Made by DATEXIS (Data Science and Text-based Information Systems) at Beuth University of Applied Sciences Berlin
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
A variety of causes may lead to dacrocystitis. Most notably, obstruction of the nasolacrimal duct leads to stasis of the nasolacrimal fluid, which predisposes to infection. Staphylococcus aureus is a common bacterial pathogen causing infectious dacrocystitis. Sometimes, especially in women, stones may develop in the lacrimal gland, causing recurrent bouts of dacrocystitis; this condition is called "acute dacryocystic retention syndrome."
Also due to pneumococcus, infection due to surrounding structure such as paranasal sinuses.
Most patients will fully recover from dacryoadenitis. For conditions with more serious causes, such as sarcoidosis, the prognosis is that of the underlying condition.
About 60 percent of initial attacks of dacryocystitis will recur. Individuals with a poorly functioning immune system (immunocompromised) may develop orbital cellulitis, which may lead to optic neuritis, proptosis, motility abnormalities, or blindness.
"Acute bacterial parotitis:"
is most often caused by a bacterial infection of Staphylococcus aureus but may be caused by any commensal bacteria.
"Parotitis as Extrapulmonary Tuberculosis:"
The mycobacterium that cause tuberculosis can also cause parotid infection. Those infected tend to have enlarged, nontender, but moderately painful glands. The diagnosis is made by typical chest radiograph findings, cultures, or histologic diagnosis after the gland has been removed. When diagnosed and treated with antitubercular medications, the gland may return to normal in 1–3 months.
"Acute viral parotitis (mumps):"
The most common viral cause of parotitis is mumps. Routine vaccinations have dropped the incidence of mumps to a very low level. Mumps resolves on its own in about ten days.
"HIV parotitis:" Generalized lymphadenopathy has long been associated with HIV, but the localized enlargement of the parotid gland is less well known.
Mumps can be prevented by immunization. Gonococcus, bacteria can be avoided by the use of condoms. Most other causes cannot be prevented.
These are also collectively known as chronic punctate parotitis or chronic autoimmune parotitis.
"Sjögren's syndrome:"
Chronic inflammation of the salivary glands may also be an autoimmune disease known as Sjögren's syndrome. The disease most commonly appears in people aged 40–60 years, but it may affect small children. In Sjögren syndrome, the prevalence of parotitis in women versus men is approximately 9:1. The involved parotid gland is enlarged and tender at times. The cause is unknown. The syndrome is often characterized by excessive dryness in the eyes, mouth, nose, vagina, and skin.
"Lymphoepithelial lesion of Godwin:"
Most frequently associated with a circumscribed tumor with the histologic features of Sjögren syndrome. This designation has also fallen out of favour.
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.
Inflammatory abnormalities are a large group of disorders that underlie a vast variety of human diseases. The immune system is often involved with inflammatory disorders, demonstrated in both allergic reactions and some myopathies, with many immune system disorders resulting in abnormal inflammation. Non-immune diseases with causal origins in inflammatory processes include cancer, atherosclerosis, and ischemic heart disease.
Examples of disorders associated with inflammation include:
- Acne vulgaris
- Asthma
- Autoimmune diseases
- Autoinflammatory diseases
- Celiac disease
- Chronic prostatitis
- Colitis
- Diverticulitis
- Glomerulonephritis
- Hidradenitis suppurativa
- Hypersensitivities
- Inflammatory bowel diseases
- Interstitial cystitis
- Mast Cell Activation Syndrome
- Mastocytosis
- Otitis
- Pelvic inflammatory disease
- Reperfusion injury
- Rheumatic fever
- Rheumatoid arthritis
- Rhinitis
- Sarcoidosis
- Transplant rejection
- Vasculitis
Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.
Granulomatous disease, including sarcoidosis, granulomatosis with polyangiitis, and midline granuloma, may also lead to NLD obstruction.
IOI or orbital pseudotumor is the second most common cause of exophthalmos following Grave’s orbitopathy and the third most common orbital disorder following thyroid orbitopathy and lymphoproliferative disease accounting for 5–17.6% of orbital disorders, There is no age, sex, or race predilection, but it is most frequently seen in middle-aged individuals. Pediatric cases account for about 17% of all cases of IOI.
The exact cause of IOI is unknown, but infectious and immune-mediated mechanisms have been proposed. Several studies have described cases where onset of orbital pseudotumor was seen simultaneously or several weeks after upper respiratory infections. Another study by Wirostko et al. proposes that organisms resembling Mollicutes cause orbital inflammation by destroying the cytoplasmic organelles of parasitized cells.
Orbital pseudotumor has also been observed in association with Crohn’s disease, systemic lupus erythematosus, rheumatoid arthritis, diabetes mellitus, myasthenia gravis, and ankylosing spondylitis all of which strengthen the basis of IOI being an immune-mediated disease. Response to corticosteroid treatment and immunosuppressive agents also support this idea.
Trauma has also been seen to precede some cases of orbital pseudotumor. However, one study by Mottow-Lippe, Jakobiec, and Smith suggests that the release of circulating antigens caused by local vascular permeability triggers an inflammatory cascade in the affected tissues.
Although these mechanisms have been postulated as possible causes of IOI, their exact nature and relationships to the condition still remain unclear.
As with similar cases of canalicular obstruction, dislodged punctal and canalicular plugs can migrate to and occlude the NLD.
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%.
Once the plaque stagnation area is removed either through further complete tooth eruption or tooth removal then pericoronitis will likely never return. A non-impacted tooth may continue to erupt, reaching a position which eliminates the operculum. A transient and mild pericoronal inflammation often continues while this tooth eruption completes. With adequate space for sustained improved oral hygiene methods, pericoronitis may never return. However, when relying on just oral hygiene for impacted and partially erupted teeth, chronic pericoronitis with occasional acute exacerbation can be expected.
Dental infections such as a pericoronal abscess can develop into septicemia and be life-threatening in persons who have neutropenia. Even in people with normal immune function, pericoronitis may cause a spreading infection into the potential spaces of the head and neck. Rarely, the spread of infection from pericoronitis may compress the airway and require hospital treatment (e.g. Ludwig's angina), although the majority of cases of pericoronitis are localized to the tooth. Other potential complications of a spreading pericoronal abscess include peritonsillar abscess formation or cellulitis.
Chronic pericoronitis may be the etiology for the development of paradental cyst, an inflammatory odontogenic cyst.
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.
Pericoronitis usually occurs in young adults, around the time when wisdom teeth are erupting into the mouth. If the individual has reached their twenties without any attack of pericoronitis, it becomes substantially less likely one will occur thereafter.
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
Salivary gland aplasia (also termed salivary gland agenesis) is the congenital absence of salivary glands. Usually the term relates to the absence of some or all of the major salivary glands.
It is a rare condition, and most known cases have been in association with syndromes of the ectodermal tissues, particularly the lacrimal apparatus. Example syndromes which have been reported with salivary gland aplasia include hereditary ectodermal dysplasia, mandibulofacial dysostosis and hemifacial microsomia.
The main significance of the condition is a lack of saliva, causing xerostomia (dry mouth), with accompanying susceptibility to dental caries (tooth decay), infections of the mouth, and upper respiratory tract infections (e.g., candidiasis, ascending sialadenitis, laryngitis and pharyngitis). Patients with salivary gland aplasia typically require regular application of topical fluoride to prevent tooth decay.
The exact cause of nasal polyps is unclear. They are, however, commonly associated with conditions that cause long term inflammation of the sinuses. This includes chronic rhinosinusitis, asthma, aspirin sensitivity, and cystic fibrosis.
Various additional diseases associated with polyp formation include:
Chronic rhinosinusitis is a common medical condition characterized by symptoms of sinus inflammation lasting at least 12 weeks. The cause is unknown and the role of microorganisms remains unclear. It can be classified as either with or without nasal polyposis.
Cystic fibrosis (CF) is the most common cause of nasal polyps in children. Therefore, any child under 12 to 20 years old with nasal polyps should be tested for CF. Half of people with CF will experience extensive polyps leading to nasal obstruction and requiring aggressive management.
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.
IgG4-related ophthalmic disease (IgG4-ROD) is the recommended term to describe orbital (eye socket) manifestations of the systemic condition IgG4-related disease, which is characterised by infiltration of lymphocytes and plasma cells and subsequent fibrosis in involved structures. It can involve one or more of the orbital structures.
Frequently involved structures include the lacrimal glands, extraocular muscles, infraorbital nerve, supraorbital nerve and eyelids. It has also been speculated that ligneous conjunctivitis may be a manifestation of IgG4-related disease (IgG4-RD).
As is the case with other manifestations of IgG4-related disease, a prompt response to steroid therapy is a characteristic feature of IgG4-ROD in most cases, unless significant fibrosis has already occurred.
If caused by a head injury, rhinorrhea can be a much more serious condition. A basilar skull fracture can result in a rupture of the barrier between the sinonasal cavity and the anterior cranial fossae or the middle cranial fossae. This rupture can cause the nasal cavity to fill with cerebrospinal fluid. This condition, known as cerebrospinal fluid rhinorrhoea or CSF rhinorrhea, can lead to a number of serious complications and possibly death if not addressed properly.
Symptoms, if any, can be mild even in the presence of significant swelling or masses.
Lacrimal gland involvement may cause swelling of the upper eyelid, or proptosis if there is severe swelling. Other orbital masses or inflammation can result in visual disturbance (blurred vision, double vision, visual field impairment), restricted eye movements, pain or discomfort, numbness in the distribution of the supraorbital and/or infraorbital nerves, or proptosis.
IgG4-related ophthalmic disease has been estimated to account for approximately 25% of all cases of proptosis, eyelid swelling and other features of orbital swelling.