A chalazion (/kəˈleɪziən/; plural chalazia /kəˈleɪziə/), also known as a meibomian gland lipogranuloma, is a cyst in the eyelid that is caused by inflammation of a blocked meibomian gland, usually on the upper eyelid. Chalazia differ from styes (hordeola) in that they are subacute and usually painless nodules. They may become acutely inflamed, but unlike a stye, chalazia usually sit inside the lid rather than on the lid margin.
A submucous cleft palate is one type of cleft palate. The word “palate” refers to the roof of the mouth and the term “cleft” indicates a split in the palate. The palate consists of both a bony portion (hard palate) and a muscular portion (soft palate). At the end of the soft palate, the small finger-like projection of tissue that hangs down is called the “uvula”. The term “submucous” refers to the fact that the cleft is covered over by the lining (mucous membrane) of the roof of the mouth. This covering of mucosa makes the cleft difficult to see when looking in the mouth.
A submucous cleft of the soft palate is characterized by a midline deficiency or lack of muscular tissue and incorrect positioning of the muscles. A submucous cleft of the hard palate is defined as a bony defect in the midline or center of the bony palate. This can sometimes be felt as a notch or depression in the bony palate when the palate is palpated with a finger. Often a submucous cleft palate is associated with a bifid or cleft uvula.
A branchial cleft cyst is a congenital epithelial cyst that arises on the lateral part of the neck due to failure of obliteration of the second branchial cleft (or failure of fusion of the second and third branchial arches) in embryonic development.
The cyst wall is composed of either squamous or columnar cells with lymphoid infiltrate, often with prominent germinal centers. The cyst may contain granular and keratinaceous cellular debris. Cholesterol crystals may be found in the fluid extracted from a branchial cyst. If the cyst connects to the either the skin on the outside or mucous membrane on the inside it is called a sinus. If it connects to both it is called a fistula.
Branchial cleft cysts are remnants of embryonic development and result from a failure of obliteration of one of the branchial clefts, which in fish develop into gills.
First branchial cleft fistulae typically originate in the angle of the mandible and extend to the external auditory canal. They are often associated with the facial nerve. Rare ~5%.
Second branchial cleft fistulae are most common (~95%). They are found along the anterior border of the Sternocleidomastoid muscle, pass through the carotid bifurcation and into the tonsillar pillar.
Third and fourth branchial cleft fistulae are rare. The external opening occurs about 2/3 of the way down the SCM anteriorly, similar to second branchial cleft cysts. The tract ascends along the carotid sheath posteriorly to the internal carotid artery, under the glossopharyngeal nerve, and over the vagus nerve and hypoglossal nerve to open into the piriform sinus.
Most branchial cleft fistulae are asymptomatic, but they may become infected. The cyst, however, usually presents as a smooth, slowly enlarging lateral neck mass that may increase in size after an upper respiratory tract infection.
Bilateral branchial cleft sinuses during surgery. Conservative (i.e. no treatment), or surgical excision. As complete surgical excision may be difficult (due to the close proximity of the internal jugular vein and carotid vessels that lie deep to the swelling), they can recur.
Frontal sinusotomy is a broad term which encompasses both external and intranasal approaches to open and/or create a permanent communication from the sinus to the nose.
Endoscopic frontal sinusotomy is defined as creating a permanent opening from the frontal sinus into the nose. This simple definition includes a range from relatively simple to highly complex procedures (Weber, 2001). The complexity of endoscopic frontal sinusotomy is determined by the site of obstruction to the outflow tract or disease within the sinus, and variations in frontal and ethmoid sinus anatomy.
I think most of us ENTs (in independent practice) would open our offices after hours for a colleague with a nosebleed. I’d much rather treat a nosebleed in my office than the ED (no offense meant toward my ED colleagues). I have most of the instruments and lighting that I would need there, ready to go. Definitely would favor an ED rather than a UCC.
Some “anterior” nosebleeds can bleed like stink. This is because bleeding is from a higher pressure arteriole. If you have Afrin or Neosynephrine at home (and it’s actively bleeding), I would advise using (after blowing to evacuate clots, as clot begets bleeding by depleting the clotting factors). Then firmly pinch the lower collapsible soft part of the nose (thumb and finger, tongue blades, clothes pin, I’ve even seen patients use a “chip clip”) for 10-15 minutes BY THE CLOCK. (Remember normal Ivy bleeding time is 3-10 minutes — but bleeding times are sadly no longer being done most places.)
If you have a bit of knowledge of internal nasal anatomy, you could try wetting an appropriate sized piece of cotton with decongestant and carefully slipping it into the nostril before pinching the nose. Keep the head elevated. Pressure on the upper lip below the nose can decrease the blood pressure in anterior septal arterioles. Ice on the forehead and/or back of the neck might help. If you are in the ER, use their LET Solution on a cotton ball—has the topical 1:1000 epi and is incredibly effective at constricting the offending arterioles.
Finally, and I’ve brought this up on other threads before, if you have some bacon (and no religious objections) you could cut off a generous portion (as fatty as possible) and gently stuff it snuggly into the nostril before going to the ED. Pork fat has a water soluble compound that promotes platelet adhesion (making them “super platelets”) and I have used salt pork with a number of patients on anti-coagulants as well as with thrombocytopenia. It has not failed me yet — this is after other, more “traditional” methods have failed.
Try to avoid sticking dry or abrasive materials into the nose (e.g. Kleenex, toilet paper, or even dry cotton). To prevent future bleeds I recommend: humidification, avoidance of NSAIDs (especially Toradol.
Take 250-500mg Vitamin C daily (promotes hydroxylation of proline and collagen formation).
Despite being benign, ameloblastoma can be very aggressive, growing into the jawbone and causing swelling and pain. Very rarely, ameloblastoma cells can spread to other areas of the body, such as the lymph nodes in the neck and the lungs.
Ameloblastoma is the most common type of odontogenic lesion.
There are over 200 known serotypes of HPV. About 79 million Americans are currently infected with HPV. About 7% of adults have HPV in their oral cavity. Only about 3,000 to 13,000 patients in the United States have Recurrent Respiratory Papilllomatosis. Virtually all of them have active HPV in thier oral cavity. These patients are afflicted with HPV 6 and 11, which affects primarily mucous membranes. It is looking more and more like oral to oral transmission trumps oral genital transmission. It seems to be a different animal all together than cervical HPV. Serotypes 16 and 18 are the types associated with carcinogenesis. There currently is no evidence that spouses should be vaccinated and it does not really seem to be easily transmitted between adults.PRIMARILY HPV 6 & 11 (RARELY TYPE 16 & 18).
This disease has become epidemic, however the treatments and the preventative measures are also gaining momentum. HPV is the whole reason we really did PAP smears. The viral changes led to cervical uterine dysplasian and even carcinogenesis. It was even suggested to consider C-section in women with active infections.
Adjuvant therapies such as Acyclovir, MTX, Ribavarin, Mumps vaccine, PPI, Alpha Interferon, Hsp E7, Retinoids, and Intralesional Cidofovir have been touted, but lack strong prospective efficacy studies. Typically I use the CO2 laser. Have patients eat green leafy vegetables (Indole-3-carbinols) modulates estrogen metabolism and 1/3 of patients respond. Inject about 75 mg of Cidofovir in 1 cc after the resection. I may consider placing on Celebrex (Cox 2 inhibitor) which modulates the over expression of epidermal growth factor by inhibiting cyclooxygenase-2 and prostaglandin E2. I also may consider injecting Avastin (Bevacizumab) recombinant monoclonal antibody against vascular endothelial growth factor.
Alpha-gal allergies are a reaction to Galactose-alpha-1,3-galactose, whereby the body is overloaded with immunoglobulin E antibodies on contact with the carbohydrate. Alpha-gal is found in all mammals apart from primates (including humans). Bites from the lone star tick, which transfer this carbohydrate to the victim, have been implicated in the development of this delayed allergic response which is triggered by the consumption of mammalian meat products. Despite myths to the contrary, an alpha-gal allergy does not require the afflicted to become a vegetarian, as poultry and fish do not trigger a reaction.
The allergy most often occurs in the central and southern United States, which corresponds to the distribution of the lone star tick. In the Southern United States, where the tick is most prevalent, allergy rates are 32% higher than elsewhere. However, as doctors are not required to report the number of patients suffering the alpha-gal allergies, the true number of affected individuals is unknown.
The allergy was first formally identified as originating from tick bites in a 2007 paper by Sheryl van Nunen. Prior to the paper’s publication, Thomas Platts-Mills and Scott Commins, were attempting to discover why some patients were reacting negatively to the carbohydrate in the cancer drug Cetuximab. They had previously hypothesized that a fungal infection or parasite could lead to the allergy. It wasn’t until Platts-Mills was bitten by a tick and developed alpha-gal allergies, that his team also came to the conclusion that there was a link between tick bites and the allergy.
Alpha-gal allergies are very similar to Pork-Cat Syndrome and hence misidentification can occur.
Alpha-gal allergies develop after a person has been bitten by the Lone Star Tick in the United States, the European Castor Bean Tick, and the Paralysis Tick in Australia. Alpha-gal is not naturally present in apes (including humans), but is in all other mammals. If a tick feeds on another mammal, the alpha-gal will remain in its alimentary tract. The tick will then inject the alpha-gal into a person’s skin, which in turn will cause the immune system to release a flood of immunoglobulin E antibodies (a.k.a. IgE) to fight off the foreign carbohydrate. Researchers still do not know which specific component of tick saliva causes the reaction.
A 2012 preliminary study found unexpectedly high rates of alpha-gal allergies in the Western and North Central parts of the United States, which suggests that the allergy may be spread by unknown tick species. Examples of alpha-gal allergies were even present in Hawaii, where none of the ticks identified with the allergies live. Human factors were suggested but no specific examples were provided.
A typical allergic reaction to alpha gal has a delayed onset, occurring 4–8 hours after the consumption of mammalian meat products, instead of the typical rapid onset with most food allergies. After the delayed onset, the allergic response is typical of most food allergies, and especially an IgE mediated allergy, including severe whole-body itching, hives, angioedema, gastrointestinal upset, and possible anaphylaxis. These symptoms are caused by too many IgE antibodies attacking the allergen, in this case the alpha-gal. In 70% of cases the reaction is accompanied by respiratory distress and as such is particularly harmful to those with asthma.
Alpha-gal allergies are the first food allergies to come with the possibility of delayed anaphylaxis. It is also the first food-related allergy to be associated with a carbohydrate, rather than a protein.
Treatment and medical issues
Blood tests for IgE response indicating alpha gal allergy have not been approved by the U.S. Food and Drug Administration (FDA), and must usually be purchased by private individuals, but are available and are in use.
There has been at least one instance of a man with an alpha-gal allergy going into anaphylaxis after receiving a heart-valve. Some researchers have suggested that the alpha-gal which is prevalent in pig’s tissue, and used for xenografts, may contribute to organ rejection.
Unlike most food allergies, the alpha-gal allergy will recede with time, as long as the person is not bitten by another tick. The recovery period can take anywhere from eight months to five years.
A new type of cancer treatment called HyperAcute immunotherapies, which utilizes humans’ usual immunity to alpha-gal is being tested by NewLink Genetics Corporation. The treatment uses modified alpha-gal cells to provoke a strong reaction in the immune system, but targeted towards cancer, rather than attacking the alpha-gal cells themselves. As of November 2013, the treatment was in a Phase 3 Trial with the FDA.