, India

1. Diagnostic Imaging- Head & Neck, Harnsberger, 1st edition, 2004.
2. S. Arya, V. Rao, S. Juvekar, A.K. Dcruz. Carotid Body Tumors: Objective Criteria to Predict the Shamblin Group on MR Imaging. AJNR 2008 29:1349-1354.
3. Nader M.A et al. Carotid Body Paraganglioma Management and Outcome. European Journal of Scientific Research 2009, 37; 4:567-574.
4. Aschenbach R, Basche S et al. Diffusion weighted imaging and ADC mapping of head and neck paragangliomas. Clin Neuroradiol 2009;19:215-9.

A 24-year-old female with painless, slowly enlarging mass lesion at the angle of mandible on right side 14 months duration.