While alkaline (battery) injuries are usually deeper and worse than acid injuries, it is because the alkali sets up a type of necrosis called liquefactive necrosis.  Acids cause coagulative necrosis.  Alkaline ingestions cause tissue injury by liquefactive necrosis, a process that involves saponification of fats and solubilization of proteins. Cell death occurs from emulsification and disruption of cellular membranes. The hydroxide ion of the alkaline agent reacts with tissue collagen and causes it to swell and shorten. Small vessel thrombosis and heat production occurs.

Yesterday, the FDA Allergenic Products Advisory Committee supported approval for a new sublingual allergy tablets (Ragwitek) that work the same way allergy shots do… but instead is dissolved under the tongue at home instead of a shot in the arm in a medical office. Given this is only a panel recommendation, final “official” FDA approval may not occur for another year or so for sale/distribution under prescription in the United States.

Ragwitek is made by ALK-Abello and Merck and treats patients aged 18-65 years who are allergic to only short ragweed pollen. The way Ragwitek is taken is placement of 1 sublingual tablet daily starting 12 weeks before and continued until the end of the ragweed pollen season. The first dose is given in a medical office to ensure safety with all other doses taken at home. The tablet dissolves in less than 10 seconds.

Epipen needs to be available at home due to possible risk of anaphylaxis. As with allergy shots, patients on beta-blockers for high blood pressure are not eligible to undergo this treatment.

Ragwitek is similar to Oralair and Grastek which treat only grass allergy. Oralair and Grastek were both recommended by the FDA panel last year.

Grass Pill

Angioedema (or Quincke’s edema) is inflammation of the deep dermis or submucosa. It is non pitting, non dependent, non tender, non erythematous, usually assymmetric.  The term angiioneurotic oedema was a misnomer as it was initially thought to be a nervous system disorder. It can be life threatening if it involves the airway. It can be congenital, idiopathic, or drug induced. Ace inhibitor blood pressure medications are common offenders causing this condition. NSAIDS and food allergies are the other big culprit. A thorough allergy history and testing are paramount. Exciting new drugs are on the horizon for this condition.

Heinrich IrenaeusQuincke (26 August 1842 – 19 May 1922) was a German internist and surgeon who internist and surgeon.  He was perhaps the first (1882) to recognize angioedema which is often referred to as “Quincke’s edema”.[1] “Quincke’s pulse”, with redness and pallor seen under the fingernails, is one of the signs of aortic insufficiency.“Quincke’s puncture” is a somewhat outdated eponym for lumbar puncture, used for the examination of the cerebrospinal fluid in numerous diseases such as meningitis and multiple sclerosis. In 1893 he described what is now known as idiopathic intracranial hypertension, which he labeled “serous meningitis”.

Discoveries

He was perhaps the first (1882) to recognize angioedema which is often referred to as “Quincke’s edema”.[1] “Quincke’s pulse”, with redness and pallor seen under the fingernails, is one of the signs of aortic insufficiency.[2] “Quincke’s puncture” is a somewhat outdated eponym for lumbar puncture,[3][4] used for the examination of the cerebrospinal fluid in numerous diseases such as meningitis and multiple sclerosis. In 1893 he described what is now known as idiopathic intracranial hypertension, which he labeled “serous meningitis”.[5]

Congenital or Hereditary Angioedema is relatively rare. It usually shows up in childhood. It is essentially caused from either absent of non functioning complement factors. Primarily C1 Esterase Inhibitor. Acquired or hereditary angioedema do not typically respond to antihistamines or steroids, so the fact that he got better with these medications argues against this. It is bradykinin mediated and inflammation peaks in about 12 hours. Also, Hereditary Angioedema does not Urticate (No Hives). Nevertheless, checking labs would put these (remote) possibilities to rest. A good laboratory screen would be aC2, C3, C4, C1q, and C1-INH level and function, ESR, ANA, RF, hepatic transaminases, TSH, T4, anti-thyroglobulin antibodies, anti-thyroid peroxidase antibodies, CBC/diff and CU index (available thru Quest and Labcorp).  If your patient has had a recent reaction, then simple doing a C4 assay will rule out a hereditary etiology.  I have yet to diagnose a case of this.  The drug company that manufactures cinryze is a human derived C1 esterase inhibitor and has to be given IV every few days and cost nearly 300k per year.  Given androgens on a regular basis is the other option for this chronic condition.

The vast majority of Angioedema is idiopathic and often drug induced. It is essentially a deeper (subdermal or submucosal) version of urticaria and is similarly most often idiopathic. It usually manifests in adulthood. Medications started within the past several months are most likely. However, ACE inhibitors are notorious for causing these reactions even after years of safe use. Aspirin and NSAIDs are also frequent causes or exacerbating factors. Less commonly, underlying problems like thyroid disease, liver disease, autoimmune disease or occult malignancy can be responsible. About half of patients with otherwise “idiopathic” chronic urticaria/angioedema make IgG autoantibodies against the high affinity IgE receptor on mast cells. Foods are uncommon offenders, but should be considered. Routine allergy testing and diet diary are appropriate.  Non hereditary forms are histaminic and thus respond better to allergy medications such as antihistamines, epinephrine, and steroids.

Treatment is largely symptomatic. Symptoms wax and wane for weeks and even months. Unfortunately up to 95% of patients will never find the etiology. I often suggest a daily 24 hour acting antihistamine to prevent/suppress episodes, such as Zyrtec 10 mg qd. If symptoms persist, you can add Allegra 180 mg qam and take Zyrtec 10 mg qhs. If symptoms STILL persist, you can continue Allegra and switch Zyrtec to Atarax, titrated as needed to suppress episodes while minimizing (hopefully) daytime sedation. I also often add a type 2 antihistamine such as Zantac. Steroids of course are helpful, however one should be cautious of rebound inflammation.

Denervation as a therapy for vasomotor rhinitis has often been considered.  With the advent of topical therapies, Dr Templer referred to this a complex procedure in search of an indication.  By transecting the Sphenopalatine Artery, we are in essence dividing the more distal nerve and thus attaining our objectives.

Most of us give our patients oral steroids such as prednisone or methylprednisolone.  Convenience, compliance, and side effects are the reasons we might consider injecting over oral administration.  60 mg of Kenalog seems to give patients a good measure of relief with very little side effects.  There is also no question of compliance with this.  The site of injection seems to matter very little, however, as we see with our tip rhinoplasty patients local atrophy is real and might actually be a beneficial side effect if we consider the inferior turbinate.  Safety in regards to micro emboli need to be considered, however, this seems very unlikely with our improved techniques and visualization.

Utilizing Flovent 220 with a modified baby nipple in the nose might be a significant adjuvant tool for refractory polyp patients. In talking with other allergists and sinus physicians I am always excited to steal from others and add to my own bag of tricks.

The biggest fear in allergy shots is the severe, or even fatal, reaction.  Each year 3-4 people die from a severe allergic reaction to allergy shots.  The biggest risk seems to be poorly controlled asthma.  Epinephrine given immediately is the most important intervention.  The reaction can happen up to 30 minutes after the shot, however, the vast majority happen within 15 minutes.  If an epinephrine injection is given, the patient should be ready to need another treatment.  Biphasic reactions are common and can happen hours later.  Drawing a tryptase level and instituting steroids seems appropriate.  Interestingly, large local reactions do not clearly predict systemic reactions.  However, they may still require a dose reduction.

Pertussis, also known as whooping cough, is a highly contagious respiratory disease. It is caused by the bacterium Bordetella pertussis.

Pertussis is known for uncontrollable, violent coughing which often makes it hard to breathe. After fits of many coughs, someone with pertussis often needs to take deep breathes which result in a “whooping” sound. Pertussis most commonly affects infants and young children and can be fatal, especially in babies less than 1 year of age.  In adults it often manifests as the “100 days cough.”

The classic symptoms of pertussis are a paroxysmal cough, inspiratory whoop, and fainting and/or vomiting after coughing.[5] The cough from pertussis has been documented to cause subconjunctival hemorrhages, rib fractures, urinary incontinence, hernias, post-cough fainting, and vertebral artery dissection.[5] Violent coughing can cause the pleura to rupture, leading to a pneumothorax. If there is vomiting after a coughing spell or an inspiratory whooping sound on coughing, the likelihood almost doubles that the illness is pertussis. On the other hand, the absence of a paroxysmal cough or posttussive emesis makes it almost half as likely.[5]
The incubation period is typically seven to ten days with a range of four to 21 days and rarely may be as long as 42 days,[6] after which there are usually mild respiratory symptoms, mild coughing, sneezing, or runny nose. This is known as the catarrhal stage. After one to two weeks, the coughing classically develops into uncontrollable fits, each with five to ten forceful coughs, followed by a high-pitched “whoop” sound in younger children, or a gasping sound in older children, as the patient struggles to breathe in afterwards (paroxysmal stage).
Fits can occur on their own or can be triggered by yawning, stretching, laughing, eating or yelling; they usually occur in groups, with multiple episodes every hour around the clock. This stage usually lasts two to eight weeks, or sometimes longer. A gradual transition then occurs to the convalescent stage, which usually lasts one to two weeks. This stage is marked by a decrease in paroxysms of coughing, both in frequency and severity, and a cessation of vomiting. A tendency to produce the “whooping” sound after coughing may remain for a considerable period after the disease itself has cleared up.

The best way to protect against pertussis is immunization.  The immunization is primarily given as the DPT vaccine and is generally considered safe and cost effective.  Treatment with a macrolide or Bactrim is  first line.  Diagnosis is made with a nasopharyngeal swab cultured in Bordet-Gengou medium.

The Chronic Cough is a very common complaint in both our adult and pediatric patients.  History and Physical exam are paramount and ruling out a worrisome etiology is our initial objective.  After this is accomplished the etiology is almost always multifactorial.  LPR, Cough variant asthma, PND associated with Allergic rhinitis, and Infectious etiologies are highest on our differential.

The Delphian (DL) node, also called the prelaryngeal or cricothyroid node, is a lymph node located on the fascia above the cricothyroid membrane. The DL node receives afferent lymphatic drainage from the larynx (supraglottis and subglottis via the anterior commissure) and the thyroid gland (upper and anterior portions of both lobes and isthmus). The DL node has two main efferent lymphatic drainage routes: one flows toward the pretracheal (sub-DL), mediastinal, supraclavicular nodes and the other to the paratracheal and lower jugular (Level IV) nodes (Fig. 1). The expression ‘Delphian’ was first used by R. Randall, at the time a medical student at Harvard, because a metastasis to the DL node may predict the prognostic outcome of laryngeal and thyroid cancers, in the same way the prophecy of Apollo at temple of Delphi foretold the future in ancient Greece.  The Oracle of Delphi in this case would make the dire prediction that death from Squamous Cell or Thyroid Cell carcinoma is pending.