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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)
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Those working in industry, in the military, or as first responders may be required to wear personal protective equipment (PPE) against hazards such as chemical agents, gases, fire, small arms and even Improvised Explosive Devices (IEDs). PPE includes a range of hazmat suits, firefighting turnout gear, body armor and bomb suits, among others. Depending on design, the wearer may be encapsulated in a microclimate, due to an increase in thermal resistance and decrease in vapor permeability. As physical work is performed, the body’s natural thermoregulation (i.e., sweating) becomes ineffective. This is compounded by increased work rates, high ambient temperature and humidity levels, and direct exposure to the sun. The net effect is that desired protection from some environmental threats inadvertently increases the threat of heat stress.
The effect of PPE on hyperthermia has been noted in fighting the 2014 Ebola virus epidemic in Western Africa. Doctors and healthcare workers were only able to work 40 minutes at a stretch in their protective suits, fearing heat strokes.
In the UK, 28,354 cases of hypothermia were treated in 2012-13 – an increase of 25% from the previous year. Some cases of hypothermia death, as well as other preventable deaths, happen because poor people cannot easily afford to keep warm. Rising fuel bills have increased the numbers who have difficulty paying for adequate heating in the UK. Some pensioners and disabled people are at risk because they do not work and cannot easily get out of their homes. Better heat insulation can help.
Alcohol consumption increases the risk of hypothermia by its action as a vasodilator. It increases blood flow to the skin and extremities, making a person "feel" warm, while increasing heat loss. Between 33% and 73% of hypothermia cases are complicated by alcohol.
Some drugs cause excessive internal heat production. The rate of drug-induced hyperthermia is higher where use of these drugs is higher.
- Many psychotropic medications, such as selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs), and tricyclic antidepressants, can cause hyperthermia. Serotonin syndrome is a rare adverse reaction to overdose of these medications or the use of several simultaneously. Similarly, neuroleptic malignant syndrome is an uncommon reaction to neuroleptic agents. These syndromes are differentiated by other associated symptoms, such as tremor in serotonin syndrome and "lead-pipe" muscle rigidity in neuroleptic malignant syndrome.
- Various stimulant drugs, including amphetamines and cocaine, and hallucinogenic drugs, including PCP, LSD, and MDMA can produce hyperthermia as an adverse effect.
- Malignant hyperthermia is a rare reaction to common anesthetic agents (such as halothane) or the paralytic agent succinylcholine. Those who have this reaction, which is potentially fatal, have a genetic predisposition.
- The use of anticholinergics, more specifically muscarinic antagonists are thought to cause mild hyperthermic episodes due to its parasympatholytic effects. The sympathetic nervous system a.k.a. the "Fight or Flight Response" dominates by raising catecholamine levels by the blocked action of the Rest and Digest System.
- Drugs that decouple oxidative phosphorylation may also cause hyperthermia. From this group of drugs the most well known is 2,4-Dinitrophenol which was used as a weight loss drug until dangers from its use became apparent.
Postanesthetic shivering (PAS) is shivering after anesthesia.
The intensity of PAS may be graded using the scale described by Crossley and Mahajan:
Postanesthetic shivering is one of the leading causes of discomfort in patients recovering from general anesthesia. It usually results due to the anesthetic inhibiting the body's thermoregulatory capability, although cutaneous vasodilation (triggered by post-operative pain) may also be a causative factor. First-line treatment consists of warming the patient; more persistent/severe cases may be treated with medications such as tramadol, pethidine, clonidine and nefopam, which work by reducing the shivering threshold temperature and reducing the patient's level of discomfort. As these medications may react and/or synergize with the anesthetic agents employed during the surgery, their use is generally avoided when possible.
Postpartum chills is a physiological response that occurs within two hours of childbirth. It appears as uncontrollable shivering that is not under voluntary control. It is seen in many women after delivery and can be unpleasant. It lasts for a short time. It is thought to be a result of a nervous system response. It may also be related to fluid shifts and the actual strenuous work of labor. It is considered a normal response and there is no accompanying fever. If a fever does develop further assessments may reveal the presence of an infection. Treatment consists of an explanation from clinicians that the shivering is a normal response and that it only lasts for a short time. Warm blankets are given to the women and fluid replacement is encouraged. It has been described as a fairly common and normal occurrence.
After discharge to home with the baby, chills that accompany uncontrolled bleeding, shortness of breath, cold clammy skin, dizziness, heart pain, and racing heart can be a sign of shock that needs immediate medical attention. Mastitis can also cause shivering.
Physicians, Nurse Practitioners, Physician Assistants, Nurses and Midwives will typically ask for the need of relief. Women in labor have many pain relief options that work well and pose small risks when given by a trained and experienced clinician. Clinicians also can use different methods for pain relief at different stages of labor. Still, not all options are available at every hospital and birthing center. Depending on the health history of the mother, the presence of allergies or other concerns, some choices will work better than others.
There are many methods of relieving pain used for labor. Rare and unpredictable, serious complications sometimes occur. Also, most medicines used to manage pain during labor pass freely into the placenta to the baby. Asking questions about the procedures and medications might affect the baby are valid questions.
More and more women in the United States are using water to find comfort during labor. This is called hydrotherapy. Laboring in a tub of warm water helps women feel physically supported, and keeps them warm and relaxed. Plus, it is easier for laboring women to move and find comfortable positions in the water.
In waterbirthing, a woman remains in the water for delivery. The American Academy of Pediatrics has expressed concerns about delivering in water because of a lack of studies showing its safety and because of the rare but reported chance of complications. Ask your doctor or midwife if you want to know more about waterbirthing.
Epidemiological studies of serotonin syndrome are difficult as many physicians are unaware of the diagnosis or they may miss the syndrome due to its variable manifestations. In 1998 a survey conducted in England found that 85% of the general practitioners that had prescribed the antidepressant nefazodone were unaware of serotonin syndrome. The incidence may be increasing as a larger number of pro-serotonergic drugs (drugs which increase serotonin levels) are now being used in clinical practice. One postmarketing surveillance study identified an incidence of 0.4 cases per 1000 patient-months for patients who were taking nefazodone. Additionally, around 14 to 16 percent of persons who overdose on SSRIs are thought to develop serotonin syndrome.
Upon the discontinuation of serotonergic drugs, most cases of serotonin syndrome resolve within 24 hours, although in some cases delirium may persist for a number of days. Symptoms typically persist for a longer time frame in patients taking drugs which have a long elimination half-life, active metabolites, or a protracted duration of action.
Cases have reported muscle pain and weakness persisting for months, and antidepressant discontinuation may contribute to ongoing features. Following appropriate medical management, serotonin syndrome is generally associated with a favorable prognosis.
Narcosis is potentially one of the most dangerous conditions to affect the scuba diver below about . Except for occasional amnesia of events at depth, the effects of narcosis are entirely removed on ascent and therefore pose no problem in themselves, even for repeated, chronic or acute exposure. Nevertheless, the severity of narcosis is unpredictable and it can be fatal while diving, as the result of illogical behavior in a dangerous environment.
Tests have shown that all divers are affected by nitrogen narcosis, though some experience lesser effects than others. Even though it is possible that some divers can manage better than others because of learning to cope with the subjective impairment, the underlying behavioral effects remain. These effects are particularly dangerous because a diver may feel they are not experiencing narcosis, yet still be affected by it.
Inactivity and starvation in mammals lead to atrophy of skeletal muscle, accompanied by a smaller number and size of the muscle cells as well as lower protein content. In humans, prolonged periods of immobilization, as in the cases of bed rest or astronauts flying in space, are known to result in muscle weakening and atrophy. Such consequences are also noted in small hibernating mammals like the golden-mantled ground squirrels and brown bats.
Bears are an exception to this rule; species in the family Ursidae are famous for their ability to survive unfavorable environmental conditions of low temperatures and limited nutrition availability during winter by means of hibernation. During that time, bears go through a series of physiological, morphological and behavioral changes. Their ability to maintain skeletal muscle number and size at time of disuse is of significant importance.
During hibernation, bears spend four to seven months of inactivity and anorexia without undergoing muscle atrophy and protein loss. There are a few known factors that contribute to the sustaining of muscle tissue. During the summer period, bears take advantage of the nutrition availability and accumulate muscle protein. The protein balance at time of dormancy is also maintained by lower levels of protein breakdown during the winter time. At times of immobility, muscle wasting in bears is also suppressed by a proteolytic inhibitor that is released in circulation. Another factor that contributes to the sustaining of muscle strength in hibernating bears is the occurrence of periodic voluntary contractions and involuntary contractions from shivering during torpor. The three to four daily episodes of muscle activity are responsible for the maintenance of muscle strength and responsiveness in bears during hibernation.
Methods of measuring blood loss associated with childbirth vary, complicating comparison of prevalence rates. A systematic review reported the highest rates of PPH in Africa (27.5%), and the lowest in Oceania (7.2%), with an overall rate globally of 10.8%. The rate in both Europe and North America was around 13%. The rate is higher for multiple pregnancies (32.4% compared with 10.6% for singletons), and for first-time mothers (12.9% compared with 10.0% for women in subsequent pregnancies). The overall rate of severe PPH (>1000 ml) was much lower at an overall rate of 2.8%, again with the highest rate in Africa (5.1%).
Postpartum bleeding or postpartum hemorrhage (PPH) is often defined as the loss of more than 500 ml or 1,000 ml of blood within the first 24 hours following childbirth. Some have added the requirement that there also be signs or symptoms of low blood volume for the condition to exist. Signs and symptoms may initially include: an increased heart rate, feeling faint upon standing, and an increased breath rate. As more blood is lost the women may feel cold, their blood pressure may drop, and they may become restless or unconscious. The condition can occur up to six weeks following delivery.
The most common cause is poor contraction of the uterus following childbirth. Not all of the placenta being delivered, a tear of the uterus, or poor blood clotting are other possible causes. It occurs more commonly in those who: already have a low amount of red blood, are Asian, with bigger or more than one baby, are obese or are older than 40 years of age. It also occurs more commonly following caesarean sections, those in whom medications are used to start labor, and those who have an episiotomy.
Prevention involves decreasing known risk factors including if possible procedures associated with the condition and giving the medication oxytocin to stimulate the uterus to contract shortly after the baby is born. Misoprostol may be used instead of oxytocin in resource poor settings. Treatments may include: intravenous fluids, blood transfusions, and the medication ergotamine to cause further uterine contraction. Efforts to compress the uterus using the hands may be effective if other treatments do not work. The aorta may also be compressed by pressing on the abdomen. The World Health Organization has recommended non-pneumatic anti-shock garment to help until other measures such as surgery can be carried out. In 2017 study found that tranexamic acid decreased a woman's risk of death.
In the developing world about 1.2% of deliveries are associated with PPH and when PPH occurred about 3% of women died. Globally it occurs about 8.7 million times and results in 44,000 to 86,000 deaths per year making it the leading cause of death during pregnancy. About 0.4 women per 100,000 deliveries die from PPH in the United Kingdom while about 150 women per 100,000 deliveries die in sub-Saharan Africa. Rates of death have decreased substantially since at least the late 1800s in the United Kingdom.
Muscle atrophy is defined as a decrease in the mass of the muscle; it can be a partial or complete wasting away of muscle, and is most commonly experienced when persons suffer temporary disabling circumstances such as being restricted in movement and/or confined to bed as when hospitalized. When a muscle atrophies, this leads to muscle weakness, since the ability to exert force is related to mass. Modern medicine's understanding of the quick onset of muscle atrophy is a major factor behind the practice of getting hospitalized patients out of bed and moving about as active as possible as soon as is feasible, despite sutures, wounds, broken bones and pain.
Muscle atrophy results from a co-morbidity of several common diseases, including cancer, AIDS, congestive heart failure, COPD (chronic obstructive pulmonary disease), renal failure, and severe burns; patients who have "cachexia" in these disease settings have a poor prognosis. Moreover, starvation eventually leads to muscle atrophy.
Disuse of the muscles, such as when muscle tissue is immobilized for even a few days of unuse – when the patient has a primary injury such as an immobilized broken bone (set in a cast or immobilized in traction), for example – will also lead rapidly to disuse atrophy. Minimizing such occurrences as soon as possible is a primary mission of occupational and physical therapists employed within hospitals working in co-ordination with orthopedic surgeons.
Neurogenic atrophy, which has a similar effect, is muscle atrophy resulting from damage to the nerve which stimulates the muscle, causing a shriveling around otherwise healthy limbs. Also, time in a circa zero g environment without exercise will lead to atrophy. This is partially due to the smaller amount of exertion needed to move about, and the fact that muscles are not used to maintain posture. In a similar effect, patients with a broken leg joint undergoing as little as three weeks of traction can lose enough back and buttocks muscle mass and strength as to have difficulty sitting without assistance, and experience pain, stress and burning even after a very short ten-minute exposure, when such positioning is contrived during recovery.
The cause of narcosis is related to the increased solubility of gases in body tissues, as a result of the elevated pressures at depth (Henry's law). Modern theories have suggested that inert gases dissolving in the lipid bilayer of cell membranes cause narcosis. More recently, researchers have been looking at neurotransmitter receptor protein mechanisms as a possible cause of narcosis. The breathing gas mix entering the diver's lungs will have the same pressure as the surrounding water, known as the ambient pressure. After any change of depth, the pressure of gases in the blood passing through the brain catches up with ambient pressure within a minute or two, which results in a delayed narcotic effect after descending to a new depth. Rapid compression potentiates narcosis owing to carbon dioxide retention.
A divers' cognition may be affected on dives as shallow as , but the changes are not usually noticeable. There is no reliable method to predict the depth at which narcosis becomes noticeable, or the severity of the effect on an individual diver, as it may vary from dive to dive even on the same day.
Significant impairment due to narcosis is an increasing risk below depths of about , corresponding to an ambient pressure of about . Most sport scuba training organizations recommend depths of no more than because of the risk of narcosis. When breathing air at depths of – an ambient pressure of about – narcosis in most divers leads to hallucinations, loss of memory, and unconsciousness. A number of divers have died in attempts to set air depth records below . Because of these incidents, "Guinness World Records" no longer reports on this figure.
Narcosis has been compared with altitude sickness regarding its variability of onset (though not its symptoms); its effects depend on many factors, with variations between individuals. Thermal cold, stress, heavy work, fatigue, and carbon dioxide retention all increase the risk and severity of narcosis. Carbon dioxide has a high narcotic potential and also causes increased blood flow to the brain, increasing the effects of other gases. Increased risk of narcosis results from increasing the amount of carbon dioxide retained through heavy exercise, shallow or skip breathing, or because of poor gas exchange in the lungs.
Narcosis is known to be additive to even minimal alcohol intoxication, and also to the effects of other drugs such as cannabis (which is more likely than alcohol to have effects that last into a day of abstinence from use). Other sedative and analgesic drugs, such as opiate narcotics and benzodiazepines, add to narcosis.
Delirium tremens is mainly caused by a long period of drinking being stopped abruptly. Withdrawal leads to a biochemical regulation cascade. It may also be triggered by head injury, infection, or illness in people with a history of heavy use of alcohol.
Another cause of delirium tremens is abrupt stopping of tranquilizer drugs of the barbiturate or benzodiazepine classes in a person with a relatively strong addiction to them. Because these tranquilizers' primary pharmacological and physiological effects stem from their manipulation of the GABA chemical and transmitter somatic system, the same neurotransmitter system affected by alcohol, delirium tremens can occur upon abrupt decrease of dosage in those who are heavily dependent. These DTs are much the same as those caused by alcohol and so is the attendant withdrawal syndrome of which they are a manifestation. That is the primary reason benzodiazepines are such an effective treatment for DTs, despite also being the cause of them in many cases. Because ethanol and tranquilizers such as barbiturates and benzodiazepines function as positive allosteric modulators at GABA receptors, the brain, in its desire to equalize an unbalanced chemical system, triggers the abrupt stopping of the production of endogenous GABA. This decrease becomes more and more marked as the addiction becomes stronger and as higher doses are needed to cause intoxication. In addition to having sedative properties, GABA is an immensely important regulatory neurotransmitter that controls the heart rate, blood pressure, and seizure threshold among myriad other important autonomic nervous subsystems.
Delirium tremens is most common in people who have a history of alcohol withdrawal, especially in those who drink the equivalent of of beer or of distilled beverage daily. Delirium tremens also commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years.
Delirium tremens (DTs) is a rapid onset of confusion usually caused by withdrawal from alcohol. When it occurs, it is often three days into the withdrawal symptoms and lasts for two to three days. Physical effects may include shaking, shivering, irregular heart rate, and sweating. People may also see or hear things other people do not. Occasionally, a very high body temperature or seizures may result in death. Alcohol is one of the most dangerous drugs from which to withdraw.
Delirium tremens typically only occurs in people with a high intake of alcohol for more than a month. A similar syndrome may occur with benzodiazepine and barbiturate withdrawal. Withdrawal from stimulants such as cocaine does not have major medical complications. In a person with delirium tremens it is important to rule out other associated problems such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.
Prevention is by treating withdrawal symptoms. If delirium tremens occurs, aggressive treatment improves outcomes. Treatment in a quiet intensive care unit with sufficient light is often recommended. Benzodiazepines are the medication of choice with diazepam, lorazepam, chlordiazepoxide, and oxazepam all commonly used. They should be given until a person is lightly sleeping. The antipsychotic haloperidol may also be used. The vitamin thiamine is recommended. Mortality without treatment is between 15% and 40%. Currently death occurs in about 1% to 4% of cases.
About half of people with alcoholism will develop withdrawal symptoms upon reducing their use. Of these, three to five percent develop DTs or have seizures. The name delirium tremens was first used in 1813; however, the symptoms were well described since the 1700s. The word "delirium" is Latin for "going off the furrow," a plowing metaphor. It is also called shaking frenzy and Saunders-Sutton syndrome. Nicknames include the shakes, barrel-fever, blue horrors, bottleache, bats, drunken horrors, elephants, gallon distemper, quart mania, and pink spiders, among others.
Hypoadrenocorticism is typically a disease of young to middle-aged female dogs, although Standard Poodles and Bearded Collies of both sexes are prone to the condition.
Hypoadrenocorticism is an inherited disease in the following breeds (and therefore a higher proportion of dogs within these breeds are affected, compared to other breeds):
- Bearded Collie
- Nova Scotia Duck Tolling Retriever
- Portuguese Water Dog
- Standard Poodle
Some breeds are at increased risk of hypoadrenocorticism:
- Airedale Terrier
- Basset Hound
- Bearded Collie
- Great Dane
- Rottweiler
- Springer Spaniels: English Springer Spaniel and Welsh Springer Spaniel
- Saint Bernard
- Soft-Coated Wheaten Terrier
- West Highland white terrier
Some breeds have a reduced risk of hypoadrenocorticism:
- Boxer
- Cocker Spaniel
- Golden Retriever
- Pit Bull Terrier
- Lhasa Apso
- Yorkshire Terrier
Aggressiveness of therapy depends on the clinical status of the patient and the nature of the insufficiency (glucocorticoid, mineralocorticoid, or both). Many dogs and cats with primary adrenal insufficiency are presented in Addisonian crisis and require immediate, aggressive therapy. In contrast, secondary insufficiency often has a chronic course.
Hypoadrenocorticism is treated with fludrocortisone (trade name Florinef) or a monthly injection of Percorten-V (desoxycorticosterone pivalate, DOCP) and prednisolone or Zycortal. Routine blood work is necessary in the initial stages until a maintenance dose is established. Most of the medications used in the therapy of hypoadrenocorticism cause excessive thirst and urination. It is absolutely vital to provide fresh drinking water for a canine suffering from this disorder.
If the owner knows about an upcoming stressful situation (shows, traveling etc.), the animals generally need an increased dose of prednisone to help deal with the added stress. Avoidance of stress is important for dogs with hypoadrenocorticism. Physical illness also stresses the body and may mean that the medication(s) need to be adjusted during this time. Most dogs with hypoadrenocorticism have an excellent prognosis after proper stabilization and treatment.
Locoregional complications include pancreatic pseudocyst (Most common, occurring in up to 25% of all cases) and phlegmon / abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis, pancreatic ascites, pleural effusion, sterile/infected pancreatic necrosis.
In the United States, the annual incidence is 18 cases of acute pancreatitis per 100,000 population, and it accounts for 220,000 hospitalizations in the US. In a European cross-sectional study, incidence of acute pancreatitis increased from 12.4 to 15.9 per 100,000 annually from 1985 to 1995; however, mortality remained stable as a result of better outcomes. Another study showed a lower incidence of 9.8 per 100,000 but a similar worsening trend (increasing from 4.9 in 1963-74) over time.
In Western countries, the most common cause is alcohol, accounting for 65 percent of acute pancreatitis cases in the US, 20 percent of cases in Sweden, and 5 percent of those in the United Kingdom. In Eastern countries, gallstones are the most common cause of acute pancreatitis. The causes of acute pancreatitis also varies across age groups, with trauma and systemic disease (such as infection) being more common in children. Mumps is a more common cause in adolescents and young adults than in other age groups.
A breast abscess is a collection of pus that develops into the breast with different causes. During lactation, breast abscess develops only rarely, most sources cite about 0.4–0.5% of breastfeeding women. Known risk factors are age over 30, primiparous and late delivery. No correlation was found with smoking status however this may be in part because much fewer smoking women choose to breastfeed. Antibiotics were not shown effective in prevention of lactation abscess but are useful to treat a secondary infection (see the section on the treatment of breast abscess in this article).
Keratinizing squamous metaplasia of lactiferous ducts may play a similar role in the pathogenesis of nonpuerperal subareolar abscess.
Since the 1980s mastitis has often been divided into non-infectious and infectious sub-groups. However, recent research suggests that it may not be feasible to make divisions in this way. It has been shown that types and amounts of potentially pathogenic bacteria in breast milk are not correlated to the severity of symptoms. Moreover, although only 15% of women with mastitis in Kvist et al.'s study were given antibiotics, all recovered and few had recurring symptoms. Many healthy breastfeeding women wishing to donate breast milk have potentially pathogenic bacteria in their milk but have no symptoms of mastitis.
In the post-antibiotic era pattern of frequency is changing. In older studies anaerobes were found in up to 90% cases but they are much less frequent now.