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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
Adenoiditis occurs mainly in childhood, often associated with acute tonsillitis. Incidence decreases with age, with adenoiditis being rare in children over 15 years due to physiological atrophy of the adenoid tissue.
Viruses that may cause adenoiditis include adenovirus, rhinovirus and paramyxovirus. Bacterial causes include Streptococcus pyogenes, Streptococcus pneumoniae, Moraxella catarrhalis and various species of Staphylococcus including Staphylococcus aureus.
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.
By definition chronic sinusitis lasts longer than 12 weeks and can be caused by many different diseases that share chronic inflammation of the sinuses as a common symptom. Symptoms of chronic sinusitis may include any combination of the following: nasal congestion, facial pain, headache, night-time coughing, an increase in previously minor or controlled asthma symptoms, general malaise, thick green or yellow discharge, feeling of facial 'fullness' or 'tightness' that may worsen when bending over, dizziness, aching teeth, and/or bad breath. Each of these symptoms has multiple other possible causes, which should be considered and investigated as well. Often chronic sinusitis can lead to anosmia, the inability to smell objects. In a small number of cases, acute or chronic maxillary sinusitis is associated with a dental infection. Vertigo, lightheadedness, and blurred vision are not typical in chronic sinusitis and other causes should be investigated.
Chronic sinusitis cases are subdivided into cases with polyps and cases without polyps. When polyps are present, the condition is called chronic hyperplastic sinusitis; however, the causes are poorly understood and may include allergy, environmental factors such as dust or pollution, bacterial infection, or fungus (either allergic, infective, or reactive).
Chronic rhinosinusitis represents a multifactorial inflammatory disorder, rather than simply a persistent bacterial infection. The medical management of chronic rhinosinusitis is now focused upon controlling the inflammation that predisposes patients to obstruction, reducing the incidence of infections. However, all forms of chronic rhinosinusitis are associated with impaired sinus drainage and secondary bacterial infections. Most individuals require initial antibiotics to clear any infection and intermittently afterwards to treat acute exacerbations of chronic rhinosinusitis.
A combination of anaerobic and aerobic bacteria are detected in conjunction with chronic sinusitis. Also isolated are "Staphylococcus aureus" (including methicilin resistant "S.aureus" ) and coagulase-negative "Staphylococci" and Gram negative enteric organisms can be isolated.
Attempts have been made to provide a more consistent nomenclature for subtypes of chronic sinusitis. The presence of eosinophils in the mucous lining of the nose and paranasal sinuses has been demonstrated for many patients, and this has been termed eosinophilic mucin rhinosinusitis (EMRS). Cases of EMRS may be related to an allergic response, but allergy is not often documented, resulting in further subcategorization into allergic and non-allergic EMRS.
A more recent, and still debated, development in chronic sinusitis is the role that fungi play in this disease. It remains unclear if fungi are a definite factor in the development of chronic sinusitis and if they are, what the difference may be between those who develop the disease and those who remain free of symptoms. Trials of antifungal treatments have had mixed results.
Recent theories of sinusitis indicate that it often occurs as part of a spectrum of diseases that affect the respiratory tract ("i.e.", the "one airway" theory) and is often linked to asthma. All forms of sinusitis may either result in, or be a part of, a generalized inflammation of the airway, so other airway symptoms, such as cough, may be associated with it.
Both smoking and secondhand smoke are associated with chronic rhinosinusitis.
Bacterial infections of the orbit have long been associated with a risk of catastrophic local
sequelae and intracranial spread.
The natural course of the disease, as documented by Gamble (1933), in the pre-antibiotic era,
resulted in death in 17% of patients and permanent blindness in 20%.
Some cases of pharyngitis are caused by fungal infection such as Candida albicans causing oral thrush.
Pharyngitis may also be caused by mechanical, chemical or thermal irritation, for example cold air or acid reflux. Some medications may produce pharyngitis such as pramipexole and antipsychotics.
Cavernous sinus thrombosis has a mortality rate of less than 20% in areas with access to antibiotics. Before antibiotics were available, the mortality was 80–100%. Morbidity rates also dropped from 70% to 22% due to earlier diagnosis and treatment.
Complications include hearing loss, blood infection, meningitis, cavernous sinus thrombosis, and optic nerve damage (which could lead to blindness).
Sinusitis is inflammation of the paranasal air sinuses. Infections associated with teeth may be responsible for approximately 20% of cases of maxillary sinusitis. The cause of this situation is usually a periapical or periodontal infection of a maxillary posterior tooth, where the inflammatory exudate has eroded through the bone superiorly to drain into the maxillary sinus. Once an odontogenic infection involves the maxillary sinus, it is possible that it may then spread to the orbit or to the ethmoid sinus.
Though it is widely held that fungal infections of the nose and paranasal sinuses are not common, most agree that their frequency has been increasing over past decades.
An odontogenic infection is an infection that originates within a tooth or in the closely surrounding tissues. The term is derived from "" (from ancient Greek "odous" - "tooth") and "" (from Greek "genos" - "birth"). Odontogenic infections may remain localized to the region where they started, or spread into adjacent or distant areas.
It is estimated that 90-95% of all orofacial infections originate from the teeth or their supporting structures. Furthermore, about 70% of odontogenic infections occur as periapical inflammation, i.e. acute periapical periodontitis or a periapical abscess. The next most common form of odontogenic infection is the periodontal abscess.
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.
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.
Rhinorrhea can also occur when individuals with allergies to certain substances, such as pollen, dust, latex, soy, shellfish, or animal dander, are exposed to these allergens. In people with sensitized immune systems, the inhalation of one of these substances triggers the production of the antibody immunoglobulin E (IgE), which binds to mast cells and basophils. IgE bound to mast cells are stimulated by pollen and dust, causing the release of inflammatory mediators such as histamine. In turn, this causes, among other things, inflammation and swelling of the tissue of the nasal cavities as well as increased mucus production. Particulate matter in polluted air and chemicals such as chlorine and detergents, which can normally be tolerated, can make the condition considerably worse.
Recognizing the primary source of infection (i.e., facial cellulitis, middle ear, and sinus infections) and treating the primary source expeditiously is the best way to prevent cavernous sinus thrombosis.
Rhinorrhea is also associated with shedding tears, whether from emotional events or from eye irritation. When excess tears are produced, the liquid drains through the inner corner of the eyelids, through the nasolacrimal duct, and into the nasal cavities. As more tears are shed, more liquid flows into the nasal cavities, both stimulating mucus production and hydrating any dry mucus already present in the nasal cavity. The buildup of fluid is usually resolved via mucus expulsion through the nostrils.
Antibiotics are aimed at gram positive bacteria. Medical attention should be sought if symptoms persist beyond 2–3 days.
"Staphylococcus aureus", "Streptococcus pneumoniae", other streptococci, and anaerobes are the most common causes, depending on the origin of the infection.
The advent of the "Haemophilus influenzae" vaccine has dramatically decreased the incidence.
Causes can be remembered by mnemonic HERNIA:
- Hereditary factors: the disease runs in families
- Endocrine imbalance: the disease tends to start at puberty and mostly involves females
- Racial factors: whites are more susceptible than natives of equatorial Africa
- Nutritional deficiency: vitamins A or D, or iron
- Infection: "Klebsiella ozaenae", diphtheroids, "Proteus vulgaris", "E. coli", etc.
- Autoimmune factors: viral infection or some other unidentified insult may trigger antigenicity of the nasal mucosa.
Treatment for fungal sinusitis can include surgical debridement; helps by slowing progression of disease thus allowing time for recovery additionally we see the options below:
- In the case of invasive fungal sinusitis, echinocandins, voriconazole, and amphoterecin (via IV) may be used
- For allergic fungal sinusitis, systemic corticosteroids like prednisolone, methylprednisolone are added for their anti-inflammatory effect, bronchodilators and expectorants help to clear secretions in the sinuses.
Some strains of group A streptococci (GAS) cause severe infection. Severe infections are usually invasive, meaning that the bacteria has entered parts of the body where bacteria are not usually found, such as the blood, lungs, deep muscle or fat tissue. Those at greatest risk include children with chickenpox; persons with suppressed immune systems; burn victims; elderly persons with cellulitis, diabetes, vascular disease, or cancer; and persons taking steroid treatments or chemotherapy. Intravenous drug users also are at high risk. GAS is an important cause of puerperal fever worldwide, causing serious infection and, if not promptly diagnosed and treated, death in newly delivered mothers. Severe GAS disease may also occur in healthy persons with no known risk factors.
All severe GAS infections may lead to shock, multisystem organ failure, and death. Early recognition and treatment are critical. Diagnostic tests include blood counts and urinalysis as well as cultures of blood or fluid from a wound site.
Severe Group A streptococcal infections often occur sporadically but can be spread by person-to-person contact.
Public Health policies internationally reflect differing views of how the close contacts of people affected by severe Group A streptococcal infections should be treated. Health Canada and the US CDC recommend close contacts see their doctor for full evaluation and may require antibiotics; current UK Health Protection Agency guidance is that, for a number of reasons, close contacts should not receive antibiotics unless they are symptomatic but that they should receive information and advice to seek immediate medical attention if they develop symptoms. However, guidance is clearer in the case of mother-baby pairs: both mother and baby should be treated if either develops an invasive GAS infection within the first 28 days following birth (though some evidence suggests that this guidance is not routinely followed in the UK).
Most patients have persistent headaches, although about 15% will remit, and 8% will have a relapsing-remitting type. It is not infrequent for NDPH to be an intractable headache disorder that is unresponsive to standard headache therapies.
Specific infections, such as syphilis, lupus, leprosy and rhinoscleroma, may cause destruction of the nasal structures leading to atrophic changes. Atrophic rhinitis can also result from long-standing purulent sinusitis or radiotherapy of the nose, or as a complication of surgery of the turbinates. The United Kingdom National Health Service has stated that "Most cases of atrophic rhinitis in the UK occur when the turbinates are damaged or removed during surgery". Some authors refer to as Atrophic rhinitis secondary to sinus surgery as the empty nose syndrome.
Acute rheumatic fever (ARF) is a complication of respiratory infections caused by GAS. The M-protein generates antibodies that cross-react with autoantigens on interstitial connective tissue, in particular of the endocardium and synovium, that can lead to significant clinical illness.
Although common in developing countries, ARF is rare in the United States, possibly secondary to improved antibiotic treatment, with small isolated outbreaks reported only occasionally. It is most common among children between 5 and 15 years old and occurs 1–3 weeks after an untreated GAS pharyngitis.
ARF is often clinically diagnosed based on Jones Criteria, which include: pancarditis, migratory polyarthritis of large joints, subcutaneous nodules, erythema marginatum, and sydenham chorea (involuntary, purposeless movement). The most common clinical finding is a migratory arthritis involving multiple joints.
Other indicators of GAS infection such as a DNAase or ASO serology test must confirm the GAS infection. Other minor Jones Criteria are fever, elevated ESR and arthralgia. One of the most serious complications is pancarditis, or inflammation of all three heart tissues. A fibrinous pericarditis can develop with a classic friction rub that can be auscultated. This will give increasing pain upon reclining.
Further endocarditis can develop with aseptic vegetations along the valve closure lines, in particular the mitral valve. Chronic rheumatic heart disease mostly affects the mitral valve, which can become thickened with calcification of the leaflets, often causing fusion of the commissures and chordae tendineae.
Other findings of ARF include erythema marginatum (usually over the spine or other bony areas) and a red expanding rash on the trunk and extremities that recurs over weeks to months. Because of the different ways ARF presents itself, the disease may be difficult to diagnose.
A neurological disorder, Sydenham chorea, can occur months after an initial attack, causing jerky involuntary movements, muscle weakness, slurred speech, and personality changes. Initial episodes of ARF as well as recurrences can be prevented by treatment with appropriate antibiotics.
It is important to distinguish ARF from rheumatic heart disease. ARF is an acute inflammatory reaction with pathognomonic Aschoff bodies histologically and RHD is a non-inflammatory sequela of ARF.