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Large doses of glucocorticoids are the treatment of choice, and are administered until the signs have resolved. In uncomplicated cases, this can take up to a month. If dogs are not treated promptly and with high doses of steroids, severe scarring may occur. If there is evidence of secondary bacterial infection, treatment with antibiotics is required.
Treatment is often with a steroids. This can be either applied as a cream or taken by mouth. As the condition tends to get better on its own taking steroids by mouth should generally only be tried if the rash covers a large area and it does not get better with other measures.
Antibiotics are usually prescribed, with the agent selected based on suspected organism and presence or absence of purulence, although the best treatment choice is unclear. If an abscess is also present, surgical drainage is usually indicated, with antibiotics often prescribed for co-existent cellulitis, especially if extensive. Pain relief is also often prescribed, but excessive pain should always be investigated, as it is a symptom of necrotizing fasciitis. Elevation of the affected area is often recommended.
Steroids may speed recovery in those on antibiotics.
Antibiotic creams are the preferred treatment for mild cases of impetigo, despite their limited systemic absorption. Such prescribed ointments include neosporin, fusidic acid, chloramphenicol and mupirocin. More severe cases of impetigo however (especially bullous impetigo) will likely require oral agents with better systemic bioavailability, such as cephalexin. Cases that do not resolve with initial antibiotic therapy or require hospitalization may also be indicative an MRSA infection, which would require the use of agents specifically able to treat it, such as clindamycin.
Antibiotic treatment typically last 7–10 days, and although highly effective some cases of methicillin resistant S. aureus (MRSA) may require longer therapy depending on the severity of infection and how much it has spread.
For generations, the disease was treated with an application of the antiseptic gentian violet. Today, topical or oral antibiotics are usually prescribed. Mild cases may be treated with bactericidal ointment, such as mupirocin. In 95% of cases, a single antibiotic course results in resolution in children. It has been advocated that topical disinfectants are not nearly as efficient as antibiotics, and therefore should be avoided.
More severe cases require oral antibiotics, such as dicloxacillin, flucloxacillin, or erythromycin. Alternatively, amoxicillin combined with clavulanate potassium, cephalosporins (first-generation) and many others may also be used as an antibiotic treatment. Alternatives for people who are seriously allergic to penicillin or infections with MRSA include doxycycline, clindamycin, and SMX-TMP. When streptococci alone are the cause, penicillin is the drug of choice.
When the condition presents with ulcers, valacyclovir, an antiviral, may be given in case a viral infection is causing the ulcer.
Antibiotics choices depend on regional availability, but a penicillinase-resistant semisynthetic penicillin or a first-generation cephalosporin is currently recommended for cellulitis without abscess. A course of antibiotics is not effective in between 6 and 37% of cases.
There is not enough evidence to recommend alternative medicine such as tea tree oil or honey.
Treatments include class I topical steroids (clobetasol, halobetasol, etc.) which in some studies have proven to be equally effective as systemic, or pill, therapy and somewhat safer. However, in difficult-to-manage or widespread cases, systemic prednisone and powerful steroid-free immunosuppressant medications, such as methotrexate, azathioprine or mycophenolate mofetil, may be appropriate. Antibiotics such as tetracycline or erythromycin may also control the disease, particularly in patients who cannot use corticosteroids. The anti-CD20 monoclonal antibody rituximab has been found to be effective in treating some otherwise refractory cases of bullous pemphigoid.
IgA-mediated pemphigoid can often be difficult to treat even with usually effective medications such as rituximab.
Since the common pathogens involved with impetigo are bacteria naturally found on the skin, most prevention (especially in children), is targeted towards appropriate hygiene, wound cleaning, and minimizing scratching (i.e. by keeping nails trimmed and short). Avoiding close contact and sharing of items such as towels with potentially infected individuals is also recommended.
Although orbital cellulitis is considered an ophthalmic emergency the prognosis is good if prompt medical treatment is received.
Immediate treatment is very important for someone with orbital cellulitis. Treatment typically involves intravenous (IV) antibiotics in the hospital and frequent observation (every 4–6 hours). Along with this several laboratory tests are run including a complete blood count, differential, and blood culture.
- Antibiotic therapy – Since orbital cellulitis is commonly caused by "Staphylococcus" and "Streptococcus" species both penicillins and cephalosporins are typically the best choices for IV antibiotics. However, due to the increasing rise of MRSA (methicillin-resistant "Staphylococcus aureus") orbital cellulitis can also be treated with Vancomycin, Clindamycin, or Doxycycline. If improvement is noted after 48 hours of IV antibiotics, healthcare professions can then consider switching a patient to oral antibiotics (which must be used for 2–3 weeks).
- Surgical intervention – An abscess can threaten the vision or neurological status of a patient with orbital cellulitis, therefore sometimes surgical intervention is necessary. Surgery typically requires drainage of the sinuses and if a subperiosteal abscess is present in the medial orbit, drainage can be performed endoscopically. Post-operatively, patients must follow up regularly with their surgeon and remain under close observation.
Treatment is directed toward the underlying cause. However, in primary eosinophilia, or if the eosinophil count must be lowered, corticosteroids such as prednisone may be used. However, immune suppression, the mechanism of action of corticosteroids, can be fatal in patients with parasitosis.
The culprit can be both a prescription drug or an over-the-counter medication.
Examples of common drugs causing drug eruptions are antibiotics and other antimicrobial drugs, sulfa drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), biopharmaceuticals, chemotherapy agents, anticonvulsants, and psychotropic drugs. Common examples include photodermatitis due to local NSAIDs (such as piroxicam) or due to antibiotics (such as minocycline), fixed drug eruption due to acetaminophen or NSAIDs (Ibuprofen), and the rash following ampicillin in cases of mononucleosis.
Certain drugs are less likely to cause drug eruptions (rates estimated to be ≤3 per 1000 patients exposed). These include: digoxin, aluminum hydroxide, multivitamins, acetaminophen, bisacodyl, aspirin, thiamine, prednisone, atropine, codeine, hydrochlorothiazide, morphine, insulin, warfarin, and spironolactone.
Corticosteroids remain the main treatment modality for IOI. There is usually a dramatic response to this treatment and is often viewed as pathognomonic for this disease. Although response is usually quick, many agree that corticosteroids should be continued on a tapering basis to avoid breakthrough inflammation.
Although many respond to corticosteroid treatment alone, there are several cases in which adjuvant therapy is needed. While many alternatives are available, there is no particular well-established protocol to guide adjuvant therapy. Among the available options there is: surgery, alternative corticosteroid delivery, radiation therapy, non-steroidal anti-inflammatory drugs, cytotoxic agents (chlorambucil, cyclophosphamide), corticosteroid sparing immunosuppressants (methotrexate, cyclosporine, azathioprine), IV immune-globin, plasmapheresis, and biologic treatments (such as TNF-α inhibitors).
Due to its rarity, no comprehensive treatment studies on eosinophilic myocarditis have been conducted. Small studies and case reports have directed efforts towards: a) supporting cardiac function by relieving heart failure and suppressing life-threatening abnormal heart rhythms; b) suppressing eosinophil-based cardiac inflammation; and c) treating the underlying disorder. In all cases of symptomatic eosinophilic myocarditis that lack specific treatment regimens for the underlying disorder, available studies recommend treating the inflammatory component of this disorder with non-specific immunosuppressive drugs, principally high-dosage followed by slowly-tapering to a low-dosage maintenance corticosteroid regimens. It is recommended that afflicted individuals who fail this regimen or present with cardiogenic shock be treated with other non-specific immunosuppressive drugs viz., azathioprine or cyclophosphamide, as adjuncts to, or replacements for, corticosteroids. However, individuals with an underlying therapeutically accessible disease should be treated for this disease; in seriously symptomatic cases, such individuals may be treated concurrently with a corticosteroid regimen. Examples of diseases underlying eosinophilic myocarditis that are recommended for treatments directed at the underlying disease include:
- Infectious agents: specific drug treatment of helminth and protozoan infections typically takes precedence over non-specific immunosuppressive therapy, which, if used without specific treatment, could worsen the infection. In moderate-to-severe cases, non-specific immunosuppression is used in combination with specific drug treatment.
- Toxic reactions to ingested agents: discontinuance of the ingested agent plus corticosteroids or other non-specific immunosuppressive regimens.
- Clonal eosinophilia caused by mutations in genes that are highly susceptible to tyrosine kinase inhibitors such as "PDGFRA", "PDGFRB", or possibly "FGFR1": first generation tyrosine kinase inhibitors (e.g. imatinib) are recommended for the former two mutations; a later generation tyrosine kinase inhibitors, ponatinib, alone or combined with bone marrow transplantation, may be useful for treating the FGFR1 mutations.
- Clonal hypereosinophilia due to mutations in other genes or primary malignancies: specific treatment regimens used for these pre-malignant or malignant diseases may be more useful and necessary than non-specific immunosuppression.
- Allergic and autoimmune diseases: non-specific treatment regimens used for these diseases may be useful in place of a simple corticosteroid regimen. For example, eosinophilic granulomatosis with polyangiitis can be successfully treated with mepolizumab.
- Idiopathic hypereosinphilic syndrome and lymphocyte-variant hypereosinophilia: corticosteroids; for individuals with these hypereosinophilias that are refractory to or break through corticosteroid therapy and individuals requiring corticosteroid-sparing therapy, recommended alternative drug therapies include hydroxyurea, Pegylated interferon-α, and either one of two tyrosine kinase inhibitors viz., imatinib and mepolizumab).
Treatment primarily consists of reducing eosinophil levels and preventing further damage to organs. Corticosteroids, such as Prednisone, are good for reducing eosinophil levels and antineoplastics are useful for slowing eosinophil production. Surgical therapy is rarely utilised, however splenectomy can reduce the pain due to spleen enlargement. If damage to the heart (in particular the valves), then prosthetic valves can replace the current organic ones. Follow-up care is vital for the survival of the patient, as such the patient should be checked for any signs of deterioration regularly. After promising results in drug trials (95% efficiency in reducing blood eosinophil count to acceptable levels) it is hoped that in the future hypereosinophilic syndrome, and diseases related to eosinophils such as asthma and eosinophilic granulomatosis with polyangiitis, may be treated with the monoclonal antibody Mepolizumab currently being developed to treat the disease. If this becomes successful, it may be possible for corticosteroids to be eradicated and thus reduce the amount of side effects encountered.
Treatment involves appropriate antibiotic medications, monitoring and protection of the airway in severe cases, and, where appropriate, urgent Otolaryngology-Head and Neck Surgery, maxillo-facial surgery and/or dental consultation to incise and drain the collections. The antibiotic of choice is from the penicillin group.
Incision and drainage of the abscess may be either intraoral or external. An intraoral incision and drainage procedure is indicated if the infection is localized to the sublingual space. External incision and drainage is performed if infection involves the perimandibular spaces.
A nasotracheal tube is sometimes warranted for ventilation if the tissues of the mouth make insertion of an oral airway difficult or impossible.
In cases where the patency of the airway is compromised, skilled airway management is mandatory. Fiberoptic intubation is common.
Ludwig's angina is a life-threatening condition, and carries a fatality rate of about 5%.
Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin, or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal.
Because of the risk of reinfection, prophylactic antibiotics are sometimes used after resolution of the initial condition. However, this approach does not always stop reinfection.
Eosinophilic cellulitis, also known as Wells' syndrome, is a skin disease that presents with painful, red, raised, and warm patches of skin. The rash comes on suddenly, lasts for a few weeks, and often repeatedly comes back. Scar formation does not typically occur.
Eosinophilic cellulitis is of unknown cause. It is suspected to be an autoimmune disorder. It may be triggered by bites from insects such as spiders, fleas, or ticks, or from medications or surgery. Diagnosis is made after other potential cases are ruled out. Skin biopsy of the affected areas may show an increased number of eosinophils. Other conditions that may appear similar include cellulitis, contact dermatitis, and severe allergic reactions such as anaphylaxis.
Treatment is often with a corticosteroids. Steroids applied as a cream is generally recommended over the use of steroids by mouth. Antihistamines may be used to help with itchiness. Many times the condition goes away after a few weeks without treatment. The condition is uncommon with about 200 described cases. It affects both sexes with the same frequency. It was first described by George Crichton Wells in 1971.
Antibiotics are aimed at gram positive bacteria. Medical attention should be sought if symptoms persist beyond 2–3 days.
The cause of juvenile cellulitis is unknown. Cytologic examination of aspirates of affected lymph nodes, pustules, abscesses, and joint fluid rarely reveal bacteria, and culture results of intact lesion are always negative for bacterial growth, suggesting a nonbacterial etiology. As signs resolve following treatment with glucocorticoids, the cause is likely to be an immune disorder.
Oral retinoids have proven effective in treating this disorder. Depending on the side effects they may improve the quality of life. Examples are etretinate, acitretin, isotretinoin
Bullous pemphigoid may be self-resolving in a period ranging from several months to many years even without treatment. Poor general health related to old age is associated with a poorer prognosis.
Pemphigoid is usually considered to be mediated by IgG, but IgA-mediated forms have also been described.
IgA-mediated immunobullous diseases can often be difficult to treat even with usually effective medications such as rituximab.
Drugs that commonly induce DRESS syndrome include phenobarbital, carbamazepine, phenytoin, lamotrigine, minocycline, sulfonamides, allopurinol, modafinil, dapsone, ziprasidone, vancomycin, and most recently olanzapine.
It has been associated with HHV-6 reactivation.