title: Occupational therapy

text: Occupational alienation: The imposition of an occupation that does not hold meaning for that person. In the OT profession, this manifests in the provision of rote activities that do not really relate to the goals or the client's interests.


title: Occupational therapy

text: • OTs can develop individualized activities tailored to the interests of the individual to maximize their potential.


title: Occupational therapy

text: • OTs can design, develop and promote programs that can be inclusive and provide a variety of choices that the individual can engage in.


title: Occupational therapy

text: Within occupational therapy practice, injustice may ensue in situations wherein professional dominance, standardized treatments, laws and political conditions create a negative impact on the occupational engagement of our clients. Awareness of these injustices will enable the therapist to reflect on his own practice and think of ways in approaching their client's problems while promoting occupational justice.


title: Occupational therapy

text: As occupational therapy (OT) has grown and developed, community-based practice has blossomed from an emerging area of practice to a fundamental part of occupational therapy practice (Scaffa & Reitz, 2013). Community-based practice allows for OTs to work with clients and other stakeholders such as families, schools, employers, agencies, service providers, stores, day treatment and day care and others who may influence the degree of success the client will have in participating. It also allows the therapist to see what is actually happening in the context and design interventions relevant to what might support the client in participating and what is impeding her or him from participating. Community-based practice crosses all of the categories within which OTs practice from physical to cognitive, mental health to spiritual, all types of clients may be seen in community-based settings. The role of the OT also may vary, from advocate to consultant, direct care provider to program designer, adjunctive services to therapeutic leader.


title: Occupational therapy

text: Worldwide, there is a range of qualifications required to practice as an occupational therapist or occupational therapy assistant. Depending on the country and expected level of practice, degree options include associate degree, Bachelor's degree, entry-level master's degree, post-professional master's degree, entry-level Doctorate (OTD), post-professional Doctorate (OTD), Doctor of Clinical Science in OT (CScD), Doctor of Philosophy in Occupational Therapy (PhD), and combined OTD/PhD degrees.


title: Occupational therapy

text: Both occupational therapist and occupational therapy assistant roles exist internationally. Currently in the United States, dual points of entry exist for both OT and OTA programs. For OT, that is entry-level Master's or entry-level Doctorate. For OTA, that is associate degree or bachelor's degree.


title: Occupational therapy

text: The World Federation of Occupational Therapists (WFOT) has minimum standards for the education of OTs, which was revised in 2016. All of the educational programs around the world need to meet these minimum standards. These standards are subsumed by and can be supplemented with academic standards set by a country's national accreditation organization. As part of the minimum standards, all programs must have a curriculum that includes practice placements (fieldwork). Examples of fieldwork settings include: acute care, inpatient hospital, outpatient hospital, skilled nursing facilities, schools, group homes, early intervention, home health, and community settings.


title: Occupational therapy

text: The profession of occupational therapy is based on a wide theoretical and evidence based background. The OT curriculum focuses on the theoretical basis of occupation through multiple facets of science, including occupational science, anatomy, physiology, biomechanics, and neurology. In addition, this scientific foundation is integrated with knowledge from psychology, sociology and more.


title: Occupational therapy

text: In the United States, Canada, and other countries around the world, there is a licensure requirement. In order to obtain an OT or OTA license, one must graduate from an accredited program, complete fieldwork requirements, and pass a national certification examination.


title: Occupational therapy

text: A distinguishing facet of occupational therapy is that therapists often espouse the use theoretical frameworks to frame their practice. Many have argued that the use of theory complicates everyday clinical care and is not necessary to provide patient-driven care.


title: Occupational therapy

text: Note that terminology differs between scholars. An incomplete list of theoretical bases for framing a human and their occupations include the following:


title: Occupational therapy

text: Generic models are the overarching title given to a collation of compatible knowledge, research and theories that form conceptual practice. More generally they are defined as "those aspects which influence our perceptions, decisions and practice".


title: Occupational therapy

text: Frames of reference are an additional knowledge base for the occupational therapist to develop their treatment or assessment of a patient or client group. Though there are conceptual models (listed above) that allow the therapist to conceptualise the occupational roles of the patient, it is often important to use further reference to embed clinical reasoning. Therefore, many occupational therapists will use additional frames of reference to both assess and then develop therapy goals for their patients or service users.


title: Occupational therapy

text: The International Classification of Functioning, Disability and Health (ICF) is a framework to measure health and ability by illustrating how these components impact one's function. This relates very closely to the Occupational Therapy Practice Framework, as it is stated that "the profession's core beliefs are in the positive relationship between occupation and health and its view of people as occupational beings". The ICF is built into the 2nd edition of the practice framework. Activities and participation examples from the ICF overlap Areas of Occupation, Performance Skills, and Performance Patterns in the framework. The ICF also includes contextual factors (environmental and personal factors) that relate to the framework's context. In addition, body functions and structures classified within the ICF help describe the client factors described in the Occupational Therapy Practice Framework. Further exploration of the relationship between occupational therapy and the components of the ICIDH-2 (revision of the original International Classification of Impairments, Disabilities, and Handicaps (ICIDH), which later became the ICF) was conducted by McLaughlin Gray.


title: Occupational therapy

text: It is noted in the literature that occupational therapists should use specific occupational therapy vocabulary along with the ICF in order to ensure correct communication about specific concepts. The ICF might lack certain categories to describe what occupational therapists need to communicate to clients and colleagues. It also may not be possible to exactly match the connotations of the ICF categories to occupational therapy terms. The ICF is not an assessment and specialized occupational therapy terminology should not be replaced with ICF terminology. The ICF is an overarching framework for current therapy practices.


title: Occupational therapy

text: Occupational therapy is practiced around the world and can be translated in practice to many different cultures and environments. The construct of occupation is shared throughout the profession regardless of country, culture and context. Occupation and the active participation in occupation is now seen as a human right and is asserted as a strong influence in health and well-being.


title: Occupational therapy

text: As the profession grows there is a lot of people who are travelling across countries to work as occupational therapists for better work or opportunities. Under this context, every occupational therapist is required to adapt to a new culture, foreign to their own. Understanding cultures and its communities are crucial to occupational therapy ethos. Effective occupational therapy practice includes acknowledging the values and social perspectives of each client and their families. Harnessing culture and understanding what is important to the client is truly a faster way towards independence.


title: Occupational therapy

text: The World Federation of Occupational Therapists is an international voice of the profession and is a membership network of occupational therapists worldwide. WFOT supports the international practice of occupational therapy through collaboration across countries. WFOT currently includes over 100 member country organizations, 550,000 occupational therapy practitioners, and 900 approved educational programs.


title: Occupational therapy

text: The profession celebrates World Occupational Therapy Day on the 27th of October annually to increase visibility and awareness of the profession, promoting the profession's development work at a local, national and international platform. WFOT has been in close collaboration with the World Health Organization (WHO) since 1959, working together in programmes that aim to improve world health. WFOT supports the vision for healthy people, in alignment with the United Nations 17 Sustainable Development Goals, which focuses on "ending poverty, fighting inequality and injustice, tackling climate change and promoting health". Occupational therapy is a major player in enabling individuals and communities to engage in "chosen and necessary occupations" and in "the creation of more meaningful lives".


title: Beach House

text: Beach House is an American musical duo formed in Baltimore, Maryland in 2004. The band consists of vocalist and keyboardist Victoria Legrand and guitarist, keyboardist, and backup vocalist Alex Scally.


title: Beach House

text: Their self-titled debut album was released in 2006 to critical acclaim and has been followed by "Devotion" (2008), "Teen Dream" (2010), "Bloom" (2012), "Depression Cherry" (2015), "Thank Your Lucky Stars" (2015), "B-sides and Rarities" (2017), "7" (2018), and "Once Twice Melody" (2022).


title: Beach House

text: Vocalist and organist Victoria Legrand, who graduated from Vassar College in 2003, and guitarist Alex Scally, who graduated from Oberlin College in 2004, formed the band in 2004 after meeting in Baltimore's indie rock scene, producing music composed largely of organ, programmed drums, and steel guitar. Of the origins of the band name Scally said: "We’d been writing music, and we had all these songs, and then there was that moment where you say ‘what do we call ourselves?’ We tried to intellectualize it, and it didn’t work. There were different plant-names, Wisteria, that kind of thing. Stupid stuff. But, once we stopped trying, it just came out, it just happened. And it just seemed perfect." In an interview with Pitchfork, Legrand addressed their being a two-member status thus: "[I]t's a way to challenge ourselves: What do you do when it's just the two of you? ... [O]ne of the reasons this has been such a fulfilling experience for me is that with two people, it's so much easier to achieve things that feel exciting and new."


title: Beach House

text: In August 2006, their song "Apple Orchard" was featured on a Pitchfork MP3 mixtape. By October 2006 the band's self-titled debut album, "Beach House", was released through Carpark Records, and was ranked 16th on Pitchfork's Best Albums of that year. The album was recorded on a 4-track over a two day period in Scally's basement.


title: Beach House

text: Beach House's second album, "Devotion", was released on February 26, 2008. It was received with similar acclaim as the first album and was included in Pitchfork's Best Albums of 2008 list. On October 21, 2008, the group released the single "Used to Be".


title: Beach House

text: Beach House also recorded a cover of Queen's "Play the Game" for the iTunes Store release of the Red Hot Organization's 2009 compilation "Dark Was The Night".


title: Beach House

text: In 2009, Legrand provided backing vocals on the song "Two Weeks" by the indie rock band Grizzly Bear. She later collaborated with the band again by providing vocals to "Slow Life", the band's contribution to the "Twilight: New Moon".


title: Beach House

text: In October 2010, the band contributed a charity T-shirt for the Yellow Bird Project to raise money for the House of Ruth women's shelter in Maryland for victims of domestic violence.


title: Beach House

text: "Teen Dream", the duo's "dynamic and intense" third album, was released on Sub Pop on January 26, 2010. It was released in the UK by Bella Union and in Mexico by Arts & Crafts. It contains a newer version of their 2008 single "Used to Be". Meanwhile, "Norway", the first single off <nowiki>"</nowiki>Teen Dream<nowiki>"</nowiki>, was made available as a free download on the band's website on November 17, 2009; it was later promoted on iTunes as the Free Single of the Week starting January 12, 2010. The album was produced and engineered by Chris Coady (Yeah Yeah Yeahs, TV on the Radio, Grizzly Bear). Music videos were made both for songs, "Silver Soul" and "Real Love", created by famed collective, The Masses. The album's unanimously positive reviews garnered the band a larger fan base, with Jay-Z and Beyoncé being spotted at the band's shows.


title: Beach House

text: Of the success of the album and it being dubbed the group's "breakout" record by numerous publications, Legrand stated: "I see this as just another step in a direction. I would not want to say that 2010 will be our year, necessarily, I hope it’s just another year in which we do good work. I don’t want to be defined by this year, I want it to just be a beginning."


title: Beach House

text: On March 7, 2012, the band streamed a new song, "Myth", from their website. The album "Bloom" was released on May 15, 2012, via Sub Pop. A second song from the album, "Lazuli", was released on April 13, 2012. Beach House was featured on the cover of Issue #80 of "the Fader". A music video for "Lazuli" was released on June 6, 2012. It was directed by Allen Cordell, who also directed the video for "Walk in the Park" from "Teen Dream". A music video for the track "Wild" has also been released. A music video for "Wishes" directed by Eric Wareheim and starring Ray Wise was released on March 7, 2013.


title: Beach House

text: The band released a short film, "Forever Still", on February 4, 2013. The film, directed by the band and Max Goldman, was inspired by Pink Floyd's and features the band performing songs from "Bloom" at various sites around Tornillo, Texas, where the album was recorded. The idea for the film came from the band's desire to make quality promotional content they could control artistically: "We had previously been involved in too many live sessions, radio tapings, photoshoots, etc., where the outcome was far below our personal artistic standards. We also felt a need to distance ourselves from the 'content' culture of the internet that rewards quantity over quality and shock over nuance."


title: Beach House

text: On May 26, 2015, the band announced their fifth album "Depression Cherry". It was released on August 28 via Sub Pop (on Bella Union in the UK) and the band announced a world tour in support. Talking about the direction of the new album, the band said, "In general, this record shows a return to simplicity, with songs structured around a melody and a few instruments, with live drums playing a far lesser role. With the growing success of "Teen Dream" and "Bloom", the larger stages and bigger rooms naturally drove us towards a louder, more aggressive place; a place farther from our natural tendencies. Here, we continue to let ourselves evolve while fully ignoring the commercial context in which we exist." "I think, this album continues to change meaning for me. But if anything, it's full of many things. Love, pain, getting older, dealing with loss, letting go. It's really ultimately whatever the listener feels in response to it," has Legrand described. "The name Depression Cherry is like a dance between these two energies. That very abstract feeling summed up the energy field of the record for us," specifies Victoria. This LP received praise from critics.


title: Beach House

text: On October 7, 2015, the band announced a sixth album, "Thank Your Lucky Stars", which was released on October 16, 2015. The record was co-produced by the band and Chris Coady. It received favorable praise from critics. Though the album was recorded alongside "Depression Cherry", the band felt that the records should be seen as distinct unconnected works.


title: Beach House

text: On September 28, 2015, popular music webzine "Spin" reported that the band had performed a new song called "Helicopter Dream (I'm Awake)" on Flaming Lips frontman Wayne Coyne's new podcast. Other music webzines also reported on the purported new track, including "Consequence of Sound", "Fact", and "Stereogum" However, according to the band's representatives, the song was a fake. In an email to "Spin", their representatives state, "It is not a new song. Not even their voices on that podcast. Sorry!" This led to a thinkpiece from the gossip blog "Gawker", which used the hoax as an example of "how easy it is to fool a blogger".


title: Beach House

text: Notably, reaction to the fake track was largely favorable, with "Spin" calling it a "fuzzy space-odyssey" and "Consequence of Sound" describing it as "a reverb-soaked number." Even the band itself gave a positive review, tweeting, "To whoever made that fake podcast interview, we like your helicopter dream song." The fake song and podcast hoax was named by Vice's Noisey as one of "The Best Trolls of 2015."


title: Beach House

text: On January 31, 2017, the band announced a North American tour. In addition, they announced that they were working on a compilation of B-Sides and rarities. The compilation, "B-Sides and Rarities", was eventually released on June 30, 2017, and was supported by a new song, "Chariot", which served as the lead single of the compilation and one of the two previously unreleased songs on it. In a promotional bio, the band wrote, "["B-Sides and Rarities"] felt like a good step for us. It helped us clean the creative closet, put the past to bed, and start anew."


title: Beach House

text: On February 15, 2018, the band released a new song, "Lemon Glow," and announced it as the lead single from their then-upcoming album which they said would be released "later this spring." On March 7, the band released another single from the album, "Dive", alongside an announcement of the album's title.


title: Beach House

text: "7" is the seventh studio album by Beach House, released on May 11, 2018, through Sub Pop. It follows the "B-Sides and Rarities" compilation album released in 2017, which served as a proverbial "cleaning out the closet" to pave the way for a new creative process.


title: Beach House

text: The album saw the group's departure from longtime producer Chris Coady. "7" was co-produced by Beach House and Pete “Sonic Boom” Kember. His work with Spacemen 3 and Spectrum impressed the band to reach out and see if he might like to co-produce the album with them. The record also features drums from James Barone, the band's longtime live drummer.


title: Beach House

text: Throughout the process of recording "7", the band's goal was rebirth and rejuvenation. They wanted to rethink old methods and shed some self-imposed limitations. In the past, they've often limited their writing to parts that they can perform live. On "7", they decided to follow whatever came naturally. As a result, there are some songs with no guitar, and some without keyboard. There are songs with layers and production that they could never recreate live, and that was exciting to them. Basically, letting creative moods, instead of instrumentation, dictate the album’s feel.


title: Beach House

text: ‘’This album felt really kinetic. We tend to make pretty still music, and this record felt like we were really excited by the kind of bubbling, chaotic, discordant energy field. … The vibe and the show are getting more energetic and messy, but in what I think is a cool way. Maybe a little bit more “rock and roll,” to use the old term,’’ adds Scally.


title: Beach House

text: On October 23, 2018, the band released a limited edition 7-inch vinyl of "Lose Your Smile" from "7" as the A-side and a new track from the recording sessions of "7" titled "Alien" as the B-side. The vinyl was originally sold on the band's European tour in dates from September to October. In addition, "Alien" was released as a standalone single to digital download and streaming services.


title: Beach House

text: In November 2021, the band announced their eighth studio album "Once Twice Melody", released on February 18, 2022. The 18-track double album was released in four "chapters". The first chapter was released on November 10, 2021, with the following three chapters released on December 8, 2021, January 19, 2022, and February 18, 2022. The band toured in support the album throughout 2022.


title: Beach House

text: In 2021, Beach House collaborated with Meow Wolf, an immersive arts production company based in Santa Fe, NM. The band scored a short film called "Marin's Dreams" and created soundscapes for Meow Wolf's new permanent installation in Las Vegas called Omega Mart. The band composed music for three rooms within the installation — "Upload Ghost," a sculpture designed by Stephen Hendee, "Goblin Computer," and "Marin and Rose's Dwelling."


title: Beach House

text: Beach House scored three trailers that ran before each film screening at the 2020 Sundance Film Festival.


title: Beach House

text: In March 2022, it was announced that Beach House would provide the score to Sofia Alvarez's Netflix film "Along for the Ride".


title: Beach House

text: Although Beach House is most often referred to as a dream pop band, their musical style has changed throughout their discography. Earlier material heard on "Beach House", "Devotion", and "Teen Dream" has been described as indie pop and lo-fi, whilst later material heard on "Bloom", "Depression Cherry", "Thank Your Lucky Stars", and "7" has been described as neo-psychedelia, ambient, and shoegazing.


title: Beach House

text: Singer Victoria Legrand's vocals have often been compared to those of Nico. Some music outlets have also compared Legrand's vocals to 1980s psychedelic rock vocalist Kendra Smith of the band Opal. Guitarist Alex Scally plays a Fender Stratocaster guitar in an E♭ Tuning. The group's influences include This Mortal Coil, Cocteau Twins, The Zombies, Brian Wilson, Françoise Hardy, Neil Young, Big Star, Tony, Caro and John and Chris Bell.


title: Beach House

text: Beach House re-recorded the Tony, Caro and John song "Snowdon Song" and renamed it "Lovelier Girl". The song was released on the band's self-titled album with no attribution. Initially, Tony Dore of Tony, Caro and John stated, "I haven't seen much yet in terms of royalties or acknowledgement of authorship". Several months later, however, Dore disclosed that discussions had taken place to apply proper attribution on re-releases of the self-titled album.


title: Beach House

text: Legrand has described creating new music and releasing albums as a necessity for the band, saying, "When we decide that a record is finished, I think it's really about coming to terms with saying 'OK, I think we've done everything that we could do, and now it's time to let these things go.' Because if we hold onto them, we might destroy them or they might never come out. There are all different types of artists and I think that some people like to hold onto things and they get very perfectionistic. But perfectionism is kind of a synonym for destruction. It can really be a deterrent for one's evolution. Alex and I have always felt that putting records out is very necessary. It's a gut feeling we have."


title: Beach House

text: Beach House's music has been sampled by prominent hip-hop and R&B artists. In 2011, The Weeknd sampled "Master of None" and "Gila" in his songs "The Party & the After Party" and "Loft Music," respectively. Kendrick Lamar sampled "Silver Soul" for his hit "Money Trees." The rap group G-Side sampled "10 Mile Stereo" in their song "How Far."


title: Beach House

text: Beach House has also inspired songs and musicians. Pop duo The Chainsmokers wrote "Beach House" as an ode to listening to Beach House. Wayne Coyne of the Flaming Lips listed Beach House's album "Bloom" as one of the ten records that changed his life.


title: Beach House

text: The band has toured extensively worldwide. Of touring, Legrand stated: "[W]e love touring. That's when you get to get into a rhythm, playing every night. It can be really fun. And I think you learn where you want to go with your music."


title: Beach House

text: Beach House is famous for its visual-heavy live shows that elevate their sound to a new level. Scally believes that playing live music is the best way to connect with fans. The band’s innovation in tour décor began with lightboxes with disco balls in them that Scally and Legrand made for their first tour.


title: Beach House

text: In March 2009, the band was featured at the SXSW festival in Austin, Texas. In April 2010, the band performed at the Coachella Festival in Indio, California. In June 2010, the band surmounted "technical difficulties due to too much MDMA" while playing a set on The Park Stage at Glastonbury. In August 2010, the band joined Vampire Weekend on tour as one of their two opening acts, the other being the Dum Dum Girls. In October 2010, Beach House played at the Austin City Limits Music Festival. On December 20, 2010, the band performed on "Conan".


title: Beach House

text: The band was chosen by Animal Collective to perform at the All Tomorrow's Parties festival they curated in May 2011, and also by Portishead to perform at the ATP I'll Be Your Mirror festival that they curated in July 2011 at London's Alexandra Palace. On May 29, 2011, the band played at the Sasquatch! Music Festival. On July 31, 2011, the band played at the Fuji Rock music festival in Niigata, Japan. On October 16, 2011, the band played at the Treasure Island Music Festival. On May 18, 2012, they appeared on the "Late Show with David Letterman" and on Sunday, July 15, 2012, they performed the closing set on the Red Stage during the Pitchfork Music Festival.


title: Beach House

text: In May 2012, the band appeared on "Later... with Jools Holland" playing "Myth" and "Lazuli" from their 2012 album, "Bloom".


title: Beach House

text: On July 26, 2012, they performed the "Bloom" cuts "Wild" and "Wishes" on "Late Night with Jimmy Fallon".


title: Beach House

text: On October 17, 2015, the band performed "One Thing" from their album "Thank Your Lucky Stars" (which debuted the same night) on "The Late Show with Stephen Colbert".


title: Beach House

text: Beach House performed at Coachella 2016 as well as Pickathon 2016 outside of Portland, Oregon and FYF Fest 2016 in Los Angeles, California. On July 15, 2016, the band headlined the Pitchfork Music Festival in Chicago, Illinois. On August 13 the band played at the Eaux Claires music festival in Eau Claire, Wisconsin.


title: Beach House

text: “I believe that our show now with 7 material, visually and musically, is the best it’s ever been. It evolved over a long period of time and it’s a vision now. At first, it was just an idea, but now it’s an experience…. We want to make people leave themselves. Any good artistic experience is like that,” adds Scally.


title: Beach House

text: In March 2018, the band announced an extensive tour itinerary that started at the end of April in the States and took them through the fall to Europe. In August 2019, Beach House added new tour dates in the US, including stops in Burlington and Cleveland, as well as Grand Rapids and Milwaukee, appearing at Osheaga festival in Montreal, Psycho Fest in Las Vegas, and Bellwether Music Festival in Waynesville, OH.


title: Beach House

text: Delivered since 2010, the GAFFA Awards (Swedish: GAFFA Priset) are a Swedish award that rewards popular music awarded by the magazine of the same name.


title: Deep vein thrombosis

text: Deep vein thrombosis (DVT) is a type of venous thrombosis involving the formation of a blood clot in a deep vein, most commonly in the legs or pelvis. A minority of DVTs occur in the arms. Symptoms can include pain, swelling, redness, and enlarged veins in the affected area, but some DVTs have no symptoms. The most common life-threatening concern with DVT is the potential for a clot to embolize (detach from the veins), travel as an embolus through the right side of the heart, and become lodged in a pulmonary artery that supplies blood to the lungs. This is called a pulmonary embolism (PE). DVT and PE comprise the cardiovascular disease of venous thromboembolism (VTE). About two-thirds of VTE manifests as DVT only, with one-third manifesting as PE with or without DVT. The most frequent long-term DVT complication is post-thrombotic syndrome, which can cause pain, swelling, a sensation of heaviness, itching, and in severe cases, ulcers. Recurrent VTE occurs in about 30% of those in the ten years following an initial VTE.


title: Deep vein thrombosis

text: The mechanism behind DVT formation typically involves some combination of decreased blood flow, increased tendency to clot, changes to the blood vessel wall, and inflammation. Risk factors include recent surgery, older age, active cancer, obesity, infection, inflammatory diseases, antiphospholipid syndrome, personal history and family history of VTE, trauma, injuries, lack of movement, hormonal birth control, pregnancy, and the period following birth. VTE has a strong genetic component, accounting for approximately 50 to 60% of the variability in VTE rates. Genetic factors include non-O blood type, deficiencies of antithrombin, protein C, and protein S and the mutations of factor V Leiden and prothrombin G20210A. In total, dozens of genetic risk factors have been identified.


title: Deep vein thrombosis

text: People suspected of having DVT can be assessed using a prediction rule such as the Wells score. A D-dimer test can also be used to assist with excluding the diagnosis or to signal a need for further testing. Diagnosis is most commonly confirmed by ultrasound of the suspected veins. VTE becomes much more common with age. The condition is rare in children, but occurs in almost 1% of those ≥ age 85 annually. Asian, Asian-American, Native American, and Hispanic individuals have a lower VTE risk than Whites or Blacks. Populations in Asia have VTE rates at 15 to 20% of what is seen in Western countries.


title: Deep vein thrombosis

text: Using blood thinners is the standard treatment. Typical medications include rivaroxaban, apixaban, and warfarin. Beginning warfarin treatment requires an additional non-oral anticoagulant, often injections of heparin. Prevention of VTE for the general population includes avoiding obesity and maintaining an active lifestyle. Preventive efforts following low-risk surgery include early and frequent walking. Riskier surgeries generally prevent VTE with a blood thinner or aspirin combined with intermittent pneumatic compression.


title: Deep vein thrombosis

text: Symptoms classically affect a leg and typically develop over hours or days, though they can develop suddenly or over a matter of weeks. The legs are primarily affected, with 4–10% of DVT occurring in the arms. Despite the signs and symptoms being highly variable, the typical symptoms are pain, swelling, and redness. However, these symptoms might not manifest in the lower limbs of those unable to walk. In those who are able to walk, DVT can reduce one's ability to do so. The pain can be described as throbbing and can worsen with weight-bearing, prompting one to bear more weight with the unaffected leg. Additional signs and symptoms include tenderness, pitting edema ("see image"), dilation of surface veins, warmth, discoloration, a "pulling sensation", and even cyanosis (a blue or purplish discoloration) with fever. DVT can also exist without causing any symptoms. Signs and symptoms help in determining the likelihood of DVT, but they are not used alone for diagnosis.


title: Deep vein thrombosis

text: At times, DVT can cause symptoms in both arms or both legs, as with bilateral DVT. Rarely, a clot in the inferior vena cava can cause both legs to swell. Superficial vein thrombosis, also known as superficial thrombophlebitis, is the formation of a blood clot (thrombus) in a vein close to the skin. It can co-occur with DVT and can be felt as a "palpable cord". Migratory thrombophlebitis (Trousseau's syndrome) is a noted finding in those with pancreatic cancer and is associated with DVT.


title: Deep vein thrombosis

text: A pulmonary embolism (PE) occurs when a blood clot from a deep vein (a DVT) detaches from a vein (embolizes), travels through the right side of the heart, and becomes lodged as an embolus in a pulmonary artery that supplies deoxygenated blood to the lungs for oxygenation. Up to one-fourth of PE cases are thought to result in sudden death. When not fatal, PE can cause symptoms such as sudden onset shortness of breath or chest pain, coughing up blood (hemoptysis), and fainting (syncope). The chest pain can be pleuritic (worsened by deep breaths) and can vary based upon where the embolus is lodged in the lungs. An estimated 30–50% of those with PE have detectable DVT by compression ultrasound.


title: Deep vein thrombosis

text: A rare and massive DVT that causes significant obstruction and discoloration (including cyanosis) is phlegmasia cerulea dolens. It is life-threatening, limb-threatening, and carries a risk of venous gangrene. Phlegmasia cerulea dolens can occur in the arm but more commonly affects the leg. If found in the setting of acute compartment syndrome, an urgent fasciotomy is warranted to protect the limb. Superior vena cava syndrome is a rare complication of arm DVT.


title: Deep vein thrombosis

text: DVT is thought to be able to cause a stroke in the presence of a heart defect. This is called a paradoxical embolism because the clot abnormally travels from the pulmonary circuit to the systemic circuit while inside the heart. The defect of a patent foramen ovale is thought to allow clots to travel through the interatrial septum from the right atrium into the left atrium.


title: Deep vein thrombosis

text: In most suspected cases, DVT is ruled out after evaluation. Cellulitis is a frequent mimic of DVT, with its triad of pain, swelling, and redness. Symptoms concerning for DVT are more often due to other causes, including cellulitis, ruptured Baker's cyst, hematoma, lymphedema, and chronic venous insufficiency. Other differential diagnoses include tumors, venous or arterial aneurysms, connective tissue disorders, superficial vein thrombosis, muscle vein thrombosis, and varicose veins.


title: Deep vein thrombosis

text: DVT and PE are the two manifestations of the cardiovascular disease venous thromboembolism (VTE). VTE can occur as DVT only, DVT with PE, or PE only. About two-thirds of VTE manifests as DVT only, with one-third manifesting as PE with or without DVT. VTE, along with superficial vein thrombosis, are common types of venous thrombosis.


title: Deep vein thrombosis

text: DVT is classified as acute when the clots are developing or have recently developed, whereas chronic DVT persists more than 28 days. Differences between these two types of DVT can be seen with ultrasound. An episode of VTE after an initial one is classified as recurrent. Bilateral DVT refers to clots in both limbs while unilateral means only a single limb is affected.


title: Deep vein thrombosis

text: DVT in the legs is proximal when above the knee and distal (or calf) when below the knee. DVT below the popliteal vein, a proximal vein behind the knee, is classified as distal and has limited clinical significance compared to proximal DVT. Calf DVT makes up about half of DVTs. Iliofemoral DVT has been described as involving either the iliac or common femoral vein; elsewhere, it has been defined as involving at a minimum the common iliac vein, which is near the top of the pelvis.


title: Deep vein thrombosis

text: DVT can be classified into provoked and unprovoked categories. For example, DVT that occurs in association with cancer or surgery can be classified as provoked. However, the European Society of Cardiology in 2019 urged for this dichotomy to be abandoned to encourage more personalized risk assessments for recurrent VTE. The distinction between these categories is not always clear.


title: Deep vein thrombosis

text: Traditionally, the three factors of Virchow's triad—venous stasis, hypercoagulability, and changes in the endothelial blood vessel lining—contribute to VTE and were used to explain its formation. More recently, inflammation has been identified as playing a clear causal role. Other related causes include activation of immune system components, the state of microparticles in the blood, the concentration of oxygen, and possible platelet activation. Various risk factors contribute to VTE, including genetic and environmental factors, though many with multiple risk factors never develop it.


title: Deep vein thrombosis

text: Acquired risk factors include the strong risk factor of older age, which alters blood composition to favor clotting. Previous VTE, particularly unprovoked VTE, is a strong risk factor. A leftover clot from a prior DVT increases the risk of a subsequent DVT. Major surgery and trauma increase risk because of tissue factor from outside the vascular system entering the blood. Minor injuries, lower limb amputation, hip fracture, and long bone fractures are also risks. In orthopedic surgery, venous stasis can be temporarily provoked by a cessation of blood flow as part of the procedure. Inactivity and immobilization contribute to venous stasis, as with orthopedic casts, paralysis, sitting, long-haul travel, bed rest, hospitalization, catatonia, and in survivors of acute stroke. Conditions that involve compromised blood flow in the veins are May–Thurner syndrome, where a vein of the pelvis is compressed, and venous thoracic outlet syndrome, which includes Paget–Schroetter syndrome, where compression occurs near the base of the neck.


title: Deep vein thrombosis

text: Infections, including sepsis, COVID-19, HIV, and active tuberculosis, increase risk. Chronic inflammatory diseases and some autoimmune diseases, such as inflammatory bowel disease, systemic sclerosis, Behçet's syndrome, primary antiphospholipid syndrome, and systemic lupus erythematosus (SLE) increase risk. SLE itself is frequently associated with secondary antiphospholipid syndrome.


title: Deep vein thrombosis

text: Cancer can grow in and around veins, causing venous stasis, and can also stimulate increased levels of tissue factor. Cancers of the blood, lung, pancreas, brain, stomach, and bowel are associated with high VTE risk. Solid tumors such as adenocarcinomas can contribute to both VTE and disseminated intravascular coagulation. In severe cases, this can lead to simultaneous clotting and bleeding. Chemotherapy treatment also increases risk. Obesity increases the potential of blood to clot, as does pregnancy. In the postpartum, placental tearing releases substances that favor clotting. Oral contraceptives and hormonal replacement therapy increase the risk through a variety of mechanisms, including altered blood coagulation protein levels and reduced fibrinolysis.


title: Deep vein thrombosis

text: Dozens of genetic risk factors have been identified, and they account for approximately 50 to 60% of the variability in VTE rates. As such, family history of VTE is a risk factor for a first VTE. Factor V Leiden, which makes factor V resistant to inactivation by activated protein C, mildly increases VTE risk by about three times. Deficiencies of three proteins that normally prevent blood from clotting—protein C, protein S, and antithrombin—contribute to VTE. These deficiencies in antithrombin, protein C, and protein S are rare but strong, or moderately strong, risk factors. They increase risk by about 10 times. Having a non-O blood type roughly doubles VTE risk. Non-O blood type is common globally, making it an important risk factor. Individuals without O blood type have higher blood levels of von Willebrand factor and factor VIII than those with O blood type, increasing the likelihood of clotting. Those homozygous for the common fibrinogen gamma gene variant rs2066865 have about a 1.6 times higher risk of VTE. The genetic variant prothrombin G20210A, which increases prothrombin levels, increases risk by about 2.5 times. Additionally, approximately 5% of people have been identified with a background genetic risk comparable to the factor V Leiden and prothrombin G20210A mutations.


title: Deep vein thrombosis

text: Blood alterations including dysfibrinogenemia, low free protein S, activated protein C resistance, homocystinuria, hyperhomocysteinemia, high fibrinogen levels, high factor IX levels, and high factor XI levels are associated with increased risk. Other associated conditions include heparin-induced thrombocytopenia, catastrophic antiphospholipid syndrome, paroxysmal nocturnal hemoglobinuria, nephrotic syndrome, chronic kidney disease, polycythemia vera, essential thrombocythemia, intravenous drug use, and smoking.


title: Deep vein thrombosis

text: Some risk factors influence the location of DVT within the body. In isolated distal DVT, the profile of risk factors appears distinct from proximal DVT. Transient factors, such as surgery and immobilization, appear to dominate, whereas thrombophilias and age do not seem to increase risk. Common risk factors for having an upper extremity DVT include having an existing foreign body (such as a central venous catheter, a pacemaker, or a triple-lumen PICC line), cancer, and recent surgery.


title: Deep vein thrombosis

text: Blood has a natural tendency to clot when blood vessels are damaged (hemostasis) to minimize blood loss. Clotting is activated by the coagulation cascade and the clearing of clots that are no longer needed is accomplished by the process of fibrinolysis. Reductions in fibrinolysis or increases in coagulation can increase the risk of DVT.


title: Deep vein thrombosis

text: DVT often develops in the calf veins and "grows" in the direction of venous flow, towards the heart. DVT most frequently affects veins in the leg or pelvis including the popliteal vein (behind the knee), femoral vein (of the thigh), and iliac veins of the pelvis. Extensive lower-extremity DVT can even reach into the inferior vena cava (in the abdomen). Upper extremity DVT most commonly affects the subclavian, axillary, and jugular veins.


title: Deep vein thrombosis

text: The process of fibrinolysis, where DVT clots can be dissolved back into the blood, acts to temper the process of thrombus growth. This is the preferred process. Aside from the potentially deadly process of embolization, a clot can resolve through organization, which can damage the valves of veins, cause vein fibrosis, and result in non-compliant veins. Organization of a thrombus into the vein can occur at the third stage of its pathological development, in which collagen becomes the characteristic component. The first pathological stage is marked by red blood cells, and the second is characterized by medium-textured fibrin.


title: Deep vein thrombosis

text: In arterial thrombosis, blood vessel wall damage is required, as it initiates coagulation, but clotting in the veins mostly occurs without any such mechanical damage. The beginning of venous thrombosis is thought to arise from "activation of endothelial cells, platelets, and leukocytes, with initiation of inflammation and formation of microparticles that trigger the coagulation system" via tissue factor. Vein wall inflammation is likely the inciting event. Importantly, the activated endothelium of veins interacts with circulating white blood cells (leukocytes). While leukocytes normally help prevent blood from clotting (as does normal endothelium), upon stimulation, leukocytes facilitate clotting. Neutrophils are recruited early in the process of venous thrombi formation. They release pro-coagulant granules and neutrophil extracellular traps (NETs) or their components, which play a role in venous thrombi formation. NET components are pro-thrombotic through both the intrinsic and extrinsic coagulation pathways. NETs provide "a scaffold for adhesion" of platelets, red blood cells, and multiple factors that potentiate platelet activation. In addition to the pro-coagulant activities of neutrophils, multiple stimuli cause monocytes to release tissue factor. Monocytes are also recruited early in the process.


title: Deep vein thrombosis

text: Tissue factor, via the tissue factor–factor VIIa complex, activates the extrinsic pathway of coagulation and leads to conversion of prothrombin to thrombin, followed by fibrin deposition. Fresh venous clots are red blood cell and fibrin rich. Platelets and white blood cells are also components. Platelets are not as prominent in venous clots as they are in arterial ones, but they can play a role. In cancer, tissue factor is produced by cancer cells. Cancer also produces unique substances that stimulate factor Xa, cytokines that promote endothelial dysfunction, and plasminogen activator inhibitor-1, which inhibits the breakdown of clots (fibrinolysis).


title: Deep vein thrombosis

text: Often, DVT begins in the valves of veins. The blood flow pattern in the valves can cause low oxygen concentrations in the blood (hypoxemia) of a valve sinus. Hypoxemia, which is worsened by venous stasis, activates pathways—ones that include hypoxia-inducible factor-1 and early-growth-response protein 1. Hypoxemia also results in the production of reactive oxygen species, which can activate these pathways, as well as nuclear factor-κB, which regulates hypoxia-inducible factor-1 transcription. Hypoxia-inducible factor-1 and early-growth-response protein 1 contribute to monocyte association with endothelial proteins, such as P-selectin, prompting monocytes to release tissue factor-filled microvesicles, which presumably begin clotting after binding to the endothelial surface.


title: Deep vein thrombosis

text: D-dimers are a fibrin degradation product, a natural byproduct of fibrinolysis that is typically found in the blood. An elevated level can result from plasmin dissolving a clot—or other conditions. Hospitalized patients often have elevated levels for multiple reasons. Anticoagulation, the standard treatment for DVT, prevents further clot growth and PE, but does not act directly on existing clots.


title: Deep vein thrombosis

text: A clinical probability assessment using the Wells score (see column in the table below) to determine if a potential DVT is "likely" or "unlikely" is typically the first step of the diagnostic process. The score is used in suspected first lower extremity DVT (without any PE symptoms) in primary care and outpatient settings, including the emergency department. The numerical result (possible score −2 to 9) is most commonly grouped into either "unlikely" or "likely" categories. A Wells score of two or more means DVT is considered "likely" (about a 28% chance), while those with a lower score are considered "unlikely" to have DVT (about a 6% chance). In those unlikely to have DVT, a diagnosis is excluded by a negative D-dimer blood test. In people with likely DVT, ultrasound is the standard imaging used to confirm or exclude a diagnosis. Imaging is also needed for hospital inpatients with suspected DVT and those initially categorized as unlikely to have DVT but who have a positive D-dimer test.


title: Deep vein thrombosis

text: While the Wells score is the predominant and most studied clinical prediction rule for DVT, it does have drawbacks. The Wells score requires a subjective assessment regarding the likelihood of an alternate diagnosis and performs less well in the elderly and those with a prior DVT. The Dutch Primary Care Rule has also been validated for use. It contains only objective criteria but requires obtaining a D-dimer value. With this prediction rule, three points or less means a person is at low risk for DVT. A result of four or more points indicates an ultrasound is needed. Instead of using a prediction rule, experienced physicians can make a DVT pre-test probability assessment using clinical assessment and gestalt, but prediction rules are more reliable.


title: Deep vein thrombosis

text: Compression ultrasonography for suspected deep vein thrombosis is the standard diagnostic method, and it is highly sensitive for detecting an initial DVT. A compression ultrasound is considered positive when the vein walls of normally compressible veins do not collapse under gentle pressure. Clot visualization is sometimes possible, but is not required. Three compression ultrasound scanning techniques can be used, with two of the three methods requiring a second ultrasound some days later to rule out the diagnosis. Whole-leg ultrasound is the option that does not require a repeat ultrasound, but proximal compression ultrasound is frequently used because distal DVT is only rarely clinically significant. Ultrasound methods including duplex and color flow Doppler can be used to further characterize the clot and Doppler ultrasound is especially helpful in the non-compressible iliac veins.


title: Deep vein thrombosis

text: CT scan venography, MRI venography, or a non-contrast MRI are also diagnostic possibilities. The gold standard for judging imaging methods is contrast venography, which involves injecting a peripheral vein of the affected limb with a contrast agent and taking X-rays, to reveal whether the venous supply has been obstructed. Because of its cost, invasiveness, availability, and other limitations, this test is rarely performed.


title: Deep vein thrombosis

text: Treatment for DVT is warranted when the clots are either proximal, distal and symptomatic, or upper extremity and symptomatic. Providing anticoagulation, or blood-thinning medicine, is the typical treatment after patients are checked to make sure they are not subject to bleeding. However, treatment varies depending upon the location of DVT. For example, in cases of isolated distal DVT, ultrasound surveillance (a second ultrasound after 2 weeks to check for proximal clots), might be used instead of anticoagulation. Although, those with isolated distal DVT at a high-risk of VTE recurrence are typically anticoagulated as if they had proximal DVT. Those at a low-risk for recurrence might receive a four to six week course of anticoagulation, lower doses, or no anticoagulation at all. In contrast, those with proximal DVT should receive at least 3 months of anticoagulation.


title: Deep vein thrombosis

text: Some anticoagulants can be taken by mouth, and these oral medicines include warfarin (a vitamin K antagonist), rivaroxaban (a factor Xa inhibitor), apixaban (a factor Xa inhibitor), dabigatran (a direct thrombin inhibitor), and edoxaban (a factor Xa inhibitor). Other anticoagulants cannot be taken by mouth. These parenteral (non-oral) medicines include low-molecular-weight heparin, fondaparinux, and unfractionated heparin. Some oral medicines are sufficient when taken alone, while others require the use of an additional parenteral blood thinner. Rivaroxaban and apixaban are the typical first-line medicines, and they are sufficient when taken orally. Rivaroxaban is taken once daily, and apixaban is taken twice daily. Warfarin, dabigatran, and edoxaban require the use of a parenteral anticoagulant to initiate oral anticoagulant therapy. When warfarin is initiated for VTE treatment, a 5-day minimum of a parenteral anticoagulant together with warfarin is given, which is followed by warfarin-only therapy. Warfarin is taken to maintain an international normalized ratio (INR) of 2.0–3.0, with 2.5 as the target. The benefit of taking warfarin declines as the duration of treatment extends, and the risk of bleeding increases with age. Periodic INR monitoring is not necessary when first-line direct oral anticoagulants are used. Overall, anticoagulation therapy is complex and many circumstances can affect how these therapies are managed.


title: Deep vein thrombosis

text: The duration of anticoagulation therapy (whether it will last 4 to 6 weeks, 6 to 12 weeks, 3 to 6 months, or indefinitely) is a key factor in clinical decision making. When proximal DVT is provoked by surgery or trauma a 3-month course of anticoagulation is standard. When a first VTE is proximal DVT that is either unprovoked or associated with transient non-surgical risk factor, low-dose anticoagulation beyond 3 to 6 months might be used. In those with an annual risk of VTE in excess of 9%, as after an unprovoked episode, extended anticoagulation is a possibility. Those who finish warfarin treatment after idiopathic VTE with an elevated D-dimer level show an increased risk of recurrent VTE (about 9% vs about 4% for normal results), and this result might be used in clinical decision making. Thrombophilia test results rarely play a role in the length of treatment.


title: Deep vein thrombosis

text: Treatment for acute leg DVT is suggested to continue at home for uncomplicated DVT instead of hospitalization. Factors that favor hospitalization include severe symptoms or additional medical issues. Early walking is suggested over bedrest. Graduated compression stockings—which apply higher pressure at the ankles and a lower pressure around the knees can be trialed for symptomatic management of acute DVT symptoms, but they are not recommended for reducing the risk of post-thrombotic syndrome, as the potential benefit of using them for this goal "may be uncertain". Nor are compression stockings likely to reduce VTE recurrence. They are, however, recommended in those with isolated distal DVT.


title: Deep vein thrombosis

text: If someone decides to stop anticoagulation after an unprovoked VTE instead of being on lifelong anticoagulation, aspirin can be used to reduce the risk of recurrence, but it is only about 33% as effective as anticoagulation in preventing recurrent VTE. Statins have also been investigated for their potential to reduce recurrent VTE rates, with some studies suggesting effectiveness.


title: Deep vein thrombosis

text: An unprovoked VTE might signal the presence of an unknown cancer, as it is an underlying condition in up to 10% of unprovoked cases. A thorough clinical assessment is needed and should include a physical examination, a review of medical history, and universal cancer screening done in people of that age. A review of prior imaging is considered worthwhile, as is "reviewing baseline blood test results including full blood count, renal and hepatic function, PT and APTT." It is not recommended practice to obtain tumor markers or a CT of the abdomen and pelvis in asymptomatic individuals. NICE recommends that further investigations are unwarranted in those without relevant signs or symptoms.


title: Deep vein thrombosis

text: Thrombolysis is the injection of an enzyme into the veins to dissolve blood clots, and while this treatment has been proven effective against the life-threatening emergency clots of stroke and heart attacks, randomized controlled trials have not established a net benefit in those with acute proximal DVT. Drawbacks of catheter-directed thrombolysis (the preferred method of administering the clot-busting enzyme) include a risk of bleeding, complexity, and the cost of the procedure. Although, while anticoagulation is the preferred treatment for DVT, thrombolysis is a treatment option for those with the severe DVT form of phlegmasia cerula dorens ("bottom left image") and in some younger patients with DVT affecting the iliac and common femoral veins. Of note, a variety of contraindications to thrombolysis exist. In 2020, NICE kept their 2012 recommendations that catheter-directed thrombolysis should be considered in those with iliofemoral DVT who have "symptoms lasting less than 14 days, good functional status, a life expectancy of 1 year or more, and a low risk of bleeding."


title: Deep vein thrombosis

text: A mechanical thrombectomy device can remove DVT clots, particularly in acute iliofemoral DVT (DVT of the major veins in the pelvis), but there is limited data on its efficacy. It is usually combined with thrombolysis, and sometimes temporary IVC filters are placed to protect against PE during the procedure. Catheter-directed thrombolysis with thrombectomy against iliofemoral DVT has been associated with a reduction in the severity of post-thrombotic syndrome at an estimated cost-effectiveness ratio of about $138,000 per gained QALY. Phlegmasia cerulea dolens might be treated with catheter-directed thrombolysis and/or thrombectomy.


title: Deep vein thrombosis

text: In DVT in the arm, the first (topmost) rib can be surgically removed as part of the typical treatment when the DVT is due to thoracic outlet syndrome or Paget–Schroetter syndrome. This treatment involves initial anticoagulation followed by thrombolysis of the subclavian vein and staged first rib resection to relieve the thoracic outlet compression and prevent recurrent DVT.


title: Deep vein thrombosis

text: The placement of an inferior vena cava filter (IVC filter) is possible when either the standard treatment for acute DVT, anticoagulation, is absolutely contraindicated (not possible), or if someone develops a PE despite being anticoagulated. However, a 2020 NICE review found "little good evidence" for their use. A 2018 study associated IVC filter placement with a 50% reduction in PE, a 70% increase in DVT, and an 18% increase in 30 day mortality when compared to no IVC placement. Other studies including a systematic review and meta-analysis did not find a difference in mortality with IVC placement. If someone develops a PE despite being anticoagulated, care should be given to optimize anticoagulation treatment and address other related concerns before considering IVC filter placement.


title: Deep vein thrombosis

text: Patients with a history of DVT might be managed by primary care, general internal medicine, hematology, cardiology, vascular surgery, or vascular medicine. Patients suspected of having an acute DVT are often referred to the emergency department for evaluation. Interventional radiology is the specialty that typically places and retrieves IVC filters, and vascular surgery might do catheter directed thrombosis for some severe DVTs.


title: Deep vein thrombosis

text: For the prevention of blood clots in the general population, incorporating leg exercises while sitting down for long periods, or having breaks from a sitting position and walking around, having an active lifestyle, and maintaining a healthy body weight are recommended. Walking increases blood flow through the leg veins. Excess body weight is modifiable unlike most risk factors, and interventions or lifestyle modifications that help someone who is overweight or obese lose weight reduce DVT risk. Avoiding both smoking and a Western pattern diet are thought to reduce risk. Statins have been investigated for primary prevention (prevention of a first VTE), and the JUPITER trial, which used rosuvastatin, has provided some tentative evidence of effectiveness. Of the statins, rosuvastatin appears to be the only one with the potential to reduce VTE risk. If so, it appears to reduce risk by about 15%. However, the number needed to treat to prevent one initial VTE is about 2000, limiting its applicability.


title: Deep vein thrombosis

text: Acutely ill hospitalized patients are suggested to receive a parenteral anticoagulant, although the potential net benefit is uncertain. Critically ill hospitalized patients are recommended to either receive unfractionated heparin or low-molecular weight heparin instead of foregoing these medicines.


title: Deep vein thrombosis

text: Major orthopedic surgery—total hip replacement, total knee replacement, or hip fracture surgery—has a high risk of causing VTE. If prophylaxis is not used after these surgeries, symptomatic VTE has about a 4% chance of developing within 35 days. Following major orthopedic surgery, a blood thinner or aspirin is typically paired with intermittent pneumatic compression, which is the preferred mechanical prophylaxis over graduated compression stockings.


title: Deep vein thrombosis

text: Options for VTE prevention in people following non-orthopedic surgery include early walking, mechanical prophylaxis, and blood thinners (low-molecular-weight heparin and low-dose-unfractionated heparin) depending upon the risk of VTE, risk of major bleeding, and person's preferences. After low-risk surgeries, early and frequent walking is the best preventive measure.


title: Deep vein thrombosis

text: The risk of VTE is increased in pregnancy by about four to five times because of a more hypercoagulable state that protects against fatal postpartum hemorrhage. Preventive measures for pregnancy-related VTE were suggested by the American Society of Hematology in 2018. Warfarin, a common vitamin K antagonist, can cause birth defects and is not used for prevention during pregnancy.


title: Deep vein thrombosis

text: Travelling "is an often cited yet relatively uncommon" cause of VTE. Suggestions for at-risk long-haul travelers include calf exercises, frequent walking, and aisle seating in airplanes to ease walking. Graduated compression stockings have sharply reduced the levels of asymptomatic DVT in airline passengers, but the effect on symptomatic DVT, PE, or mortality is unknown, as none of the individuals studied developed these outcomes. However, graduated compression stockings are not suggested for long-haul travelers (>4 hours) without risk factors for VTE. Likewise, neither aspirin nor anticoagulants are suggested in the general population undertaking long-haul travel. Those with significant VTE risk factors undertaking long-haul travel are suggested to use either graduated compression stockings or LMWH for VTE prevention. If neither of these two methods are feasible, then aspirin is suggested.


title: Deep vein thrombosis

text: DVT is most frequently a disease of older age that occurs in the context of nursing homes, hospitals, and active cancer. It is associated with a 30-day mortality rate of about 6%, with PE being the cause of most of these deaths. Proximal DVT is frequently associated with PE, unlike distal DVT, which is rarely if ever associated with PE. Around 56% of those with proximal DVT also have PE, although a chest CT is not needed simply because of the presence of DVT. If proximal DVT is left untreated, in the following 3 months approximately half of people will experience symptomatic PE.


title: Deep vein thrombosis

text: Another frequent complication of proximal DVT, and the most frequent chronic complication, is post-thrombotic syndrome, where individuals have chronic venous symptoms. Symptoms can include pain, itching, swelling, paresthesia, a sensation of heaviness, and in severe cases, leg ulcers. After proximal DVT, an estimated 20–50% of people develop the syndrome, with 5–10% experiencing severe symptoms. Post-thrombotic syndrome can also be a complication of distal DVT, though to a lesser extent than with proximal DVT.


title: Deep vein thrombosis

text: In the 10 years following an initial VTE, about 30% of people will have a recurrence. VTE recurrence in those with prior DVT is more likely to recur as DVT than PE. Cancer and unprovoked DVT are strong risk factors for recurrence. After initial proximal unprovoked DVT with and without PE, 16–17% of people will have recurrent VTE in the 2 years after they complete their course of anticoagulants. VTE recurrence is less common in distal DVT than proximal DVT. In upper extremity DVT, annual VTE recurrence is about 2–4%. After surgery, a provoked proximal DVT or PE has an annual recurrence rate of only 0.7%.


title: Deep vein thrombosis

text: About 1.5 out of 1000 adults a year have a first VTE in high-income countries. The condition becomes much more common with age. VTE rarely occurs in children, but when it does, it predominantly affects hospitalized children. Children in North America and the Netherlands have VTE rates that range from 0.07 to 0.49 out of 10,000 children annually. Meanwhile, almost 1% of those aged 85 and above experience VTE each year. About 60% of all VTEs occur in those 70 years of age or older. Incidence is about 18% higher in males than in females, though there are ages when VTE is more prevalent in women. VTE occurs in association with hospitalization or nursing home residence about 60% of the time, active cancer about 20% of the time, and a central venous catheter or transvenous pacemaker about 9% of the time.


title: Deep vein thrombosis

text: During pregnancy and after childbirth, acute VTE occurs in about 1.2 of 1000 deliveries. Despite it being relatively rare, it is a leading cause of maternal morbidity and mortality. After surgery with preventive treatment, VTE develops in about 10 of 1000 people after total or partial knee replacement, and in about 5 of 1000 after total or partial hip replacement. About 400,000 Americans develop an initial VTE each year, with 100,000 deaths or more attributable to PE. Asian, Asian-American, Native American, and Hispanic individuals have a lower VTE risk than Whites or Blacks. Populations in Asia have VTE rates at 15 to 20% of what is seen in Western countries, with an increase in incidence seen over time. In North American and European populations, around 4–8% of people have a thrombophilia, most commonly factor V leiden and prothrombin G20210A. For populations in China, Japan, and Thailand, deficiences in protein S, protein C, and antithrombin predominate. Non-O blood type is present in around 50% of the general population and varies with ethnicity, and it is present in about 70% of those with VTE.


title: Deep vein thrombosis

text: DVT occurs in the upper extremities in about 4–10% of cases, with an incidence of 0.4–1.0 people out of 10,000 a year. A minority of upper extremity DVTs are due to Paget–Schroetter syndrome, also called effort thrombosis, which occurs in 1–2 people out of 100,000 a year, usually in athletic males around 30 years of age or in those who do significant amounts of overhead manual labor.


title: Deep vein thrombosis

text: Being on blood thinners because of DVT can be life-changing because it can prevent lifestyle activities such as contact or winter sports to prevent bleeding after potential injuries. Head injuries prompting brain bleeds are of particular concern. This has caused NASCAR driver Brian Vickers to forego participation in races. Professional basketball players including NBA players Chris Bosh and hall of famer Hakeem Olajuwon have dealt with recurrent blood clots, and Bosh's career was significantly hampered by DVT and PE.


title: Deep vein thrombosis

text: Tennis star Serena Williams was hospitalized in 2011 for PE thought to have originated from DVT. Years later, in 2017, due to her knowledge of DVT and PE, Serena accurately advocated for herself to have a PE diagnosed and treated. During this encounter with VTE, she was hospitalized after a C-section surgery and was off of blood thinners. After feeling the sudden onset of a PE symptom, shortness of breath, she told her nurse and requested a CT scan and an IV heparin drip, all while gasping for air. She started to receive an ultrasound to look for DVT in the legs, prompting her to express dissatisfaction to the medical staff that they were not looking for clots where she had symptoms (her lungs), and they were not yet treating her presumed PE. After being diagnosed with PE and not DVT, and after receiving heparin by IV, the coughing from the PE caused her C-section surgical site to open and the heparin contributed to bleeding at the site. Serena later received an IVC filter while in the hospital.


title: Deep vein thrombosis

text: Other notable people have been affected by DVT. Former United States (US) President Richard Nixon had recurrent DVT, and so has former Secretary of State Hillary Clinton. She was first diagnosed while First Lady in 1998 and again in 2009. Dick Cheney was diagnosed with an episode while Vice President, and TV show host Regis Philbin had DVT after hip-replacement surgery. DVT has also contributed to the deaths of famous people. For example, DVT and PE played a role in rapper Heavy D's death at age 44. NBC journalist David Bloom died at age 39 while covering the Iraq War from a PE that was thought to have progressed from a missed DVT, and actor Jimmy Stewart had DVT that progressed to a PE when he was 89.


title: Deep vein thrombosis

text: The book "Sushruta Samhita", an Ayurvedic text published around 600–900 BC, contains what has been cited as the first description of DVT. In 1271, DVT symptoms in the leg of a 20-year-old male were described in a French manuscript, which has been cited as the first case or the first Western reference to DVT.


title: Deep vein thrombosis

text: In 1856, German physician and pathologist Rudolf Virchow published his analysis after the insertion of foreign bodies into the jugular veins of dogs, which migrated to the pulmonary arteries. These foreign bodies caused pulmonary emboli, and Virchow was focused on explaining their consequences. He cited three factors, which are now understood as hypercoaguability, stasis, and endothelial injury. It was not until 1950 that this framework was cited as Virchow's triad, but the teaching of Virchow's triad has continued in light of its utility as a theoretical framework and as a recognition of the significant progress Virchow made in expanding the understanding of VTE.


title: Deep vein thrombosis

text: Methods to observe DVT by ultrasound were established in the 1960s. Diagnoses were commonly performed by impedance plethysmography in the 1970s and 1980s, but ultrasound, particularly after utility of probe compression was demonstrated in 1986, became the preferred diagnostic method. Yet, in the mid-1990s, contrast venography and impedance plethysmography were still described as common.


title: Deep vein thrombosis

text: Multiple pharmacological therapies for DVT were introduced in the 20th century: oral anticoagulants in the 1940s, subcutaneous injections of LDUH in 1962 and subcutaneous injections of LMWH in 1982. 1974 was when vascular inflammation and venous thrombosis were first proposed to be interrelated. For around 50 years, a months-long warfarin (Coumadin) regimen was the mainstay of pharmacological treatment. To avoid the blood monitoring required with warfarin and the injections required by heparin and heparin-like medicines, direct oral anticoagulants (DOACs) were developed. In the late 2000s to early 2010s, DOACs—including rivaroxaban (Xarelto), apixaban (Eliquis), and dabigatran (Pradaxa)—came to the market. "The New York Times" described a "furious battle" among the three makers of these drugs "for the prescription pads of doctors".


title: Deep vein thrombosis

text: VTE costs the US healthcare system about $7 to 10 billion dollars annually. Initial and average DVT costs for a hospitalized US patient is about $10,000 (2015 estimate). In Europe, the costs for an initial VTE hospitalization are significantly less, costing about €2000 to 4000 (2011 estimate). Post-thrombotic syndrome is a significant contributor to DVT follow-up costs. Outpatient treatment significantly reduces costs, and treatment costs for PE exceed those of DVT.


title: Deep vein thrombosis

text: A 2019 study published in "Nature Genetics" reported more than doubling the known genetic loci associated with VTE. In their updated 2018 clinical practice guidelines, the American Society of Hematology identified 29 separate research priorities, most of which related to patients who are acutely or critically ill. Inhibition of factor XI, P-selectin, E-selectin, and a reduction in formation of neutrophil extracellular traps are potential therapies that might treat VTE without increasing bleeding risk.


title: Formula One engines

text: Since its inception in 1947, Formula One has used a variety of engine regulations. "Formulae" limiting engine capacity had been used in Grand Prix racing on a regular basis since after World War I. The engine formulae are divided according to era.


title: Formula One engines

text: Formula One currently uses 1.6 litre four-stroke turbocharged 90 degree V6 double-overhead camshaft (DOHC) reciprocating engines. They were introduced in 2014 and have been developed over the subsequent seasons.


title: Formula One engines

text: The power a Formula One engine produces is generated by operating at a very high rotational speed, up to 20,000 revolutions per minute (rpm). However, they are electronically limited to 15,000 as of 2021 season. This contrasts with road car engines of a similar size, which typically operate at less than 6,000 rpm. The basic configuration of a naturally aspirated Formula One engine had not been greatly modified since the 1967 Ford Cosworth DFV and the mean effective pressure had stayed at around 14 bar. Until the mid-1980s Formula One engines were limited to around 12,000 rpm due to the traditional metal springs used to close the valves. The speed required to operate the engine valves at a higher rpm called for ever stiffer springs, which increased the power required to drive the camshaft and the valves to the point where the loss nearly offset the power gain through the increase in rpm. They were replaced by pneumatic valve springs introduced by Renault in 1986, which inherently have a rising rate (progressive rate) that allowed them to have an extremely high spring rate at larger valve strokes without much increasing the driving power requirements at smaller strokes, thus lowering the overall power loss. Since the 1990s, all Formula One engine manufacturers used pneumatic valve springs with the pressurised air allowing engines to reach speeds of over 20,000 rpm.


title: Formula One engines

text: Formula One cars use short-stroke engines. To operate at high engine speeds, the stroke must be relatively short to prevent catastrophic failure, usually from the connecting rod, which is under very large stresses at these speeds. Having a short stroke means a relatively large bore is required to reach a 1.6-litre displacement. This results in a less efficient combustion stroke, especially at lower rpm.


title: Formula One engines

text: In addition to the use of pneumatic valve springs, a Formula One engine's high rpm output has been made possible due to advances in metallurgy and design, allowing lighter pistons and connecting rods to withstand the accelerations necessary to attain such high speeds. Improved design also allows narrower connecting rod ends and so narrower main bearings. This permits higher rpm with less bearing-damaging heat build-up. For each stroke, the piston goes from a virtual stop to almost twice the mean speed (approximately 40 m/s), then back to zero. This occurs once for each of the four strokes in the cycle: one Intake (down), one Compression (up), one Power (ignition-down), one Exhaust (up). Maximum piston acceleration occurs at top dead center and is in the region of 95,000 m/s, about 10,000 times standard gravity (10,000 "g").


title: Formula One engines

text: Formula One engines have come through a variety of regulations, manufacturers and configurations through the years.


title: Formula One engines

text: This era used pre-war voiturette engine regulations, with 4.5 L atmospheric and 1.5 L supercharged engines. The Indianapolis 500 (which was a round of the World Drivers' Championship from 1950 onwards) used pre-war Grand Prix regulations, with 4.5 L atmospheric and 3.0 L supercharged engines. The power range was up to , though the BRM Type 15 of 1953 reportedly achieved with a 1.5 L supercharged engine.


title: Formula One engines

text: In 1952 and 1953, the World Drivers' Championship was run to Formula Two regulations, but the existing Formula One regulations remained in force and a number of Formula One races were still held in those years.


title: Formula One engines

text: Naturally-aspirated engine size was reduced to 2.5 L and supercharged cars were limited to 750 cc. No constructor built a supercharged engine for the World Championship. The Indianapolis 500 continued to use old pre-war regulations. The power range was up to .


title: Formula One engines

text: Introduced in 1961 amidst some criticism, the new reduced engine 1.5 L formula took control of F1 just as every team and manufacturer switched from front to mid-engined cars. Although these were initially underpowered, by 1965 average power had increased by nearly 50% and lap times were faster than in 1960. The old 2.5 L formula had been retained for International Formula racing, but this did not achieve much success until the introduction of the Tasman Series in Australia and New Zealand during the winter season, leaving the 1.5 L cars as the fastest single seaters in Europe during this time. The power range was between and .


title: Formula One engines

text: In 1966, with sports cars capable of outrunning Formula One cars thanks to much larger and more powerful engines, the FIA increased engine capacity to 3.0 L atmospheric and 1.5 L compressed engines. Although a few manufacturers had been clamouring for larger engines, the transition was not smooth and 1966 was a transitional year, with 2.0 L versions of the BRM and Coventry-Climax V8 engines being used by several entrants. The appearance of the standard-produced Cosworth DFV in 1967 made it possible for small manufacturers to join the series with a chassis designed in-house. Compression devices were allowed for the first time since 1960, but it was not until 1977 that a company actually had the finance and interest of building one, when Renault debuted their new Gordini V6 turbocharged engine at that year's British Grand Prix at Silverstone. This engine had a considerable power advantage over the naturally-aspirated Cosworth DFV, Ferrari and Alfa Romeo engines. By the start of the 1980s, Renault had proved that turbocharging was the way to go in order to stay competitive in Formula One, particularly at high-altitude circuits like Kyalami in South Africa and Interlagos in Brazil. Ferrari introduced their all-new V6 turbocharged engine in 1981, before Brabham owner Bernie Ecclestone managed to persuade BMW to manufacture straight-4 turbos for his team from 1982 onwards. In 1983, Alfa Romeo introduced a V8 turbo, and by the end of that year Honda and Porsche had introduced their own V6 turbos (the latter badged as TAG in deference to the company that provided the funding). Cosworth and the Italian Motori Moderni concern also manufactured V6 turbos during the 1980s, while Hart Racing Engines manufactured their own straight-4 turbo. By mid-1985, every Formula One car was running with a turbocharged engine. BMW's straight-4 turbo, the M12/13, produced around at over 5 bar of boost in qualifying trim, but was detuned to produce between in race spec. It powered the Brabham BT52 of , with which Nelson Piquet won that year's Drivers' Championship. By 1986, power figures were reaching unprecedented levels, with all engines reaching over during qualifying with unrestricted turbo boost pressures. This was especially seen with the BMW engines of Benetton's cars, reaching around 1,400 hp (1,040 kW) at a 5.5 bar boost pressure during qualifying. However, these engines and gearboxes were very unreliable because of the engine's immense power, and would only last about four laps. For the race, the turbocharger's boost was restricted to ensure engine reliability; but the engines still produced during the race. The power range from 1966 to 1986 was between to , turbos to in race trim, and in qualifying, up to . Following their experiences at Indianapolis, in 1971 Lotus made a few unsuccessful experiments with a Pratt & Whitney turbine fitted to chassis which also had four-wheel-drive.


title: Formula One engines

text: Following the turbo domination, forced induction was allowed for two seasons before its eventual ban. The FIA regulations limited boost pressure, to 4 bar in qualifying in 1987 for 1.5 L turbo; and allowed a larger 3.5 L formula. These seasons were still dominated by turbocharged engines, the Honda RA167E V6 supplying Nelson Piquet winning the 1987 Formula One season on a Williams also winning the constructors championship, followed by TAG-Porsche P01 V6 in McLaren then Honda again with the previous RA166E for Lotus then Ferrari's own 033D V6.


title: Formula One engines

text: The rest of the grid was powered by the Ford GBA V6 turbo in Benetton, with the only naturally-aspirated engine, the DFV-derived Ford-Cosworth DFZ 3.5 L V8 outputting in Tyrrell, Lola, AGS, March and Coloni. The massively powerful BMW M12/13 inline-four found in the Brabham BT55 tilted almost horizontally, and in upright position under the Megatron brand in Arrows and Ligier, producing at 3.8 bar in race trim, and an incredible at 5.5 bar of boost in qualifying spec. Zakspeed was building its own turbo inline-four, Alfa Romeo was to power the Ligiers with an inline-four but the deal fell through after initial testing had been carried out. Alfa was still represented by its old 890T V8 used by Osella, and Minardi was powered by a Motori Moderni V6.


title: Formula One engines

text: In , six teams – McLaren, Ferrari, Lotus, Arrows, Osella and Zakspeed – continued with turbocharged engines, now limited to 2.5 bar. Honda's V6 turbo, the RA168E, which produced at 12,300 rpm in qualifying, powered the McLaren MP4/4 with which Ayrton Senna and Alain Prost won fifteen of the sixteen races between them. The Italian Grand Prix was won by Gerhard Berger in the Ferrari F1/87/88C, powered by the team's own V6 turbo, the 033E, with about at 12,000 rpm in qualifying. The Honda turbo also powered Lotus's 100T, while Arrows continued with the Megatron-badged BMW turbo, Osella continued with the Alfa Romeo V8 (now badged as an Osella) and Zakspeed continued with their own straight-4 turbo. All the other teams used naturally aspirated 3.5 L V8 engines: Benetton used the Cosworth DFR, which produced at 11,000 rpm; Williams, March and Ligier used the Judd CV, producing ; and the rest of the grid used the previous year's Cosworth DFZ.


title: Formula One engines

text: Turbochargers were banned from the 1989 Formula One season, leaving only a naturally aspirated 3.5 L formula. Honda was still dominant with their RA109E 72° V10 giving @ 13,500 rpm on McLaren cars, enabling Prost to win the championship in front of his teammate Senna. Behind were the Renault RS1-powered Williams, a 67° V10 giving @ 12,500 rpm. Ferrari with its 035/5 65° V12 giving at 13,000 rpm. Behind, the grid was powered mainly by Ford Cosworth DFR V8 giving @ 10,750 rpm except for a few Judd CV V8 in Lotus, Brabham and EuroBrun cars, and two oddballs: the Lamborghini 3512 80° V12 powering Lola, and the Yamaha OX88 75° V8 in Zakspeed cars. Ford started to try its new design, the 75° V8 HBA1 with Benetton.


title: Formula One engines

text: The 1990 Formula One season was again dominated by Honda in McLarens with the @ 13,500 rpm RA100E powering Ayrton Senna and Gerhard Berger ahead of the @ 12,750 rpm Ferrari Tipo 036 of Alain Prost and Nigel Mansell. Behind them the Ford HBA4 for Benetton and Renault RS2 for Williams with @ 12,800 rpm were leading the pack powered by Ford DFR and Judd CV engines. The exceptions were the Lamborghini 3512 in Lola and Lotus, and the new Judd EV 76° V8 giving @ 12,500 rpm in Leyton House and Brabham cars. The two new contenders were the Life which built for themselves an F35 W12 with three four cylinders banks @ 60°, and Subaru giving Coloni a 1235 flat-12 from Motori Moderni


title: Formula One engines

text: Honda was still leading the 1991 Formula One season in Senna's McLaren with the @ 13,500–14,500 rpm 60° V12 RA121E, just ahead of the Renault RS3 powered Williams benefiting from @ 12,500–13,000 rpm. Ferrari was behind with its Tipo 037, a new 65° V12 giving @ 13,800 rpm also powering Minardi, just ahead the Ford HBA4/5/6 in Benetton and Jordan cars. Behind, Tyrrell was using the previous Honda RA109E, Judd introduced its new GV with Dallara leaving the previous EV to Lotus, Yamaha were giving its OX99 70° V12 to Brabham, Lamborghini engines were used by Modena and Ligier. Ilmor introduced its LH10, a @ 13,000 rpm V10 which eventually became the Mercedes with Leyton House and Porsche sourced a little successful 3512 V12 to Footwork Arrows; the rest of the field was Ford DFR powered.


title: Formula One engines

text: In 1992, the Renault engines became dominant, even more so following the departure from the sport of Honda at the end of 1992. The 3.5 L Renault V10 engines powering the Williams F1 team produced a power output between @ 13,000–14,300 rpm toward the end of the 3.5 L naturally-aspirated era, between 1992 and 1994. Renault-engined cars won the last three consecutive world constructors' championships of the 3.5 L formula era with Williams (1992–1994).


title: Formula One engines

text: The Peugeot A4 V10, used by the McLaren Formula One team in 1994, initially developed @ 14,250 rpm. It was later further developed into the A6, which produced even more power, developing @ 14,500 rpm.


title: Formula One engines

text: The "EC Zetec-R" V8, which powered the championship-winning Benetton team and Michael Schumacher in 1994, produced between @ 14,500 rpm.


title: Formula One engines

text: By the end of the 1994 season, Ferrari's "Tipo 043" V12 was putting out around @ 15,800 rpm, which is to date the most-powerful naturally-aspirated V12 engine ever used in Formula One. This was also the most powerful engine of 3.5-litre engine regulation era, before a reduction in engine capacity to 3 litres in 1995.


title: Formula One engines

text: This era used a 3.0 L formula, with the power range varying (depending on engine tuning) between and , between 13,000 rpm and 20,000 rpm, and from eight to twelve cylinders. Despite engine displacement being reduced from 3.5 L, power figures and RPMs still managed to climb. Renault was the initial dominant engine supplier from 1995 until 1997, winning the first three world championships with Williams and Benetton in this era. The championship-winning 1995 Benetton B195 produced a power output of @ 15,200 rpm, and the 1996 championship-winning Williams FW18 produced @ 16,000 rpm; both from a shared Renault RS9 3.0 L V10 engine. The 1997 championship-winning FW19 produced between @ 16,000 rpm, from its Renault RS9B 3.0 L V10. Ferrari's last V12 engine, the "Tipo 044/1", was used in . The engine's design was largely influenced by major regulation changes imposed by the FIA after the dreadful events during the year before: the V12 engine was reduced from 3.5 to 3.0 litres. The 3.0-litre engine produced around 700 hp (522 kW) 17,000 rpm in race trim; but was reportedly capable of producing up to 760 hp (567 kW) in its highest state of tune for qualification mode. Between 1995 and 2000, cars using this 3.0 L engine formula, imposed by the FIA, produced a constant power range (depending on engine type and tuning), varying between 600 hp and 815 hp. Most Formula One cars during the season comfortably produced a consistent power output of between , depending on whether a V8 or V10 engine configuration was used. From 1998 to 2000 it was Mercedes' power that ruled, giving Mika Häkkinen two world championships. The 1999 McLaren MP4/14 produced between 785 and 810 hp @ 17,000 rpm. Ferrari gradually improved their engine. In , they changed from their traditional V12 engine to a smaller and lighter V10 engine. They preferred reliability to power, losing out to Mercedes in terms of outright power initially. Ferrari's first V10 engine, in 1996, produced @ 15,550 rpm, down on power from their most powerful 3.5 L V12 (in 1994), which produced over @ 15,800 rpm, but up on power from their last 3.0 L V12 (in 1995), which produced @ 17,000 rpm. At the 1998 Japanese GP, Ferrari's 047D engine spec was said to produce over , and from 2000 onward, they were never short of power or reliability. To keep costs down, the 3.0 L V10 engine configuration was made fully mandatory for all teams in 2000 so that engine builders would not develop and experiment with other configurations. The V10 configuration had been the most popular since the banning of turbocharged engines in 1989, and no other configuration had been used since 1998.


title: Formula One engines

text: BMW started supplying its engines to Williams from 2000. The engine was very reliable in the first season though slightly short of power compared to Ferrari and Mercedes units. The BMW E41-powered Williams FW22 produced around 810 hp @ 17,500 rpm, during the 2000 season. BMW went straight forward with its engine development. The P81, used during the 2001 season, was able to hit 17,810 rpm. Unfortunately, reliability was a large issue with several blowups during the season.


title: Formula One engines

text: The BMW P82, the engine used by the BMW WilliamsF1 Team in 2002, had hit a peak speed of 19,050 rpm in its final evolutionary stage. It was also the first engine in the 3.0 litre V10-era to break through the 19,000 rpm wall, during the 2002 Italian Grand Prix's qualifying. BMW's P83 engine used in 2003 season managed an impressive 19,200 rpm and cleared the mark, at around 940 bhp, and weighs less than . Honda's "RA003E" V10 also cleared the mark at the 2003 Canadian Grand Prix.


title: Formula One engines

text: In 2005, the 3.0 L V10 engine was permitted no more than 5 valves per cylinder. Also, the FIA introduced new regulations limiting each car to one engine per two Grand Prix weekends, putting the emphasis on increased reliability. In spite of this, power outputs continued to rise. Mercedes engines had about in this season. Cosworth, Mercedes, Renault, and Ferrari engines all produced around to @ 19,000 rpm. Honda had over . The BMW engine made over . Toyota engines had over , according to Toyota Motorsport's executive Vice President, Yoshiaki Kinoshita. However, for reliability and longevity purposes, this power figure may have been detuned to around for races.


title: Formula One engines

text: For 2006, the engines had to be 90° V8 of 2.4 litres maximum capacity with a circular bore of maximum, which implies a stroke at maximum bore. The engines must have two inlet and two exhaust valves per cylinder, be naturally aspirated and have a minimum weight. The previous year's engines with a rev-limiter were permitted for 2006 and 2007 for teams who were unable to acquire a V8 engine, with Scuderia Toro Rosso using a Cosworth V10, after Red Bull's takeover of the former Minardi team did not include the new engines. The 2006 season saw the highest rev limits in the history of Formula One, at well over 20,000 rpm; before a 19,000 rpm mandatory rev limiter was implemented for all competitors in 2007. Cosworth was able to achieve just over 20,000 rpm with their V8, and Renault around 20,500 rpm. Honda did the same; albeit only on the dynamometer.


title: Formula One engines

text: Pre-cooling air before it enters the cylinders, injection of any substance other than air and fuel into the cylinders, variable-geometry intake and exhaust systems, and variable valve timing were forbidden. Each cylinder could have only one fuel injector and a single plug spark ignition. Separate starting devices were used to start engines in the pits and on the grid. The crankcase and cylinder block had to be made of cast or wrought aluminium alloys. The crankshaft and camshafts had to be made from an iron alloy, pistons from an aluminium alloy, and valves from alloys based on iron, nickel, cobalt or titanium. These restrictions were in place to reduce development costs on the engines.


title: Formula One engines

text: The reduction in capacity was designed to give a power reduction of around 20% from the three-litre engines, to reduce the increasing speeds of Formula One cars. Despite this, in many cases the performance of the car improved. In 2006 Toyota F1 announced an approximate output at 18,000 rpm for its new RVX-06 engine, but real figures are of course difficult to obtain. Most cars from this period (2006–2008) produced a regular power output of approximately between 720 and 800 hp @ 19,000 rpm (over 20,000 rpm for the season).


title: Formula One engines

text: The engine specification was frozen in 2007 to keep development costs down. The engines which were used in the 2006 Japanese Grand Prix were used for the 2007 and 2008 seasons and they were limited to 19,000 rpm. In 2009 the limit was reduced to 18,000 rpm with each driver allowed to use a maximum of 8 engines over the season. Any driver needing an additional engine is penalised 10 places on the starting grid for the first race the engine is used. This increases the importance of reliability, although the effect is only seen towards the end of the season. Certain design changes intended to improve engine reliability may be carried out with permission from the FIA. This has led to some engine manufacturers, notably Ferrari and Mercedes, exploiting this ability by making design changes which not only improve reliability but also boost engine power output as a side effect. As the Mercedes engine was proven to be the strongest, re-equalisations of engines were allowed by the FIA to allow other manufacturers to match the power.


title: Formula One engines

text: 2009 saw the exit of Honda from Formula One. The team was acquired by Ross Brawn, creating Brawn GP and the BGP 001. With the absence of the Honda engine, Brawn GP retrofitted the Mercedes engine to the BGP 001 chassis. The newly branded team won both the Constructors' Championship and the Drivers' Championship from better-known and better-established contenders Ferrari, McLaren-Mercedes, and Renault.


title: Formula One engines

text: Cosworth, absent since the 2006 season, returned in 2010. New teams Lotus Racing, HRT, and Virgin Racing, along with the established Williams, used this engine. The season also saw the withdrawal of the BMW and Toyota engines, as the car companies withdrew from Formula One due to the recession.


title: Formula One engines

text: In 2009, constructors were allowed to use kinetic energy recovery systems (KERS), also called regenerative brakes. Energy can either be stored as mechanical energy (as in a flywheel) or as electrical energy (as in a battery or supercapacitor), with a maximum power of 81 hp (60 kW; 82 PS) deployed by an electric motor, for a little over 6 seconds per lap. Four teams used it at some point in the season: Ferrari, Renault, BMW, and McLaren.


title: Formula One engines

text: Although KERS was still legal in F1 in the 2010 season, all the teams agreed not to use it. KERS returned for the 2011 season, when only three teams elected not to use it. For the 2012 season, only Marussia and HRT raced without KERS, and in 2013 all teams on the grid had KERS. From 2010 to 2013 cars have a regular power of 700–800 hp, averaging around 750 hp @ 18,000 rpm.


title: Formula One engines

text: The FIA announced to change the 2.4-litre V8 to 1.6-litre V6 hybrid engines for the 2014 season. The new regulations allow kinetic and heat energy recovery systems. Forced induction is now allowed, and instead of limiting the boost level, fuel flow restriction at 100 kg of petrol per hour maximum is introduced. The engines sounded very different due to the lower rev limit (15,000 rpm) and the turbocharger. While superchargers are allowed, all constructors opted to use a turbo.


title: Formula One engines

text: The new formula allows turbocharged engines, which last appeared in . These have their efficiency improved through turbo-compounding by recovering energy from exhaust gases. The original proposal for four-cylinder turbocharged engines was not welcomed by the racing teams, in particular Ferrari. Adrian Newey stated during the 2011 European Grand Prix that the change to a V6 enables teams to carry the engine as a stressed member, whereas an inline-4 would have required a space frame. A compromise was reached, allowing V6 forced induction engines instead. The engines rarely exceed 12,000 rpm during qualifying and race, due to the new fuel flow restrictions.


title: Formula One engines

text: Energy recovery systems such as KERS had a boost of and 2 megajoules per lap. KERS was renamed Motor Generator Unit–Kinetic (). Heat energy recovery systems were also allowed, under the name Motor Generator Unit–Heat ()


title: Formula One engines

text: The 2015 season was an improvement on 2014, adding about 30–50 hp (20–40 kW) to most engines, the Mercedes engine being the most powerful with 870 hp (649 kW). In 2019, Renault's engine was claimed to have hit 1,000 hp in qualifying trim.


title: Formula One engines

text: Of the previous manufacturers, only Mercedes, Ferrari and Renault produced engines to the new formula in 2014, whereas Cosworth stopped supplying engines. Honda returned in 2015 with their own engine, while McLaren used Honda power, changing from Mercedes power in 2014. In 2019, Red Bull switched from using a Renault engine to Honda power. Honda supplies both Red Bull and AlphaTauri. Honda are due to withdraw as a power unit supplier at the end of , with Red Bull taking over the project and producing the engine in-house.