Tag Archives: ENT

Ear Development

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Ear development

The ear is a fascinating and complex appendage and organ. Formation is from structures called branchial arches. Branchial (from Greek branchia gills) arches are composed of endoderm on the internal aspect, by clefts composed of ectoderm on the external side with the central mesoderm containing the muscle, cartilage, vessels and nerves that will ultimately supply and establish the surrounding anatomic structures. Molecular signaling from the ectoderm leads the mesenchyme from the mesodermal (central) layer to eventually, if it works out as planned, to obliterate the clefts and and pouches. If clefts persist, they are given names, such as Type I branchial cleft cyst. When this signaling goes wrong, there are different degrees of anomalies, from absence of specific auricle components to microtia or even anotia if there is complete failure.

The ear begins to form the otic placode and vestibulocochlear ganglia at 3 weeks of gestation. The external canal then develops from the first branchial cleft at 4 weeks. By 28 weeks there is a fully open external canal. Failure to canalize can result in membranous or bony stenosis or atresia (from Latin a = no and Greek trēsisperforation, from tetrainein to pierce). Development of the auricle (external ear) begins at 5 weeks gestation with development of the auricular hillocks numbered from 1 through 6, derived from the first (mandibular) and second (hyoid) branchial arches. So the inner ear has already formed when the external ear begins.

The ear develops in a predictable manner, with various alterations in development resulting in predictable deformities when the process is interrupted. Knowledge of auricular development as well as normal external anatomy allows for precise evaluation of the ear and assists in selecting appropriate reconstructive techniques to optimize the complex 3-dimensional anatomical outcomes.

If you have a ear question, please do not hesitate to call me for an appointment. Office number is 989-839-6201, fax is 989-839-6202. Providers can page me through the Midland hospital operator. Patients can reach me by way of the patient portal.

Let me know how I can be of help to you.

Philip Harris, MD FARS
Ear Nose Throat and Cancer of the Head and Neck
Serving Gladwin, Clare, Midland and Alpena
Call for appointment and ask to see Dr. Harris


Is Being Fat Killing Us?

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A new report addresses many novel and intriguing aspects of the relationship between cancer, cancer stem cells, and adipocytes (fat cells).

Fat (adipose) tissue has been suggested to play a direct role in resistance to cancer treatment. Obese (body mass index or BMI > 25) patients with leukemia have shown poor survival outcomes relative to non-obese patients (see 2010 ,M.A. Lichtman Oncologist, 15, pp. 1083–110). When one has cancer, traditionally there was weight loss. This was termed cachexia,a common and historically long-recognized hallmark of advanced cancer. Breakdown of adipose tissue through the action of pro-inflammatory cytokines leading to tissue atrophy occurs as part of cancer-induced cachexia. This dramatic metabolic disturbance was assumed to benefit the tumor at the expense of the normal tissue. These changes are only beginning to be more fully explored.

A recent mouse study found that leukemia cells utilized fat to hide away from the immune system. Numerous leukemia cells were found in gonadal addipose tissue (GAT), which is the largest visceral fat depot in mice, but not in subcutaneous fat deposits. The leukemia cells were located directly adjacent to adipocytes throughout the tissue. Even more worrisome, these phenotypically defined GAT-resident leukemic stem cells gave rise to leukemia at frequencies comparable to bone-marrow-derived leukemia stem cells. This established that adipose (fat) tissue can function as a reservoir for this cancer. As the mice’s leukemia progressed, atrophy of GAT was noted before the development of full-blown cachexia (weight loss).

Adipose tissue has previously been identified as an extra-medullary reservoir for normal hematopoietic stem cells (HSCs) and may promote tumor development.

As a cancer survivor and as a surgeon who treats head and neck cancer, I encourage you to be lean and fit. Maybe it will keep that cancer at bay or from recurring? You will feel and look better while fighting to keep away a disease that 50% of the population will get, cancer.


Basal Cell Carcinoma

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Skin cancer in general is a very large topic and difficult to address in a blog. As a head and neck surgeon, I commonly see skin cancer on referral for surgical treatment.

I would reference the reader to two recent and good articles to review.

JNCCN May 2016 Basal Cell Skin Cancer, Version 1.2016, NCCN Clinical Practice Guidelines in Oncology  and

European Journal of Cancer November 2014 Surgical excision versus Mohs’ micrographic surgery for basal cell carcinoma of the face: A randomised clinical trial with 10 year follow-up

Basal cell carcinoma (BCC) is a common form of cancer. The incidence has increased over the past decades and is predicted to continue rising. The disease related mortality is very low due to the low rates of metastatic disease but morbidity can be high due to local tissue destruction, especially since most tumors occur in functional areas such as the head and neck.

Known risk factors for development of BCC are sunlight (relationship between sun exposure and BCC is complex, depending on timing, pattern, and amount of ultraviolet radiation), fair skin, red or blond hair, light eye color, and radiation treatment for other conditions, especially at a young age. BCC tends to occur in the head and neck area and within the treatment field of prior radiation therapy. BCCs that develop in the head and neck area are more likely to recur than those developing on the trunk and extremities. BCC located in the H-zone of the face, with positive excision margins in previous resections or with an aggressive histological growth pattern show higher recurrence rates. Compared with squamous cell carcinoma, BCCs are much less likely to metastasize

Workup begins with a history and physical examination. A skin biopsy may then be performed on a suspicious lesion. The biopsy needs to include deep reticular dermis if the lesion is suspected to be more than a superficial process.  Imaging studies may be considered when extensive disease such as bone involvement, perineural invasion, or deep soft tissue involvement is suspected. MRI has greater sensitivity for perineural disease.

Many therapeutic options are available today, standard surgical excision (SE) is still the most common form of treatment for BCCs and Mohs’ micrographic surgery (MMS), a specialized surgical technique where available. The difference between both treatments is the method of histological margin examination primarily. In standard SE, surgical margins are mostly examined on random vertical sections whereas in MMS, the specimen is flattened and sliced horizontally offering the possibility to examine 100% of the resection margins. Treatment of BCC is primarily surgical with radiation as an alternate and / or adjuvant treatment. Radiation is not the primary treatment choice. Superficial therapies for BCC have been explored (topicals, cryosurgery, and photodynamic therapy). Two hedgehog pathway inhibitors are approved by the FDA for systemic treatment of advanced and metastatic BCC. Recurrences are more common when tumors in high-risk locations are 6 mm or more in diameter and when tumors in moderate-risk locations are 10 mm or more in diameter. immunosuppression, such as organ transplantation and long-term use of psoralen and UV-A light (PUVA), increase the incidence of BCC. Tumors developing in sites of prior radiotherapy are high risk. Tumors with perineural involvement poses a greatly increased risk of recurrence. Associated risk factors for perineural spread include previous recurrent tumors, high-grade, larger lesion size, and infiltrating, morpheic, and basosquamous subtypes.

In most patients the removal is performed under local anesthesia.  Surgical excision is currently with a 4-5 mm clinically tumor free resection margin at a 90° angle into the subcutaneous fat (for well-circumscribed BCC lesions less than 2 cm in diameter, excision with 4-mm clinical margins should result in complete removal in more than 95% of cases). For Mohs micrognathic surgery, the tumor is excised with the same clinically tumor free resection margin at a 45° angle in order to obtain a bowl-shaped excision sample (the preferred surgical technique for high-risk BCC because it allows intraoperative analysis, of 100% of the excision margin). In the Netherland study noted above, the excisions were at previously recommended margins of 3 mm. The benefit of larger margins must always be carefully weighed against the disadvantage of larger defects. A larger defect worsens aesthetic outcome and may in some cases lead to reduced functionality. The costs of MMS are higher than costs of SE and should be reserved for high risk facial primary BCC and facial recurrent BCC for example. A high risk facial primary BCC would be defined as a BCC of at least 1 cm diameter either located in the H-zone of the face or being of an aggressive histological subtype. For these lesions, we consider MMS superior to SE.  Recurrences after surgical treatment can still occur up to and even after 10-years post treatment. In BCC treated with MMS, fewer tumors do recoccur during long-term follow-up.

A brief discussion of local treatments for the reader includes use of curettage and electrodesiccation, standard surgical excision followed by postoperative pathologic evaluation of margins, MOHS, cryosurgery, radiation, topical therapy and photodynamic therapy.

Curettage and electrodesiccation is the process of alternatively scraping away tumor tissue with a curette down to a firm layer of normal dermis and denaturing the area by electrodessication. Up to 3 cycles may be performed in a session. It is a fast and cost-effective technique for superficial lesions but does not allow histologic margin assessment. A skilled practitioner is required as it is highly operator dependent. If the subcutaneous layer is reached during the course of surgery, surgical excision should generally be performed instead.

Radiation therapy, as a primary treatment, results in higher recurrence rates than surgery, poorer cosmetic outcomes, and more postoperative complications.

Superficial therapies (cryotherapy, photodynamic therapy) should be reserved for patients for whom surgery or radiation therapy is contraindicated or impractical. Cure rates are lower with superficial therapies. A key limitation of cryotherapy is poorer cosmetic outcomes, operator dependent result, and lack of specimen for pathological assessment.

Recommendations for low risk BCC include curettage and electrodissection in areas without hair growth, standard excision with 4 mm margin, radiotherapy for nonsurgical candidates (generally limited to those over age 60 years due to risk of long term toxicity), and pursuit of Mohs if margins are positive after standard excision or re-resection based on pathology. High risk BCC are advised standard excision with wider margins, Mohs, or radiation therapy for non-surgical candidates. Adjuvant radiation therapy advised for large nerve or extensive perineural involvement and in case of positive margin. Hedgehog pathway inhibitors an be offered for systemic therapy after multidisciplinary consultation.

The subtypes encompassed by the term “aggressive growth pattern” including micronodular, infiltrative, sclerosing, and morpheaform (or desmoplastic) patterns are more likely to recur than nodular and superficial BCC.Non-aggressive subtypes include the keratotic variant, infundibulocystic variant, and fibroepithelioma of Pinkus.

All patients who have had skin cancer need continuous followup and monitoring.  30% to 50% of patients will develop another BCC within 5 years. Patients with a prior BCC are also at increased risk of developing SCC and cutaneous melanoma. Continued long-term surveillance is essential, as is education about the values of sun protection and regular self-examination of the skin.

Resources for you and your patients: