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SOBRE NOTICIAS EN ESPAÑOLNoticias en español es una sección de Kaiser Health News que contiene traducciones de artículos de gran interés para la comunidad hispanohablante, y contenido original enfocado buy furosemide online without a prescription en la población hispana que vive en los Estados Unidos. Use Nuestro Contenido Este buy furosemide online without a prescription contenido puede usarse de manera gratuita (detalles). El doctor Chris Kjolhede está enfocado en los niños del centro de Nueva York.Como codirector de los centros de salud escolares de Bassett Healthcare Network, el pediatra supervisa alrededor de 21 clínicas de salud escolares en toda la región, una zona rural pobre conocida por sus fábricas y paralizada por la epidemia de opioides. Desde un esguince de tobillo en el buy furosemide online without a prescription recreo hasta preguntas sobre el control de la natalidad, las clínicas sirven como proveedoras de atención primaria para muchos estudiantes, dentro y fuera del aula.La meta principal es asegurarse que los niños estén al día con las vacunas obligatorias, dijo Kjolhede.Pero, en marzo, COVID revocó el acuerdo cuando obligó a cerrar las escuelas.Lo primero que me pregunté, dijo Kjolhede, fue.

€œÂ¿qué va a pasar ahora?. €.Las escuelas juegan un papel fundamental en los buy furosemide online without a prescription esfuerzos de vacunación en los Estados Unidos. Las leyes requieren que los niños tengan ciertas vacunas para inscribirse y asistir a clases.Pero para evitar que COVID-19 no siguiera propagándose, muchos distritos escolares han optado por comenzar el año académico en internet.La decisión neutraliza en muchos casos el impulso de los padres por vacunar a sus hijos para el regreso a la escuela, dijo el doctor Nathaniel Beers, miembro del Consejo de Salud Escolar de la Academia Americana de Pediatría.Beers, quien también ocupó varios roles en el sistema de Escuelas Públicas del Distrito de Columbia, agregó que si la educación no es en persona, “es más difícil de hacer cumplir los requisitos”.Los funcionarios de salud pública han confiado en las escuelas como un medio para controlar las enfermedades prevenibles por vacunas durante más de un siglo. Las leyes de vacunación surgieron por primera vez buy furosemide online without a prescription en la década de 1850 en Massachusetts como un medio para controlar la viruela, según cuentan los Centros para el Control y Prevención de Enfermedades (CDC).Todos los estados requieren que los niños reciban ciertas vacunas contra enfermedades como la poliomielitis, las paperas y el sarampión antes de empezar el año escolar o al jardín de infantes, al menos que el niño tenga una exención médica.Algunos estados permiten a las personas optar por no vacunar a los niños por razones religiosas o filosóficas, aunque estas exenciones se han asociado con brotes de enfermedades que de otro modo estarían bien controladas, como por ejemplo el sarampión.“Cuando entran al sistema, en preescolar, es donde se detecta si están atrasados con sus vacunas”, dijo Claire Hannan, directora ejecutiva de la Asociación de Administradores de Inmunización.A nivel local, la responsabilidad de rastrear si los estudiantes cumplen con los requisitos de vacunación generalmente recae en la enfermera de la escuela.

Si no, un oficinista o administrador hace el trabajo, dijo Linda Mendonca, presidenta electa de la Asociación Nacional de Enfermeras Escolares.Si no los cumplen, algunas escuelas trabajan con los padres para programar citas con un proveedor de salud. Otras aíslan a los niños en buy furosemide online without a prescription el aula, y otras son tan estrictas que “ni siquiera puedes cruzar la puerta a menos que estés debidamente inmunizado”, dijo Beers.La pandemia de COVID-19 ha provocado una baja dramática en la vacunación. En mayo, un informe de los CDC mostró una fuerte caída en la cantidad de pedidos al programa Vaccines For Children, una iniciativa federal que compra vacunas para la mitad de los niños del país.Un segundo comunicado reveló tendencias similares. La cobertura de vacunación en Michigan disminuyó entre todas buy furosemide online without a prescription las edades, con la excepción de las vacunas que se administran al nacer, que generalmente se dan en el hospital.En Pennsylvania, por ejemplo, el Departamento de Salud estatal suspendió en julio los requisitos de vacunas durante dos meses después del inicio del año escolar.“El departamento no puede enfatizar más que hay que vacunarse lo antes posible”, dijo Nate Wardle, secretario de prensa del departamento de salud de ese estado, en una declaración escrita.

Sin embargo, la orden de permanecer en casa por COVID hizo que durante meses los consultorios pediátricos no hicieran citas con niños sanos.Beers reconoció que el cierre de las escuelas, entre otras acciones como restringir los viajes y cerrar grandes espacios de reunión, hace que los niños sean menos propensos a contraer o propagar enfermedades que generalmente se incuban en las aulas. Por ejemplo, según los datos buy furosemide online without a prescription de los CDC, el sarampión prácticamente ha desaparecido. Se habían reportado 12 casos hasta el 19 de agosto de este año, en comparación con 1,282 en 2019.“Lo que sería una gran vergüenza es que las escuelas vuelvan a abrir en persona y los niños vuelvan a estar juntos y empecemos a tener brotes de otras enfermedades que se pueden prevenir con vacunas”, agregó.Los centros de salud de buy furosemide online without a prescription las escuelas de Nueva York se están comunicando activamente con los padres sobre las vacunas. En Cooperstown, Kjolhede se acercó a todos los superintendentes poco después del cierre en marzo para preguntar si la clínica podía permanecer abierta.

Todos menos uno dijeron que buy furosemide online without a prescription no.Luego, el personal concertó citas de telesalud y llamó a los estudiantes que necesitaban atención en persona para concertar visitas, incluidos aquellos que necesitaban una vacuna antes del comienzo de este año escolar, dijo. Afortunadamente, el centro de salud que permaneció abierto tenía una puerta que permitía a los pacientes ingresar a la clínica sin caminar por la escuela.A varias horas de distancia, la doctora Lisa Handwerker está lidiando con la forma de abordar el problema de que cientos de estudiantes en sus seis clínicas de salud en las escuelas de la ciudad de Nueva York no han recibido vacunas mandatorias.El departamento de salud de la ciudad le dio una lista de estudiantes bajo su cuidado que necesitaban vacunas adicionales, dijo. A más de 400 niños les faltaba la buy furosemide online without a prescription segunda dosis para prevenir la meningitis meningocócica, que generalmente se administra a adolescentes y adultos jóvenes de 16 a 23 años. Debido a que el departamento usó datos del último año académico para compilar la lista, Handwerker no tiene información sobre nuevos estudiantes.

Algunas familias abandonaron la ciudad por la falta de ingresos y recursos provocada buy furosemide online without a prescription por la pandemia.“Tuvimos dificultades con al menos la mitad de los niños en nuestra lista de vacunas”, dijo Handwerker. €œLuego, cuando hablamos a las familias, se mostraron reacias a salir de sus casas”.Ese no fue el caso de Tracey Wolf, una madre de dos hijos que visitó al médico recientemente para vacunar a su hijo Jordan contra el sarampión, las paperas, la rubéola y el VPH antes de comenzar el séptimo grado. Asistirá a la escuela secundaria en buy furosemide online without a prescription Dunedin, Florida, en persona, dijo Wolf, de 38 años.Parecía una tontería mantener a Jordan, de 13 años, alejado de sus compañeros de clase cuando ya juega béisbol y sale con sus amigos, dijo. Sus calificaciones también bajaron la primavera pasada cuando la amenaza COVID transformó su salón de clases en una computadora.También llevó a su hijo de 6 meses a recibir sus vacunas.

Cuando se le preguntó si buy furosemide online without a prescription tenía miedo de ir al consultorio de su médico, respondió. €œNo más que ir al supermercado”.Independientemente de si un niño comienza la escuela en casa o en el aula, los expertos en inmunización enfatizaron la importancia de vacunar siguiendo el calendario de inmunizaciones. Esas fechas tienen en cuenta la etapa de desarrollo del niño para maximizar la eficacia de buy furosemide online without a prescription la vacuna. Dicho esto, es preferible que los niños reciban las vacunas de su médico habitual para evitar la pérdida de los registros de vacunación y las vacunas adicionales, completó Beers.Sin embargo, el 19 de agosto, el Departamento de Salud y Servicios Humanos (HHS) emitió una declaración que permite a los farmacéuticos administrar vacunas infantiles a niños y adolescents de 3 a 18 buy furosemide online without a prescription años.

Carmen Heredia Rodriguez. CarmenH@kff.org, @ByCHRodriguez Related Topics buy furosemide online without a prescription Noticias En Español Public Health Children's Health COVID-19 VaccinesAlthough the coronavirus pandemic shut down many organizations and businesses across the nation, KHN has never been busier ― and health coverage has never been more vital. We’ve revamped our Behind the Byline YouTube series and brought it to Instagram TV.Journalists and producers from across KHN’s newsrooms take you behind the scenes in these bite-size videos to show the ways they are following the story, connecting with sources and sorting through facts — all while staying safe.Heidi de Marco — “At Least I Got the Shot” Photojournalist Heidi de Marco’s stunning images transport viewers to two California hospitals near the U.S.-Mexico border where the influx of patients with COVID-19 overwhelmed local intensive care units in late May. To capture these scenes at El Centro Regional Medical Center in Imperial County and Scripps Mercy Hospital Chula buy furosemide online without a prescription Vista in San Diego County, de Marco donned personal protective equipment and followed each facility’s safety guidelines.

Still, she acknowledges, the work increased her risk of exposure to the coronavirus. She also risked bringing the virus home to her family buy furosemide online without a prescription. For her it was worth the risk, in order to give readers a window on health care in the midst of a pandemic — and to share her work with the world. This KHN buy furosemide online without a prescription story first published on California Healthline, a service of the California Health Care Foundation.

Heidi de Marco. heidid@kff.org, @Heidi_deMarco Related Topics California Multimedia Public Health States Behind The Byline COVID-19Can’t see the audio buy furosemide online without a prescription player?. Click here to listen. About This Podcast Health care — and how much it costs — buy furosemide online without a prescription is scary.

But you’re not alone with this stuff, and knowledge is power. €œAn Arm and a Leg” is a podcast buy furosemide online without a prescription about these issues, and its second season is co-produced by KHN. Barbara Faubion’s boss, an buy furosemide online without a prescription insurance broker, used to tell clients. €œListen, you don’t need to be on the phone for four hours with Blue Cross Blue Shield.

Let us buy furosemide online without a prescription do that. I have a person.”Faubion was that person. And she got up every buy furosemide online without a prescription day psyched to go to work, which she said puzzled her friends.“They’d go, ‘You love your job?. !.

?. You spend your whole day talking to an insurance company. Are you kidding me?. €™â€She was not kidding.

Faubion loved to win — and she was really, really good at untangling other people’s health insurance problems.Now she’s going to teach us some of what she knows.So why doesn’t every health insurance broker have someone like Faubion on staff?. ProPublica reporter Marshall Allen has that answer. There are big clues in his 2019 story about industry commissions and bonuses.“An Arm and a Leg” is a co-production of Kaiser Health News and Public Road Productions.To keep in touch with “An Arm and a Leg,” subscribe to the newsletter. You can also follow the show on Facebook and Twitter.

And if you’ve got stories to tell about the health care system, the producers would love to hear from you.To hear all Kaiser Health News podcasts, click here.And subscribe to “An Arm and a Leg” on iTunes, Pocket Casts, Google Play or Spotify. Related Topics Cost and Quality Health Care Costs Health Industry Insurance Multimedia An Arm and a Leg PodcastsThis story also ran on USA Today. This story can be republished for free (details). Dr. Chris Kjolhede is focused on the children of central New York.As co-director of school-based health centers at Bassett Healthcare Network, the pediatrician oversees about 21 school-based health clinics across the region — a poor, rural area known for manufacturing and crippled by the opioid epidemic.From ankles sprained during recess to birth control questions, the clinics serve as the primary care provider for many children both in and out of the classroom. High on the to-do list is making sure kids are up to date on required vaccinations, said Kjolhede.But, in March, COVID upended the arrangement when it forced schools to close.“It was like, holy smokes,” he said, “what’s going to happen now?.

€ Email Sign-Up Subscribe to KHN’s free Morning Briefing. Schools play a pivotal role in U.S. Vaccination efforts. Laws require children to have certain immunizations to enroll and attend classes.But this academic year, to prevent COVID-19 from spreading, many school districts have opted to start classes online.

The decision takes away much of the back-to-school leverage pushing parents to stay current on their children’s shots, said Dr. Nathaniel Beers, member of the Council on School Health for the American Academy of Pediatrics. If schooling is not happening in person, said Beers, who also led multiple roles in the District of Columbia Public Schools system, “it is harder to enforce.”Public health officials have relied on schools as a means to control vaccine-preventable diseases for over a century. Vaccination laws that require immunizations to enter school first emerged in the 1850s in Massachusetts as a means to control smallpox, as the Centers for Disease Control and Prevention has noted.Every state requires children to receive certain vaccinations against illnesses like polio, mumps and measles before entering the classroom or a child care center, unless the child has a medical exemption.

Some states allow people to opt children out of vaccinations for religious or philosophical reasons, although these exemptions have been associated with outbreaks of otherwise well-controlled diseases like measles.“If they get behind or they don’t get specific vaccines they need, kindergarten is a real catch point to get them up to speed and make sure they’re up to date,” said Claire Hannan, executive director of the Association of Immunization Managers.At the local level, the responsibility of tracking whether students are compliant generally falls on the school nurse. If one is not present, a clerical worker or administrator does the job, said Linda Mendonca, president-elect of the National Association of School Nurses. Usually, school systems face a deadline for checking every child’s record and reporting compliance to government health officials, she said.How districts choose to hold noncompliant children accountable varies, Beers said. Some schools work with parents to set up appointments with a provider.

Some isolate children in a classroom, he said, and some are so strict that “you can’t even walk through the door unless you are appropriately immunized.”The COVID-19 pandemic has resulted in steep declines in vaccinations. In May, a report from the CDC showed a sharp drop in the number of orders submitted to the Vaccines For Children program, a federal initiative that purchases vaccines for half the children in the U.S. A second release revealed similar trends — vaccination coverage in Michigan declined among all milestone ages, with the exception of immunizations given at birth, which are generally done in a hospital.Making Backup PlansIn Pennsylvania, for instance, the state health department in July suspended vaccine requirements for two months after the start of the school year. In addition to causing delays in doctors’ offices, the state said, the pandemic may also prevent school and public health nurses from holding in-school “catch-up” vaccination clinics.“The department cannot stress enough that as soon as children can be vaccinated, they should be,” said Nate Wardle, press secretary for the state’s health department, in a written statement.

However, the lockdown order prompted by COVID meant “that there was a several month period in some parts of the state where well-child visits were not occurring.”Members of the American Academy of Pediatrics, the National Association of School Nurses and the Association of Immunization Managers said the grace periods are a prudent step to account for the pandemic’s effect on pediatric care. The majority of children already have some protection from diseases from previous vaccines, they said.Additionally, Beers acknowledged that closing schools — among other actions like restricting travel and shuttering large gathering spaces — make children less likely to contract or spread illnesses that typically incubate in classrooms. For example, according to CDC data, measles has essentially disappeared — 12 cases had been reported as of Aug. 19 this year, compared with 1,282 throughout 2019.However, schooling will eventually resume in person, which will also bring back the risks of illnesses moving through classrooms, Beers said.

And school systems may be less forgiving of children who enter the classroom without the needed vaccinations.“What would be an immense shame is if schools reopen in person and children are back together and we start getting outbreaks of other diseases that are preventable based on immunizations,” he said.School-based health centers in New York are actively contacting parents about vaccinations. In Cooperstown, Kjolhede reached out to every superintendent soon after the lockdown in March to ask if the clinic could remain open. All but one said no.The staff then set up telehealth appointments and phoned students who needed in-person care to arrange visits — including those who needed a vaccine before the start of this school year, he said. Luckily, the health center that remained open had a door that allowed patients to enter the clinic without walking through the school.Several hours away, Dr.

Lisa Handwerker is grappling with how to tackle the problem that hundreds of students across her six school-based health clinics in New York City have missed a required vaccine.The city’s health department gave her a list of students in her care who needed additional immunizations, she said. Over 400 children were missing the second dose to prevent meningococcal meningitis, generally given to teens and young adults ages 16 to 23. Because the department used data from the last academic year to compile the list, Handwerker has no information about new students. Some families left the city because of the lack of income and resources caused by the pandemic.“We had difficulty with at least half of the kids on our vaccine list,” Handwerker said.

€œThen when we reached families, they were reluctant to leave their houses.”A Shot at NormalcyThat wasn’t the case for Tracey Wolf, a mother of two who visited the doctor recently to get her son Jordan vaccinated for measles, mumps, rubella and HPV before starting the seventh grade. He will be attending middle school in Dunedin, Florida, in person, said Wolf, 38.It seemed nonsensical to keep Jordan, 13, from his classmates when he already plays baseball and hangs out with his friends, she said. His grades also slipped last spring when the COVID threat transformed his classroom into a computer.She also took her 6-month-old Ethan for his immunizations. When asked whether she was afraid of going into her doctor’s office, she replied, “Not more than going to the grocery store.”Regardless of whether a child starts school at home or in the classroom, immunization experts stressed the importance of vaccinating a child on time.

The schedules factor in a child’s stage of development to maximize the vaccine’s effectiveness. That said, it is preferable that children get their vaccines from their regular doctor to prevent lost immunization records and additional shots, said Beers.Yet on Aug. 19, the Department of Health and Human Services released a statement allowing pharmacists to provide childhood immunizations for children ages 3 to 18. Carmen Heredia Rodriguez.

CarmenH@kff.org, @ByCHRodriguez Related Topics Public Health Children's Health COVID-19 Vaccines.

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Influenza affects millions of people each year, and because of the furosemide mylan 40mg COVID-19 pandemic, many physicians and health experts are concerned that this year’s flu season will hit with full force. In the Lone Star State, it’s important for Texans to be proactive about their health by getting the yearly flu vaccination. One of the worst things that could happen would be having many people sick with the flu while many are ill with coronavirus.Flu furosemide mylan 40mg vaccination is the best way to reduce the risk of getting and spreading the flu. This year, it also will help keep hospitalizations down as physicians, nurses, and other medical staff continue to care for COVID-19 patients.

Traditionally, Texas falls behind on flu vaccination furosemide mylan 40mg. According to the Centers for Disease Control and Prevention (CDC), only 43.3% of Texas adults got a flu shot in 2018-2019, compared to the national average of 45.3%.Although influenza viruses circulate throughout the year, flu season usually starts in the fall and winter, and peaks between December and February.Like COVID-19, the flu is contagious. Both have some furosemide mylan 40mg similar symptoms, including fever, chills, cough, fatigue, body aches, vomiting, and diarrhea. People with the flu may not experience symptoms until one to four days after catching the virus.

The CDC outlines key similarities and differences between influenza and COVID-19 here.While most people recover from the flu, many can experience complications, especially older adults, people with pre-existing medical furosemide mylan 40mg conditions, young children, and pregnant women. If left untreated, infected patients can develop pneumonia, inflammation of the heart, brain, or muscle tissues, organ failure, sepsis, or they could even die. In Texas, more than 21,000 people died from the flu in the past two furosemide mylan 40mg years. To put that into perspective, that is the population of Katy!.

Everyone 6 furosemide mylan 40mg months or older is encouraged to get the flu vaccine each year – especially adults aged 65 and older, pregnant women, young children, and people who have chronic illnesses such as diabetes, asthma, and heart disease. The CDC is urging the public to get the flu vaccine while maintaining social distancing, wearing a mask in public, and practicing good hygiene.People who receive the flu shot may experience some mild side effects like aches and a mild fever, but they can’t get the flu from the shot. Those who get the flu after being vaccinated might have been exposed to the virus beforehand. The flu vaccination can help lessen flu symptoms and severity, helping reduce the amount of time spent away from work and school.In a time when community health furosemide mylan 40mg is front and center, getting a flu shot is more important than ever.

The Texas Medical Association’s Be Wise Immunize℠ program recently created a downloadable poster below in English and Spanish with key takeaways about the flu vaccination. You can print furosemide mylan 40mg the poster, or save it and share it on social media. Be Wise – Immunize is funded in 2020 by the TMA Foundation, thanks to major support from H-E-B and Permian Basin Youth Chavarim.Be Wise – Immunize is a service mark of the Texas Medical Association.Lauren Gambill, MDPediatrician, AustinMember, Texas Medical Association (TMA) Committee on Child and Adolescent HealthExecutive Board Member, Texas Pediatric SocietyDoctors are community leaders. This role has become even more important during the furosemide mylan 40mg COVID-19 pandemic.

As patients navigate our new reality, they are looking to us to determine what is safe, how to protect their families, and the future of their health care. As more Texans lose their jobs, their health insurance, or even their homes, it is crucial that Texas receives furosemide mylan 40mg the resources it needs to uphold our social safety net. The U.S. Census helps determine funding for those resources, and that is why it is of the upmost importance that each and furosemide mylan 40mg every Texan, no matter address, immigration status, or age, respond to the 2020 U.S.

Census. The deadline has been cut short one month and furosemide mylan 40mg now closes Sept. 30.COVID-19 has only increased the importance of completing the census to help our local communities and economies recover. The novel coronavirus has inflicted unprecedented strain on patients and exacerbated inequality as more people are out of work and are many in need of help with food, health care, housing, and more.

Schools also have been stretched thin, with teachers furosemide mylan 40mg scrambling to teach students online. Yet, the amount of federal funding Texas has available today to help weather this emergency was driven in part by the census responses made a decade ago. Getting an accurate count in 2020 will help Texans prepare for the decade to follow, the first few years of which most certainly will be spent rebuilding from furosemide mylan 40mg the pandemic’s fallout. Therefore, it is vital that all Texans be counted.The federal dollars Texas receives generally depends on our population.

A George Washington University study recently found that even a 1% undercount can lead to a furosemide mylan 40mg $300 million loss in funding.Take Medicaid, for example. Federal funds pay for 60% of the state’s program, which provides health coverage for two out of five Texas children, one in three individuals with disabilities, and 53% of all births. The complicated formula used to calculate furosemide mylan 40mg the federal portion of this funding depends on accurate census data. If Texas’ population is undercounted, Texans may appear better off financially than they really are, resulting in Texas getting fewer federal Medicaid dollars.

If that happens, lawmakers will have to make up the difference, with furosemide mylan 40mg cuts in services, program eligibility, or physician and provider payments, any of which are potentially detrimental.The census data also is key to funding other aspects of a community’s social safety net:Health careThe Children’s Health Insurance Program (CHIP) provides low-cost health insurance to children whose parents make too much to qualify for Medicaid, but not enough to afford quality coverage. Like Medicaid, how much money the federal government reimburses the state for the program depends in part on the census.Maternal and child health programs that promote public health and help ensure children are vaccinated relies on data from the census. Texas also uses this federal funding to study and respond to maternal mortality and perinatal depression.Food and housing As unemployment rises and families struggle financially, many live with uncertainty as to where they will find furosemide mylan 40mg their next meal. Already, one in seven Texans experiences food insecurity, and 20% of Texas children experience hunger.

Food insecurity is rising in Texas as the pandemic continues. The Central Texas Food Bank saw a 206% rise furosemide mylan 40mg in clients in March. Funding for the Supplemental Nutrition Assistance Program and school lunch programs are both determined by the census. Funding for local housing programs also is calculated via furosemide mylan 40mg the census.

An accurate count will help ensure that people who lose their homes during this economic crisis have better hope of finding shelter while our communities recover. Homelessness is closely connected with declines in overall physical and mental health.Childcare and educationAs we navigate the new reality brought on by coronavirus, more parents are taking on roles as breadwinner, furosemide mylan 40mg parent, teacher, and caretaker. This stress highlights the desperate need for affordable childcare. The census determines funding for programs like Head Start that provide comprehensive early childhood furosemide mylan 40mg education to low-income families.

The good news is you still have time to complete the census. Visit 2020census.gov to take furosemide mylan 40mg it. It takes less than five minutes to complete. Then talk to your family, neighbors, and colleagues about doing furosemide mylan 40mg the same.

If you are wondering who counts, the answer is everyone, whether it’s a newborn baby, child in foster care, undocumented immigrant, or an individual experiencing homelessness.Completing the census is one of the best things that you can do for the health of your community, especially during the pandemic. Thank you for helping Texas heal and for supporting these essential safety net programs..

Influenza affects millions of people each year, and because of the COVID-19 pandemic, many physicians and buy furosemide online without a prescription health experts are concerned that this year’s flu season will hit with full force. In the Lone Star State, it’s important for Texans to be proactive about their health by getting the yearly flu vaccination. One of the worst things that could happen would be having many people sick with the flu while many are ill with coronavirus.Flu vaccination is the buy furosemide online without a prescription best way to reduce the risk of getting and spreading the flu. This year, it also will help keep hospitalizations down as physicians, nurses, and other medical staff continue to care for COVID-19 patients. Traditionally, Texas buy furosemide online without a prescription falls behind on flu vaccination.

According to the Centers for Disease Control and Prevention (CDC), only 43.3% of Texas adults got a flu shot in 2018-2019, compared to the national average of 45.3%.Although influenza viruses circulate throughout the year, flu season usually starts in the fall and winter, and peaks between December and February.Like COVID-19, the flu is contagious. Both have buy furosemide online without a prescription some similar symptoms, including fever, chills, cough, fatigue, body aches, vomiting, and diarrhea. People with the flu may not experience symptoms until one to four days after catching the virus. The CDC outlines key similarities and differences between influenza and buy furosemide online without a prescription COVID-19 here.While most people recover from the flu, many can experience complications, especially older adults, people with pre-existing medical conditions, young children, and pregnant women. If left untreated, infected patients can develop pneumonia, inflammation of the heart, brain, or muscle tissues, organ failure, sepsis, or they could even die.

In Texas, buy furosemide online without a prescription more than 21,000 people died from the flu in the past two years. To put that into perspective, that is the population of Katy!. Everyone 6 months or older is encouraged to get the flu buy furosemide online without a prescription vaccine each year – especially adults aged 65 and older, pregnant women, young children, and people who have chronic illnesses such as diabetes, asthma, and heart disease. The CDC is urging the public to get the flu vaccine while maintaining social distancing, wearing a mask in public, and practicing good hygiene.People who receive the flu shot may experience some mild side effects like aches and a mild fever, but they can’t get the flu from the shot. Those who get the flu after being vaccinated might have been exposed to the virus beforehand.

The flu vaccination can help lessen flu symptoms buy furosemide online without a prescription and severity, helping reduce the amount of time spent away from work and school.In a time when community health is front and center, getting a flu shot is more important than ever. The Texas Medical Association’s Be Wise Immunize℠ program recently created a downloadable poster below in English and Spanish with key takeaways about the flu vaccination. You can print the poster, or save it and share it buy furosemide online without a prescription on social media. Be Wise – Immunize is funded in 2020 by the TMA Foundation, thanks to major support from H-E-B and Permian Basin Youth Chavarim.Be Wise – Immunize is a service mark of the Texas Medical Association.Lauren Gambill, MDPediatrician, AustinMember, Texas Medical Association (TMA) Committee on Child and Adolescent HealthExecutive Board Member, Texas Pediatric SocietyDoctors are community leaders. This role buy furosemide online without a prescription has become even more important during the COVID-19 pandemic.

As patients navigate our new reality, they are looking to us to determine what is safe, how to protect their families, and the future of their health care. As more buy furosemide online without a prescription Texans lose their jobs, their health insurance, or even their homes, it is crucial that Texas receives the resources it needs to uphold our social safety net. The U.S. Census helps determine funding for those resources, and that is why it is of the upmost importance buy furosemide online without a prescription that each and every Texan, no matter address, immigration status, or age, respond to the 2020 U.S. Census.

The deadline has been cut short one month buy furosemide online without a prescription and now closes Sept. 30.COVID-19 has only increased the importance of completing the census to help our local communities and economies recover. The novel coronavirus has inflicted unprecedented strain on patients and exacerbated inequality as more people are out of work and are many in need of help with food, health care, housing, and more. Schools also have been stretched thin, with teachers scrambling to teach buy furosemide online without a prescription students online. Yet, the amount of federal funding Texas has available today to help weather this emergency was driven in part by the census responses made a decade ago.

Getting an accurate count in 2020 will help Texans prepare buy furosemide online without a prescription for the decade to follow, the first few years of which most certainly will be spent rebuilding from the pandemic’s fallout. Therefore, it is vital that all Texans be counted.The federal dollars Texas receives generally depends on our population. A George Washington University study recently found that even a buy furosemide online without a prescription 1% undercount can lead to a $300 million loss in funding.Take Medicaid, for example. Federal funds pay for 60% of the state’s program, which provides health coverage for two out of five Texas children, one in three individuals with disabilities, and 53% of all births. The complicated formula used to buy furosemide online without a prescription calculate the federal portion of this funding depends on accurate census data.

If Texas’ population is undercounted, Texans may appear better off financially than they really are, resulting in Texas getting fewer federal Medicaid dollars. If that happens, lawmakers will have to make up buy furosemide online without a prescription the difference, with cuts in services, program eligibility, or physician and provider payments, any of which are potentially detrimental.The census data also is key to funding other aspects of a community’s social safety net:Health careThe Children’s Health Insurance Program (CHIP) provides low-cost health insurance to children whose parents make too much to qualify for Medicaid, but not enough to afford quality coverage. Like Medicaid, how much money the federal government reimburses the state for the program depends in part on the census.Maternal and child health programs that promote public health and help ensure children are vaccinated relies on data from the census. Texas also buy furosemide online without a prescription uses this federal funding to study and respond to maternal mortality and perinatal depression.Food and housing As unemployment rises and families struggle financially, many live with uncertainty as to where they will find their next meal. Already, one in seven Texans experiences food insecurity, and 20% of Texas children experience hunger.

Food insecurity is rising in Texas as the pandemic continues. The Central Texas Food Bank saw a 206% rise in clients in March buy furosemide online without a prescription. Funding for the Supplemental Nutrition Assistance Program and school lunch programs are both determined by the census. Funding for local buy furosemide online without a prescription housing programs also is calculated via the census. An accurate count will help ensure that people who lose their homes during this economic crisis have better hope of finding shelter while our communities recover.

Homelessness is closely connected with declines in overall physical and mental health.Childcare and educationAs we navigate the new buy furosemide online without a prescription reality brought on by coronavirus, more parents are taking on roles as breadwinner, parent, teacher, and caretaker. This stress highlights the desperate need for affordable childcare. The census determines funding for programs like Head Start that provide comprehensive early childhood education buy furosemide online without a prescription to low-income families. The good news is you still have time to complete the census. Visit 2020census.gov buy furosemide online without a prescription to take it.

It takes less than five minutes to complete. Then talk buy furosemide online without a prescription to your family, neighbors, and colleagues about doing the same. If you are wondering who counts, the answer is everyone, whether it’s a newborn baby, child in foster care, undocumented immigrant, or an individual experiencing homelessness.Completing the census is one of the best things that you can do for the health of your community, especially during the pandemic. Thank you for helping Texas heal and for supporting these essential safety net programs..

Furosemide solution

First-of-its-kind study, based on a mouse model, finds living in a polluted environment could be comparable to eating a high-fat diet, leading to a pre-diabetic state CLEVELAND—Air pollution is the world’s leading environmental risk factor, and causes more than nine million deaths per furosemide solution year. New research published in the Journal of Clinical Investigation shows air pollution may play a role in the development of cardiometabolic diseases, such as diabetes. Importantly, the effects were reversible with furosemide solution cessation of exposure.

Researchers found that air pollution was a “risk factor for a risk factor” that contributed to the common soil of other fatal problems like heart attack and stroke. Similar to how an unhealthy diet and lack of exercise can lead to disease, exposure to air pollution could be added to this risk factor list as well. “In this study, we created an environment that mimicked a polluted day in New Delhi or Beijing,” said Sanjay Rajagopalan, MD, first author on the study, Chief of Cardiovascular Medicine at University Hospitals Harrington Heart and Vascular Institute, and Director of the Case Western Reserve University Cardiovascular Research Institute furosemide solution.

€œWe concentrated fine particles of air pollution, called PM2.5 (particulate matter component <. 2.5 microns) furosemide solution. Concentrated particles like this develop from human impact on the environment, such as automobile exhaust, power generation and other fossil fuels.” These particles have been strongly connected to risk factors for disease.

For example, cardiovascular effects of air pollution can lead to heart attack and stroke. The research team has shown exposure to air pollution can increase the likelihood of the same risk factors that furosemide solution lead to heart disease, such as insulin resistance and type 2 diabetes. In the mouse model study, three groups were observed.

A control group receiving clean filtered air, a group exposed to polluted air for 24 weeks, and a group fed a high-fat diet. Interestingly, the researchers found that furosemide solution being exposed to air pollution was comparable to eating a high-fat diet. Both the air pollution and high-fat diet groups showed insulin resistance and abnormal metabolism – just like one would see in a pre-diabetic state.

These changes were associated with changes in the epigenome, a layer of control that can masterfully turn on and turn off thousands of furosemide solution genes, representing a critical buffer in response to environmental factors. This study is the first-of-its-kind to compare genome-wide epigenetic changes in response to air pollution, compare and contrast these changes with that of eating an unhealthy diet, and examine the impact of air pollution cessation on these changes.“The good news is that these effects were reversible, at least in our experiments” added Dr. Rajagopalan.

€œOnce the air furosemide solution pollution was removed from the environment, the mice appeared healthier and the pre-diabetic state seemed to reverse.” Dr. Rajagopalan explains that if you live in a densely polluted environment, taking actions such as wearing an N95 mask, using portable indoor air cleaners, utilizing air conditioning, closing car windows while commuting, and changing car air filters frequently could all be helpful in staying healthy and limiting air pollution exposure.Next steps in this research involve meeting with a panel of experts, as well as the National Institutes of Health, to discuss conducting clinical trials that compare heart health and the level of air pollution in the environment. For example, if someone has a heart attack, should they be wearing an N95 mask or using a portable air filter at home during recovery?.

Dr furosemide solution. Rajagopalan and his team believe that it is important to address the environment as a population health risk factor and continue to diligently research these issues. The authors also note that these findings should encourage policymakers to enact measures aimed at reducing air pollution.Shyam Biswal, PhD, Professor in the Department of Environmental Health and Engineering at Johns Hopkins University School of Public Health, is the joint senior furosemide solution author on the study.

Drs. Rajagopalan and Biswal are co-PIs on the NIH grant that supported this work.###Rajagopalan, S., Biswal, S., et al. €œMetabolic effects of air pollution exposure and reversibility.” Journal of Clinical furosemide solution Investigation.

DOI. 10.1172/JCI137315. This work was supported by the National Institute of Environmental Health Sciences TaRGET II Consortium grant U01ES026721, as well as grants R01ES015146 and R01ES019616.About one in five women experience some form of depression during pregnancy, with poorly understood effects on the fetus.

Prenatal depression is linked to behavioural and developmental issues in children as well as an increased risk for depression as young adults. But how prenatal depression leads to these changes remains unclear. UCalgary researcher Dr.

Catherine Lebel, PhD, is helping understand what may be happening in the developing brains of these children. The research team has shown that young children whose mothers experienced more numerous symptoms of depression in pregnancy have weakened connectivity in brain pathways involved in emotion. These structural changes can be related to increased hyperactivity and aggression in boys.

The research is based on diffusion magnetic resonance imaging, an imaging technique that probes the strength of structural connections between brain regions. The findings are published in The Journal of Neuroscience. Catherine Lebel, senior author and investigator.

Riley Brandt, University of Calgary “The results help us understand how depression can have multigenerational impacts, and speaks to the importance of helping mothers who may be experiencing depression during pregnancy,” says Lebel, an associate professor at the Cumming School of Medicine, and researcher in the Alberta Children’s Hospital Research Institute. She holds the Canada Research Chair in Paediatric Neuroimaging. Lebel and her team studied 54 Calgary mothers and their children.

They were enrolled from the ongoing, prospective study called the Alberta Pregnancy Outcomes and Nutrition study. Mothers answered a survey about their depression symptoms at several points during their pregnancy. Their children were followed after birth and undertook an MRI scan at the Alberta Children’s Hospital at around age four.

As well, the children’s behaviour was assessed within six months of their MRI scan. The team found a significant reduction in structural brain connectivity between the amygdala, a structure essential for emotional processing, and the frontal cortex. Weakened connectivity between the amygdala and frontal cortex is associated with disruptive behaviours and vulnerability to depression.

The first author on the study, Dr. Rebecca Hay, MD, stresses the importance of recognition of depression and intervention in prenatal health. €œThese results suggest complex associations between the prenatal environment and children’s brain development, and may help us to understand why children of depressed mothers are more vulnerable to depression themselves,” says Hay, a resident physician in paediatrics and recent Cumming School of Medicine graduate.

The main clinical takeaway from this is to emphasize the importance of recognizing, treating prenatal depression and supporting mothers, both for better maternal outcomes and to help future child development. Rebecca Hay, the study's first author. Courtesy Rebecca Hay Current study looks at stress during pandemic Lebel and her research team are currently trying to understand how stress and mental health are affecting pregnant women during the COVID-19 pandemic.

She is examining how factors such as social supports might mitigate stress, and how this may influence pregnancy and birth outcomes. If you are interested, you can get involved here in the Pregnancy During the COVID-19 Pandemic study at the University of Calgary. So far, approximately 7,500 women from across Canada are enrolled and supplying information through questionnaires.

€œIt is critical to appropriately recognize and treat prenatal maternal mental health problems, both for the mothers and to improve child outcomes,” says Lebel. €œNow more than ever, with increased stress, anxiety and depression during the COVID-19 pandemic, we should do more to support mothers to positively impact the health of their children.” Lebel is an associate professor in the Department of Radiology at the Cumming School of Medicine, adjunct associate professor in the Werklund School of Education and a member of The Mathison Centre for Mental Health Research &. Education, Owerko Centre at ACHRI, Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute.

The study was funded by the Canadian Institute of Health Research, Alberta Innovates - Health Solutions, the Alberta Children's Hospital Foundation, the National Institute of Environmental Health Sciences, the Mach-Gaensslen Foundation, and an Eyes High University of Calgary Postdoctoral Scholar. Led by the Hotchkiss Brain Institute, Brain and Mental Health is one of six research strategies guiding the University of Calgary toward its Eyes High goals. The strategy provides a unifying direction for brain and mental health research at the university..

First-of-its-kind study, based on a mouse model, finds living in a polluted environment could be comparable buy furosemide online without a prescription to eating a high-fat diet, leading to a pre-diabetic state CLEVELAND—Air pollution is the world’s leading environmental risk factor, and causes more than nine million deaths per year. New research published in the Journal of Clinical Investigation shows air pollution may play a role in the development of cardiometabolic diseases, such as diabetes. Importantly, the buy furosemide online without a prescription effects were reversible with cessation of exposure. Researchers found that air pollution was a “risk factor for a risk factor” that contributed to the common soil of other fatal problems like heart attack and stroke.

Similar to how an unhealthy diet and lack of exercise can lead to disease, exposure to air pollution could be added to this risk factor list as well. “In this study, buy furosemide online without a prescription we created an environment that mimicked a polluted day in New Delhi or Beijing,” said Sanjay Rajagopalan, MD, first author on the study, Chief of Cardiovascular Medicine at University Hospitals Harrington Heart and Vascular Institute, and Director of the Case Western Reserve University Cardiovascular Research Institute. €œWe concentrated fine particles of air pollution, called PM2.5 (particulate matter component <. 2.5 microns) buy furosemide online without a prescription.

Concentrated particles like this develop from human impact on the environment, such as automobile exhaust, power generation and other fossil fuels.” These particles have been strongly connected to risk factors for disease. For example, cardiovascular effects of air pollution can lead to heart attack and stroke. The research team has shown exposure to air pollution can increase the likelihood of the same risk factors that lead to heart buy furosemide online without a prescription disease, such as insulin resistance and type 2 diabetes. In the mouse model study, three groups were observed.

A control group receiving clean filtered air, a group exposed to polluted air for 24 weeks, and a group fed a high-fat diet. Interestingly, the researchers found that being exposed to buy furosemide online without a prescription air pollution was comparable to eating a high-fat diet. Both the air pollution and high-fat diet groups showed insulin resistance and abnormal metabolism – just like one would see in a pre-diabetic state. These changes were associated with changes in the epigenome, a layer of control that can masterfully turn buy furosemide online without a prescription on and turn off thousands of genes, representing a critical buffer in response to environmental factors.

This study is the first-of-its-kind to compare genome-wide epigenetic changes in response to air pollution, compare and contrast these changes with that of eating an unhealthy diet, and examine the impact of air pollution cessation on these changes.“The good news is that these effects were reversible, at least in our experiments” added Dr. Rajagopalan. €œOnce the air pollution was removed buy furosemide online without a prescription from the environment, the mice appeared healthier and the pre-diabetic state seemed to reverse.” Dr. Rajagopalan explains that if you live in a densely polluted environment, taking actions such as wearing an N95 mask, using portable indoor air cleaners, utilizing air conditioning, closing car windows while commuting, and changing car air filters frequently could all be helpful in staying healthy and limiting air pollution exposure.Next steps in this research involve meeting with a panel of experts, as well as the National Institutes of Health, to discuss conducting clinical trials that compare heart health and the level of air pollution in the environment.

For example, if someone has a heart attack, should they be wearing an N95 mask or using a portable air filter at home during recovery?. Dr buy furosemide online without a prescription. Rajagopalan and his team believe that it is important to address the environment as a population health risk factor and continue to diligently research these issues. The authors also note that buy furosemide online without a prescription these findings should encourage policymakers to enact measures aimed at reducing air pollution.Shyam Biswal, PhD, Professor in the Department of Environmental Health and Engineering at Johns Hopkins University School of Public Health, is the joint senior author on the study.

Drs. Rajagopalan and Biswal are co-PIs on the NIH grant that supported this work.###Rajagopalan, S., Biswal, S., et al. €œMetabolic effects of air pollution exposure and reversibility.” buy furosemide online without a prescription Journal of Clinical Investigation. DOI.

10.1172/JCI137315. This work was supported by the National Institute of Environmental Health Sciences TaRGET II Consortium grant U01ES026721, as well as grants R01ES015146 and R01ES019616.About one in five women experience some form of depression during pregnancy, with poorly understood effects on the fetus. Prenatal depression is linked to behavioural and developmental issues in children as well as an increased risk for depression as young adults. But how prenatal depression leads to these changes remains unclear.

UCalgary researcher Dr. Catherine Lebel, PhD, is helping understand what may be happening in the developing brains of these children. The research team has shown that young children whose mothers experienced more numerous symptoms of depression in pregnancy have weakened connectivity in brain pathways involved in emotion. These structural changes can be related to increased hyperactivity and aggression in boys.

The research is based on diffusion magnetic resonance imaging, an imaging technique that probes the strength of structural connections between brain regions. The findings are published in The Journal of Neuroscience. Catherine Lebel, senior author and investigator. Riley Brandt, University of Calgary “The results help us understand how depression can have multigenerational impacts, and speaks to the importance of helping mothers who may be experiencing depression during pregnancy,” says Lebel, an associate professor at the Cumming School of Medicine, and researcher in the Alberta Children’s Hospital Research Institute.

She holds the Canada Research Chair in Paediatric Neuroimaging. Lebel and her team studied 54 Calgary mothers and their children. They were enrolled from the ongoing, prospective study called the Alberta Pregnancy Outcomes and Nutrition study. Mothers answered a survey about their depression symptoms at several points during their pregnancy.

Their children were followed after birth and undertook an MRI scan at the Alberta Children’s Hospital at around age four. As well, the children’s behaviour was assessed within six months of their MRI scan. The team found a significant reduction in structural brain connectivity between the amygdala, a structure essential for emotional processing, and the frontal cortex. Weakened connectivity between the amygdala and frontal cortex is associated with disruptive behaviours and vulnerability to depression.

The first author on the study, Dr. Rebecca Hay, MD, stresses the importance of recognition of depression and intervention in prenatal health. €œThese results suggest complex associations between the prenatal environment and children’s brain development, and may help us to understand why children of depressed mothers are more vulnerable to depression themselves,” says Hay, a resident physician in paediatrics and recent Cumming School of Medicine graduate. The main clinical takeaway from this is to emphasize the importance of recognizing, treating prenatal depression and supporting mothers, both for better maternal outcomes and to help future child development.

Rebecca Hay, the study's first author. Courtesy Rebecca Hay Current study looks at stress during pandemic Lebel and her research team are currently trying to understand how stress and mental health are affecting pregnant women during the COVID-19 pandemic. She is examining how factors such as social supports might mitigate stress, and how this may influence pregnancy and birth outcomes. If you are interested, you can get involved here in the Pregnancy During the COVID-19 Pandemic study at the University of Calgary.

So far, approximately 7,500 women from across Canada are enrolled and supplying information through questionnaires. €œIt is critical to appropriately recognize and treat prenatal maternal mental health problems, both for the mothers and to improve child outcomes,” says Lebel. €œNow more than ever, with increased stress, anxiety and depression during the COVID-19 pandemic, we should do more to support mothers to positively impact the health of their children.” Lebel is an associate professor in the Department of Radiology at the Cumming School of Medicine, adjunct associate professor in the Werklund School of Education and a member of The Mathison Centre for Mental Health Research &. Education, Owerko Centre at ACHRI, Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute.

The study was funded by the Canadian Institute of Health Research, Alberta Innovates - Health Solutions, the Alberta Children's Hospital Foundation, the National Institute of Environmental Health Sciences, the Mach-Gaensslen Foundation, and an Eyes High University of Calgary Postdoctoral Scholar. Led by the Hotchkiss Brain Institute, Brain and Mental Health is one of six research strategies guiding the University of Calgary toward its Eyes High goals. The strategy provides a unifying direction for brain and mental health research at the university..

Furosemide over the counter equivalent

Rheumatic feverIs there any disease group furosemide over the counter equivalent more ’deserving’ of a place at the neglected tropical disease table than the post streptococcal illnesses, glomerulonephritis and rheumatic fever?. These dropped off the radar of most high income countries in the second half of the 20th century but have continued to smoulder, largely unchecked, in low and middle income countries (LMICs). The burden is furosemide over the counter equivalent frightening. 300 000 incident cases per year and 30 million prevalent cases, the damage from chronic carditis resulting, in so many, in heart failure and stroke.There are a number of approaches.

Primary prevention (vaccination) remains a work in progress. Secondary prevention (prompt treatment) is largely dependent on diagnosis which depends on a positive throat swab or serological evidence in the form of the ASOT and ADB titres and furosemide over the counter equivalent this is where the complexities begin. Tertiary prevention, early diagnosis of heart disease by echo screening and prophylaxis has promise but is gestational. The range of population norms depends on exposure and furosemide over the counter equivalent threshold levels in one country might not be applicable elsewhere inevitably resulting in false positive and false negative results.

Okello et al establishes a range of ASOT levels in urban Uganda and shows much higher mean titres than other comparable populations. Joshua Osowicki and Andrew Steer discuss the implications of these findings in the context of a multipronged approach to rheumatic fever during the wait for the long yearned-for group A streptococcal vaccine. See pages 825 and 813Febrile neutropaeniaOncological treatment is prolonged and draining for furosemide over the counter equivalent both a child and their family. A major contributor to the fatigue is the need for recurrent admissions for chemotherapy induced febrile neutropenia (FN).

Though evidence of benefit is scanty to furosemide over the counter equivalent non-existent, it is traditional to keep children in hospital on IV antibiotic treatment for several days irrespective of culture results and clinical appearance. Sereveratne and colleagues assess the safety of a more flexible approach in a tertiary oncology centre, allowing discharge at 48 hours, even if culture positive as long as ‘wellness’ and social criteria were metIn total, 179 episodes of FN were reviewed from 47 patients. In 70% (125/179) of episodes, patients were discharged safely once 48 hours microbiology results were available, with only 5.6% (7/125) resulting in readmission in the 48 hours following discharge. There were no deaths from furosemide over the counter equivalent sepsis.

This approach won’t work for all episodes of febrile neutropenia, but, probably applies to the majority and the differences to quality of life if adopted widely are hard to overstate. See page furosemide over the counter equivalent 881Infectious disease mortalityTrends in infectious disease mirror changes in vaccination programmes, society and the environment, diagnostics and microbiological epidemiology. Ferreras-Antolin examines Public Health England data over two eras, 2003 to 2005 and 2013 to 2015. In the latter period, there were 5088 death registrations recorded in children aged 28 days to <15 years in England and Wales (17.6 deaths/100 000 children annually) and, in the first 6897 (23.9/100 000).

The incidence rate furosemide over the counter equivalent ratio (IRR) of 0.74 (95% CI 0.71 to 0.77) fell significantly and the stories behind these data are revealing. There is little doubt that PCV vaccination has played a role though, in this series, it is too early to assess the contribution of the (2015 launched) meningococcal B programme. The raw data also mask the rise of (the still non-vaccine preventable) invasive group A streptococcal disease (one of the arguments for varicella vaccination) and the future role for Group B streptococcal immunisation. Influenza deaths were rare and, despite furosemide over the counter equivalent a reduction between the eras was not a major explanator.

See page 857Fibre and constipationOne of the more entrenched tenets of child nutrition folklore is that of the association between fibre and constipation. In a re-analysis of data from the latest NICE review, information from the ALSPAC cohort (in which stool consistency pre-weaning was established) and monozygotic twin studies, Tappin persuasively argues (through triangulation analysis) that fibre is the result of and confounded by parental response to hard stool and is neither a cause of constipation or a furosemide over the counter equivalent treatment. Laxation (as advocated) should be the first line and used early to prevent the all too familiar chronic issues with undertreatment. Soiling.

Loss of self esteem furosemide over the counter equivalent. Poor mood and loss of appetite. See page 864Drowning and autismDrowning is a major cause of global child furosemide over the counter equivalent mortality, particularly in low and middle income country settings. Interventions such as fencing off access and swimming lessons have partially ameliorated the risk, but progress has been slow and awareness probably still the single best form of prophylaxis.

Autistic children represent a high risk group due to their inherent communication and behavioural issues. Peden assesses the association between autism furosemide over the counter equivalent and drowning in Australia from coronial certificates between 2002 and 2018. Of the 667 cases of drowning among 0–19 year olds (with known history), 27 (4%) had an ASD diagnosis, relative risk 2.85 (95% CI 0.61 to 13.24). Children and adolescents with ASD were significantly furosemide over the counter equivalent more likely to drown when compared with those without ASD.

If aged 5–9 years (44.4% of ASD cases. 13.3% of non ASD cases). In a lake or dam (25.9% vs furosemide over the counter equivalent 10.0%) and during winter (37.0% vs 13.1%). These sobering figures are likely to be an underestimate as the diagnosis of ASD is often not made until the age of 5 years, past the highest drowning risk preschool group.

Rheumatic feverIs there any disease group more ’deserving’ of a place at the neglected tropical disease table buy furosemide online without a prescription than the post streptococcal illnesses, glomerulonephritis and rheumatic fever?. These dropped off the radar of most high income countries in the second half of the 20th century but have continued to smoulder, largely unchecked, in low and middle income countries (LMICs). The burden buy furosemide online without a prescription is frightening. 300 000 incident cases per year and 30 million prevalent cases, the damage from chronic carditis resulting, in so many, in heart failure and stroke.There are a number of approaches. Primary prevention (vaccination) remains a work in progress.

Secondary prevention (prompt treatment) is largely dependent on buy furosemide online without a prescription diagnosis which depends on a positive throat swab or serological evidence in the form of the ASOT and ADB titres and this is where the complexities begin. Tertiary prevention, early diagnosis of heart disease by echo screening and prophylaxis has promise but is gestational. The range of population norms depends on exposure and threshold levels in one country might not be applicable elsewhere inevitably resulting in false positive and false negative buy furosemide online without a prescription results. Okello et al establishes a range of ASOT levels in urban Uganda and shows much higher mean titres than other comparable populations. Joshua Osowicki and Andrew Steer discuss the implications of these findings in the context of a multipronged approach to rheumatic fever during the wait for the long yearned-for group A streptococcal vaccine.

See pages 825 and 813Febrile neutropaeniaOncological treatment is prolonged and draining buy furosemide online without a prescription for both a child and their family. A major contributor to the fatigue is the need for recurrent admissions for chemotherapy induced febrile neutropenia (FN). Though evidence of benefit is scanty buy furosemide online without a prescription to non-existent, it is traditional to keep children in hospital on IV antibiotic treatment for several days irrespective of culture results and clinical appearance. Sereveratne and colleagues assess the safety of a more flexible approach in a tertiary oncology centre, allowing discharge at 48 hours, even if culture positive as long as ‘wellness’ and social criteria were metIn total, 179 episodes of FN were reviewed from 47 patients. In 70% (125/179) of episodes, patients were discharged safely once 48 hours microbiology results were available, with only 5.6% (7/125) resulting in readmission in the 48 hours following discharge.

There were buy furosemide online without a prescription no deaths from sepsis. This approach won’t work for all episodes of febrile neutropenia, but, probably applies to the majority and the differences to quality of life if adopted widely are hard to overstate. See page 881Infectious disease mortalityTrends in infectious disease mirror changes in vaccination buy furosemide online without a prescription programmes, society and the environment, diagnostics and microbiological epidemiology. Ferreras-Antolin examines Public Health England data over two eras, 2003 to 2005 and 2013 to 2015. In the latter period, there were 5088 death registrations recorded in children aged 28 days to <15 years in England and Wales (17.6 deaths/100 000 children annually) and, in the first 6897 (23.9/100 000).

The incidence buy furosemide online without a prescription rate ratio (IRR) of 0.74 (95% CI 0.71 to 0.77) fell significantly and the stories behind these data are revealing. There is little doubt that PCV vaccination has played a role though, in this series, it is too early to assess the contribution of the (2015 launched) meningococcal B programme. The raw data also mask the rise of (the still non-vaccine preventable) invasive group A streptococcal disease (one of the arguments for varicella vaccination) and the future role for Group B streptococcal immunisation. Influenza deaths were rare and, despite a reduction between the eras was not a buy furosemide online without a prescription major explanator. See page 857Fibre and constipationOne of the more entrenched tenets of child nutrition folklore is that of the association between fibre and constipation.

In a re-analysis of data from the latest NICE review, information from the ALSPAC cohort (in which stool consistency pre-weaning was established) and monozygotic twin studies, Tappin persuasively argues (through triangulation analysis) that fibre is the result of and confounded by parental response to hard stool and is buy furosemide online without a prescription neither a cause of constipation or a treatment. Laxation (as advocated) should be the first line and used early to prevent the all too familiar chronic issues with undertreatment. Soiling. Loss of buy furosemide online without a prescription self esteem. Poor mood and loss of appetite.

See page 864Drowning and autismDrowning is a buy furosemide online without a prescription major cause of global child mortality, particularly in low and middle income country settings. Interventions such as fencing off access and swimming lessons have partially ameliorated the risk, but progress has been slow and awareness probably still the single best form of prophylaxis. Autistic children represent a high risk group due to their inherent communication and behavioural issues. Peden assesses the association between autism and drowning in Australia from coronial buy furosemide online without a prescription certificates between 2002 and 2018. Of the 667 cases of drowning among 0–19 year olds (with known history), 27 (4%) had an ASD diagnosis, relative risk 2.85 (95% CI 0.61 to 13.24).

Children and adolescents with buy furosemide online without a prescription ASD were significantly more likely to drown when compared with those without ASD. If aged 5–9 years (44.4% of ASD cases. 13.3% of non ASD cases). In a lake or dam (25.9% vs 10.0%) buy furosemide online without a prescription and during winter (37.0% vs 13.1%). These sobering figures are likely to be an underestimate as the diagnosis of ASD is often not made until the age of 5 years, past the highest drowning risk preschool group.

Furosemide and chronic kidney disease

Imaging the furosemide and chronic kidney disease encephalopathy of prematurityJulia Kline and colleagues assessed MRI findings at term in 110 preterm infants born before 32 weeks’ gestation and cared for in four neonatal units in Columbus, Ohio. Using automated cortical and sub-cortical segmentation they analysed cortical surface area, sulcal depth, gyrification index, inner cortical curvature and thickness. These measures of brain development and maturation were related to the furosemide and chronic kidney disease outcomes of cognitive and language testing undertaken at 2 years corrected age using the Bayley-III. Increased surface area in nearly every brain region was positively correlated with Bayley-III cognitive and language scores. Increased inner cortical curvature was negatively correlated with both outcomes.

Gyrification index and sulcal depth furosemide and chronic kidney disease did not follow consistent trends. These metrics retained their significance after sex, gestational age, socio-economic status and global injury score on structural MRI were included in the analysis. Surface area and inner cortical curvature explained approximately one-third of the variance in Bayley-III scores.In an accompanying editorial, David Edwards characterises the complexity of imaging and interpreting the combined effects of injury and dysmaturation on the developing brain. Major structural lesions are present in a minority of infants and the problems observed in later childhood require a much broader understanding of the furosemide and chronic kidney disease effects of prematurity on brain development. Presently these more sophisticated image-analysis techniques provide insights at a population level but the variation between individuals is such that they are not sufficiently predictive at an individual patient level to be of practical use to parents or clinicians in prognostication.

Studies like this highlight the importance of follow-up programmes and help clinicians to avoid falling into the trap of equating normal (no major structural lesion) imaging studies with normal long term outcomes. See pages F460 and F458Drift at 10 yearsKaren Luuyt and colleagues report the cognitive outcomes at 10 years of the DRIFT (drainage, irrigation furosemide and chronic kidney disease and fibrinolytic therapy) randomised controlled trial of treatment for post haemorrhagic ventricular dilatation. They are to be congratulated for continuing to track these children and confirming the persistence of the cognitive advantage of the treatment that was apparent from earlier follow-up. Infants who received DRIFT were almost twice as likely to survive without severe cognitive disability than those who received standard treatment furosemide and chronic kidney disease. While the confidence intervals were wide, the point estimate suggests that the number needed to treat for DRIFT to prevent one death or one case of severe cognitive disability was 3.

The original trial took place between 2003 and 2006 and was stopped early because of concerns about secondary intraventricular haemorrhage and it was only on follow-up that the advantages of the treatment became apparent. The study shows that secondary brain injury furosemide and chronic kidney disease can be reduced by washing away the harmful debris of IVH. No other treatment for post-haemorrhagic ventricular dilatation has been shown to be beneficial in a randomised controlled trial. Less invasive approaches to CSF drainage at different thresholds of ventricular enlargement later in the clinical course have not been associated with similar advantage. However the DRIFT treatment is complex and invasive and could only be provided in a small number of specialist referral centres and logistical furosemide and chronic kidney disease challenges will need to be overcome to evaluate the treatment approach further.

See page F466Chest compressionsWith a stable infant in the neonatal unit, it is common to review the events of the initial stabilisation and to speculate on whether chest compressions were truly needed to establish an effective circulation, or whether their use reflected clinician uncertainty in the face of other challenges. Anne Marthe Boldinge and colleagues provide some objective data on the subject. They analysed videos that were recorded during neonatal stabilisation in a single centre with 5000 births per furosemide and chronic kidney disease annum. From a birth population of almost 1200 infants there were good quality video recordings from 327 episodes of initial stabilisation where positive pressure ventilation was provided and 29 of these episodes included the provision of chest compressions, mostly in term infants. 6/29 of the infants who received chest compressions were retrospectively judged to have needed them.

8/29 had adequate furosemide and chronic kidney disease spontaneous respiration. 18/29 received ineffective positive pressure ventilation prior to chest compressions. 5/29 had a heart furosemide and chronic kidney disease rate greater than 60 beats per minute at the time of chest compressions. A consistent pattern of ventilation corrective actions was not identified. One infant received chest compressions without prior heart rate assessment.

See page 545Propofol for neonatal endotracheal intubationMost clinicians provide sedation/analgesia for neonatal intubations but there is still a lot of uncertainty about furosemide and chronic kidney disease the best approach. Ellen de Kort and colleagues set out to identify the dose of propofol that would provide adequate sedation for neonatal intubation without side-effects. They conducted a dose-finding trial which evaluated a range of doses in infants of different gestations. They ended their study after 91 infants furosemide and chronic kidney disease because they only achieved adequate sedation without side effects in 13% of patients. Hypotension (mean blood pressure below post-mentrual age in the hour after treatment) was observed in 59% of patients.

See page 489Growth to early adulthood following extremely preterm birthThe EPICure cohort comprised all babies born at 25 completed weeks of gestation or less in all 276 maternity units in the UK and Ireland from March to December 1995. Growth data into adulthood are furosemide and chronic kidney disease sparse for such immature infants. Yanyan Ni and colleagues report the growth to 19 years of 129 of the cohort in comparison with contemporary term born controls. The extremely preterm infants were on furosemide and chronic kidney disease average 4.0 cm shorter and 6.8 kg lighter with a 1.5 cm smaller head circumference relative to controls at 19 years. Body mass index was significantly elevated to +0.32 SD.

With practice changing to include the provision of life sustaining treatment to greater numbers of infants born at 22 and 23 weeks of gestation there is a strong case for further cohort studies to include this population of infants. See page F496Premature birth is a worldwide problem, and the furosemide and chronic kidney disease most significant cause of loss of disability-adjusted life years in children. Impairment and disability among survivors are common. Cerebral palsy is diagnosed in around 10% of infants born before 33 weeks of gestation, although the rates approximately double in the smallest and most vulnerable infants, and other motor disturbances are being detected in 25%–40%. Cognitive, socialisation and behavioural problems are apparent in around half of furosemide and chronic kidney disease preterm infants, and there is increased incidence of neuropsychiatric disorders, which develop as the children grow older.

Adults born preterm are approximately seven times more likely to be diagnosed with bipolar disease.1 2The neuropathological basis for these long-term and debilitating disorders is often unclear. Brain imaging by ultrasound or MRI shows that only a relatively small proportion of infants have significant destructive brain lesions, and these major lesions are not detected commonly enough to account for the prevalence of long-term impairments. However, abnormalities of brain growth and maturation are common, and it is now apparent that, in addition to recognisable cerebral damage, adverse neurological, cognitive and psychiatric outcomes furosemide and chronic kidney disease are consistently associated with abnormal cerebral maturation and development.Currently, most clinical decision-making remains focused around a number of well-described cerebral lesions usually detected in routine practice using cranial ultrasound. Periventricular haemorrhage is common. Severe haemorrhages are associated with long-term adverse outcomes, and in infants born before 33 weeks of gestation, haemorrhagic parenchymal infarction predicts motor deficits ….

Imaging the encephalopathy of prematurityJulia Kline and colleagues assessed MRI findings at term in 110 preterm infants born before 32 weeks’ gestation and cared for buy furosemide online without a prescription in four neonatal units in Columbus, Ohio. Using automated cortical and sub-cortical segmentation they analysed cortical surface area, sulcal depth, gyrification index, inner cortical curvature and thickness. These measures of brain development and maturation were related to the outcomes of cognitive and language testing undertaken at buy furosemide online without a prescription 2 years corrected age using the Bayley-III. Increased surface area in nearly every brain region was positively correlated with Bayley-III cognitive and language scores. Increased inner cortical curvature was negatively correlated with both outcomes.

Gyrification index and sulcal depth did not follow buy furosemide online without a prescription consistent trends. These metrics retained their significance after sex, gestational age, socio-economic status and global injury score on structural MRI were included in the analysis. Surface area and inner cortical curvature explained approximately one-third of the variance in Bayley-III scores.In an accompanying editorial, David Edwards characterises the complexity of imaging and interpreting the combined effects of injury and dysmaturation on the developing brain. Major structural lesions are present in a minority of infants and the problems observed in later childhood require a buy furosemide online without a prescription much broader understanding of the effects of prematurity on brain development. Presently these more sophisticated image-analysis techniques provide insights at a population level but the variation between individuals is such that they are not sufficiently predictive at an individual patient level to be of practical use to parents or clinicians in prognostication.

Studies like this highlight the importance of follow-up programmes and help clinicians to avoid falling into the trap of equating normal (no major structural lesion) imaging studies with normal long term outcomes. See pages F460 and F458Drift at 10 yearsKaren Luuyt and colleagues report the cognitive outcomes at 10 years buy furosemide online without a prescription of the DRIFT (drainage, irrigation and fibrinolytic therapy) randomised controlled trial of treatment for post haemorrhagic ventricular dilatation. They are to be congratulated for continuing to track these children and confirming the persistence of the cognitive advantage of the treatment that was apparent from earlier follow-up. Infants who received DRIFT were almost twice as likely to survive without severe cognitive disability buy furosemide online without a prescription than those who received standard treatment. While the confidence intervals were wide, the point estimate suggests that the number needed to treat for DRIFT to prevent one death or one case of severe cognitive disability was 3.

The original trial took place between 2003 and 2006 and was stopped early because of concerns about secondary intraventricular haemorrhage and it was only on follow-up that the advantages of the treatment became apparent. The study shows buy furosemide online without a prescription that secondary brain injury can be reduced by washing away the harmful debris of IVH. No other treatment for post-haemorrhagic ventricular dilatation has been shown to be beneficial in a randomised controlled trial. Less invasive approaches to CSF drainage at different thresholds of ventricular enlargement later in the clinical course have not been associated with similar advantage. However the buy furosemide online without a prescription DRIFT treatment is complex and invasive and could only be provided in a small number of specialist referral centres and logistical challenges will need to be overcome to evaluate the treatment approach further.

See page F466Chest compressionsWith a stable infant in the neonatal unit, it is common to review the events of the initial stabilisation and to speculate on whether chest compressions were truly needed to establish an effective circulation, or whether their use reflected clinician uncertainty in the face of other challenges. Anne Marthe Boldinge and colleagues provide some objective data on the subject. They analysed videos that buy furosemide online without a prescription were recorded during neonatal stabilisation in a single centre with 5000 births per annum. From a birth population of almost 1200 infants there were good quality video recordings from 327 episodes of initial stabilisation where positive pressure ventilation was provided and 29 of these episodes included the provision of chest compressions, mostly in term infants. 6/29 of the infants who received chest compressions were retrospectively judged to have needed them.

8/29 had adequate buy furosemide online without a prescription spontaneous respiration. 18/29 received ineffective positive pressure ventilation prior to chest compressions. 5/29 had a heart rate greater than 60 beats per minute at the buy furosemide online without a prescription time of chest compressions. A consistent pattern of ventilation corrective actions was not identified. One infant received chest compressions without prior heart rate assessment.

See page 545Propofol for neonatal endotracheal intubationMost clinicians provide sedation/analgesia for neonatal intubations but there is still a lot of uncertainty about the best approach buy furosemide online without a prescription. Ellen de Kort and colleagues set out to identify the dose of propofol that would provide adequate sedation for neonatal intubation without side-effects. They conducted a dose-finding trial which evaluated a range of doses in infants of different gestations. They ended their buy furosemide online without a prescription study after 91 infants because they only achieved adequate sedation without side effects in 13% of patients. Hypotension (mean blood pressure below post-mentrual age in the hour after treatment) was observed in 59% of patients.

See page 489Growth to early adulthood following extremely preterm birthThe EPICure cohort comprised all babies born at 25 completed weeks of gestation or less in all 276 maternity units in the UK and Ireland from March to December 1995. Growth data into adulthood are sparse for buy furosemide online without a prescription such immature infants. Yanyan Ni and colleagues report the growth to 19 years of 129 of the cohort in comparison with contemporary term born controls. The extremely preterm infants were on average 4.0 cm shorter and 6.8 kg lighter with a buy furosemide online without a prescription 1.5 cm smaller head circumference relative to controls at 19 years. Body mass index was significantly elevated to +0.32 SD.

With practice changing to include the provision of life sustaining treatment to greater numbers of infants born at 22 and 23 weeks of gestation there is a strong case for further cohort studies to include this population of infants. See page F496Premature birth is a worldwide problem, and the most significant cause of loss of disability-adjusted life years in buy furosemide online without a prescription children. Impairment and disability among survivors are common. Cerebral palsy is diagnosed in around 10% of infants born before 33 weeks of gestation, although the rates approximately double in the smallest and most vulnerable infants, and other motor disturbances are being detected in 25%–40%. Cognitive, socialisation and behavioural problems are apparent in around half of preterm infants, and there is increased buy furosemide online without a prescription incidence of neuropsychiatric disorders, which develop as the children grow older.

Adults born preterm are approximately seven times more likely to be diagnosed with bipolar disease.1 2The neuropathological basis for these long-term and debilitating disorders is often unclear. Brain imaging by ultrasound or MRI shows that only a relatively small proportion of infants have significant destructive brain lesions, and these major lesions are not detected commonly enough to account for the prevalence of long-term impairments. However, abnormalities of brain growth and maturation are common, and it is now apparent that, in addition to recognisable cerebral damage, adverse neurological, cognitive and psychiatric outcomes are consistently associated with abnormal cerebral maturation and development.Currently, most clinical decision-making remains focused around a number of well-described cerebral lesions usually buy furosemide online without a prescription detected in routine practice using cranial ultrasound. Periventricular haemorrhage is common. Severe haemorrhages are associated with long-term adverse outcomes, and in infants born before 33 weeks of gestation, haemorrhagic parenchymal infarction predicts motor deficits ….

Furosemide blood sugar

Over 12,000 home health agencies served 5 million disabled and older Americans in 2018 furosemide blood sugar. Home health aides help their clients with the tasks of daily living, like eating and showering, as well as with clinical tasks, like taking blood pressure and leading physical therapy exercises. Medicare relies on home health care services because they help patients discharged furosemide blood sugar from the hospital and skilled nursing facilities recover but at a much lower cost. Together, Medicare and Medicaid make up 76% of all home health spending.Home health care workers serve a particularly important role in rural areas.

As rural areas lose physicians and hospitals, home health agencies furosemide blood sugar often replace primary care providers. The average age of residents living in rural counties is seven years older than in urban counties, and this gap is growing. The need for home health agencies serving the elderly in rural areas will continue to grow over the coming decades.Rural home health agencies face unique challenges. Low concentrations of people are dispersed over large geographic areas leading to long travel times for workers to drive to clients’ homes furosemide blood sugar.

Agencies in rural areas also have difficulties recruiting and maintaining a workforce. Due to these difficulties, agencies may not be able to serve all rural beneficiaries, initiate care on time, or deliver all covered services.Congress has supported measures to encourage home health agencies to work in rural areas since furosemide blood sugar the 1980s by using rural add-on payments. A rural add-on is a percentage increase on top of per visit and episode-of-care payments. When a home health aide works in a rural county, Medicare pays their home health agency a standard fee plus furosemide blood sugar a rural add-on.

With a 5% add-on, Medicare would pay $67.78 for an aide home visit in a city and $71.17 for the same care in a rural area.Home health care workers serve a particularly important role in rural areas. As rural areas lose physicians and hospitals, home health agencies often replace primary care providers.Rural add-on payments have fluctuated based on Congressional budgets and political priorities. From 2003 to 2019, the amount Medicare paid agencies changed furosemide blood sugar eight times. For instance, the add-on dropped from 10% to nothing in April 2003.

Then, in April furosemide blood sugar 2004, Congress set the rural add-on to 5%.The variation in payments created a natural experiment for researchers. Tracy Mroz and colleagues assessed how rural add-ons affected the supply of home health agencies in rural areas. They asked if the number of agencies in urban and rural counties varied depending on the presence and dollar amount of rural add-ons between 2002 and 2018. Though rural add-ons have been furosemide blood sugar in place for over 30 years, researchers had not previously investigated their effect on the availability of home healthcare.The researchers found that rural areas adjacent to urban areas were not affected by rural add-ons.

They had similar supply to urban areas whether or not add-ons were in place. In contrast, isolated rural furosemide blood sugar areas were affected substantially by add-ons. Without add-ons, the number of agencies in isolated rural areas lagged behind those in urban areas. When the add-ons were at least 5%, the availability of home health in isolated rural areas was comparable to urban areas.In 2020, Congress implemented a system of payment reform that reimburses home health agencies in rural counties by population density and furosemide blood sugar home health use.

Under the new system, counties with low population densities and low home health use will receive the greatest rural add-on payments. These payments aim to increase and maintain the availability of care in the most vulnerable rural home health markets. Time will tell if this approach gives sufficient incentive to ensure access to quality care in the nation’s most isolated furosemide blood sugar areas.Photo via Getty ImagesStart Preamble Correction In proposed rule document 2020-13792 beginning on page 39408 in the issue of Tuesday, June 30, 2020, make the following correction. On page 39408, in the first column, in the DATES section, “August 31, 2020” should read “August 24, 2020”.

End Preamble [FR Doc furosemide blood sugar. C1-2020-13792 Filed 7-17-20. 8:45 am]BILLING CODE 1301-00-D.

Over 12,000 home health buy furosemide online without a prescription agencies served 5 million disabled and older Americans in 2018. Home health aides help their clients with the tasks of daily living, like eating and showering, as well as with clinical tasks, like taking blood pressure and leading physical therapy exercises. Medicare relies on home health buy furosemide online without a prescription care services because they help patients discharged from the hospital and skilled nursing facilities recover but at a much lower cost. Together, Medicare and Medicaid make up 76% of all home health spending.Home health care workers serve a particularly important role in rural areas.

As rural areas lose physicians buy furosemide online without a prescription and hospitals, home health agencies often replace primary care providers. The average age of residents living in rural counties is seven years older than in urban counties, and this gap is growing. The need for home health agencies serving the elderly in rural areas will continue to grow over the coming decades.Rural home health agencies face unique challenges. Low concentrations of people are dispersed over large geographic areas buy furosemide online without a prescription leading to long travel times for workers to drive to clients’ homes.

Agencies in rural areas also have difficulties recruiting and maintaining a workforce. Due to these difficulties, agencies may not be able to serve all buy furosemide online without a prescription rural beneficiaries, initiate care on time, or deliver all covered services.Congress has supported measures to encourage home health agencies to work in rural areas since the 1980s by using rural add-on payments. A rural add-on is a percentage increase on top of per visit and episode-of-care payments. When a home health aide works in a rural county, buy furosemide online without a prescription Medicare pays their home health agency a standard fee plus a rural add-on.

With a 5% add-on, Medicare would pay $67.78 for an aide home visit in a city and $71.17 for the same care in a rural area.Home health care workers serve a particularly important role in rural areas. As rural areas lose physicians and hospitals, home health agencies often replace primary care providers.Rural add-on payments have fluctuated based on Congressional budgets and political priorities. From 2003 to 2019, the amount Medicare buy furosemide online without a prescription paid agencies changed eight times. For instance, the add-on dropped from 10% to nothing in April 2003.

Then, in April buy furosemide online without a prescription 2004, Congress set the rural add-on to 5%.The variation in payments created a natural experiment for researchers. Tracy Mroz and colleagues assessed how rural add-ons affected the supply of home health agencies in rural areas. They asked if the number of agencies in urban and rural counties varied depending on the presence and dollar amount of rural add-ons between 2002 and 2018. Though rural add-ons have been in place for over 30 years, researchers had buy furosemide online without a prescription not previously investigated their effect on the availability of home healthcare.The researchers found that rural areas adjacent to urban areas were not affected by rural add-ons.

They had similar supply to urban areas whether or not add-ons were in place. In contrast, isolated rural areas were affected substantially by add-ons buy furosemide online without a prescription. Without add-ons, the number of agencies in isolated rural areas lagged behind those in urban areas. When the buy furosemide online without a prescription add-ons were at least 5%, the availability of home health in isolated rural areas was comparable to urban areas.In 2020, Congress implemented a system of payment reform that reimburses home health agencies in rural counties by population density and home health use.

Under the new system, counties with low population densities and low home health use will receive the greatest rural add-on payments. These payments aim to increase and maintain the availability of care in the most vulnerable rural home health markets. Time will tell if this approach gives sufficient incentive to ensure access to quality care in the nation’s most isolated areas.Photo via Getty buy furosemide online without a prescription ImagesStart Preamble Correction In proposed rule document 2020-13792 beginning on page 39408 in the issue of Tuesday, June 30, 2020, make the following correction. On page 39408, in the first column, in the DATES section, “August 31, 2020” should read “August 24, 2020”.

End Preamble buy furosemide online without a prescription [FR Doc. C1-2020-13792 Filed 7-17-20. 8:45 am]BILLING CODE 1301-00-D.

What are furosemide used for

How to what are furosemide used for cite this article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the what are furosemide used for highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide.

As expected, the media went into a frenzy as newspapers, news what are furosemide used for channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated what are furosemide used for with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started what are furosemide used for getting distress calls from their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental what are furosemide used for Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were what are furosemide used for full of speculations about the person's mental condition and illness and also his relationships and finances. Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him.

The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for what are furosemide used for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals what are furosemide used for were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate what are furosemide used for stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we what are furosemide used for have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should what are furosemide used for familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media.

Till then, it is desirable to be guided by what are furosemide used for the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr. O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli what are furosemide used for Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage.

This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods.

These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies. And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain.

However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords. Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time.

Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions.

These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT. Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past. In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT.

In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes.

A single study by Coffey et al. Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h. This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies.

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al. Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al.

That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala. In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms.

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression.

It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus. The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe.

It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT. In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage.

Metabolic Neuroimaging Studies. Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower.

However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover. Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable. The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT.

Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations.

The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT. Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT.

Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT.

This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al. In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al.

In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied. In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus.

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder.

The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration. However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory.

Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia. It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT.

One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al. In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail.

And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this. These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered.

However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons. Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect.

This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT. However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question.

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50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity. The synaptic consolidation hypothesis. Prog Neurobiol 2005;76:99-125.

51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders. Biol Psychiatry 2006;59:1116-27. 52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al.

Serum and plasma BDNF levels in major depression. A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

A systematic review and meta-analysis of clinical studies on major depression and BDNF levels. Implications for the role of neuroplasticity in depression. Int J Neuropsychopharmacol 2008;11:1169-80. 54.Rocha RB, Dondossola ER, Grande AJ, Colonetti T, Ceretta LB, Passos IC, et al.

Increased BDNF levels after electroconvulsive therapy in patients with major depressive disorder. A meta-analysis study. J Psychiatr Res 2016;83:47-53. 55.UK ECT Review Group.

Efficacy and safety of electroconvulsive therapy in depressive disorders. A systematic review and meta-analysis. Lancet 2003;361:799-808. 56.57.Semkovska M, McLoughlin DM.

Objective cognitive performance associated with electroconvulsive therapy for depression. A systematic review and meta-analysis. Biol Psychiatry 2010;68:568-77. 58.Tulving E, Madigan SA.

Memory and verbal learning. Annu Rev Psychol 1970;21:437-84. 59.Rose D, Fleischmann P, Wykes T, Leese M, Bindman J. Patients' perspectives on electroconvulsive therapy.

Systematic review. BMJ 2003;326:1363. 60.Semkovska M, McLoughlin DM. Measuring retrograde autobiographical amnesia following electroconvulsive therapy.

Historical perspective and current issues. J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP. The effect of electroconvulsive therapy on autobiographical memory.

A systematic review. J ECT 2008;24:10-7. 62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy.

Arch Gen Psychiatry 1975;32:1557-64. 63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction. A prospective three-year follow-up study.

Br J Psychiatry 1983;142:1-8. 64.Squire LR, Slater PC, Miller PL. Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up.

Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC. Memory complaint after electroconvulsive therapy. Assessment with a new self-rating instrument.

Biol Psychiatry 1979;14:791-801. 66.Calev A, Nigal D, Shapira B, Tubi N, Chazan S, Ben-Yehuda Y, et al. Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. J Nerv Ment Dis 1991;179:526-33.

67.Sackeim HA, Prudic J, Devanand DP, Nobler MS, Lisanby SH, Peyser S, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities. Arch Gen Psychiatry 2000;57:425-34. 68.Abrams R.

Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3. 69.Peretti CS, Danion JM, Grangé D, Mobarek N. Bilateral ECT and autobiographical memory of subjective experiences related to melancholia.

A pilot study. J Affect Disord 1996;41:9-15. 70.Weiner RD, Rogers HJ, Davidson JR, Squire LR. Effects of stimulus parameters on cognitive side effects.

Ann N Y Acad Sci 1986;462:315-25. 71.Prudic J, Peyser S, Sackeim HA. Subjective memory complaints. A review of patient self-assessment of memory after electroconvulsive therapy.

J ECT 2000;16:121-32. 72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46.

73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ. Effects of ECT and depression on various aspects of memory. Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al.

Efficacy and cognitive effects of right unilateral electroconvulsive therapy. J ECT 2000;16:370-9. 75.Coleman EA, Sackeim HA, Prudic J, Devanand DP, McElhiney MC, Moody BJ. Subjective memory complaints prior to and following electroconvulsive therapy.

Biol Psychiatry 1996;39:346-56. 76.Berggren Š, Gustafson L, Höglund P, Johanson A. A long-term longitudinal follow-up of depressed patients treated with ECT with special focus on development of dementia. J Affect Disord 2016;200:15-24.

77.Brodaty H, Hickie I, Mason C, Prenter L. A prospective follow-up study of ECT outcome in older depressed patients. J Affect Disord 2000;60:101-11. 78.Osler M, Rozing MP, Christensen GT, Andersen PK, Jørgensen MB.

Electroconvulsive therapy and risk of dementia in patients with affective disorders. A cohort study. Lancet Psychiatry 2018;5:348-56. Correspondence Address:Dr.

Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

How to cite this buy furosemide online without a prescription article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one buy furosemide online without a prescription of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide.

As expected, buy furosemide online without a prescription the media went into a frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, buy furosemide online without a prescription and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from their patients in despair buy furosemide online without a prescription with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental buy furosemide online without a prescription Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and buy furosemide online without a prescription also his relationships and finances. Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him.

The Indian Psychiatric Society has written to the Press buy furosemide online without a prescription Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental buy furosemide online without a prescription health professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and buy furosemide online without a prescription injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact buy furosemide online without a prescription with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, buy furosemide online without a prescription and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media.

Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and buy furosemide online without a prescription limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr. O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, buy furosemide online without a prescription Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage.

This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods.

These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies. And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain.

However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords. Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time.

Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions.

These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT. Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past. In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT.

In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes.

A single study by Coffey et al. Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h. This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies.

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al. Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al.

That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala. In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms.

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression.

It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus. The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe.

It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT. In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage.

Metabolic Neuroimaging Studies. Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower.

However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover. Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable. The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT.

Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations.

The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT. Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT.

Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT.

This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al. In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al.

In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied. In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus.

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder.

The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration. However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory.

Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia. It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT.

One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al. In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail.

And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this. These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered.

However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons. Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect.

This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT. However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question.

However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J. Electroconvulsive therapy. Part I.

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Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

Furosemide in sports

A hearing aid is a small electronic device worn behind the ear or in the ear furosemide in sports canal. It amplifies sound so that a person with hearing loss can hear sound better. Hearing devices have three components. A microphone, amplifier and speaker furosemide in sports. Sound comes through the microphone and is converted into an electrical signal and sent to the amplifier.

The amplifier increases the power of the signals and sends them to the ear through the speaker. Today’s hearing aid is much smaller and more furosemide in sports powerful than the hearing devices our parents and grandparents wore even 10 years ago. Advances in digital technology make them better able to distinguish conversation in noisy environments. Many are Bluetooth capable and connect with smartphones and other personal electronic devices we now use on a daily basis. More.

See the different types and styles of hearing aids Can hearing aids improve my hearing?. That depends on what type of hearing loss you have. Sensorineural hearing loss is caused by damage to the sensory hair cells of the inner ear. This damage can be caused by exposure to loud noise, illness, medication, injury or age. If your hearing healthcare professional determines you have sensorineural hearing loss, you will probably benefit from wearing a hearing aid.

Age-related hearing loss, generally a subset of sensorineural, is the loss of hearing that occurs in most people as they age. This condition, known medically as presbycusis, is common and can often be improved with hearing aids. Conductive hearing loss, however is usually caused by an obstruction in the ear canal, such as swelling due to an ear infection or a benign tumor. If your hearing healthcare professional determines your hearing loss is conductive, your hearing may return to normal once the obstruction has been removed. If your hearing does not return to normal, you may benefit from wearing a hearing aid, cochlear implant or bone-anchored hearing system.

What should I look for when choosing a hearing aid?. That depends on your lifestyle and your budget. An active person who enjoys traveling and athletic activities will most likely need a different model of hearing aid than someone who spends most of their time at home watching television. Your hearing healthcare professional will ask a variety of questions to help you determine what type of amplification you need, then work with you to make sure your hearing device works properly to help you hear the sounds that are most important to you. Remember that friend who told you they keep their hearing aids in the dresser drawer?.

That just might be because they weren’t honest with their hearing healthcare professional about their expectations and lifestyle, or didn’t schedule follow-up visits as requested. How long will it take for me to adjust to wearing hearing aids?. Wondering what to expect from new hearing aids?. Adjusting to hearing aids varies from person to person and depends upon how long you waited to treat your hearing loss as well as its severity. Although our ears collect noise from our environment, it’s actually our brain that translates it into recognizable sound.

If hearing loss is left untreated, the auditory part of your brain can actually atrophy, in which case your rehabilitation may take a while longer. You’ll also want to wear them as recommended. Following your doctor’s orders improves your chances for success. More. 7 tips for getting used to hearing aids How long do hearing aids last?.

With proper use and maintenance, hearing aids typically last between three and five years. Can I return my hearing aids if I’m not satisfied?. Many hearing centers offer a trial period to ensure you are satisfied. Be sure to ask your hearing healthcare professional about their policies before you purchase any hearing device. How can I find out if I need a hearing aid?.

The best way to find out if you need a hearing aid is to have your hearing tested by a hearing healthcare professional. A thorough hearing test will take approximately an hour of your time during which you will most likely be asked to provide your health history, undergo a series of hearing assessments, and discuss your lifestyle and expectations for better hearing. Afterward, a hearing healthcare professional will discuss the results of your test with you and, if its determined that your hearing can benefit from amplification, discuss next steps. If your hearing has changed recently or you suspect you have hearing loss, make an appointment to see a hearing healthcare professional in your community as soon as possible. There’s a lot to hear in this world – laughing children, music, the sound of someone you love calling your name – and hearing aids may be able to help you hear them.When deciding on a new pair of hearing aids, you should consider how long they will last.

Just like buying a car, the actual mileage may vary.Most modern high-quality hearing aids have a life expectancy on average between three and seven years. However, keep in mind that two people can buy exactly the same hearing aids and have them last vastly different amounts of time. Here's why. New hearing aids generally last aroundfive years, but this depends on a lotof different factors. Factors impacting how long hearing aids will last There are at least nine factors that impact the average lifespan of a hearing aid.

Materials used to make hearing aids Frequency of cleaning Where hearing aids are worn How hearing aids are stored Hearing aid style A person's body physiology Frequency of maintenance Technological advancements Unique hearing needs 1. Materials used to make hearing aids Although they are designed to be durable, hearing aids are made of plastic, metal, silicon, polymers and other materials that may be subject to some degree of structural degradation over time. Most hearing aids sold today have a protective nanocoating on them to resist water, dust and moisture, but you should still treat them gently to protect them from shock and impacts. 2. Frequency of cleaning Most people would never dream of going months without washing their hair, face or body.

However, they forget their hearing aids are exposed to the same environment—moisture, dust, skin oils and sweat, extreme temperatures and sunlight. All this occurs in addition to the earwax generated by your ear canal in its natural cleaning process. Some wearers only have their hearing aids professionally cleaned twice a year or so. This takes a toll on hearing aids and can significantly reduce their life expectancy. To help your hearing aids life expectancy, clean them daily as directed by your hearing care practitioner and have them professionally cleaned in the hearing clinic every three to four months.

3. Where hearing aids are worn Hearing aids that are consistently in damp or dusty environments often have more performance issues than other hearing aids. If you’re concerned about the environments in which you wear your hearing aids, consult your hearing care professional for ideas about protective measures. You may need to use protective sleeves or schedule more frequent professional cleanings to extend the life of your hearing aids. 4.

How hearing aids are stored The way hearing aids are stored when you’re not wearing them can also be a factor in hearing aid life expectancy. For hearing aids with disposable batteries, storing hearing aids with the battery door open will keep them safer. A case with a dehumidifier will keep them drier as well, which will also help them last longer. Ask your hearing care practitioner what type of storage case or dehumidifier options would work best for your hearing aids. For rechargeable hearing aids, lithium batteries last about four to five years.

Just like with smartphones, the battery lifespan gets shorter the longer you own the device. If you notice your battery draining faster than usual, speak to your hearing care provider about whether new rechargeable batteries will help, or if you should get new devices. 5. Style of hearing aids Conventional wisdom in the hearing aid industry is that behind-the-ear (BTE) styles tend to have a long lifespan than in-the-ear (ITE) styles. The reason behind this wisdom is more of the electronic components sit in the damp environment of the ear canal with ITE styles.

However, recent technical advancements in nanocoatings on internal and external components may soon make this durability difference a thing of the past. 6. Your body’s physiology Some body chemistries are harder on the plastic and metal components of hearing aids and tend to discolor or degrade parts much faster than others. Some people have very oily skin, produce a lot of earwax or sweat profusely–all of these factors can impact hearing aid life, too. You can’t control these things, of course, but if you have any of these issues you should discuss them with your hearing care practitioner when you’re selecting hearing aids.

7. Frequency of maintenance Most hearing aids have some readily-replaceable parts, such as wax guards, earmold tubing and silicone dome earpiece tips. These parts are regularly replaced during routine maintenance visits with your hearing care practitioner. There are other parts which can usually be replaced or repaired in the clinic if they become damaged or nonfunctional, like battery doors, earmolds, external speakers and microphone covers. These types of maintenance activities are very important for making your hearing aids last as long as possible.

8. Technological advancements Hearing aid technology changes often.Many new hearing aids can connectto phones via Bluetooth, for example. Obsolescence can become an issue for very old hearing aids. After several years (usually between five and 10), hearing aid manufacturers may stop making replacement parts for a particular aid, which may make repairs on old hearing aids difficult or impossible. Software used to program hearing aids also changes over time and eventually becomes obsolete.

This often makes it difficult to reprogram very old hearing aids. Hearing aid performance and features advance very rapidly. The technology in the most advanced hearing aids available six or seven years ago would be considered basic today. While some folks are content to stick with what they have if it still performs for them, many people who buy hearing aids find themselves wanting to benefit from the new technology that becomes available four or five years down the road. 9.

Changing needs Everything described up to this point focuses on the hearings aids themselves. Changing needs of the wearer can also affect how long hearing aids last. Sometimes after several years, a person's hearing loss can progress to the point where a more powerful hearing aid would suit them better. A person's lifestyle could change and require a hearing aid with more—or fewer—features. In cases where a hearing aid is replaced while it’s still functional, your hearing care practitioner can assist you in donating the used hearing aids to a worthy cause.

Hearing devices buy furosemide online without a prescription have three components. A microphone, amplifier and speaker. Sound comes through the microphone and is converted into an electrical signal and sent to the amplifier. The amplifier increases the power buy furosemide online without a prescription of the signals and sends them to the ear through the speaker. Today’s hearing aid is much smaller and more powerful than the hearing devices our parents and grandparents wore even 10 years ago.

Advances in digital technology make them better able to distinguish conversation in noisy environments. Many are Bluetooth capable and connect with smartphones and other personal buy furosemide online without a prescription electronic devices we now use on a daily basis. More. See the different types and styles of hearing aids Can hearing aids improve my hearing?. That depends on what buy furosemide online without a prescription type of hearing loss you have.

Sensorineural hearing loss is caused by damage to the sensory hair cells of the inner ear. This damage can be caused by exposure to loud noise, illness, medication, injury or age. If your hearing healthcare professional determines you have sensorineural hearing loss, you will probably benefit from wearing a hearing aid buy furosemide online without a prescription. Age-related hearing loss, generally a subset of sensorineural, is the loss of hearing that occurs in most people as they age. This condition, known medically as presbycusis, is common and can often be improved with hearing aids.

Conductive hearing loss, however is usually caused by an obstruction in the ear canal, such as swelling buy furosemide online without a prescription due to an ear infection or a benign tumor. If your hearing healthcare professional determines your hearing loss is conductive, your hearing may return to normal once the obstruction has been removed. If your hearing does not return to normal, you may benefit from wearing a hearing aid, cochlear implant or bone-anchored hearing system. What should I look for buy furosemide online without a prescription when choosing a hearing aid?. That depends on your lifestyle and your budget.

An active person who enjoys traveling and athletic activities will most likely need a different model of hearing aid than someone who spends most of their time at home watching television. Your hearing healthcare professional will ask a variety of questions to help you determine what type of amplification you need, then work with you to make sure your hearing device works properly to buy furosemide online without a prescription help you hear the sounds that are most important to you. Remember that friend who told you they keep their hearing aids in the dresser drawer?. That just might be because they weren’t honest with their hearing healthcare professional about their expectations and lifestyle, or didn’t schedule follow-up visits as requested. How long will it buy furosemide online without a prescription take for me to adjust to wearing hearing aids?.

Wondering what to expect from new hearing aids?. Adjusting to hearing aids varies from person to person and depends upon how long you waited to treat your hearing loss as well as its severity. Although our ears buy furosemide online without a prescription collect noise from our environment, it’s actually our brain that translates it into recognizable sound. If hearing loss is left untreated, the auditory part of your brain can actually atrophy, in which case your rehabilitation may take a while longer. You’ll also want to wear them as recommended.

Following your buy furosemide online without a prescription doctor’s orders improves your chances for success. More. 7 tips for getting used to hearing aids How long do hearing aids last?. With proper use and maintenance, hearing aids buy furosemide online without a prescription typically last between three and five years. Can I return my hearing aids if I’m not satisfied?.

Many hearing centers offer a trial period to ensure you are satisfied. Be sure to ask your hearing healthcare professional about their policies before you purchase any hearing device buy furosemide online without a prescription. How can I find out if I need a hearing aid?. The best way to find out if you need a hearing aid is to have your hearing tested by a hearing healthcare professional. A thorough hearing test will take approximately an hour of your time during which you will most likely be asked to provide your health history, undergo a series of hearing assessments, and discuss your lifestyle buy furosemide online without a prescription and expectations for better hearing.

Afterward, a hearing healthcare professional will discuss the results of your test with you and, if its determined that your hearing can benefit from amplification, discuss next steps. If your hearing has changed recently or you suspect you have hearing loss, make an appointment to see a hearing healthcare professional in your community as soon as possible. There’s a lot to hear in this world – laughing children, music, the sound of someone you love calling your name – and hearing aids may be able buy furosemide online without a prescription to help you hear them.When deciding on a new pair of hearing aids, you should consider how long they will last. Just like buying a car, the actual mileage may vary.Most modern high-quality hearing aids have a life expectancy on average between three and seven years. However, keep in mind that two people can buy exactly the same hearing aids and have them last vastly different amounts of time.

Here's why buy furosemide online without a prescription. New hearing aids generally last aroundfive years, but this depends on a lotof different factors. Factors impacting how long hearing aids will last There are at least nine factors that impact the average lifespan of a hearing aid. Materials used to make hearing aids Frequency buy furosemide online without a prescription of cleaning Where hearing aids are worn How hearing aids are stored Hearing aid style A person's body physiology Frequency of maintenance Technological advancements Unique hearing needs 1. Materials used to make hearing aids Although they are designed to be durable, hearing aids are made of plastic, metal, silicon, polymers and other materials that may be subject to some degree of structural degradation over time.

Most hearing aids sold today have a protective nanocoating on them to resist water, dust and moisture, but you should still treat them gently to protect them from shock and impacts. 2 buy furosemide online without a prescription. Frequency of cleaning Most people would never dream of going months without washing their hair, face or body. However, they forget their hearing aids are exposed to the same environment—moisture, dust, skin oils and sweat, extreme temperatures and sunlight. All this occurs in addition buy furosemide online without a prescription to the earwax generated by your ear canal in its natural cleaning process.

Some wearers only have their hearing aids professionally cleaned twice a year or so. This takes a toll on hearing aids and can significantly reduce their life expectancy. To help your hearing aids life expectancy, clean them daily as directed by your hearing care practitioner and have them professionally cleaned in the buy furosemide online without a prescription hearing clinic every three to four months. 3. Where hearing aids are worn Hearing aids that are consistently in damp or dusty environments often have more performance issues than other hearing aids.

If you’re concerned buy furosemide online without a prescription about the environments in which you wear your hearing aids, consult your hearing care professional for ideas about protective measures. You may need to use protective sleeves or schedule more frequent professional cleanings to extend the life of your hearing aids. 4. How hearing aids are stored The way hearing aids are stored when you’re buy furosemide online without a prescription not wearing them can also be a factor in hearing aid life expectancy. For hearing aids with disposable batteries, storing hearing aids with the battery door open will keep them safer.

A case with a dehumidifier will keep them drier as well, which will also help them last longer. Ask your hearing care practitioner what type buy furosemide online without a prescription of storage case or dehumidifier options would work best for your hearing aids. For rechargeable hearing aids, lithium batteries last about four to five years. Just like with smartphones, the battery lifespan gets shorter the longer you own the device. If you notice your buy furosemide online without a prescription battery draining faster than usual, speak to your hearing care provider about whether new rechargeable batteries will help, or if you should get new devices.

5. Style of hearing aids Conventional wisdom in the hearing aid industry is that behind-the-ear (BTE) styles tend to have a long lifespan than in-the-ear (ITE) styles. The reason behind this buy furosemide online without a prescription wisdom is more of the electronic components sit in the damp environment of the ear canal with ITE styles. However, recent technical advancements in nanocoatings on internal and external components may soon make this durability difference a thing of the past. 6.

Your body’s physiology Some body chemistries are harder on the plastic and buy furosemide online without a prescription metal components of hearing aids and tend to discolor or degrade parts much faster than others. Some people have very oily skin, produce a lot of earwax or sweat profusely–all of these factors can impact hearing aid life, too. You can’t control these things, of course, but if you have any of these issues you should discuss them with your hearing care practitioner when you’re selecting hearing aids. 7. Frequency of maintenance Most hearing aids have some readily-replaceable parts, such as wax guards, earmold tubing and silicone dome earpiece tips.

These parts are regularly replaced during routine maintenance visits with your hearing care practitioner. There are other parts which can usually be replaced or repaired in the clinic if they become damaged or nonfunctional, like battery doors, earmolds, external speakers and microphone covers. These types of maintenance activities are very important for making your hearing aids last as long as possible. 8. Technological advancements Hearing aid technology changes often.Many new hearing aids can connectto phones via Bluetooth, for example.

Obsolescence can become an issue for very old hearing aids. After several years (usually between five and 10), hearing aid manufacturers may stop making replacement parts for a particular aid, which may make repairs on old hearing aids difficult or impossible. Software used to program hearing aids also changes over time and eventually becomes obsolete. This often makes it difficult to reprogram very old hearing aids. Hearing aid performance and features advance very rapidly.

The technology in the most advanced hearing aids available six or seven years ago would be considered basic today. While some folks are content to stick with what they have if it still performs for them, many people who buy hearing aids find themselves wanting to benefit from the new technology that becomes available four or five years down the road. 9. Changing needs Everything described up to this point focuses on the hearings aids themselves. Changing needs of the wearer can also affect how long hearing aids last.

Sometimes after several years, a person's hearing loss can progress to the point where a more powerful hearing aid would suit them better. A person's lifestyle could change and require a hearing aid with more—or fewer—features. In cases where a hearing aid is replaced while it’s still functional, your hearing care practitioner can assist you in donating the used hearing aids to a worthy cause. How do you determine which factors will affect your hearing aids?. Hearing aid durability is impacted by a variety of factors, many of which you can work with your hearing care practitioner to control.