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
In almost all cases, recluse bites are self-limited and typically heal without any medical intervention. Recommendations to limit the extent of damage include elevation and immobilization of the affected limb, application of ice. Both local wound care, and tetanus prophylaxis are simple standards. There is no established treatment for more extensive necrosis. Many therapies have been used including hyperbaric oxygen, dapsone, antihistamines (e.g., cyproheptadine), antibiotics, dextran, glucocorticoids, vasodilators, heparin, nitroglycerin, electric shock, curettage, surgical excision, and antivenom. None of these treatments conclusively show benefit. Studies have shown surgical intervention is ineffective and may worsen outcome. Excision may delay wound healing, cause abscesses, and lead to objectionable scarring.
Dapsone, an antibiotic, is commonly used in the United States and Brazil for the treatment of necrosis. There have been conflicting reports with some supporting its efficacy and others have suggested it should no longer be used routinely, if at all.
Use of antivenom for severe spider bites may be indicated, especially in the case of neurotoxic venoms. Effective antivenoms exist for "Latrodectus", "Atrax", and "Phoneutria" venom. Antivenom in the United States is in intravenous form but is rarely used, as anaphylactic reaction to the antivenom has resulted in deaths. In Australia, antivenom in intramuscular form was once commonly used, but use has declined. In 2014 some doubt as to antivenom effectiveness has been raised. In South America an antivenom is available for "Loxosceles" bites, and it appears antivenom may be the most promising therapy four recluse bites. However, in experimental trials recluse antivenom is more effective when given early, and patients often do not present for 24 or more hours after envenomation, possibly limiting the effect of such intervention.
No specific treatment for CTF is yet available. The first action is make sure the tick is fully removed from the skin, then acetaminophen and analgesics can be used to help relieve the fever and pain. Aspirin is not recommended for children, as it has been linked to Reye’s syndrome in some viral illnesses. Salicylates should not be used because of thrombocytopenia, and the rare occurrence of bleeding disorders. People who suspect they have been bitten by a tick or are starting to show signs of CTF should contact their physicians immediately.
Ticks should be removed promptly and carefully with tweezers and by applying gentle, steady traction. The tick's body should not be crushed when it is removed and the tweezers should be placed as close to the skin as possible to avoid leaving tick mouthparts in the skin; mouthparts left in the skin can allow secondary infections. Ticks should not be removed with bare hands. Hands should be protected by gloves and/or tissues and thoroughly washed with soap and water after the removal process.
A match or flame should not be used to remove a tick. This method, once thought safe, can cause the tick to regurgitate, expelling any disease it may be carrying into the bite wound.
Topical 5-fluorouracil (5-FU, Efudex, Carac) has been shown to be an effective therapy for diffuse, but minor actinic cheilitis. 5-fluorouracil works by blocking DNA synthesis. Cells that are rapidly growing need more DNA, so they accumulate more 5-fluorouracil, resulting in their death. Normal skin is much less affected. The treatment usually takes 2–4 weeks depending on the response. The typical response includes an inflammatory phase, followed by redness, burning, oozing, and finally erosion. Treatment is stopped when ulceration and crusting appear. There is minimal scarring. Complete clearance has been reported in about 50% of patients.
Imiquimod (Aldara) is an immune response modifier that has been studied for the treatment of actinic cheilitis. It promotes an immune response in the skin leading to apoptosis (death) of the tumor cells. It causes the epidermis to be invaded by macrophages, which leads to epidermal erosion. T-cells are also activated as a result of imiquimod treatment. Imiquimod appears to promote an “immune memory” that reduces the recurrence of lesions. There is minimal scarring. Complete clearance has been demonstrated in up to 45% of patients with actinic keratoses. However, the dose and duration of therapy, as well as the long-term efficacy, still need to be established in the treatment of actinic cheilitis.
This condition is considered premalignant because it may lead to squamous cell carcinoma in about 10% of all cases. It is not possible to predict which cases will progress into SCC, so the current consensus is that all lesions should be treated.
Treatment options include 5-fluorouracil, imiquimod, scalpel vermillionectomy, chemical peel, electrosurgery, and carbon dioxide laser vaporization. These curative treatments attempt to destroy or remove the damaged epithelium. All methods are associated with some degree of pain, edema, and a relatively low rate of recurrence.
Conjunctival auto-grafting is a surgical technique that is an effective and safe procedure for pterygium removal. When the pterygium is removed, the tissue that covers the sclera known as the Tenons layer is also removed. Auto-grafting covers the bare sclera with conjunctival tissue that is surgically removed from an area of healthy conjunctiva. That “self-tissue” is then transplanted to the bare sclera and is fixated using sutures or tissue adhesive.
A Cochrane review found conjunctival autograft surgery was less likely to have reoccurrence of the pterygium at 6 months compared to amniotic membrane transplant. More research is needed to determine which type of surgery resulted in better vision or quality of life. The additional use of mitomycin C is of unclear effect. Radiotherapy has also be used in an attempt to reduce the risk of recurrence.
Treatments for the various forms of hair loss have limited success. Three medications have evidence to support their use in male pattern hair loss: minoxidil, finasteride, and dutasteride. They typically work better to prevent further hair loss, than to regrow lost hair.
- Minoxidil (Rogaine) is a nonprescription medication approved for male pattern baldness and alopecia areata. In a liquid or foam, it is rubbed into the scalp twice a day. Some people have an allergic reaction to the propylene glycol in the minoxidil solution and a minoxidil foam was developed without propylene glycol. Not all users will regrow hair. The longer the hair has stopped growing, the less likely minoxidil will regrow hair. Minoxidil is not effective for other causes of hair loss. Hair regrowth can take 1 to 6 months to begin. Treatment must be continued indefinitely. If the treatment is stopped, hair loss resumes. Any regrown hair and any hair susceptible to being lost, while Minoxidil was used, will be lost. Most frequent side effects are mild scalp irritation, allergic contact dermatitis, and unwanted hair in other parts of the body.
- Finasteride (Propecia) is used in male-pattern hair loss in a pill form, taken 1 milligram per day. It is not indicated for women and is not recommended in pregnant women. Treatment is effective starting within 6 weeks of treatment. Finasteride causes an increase in hair retention, the weight of hair, and some increase in regrowth. Side effects in about 2% of males, include decreased sex drive, erectile dysfunction, and ejaculatory dysfunction. Treatment should be continued as long as positive results occur. Once treatment is stopped, hair loss resumes.
- Corticosteroids injections into the scalp can be used to treat alopecia areata. This type of treatment is repeated on a monthly basis. Oral pills for extensive hair loss may be used for alopecia areata. Results may take up to a month to be seen.
- Immunosuppressants applied to the scalp have been shown to temporarily reverse alopecia areata, though the side effects of some of these drugs make such therapy questionable.
- There is some tentative evidence that anthralin may be useful for treating alopecia areata.
- Hormonal modulators (oral contraceptives or antiandrogens such as spironolactone and flutamide) can be used for female-pattern hair loss associated with hyperandrogenemia.
Antibiotics are the primary treatment. The specific approach to their use is dependent on the individual affected and the stage of the disease. For most people with early localized infection, oral administration of doxycycline is widely recommended as the first choice, as it is effective against not only "Borrelia" bacteria but also a variety of other illnesses carried by ticks. Doxycycline is contraindicated in children younger than eight years of age and women who are pregnant or breastfeeding; alternatives to doxycycline are amoxicillin, cefuroxime axetil, and azithromycin. Individuals with early disseminated or late infection may have symptomatic cardiac disease, refractory Lyme arthritis, or neurologic symptoms like meningitis or encephalitis. Intravenous administration of ceftriaxone is recommended as the first choice in these cases; cefotaxime and doxycycline are available as alternatives.
These treatment regimens last from one to four weeks. If joint swelling persists or returns, a second round of antibiotics may be considered. Outside of that, a prolonged antibiotic regimen lasting more than 28 days is not recommended as no clinical evidence shows it to be effective. IgM and IgG antibody levels may be elevated for years even after successful treatment with antibiotics. As antibody levels are not indicative of treatment success, testing for them is not recommended.
Naltrexone is used for the treatment of opioid addiction. It works by blocking the physiological, euphoric, and reinforcing effects of opioids. Non-compliance with naltrexone therapy is a concern with oral formulations because of its daily dosing, and although the alternative intramuscular (IM) injection has better compliance due to its monthly dosing, attempts to override the blocking effect with higher doses and stronger drugs have proven dangerous. Naltrexone monthly IM injections received FDA approval in 2010 for the treatment of opioid dependence in abstinent opioid users.
In terms of a cure there is currently none available, however for the disease to manifest itself, it requires mutant gene expression. Manipulating the use of protein homoestasis regulators can be therapuetic agents, or a treatment to try and correct an altered function that makes up the pathology is one current idea put forth by Bushart, et al. There is some evidence that for SCA1 and two other polyQ disorders that the pathology can be reversed after the disease is underway. There is no effective treatments that could alter the progression of this disease, therefore care is given, like occupational and physical therapy for gait dysfunction and speech therapy.
Palinopsia from cerebrovascular accidents generally resolves spontaneously, and treatment should be focused on the vasculopathic risk factors. Palinopsia from neoplasms, AVMs, or abscesses require treatment of the underlying condition, which usually also resolves the palinopsia. Palinopsia due to seizures generally resolves after correcting the primary disturbance and/or treating the seizures. In persistent hallucinatory palinopsia, a trial of an anti-epileptic drug can be attempted. Anti-epileptics reduce cortical excitability and could potentially treat palinopsia caused by cortical deafferentation or cortical irritation. Patients with idiopathic hallucinatory palinopsia should have close follow-up.
Buprenorphine sublingual preparations are often used to manage opioid dependence (that is, dependence on heroin, oxycodone, hydrocodone, morphine, oxymorphone, fentanyl or other opioids). Preparations were approved for this indication by the United States Food and Drug Administration in October 2002. Some formulations of buprenorphine incorporate the opiate antagonist naloxone during the production of the pill form to prevent people from crushing the tablets and injecting them, instead of using the sublingual (under the tongue) route of administration.
Dietary supplements are not typically recommended. There is only one small trial of saw palmetto which shows tentative benefit in those with mild to moderate androgenetic alopecia. There is no evidence for biotin. Evidence for most other produces is also insufficient. There was no good evidence for gingko, aloe vera, ginseng, bergamot, hibiscus, or sorphora as of 2011.
Many people use unproven treatments. Egg oil, in Indian, Japanese, Unani (Roghan Baiza Murgh) and Chinese traditional medicine, was traditionally used as a treatment for hair loss.
The onset of Wernicke's encephalopathy is considered a medical emergency, and thus thiamine administration should be initiated immediately when the disease is suspected. Prompt administration of thiamine to patients with Wernicke's encephalopathy can prevent the disorder from developing into Wernicke–Korsakoff syndrome, or reduce its severity. Treatment can also reduce the progression of the deficits caused by WKS, but will not completely reverse existing deficits. WKS will continue to be present, at least partially, in 80% of patients. Patients suffering from WE should be given a minimum dose of 500 mg of thiamine hydrochloride, delivered by infusion over a 30-minute period for two to three days. If no response is seen then treatment should be discontinued but for those patients that do respond, treatment should be continued with a 250 mg dose delivered intravenously or intramuscularly for three to five days unless the patient stops improving. Such prompt administration of thiamine may be a life-saving measure. Banana bags, a bag of intravenous fluids containing vitamins and minerals, is one means of treatment.
As described, Korsakoff 's syndrome usually follows or accompanies Wernicke's encephalopathy. If treated quickly, it may be possible to prevent the development of Korsakoff's syndrome with thiamine treatments. This treatment is not guaranteed to be effective and the thiamine needs to be administered adequately in both dose and duration. A study on Wernicke-Korsakoff's syndrome showed that with consistent thiamine treatment there were noticeable improvements in mental status after only 2–3 weeks of therapy. Thus, there is hope that with treatment Wernicke's encephalopathy will not necessarily progress to WKS.
In order to reduce the risk of developing WKS it is important to limit the intake of alcohol or drink in order to ensure that proper nutrition needs are met. A healthy diet is imperative for proper nutrition which, in combination with thiamine supplements, may reduce the chance of developing WKS. This prevention method may specifically help heavy drinkers who refuse to or are unable to quit.
Other prescription drugs are also used, if other methods are not effective. Before the introduction of SSRIs, monoamine oxidase inhibitors (MAOIs) such as phenelzine were frequently used in the treatment of social anxiety. Evidence continues to indicate that MAOIs are effective in the treatment and management of social anxiety disorder and they are still used, but generally only as a last resort medication, owing to concerns about dietary restrictions, possible adverse drug interactions and a recommendation of multiple doses per day. A newer type of this medication, Reversible inhibitors of monoamine oxidase subtype A (RIMAs) such as the drug moclobemide, bind reversibly to the MAO-A enzyme, greatly reducing the risk of hypertensive crisis with dietary tyramine intake.
Benzodiazepines such as clonazepam are an alternative to SSRIs. These drugs are often used for short-term relief of severe, disabling anxiety. Although benzodiazepines are still sometimes prescribed for long-term everyday use in some countries, there is concern over the development of drug tolerance, dependency and misuse. It has been recommended that benzodiazepines be considered only for individuals who fail to respond to other medications. Benzodiazepines augment the action of GABA, the major inhibitory neurotransmitter in the brain; effects usually begin to appear within minutes or hours. In most patients, tolerance rapidly develops to the sedative effects of benzodiazepines, but not to the anxiolytic effects. Long-term use of benzodiazepine may result in physical dependence, and abrupt discontinuation of the drug should be avoided due to high potential for withdrawal symptoms (including tremor, insomnia, and in rare cases, seizures). A gradual tapering of the dose of clonazepam (a decrease of 0.25 mg every 2 weeks), however, has been shown to be well tolerated by patients with social anxiety disorder. Benzodiazepines are not recommended as monotherapy for patients who have major depression in addition to social anxiety disorder and should be avoided in patients with a history of substance abuse.
Certain anticonvulsant drugs such as gabapentin are effective in social anxiety disorder and may be a possible treatment alternative to benzodiazepines.
Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine have shown similar effectiveness to the SSRIs. In Japan, Milnacipran is used in the treatment of Taijin kyofusho, a Japanese variant of social anxiety disorder. The atypical antidepressants mirtazapine and bupropion have been studied for the treatment of social anxiety disorder, and rendered mixed results.
Some people with a form of social phobia called performance phobia have been helped by beta-blockers, which are more commonly used to control high blood pressure. Taken in low doses, they control the physical manifestation of anxiety and can be taken before a public performance.
A novel treatment approach has recently been developed as a result of translational research. It has been shown that a combination of acute dosing of d-cycloserine (DCS) with exposure therapy facilitates the effects of exposure therapy of social phobia. DCS is an old antibiotic medication used for treating tuberculosis and does not have any anxiolytic properties per se. However, it acts as an agonist at the glutamatergic N-methyl-D-aspartate (NMDA) receptor site, which is important for learning and memory.
Kava-kava has also attracted attention as a possible treatment, although safety concerns exist.
For "T. b. gambiense" the combination of nifurtimox and eflornithine (NECT) or eflornithine alone appear to be more effective and result in fewer side effects. These treatments may replace melarsoprol when available with the combination being first line. NECT has the benefit of requiring less injections of eflornithine.
Intravenous melarsoprol was previously the standard treatment for second-stage (neurological phase) disease and is effective for both types. Melarsoprol is the only treatment for second stage "T. b. rhodesiense"; however, it causes death in 5% of people who take it. Resistance to melarsoprol can occur.
The current treatment for first-stage disease is intravenous or intramuscular pentamidine for "T. b. gambiense" or intravenous suramin for "T. b. rhodesiense".
Treatment of APD typically focuses on three primary areas: changing learning environment, developing higher-order skills to compensate for the disorder, and remediation of the auditory deficit itself. However, there is a lack of well-conducted evaluations of intervention using randomized controlled trial methodology. Most evidence for effectiveness adopts weaker standards of evidence, such as showing that performance improves after training. This does not control for possible influences of practice, maturation, or placebo effects. Recent research has shown that practice with basic auditory processing tasks (i.e. auditory training) may improve performance on auditory processing measures and phonemic awareness measures. Changes after auditory training have also been recorded at the physiological level. Many of these tasks are incorporated into computer-based auditory training programs such as Earobics and Fast ForWord, an adaptive software available at home and in clinics worldwide, but overall, evidence for effectiveness of these computerised interventions in improving language and literacy is not impressive. One small-scale uncontrolled study reported successful outcomes for children with APD using auditory training software.
Treating additional issues related to APD can result in success. For example, treatment for phonological disorders (difficulty in speech) can result in success in terms of both the phonological disorder as well as APD. In one study, speech therapy improved auditory evoked potentials (a measure of brain activity in the auditory portions of the brain).
While there is evidence that language training is effective for improving APD, there is no current research supporting the following APD treatments:
- Auditory Integration Training typically involves a child attending two 30-minute sessions per day for ten days.
- Lindamood-Bell Learning Processes (particularly, the Visualizing and Verbalizing program)
- Physical activities that require frequent crossing of the midline (e.g., occupational therapy)
- Sound Field Amplification
- Neuro-Sensory Educational Therapy
- Neurofeedback
However, use of a FM transmitter has been shown to produce significant improvements over time with children.
Selective serotonin reuptake inhibitors (SSRIs), a class of antidepressants, are first choice medication for generalized social phobia but a second line treatment. Compared to older forms of medication, there is less risk of tolerability and drug dependency associated with SSRIs.
In a 1995 double-blind, placebo-controlled trial, the SSRI paroxetine was shown to result in clinically meaningful improvement in 55 percent of patients with generalized social anxiety disorder, compared with 23.9 percent of those taking placebo. An October 2004 study yielded similar results. Patients were treated with either fluoxetine, psychotherapy, or a placebo. The first four sets saw improvement in 50.8 to 54.2 percent of the patients. Of those assigned to receive only a placebo, 31.7 percent achieved a rating of 1 or 2 on the Clinical Global Impression-Improvement scale. Those who sought both therapy and medication did not see a boost in improvement.
General side-effects are common during the first weeks while the body adjusts to the drug. Symptoms may include headaches, nausea, insomnia and changes in sexual behavior. Treatment safety during pregnancy has not been established. In late 2004 much media attention was given to a proposed link between SSRI use and suicidality [a term that encompasses suicidal ideation and attempts at suicide as well as suicide]. For this reason, [although evidential causality between SSRI use and actual suicide has not been demonstrated] the use of SSRIs in pediatric cases of depression is now recognized by the Food and Drug Administration as warranting a cautionary statement to the parents of children who may be prescribed SSRIs by a family doctor. Recent studies have shown no increase in rates of suicide. These tests, however, represent those diagnosed with depression, not necessarily with social anxiety disorder.
In addition, studies show that more socially phobic patients treated with anti-depressant medication develop hypomania than non-phobic controls. The hypomania can be seen as the medication creating a new problem.
Some medications that can be used for erethism are Traid and Ritalin. Methylphenidate (Ritalin) is a stimulant drug approved for therapy of attention-deficit hyperactivity disorder, postural orthostatic tachycardia syndrome and narcolepsy. It may also be prescribed for off-label use in treatment-resistant cases of lethargy, depression (mood), or neural insult.
One treatment of mercury poisoning was to admit fresh air to the patient by having him go outside daily as much as possible. Stimulants such as ammonia have also been documented to help restore pulse to a normal rhythm. For a more comprehensive reading of treatment, see Mercury poisoning, 'Treatment' section.
Prevention includes avoiding exposure to the sun and wearing sun block on the affected area.
- Cover up: wear long sleeves, slacks, and a wide-brimmed hat whenever harsh exposure is probable
- Avoid chemicals that may trigger a reaction
- Wear sunscreen at least factor 30 with a high UVA protection level
- Wear gloves and/or remain indoors after handling fruits or plants which increase sensitivity to light
Many medications and conditions can cause sun sensitivity, including:
- Sulfa used in some drugs, among them some antibiotics, diuretics, COX-2 inhibitors, and diabetes drugs.
- Psoralens, coal tars, photo-active dyes (eosin, acridine orange)
- Musk ambrette, methylcoumarin, lemon oil (may be present in fragrances)
- PABA (found in sunscreens)
- Oxybenzone (UVA and UVB chemical blocker also in sunscreens)
- Salicylanilide (found in industrial cleaners)
- St John's Wort, used to treat clinical depression
- Hexachlorophene (found in some ℞ antibacterial soaps)
- Contact with sap from Giant Hogweed. Common Rue (Ruta graveolens) is another phototoxic plant commonly found in gardens. Phototoxicity caused by plants is called phytophotodermatitis.
- Tetracycline antibiotics (e.g., tetracycline, doxycycline, minocycline)
- Benzoyl peroxide
- Retinoids (e.g., isotretinoin)
- Some NSAIDs (e.g., ibuprofen, naproxen sodium)
- Fluoroquinolone antibiotic: Sparfloxacin in 2% of cases
- Amiodarone, used to treat atrial fibrillation
- Pellagra
Photo dermatitis can also be caused by plants like the Dictamnus (commonly known as the "Burning Bush") which is a genus of the flowering plant in the Rutaceae family. This is called phytophotodermatitis.