<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Traffic collision and explain in detail? [/INST] A traffic collision, also called a motor vehicle collision, car accident or car crash, occurs when a vehicle collides with another vehicle, pedestrian, animal, road debris, or other stationary obstruction, such as a tree, pole or building. Traffic collisions often result in injury, disability, death, and property damage as well as financial costs to both society and the individuals involved. Road transport is the most dangerous situation people deal with on a daily basis, but casualty figures from such incidents attract less media attention than other, less frequent types of tragedy.A number of factors contribute to the risk of collisions, including vehicle design, speed of operation, road design, weather, road environment, driving skills, impairment due to alcohol or drugs, and behavior, notably aggressive driving, distracted driving, speeding and street racing.

In 2013, 54 million people worldwide sustained injuries from traffic collisions. This resulted in 1.4 million deaths in 2013, up from 1.1 million deaths in 1990. About 68,000 of these occurred with children less than five years old. Almost all high-income countries have decreasing death rates, while the majority of low-income countries have increasing death rates due to traffic collisions. Middle-income countries have the highest rate with 20 deaths per 100,000 inhabitants, accounting for 80% of all road fatalities with 52% of all vehicles. While the death rate in Africa is the highest (24.1 per 100,000 inhabitants), the lowest rate is to be found in Europe (10.3 per 100,000 inhabitants).

Terminology
Traffic collisions can be classified by general types. Types of collision include head-on, road departure, rear-end, side collisions, and rollovers.
Many different terms are commonly used to describe vehicle collisions. The World Health Organization uses the term road traffic injury, while the U.S. Census Bureau uses the term motor vehicle accidents (MVA), and Transport Canada uses the term "motor vehicle traffic collision" (MVTC). Other common terms include auto accident, car accident, car crash, car smash, car wreck, motor vehicle collision (MVC), personal injury collision (PIC), road accident, road traffic accident (RTA), road traffic collision (RTC), and road traffic incident (RTI) as well as more unofficial terms including smash-up, pile-up, and fender bender.
Some organizations have begun to avoid the term accident, instead preferring terms such as collision, crash or incident. This is because the term accident implies that there is no one to blame, whereas most traffic collisions are the result of driving under the influence, excessive speed, distractions such as mobile phones or other risky behavior.Historically, in the United States, the use of terms other than accident had been criticized for holding back safety improvements, based on the idea that a culture of blame may discourage the involved parties from fully disclosing the facts, and thus frustrate attempts to address the real root causes.

Health effects
Physical
A number of physical injuries can commonly result from the blunt force trauma caused by a collision, ranging from bruising and contusions to catastrophic physical injury (e.g., paralysis), traumatic or non-traumatic cardiac arrest and death.

Psychological
Following collisions, long-lasting psychological trauma may occur. These issues may make those who have been in a crash afraid to drive again. In some cases, psychological trauma may affect individuals lives, causing difficulty going to work, attending school, or performing family responsibilities.

Causes
Road incidents are caused by a large number of human factors such as failing to act according to weather conditions, road design, signage, speed limits, lighting conditions, pavement markings, and roadway obstacles. A 1985 study by K. Rumar, using British and American crash reports as data, suggested 57% of crashes were due solely to driver factors, 27% to combined roadway and driver factors, 6% to combined vehicle and driver factors, 3% solely to roadway factors, 3% to combined roadway, driver, and vehicle factors, 2% solely to vehicle factors, and 1% to combined roadway and vehicle factors. Reducing the severity of injury in crashes is more important than reducing incidence and ranking incidence by broad categories of causes is misleading regarding severe injury reduction. Vehicle and road modifications are generally more effective than behavioral change efforts with the exception of certain laws such as required use of seat belts, motorcycle helmets, and graduated licensing of teenagers.

Human factors
Human factors in vehicle collisions include anything related to drivers and other road users that may contribute to a collision. Examples include driver behavior, visual and auditory acuity, decision-making ability, and reaction speed.
A 1985 report based on British and American crash data found driver error, intoxication, and other human factors contribute wholly or partly to about 93% of crashes. A 2019 report from the U.S. National Highway Traffic Safety Administration found that leading contributing factors for fatal crashes included driving too fast for conditions or in excess of the speed limit, operating under the influence, failure to yield right of way, failure to keep within the proper lane, operating a vehicle in a careless manner, and distracted driving.Drivers distracted by mobile devices had nearly four times greater risk of crashing their cars than those who were not. Research from the Virginia Tech Transportation Institute has found that drivers who are texting while driving are 23 times more likely to be involved in a crash as non-texting drivers. Dialing a phone is the most dangerous distraction, increasing a drivers chance of crashing by 12 times, followed by reading or writing, which increased the risk by ten times.An RAC survey of British drivers found 78% of drivers thought they were highly skilled at driving, and most thought they were better than other drivers, a result suggesting overconfidence in their abilities. Nearly all drivers who had been in a crash did not believe themselves to be at fault. One survey of drivers reported that they thought the key elements of good driving were:
controlling a car including a good awareness of the cars size and capabilities
reading and reacting to road conditions, weather, road signs, and the environment
alertness, reading and anticipating the behavior of other drivers.Although proficiency in these skills is taught and tested as part of the driving exam, a "good" driver can still be at a high risk of crashing because:

the feeling of being confident in more and more challenging situations is experienced as evidence of driving ability, and that proven ability reinforces the feelings of confidence. Confidence feeds itself and grows unchecked until something happens – a near-miss or an accident.
An Axa survey concluded Irish drivers are very safety-conscious relative to other European drivers. However, this does not translate to significantly lower crash rates in Ireland.Accompanying changes to road designs have been wide-scale adoptions of rules of the road alongside law enforcement policies that included drink-driving laws, setting of speed limits, and speed enforcement systems such as speed cameras. Some countries driving tests have been expanded to test a new drivers behavior during emergencies, and their hazard perception.
There are demographic differences in crash rates. For example, although young people tend to have good reaction times, disproportionately more young male drivers feature in collisions, with researchers observing that many exhibit behaviors and attitudes to risk that can place them in more hazardous situations than other road users. This is reflected by actuaries when they set insurance rates for different age groups, partly based on their age, sex, and choice of vehicle. Older drivers with slower reactions might be expected to be involved in more collisions, but this has not been the case as they tend to drive less and, apparently, more cautiously. Attempts to impose traffic policies can be complicated by local circumstances and driver behavior. In 1969 Leeming warned that there is a balance to be struck when "improving" the safety of a road.Conversely, a location that does not look dangerous may have a high crash frequency. This is, in part, because if drivers perceive a location as hazardous, they take more care. Collisions may be more likely to happen when hazardous road or traffic conditions are not obvious at a glance, or where the conditions are too complicated for the limited human machine to perceive and react in the time and distance available. High incidence of crashes is not indicative of high injury risk. Crashes are common in areas of high vehicle congestion, but fatal crashes occur disproportionately on rural roads at night when traffic is relatively light.
This phenomenon has been observed in risk compensation research, where the predicted reductions in collision rates have not occurred after legislative or technical changes. One study observed that the introduction of improved brakes resulted in more aggressive driving, and another argued that compulsory seat belt laws have not been accompanied by a clearly attributed fall in overall fatalities. Most claims of risk compensation offsetting the effects of vehicle regulation and belt use laws have been discredited by research using more refined data.In the 1990s, Hans Mondermans studies of driver behavior led him to the realization that signs and regulations had an adverse effect on a drivers ability to interact safely with other road users. Monderman developed shared space principles, rooted in the principles of the woonerven of the 1970s. He concluded that the removal of highway clutter, while allowing drivers and other road users to mingle with equal priority, could help drivers recognize environmental clues. They relied on their cognitive skills alone, reducing traffic speeds radically and resulting in lower levels of road casualties and lower levels of congestion.Some crashes are intended; staged crashes, for example, involve at least one party who hopes to crash a vehicle in order to submit lucrative claims to an insurance company. In the United States during the 1990s, criminals recruited Latin American immigrants to deliberately crash cars, usually by cutting in front of another car and slamming on the brakes. It was an illegal and risky job, and they were typically paid only $100. Jose Luis Lopez Perez, a staged crash driver, died after one such maneuver, leading to an investigation that uncovered the increasing frequency of this type of crash.

Motor vehicle speed
The U.S. Department of Transportations Federal Highway Administration review research on traffic speed in 1998.  The summary says:

The evidence shows the risk of having a crash is increased both for vehicles traveling slower than the average speed, and for those traveling above the average speed.
The risk of being injured increases exponentially with speeds much faster than the median speed.
The severity / lethality of a crash depends on the vehicle speed change at impact.
There is limited evidence suggesting lower speed limits result in lower speeds on a system-wide basis.
Most crashes related to speed involve speed too fast for the conditions.
More research is needed to determine the effectiveness of traffic calming.In the U.S. in 2018, 9,378 people were killed in motor vehicle crashes involving at least one speeding driver, which accounted for 26% of all traffic-related deaths for the year.In Michigan in 2019, excessive speed was a factor in 18.8% of the fatalities that resulted from fatal motor vehicle crashes and in 15.6% of the suspected serious injuries resulting from crashes.The Road and Traffic Authority (RTA) of the Australian state of New South Wales (NSW) asserts speeding (traveling too fast for the prevailing conditions or above the posted speed limit) is a factor in about 40 percent of road deaths. The RTA also say speeding increases the risk of a crash and its severity.  On another web page, the RTA qualify their claims by referring to one specific piece of research from 1997, and writes "research has shown that the risk of a crash causing death or injury increases rapidly, even with small increases above an appropriately set speed limit."The contributory factor report in the official British road casualty statistics show for 2006, that "exceeding speed limit" was a contributory factor in 5% of all casualty crashes (14% of all fatal crashes), and "traveling too fast for conditions" was a contributory factor in 11% of all casualty crashes (18% of all fatal crashes).In France, in 2018, the speed limit was reduced from 90 km/h to 80 km/h on a large part of the local outside built-up area road network in the sole aim to reduce the number of road fatalities.

Assured clear distance ahead
A common cause of collisions is driving faster than one can stop within their field of vision. Such practice is illegal and is particularly responsible for an increase of fatalities at night – when it occurs most.

Driver impairment
Driver impairment describes factors that prevent the driver from driving at their normal level of skill. Common impairments include:

Alcohol
According to the Government of Canada, coroner reports from 2008 suggested almost 40% of fatally injured drivers consumed some quantity of alcohol before the collision.
Physical impairment
Poor eyesight and/or physical impairment, with many jurisdictions setting simple sight tests and/or requiring appropriate vehicle modifications before being allowed to drive.
Youth
Insurance statistics demonstrate a notably higher incidence of collisions and fatalities among drivers aged in their teens or early twenties, with insurance rates reflecting this data. These drivers have the highest incidence of both collisions and fatalities among all driver age groups, a fact that was observed well before the advent of mobile phones.Females in this age group exhibit somewhat lower collision and fatality rates than males but still register well above the median for drivers of all ages. Also within this group, the highest collision incidence rate occurs within the first year of licensed driving. For this reason, many US states have enacted a zero-tolerance policy wherein receiving a moving violation within the first six months to one year of obtaining a license results in automatic license suspension. South Dakota is the only state that allows fourteen year-olds to obtain drivers licenses.
Old age
Old age, with some jurisdictions requiring driver retesting for reaction speed and eyesight after a certain age.
Sleep deprivationVarious factors such as fatigue or sleep deprivation might increase the risk, or numbers of hours driving might increase the risk of an incident. 41% of drivers self report having fallen asleep at the wheel.: 41  It is estimated that 15% of fatal crashes involve drowsiness (10% of day time crashes, and 24% of night time crashes). Work factors can increase the risk of drowsy driving such as long or irregular hours or driving at night.
Drug use
Including some prescription drugs, over the counter drugs (notably antihistamines, opioids and muscarinic antagonists), and illegal drugs.
Distraction
Research suggests that the drivers attention is affected by distracting sounds such as conversations and operating a mobile phone while driving. Many jurisdictions now restrict or outlaw the use of some types of phone within the car. Recent research conducted by British scientists suggests that music can also have an effect; classical music is considered to be calming, yet too much could relax the driver to a condition of distraction. On the other hand, hard rock may encourage the driver to step on the acceleration pedal, thus creating a potentially dangerous situation on the road.Cell phone use is an increasingly significant problem on the roads and as the U.S. National Safety Council compiled more than 30 studies postulating that hands-free is not a safer option, because the brain remains distracted by the conversation and cannot focus solely on the task of driving.

Intent
Some traffic collisions are caused intentionally by a driver. For example, a collision may be caused by a driver who intends to commit vehicular suicide. Collisions may also be intentionally caused by people who hope to make an insurance claim against the other driver, or may be staged for such purposes as insurance fraud. Motor vehicles may also be involved in collisions as part of a deliberate effort to hurt other people, such as in a vehicle-ramming attack.

Combinations of factors
Several conditions can combine to create a much worse situation, for example:

Combining low doses of alcohol and cannabis has a more severe effect on driving performance than either cannabis or alcohol in isolation.
Taking recommended doses of several drugs together, which individually do not cause impairment, may combine to bring on drowsiness or other impairment. This could be more pronounced in an elderly person whose renal function is less efficient than a younger persons.Thus, there are situations when a person may be impaired, but still legally allowed to drive, and becomes a potential hazard to themselves and other road users. Pedestrians or cyclists are affected in the same way and can similarly jeopardize themselves or others when on the road.

Road design
A 1985 US study showed that about 34% of serious crashes had contributing factors related to the roadway or its environment. Most of these crashes also involved a human factor. The road or environmental factor was either noted as making a significant contribution to the circumstances of the crash, or did not allow room to recover. In these circumstances, it is frequently the driver who is blamed rather than the road; those reporting the collisions have a tendency to overlook the human factors involved, such as the subtleties of design and maintenance that a driver could fail to observe or inadequately compensate for.Research has shown that careful design and maintenance, with well-designed intersections, road surfaces, visibility and traffic control devices, can result in significant improvements in collision rates.

Individual roads also have widely differing performance in the event of an impact. In Europe, there are now EuroRAP tests that indicate how "self-explaining" and forgiving a particular road and its roadside would be in the event of a major incident.
In the UK, research has shown that investment in a safe road infrastructure program could yield a 1⁄3 reduction in road deaths, saving as much as £6 billion per year. A consortium of 13 major road safety stakeholders have formed the Campaign for Safe Road Design, which is calling on the UK Government to make safe road design a national transport priority.

Vehicle design and maintenance
Seat beltsResearch has shown that, across all collision types, it is less likely that seat belts were worn in collisions involving death or serious injury, rather than light injury; wearing a seat belt reduces the risk of death by about 45 percent.  Seat belt use is controversial, with notable critics such as Professor John Adams suggesting that their use may lead to a net increase in road casualties due to a phenomenon known as risk compensation. However, actual observation of driver behaviors before and after seat belt laws does not support the risk compensation hypothesis.
Several important driving behaviors were observed on the road before and after the belt use law was enforced in Newfoundland, and in Nova Scotia during the same period without a law. Belt use increased from 16 percent to 77 percent in Newfoundland and remained virtually unchanged in Nova Scotia. Four driver behaviors (speed, stopping at intersections when the control light was amber, turning left in front of oncoming traffic, and gaps in following distance) were measured at various sites before and after the law. Changes in these behaviors in Newfoundland were similar to those in Nova Scotia, except that drivers in Newfoundland drove slower on expressways after the law, contrary to the risk compensation theory.
MaintenanceA well-designed and well-maintained vehicle, with good brakes, tires and well-adjusted suspension will be more controllable in an emergency and thus be better equipped to avoid collisions. Some mandatory vehicle inspection schemes include tests for some aspects of roadworthiness, such as the UKs MOT test or German TÜV conformance inspection.
The design of vehicles has also evolved to improve protection after collision, both for vehicle occupants and for those outside of the vehicle. Much of this work was led by automotive industry competition and technological innovation, leading to measures such as Saabs safety cage and reinforced roof pillars of 1946, Fords 1956 Lifeguard safety package, and Saab and Volvos introduction of standard fit seatbelts in 1959. Other initiatives were accelerated as a reaction to consumer pressure, after publications such as Ralph Naders 1965 book Unsafe at Any Speed accused motor manufacturers of indifference towards safety.
In the early 1970s, British Leyland started an intensive programme of vehicle safety research, producing a number of prototype experimental safety vehicles demonstrating various innovations for occupant and pedestrian protection such as air bags, anti-lock brakes, impact-absorbing side-panels, front and rear head restraints, run-flat tires, smooth and deformable front-ends, impact-absorbing bumpers, and retractable headlamps. Design has also been influenced by government legislation, such as the Euro NCAP impact test.
Common features designed to improve safety include thicker pillars, safety glass, interiors with no sharp edges, stronger bodies, other active or passive safety features, and smooth exteriors to reduce the consequences of an impact with pedestrians.
The UK Department for Transport publish road casualty statistics for each type of collision and vehicle through its Road Casualties Great Britain report.
These statistics show a ten to one ratio of in-vehicle fatalities between types of car. In most cars, occupants have a 2–8% chance of death in a two-car collision.

Center of gravitySome crash types tend to have more serious consequences. Rollovers have become more common in recent years, perhaps due to increased popularity of taller SUVs, people carriers, and minivans, which have a higher center of gravity than standard passenger cars. Rollovers can be fatal, especially if the occupants are ejected because they were not wearing seat belts (83% of ejections during rollovers were fatal when the driver did not wear a seat belt, compared to 25% when they did).
After a new design of Mercedes Benz notoriously failed a moose test (sudden swerving to avoid an obstacle), some manufacturers enhanced suspension using stability control linked to an anti-lock braking system to reduce the likelihood of rollover. After retrofitting these systems to its models in 1999–2000, Mercedes saw its models involved in fewer crashes.Now, about 40% of new US vehicles, mainly the SUVs, vans and pickup trucks that are more susceptible to rollover, are being produced with a lower center of gravity and enhanced suspension with stability control linked to its anti-lock braking system to reduce the risk of rollover and meet US federal requirements that mandate anti-rollover technology by September 2011.
MotorcyclesMotorcyclists and pillion-riders have little protection other than their clothing and helmets.  This difference is reflected in the casualty statistics, where they are more than twice as likely to suffer severely after a collision. In 2005, there were 198,735 road crashes with 271,017 reported casualties on roads in Great Britain. This included 3,201 deaths (1.1%) and 28,954 serious injuries (10.7%) overall.
Of these casualties 178,302 (66%) were car users and 24,824 (9%) were motorcyclists, of whom 569 were killed (2.3%) and 5,939 seriously injured (24%).

Sociological factors
Studies in United States have shown that poor people have a greater risk of dying in a car crash than people who are well-off. Car deaths are also higher in poorer states.Similar studies in France or Israel have shown the same results. This may be due to working-class people having less access to secure equipment in cars, having older cars which are less protected against crash, and needing to cover more distance to go to work each day.

COVID-19 impact on traffic incidents
While the advent of the COVID lockdown meant a decrease in road traffic in the United States, the rates of incidents, speeding, and traffic fatalities rose in 2020 and 2021 (rate as measured against vehicle miles traveled). The traffic fatality rate jumped to 1.25 per 100 million vehicle miles traveled, up from 1.06 during the same period in 2019. Reasons cited for the increases are greater speeds, not wearing seatbelts, and driving while impaired.In their preliminary report covering the first six months of 2021, the US nonprofit public safety advocacy group, the National Safety Council (NSC) estimated of total motor-vehicle deaths for the first six months of 2021 were 21,450, up 16% from 2020 and up 17% from 18,384 in 2019. The estimated mileage death rate in 2021 was 1.43 deaths per 100 million vehicle miles traveled, up 3% from 1.39 in 2020 and up 24% from 1.15 in 2019.Preliminary data also show that even as traffic levels returned to normal after the onset of COVID in March–April 2020, drivers continued to drive at excessive speeds. A 2020 study conducted by INRIX, private company that analyzes traffic patters, behaviors and congestion, showed that as traffic levels returned to normal during the three-month period August to October 2020, growth in collisions (57%), outpaced the growth in miles traveled (22%) resulting in a higher than normal collision rate during this period.In France, the Ministry of Interior reported that traffic incidents, crash-related injuries, and fatalities dropped in 2020 compared with 2019. Fatalities dropped 21.4%, injuries dropped 20.9%, and incidents overall dropped 20%. In the same report, the ministry reported that the number of vehicles on the road dropped by 75%, which would indicate that the rate (incidents per vehicle-mile) in fact increased.

Other
Other possibly hazardous factors that may alter a drivers soundness on the road include:

Irritability
Following specifically distinct rules too bureaucratically, inflexibly or rigidly when unique circumstances might suggest otherwise
Sudden swerving into somebodys blind spot without first clearly making oneself visible through the wing mirror
Unfamiliarity with ones dashboard features, center console or other interior handling devices after a recent car purchase
Lack of visibility due to windshield design, dense fog or sun glare
People-watching.
Traffic safety culture, a variety of aspects of safety culture could impact on the number of crashes.

Prevention
A large body of knowledge has been amassed on how to prevent car crashes, and reduce the severity of those that do occur.

United Nations
Owing to the global and massive scale of the issue, with predictions that by 2020 road traffic deaths and injuries will exceed HIV/AIDS as a burden of death and disability, the United Nations and its subsidiary bodies have passed resolutions and held conferences on the issue. The first United Nations General Assembly resolution and debate was in 2003 The World Day of Remembrance for Road Traffic Victims was declared in 2005. In 2009 the first high level ministerial conference on road safety was held in Moscow.
The World Health Organization, a specialized agency of the United Nations Organization, in its Global Status Report on Road Safety 2009, estimates that over 90% of the worlds fatalities on the roads occur in low-income and middle-income countries, which have only 48% of the worlds registered vehicles, and predicts road traffic injuries will rise to become the fifth leading cause of death by 2030.The United Nations Sustainable Development Goal 3, target 3.6 is directed at reducing road injuries and deaths. February 2020 saw a global ministerial conference which brought the Stockholm Declaration, setting a target to reduce global traffic deaths and injuries by 50% within ten years. The decade of 2021-2030 was declared the second decade of road safety.

Collision migration
Collisions migration refers to a situation where action to reduce road traffic collisions in one place may result in those collisions resurfacing elsewhere. For example, an accident blackspot may occur at a dangerous bend. The treatment for this may be to increase signage, post an advisory speed limit, apply a high-friction road surface, add crash barriers or any one of a number of other visible interventions. The immediate result may be to reduce collisions at the bend, but the subconscious relaxation on leaving the "dangerous" bend may cause drivers to act with fractionally less care on the rest of the road, resulting in an increase in collisions elsewhere on the road, and no overall improvement over the area. In the same way, increasing familiarity with the treated area will often result in a reduction over time to the previous level of care and may result in faster speeds around the bend due to perceived increased safety (risk compensation).

Epidemiology
In 2004 50 million more were injured in motor vehicle collisions. In 2013, between 1.25 million and 1.4 million people were killed in traffic collisions, up from 1.1 million deaths in 1990. That number represents about 2.5% of all deaths. Approximately 50 million additional people were injured in traffic collisions, a number unchanged from 2004.India recorded 105,000 traffic deaths in a year, followed by China with over 96,000 deaths. This makes motor vehicle collisions the leading cause of injury and death among children worldwide 10–19 years old (260,000 children die a year, 10 million are injured) and the sixth leading preventable cause of death in the United States. In 2019, there were 36,096 people killed and 2.74 million people injured in motor vehicle traffic crashes on roadways in the United States. In the state of Texas alone, there were a total of 415,892 traffic collisions, including 3,005 fatal crashes in 2012. In Canada, they are the cause of 48% of severe injuries.

Crash rates
The safety performance of roadways is almost always reported as a rate. That is, some measure of harm (deaths, injuries, or number of crashes) divided by some measure of exposure to the risk of this harm. Rates are used so the safety performance of different locations can be compared, and to prioritize safety improvements.
Common rates related to road traffic fatalities include the number of deaths per capita, per registered vehicle, per licensed driver, or per vehicle mile or kilometer traveled. Simple counts are almost never used. The annual count of fatalities is a rate, namely, the number of fatalities per year.
There is no one rate that is superior to others in any general sense. The rate to be selected depends on the question being asked – and often also on what data are available. What is important is to specify exactly what rate is measured and how it relates to the problem being addressed. Some agencies concentrate on crashes per total vehicle distance traveled. Others combine rates. The U.S. state of Iowa, for example, selects high collision locations based on a combination of crashes per million miles traveled, crashes per mile per year, and value loss (crash severity).

Fatality
The definition of a road-traffic fatality varies from country to country. In the United States, the definition used in the Fatality Analysis Reporting System (FARS) run by the National Highway Traffic Safety Administration (NHTSA) is a person who dies within 30 days of a crash on a US public road involving a vehicle with an engine, the death being the result of the crash. In the U.S., therefore, if a driver has a non-fatal heart attack that leads to a road-traffic crash that causes death, that is a road-traffic fatality. However, if the heart attack causes death prior to the crash, then that is not a road-traffic fatality.
The definition of a road-traffic fatality can change with time in the same country. For example, fatality was defined in France as a person who dies in the six days (pre 2005) after the collision and was subsequently changed to the 30 days (post 2005) after the collision.

History
The worlds first recorded road traffic death involving a motor vehicle occurred on 31 August 1869. Irish scientist Mary Ward died when she fell out of her cousins steam car and was run over by it.The British road engineer J. J. Leeming, compared the statistics for fatality rates in Great Britain, for transport-related incidents both before and after the introduction of the motor vehicle, for journeys, including those once by water that now are undertaken by motor vehicle: For the period 1863–1870 there were: 470 fatalities per million of population (76 on railways, 143 on roads, 251 on water); for the period 1891–1900 the corresponding figures were: 348 (63, 107, 178); for the period 1931–1938: 403 (22, 311, 70) and for the year 1963: 325 (10, 278, 37). Leeming concluded that the data showed that "travel accidents may even have been more frequent a century ago than they are now, at least for men".

He also compared the circumstances around road deaths as reported in various American states before the widespread introduction of 55 mph (89 km/h) speed limits and drunk-driving laws.

They took into account thirty factors which it was thought might affect the death rate. Among these were included the annual consumption of wine, of spirits and of malt beverages—taken individually—the amount spent on road maintenance, the minimum temperature, certain of the legal measures such as the amount spent on police, the number of police per 100,000 inhabitants, the follow-up programme on dangerous drivers, the quality of driver testing, and so on. The thirty factors were finally reduced to six by eliminating those found to have small or negligible effect. The final six were:

(a) The percentage of the total state highway mileage that is rural
(b) The percent increase in motor vehicle registration
(c) The extent of motor vehicle inspection
(d) The percentage of state-administered highway that is surfaced
(e) The average yearly minimum temperature
(f) The income per capitaThese are placed in descending order of importance. These six accounted for 70% of the variations in the rate.

The rate of traffic deaths in the United States doubled from 1915 to 1921 when it reached 12 deaths per 100,000 Americans. A century later, in 2021, the annual death rate was 12.9 per 100,000. Safety focus on protecting the occupants of automobiles has victimized bicyclists and pedestrians.  From 2010 to 2019, fatalities rose 36% for bicyclists and nearly doubled for those on foot. Reasons include larger vehicles, faster driving, and digital distractions making walking and biking in the United States far more dangerous than in other comparable nations.Early 20th century "judges defended pedestrians rights in city streets. The convenience of drivers was no grounds for infringing these rights. Any motorist driving too fast to avoid injuring or killing a pedestrian was regarded as speeding.... (More recently) there has been a tacit agreement in the United States to treat the right to walk as dispensable, (tending) to attribute such deaths to individual failures for which individuals alone — reckless drivers or careless pedestrians — are responsible."The worlds first autonomous car incident resulting in the death of a pedestrian occurred on 18 March 2018 in Arizona. The pedestrian was walking her bicycle outside of the crosswalk, and died in the hospital after she was struck by a self-driving car being tested by Uber.

Society and culture
Economic costs
The global economic cost of MVCs was estimated at $518 billion per year in 2003, and $100 billion in developing countries. The Center for Disease Control and Prevention estimated the U.S. cost in 2000 at $230 billion. A 2010 US report estimated costs of $277 billion, which included lost productivity, medical costs, legal and court costs, emergency service costs (EMS), insurance administration costs, congestion costs, property damage, and workplace losses. "The value of societal harm from motor vehicle crashes, which includes both economic impacts and valuation for lost quality-of-life, was $870.8 billion in 2010. Sixty-eight percent of this value represents lost quality-of-life, while 32 percent are economic impacts."Traffic collision affect the national economy as the cost of road injuries are estimated to account for 1.0% to 2.0% of the gross national product (GNP) of every country each year. A recent study from Nepal showed that the total economic costs of road injuries were approximately $122.88 million, equivalent to 1.52% of the total Nepal GNP for 2017, indicating the growing national financial burden associate with preventable road injuries and deaths.The economic cost to the individuals involved in an MVC varies widely depending on geographic distribution, and varies largely on depth of accident insurance cover, and legislative policy. In the UK for example, a survey conducted using 500 post-accident insurance policy customers, showed an average individual financial loss of £1300.00. This is due in part to voluntary excesses that are common tactics used to reduce overall premium, and in part due to under valuation of vehicles. By contrast, Australian insurance policy holders are subject to an average financial loss of $950.00 AUD

Legal consequences
There are a number of possible legal consequences for causing a traffic collision, including:

Traffic citations: drivers who are involved in a collision may receive one or more traffic citations for improper driving conduct such as speeding, failure to obey a traffic control device, or driving under the influence of drugs or alcohol. Convictions for traffic violations are usually penalized with fines, and for more severe offenses, the suspension or revocation of driving privileges.
Civil lawsuits: a driver who causes a traffic collision may be sued for damages resulting from the accident, including damages to property and injuries to other persons.
Criminal prosecution: More severe driving misconduct, including impaired driving, may result in criminal charges against the driver. In the event of a fatality, a charge of vehicular homicide is occasionally prosecuted, especially in cases involving alcohol. Convictions for alcohol offenses may result in the revocation or long term suspension of the drivers license, and sometimes jail time, mandatory drug or alcohol rehabilitation, or both.

Fraud
Sometimes, people may make false insurance claims or commit insurance fraud by staging collisions or jumping in front of moving cars.

United Kingdom
In the United Kingdom, the Pre-Action Protocol for Low Value Personal Injury Claims in Road Traffic Accidents from 31 July 2013, otherwise known as the RTA Protocol,describes the behaviour the court expects of the parties prior to the start of proceedings where a claimant claims damages valued at no more than the Protocol upper limit as a result of a personal injury sustained by that person in a road traffic accident. As of February 2022 the "upper limit" is £25,000 for an accident which occurred on or after 31 July 2013; the limit under a previous version of the protocol was £10,000 for an accident which had occurred on or after 30 April 2010 but before 31 July 2013.

United States
Motor vehicle crashes are the leading cause of death in the workplace in the United States accounting for 35 percent of all workplace fatalities. In the United States, individuals involved in motor vehicle collisions may be held financially liable for the consequences of a collision, including property damage, and injuries to passengers and drivers. Where another drivers vehicle is damaged as the result of a crash, some states allow the owner of the vehicle to recover both the cost of repair for the diminished value of the vehicle from the at-fault driver. Because the financial liability that results from causing a crash is so high, most U.S. states require drivers to carry liability insurance to cover these potential costs. In the event of serious injuries or fatalities, it is possible for injured persons to seek compensation in excess of the at-fault drivers insurance coverage.In some cases, involving a defect in the design or manufacture of motor vehicles, such as where defective design results in SUV rollovers or sudden unintended acceleration, accidents caused by defective tires, or where injuries are caused or worsened as a result of defective airbags, it is possible that the manufacturer will face a class action lawsuit.

Art
Cars have come to represent a part of the American Dream of ownership coupled with the freedom of the road </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Rotaviral gastroenteritis and explain in detail? [/INST] Rotavirus gastroenteritis is a major cause of severe diarrhoea among infants and young children globally. It is caused by rotavirus, a genus of double-stranded RNA virus in the family Reoviridae. The diarrhea tends to be watery and is frequently accompanied by fever, vomiting and abdominal pain. By the age of five, nearly every child in the world has been infected with rotavirus at least once. However, with each infection, immunity develops, and subsequent infections are less severe; adults are rarely affected.  There are five species of this virus, referred to as A, B, C, D, and E. Rotavirus A, the most common, causes more than 90% of infections in humans.The virus is transmitted by the faecal-oral route. It infects and damages the cells that line the small intestine and causes gastroenteritis (which is often called "stomach flu" despite having no relation to influenza). Although rotavirus was discovered in 1973 and accounts for up to 50% of hospitalisations for severe diarrhoea in infants and children, its importance is still not widely known within the public health community, particularly in developing countries. In addition to its impact on human health, rotavirus also infects animals, and is a pathogen of livestock.Rotavirus is usually an easily managed disease of childhood, but worldwide nearly 500,000 children under five years of age still die from rotavirus infection each year and almost two million more become severely ill. In the United States, before initiation of  the rotavirus vaccination programme, rotavirus caused about 2.7 million cases of severe gastroenteritis in children, almost 60,000 hospitalisations, and around 37 deaths each year. Public health campaigns to combat rotavirus focus on providing oral rehydration therapy for infected children and vaccination to prevent the disease. The incidence and severity of rotavirus infections has declined significantly in countries that have added rotavirus vaccine to their routine childhood immunisation policies.

Signs and symptoms
Rotavirus gastroenteritis is a mild to severe disease characterised by vomiting, watery diarrhoea, and low-grade fever. Once a child is infected by the virus, there is an incubation period of about two days before symptoms appear. Symptoms often start with vomiting followed by profuse diarrhoea after at least four days. Dehydration is more common in rotavirus infection than in most of those caused by bacterial pathogens, and is the most common cause of death related to rotavirus infection.Rotavirus A infections can occur throughout life: the first usually produces symptoms, but subsequent infections are typically mild or asymptomatic, as the immune system provides some protection.: 106–124  Consequently, symptomatic infection rates are highest in children under two years of age and decrease progressively towards 45 years of age. Infection in newborn children, although common, is often associated with mild or asymptomatic disease; the most severe symptoms tend to occur in children six months to two years of age, the elderly, and those with  compromised or absent immune system functions. Due to immunity acquired in childhood, most adults are not susceptible to rotavirus; gastroenteritis in adults usually has a cause other than rotavirus, but asymptomatic infections in adults may maintain the transmission of infection in the community.

Virology
Transmission
Rotavirus is transmitted by the faecal-oral route, via contact with contaminated hands, surfaces and objects, and possibly by the respiratory route. The faeces of an infected person can contain more than 10 trillion infectious particles per gram;  fewer than 100 of these are required to transmit infection to another person.Rotaviruses are stable in the environment and have been found in estuary samples at levels as high as 1–5 infectious particles per US gallon. Sanitary measures adequate for eliminating bacteria and parasites seem to be ineffective in control of rotavirus, as the incidence of rotavirus infection in countries with high and low health standards is similar.

Types
There are five species of rotavirus, referred to as A, B, C, D and E. Humans are mostly infected by species A. All five species cause disease in other animals.
Within rotavirus A there are different strains, called serotypes. As with influenza virus, a dual classification system is used based on two  proteins on the surface of the virus. The glycoprotein VP7 defines the  G serotypes and the protease-sensitive protein VP4 defines P serotypes. Because the two genes that determine G-types and P-types can be passed on separately to progeny viruses, different combinations are found.

Replication
Rotaviruses replicate mainly in the gut, and infect enterocytes of the villi of the small intestine, leading to structural and functional changes of the epithelium. The triple protein coats make them resistant to the acidic pH of the stomach and the digestive enzymes in the gut.The virus enter cells by receptor mediated endocytosis and form a vesicle known as an endosome. Proteins in the third layer (VP7 and the VP4 spike) disrupt the membrane of the endosome, creating a difference in the calcium concentration. This causes the breakdown of VP7 trimers into single protein subunits, leaving the VP2 and VP6 protein coats around the viral dsRNA, forming a double-layered particle (DLP).The eleven dsRNA strands remain within the protection of the two protein shells and the viral RNA-dependent RNA polymerasecreates mRNA transcripts of the double-stranded viral genome. By remaining in the core, the viral RNA evades innate host immune responses called RNA interference that are triggered by the presence of double-stranded RNA.During the infection, rotavirus produces mRNA for both protein biosynthesis and gene replication. Most of the rotavirus proteins accumulate in viroplasm, where the RNA is replicated and the DLPs are assembled. Viroplasm is formed around the cell nucleus as early as two hours after virus infection, and consists of viral factories thought to be made by two viral nonstructural proteins: NSP5 and NSP2. Inhibition of NSP5 by RNA interference results in a sharp decrease in rotavirus replication. The DLPs migrate to the endoplasmic reticulum where they obtain their third, outer layer (formed by VP7 and VP4). The progeny viruses are released from the cell by lysis.

Pathophysiology
The diarrhoea is caused by multiple activities of the virus. Malabsorption occurs because of the destruction of gut cells called enterocytes. The toxic rotavirus protein NSP4 induces age- and calcium ion-dependent chloride secretion, disrupts SGLT1 transporter-mediated reabsorption of water, apparently reduces activity of brush-border membrane disaccharidases, and possibly activates the calcium ion-dependent secretory reflexes of the enteric nervous system. Healthy enterocytes secrete lactase into the small intestine; milk intolerance due to lactase deficiency is a symptom of rotavirus infection, which can persist for weeks. A recurrence of mild diarrhoea often follows the reintroduction of milk into the childs diet, due to bacterial fermentation of the disaccharide lactose in the gut.

Diagnosis
Diagnosis of infection with rotavirus normally follows diagnosis of gastroenteritis as the cause of severe diarrhoea. Most children admitted to hospital with gastroenteritis are tested for rotavirus A.
Specific diagnosis of infection with rotavirus A is made by finding the virus in the childs stool by enzyme immunoassay. There are several licensed test kits on the market which are sensitive, specific and detect all serotypes of rotavirus A. Other methods, such as electron microscopy and PCR, are used in research laboratories. Reverse transcription-polymerase chain reaction (RT-PCR) can detect and identify all species and serotypes of human rotavirus.

Prevention
Because improved sanitation does not decrease the prevalence of rotaviral disease, and the rate of hospitalisations remains high, despite the use of oral rehydrating medicines, the primary public health intervention is vaccination. Two rotavirus vaccines against Rotavirus A infection are safe and effective in children: Rotarix by GlaxoSmithKline and RotaTeq by Merck. Both are taken orally and contain attenuated live virus.Rotavirus vaccines are licensed in more than 100 countries, but only 17 countries have introduced routine rotavirus vaccination. Following the introduction of routine rotavirus vaccination in the US in 2006, the health burden of rotavirus gastroenteritis "rapidly and dramatically reduced" despite lower coverage levels compared to other routine infant immunizations. Clinical trials of the Rotarix  rotavirus vaccine in South Africa and Malawi, found that the vaccine significantly reduced severe diarrhoea episodes caused by rotavirus, and that the infection was preventable by vaccination.  A 2019 Cochrane systematic review of 55 clinical trials that included 216,480 participants concluded RV1 (Rotarix), RV5 (RotaTeq), and Rotavac  and  are effective vaccines. Additional rotavirus vaccines are under development. The World Health Organization(WHO) recommends that rotavirus vaccine be included in all national immunisation programmes. The incidence and severity of rotavirus infections has declined significantly in countries that have acted on this recommendation.The Rotavirus Vaccine Program is a collaboration between PATH, the  (WHO), and the U.S. Centers for Disease Control and Prevention, and is funded by the GAVI Alliance. The Program aims to reduce child morbidity and mortality from diarrhoeal disease by making a vaccine against rotavirus available for use in developing countries.

Treatment
Treatment of acute rotavirus infection is nonspecific and involves management of symptoms and, most importantly, maintenance of hydration. If untreated, children can die from the resulting severe dehydration.  Depending on the severity of diarrhea, treatment consists of oral rehydration, during which the child is given extra water to drink that contains small amounts of salt and sugar.  Some infections are serious enough to warrant hospitalisation where fluids are given by intravenous drip or nasogastric tube, and the childs electrolytes and blood sugar are monitored. Antibiotics are not recommended.

Prognosis
Rotavirus infections rarely cause other complications and for a well managed child the prognosis is excellent.

Epidemiology
Rotavirus A, which accounts for more than 90% of rotavirus gastroenteritis in humans, is endemic worldwide. Each year rotavirus causes millions of cases of diarrhoea in developing countries, almost 2 million resulting in hospitalisation and an estimated 453,000 resulting in the death of a child younger than five. This is about 40 per cent of all hospital admissions related to diarrhea in children under five worldwide.In the United States alone—before initiation of the rotavirus vaccination programme—over 2.7 million cases of rotavirus gastroenteritis occurred annually, 60,000 children were hospitalised and around 37 died from the results of the infection. The major role of rotavirus in causing diarrhoea is not widely recognised within the public health community, particularly in developing countries. Almost every child has been infected with rotavirus by age five. It is the leading single cause of severe diarrhoea among infants and children, being responsible for about 20% of cases, and accounts for 50% of the cases requiring hospitalisation. Rotavirus causes 37% of deaths attributable to diarrhoea and 5% of all deaths in children younger than five. Boys are twice as likely as girls to be admitted to hospital.
Rotavirus infections occur primarily during cool, dry seasons. The number attributable to food contamination is unknown.Outbreaks of rotavirus A diarrhoea are common among hospitalised infants, young children attending day care centres, and elderly people in nursing homes. An outbreak caused by contaminated municipal water occurred in Colorado in 1981.
During 2005, the largest recorded epidemic of diarrhoea occurred in Nicaragua. This unusually large and severe outbreak was associated with mutations in the rotavirus A genome, possibly helping the virus escape the prevalent immunity in the population. A similar large outbreak occurred in Brazil in 1977.Rotavirus B, also called adult diarrhoea rotavirus or ADRV, has caused major epidemics of severe diarrhoea affecting thousands of people of all ages in China. These epidemics occurred as a result of sewage contamination of drinking water. Rotavirus B infections also occurred in India in 1998; the causative strain was named CAL. Unlike ADRV, the CAL strain is endemic. To date, epidemics caused by rotavirus B have been confined to mainland China, and surveys indicate a lack of immunity to this species in the United States.

History
In 1943, Jacob Light and Horace Hodes proved that a filterable agent in the faeces of children with infectious diarrhoea also caused scours (livestock diarrhoea) in cattle. Three decades later, preserved samples of the agent were shown to be rotavirus. In the intervening years, a virus in mice was shown to be related to the virus causing scours. In 1973, Ruth Bishop and colleagues described related viruses found in children with gastroenteritis.In 1974, Thomas Henry Flewett suggested the name rotavirus after observing that, when viewed through an electron microscope, a rotavirus particle looks like a wheel (rota in Latin); the name was officially recognised by the International Committee on Taxonomy of Viruses four years later. In 1976, related viruses were described in several other species of animals. These viruses, all causing acute gastroenteritis, were recognised as a collective pathogen affecting humans and animals worldwide. Rotavirus serotypes were first described in 1980, and in the following year, rotavirus from humans was first grown in cell cultures derived from monkey kidneys, by adding trypsin (an enzyme found in the duodenum of mammals and now known to be essential for rotavirus to replicate) to the culture medium. The ability to grow rotavirus in culture accelerated the pace of research, and by the mid-1980s the first candidate vaccines were being evaluated.In 1998, a rotavirus vaccine was licensed for use in the United States. Clinical trials in the United States, Finland, and Venezuela had found it to be 80 to 100% effective at preventing severe diarrhoea caused by rotavirus A, and researchers had detected no statistically significant serious adverse effects. The manufacturer, however, withdrew it from the market in 1999, after it was discovered that the vaccine may have contributed to an increased risk for intussusception, a type of bowel obstruction, in one of every 12,000 vaccinated infants </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Gout and explain in detail? [/INST] Gout ( GOWT) is a form of inflammatory arthritis characterized by recurrent attacks of a red, tender, hot and swollen joint, caused by deposition of monosodium urate monohydrate crystals. Pain typically comes on rapidly, reaching maximal intensity in less than 12 hours. The joint at the base of the big toe is affected in about half of cases. It may also result in tophi, kidney stones, or kidney damage.Gout is due to persistently elevated levels of uric acid in the blood. This occurs from a combination of diet, other health problems, and genetic factors. At high levels, uric acid crystallizes and the crystals deposit in joints, tendons, and surrounding tissues, resulting in an attack of gout. Gout occurs more commonly in those who regularly drink beer or sugar-sweetened beverages or who eat foods that are high in purines such as liver, shellfish, or anchovies, or are overweight. Diagnosis of gout may be confirmed by the presence of crystals in the joint fluid or in a deposit outside the joint. Blood uric acid levels may be normal during an attack.Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, or colchicine improves symptoms. Once the acute attack subsides, levels of uric acid can be lowered via lifestyle changes and in those with frequent attacks, allopurinol or probenecid provides long-term prevention. Taking vitamin C and eating a diet high in low-fat dairy products may be preventive.Gout affects about 1 to 2% of adults in the developed world at some point in their lives. It has become more common in recent decades. This is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy, and changes in diet. Older males are most commonly affected. Gout was historically known as "the disease of kings" or "rich mans disease". It has been recognized at least since the time of the ancient Egyptians.

Signs and symptoms
Gout can present in several ways, although the most common is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint). The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases. Other joints, such as the heels, knees, wrists, and fingers, may also be affected. Joint pain usually begins during the night and peaks within 24 hours of onset. This is mainly due to lower body temperature. Other symptoms may rarely occur along with the joint pain, including fatigue and a high fever.Long-standing elevated uric acid levels (hyperuricemia) may result in other symptoms, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion. Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.

Cause
The crystallization of uric acid, often related to relatively high levels in the blood, is the underlying cause of gout. This can occur because of diet, genetic predisposition, or underexcretion of urate, the salts of uric acid. Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. About 10% of people with hyperuricemia develop gout at some point in their lifetimes. The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/L (7 and 8.9 mg/dl), the risk is 0.5% per year, while in those with a level greater than 535 μmol/L (9 mg/dL), the risk is 4.5% per year.

Lifestyle
Dietary causes account for about 12% of gout,  and include a strong association with the consumption of alcohol, sugar-sweetened beverages, meat, and seafood. Among foods richest in purines yielding high amounts of uric acid are dried anchovies, shrimp, organ meat, dried mushrooms, seaweed, and beer yeast. Chicken and potatoes also appear related. Other triggers include physical trauma and surgery.Studies in the early 2000s found that other dietary factors are not relevant. Specifically, a diet with moderate purine-rich vegetables (e.g., beans, peas, lentils, and spinach) is not associated with gout. Neither is total dietary protein. Alcohol consumption is strongly associated with increased risk, with wine presenting somewhat less of a risk than beer or spirits. Eating skim milk powder enriched with glycomacropeptide (GMP) and G600 milk fat extract may reduce pain but may result in diarrhea and nausea.Physical fitness, healthy weight, low-fat dairy products, and to a lesser extent, coffee and taking vitamin C, appear to decrease the risk of gout; however, taking vitamin C supplements does not appear to have a significant effect in people who already have established gout. Peanuts, brown bread, and fruit also appear protective. This is believed to be partly due to their effect in reducing insulin resistance.Other than dietary and lifestyle choices, the recurrence of gout attacks is also linked to the weather. High ambient temperature and low relative humidity may increase the risk of a gout attack.

Genetics
Gout is partly genetic, contributing to about 60% of variability in uric acid level. The SLC2A9, SLC22A12, and ABCG2 genes have been found to be commonly associated with gout and variations in them can approximately double the risk. Loss-of-function mutations in SLC2A9 and SLC22A12 causes low blood uric acid levels by reducing urate absorption and unopposed urate secretion. The rare genetic disorders familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase superactivity and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch–Nyhan syndrome, are complicated by gout.

Medical conditions
Gout frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance, and abnormal lipid levels, occurs in nearly 75% of cases. Other conditions commonly complicated by gout include lead poisoning, kidney failure, hemolytic anemia, psoriasis, solid organ transplants, and myeloproliferative disorders such as polycythemia. A body mass index greater than or equal to 35 increases male risk of gout threefold. Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.

Medication
Diuretics have been associated with attacks of gout, but a low dose of hydrochlorothiazide does not seem to increase risk. Other medications that increase the risk include niacin, aspirin (acetylsalicylic acid), ACE inhibitors, angiotensin receptor blockers, beta blockers, ritonavir, and pyrazinamide. The immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout, the former more so when used in combination with hydrochlorothiazide. Hyperuricemia may be induced by excessive use of Vitamin D supplements. Levels of serum uric acid have been positively associated with 25(OH) D. The incidence of hyperuricemia increased 9.4% for every 10 nmol/L increase in 25(OH) D (P < 0.001).

Pathophysiology
Gout is a disorder of purine metabolism, and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating and forming deposits (tophi) in joints, on tendons, and in the surrounding tissues. Microscopic tophi may be walled off by a ring of proteins, which blocks interaction of the crystals with cells and therefore avoids inflammation. Naked crystals may break out of walled-off tophi due to minor physical damage to the joint, medical or surgical stress, or rapid changes in uric acid levels. When they break through the tophi, they trigger a local immune-mediated inflammatory reaction in macrophages, which is initiated by the NLRP3 inflammasome protein complex. Activation of the NLRP3 inflammasome recruits the enzyme caspase 1, which converts pro-interleukin 1β into active interleukin 1β, one of the key proteins in the inflammatory cascade. An evolutionary loss of urate oxidase (uricase), which breaks down uric acid, in humans and higher primates has made this condition common.The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase. Other triggers believed to be important in acute episodes of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis, articular hydration and extracellular matrix proteins. The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected. Rapid changes in uric acid may occur due to factors including trauma, surgery, chemotherapy and diuretics. The starting or increasing of urate-lowering medications can lead to an acute attack of gout with febuxostat of a particularly high risk. Calcium channel blockers and losartan are associated with a lower risk of gout compared to other medications for hypertension.

Diagnosis
Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic acute arthritis of the base of the great toe (known as podagra). Synovial fluid analysis should be done if the diagnosis is in doubt. Plain X-rays are usually normal and are not useful for confirming a diagnosis of early gout. They may show signs of chronic gout such as bone erosion.

Synovial fluid
A definitive diagnosis of gout is based upon the identification of monosodium urate crystals in synovial fluid or a tophus. All synovial fluid samples obtained from undiagnosed inflamed joints by arthrocentesis should be examined for these crystals. Under polarized light microscopy, they have a needle-like morphology and strong negative birefringence. This test is difficult to perform and requires a trained observer. The fluid must be examined relatively soon after aspiration, as temperature and pH affect solubility.

Blood tests
Hyperuricemia is a classic feature of gout, but nearly half of the time gout occurs without hyperuricemia and most people with raised uric acid levels never develop gout. Thus, the diagnostic utility of measuring uric acid levels is limited. Hyperuricemia is defined as a plasma urate level greater than 420 μmol/L (7.0 mg/dl) in males and 360 μmol/L (6.0 mg/dl) in females. Other blood tests commonly performed are white blood cell count, electrolytes, kidney function and erythrocyte sedimentation rate (ESR). However, both the white blood cells and ESR may be elevated due to gout in the absence of infection. A white blood cell count as high as 40.0×109/l (40,000/mm3) has been documented.

Differential diagnosis
The most important differential diagnosis in gout is septic arthritis. This should be considered in those with signs of infection or those who do not improve with treatment. To help with diagnosis, a synovial fluid Gram stain and culture may be performed. Other conditions that can look similar include CPPD (pseudogout), rheumatoid arthritis, psoriatic arthritis, palindromic rheumatism, and reactive arthritis. Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma or other neoplasms.

Prevention
Risk of gout attacks can be lowered by complete abstinence from drinking alcoholic beverages, reducing the intake of fructose (e.g. high fructose corn syrup) and purine-rich foods of animal origin, such as organ meats and seafood. Eating dairy products, vitamin C-rich foods, coffee, and cherries may help prevent gout attacks, as does losing weight. Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Treatment of apnea can lessen the occurrence of attacks.

Medications
As of 2020, allopurinol is generally the recommended preventative treatment if medications are used. A number of other medications may occasionally be considered to prevent further episodes of gout, including probenecid, febuxostat, benzbromarone, and colchicine. Long term medications are not recommended until a person has had two attacks of gout, unless destructive joint changes, tophi, or urate nephropathy exist. It is not until this point that medications are cost-effective. They are not usually started until one to two weeks after an acute flare has resolved, due to theoretical concerns of worsening the attack. They are often used in combination with either an NSAID or colchicine for the first three to six months.While it has been recommended that urate-lowering measures should be increased until serum uric acid levels are below 300–360 µmol/L (5.0–6.0 mg/dl), there is little evidence to support this practice over simple putting people on a standard dose of allopurinol. If these medications are in chronic use at the time of an attack, it is recommended that they be continued. Levels that cannot be brought below 6.0 mg/dl while attacks continue indicates refractory gout.While historically it is not recommended to start allopurinol during an acute attack of gout, this practice appears acceptable. Allopurinol blocks uric acid production, and is the most commonly used agent. Long term therapy is safe and well-tolerated and can be used in people with renal impairment or urate stones, although hypersensitivity occurs in a small number of individuals.  The HLA-B*58:01 allele of the human leukocyte antigen B (HLA-B) is strongly associated with severe cutaneous adverse reactions during treatment with allopurinol and is most common among Asian subpopulations, notably those of Korean, Han-Chinese, or Thai descent.Febuxostat is only recommended in those who cannot tolerate allopurinol. There are concerns about more deaths with febuxostat compared to allopurinol. Febuxostat may also increase the rate of gout flares during early treatment. However, there is tentative evidence that febuxostat may bring down urate levels more than allopurinol.Probenecid appears to be less effective than allopurinol and is a second line agent. Probenecid may be used if undersecretion of uric acid is present (24-hour urine uric acid less than 800 mg). It is, however, not recommended if a person has a history of kidney stones. Pegloticase is an option for the 3% of people who are intolerant to other medications. It is a third line agent. Pegloticase is given as an intravenous infusion every two weeks, and reduces uric acid levels. Pegloticase is useful decreasing tophi but has a high rate of side effects and many people develop resistance to it. Using lesinurad 400 mg plus febuxostat is more beneficial for tophi resolution than lesinural 200 mL with febuxostat, with similar side effects. Lesinural plus allopurinol is not effective for tophi resolution. Potential side effects include kidney stones, anemia and joint pain. In 2016, it was withdrawn from the European market.Lesinurad reduces blood uric acid levels by preventing uric acid absorption in the kidneys. It was approved in the United States for use together with allopurinol, among those who were unable to reach their uric acid level targets. Side effects include kidney problems and kidney stones.

Treatment
The initial aim of treatment is to settle the symptoms of an acute attack. Repeated attacks can be prevented by medications that reduce serum uric acid levels. Tentative evidence supports the application of ice for 20 to 30 minutes several times a day to decrease pain. Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and glucocorticoids. While glucocorticoids and NSAIDs work equally well, glucocorticoids may be safer. Options for prevention include allopurinol, febuxostat, and probenecid. Lowering uric acid levels can cure the disease. Treatment of associated health problems is also important. Lifestyle interventions have been poorly studied. It is unclear whether dietary supplements have an effect in people with gout.

NSAIDs
NSAIDs are the usual first-line treatment for gout. No specific agent is significantly more or less effective than any other. Improvement may be seen within four hours and treatment is recommended for one to two weeks. They are not recommended for those with certain other health problems, such as gastrointestinal bleeding, kidney failure, or heart failure. While indometacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness. For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given. There is some evidence that COX-2 inhibitors may work as well as nonselective NSAIDs for acute gout attack with fewer side effects.

Colchicine
Colchicine is an alternative for those unable to tolerate NSAIDs. At high doses, side effects (primarily gastrointestinal upset) limit its usage. At lower doses, which are still effective, it is well tolerated. Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.

Glucocorticoids
Glucocorticoids have been found to be as effective as NSAIDs and may be used if contraindications exist for NSAIDs. They also lead to improvement when injected into the joint. A joint infection must be excluded, however, as glucocorticoids worsen this condition. There were no short-term adverse effects reported.

Others
Interleukin-1 inhibitors, such as canakinumab, showed moderate effectiveness for pain relief and reduction of joint swelling, but have increased risk of adverse events, such as back pain, headache, and increased blood pressure. They, however, may work less well than usual doses of NSAIDS. The high cost of this class of drugs may also discourage their use for treating gout.

Prognosis
Without treatment, an acute attack of gout usually resolves in five to seven days; however, 60% of people have a second attack within one year. Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and kidney and cardiovascular disease and thus are at increased risk of death. It is unclear whether medications that lower urate affect cardiovascular disease risks. This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi. These tophi occur in 30% of those who are untreated for five years, often in the helix of the ear, over the olecranon processes, or on the Achilles tendons. With aggressive treatment, they may dissolve. Kidney stones also frequently complicate gout, affecting between 10 and 40% of people, and occur due to low urine pH promoting the precipitation of uric acid. Other forms of chronic kidney dysfunction may occur.

Epidemiology
Gout affects around 1–2% of people in the Western world at some point in their lifetimes and is becoming more common. Some 5.8 million people were affected in 2013. Rates of gout approximately doubled between 1990 and 2010. This rise is believed to be due to increasing life expectancy, changes in diet and an increase in diseases associated with gout, such as metabolic syndrome and high blood pressure. Factors that influence rates of gout include age, race, and the season of the year. In men over 30 and women over 50, rates are 2%.In the United States, gout is twice as likely in males of African descent than those of European descent. Rates are high among Pacific Islanders and the Māori, but the disease is rare in aboriginal Australians, despite a higher mean uric acid serum concentration in the latter group. It has become common in China, Polynesia, and urban Sub-Saharan Africa. Some studies found that attacks of gout occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity, and temperature.

History
The term  "gout" was initially used by Randolphus of Bocking, around 1200 AD. It is derived from the Latin word gutta, meaning "a drop" (of liquid). According to the Oxford English Dictionary, this is derived from humorism and "the notion of the dropping of a morbid material from the blood in and around the joints".Gout has been known since antiquity. Historically, it was referred to as "the king of diseases and the disease of kings" or "rich mans disease". The Ebers papyrus and the Edwin Smith papyrus, (c. 1550 BC) each mention arthritis of the first metacarpophalangeal joint as a distinct type of arthritis. These ancient manuscripts cite (now missing) Egyptian texts about gout that are claimed to have been written 1,000 years earlier by Imhotep. Greek physician Hippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs and premenopausal women. Aulus Cornelius Celsus (30 AD) described the linkage with alcohol, later onset in women and associated kidney problems:

Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera... Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed... some have obtained lifelong security by refraining from wine, mead and venery.
Benjamin Welles, an English physician authored the first medical book on gout, A Treatise of the Gout, or Joint Evil, in 1669. In 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning and its predilection for older males:

Gouty patients are, generally, either old men or men who have so worn themselves out in youth as to have brought on a premature old age—of such dissolute habits none being more common than the premature and excessive indulgence in venery and the like exhausting passions. The victim goes to bed and sleeps in good health. About two oclock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle, or instep. The pain is like that of a dislocation and yet parts feel as if cold water were poured over them. Then follows chills and shivers and a little fever... The night is passed in torture, sleeplessness, turning the part affected and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint and being worse as the fit comes on.
Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679. In 1848, English physician Alfred Baring Garrod identified excess uric acid in the blood as the cause of gout.

Other animals
Gout is rare in most other animals due to their ability to produce uricase, which breaks down uric acid. Humans and other great apes do not have this ability; thus, gout is common. Other animals with uricase include fish, amphibians and most non-primate mammals. The Tyrannosaurus rex specimen known as "Sue" is believed to have had gout.

Research
A number of new medications are under study for treating gout, including anakinra, canakinumab, and rilonacept. Canakinumab may result in better outcomes than a low dose of a glucocorticoid, but costs five thousand times more. A recombinant uricase enzyme (rasburicase) is available but its use is limited, as it triggers an immune response. Less antigenic versions are in development.

References
External links

Gout at Curlie
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