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
Several treatment methods are available to help prevent CINV. Pharmaceutical treatment is generally separated into two types: prophylactic (preventative) treatment, given before the dose of chemotherapy agents, and rescue treatment, given to treat breakthrough nausea and vomiting.
5-HT receptor antagonists are very effective antiemetics and constitute a great advance in the management of CINV. These drugs block one or more of the nerve signals that cause nausea and vomiting. During the first 24 hours after chemotherapy, the most effective approach appears to be blocking the 5-HT nerve signal. Approved 5-HT inhibitors include dolasetron (Anzemet), granisetron (Kytril, Sancuso), and ondansetron (Zofran). Their antiemetic effect due to blockade of 5HT3 receptor on vagal afferent in the gut. in addition they also block 5-HT3 receptors in CTZ and STN. The newest 5-HT inhibitor, palonosetron (Aloxi), also prevents delayed nausea and vomiting, which can occur during the 2–5 days after treatment. Since some patients have trouble swallowing pills, these drugs are often available by injection, as orally disintegrating tablets, or as transdermal patches.
A Cochrane review found droperidol, metoclopramide, ondansetron, tropisetron, dolasetron, dexamethasone, cyclizine, and granisetron effective for preventing PONV.
Granisetron and dexamethasone is not recommended due to the higher rate of side effects.
In conjunction with antiemetic medications, at least one study has found that application to the Pericardium Meridian 6 acupressure point produced a positive effect in relieving postoperative nausea and vomiting. Another study found no statistically significant difference. The two general types of alternative pressure therapy are sham acupressure and the use of the P6 point. A 2015 study found that there is no significant difference between the use of either therapy in the treatment or prevention of PONV. In a review of 59 studies it was found that both therapies significantly affected the nausea aspect, but had no significant effect on vomiting.
Acute episodes of cannabinoid hyperemesis typically last for 24–48 hours and the problem often resolves with long term stopping of cannabis use. Improvement can take one to three months to occur.
Relapses are common, and this is thought to be possibly secondary to a lack of education as many people use or increase their use of cannabis due to their symptoms of nausea and vomiting.
Many traditional medications for nausea and vomiting are ineffective. However, treatment with lorazepam or haloperidol has provided relief for some people. Assessing for dehydration due to vomiting and hot showers is important as it can lead to cannabinoid hyperemesis acute renal failure (CHARF), and this is easily treated with IV fluids. Treatment is otherwise supportive and focuses on stopping cannabis use.
There is no known cure for CVS, but there are medications that can be used for treatment, intervention, and prevention. There is a growing body of publications on both individual cases and the experiences of the CVS cohort. Treatment is usually on an individual basis, based on trial and error.
The most common therapeutic strategies for those already in an attack are maintenance of salt balance by appropriate intravenous fluids and, in some cases, sedation. Having vomited for a long period prior to attending a hospital, patients are typically severely dehydrated. For a number of patients, potent anti-emetic drugs such as ondansetron (Zofran) or granisetron (Kytril), and dronabinol (Marinol) may be helpful in either preventing an attack, aborting an attack, or reducing the severity of an attack. Lifestyle changes may be recommended, such as extended rest and reduction of stress. Because the symptoms of CVS are similar (or perhaps identical) to those of the disease well-identified as "abdominal migraine", treatment of CVS with a regimen of anti-migraine drugs, such as topiramate and amitriptyline, is showing promise in preventing recurrent attacks.
Fitzpatrick et al. (2007) identified 41 children with CVS. The mean age of the sample was 6 years at the onset of the syndrome, 8 years at first diagnosis, and 13 years at follow-up. As many as 39% of the children had resolution of symptoms immediately or within weeks of the diagnosis. Vomiting had resolved at the time of follow-up in 61% of the sample. Many children, including those in the remitted group, continued to have somatic symptoms such as headaches (in 42%) and abdominal pain (in 37%).
Most children who have this disorder miss on average 24 school days a year. The frequency of episodes is higher for some people during times of excitement. Charitable organizations to support sufferers and their families and to promote knowledge of CVS exist in several countries.
Hypersalivation is optimally treated by treating or avoiding the underlying cause. Mouthwash and tooth brushing may have drying effects.
In the palliative care setting, anticholinergics and similar drugs that would normally reduce the production of saliva causing a dry mouth could be considered for symptom management: scopolamine, atropine, propantheline, hyoscine, amitriptyline, glycopyrrolate.
A 2008 systematic review investigated the efficacy of pharmacological interventions for patients who have too much salvia due to clozapine treatment:
There has been no specific drug therapy developed for hepatitis, with the exception of hepatitis C. Patients are advised to rest in the early stages of the illness, and to eat small, high-calorie, high-protein meals in order to battle anorexia. Larger meals are more easily tolerated in the morning, for patients often experience nausea later in the day. Although high-protein meals are recommended, protein intake should be reduced if signs of precoma — lethargy, confusion, and mental changes — develop.
In acute viral hepatitis, hospitalization is usually required only for patients with severe symptoms (severe nausea, vomiting, change in mental status, and PT greater than 3 seconds above normal) or complications. If the patient experiences continuous vomiting and is unable to maintain oral intake, parenteral nutrition may be required.
In order to relieve nausea and also prevent vomiting, antiemetics (diphenhydramine or prochlorperazine) may be given 30 minutes before meals. However, phenothiazines have a cholestatic effect and should be avoided. The resin cholestyramine may be given only for severe pruritus.
Hangovers are poorly understood from a medical point of view. Health care professionals prefer to study alcohol abuse from a standpoint of treatment and prevention, and there is a view that the hangover provides a useful, natural and intrinsic disincentive to excessive drinking.
Within the limited amount of serious study on the subject, there is debate about whether a hangover may be prevented or at least mitigated. There is also a vast body of folk medicine and simple quackery. A four-page literature review in the "British Medical Journal" concludes: "No compelling evidence exists to suggest that any conventional or complementary intervention is effective for preventing or treating alcohol hangover. The most effective way to avoid the symptoms of alcohol induced hangover is to avoid drinking." Most remedies do not significantly reduce overall hangover severity. Some compounds reduce specific symptoms such as vomiting and headache, but are not effective in reducing other common hangover symptoms such as drowsiness and fatigue
There is no evidence that any treatment for hangovers is very effective.
- Rehydration: Drinking water before going to bed or during hangover may relieve dehydration-associated symptoms such as thirst, dizziness, dry mouth, and headache.
- Non-steroidal anti-inflammatory drugs such as aspirin or ibuprofen have been proposed as a treatment for the headaches associated with a hangover. There however is no evidence to support a benefit, and there are concerns that taking alcohol and aspirin together may increase the risk of stomach bleeding and liver damage.
- Tolfenamic acid, an inhibitor of prostaglandin synthesis, in a 1983 study reduced headache, nausea, vomiting, irritation but had no effect on tiredness in 30 people.
- Pyritinol: A 1973 study found that large doses (several hundred times the recommended daily intake) of Pyritinol, a synthetic Vitamin B6 analog, can help to reduce hangover symptoms. Possible side effects of pyritinol include hepatitis (liver damage) due to cholestasis and acute pancreatitis.
- Yeast-based extracts: The difference in the change for discomfort, restlessness, and impatience were statistically significant but no significant differences on blood chemistry parameters, blood alcohol or acetaldehyde concentrations have been found, and it did not significantly improve general well-being.
Some studies support the use of ginger, but overall the evidence is limited and inconsistent. Safety concerns have been raised regarding its anticoagulant properties.
Causes of decreased clearance of saliva include:
- Infections such as tonsillitis, retropharyngeal and peritonsillar abscesses, epiglottitis and mumps.
- Problems with the jaw, e.g., fracture or dislocation
- Radiation therapy
- Neurologic disorders such as myasthenia gravis, Parkinson's disease, multiple system atrophy, rabies, bulbar paralysis, bilateral facial nerve palsy, and hypoglossal nerve palsy
Thalidomide was originally developed and prescribed as a cure for morning sickness in West Germany, but its use was discontinued when it was found to cause birth defects. The United States Food and Drug Administration never approved thalidomide for use as a cure for morning sickness.
Treatment includes dietary changes (low fiber diets) and, in some cases, restrictions on fat and/or solids. Eating smaller meals, spaced two to three hours apart has proved helpful. Avoiding foods that cause the individual problems, such as pain in the abdomen, or constipation, such as rice or beef, will help avoid symptoms.
Metoclopramide, a dopamine D receptor antagonist, increases contractility and resting tone within the GI tract to improve gastric emptying. In addition, dopamine antagonist action in the central nervous system prevents nausea and vomiting. Similarly, the dopamine receptor antagonist domperidone is also used to treat gastroparesis. Erythromycin is known to improve emptying of the stomach but its effects are temporary due to tachyphylaxis and wane after a few weeks of consistent use.
Sildenafil citrate, which increases blood flow to the genital area in men, is being used by some practitioners to stimulate the gastrointestinal tract in cases of diabetic gastroparesis.
The antidepressant mirtazapine has proven effective in the treatment of gastroparesis unresponsive to conventional treatment. This is due to its antiemetic and appetite stimulant properties. Mirtazapine acts on the same serotonin receptor (5-HT3) as does the popular anti-emetic ondansetron.
In specific cases where treatment of chronic nausea and vomiting proves resistant to drugs, implantable gastric stimulation may be utilized. A medical device is implanted that applies neurostimulation to the muscles of the lower stomach to reduce the symptoms. This is only done in refractory cases that have failed all medical management (usually at least 2 years of treatment). Medically refractory gastroparesis may also be treated with a pyloromyotomy, which widens the gastric outlet by cutting the circular pylorus muscle. This can be done laparoscopically or endoscopically.
There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. Heightened mast cell activation has been proposed to be a common factor among FGIDs, contributing to visceral hypersensitivity as well as epithelial, neuromuscular, and motility dysfunction.
Thalidomide was prescribed for treatment of HG in Europe until it was recognized that thalidomide is teratogenic and is a cause of phocomelia in neonates.
Dry bland food and oral rehydration are first-line treatments. Due to the potential for severe dehydration and other complications, HG is treated as an emergency. If conservative dietary measures fail, more extensive treatment such as the use of antiemetic medications and intravenous rehydration may be required. If oral nutrition is insufficient, intravenous nutritional support may be needed. For women who require hospital admission, thromboembolic stockings or low-molecular-weight heparin may be used as measures to prevent the formation of a blood clot.
Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.
It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves. The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease. It may also occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis.
Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery. Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.
Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.
Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men. A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.
Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCl) in order to properly empty itself of a meal.
New agents have been identified in animal studies that may have effects on intestinal radiation injury. The research approach in humans has been reviewed.
Two small randomized controlled trials (RCTs) and one larger RCT (86 subjects) tested glutamine in the prevention of platinum treatment-induced neuropathy and showed promise. As of September 2013 a larger, placebo-controlled trial is running.
A 2013 systematic review of the use of acetyl-L-carnitine, glutamine, vitamin E, glutathione, vitamin B6, omega-3 fatty acids, magnesium, calcium, alpha lipoic acid and n-acetyl cysteine as anti-CIPN adjuvants concluded that "currently no agent has shown solid beneficial evidence to be recommended for the treatment or prophylaxis of CIPN."
As possible preventative interventions, the American National Cancer Institute Symptom Management and Health-related Quality of Life Steering Committee recommends continued investigation of several dietary supplements, including glutathione, and intravenous calcium and magnesium, which have shown early promise in limited human trials; acetyl-L-carnitine, which was effective in animal models and on diabetes and HIV patients; and the anti-oxidant alpha-lipoic acid.
Alimentary toxic aleukia, or Aleukia, is a mycotoxin-induced condition characterized by nausea, vomiting, diarrhea, leukopenia (aleukia), hemorrhaging, skin inflammation, and sometimes death. Alimentary Toxic Alekia almost always refers to the human condition associated with presence of T2 Toxin.
Functional gastrointestinal disorders (FGID) include a number of separate idiopathic disorders which affect different parts of the gastrointestinal tract and involve visceral hypersensitivity and impaired gastrointestinal motility.