A Cool Evening Walk in the Streets of Calbayog

I always liked to do evening walks in every Philippine town or city that I visit. It has become a habit in me, maybe because it fascinates me to see how a city closes at the end of each busy day.

I always do this nocturnal walks everytime I visit the quiet little town of Calbayog. Usually I just stroll along in the streets trying to photograph the sceneries. This made me a very familiar tourist among the kind townsfolk. I also now speak a little of their Waray dialect. Little by little, I understand their language, and that is an essential part of understanding Waray culture.

Evenings, in Calbayog, are cool and windy because this little town is very near the sea on the west, and jungles on the east. I walk around, with my camera hung in my shoulders, and I see familiar faces. Here and there I see the same people I met from my several visits. The vendors, the trike drivers, the tinderas in the mercado, the dama players in the plaza, the common village people.

It seemed that I am no longer a stranger here, and that I, too belong to their town. The few photos below are some that I took from those cool and lovely evening walks in the lovely city of Calbayog.

Carotid body (paraganglioma) tumor

Findings

Figure 1: Axial contrast enhanced CT image of the upper neck shows a large enhancing mass in relation to the carotid space and is displacing and compressing the vessels.
Figure 2: MRI image of the upper neck shows a large enhancing mass in relation to the carotid space and is displacing and compressing the vessels. Note the multiple small flow voids within the lesion on MRI giving the "salt & pepper" appearance.


Diagnosis: Carotid body (paraganglioma) tumor


Carotid body tumor is a rare type of head and neck tumor composed of paraganglionic cells. Paraganglionic tissue can be found in the adrenal medulla and in multiple extra-adrenal sites, including at the carotid bifurcation, the aortic arch, adjacent to the jugular vein, the tympanic nerve, the facial nerve, the vagus nerve, and others. This tissue develops embryologically from neural crest tissue. These tumors are called extra-adrenal paragangliomas and sometimes as glomus tumors or chemodectomas. The function of paraganglionic tissue in the carotid body is to function as a chemoreceptor, sensing oxygen levels as well as carbon dioxide and pH levels. In head and neck, the glomus tumors are seen at the carotid bifurcation (carotid body tumor) as seen in this case, at the jugular fossa (glomus jugulare), in the middle ear (glomus tympanicum) or along the vagus nerve (glomus vagale).

Carotid body tumors are well encapsulated and highly vascular benign tumors and can occur in a wide range of ages, from childhood to the elderly, but the average age at diagnosis is around 45. There is a slight female predominance, and people who live at high altitudes are more likely to develop carotid body tumors (thought to be due to lower oxygen levels).Most cases are sporadic but familial inheritance is also described. In addition, familial syndromes such as multiple endocrine neoplasia (MEN) can contribute to the development of multiple carotid body tumors as well as tumors at multiple other paraganglionic sites in the head and neck and in the rest of the body as well. Carotid bifurcation is the second most common site for glomus tumors in head and neck, after the middle ear(glomus tymapnicum).

Carotid body tumors like all other paragangliomas are slow-growing and may be locally invasive. They can present as a lateral cervical mass which may or may not be pulsatile. These tumors can sometimes cause cranial nerve palsies, most commonly vagal nerve palsy, and if large can even erode through the skull base or other bony structures. They are rarely malignant in that they rarely metastasize, although local recurrence is not uncommon. 10% of head and neck paragangliomas are multicentric and bilaterality is most common with carotid body tumors. Synchronous and/or metachronous tumors can develop at the contralateral carotid bifurcation as well as in other paraganglionic sites, especially if a familial syndrome is present. These types of recurrences are not usually considered metastases by most sources. Carotid body tumors and other paragangliomas can actively secrete metanephrines, most commonly norepinephrine, although this is rare (3-5% of head and neck paragangliomas). Symptoms of an actively secreting carotid body tumor would include headaches, flushing, hypertension, and palpitations.

CT of the neck is helpful for diagnosis and can identify any local lymph node enlargement or bony erosions. Additionally, MR can help determine the relationship of the tumor with respect to the carotid vessels and other neck structures and if there are multiple paragangliomas present. A classic finding of the carotid body tumor is splaying of the internal and external carotid arteries. On both enhanced CT and MR, the carotid body tumors and other paragangliomas are intensely enhancing due to their extensive vascularity. Sometimes small flow voids can be seen on nonenhanced MR, causing a “speckled” or “salt and pepper” appearance of the tumor. On dynamic enhanced CT or MR, there will be a rapid enhancement, a high peak, and rapid washout due to early arteriovenous shunting of the tumor. Conventional catheter angiography reveals similar findings. In addition, embolization of the tumor can be undertaken during the angiographic exam to reduce blood loss from this highly vascular tumor during surgery. Another study that can be performed to evaluate the carotid body tumor is an Indium-111 octreotide isotope scan which is preferentially taken up by neuroendocrine tissues and can help detect presence of multiple paragangliomas.

Surgical excision is the preferred treatment of head and neck paragangliomas in most cases although it is not without risk. The main risks of excision are injury to local cranial nerves or to the carotid artery and blood loss from these highly vascular tumors. If the tumor is found to encase the carotid extensively, then temporary balloon occlusion of the common carotid artery with EEG monitoring can help determine the adequacy of collateral circulation. If the patient is not a surgical candidate, due to extensive tumor involvement or coexisting morbidities, radiation therapy is an option, although it is considered second-line therapy.

Repeat examinations advised by Radiologists-how much do they contribute to the bulk??

According to a recent article in Radiology. 2007 Mar;242(3):857-64,

From 1997 to mid-2003, MR imaging and CT repeat rates increased (0.71% per year and 1.87% per year respectively). Repeat examinations account for nearly one-third of high-cost radiology examinations and represent an increasing proportion of such examinations. Most repeat examinations are initiated clinically without a recommendation by a radiologist.

Article entitled-

Does radiologist recommendation for follow-up with the same imaging modality contribute substantially to high-cost imaging volume?

Radiology 2007 Mar;242(3):857-64.

Cubao Bus Terminal Station

Everyone seems to be leaving Manila behind to head up to the beaches and mountains. I myself am going to Mount Makiling to spend my own Holy Week there. Meantime, here are the images on how it looks like to be in the central bus station in Araneta center Cubao during this time of the year. Have a nice getaway everyone!

Nasolacrimal duct mucocele

Findings

There is a rounded hypoattenuating lesion in the medial aspect of the left orbit which extends through the left nasolacrimal duct into the left nasal cavity. There is bony expansion of the left nasolacrimal duct.

Differential diagnosis:
- Mucocele
- Intraorbital abscess
- Encephalocele
- Dermoid
- Hemangioma
- Glioma


Diagnosis: Nasolacrimal duct mucocele



Congenital nasolacrimal duct mucocele is characterized by a triad of findings:
- Mass located at the medial canthus
- Bony expansion of the nasolacrimal duct
- Intranasal mass

In neonates, there is a thin mucus membrane (plica lacrimale or valve of Hasner) at the inferior aspect of the nasolacrimal duct. In 6-12% of patients, this is imperforate at birth, but shortly after birth it typically spontaneously perforates.
Failure to perforate this membrane results in outflow obstruction with subsequent mucocele formation.
Initial presentation may include a mass at the medical canthus. A secondary infection may cause physical exam findings similar to an abscess.
Epiphora may result from blockage of nasolacrimal duct drainage.
The initial presentation may also include respiratory distress secondary to nasal obstruction, as neonates are obligate nasal breathers.
Management is typically expectant, as spontaneous perforation is typical. If there is persistent failure to perforate, or there are signs of infection, the mucocele can be marsupialized endoscopically, or a dacryocystorhinostomy may be performed.
The imaging modality of choice is CT, which can show the extent of the mass lesion within the medial canthus as well as the nasal cavity, and any associated nasolacrimal duct bony expansion.

Malignant otitis externa

Findings

Figure 1: Initial CT of the skull base on bone widows shows subtotal opacification of the mastoid air cells without bony destruction.
Figure 2: CT of the skull base on soft tissue windows shows an inflammatory soft tissue mass filling the external auditory canal extending into the surrounding soft tissues without involvement of the middle ear.
Figure 3: On subsequent CT of the skull base with soft tissue windows, the inflammatory soft tissue mass remains with partial destruction of the auricular cartilage. It now crosses the tympanic membrane and opacifies the middle ear with osteolysis of the anterior, bony portion of the external auditory canal.
Figure 4: Axial bone windows reveal destruction of the anterior wall of the mastoid air cells.
Figure 5: Sagittal reconstruction with bone windows reveals coalescing mastoiditis with destruction of the bony septae and resultant enlargement of the air cells. The inflammatory mass displaces the mandibular condyle anteriorly out of the articular fossa.
Figure 6: Coronal reconstruction with bone windows reveals soft tissue opacifying the middle ear with partial destruction of the tympanic portion of the temporal bone.


Diagnosis: Malignant otitis externa


Malignant otitis externa (MOE) also referred to as necrotizing otitis externa or skull base osteomyelitis can be defined as otitis externa with progression to skull base osteomyelitis. The causative organism is almost universally Pseudomonas, which invades via the fissures of Santorini, located in the cartilaginous, lateral 1/3 of the external auditory canal (EAC). Affected patients are typically immunocompromised, often diabetic and present with symptoms of otitis externa unresponsive to topical antibiotics. Examination demonstrates purulent otorrhea with granulation tissue in the EAC. Cranial nerve involvement in the setting of otitis externa is an ominous sign and suggests progression to malignant otitis externa. Leukocytosis and signs of systemic infection are not typically present.

When diagnosing MOE, imaging is mandatory. CT is the exam of choice, demonstrating osteolysis in association with mastoid opacification and marked soft tissue inflammation centering on the external auditory canal. CT is relatively insensitive for early disease; osteolysis is not seen until at least 30% of the bone has been destroyed. Nuclear scans are generally sensitive but not specific, and may play an adjunctive role. Due to the lack of marrow in the affected bones, MR is of limited use, but may be complimentary to demonstrate soft tissue involvement.

Imaging can only suggest the diagnosis of MOE, and biopsy is necessary for confirmation.

The anatomy of the temporal bone means that the disease may disrupt the TMJ or the middle ear. Involvement of the facial nerve may occur. Intracranial spread is more ominous still, leading to venous sinus thrombosis, meningitis and abscess formation.

The historical mortality for MOE was 77%; however with current treatment the mortality is closer to 10%. Systemic antibiotics are the mainstay of therapy however surgical debridement may be necessary.