Common issues that lead to overuse of topical decongestants:

- Deviated septum

- Upper respiratory tract infection

- Vasomotor rhinitis

- Cocaine use and other stimulant abuse

- Pregnancy (these products are not considered safe for pregnancy)

- Chronic rhinosinusitis

- Hypertrophy of the inferior turbinates

It has been hypothesized that biofilm bacterial infections may account for many cases of antibiotic-refractory chronic sinusitis. Biofilms are complex aggregates of extracellular matrix and inter-dependent microorganisms from multiple species, many of which may be difficult or impossible to isolate using standard clinical laboratory techniques. Bacteria found in biofilms have their antibiotic resistance increased up to 1000 times when compared to free-living bacteria of the same species. A recent study found that biofilms were present on the mucosa of 75% of people undergoing surgery for chronic sinusitis.

Sinusitis is a common condition, with between 24 and 31 million cases occurring in the United States annually. Chronic sinusitis affects approximately 12.5% of people.

The hygiene hypothesis attempts to explain the increased rates of asthma worldwide as a direct and unintended result of reduced exposure, during childhood, to non-pathogenic bacteria and viruses. It has been proposed that the reduced exposure to bacteria and viruses is due, in part, to increased cleanliness and decreased family size in modern societies. Exposure to bacterial endotoxin in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction. Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.

Use of antibiotics in early life has been linked to the development of asthma. Also, delivery via caesarean section is associated with an increased risk (estimated at 20–80%) of asthma—this increased risk is attributed to the lack of healthy bacterial colonization that the newborn would have acquired from passage through the birth canal. There is a link between asthma and the degree of affluence which may be related to the hygiene hypothesis as less affluent individuals often have more exposure to bacteria and viruses.

Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms. Low air quality from factors such as traffic pollution or high ozone levels has been associated with both asthma development and increased asthma severity. Over half of cases in children in the United States occur in areas with air quality below EPA standards. Low air quality is more common in low-income and minority communities.

Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association. Also, phthalates in certain types of PVC are associated with asthma in children and adults. While exposure to pesticides is linked to the development of asthma it is unclear if this is a cause and effect relationship.

There is an association between acetaminophen (paracetamol) use and asthma. The majority of the evidence does not, however, support a causal role. A 2014 review found that the association disappeared when respiratory infections were taken into account. Use by a mother during pregnancy is also associated with an increased risk as is psychological stress during pregnancy.

Asthma is associated with exposure to indoor allergens. Common indoor allergens include dust mites, cockroaches, animal dander (fragments of fur or feathers), and mold. Efforts to decrease dust mites have been found to be ineffective on symptoms in sensitized subjects. Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, may increase the risk of developing asthma when acquired as young children. Certain other infections, however, may decrease the risk.

There is low or very-low quality evidence that probiotics may be better than placebo in preventing acute URTIs. Vaccination against influenza viruses, adenoviruses, measles, rubella, "Streptococcus pneumoniae", "Haemophilus influenzae", diphtheria, "Bacillus anthracis", and "Bordetella pertussis" may prevent them from infecting the URT or reduce the severity of the infection.

Children have 2-9 viral respiratory illnesses per year. In 2013 18.8 billion cases of upper respiratory infections were reported. As of 2014, upper respiratory infections caused about 3,000 deaths down from 4,000 in 1990. In the United States, URIs are the most common infectious illness in the general population. URIs are the leading reasons for people missing work and school.

The pathophysiology of RM is unclear, although several mechanisms involving norepinephrine signaling have been proposed. RM is associated with histological changes that include: an increase in the number of lymphocytes and fibroblasts, epithelial cell denudation, epithelial edema, goblet cell hyperplasia, increased expression of the epidermal growth factor receptor, increased mucus production, nasociliary loss, inflammatory cell infiltration, and squamous cell metaplasia.

Direct acting sympathomimetic amines, such as phenylephrine stimulate alpha adrenergic receptors, while mixed-acting agents, such as pseudoephedrine can stimulate both alpha and beta adrenergic receptors directly and indirectly by releasing norepinephrine from sympathetic nerve terminals. At first, the vasoconstrictive effect of alpha-receptors dominates, but with continued use of an alpha agonist, this effect fades first, allowing the vasodilation due to beta-receptor stimulation to emerge.

2-Imidazoline derivatives, such as oxymetazoline, may participate in negative feedback on endogenous norepinephrine production. Therefore, after cessation of prolonged use, there will be inadequate sympathetic vasoconstriction in the nasal mucosa, and domination of parasympathetic activity can result in increased secretions and nasal edema. Evidence suggests that if oxymetazoline is used only nightly for allergic rhinitis (instead of more frequent dosage as may be directed on product label), it may be used longer than one week without high risk of rhinitis medicamentosa especially with use of intranasal steroid like fluticasone furoate.

There is currently a limited amount of information available on the incidence and prevalence of VCD, and the various rates reported in the literature are most likely an underestimate. Although VCD is thought to be rare overall, its prevalence among the population at large is not known.

However, numerous studies have been conducted on its incidence and prevalence among patients presenting with asthma and exertional dyspnea. A VCD incidence rate of 2% has been reported among patients whose primary complaint was either asthma or dyspnea; the same incidence rate has also been reported among patients with acute asthma exacerbation. Meanwhile, much higher VCD incidence rates have also been reported in asthmatic populations, ranging from 14% in children with refractory asthma to 40% in adults with the same complaint. It has also been reported that the VCD incidence rate is as high as 27% in non-asthmatic teenagers and young adults.

Data on the prevalence of VCD is also limited. An overall prevalence of 2.5% has been reported in patients presenting with asthma. Among adults with asthma considered "difficult to control", 10% were found to have VCD while 30% were found to have both VCD and asthma. Among children with severe asthma, a VCD prevalence rate of 14% has been reported. However, higher rates have also been reported; among one group of schoolchildren thought to suffer from exercise-induced asthma, it was found that 26.9% actually had VCD and not asthma. Among intercollegiate athletes with exercise-induced asthma, the VCD rate has been estimated at 3%.

In patients presenting with symptoms of dyspnea, prevalence rates ranging from 2.8% to 22% have been reported in various studies. It has been reported that two to three times more females than males suffer from VCD. VCD is especially common in females who suffer from psychological problems. There is an increased risk associated with being young and female. Among patients suffering from VCD, 71% are over the age of 18. In addition, 73% of those with VCD have a previous psychiatric diagnosis. VCD has also been reported in newborns with gastroesophageal reflux disorder (GERD).

Nasal polyps resulting from chronic rhinosinusitis affect approximately 4.3% of the population. Nasal polyps occur more frequently in men than women and are more common as people get older, increasing drastically after the age of 40.

Of people with chronic rhinosinusitis, 10% to 54% also have allergies. An estimated 40% to 80% of people with sensitivity to aspirin will develop nasal polyposis. In people with cystic fibrosis, nasal polyps are noted in 37% to 48%.

The following increase an individual's chances for acquiring VCD:

- Upper airway inflammation (allergic or non-allergic rhinitis, chronic sinusitis, recurrent upper respiratory infections)

- Gastroesophageal reflux disease

- Past traumatic event that involved breathing (e.g. near-drowning, suffocation)

- Severe emotional trauma or distress

- Female gender

- Playing a wind instrument

- Playing a competitive or elite sport

Empty nose syndrome has been observed to affect a small proportion of people who have undergone surgery to the nose or sinuses, particularly those who have undergone turbinectomy (a procedure that removes some of the bones in the nasal passage). The incidence of ENS is variable and has not yet been quantified, but it is considered rare.

Untreated, the condition can cause significant and longterm physical and emotional distress in some people; some of the initial presentations on the condition described people who committed suicide. It is difficult to determine what treatments are safe and effective, and to what extent, in part because the diagnosis itself is unclear.

Endoscopic sinus surgery with removal of polyps is often very effective for most people providing rapid symptom relief. Endoscopic sinus surgery is minimally-invasive and is done entirely through the nostril with the help of a camera. Surgery should be considered for those with complete nasal obstruction, uncontrolled runny nose, nasal deformity caused by polyps or continued symptoms despite medical management. Surgery serves to remove the polyps as well as the surrounding inflamed mucosa, open obstructed nasal passages, and clear the sinuses. This not only removes the obstruction caused by the polyps themselves, but allows medications such as saline irrigations and topical steroids to become more effective.

Surgery lasts approximately 45 minutes to 1 hour and can be done under general or local anesthesia. Most patients tolerate the surgery without much pain, though this can vary from patient to patient. The patient should expect some discomfort, congestion, and drainage from the nose in the first few days after surgery, but this should be mild. Complications from endoscopic sinus surgery are rare, but can include bleeding and damage to other structures in the area including the eye or brain.

Many physicians recommend a course of oral steroids prior to surgery to reduce mucosal inflammation, decrease bleeding during surgery, and help with visualization of the polyps. Nasal steroid sprays should be used preventatively after surgery to delay or prevent recurrence. People often have recurrence of polyps even following surgery. Therefore, continued follow up with a combination of medical and surgical management is preferred for the treatment of nasal polyps.

Initial treatment is similar to atrophic rhinitis, namely keeping the nasal mucosa moist with saline or oil-based lubricants and treating pain and infection as they arise; adding menthol to lubricants may be helpful in ENS, as may be use of a cool mist humidifer at home. For people with anxiety, depression, or who are obsessed with the feeling that they can't breathe, psychiatric or psychological care may be helpful.

In some people, surgery to restore missing or reduced turbinates may be beneficial.

A 2015 meta-analysis identified 128 people treated with surgery from eight studies that were useful to pool, with an age range of 18 to 64, most of whom had been suffering ENS symptoms for many years. The most common surgical approach was creating a pocket under the mucosa and implanting material - the amount and location were based on the judgement of the surgeon. In about half the cases a filler such as noncellular dermis, a medical-grade porous high-density polyethylene, or silastic was used and in about 40% cartilage taken from the person or from a cow was used. In a few cases hyaluronic acid was injected and in a few others tricalcium phosphate was used. There were no complications caused by the surgery, although one person was over-corrected and developed chronic rhinosinusitis and two people were under-corrected. The hyaluronic acid was completely resorbed in the three people who received it at the one year follow up, and in six people some of the implant came out, but this did not affect the result as enough remained. About 21% of the people had no or marginal improvement but the rest reported significant relief of their symptoms. Since none of the studies used placebo or blinding there may be a strong placebo effect or bias in reporting.

OAF is a complication of oroantral communication. Other complications may arise if left untreated. For example:

- Candidal infection

- Chronic maxillary sinus infection of bacterial origin

- Osteomyelitis

- Rhinosinusitis

- Sinus pathology

Therefore, OAF should be dealt with first, before treating the complications.

Studies have shown that sinusitis is found in about 60% of the cases on the fourth day after the manifestation of sinus. Moreover, patient may be afflicted with an acute sinus disease if OAC is not treated promptly upon detecting clear signs of sinusitis. So, early diagnosis of OAC must be conducted in order to prevent OAF from setting in.

Spontaneous healing of small perforation is expected to begin about 48 hours after tooth extraction and it remains possible during the following two weeks. Patient must consult the dentist as early as possible should a large defect of more than 7mm in diameter or a dogged opening that requires closure is discovered so that appropriate and suitable treatment can be swiftly arranged or referral to Oral Maxillofacial Surgery (OMFS) be made at the local hospital, if required.

A comprehensive preoperative radiographic evaluation is a must as the risk of OAC can increase due to one or more of the following situations :-

- Close relationship between the roots of the maxillary posterior teeth and the sinus floor

- Increased divergence or dilaceration of the roots of the tooth

- Marked pneumatization of the sinus leading to a larger size

- Peri-radicular lesions involving teeth or roots in close association with the sinus floor

Hence, in such cases:

- Avoid using too much of apical pressure during tooth extraction

- Perform surgical extraction with roots sectioning

- Consider referral to OMFS at local hospital

Drugs in systemic circulation have a certain concentration in the blood, which serves as a surrogate marker for how much drug will be delivered throughout the body (how much drug the rest of the body will "see"). There exists a minimum concentration of drug within the blood that will give rise to the intended therapeutic effect (minimum effective concentration, MEC), as well as a minimum concentration of drug that will give rise to an unintended adverse drug event (minimum toxic concentration, MTC). The difference between these two values is generally referred to as the therapeutic window. Different drugs have different therapeutic windows, and different people will have different MECs and MTCs for a given drug. If someone has a very low MTC for a drug, they are likely to experience adverse effects at drug concentrations lower than what it would take to produce the same adverse effects in the general populace; thus, the individual will experience significant toxicity at a dose that is otherwise considered "normal" for the average person. This individual will be considered "intolerant" to that drug.

There are a variety of factors that can affect the MTC, which is often the subject of clinical pharmacokinetics. Variations in MTC can occur at any point in the ADME (absorption, distribution, metabolism, and excretion) process. For example, a patient could possess a genetic defect in a drug metabolizing enzyme in the cytochrome P450 superfamily. While most individuals will possess the effective metabolizing machinery, a person with a defect will have a difficult time trying to clear the drug from their system. Thus, the drug will accumulate within the blood to higher-than-expected concentrations, reaching a MTC at a dose that would otherwise be considered normal for the average person. In other words, in a person that is intolerant to a medication, it is possible for a dose of 10 mg to "feel" like a dose of 100 mg, resulting in an overdose—a "normal" dose can be a "toxic" dose in these individuals, leading to clinically significant effects.

There is also an aspect of drug intolerance that is subjective. Just as different people have different pain tolerances, so too do people have different tolerances for dealing with the adverse effects from their medications. For example, while opioid-induced constipation may be tolerable to some individuals, other people may stop taking an opioid due to the unpleasantness of the constipation even if it brings them significant pain relief.

Intolerance to analgesics, particularly NSAIDs, is relatively common. It is thought that a variation in the metabolism of arachidonic acid is responsible for the intolerance. Symptoms include chronic rhinosinusitis with nasal polyps, asthma, gastrointestinal ulcers, angioedema, and urticaria.

NSAID or nonsteroidal anti-inflammatory drug hypersensitivity reactions encompasses a broad range of allergic or allergic-like symptoms that occur within minutes to hours after ingesting aspirin or other NSAID nonsteroidal anti-inflammatory drugs. Hypersensitivity drug reactions differ from drug toxicity reactions in that drug toxicity reactions result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual (see nonsteroidal anti-inflammatory drugs section on adverse reactions for NSAID-induced toxic reactions); hypersensitivity reactions are idiosyncratic reactions to a drug. Although the term NSAID was introduced to signal a comparatively low risk of adverse effects, NSAIDs do evoke a broad range of hypersensitivity syndromes. These syndromes have recently been classified by the European Academy of Allergy and Clinical Immunology Task Force on NSAIDs Hypersensitivity. The classification organizes the hypersensitivity reactions to NSAIDs into the following five categories:

- 1) NSAIDs-exacerbated respiratory disease (NERD) is an acute (immediate to several hours) exacerbation of bronchoconstriction and other symptoms of asthma (see aspirin-induced asthma) in individuals with a history of asthma and/or nasal congestion, rhinorrhea or other symptoms of rhinitis and sinusitis in individuals with a history of rhinosinusitis after ingestion of various NSAIDs, particularly those that act by inhibiting the COX-1 enzyme. NERD does not appear to be due to a true allergic reaction to NSAIDs but rather at least in part to the more direct effects of these drugs to promote the production and/or release of certain mediators of allergy. That is, inhibition of cellular COX activity deprives tissues of its anti-inflammatory product(s), particularly prostaglandin E2 while concurrently shuttling its substrate, arachidonic acid, into other metabolizing enzymes, particularly 5-lipoxygenase (ALOX5) to overproduce pro-inflammatory leukotriene and 5-Hydroxyicosatetraenoic acid metabolites and 15-lipoxygenase (ALOX15) to overproduce pro-inflammatory 15-Hydroxyicosatetraenoic acid metabolites, including eoxins; the condition is also associated with a reduction in the anti-inflammatory metabolite, lipoxin A4, and increases in certain pro-allergic chemokines such as eotaxin-2 and CCL7.

- 2) NSAIDs-exacerbated cutaneous disease (NECD) is an acute exacerbation of wheals and/or angioedema in individuals with a history of chronic urticaria. NECD also appears due to the non-allergic action of NSAIDs in inhibiting the production of COX anti-inflammatory metabolites while promoting the production 5-lipoxygenase and 15-lipoxygenase pro-inflammatory metabolites and the overproduction of certain pro-allergic chemokines, e.g. eotaxin-1, eotaxin-2, RANTES, and interleukin-5.

- 3) NSAIDs-induced urticarial disease (NEUD) is the acute development of wheals and/or angioedema in individuals with no history of chronic NSAIDs-induced urticaria or related diseases. The mechanism behind NEUD is unknown but may be due to the non-allergic action of NSAIDs in promoting the production and/or release of allergy mediators.

- 4) Single NSAID-induced urticarial/angioedema or anaphylaxis (SNIUAA) is the acute development of urticarial, angioedema, or anaphylaxis in response to a single type of NSAID and/or a single group of NSAIDs with a similar structure but not to other structurally unrelated NSAIDs in individuals with no history of underlying relevant chronic diseases. SNIUAA is due to a true IgE-mediated allergy reaction.

- 5 Single NSAID-induced delayed reactions (SNIDR) are a set of delayed onset (usually more than 24 hour) reactions to NSAIDs. SNIDR are most commonly skin reactions that may be relatively mild moderately severe such as maculopapular rash, fixed drug eruptions, photosensitivity reactions, delayed urticaria, and contact dermatitis or extremely severe such as the DRESS syndrome, acute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis (also termed Lyell's syndrome). SNIDR result from the drug-specific stimulation of CD4+ T lymphocytes and CD8+ cytotoxic T cells to elicit a delayed type hypersensitivity reaction.

Infants may develop respiratory symptoms as a result of exposure to a specific type of fungal mold, called Penicillium. Signs that an infant may have mold-related respiratory problems include (but are not limited to) a persistent cough and/or wheeze. Increased exposure increases the probability of developing respiratory symptoms during their first year of life. Studies have shown that a correlation exists between the probability of developing asthma and increased exposure to "Penicillium". The levels are deemed ‘no mold’ to ‘low level’ , from ‘low’ to ‘intermediate’ , and from ‘intermediate’ to ‘high’.

Mold exposures have a variety of health effects depending on the person. Some people are more sensitive to mold than others. Exposure to mold can cause a number of health issues such as; throat irritation, nasal stuffiness, eye irritation, cough and wheezing, as well as skin irritation in some cases. Exposure to mold may also cause heightened sensitivity depending on the time and nature of exposure. People at higher risk for mold allergies are people with chronic lung illnesses, which will result in more severe reactions when exposed to mold.

There has been sufficient evidence that damp indoor environments are correlated with upper respiratory tract symptoms such as coughing, and wheezing in people with asthma.

Young's syndrome, also known as azoospermia sinopulmonary infections, sinusitis-infertility syndrome and Barry-Perkins-Young syndrome, is a rare condition that encompasses a combination of syndromes such as bronchiectasis, rhinosinusitis and reduced fertility. In individuals with this syndrome, the functioning of the lungs is usually normal but the mucus is abnormally viscous. The reduced fertility (azoospermia) is due to functional obstruction of sperm transport down the genital tract at the epididymis where the sperms are found in viscous, lipid-rich fluid. The syndrome was named after Donald Young, the urologist who first made observations of the clinical signs of the syndrome in 1972. There have been several studies undertaken suggesting that contact with mercury might cause the syndrome.

A variant of Young's syndrome has been observed in an individual, showing slightly different signs and symptoms.

Symptoms of mold exposure can include:

- Nasal and sinus congestion, runny nose

- Respiratory problems, such as wheezing and difficulty breathing, chest tightness

- Cough

- Throat irritation

- Sneezing / Sneezing fits

Nasal glial heterotopia is rare, while an encephalocele is uncommon. NGH usually presents in infancy, while encephalocele may present in older children and adults. It is seen in both genders equally.

Although surgery is the treatment of choice, it must be preceded by imaging studies to exclude an intracranial connection. Potential complications include meningitis and a cerebrospinal fluid leak. Recurrences or more correctly persistence may be seen in up to 30% of patients if not completely excised.