Epididymo-orchitis

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Orchitis (or-KIE-tis) is an inflammation of one or both testicles. Bacterial or viral infections can cause orchitis, or the cause can be unknown. Orchitis is most often the result of a bacterial infection, such as a sexually transmitted infection (STI). In some cases, the mumps virus can cause orchitis.

Bacterial orchitis might be associated with epididymitis — an inflammation of the coiled tube (epididymis) at the back of the testicle that stores and carries sperm. In that case, it’s called epididymo-orchitis.

Orchitis causes pain and can affect fertility. Medication can treat the causes of bacterial orchitis and can ease some signs and symptoms of viral orchitis. But it can take several weeks for scrotal tenderness to disappear.

Acute epididymo-orchitis is a clinical syndrome consisting of pain, swelling and inflammation of the epididymis, with or without inflammation of the testes. The most common route of infection is local extension and is mainly due to infections spreading from the urethra (sexually transmitted infections (STIs)) or from the bladder[1]. Orchitis (infection limited to the testis) is much less common. Chronic epididymitis refers to epididymal pain and inflammation (usually without scrotal swelling) that lasts for more than six months.

  • Epididymitis means inflammation of the epididymis (the structure next to the testicle (testis) that is involved in making sperm).
  • Orchitis means inflammation of a testicle.

As the epididymis and testis lie next to each other, it is often difficult to tell if the epididymis, the testis, or both are inflamed. Therefore, the term epididymo-orchitis is often used.

Causes

Orchitis can be caused by a bacterial or viral infection. Sometimes a cause of orchitis can’t be determined.

Bacterial orchitis

Most often, bacterial orchitis is associated with or the result of epididymitis. Epididymitis usually is caused by an infection of the urethra or bladder that spreads to the epididymis.

Often, the cause of the infection is an STI. Other causes of infection can be related to having been born with abnormalities in your urinary tract or having had a catheter or medical instruments inserted into your penis.

Viral orchitis

The mumps virus usually causes viral orchitis. Nearly one-third of males who contract the mumps after puberty develop orchitis, usually four to seven days after onset of the mumps.

Acute Epididymitis

An “acute” case is most often caused by an infection from bacteria. The e-coli bacteria are a common cause for infection.

  • In children who haven’t reached puberty, the infection may start in the bladder or kidney. It then spreads to the testis. Some boys get more urinary tract infections, and may get this more often.
  • In men, a STD ( sexually transmitted disease) is one of the causes. Mostly from chlamydia, mycoplasma or rarely gonorrhea. These infections start in the urethra. They can then move into the testis. Sometimes there is a discharge of fluid from the urethra.

Sometimes it is caused by something else:

  • Enlarged prostate blocking the bladder
  • Infection of the prostate gland (“bacterial prostatitis”)
  • Partly blocked urethra
  • Recent catheter use

Epididymitis is sometimes caused by other things:

  • Chemical or inflammatory non-bacterial epididymitis may happen from urine flowing backwards to the epididymis. This is most often from heavy lifting. The urine causes swelling but no infection.
  • The drug “Amidarone” can be a cause but this is rare
  • An infection from the bloodstream (as with tuberculosis)
  • Other unknown causes

In any of these cases, the first sign of a problem is often pain in the back of the testis.

Chronic Epididymitis

A “chronic” case may result after acute epididymitis. It doesn’t seem to go away. It can also happen without acute symptoms or known infection. In this case, the cause is unknown.

Orchitis

Orchitis alone is mostly from a mumps virus (or other virus) infection. “Mumps orchitis” appears in about 1/3 of males who get mumps after puberty. It only occurs in boys that have mumps AFTER puberty. In some cases of mumps, interferon can be given to prevent orchitis. This infection doesn’t spread to the epididymis.

Acute Epididymo-orchitis

Acute epididymo-orchitis is most often from a bacterial infection. It can also be caused by a tuberculous infection of the epididymis, but this is rare. Rarely, it can start in the testis and spread to the epididymis.

Symptoms

Orchitis signs and symptoms usually develop suddenly and can include:

  • Swelling in one or both testicles
  • Pain ranging from mild to severe
  • Fever
  • Nausea and vomiting
  • General feeling of unwellness (malaise)

The terms “testicle pain” and “groin pain” are sometimes used interchangeably. But groin pain occurs in the fold of skin between the thigh and abdomen — not in the testicle. The causes of groin pain are different from the causes of testicle pain.

When to see a doctor

If you have pain or swelling in your scrotum, especially if the pain occurs suddenly, see your doctor right away.

A number of conditions can cause testicle pain, and some require immediate treatment. One such condition involves twisting of the spermatic cord (testicular torsion), which might cause pain similar to that caused by orchitis. Your doctor can perform tests to determine which condition is causing your pain.

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  • A study of UK general practices during the years 2003-2008 reported a highest incidence of 25/10,000 in 2004-2005. The incidence declined during the latter part of the study.
  • Acute epididymitis most commonly occurs in patients aged 15-30 years and patients older than 60 years. In the UK GP study, the incidence declined in younger age groups throughout the study period but that of males aged over 45 years was stable. Prepubertal epididymitis is rare (and testicular torsion is much more common in this age group).
  • Mumps orchitis occurs in up to 40% of postpubertal boys with mumps; it is rare in prepubertal boys. An outbreak starting in 2004 and lasting for some three years was seen in England and Wales and was attributed to a reduction in the uptake of measles-mumps-rubella (MMR) vaccine during the early to mid-1990s in children who subsequently matured.
  • Prepubertal epididymitis is thought to be more common than was once believed. It is thought to be a postviral infectious phenomenon.

Risk factors

Risk factors for nonsexually transmitted orchitis include:

  • Not being immunized against mumps
  • Having recurring urinary tract infections
  • Having surgery that involves the genitals or urinary tract
  • Being born with an abnormality in the urinary tract 

Sexual behaviors that can lead to STIs put you at risk of sexually transmitted orchitis. Those behaviors include having:

  • Multiple sexual partners
  • Sex with a partner who has an STI
  • Sex without a condom
  • A personal history of an STI

Complications

Complications of orchitis may include:

  • Testicular atrophy. Orchitis can eventually cause the affected testicle to shrink.
  • Scrotal abscess. The infected tissue fills with pus.
  • Infertility. Occasionally, orchitis can cause infertility or inadequate testosterone production (hypogonadism). But these are less likely if orchitis affects only one testicle.

Prevention

To prevent orchitis:

  • Get immunized against mumps, the most common cause of viral orchitis
  • Practice safe sex, to help protect against STIs that can cause bacterial orchitis

Treatment

Acute Epididymitis and Acute Epididymo-orchitis

Treatment often starts with a 1-2 week course of antibiotics. Most cases can be treated out of the hospital with pills. The best medicine for you will depend on the type of bacteria found. The most common antibiotics used are:

  • Doxycycline
  • Ciprofloxacin
  • Levofloxacin
  • Trimethoprim-sulfamethoxazole

For bad cases of infection, you may need to stay in the hospital for treatment. These are cases with pain that’s hard to control with vomiting, high fever and if you are not getting better with antibiotics given by mouth. Occasionally, for bad cases, narcotics are needed for a few days.

Tuberculosis epididymitis is more serious but is very rare. It is treated with anti-tuberculous drugs. If damage is bad, surgery may be needed to take out the testis and the epididymis (“orchiectomy”).

Epididymitis caused by amidarone is treated by limiting or stopping the drug. Your health care provider will tell you what to do.

For other types of non-infectious epididymitis, there’s no set treatment.

Epididymitis care involves rest for 1 – 2 days with the scrotum raised if possible. The aim is to get the inflamed area above the level of the heart. This helps blood flow, which lowers swelling and pain, and helps with healing. Putting ice on the scrotum now and then can also help. In cases due to infection, it helps to drink fluids.

Anti-inflammatory pills like ibuprofen or naproxen help ease pain. They also ease the swelling that causes the pain. If the pain is severe, a short-term narcotic pain medicine may help but is only used for a short period of time at best in most situations.

Chronic Epididymitis

Chronic epididymitis is mainly treated with drugs and comfort to ease pain. Pain medicine and applying heat are the standard treatments.

If symptoms don’t go away, your health care provider may suggest other pain medicine. Or, recommend a pain management specialist. If all else fails, the epididymis can be surgically removed (“epididymectomy”). The testis can be left in place.

Acute Orchitis

Antibiotics are often the best treatment for bacterial infections. Pain medicine may help reduce symptoms.

There’s no set care for acute mumps orchitis and this will usually resolve in time.

After Treatment

Acute Epididymitis and Acute Epididymo-orchitis

For infectious cases, it takes two to three days to start feeling better. If you don’t, and if the redness doesn’t begin to fade, call your provider. Discomfort can last for weeks to months after the full course of antibiotics is taken in some cases. It can take months for the swelling to ease. Rest with the scrotum raised for a day or two helps speed healing.

Cases of tuberculous epididymitis (without surgery) may need months to heal with medicine. The testis may shrink after treatment.

Amidarone epididymitis simply gets better after cutting the dose or stopping the drug.

Chemical epididymitis heals fully with treatment.

Please follow-up with your health care provider to make sure the problem doesn’t return.

Chronic Epididymitis

Symptoms for chronic epididymitis go away eventually or may come and go. Anti- inflammatory medicine may be needed on and off for a months or years. Symptoms are sometimes better and sometimes worse.

If surgery is done, symptoms ease in most men after a few weeks of healing. If surgery hasn’t helped, your health care provider will try drugs again. In certain cases, he/she may suggest microsurgery to block nerves on the spermatic cord.

Acute Orchitis

Pain often goes away after the acute phase. The testis often shrinks.

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prostatic hyperplasia

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Benign prostatic hyperplasia—also called BPH—is a condition in men in which the prostate gland is enlarged and not cancerous. Benign prostatic hyperplasia is also called benign prostatic hypertrophy or benign prostatic obstruction.

The prostate goes through two main growth periods as a man ages. The first occurs early in puberty, when the prostate doubles in size. The second phase of growth begins around age 25 and continues during most of a man’s life. Benign prostatic hyperplasia often occurs with the second growth phase.

As the prostate enlarges, the gland presses against and pinches the urethra. The bladder wall becomes thicker. Eventually, the bladder may weaken and lose the ability to empty completely, leaving some urine in the bladder. The narrowing of the urethra and urinary retention—the inability to empty the bladder completely—cause many of the problems associated with benign prostatic hyperplasia.

BPH is an enlarged prostate. The prostate goes through two main growth cycles during a man’s life. The first occurs early in puberty, when the prostate doubles in size. The second phase of growth starts around age 25 and goes on for most of the rest of a man’s life. BPH most often occurs during this second growth phase.

As the prostate enlarges, it presses against the urethra. The bladder wall becomes thicker. One day, the bladder may weaken and lose the ability to empty fully, leaving some urine in the bladder. Narrowing of the urethra and urinary retention – being unable to empty the bladder fully – cause many of the problems of BPH.

BPH is benign. This means it is not cancer. It does not cause or lead to cancer. However, BPH and cancer can happen at the same time.

BPH is common. About half of all men between ages 51 and 60 have BPH. Up to 90% of men over age 80 have it.

causes

The prostate gland is located beneath your bladder. The tube that transports urine from the bladder out of your penis (urethra) passes through the center of the prostate. When the prostate enlarges, it begins to block urine flow.

Most men have continued prostate growth throughout life. In many men, this continued growth enlarges the prostate enough to cause urinary symptoms or to significantly block urine flow.

It isn’t entirely clear what causes the prostate to enlarge. However, it might be due to changes in the balance of sex hormones as men grow older.

The causes of BPH are not well-understood. Some researchers believe that factors related to aging and the testicles may cause BPH. This is because BPH does not develop in men whose testicles were removed before puberty.

Throughout their lives, men produce both testosterone, a male hormone, and small amounts of estrogen, a female hormone. As men age, the amount of active testosterone in the blood lowers, leaving a higher share of estrogen. Studies have suggested that BPH may happen because the higher share of estrogen in the prostate adds to the activity of substances that start prostate cells to grow.

Another theory points to dihydrotestosterone (DHT), a male hormone that plays a role in prostate development and growth. Some research has shown that, even when testosterone levels in the blood start to fall, high levels of DHT still build up in the prostate. This may push prostate cells to continue to grow. Scientists have noted that men who do not produce DHT do not develop BPH.

Symptoms

The severity of symptoms in people who have prostate gland enlargement varies, but symptoms tend to gradually worsen over time. Common signs and symptoms of BPH include:

  • Frequent or urgent need to urinate
  • Increased frequency of urination at night (nocturia)
  • Difficulty starting urination
  • Weak urine stream or a stream that stops and starts
  • Dribbling at the end of urination
  • Inability to completely empty the bladder

Less common signs and symptoms include:

  • Urinary tract infection
  • Inability to urinate
  • Blood in the urine

The size of your prostate doesn’t necessarily determine the severity of your symptoms. Some men with only slightly enlarged prostates can have significant symptoms, while other men with very enlarged prostates can have only minor urinary symptoms.

In some men, symptoms eventually stabilize and might even improve over time.

Other possible causes of urinary symptoms

Conditions that can lead to symptoms similar to those caused by enlarged prostate include:

  • Urinary tract infection
  • Inflammation of the prostate (prostatitis)
  • Narrowing of the urethra (urethral stricture)
  • Scarring in the bladder neck as a result of previous surgery
  • Bladder or kidney stones
  • Problems with nerves that control the bladder
  • Cancer of the prostate or bladder

How common is benign prostatic hyperplasia?

Benign prostatic hyperplasia is the most common prostate problem for men older than age 50. In 2010, as many as 14 million men in the United States had lower urinary tract symptoms suggestive of benign prostatic hyperplasia.1 Although benign prostatic hyperplasia rarely causes symptoms before age 40, the occurrence and symptoms increase with age. Benign prostatic hyperplasia affects about 50 percent of men between the ages of 51 and 60 and up to 90 percent of men older than 80.

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Risk factors

Risk factors for prostate gland enlargement include:

  • Aging. Prostate gland enlargement rarely causes signs and symptoms in men younger than age 40. About one-third of men experience moderate to severe symptoms by age 60, and about half do so by age 80.
  • Family history. Having a blood relative, such as a father or a brother, with prostate problems means you’re more likely to have problems.
  • Diabetes and heart disease. Studies show that diabetes, as well as heart disease and use of beta blockers, might increase the risk of BPH.
  • Lifestyle. Obesity increases the risk of BPH, while exercise can lower your risk.

Complications

Complications of an enlarged prostate can include:

  • Sudden inability to urinate (urinary retention). You might need to have a tube (catheter) inserted into your bladder to drain the urine. Some men with an enlarged prostate need surgery to relieve urinary retention.
  • Urinary tract infections (UTIs). Inability to fully empty the bladder can increase the risk of infection in your urinary tract. If UTIs occur frequently, you might need surgery to remove part of the prostate.
  • Bladder stones. These are generally caused by an inability to completely empty the bladder. Bladder stones can cause infection, bladder irritation, blood in the urine and obstruction of urine flow.
  • Bladder damage. A bladder that hasn’t emptied completely can stretch and weaken over time. As a result, the muscular wall of the bladder no longer contracts properly, making it harder to fully empty your bladder.
  • Kidney damage. Pressure in the bladder from urinary retention can directly damage the kidneys or allow bladder infections to reach the kidneys.

Most men with an enlarged prostate don’t develop these complications. However, acute urinary retention and kidney damage can be serious health threats.

Having an enlarged prostate is not believed to increase your risk of developing prostate cancer.

diagnosis

When checking you for BPH, your doctor will usually begin by doing a physical exam and asking you about your medical history. The physical exam includes a rectal examination that allows the doctor to estimate the size and shape of your prostate. Other tests can include:

  • Urinalysis: Your urine is checked for blood and bacteria.
  • Prostatic biopsy: A small amount of prostate tissue is removed and examined for abnormalities.
  • Urodynamic test: Your bladder is filled with liquid via a catheter to measure the pressure of your bladder during urination.
  • Prostate-specific antigen (PSA) test: This blood test checks for cancer of the prostate.
  • Post-void residual: This tests the amount of urine left in your bladder after urination.
  • Cystoscopy: This is the examination of your urethra and bladder with a tiny lighted scope that is inserted into your urethra
  • Intravenous pyelography or urography: This is an X-ray exam or CT scan that is done after a dye is injected into your body. The dye highlights your entire urinary system on the images produced by the X-ray or CT.

Your doctor may also ask about medications you’re taking that might be affecting your urinary system, such as:

  • antidepressants
  • diuretics
  • antihistamines
  • sedatives

Your doctor can make any necessary medication adjustments. Don’t attempt to adjust your medications or doses yourself. Let your doctor know if you’ve taken self-care measures for your symptoms for at least two months without noticing any improvement.

treatment-

Treatment options for benign prostatic hyperplasia may include

  • lifestyle changes
  • medications
  • minimally invasive procedures
  • surgery

A health care provider treats benign prostatic hyperplasia based on the severity of symptoms, how much the symptoms affect a man’s daily life, and a man’s preferences.

Men may not need treatment for a mildly enlarged prostate unless their symptoms are bothersome and affecting their quality of life. In these cases, instead of treatment, a urologist may recommend regular checkups. If benign prostatic hyperplasia symptoms become bothersome or present a health risk, a urologist most often recommends treatment.

Lifestyle Changes

A health care provider may recommend lifestyle changes for men whose symptoms are mild or slightly bothersome. Lifestyle changes can include

  • reducing intake of liquids, particularly before going out in public or before periods of sleep
  • avoiding or reducing intake of caffeinated beverages and alcohol
  • avoiding or monitoring the use of medications such as decongestants, antihistamines, antidepressants, and diuretics
  • training the bladder to hold more urine for longer periods
  • exercising pelvic floor muscles
  • preventing or treating constipation

Medications

A health care provider or urologist may prescribe medications that stop the growth of or shrink the prostate or reduce symptoms associated with benign prostatic hyperplasia:

  • alpha blockers
  • phosphodiesterase-5 inhibitors
  • 5-alpha reductase inhibitors
  • combination medications

Alpha blockers. These medications relax the smooth muscles of the prostate and bladder neck to improve urine flow and reduce bladder blockage:

  • terazosin (Hytrin)
  • doxazosin (Cardura)
  • tamsulosin (Flomax)
  • alfuzosin (Uroxatral)
  • silodosin (Rapaflo)

Phosphodiesterase-5 inhibitors. Urologists prescribe these medications mainly for erectile dysfunction. Tadalafil (Cialis) belongs to this class of medications and can reduce lower urinary tract symptoms by relaxing smooth muscles in the lower urinary tract. Researchers are working to determine the role of erectile dysfunction drugs in the long-term treatment of benign prostatic hyperplasia.

5-alpha reductase inhibitors. These medications block the production of DHT, which accumulates in the prostate and may cause prostate growth:

  • finasteride (Proscar)
  • dutasteride (Avodart)

These medications can prevent progression of prostate growth or actually shrink the prostate in some men. Finasteride and dutasteride act more slowly than alpha blockers and are useful for only moderately enlarged prostates.

Combination medications. Several studies, such as the Medical Therapy of Prostatic Symptoms (MTOPS) study, have shown that combining two classes of medications, instead of using just one, can more effectively improve symptoms, urinary flow, and quality of life. The combinations include

  • finasteride and doxazosin
  • dutasteride and tamsulosin (Jalyn), a combination of both medications that is available in a single tablet
  • alpha blockers and antimuscarinics

A urologist may prescribe a combination of alpha blockers and antimuscarinics for patients with overactive bladder symptoms. Overactive bladder is a condition in which the bladder muscles contract uncontrollably and cause urinary frequency, urinary urgency, and urinary incontinence. Antimuscarinics are a class of medications that relax the bladder muscles.

Minimally Invasive Procedures

Researchers have developed a number of minimally invasive procedures that relieve benign prostatic hyperplasia symptoms when medications prove ineffective. These procedures include

  • transurethral needle ablation
  • transurethral microwave thermotherapy
  • high-intensity focused ultrasound
  • transurethral electrovaporization
  • water-induced thermotherapy
  • prostatic stent insertion

Minimally invasive procedures can destroy enlarged prostate tissue or widen the urethra, which can help relieve blockage and urinary retention caused by benign prostatic hyperplasia.

Urologists perform minimally invasive procedures using the transurethral method, which involves inserting a catheter—a thin, flexible tube—or cystoscope through the urethra to reach the prostate. These procedures may require local, regional, or general anesthesia. Although destroying troublesome prostate tissue relieves many benign prostatic hyperplasia symptoms, tissue destruction does not cure benign prostatic hyperplasia. A urologist will decide which procedure to perform based on the man’s symptoms and overall health.

Transurethral needle ablation. This procedure uses heat generated by radiofrequency energy to destroy prostate tissue. A urologist inserts a cystoscope through the urethra to the prostate. A urologist then inserts small needles through the end of the cystoscope into the prostate. The needles send radiofrequency energy that heats and destroys selected portions of prostate tissue. Shields protect the urethra from heat damage.

Transurethral microwave thermotherapy. This procedure uses microwaves to destroy prostate tissue. A urologist inserts a catheter through the urethra to the prostate, and a device called an antenna sends microwaves through the catheter to heat selected portions of the prostate. The temperature becomes high enough inside the prostate to destroy enlarged tissue. A cooling system protects the urinary tract from heat damage during the procedure.

High-intensity focused ultrasound. For this procedure, a urologist inserts a special ultrasound probe into the rectum, near the prostate. Ultrasound waves from the probe heat and destroy enlarged prostate tissue.

Transurethral electrovaporization. For this procedure, a urologist inserts a tubelike instrument called a resectoscope through the urethra to reach the prostate. An electrode attached to the resectoscope moves across the surface of the prostate and transmits an electric current that vaporizes prostate tissue. The vaporizing effect penetrates below the surface area being treated and seals blood vessels, which reduces the risk of bleeding.

Water-induced thermotherapy. This procedure uses heated water to destroy prostate tissue. A urologist inserts a catheter into the urethra so that a treatment balloon rests in the middle of the prostate. Heated water flows through the catheter into the treatment balloon, which heats and destroys the surrounding prostate tissue. The treatment balloon can target a specific region of the prostate, while surrounding tissues in the urethra and bladder remain protected.

Prostatic stent insertion. This procedure involves a urologist inserting a small device called a prostatic stent through the urethra to the area narrowed by the enlarged prostate. Once in place, the stent expands like a spring, and it pushes back the prostate tissue, widening the urethra. Prostatic stents may be temporary or permanent. Urologists generally use prostatic stents in men who may not tolerate or be suitable for other procedures.

Surgery

For long-term treatment of benign prostatic hyperplasia, a urologist may recommend removing enlarged prostate tissue or making cuts in the prostate to widen the urethra. Urologists recommend surgery when

  • medications and minimally invasive procedures are ineffective
  • symptoms are particularly bothersome or severe
  • complications arise

Although removing troublesome prostate tissue relieves many benign prostatic hyperplasia symptoms, tissue removal does not cure benign prostatic hyperplasia.

Surgery to remove enlarged prostate tissue includes

  • transurethral resection of the prostate (TURP)
  • laser surgery
  • open prostatectomy
  • transurethral incision of the prostate (TUIP)

A urologist performs these surgeries, except for open prostatectomy, using the transurethral method. Men who have these surgical procedures require local, regional, or general anesthesia and may need to stay in the hospital.

The urologist may prescribe antibiotics before or soon after surgery to prevent infection. Some urologists prescribe antibiotics only when an infection occurs.

Immediately after benign prostatic hyperplasia surgery, a urologist may insert a special catheter, called a Foley catheter, through the opening of the penis to drain urine from the bladder into a drainage pouch.

TURP. With TURP, a urologist inserts a resectoscope through the urethra to reach the prostate and cuts pieces of enlarged prostate tissue with a wire loop. Special fluid carries the tissue pieces into the bladder, and the urologist flushes them out at the end of the procedure. TURP is the most common surgery for benign prostatic hyperplasia and considered the gold standard for treating blockage of the urethra due to benign prostatic hyperplasia.

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school health

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School Health is:

  • a healthful environment,
  • nursing and other health services that students need to stay in school,
  • nutritious and appealing school meals,
  • opportunities for physical activity that include physical education,
  • health education that covers a range of developmentally appropriate topics taught by knowledgeable teachers,
  • programs that promote the health of school faculty and staff, and
  • counseling, psychological and social services that promote healthy social and emotional development and remove barriers to students’ learning.

Over 2.3 billion school age children spend one third of their time in schools. Schools therefore constitute a unique setting to help children and adolescents to develop a positive outlook on life and help them establish healthy lifestyles. Yet global mortality and morbidity estimates in children and adolescents suggest that school aged children have significant needs for health promotion, prevention and health care services.

For many school age children school health services are the first and the most accessible point of contact with health services, with a potential to regularly reach most school-age children with preventive, curative and supportive health interventions. School health services are a very common model of service provision in both high- and middle and low-income countries – at least 102 countries have either school-based or school-linked service provision.

School health services are part of the whole school approach that is promoted by WHO through the Global School Health Initiative launched in 1995. The initiative supports countries to implement the four pillars for Health Promoting Schools: 1) Health promoting school policies 2) Safe and healthy learning environment, 3) Skills-based health education, and 4) School-based health and nutrition services.

Recent guidance from WHO and other UN partners – the Global accelerated action for the health of adolescents (AA-HA!): guidance to support country implementation – gave a new impetus to school health by recommending that “every school should be a health promoting school”.

WHO is working to support Member States in strengthening school health services. This work will support the implementation of the WHO’s 13th General Programme of Work, and more specifically its targets of “1 billion more people benefitting from universal health coverage” and “1 billion lives made healthier” by 2023.

What are best practices in school health?

The American Cancer Society identified the basics of a high-quality school health program in a brochure Elements of Excellence. Those basic elements are:

  1. Active leadership from school administrators, a school and community health council, and a school employee with responsibility for coordination.
  2. A coordinated and collaborative approach overseen by a school health council, that sets priorities based on community needs and values, and that links with community resources.
  3. A safe and nurturing learning environment with supportive policies and practices, facilities that are hazard free, and consistent health-enhancing messages.
  4. A commitment of time, personnel, and resources.

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Committees & Initiatives

The American School Health Association values member volunteers and their contributions to our committees and initiatives. ASHA encourages engagement from a diverse group of volunteers who represent various roles, settings, student populations, and health issues.

Committees

Advocacy and Coalitions Committee

Purpose: To build partnerships with national level coalitions and other partners to influence public policy on issues of importance to ASHA’s mission. This committee also works to educate and empower the ASHA membership to act on school health policy issues at the local, state, and federal levels.

Leadership and Recognition Committee

Purpose: To help support ASHA’s efforts in building a community to support the whole child, and to activate champions of school health by recognizing leaders in school health, developing their skills, and to support academic pursuits of young school health professionals through scholarships.

Professional Development Committee

Purpose: To work in collaboration with ASHA staff to plan and implement year-round professional development opportunities for school health professionals including the annual ASHA conference, monthly webinars, self-studies, and any new opportunities that may emerge.

Research and Publications Committee

Purpose: To solicit, curate, disseminate, and promote research I the field of school health. These activities help the ASHA leadership better understand how to lead change efforts and provided the bases of how best to build communities to support school health.

Actions for country impact

WHO provides technical assistance to governments and partners to strengthen school health services as part of national school health programmes and initiatives.

The Pan American Health Organization supported Member States to conduct assessments of school health programmes, including school health services. The assessments informed the regional meeting “Improving the health and wellbeing of school-aged children and adolescents in the Americas” that took place on 11-13 June, 2019, in Washington, DC. The purpose of the meeting was to engage stakeholders from 18 LAC and Caribbean countries in a regional dialogue on the current status of school health based on the results of the regional assessment and country experiences, and to jointly identify actions to strengthen school health in the region.

The WHO Regional Office for Africa supported 29 Member States to take stock of progress made in school health in the African Region. Country teams reviewed progress and planned action to strengthen school health programmes during a regional consultation involving government officials, representatives of United Nations agencies, international NGOs, bilateral agencies, civil society organizations and young people’s organizations operating at the global, regional and national level.

Evaluation of school health services and school health programmes

WHO and partners are working towards a monitoring and evaluation framework for the Global Standards for Health Promoting Schools. A web-platform will be developed to facilitate students’ and parents’ engagement in monitoring and evaluation of the performance of their school against Global Standards. Key indicators will be aligned with existing global monitoring systems for input, process, outcome and impact indicators, such as the Global School-based Student Health Survey (GSHS), the Health Behaviour in School-aged Children (HBSC) survey, and other surveys.

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Natural and manmade disasters and disaster management

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Disaster, as defined by the United Nations, is a serious disruption of the functioning of a community or society, which involve widespread human, material, economic or environmental impacts that exceed the ability of the affected community or society to cope using its own resources . Disaster management is how we deal with the human, material, economic or environmental impacts of said disaster, it is the process of how we “prepare for, respond to and learn from the effects of major failures”. Though often caused by nature, disasters can have human origins. According to the International Federation of Red Cross & Red Crescent Societies a disaster occurs when a hazard impacts on vulnerable people. The combination of hazards, vulnerability and inability to reduce the potential negative consequences of risk results in disaster.

The impact of disasters on the environment has become more severe over the last decades. Moreover, the reported number of disasters has dramatically increased, as well as the costs to the global economy and the number of people affected . The reasons for these disasters are manifold, and the impact can be found in the increasing vulnerability of societies, infrastructure, and population. Furthermore, extreme weather events have become more common and severe.

The increasing occurrences of natural and man-made disasters lead to a growing demand for up-to-date geographic information, especially timely material on rapidly evolving events. This includes comprehensive, near-real-time Earth observation data, which offer independent coverage of wide areas for a broad spectrum of civilian crisis situations . Satellite imagery can serve as a source of information in disaster situation. Accordingly, remote sensing can provide information on various domains of the disaster management, from risk modelling and vulnerability analysis to early warning and damage assessment

Types of Disaster-

A disaster is a more serious event, defined as “A serious disruption of the functioning of a community or a society involving widespread human, material, economic or environmental losses and impacts, which exceeds the ability of the affected community or society to cope using its own resources” (United Nations Office for Disaster Risk Reduction, UNISDR Terminology and Disaster Risk Reduction, Geneva 2009).  The exceedance of the affected community’s ability to cope is a critical differential point compared to an emergency, and external help will be required to restore functioning. 

Whether an emergency results in disaster is context specific – disasters are often described as a result of the combination of: the exposure to a hazard; the conditions of vulnerability that are present; and insufficient capacity or measures to reduce or cope with the potential negative consequences (UNISDR 2009).   Resilience and response of the community can prevent an emergency becoming a full-scale disaster.

Types of emergencies:

  • ‘Man-made’ e.g. transport-related, terrorism
  • Natural e.g. flooding, earthquake
  • Can also be defined by speed of onset e.g. ‘big bang’ – sudden events such as bombings or earthquakes; ‘rising tide’ gradual events such as famine, infectious disease pandemics.

Natural Disasters

According to the International Federation of Red Cross & Red Crescent Societies Natural Disasters are naturally occurring physical phenomena caused either by rapid or slow onset events that have immediate impacts on human health and secondary impacts causing further death and suffering. These disasters can be:

  • Geophysical (e.g. Earthquakes, Landslides, Tsunamis and Volcanic Activity)
  • Hydrological (e.g. Avalanches and Floods)
  • Climatological (e.g. Extreme Temperatures, Drought and Wildfires)
  • Meteorological (e.g. Cyclones and Storms/Wave Surges)
  • Biological (e.g. Disease Epidemics and Insect/Animal Plagues)

The United Nations Office for Disaster Risk Reduction characterises Natural Disasters in relation to their magnitude or intensity, speed of onset, duration and area of extent e.g. earthquakes are of short duration and usually affect a relatively small region whereas droughts are slow to develop and fade away and often affect large regions.

Man-Made Disasters-

Man-Made Disasters as viewed by the International Federation of Red Cross & Red Crescent Societies are events that are caused by humans which occur in or close to human settlements often caused as a results of Environmental or Technological Emergencies. This can include [3]:

  • Environmental Degradation
  • Pollution
  • Accidents (e.g. Industrial, Technological and Transport usually involving the production, use or transport of hazardous materials) 

Complex Emergencies

Some disasters can result from multiple hazards, or, more often, to a complex combination of both natural and man-made causes which involve a break-down of authority, looting and attacks on strategic installations, including conflict situations and war. These can include [6]:

  • Food Insecurity
  • Epidemics
  • Armed Conflicts
  • Displaced Populations

According to ICRC these Complex Emergencies are typically characterized by [6]:

  • Extensive Violence
  • Displacements of Populations
  • Loss of Life
  • Widespread Damage to both Societies and Economies
  • Need for Large-scale, Humanitarian Assistance across Multiple Agencies
  • Political and Military Constraints which impact or prevent Humanitarian Assistance
  • Increased Security Risks for Humanitarian Relief Workers

Pandemic Emergencies

Pandemic (from Greek πᾶν pan “all” and δῆμος demos “people”) is an epidemic of infectious disease that has spread across a large region, which can occur to the human population or animal population and may affect health and disrupt services leading to economic and social costs. It may be an unusual or unexpected increase in the number of cases of an infectious disease which already exists in a certain region or population or can also refer to the appearance of a significant number of cases of an infectious disease in a region or population that is usually free from that disease. Pandemic Emergencies may occur as a consequence of natural or man-made disasters. These have included the following epidemics:

  • Ebola
  • Zika
  • Avian Flu
  • Cholera
  • Dengue Fever
  • Malaria
  • Yellow Fever
  • Coronavirus Disease (COVID-19)

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Preparedness

is the step beyond planning, implies a plan is in place, and has been tested: organisations and individuals are clear about their roles and responsibilities.

Types of responders:

In the UK, the Civil Contingencies Act 2004 (CCA) defines two categories or responders, with different roles and responsibilities when planning for and responding to emergencies:

  • Category 1 responders are agencies core to civil protection – emergency services, local government, acute hospitals and emergency departments, health service managers, public health agency, the environment agency, maritime and coastguard agency, port health authority
  • Category 2 responders have a role to co-operate to support the main effort – utility companies, highway authorities, railway, harbour and airport operators, health and safety executive, primary care organisations
  • The military are not categorised here because the Act governs responses to civil emergencies
  • Category 1 & 2 responders have a duty to cooperate and share information for the purpose of civil protection.  Category 1 responders have additional duties to put in place emergency plans, business continuity arrangements, arrangements to keep the public informed during emergencies, and to provide advice and assistance to local business and voluntary agencies about business continuity.

National organisational response to emergencies 

(Scientific advice and evidence in emergencies – UK Science and Technology Committee http://www.publications.parliament.uk/pa/cm201011/cmselect/cmsctech/498/49806.htm)

Where there are (or there is the potential to be) more than one emergency response over several regions, a further level of strategic oversight exists in the UK.  The Cabinet Office Briefing Rooms (COBR) takes the strategic lead and is a forum of Ministers and senior officials from relevant Departments and agencies, brought together to make decisions on an emergency response. External representatives and experts are invited to attend COBR meetings as appropriate; discussions are confidential.  COBR should facilitate rapid coordination of the Central Government response and effective decision-making.   In an emergency where a central response is required, a Lead Government Department (LGD) is appointed. The LGD is responsible for ensuring that appropriate plans exist to manage the emergency, for ensuring that adequate resources are available and for leading on public and parliamentary handling. LGDs are also responsible for ensuring they have effective arrangements to access scientific and technical advice in a timely fashion in an emergency.  This may involve establishing a Science Advisory Group for Emergencies (SAGE).

Acronym

M – Major Incident Declared?

E – Exact Location

T – Type of Incident

H – Hazards present or suspected

A – Access – routes that are safe to use

N – Number, type and severity of casualties

E – Emergency services present, and those required

Disaster Response / Relief-

“The provision of emergency services and public assistance during or immediately after a disaster in order to save lives, reduce health impacts, ensure public safety and meet the basic subsistence needs of the people affected”.

Focused predominantly on immediate and short-term needs, the division between this response/relief stage and the subsequent recovery stage is not clear-cut. Some response actions, such as the supply of temporary housing and water supplies, may extend well into the recovery stage. Rescue from immediate danger and stabilization of the physical and emotional condition of survivors is the primary aims of disaster response/relief, which go hand in hand with the recovery of the dead and the restoration of essential services such as water and power . 

Coordinated multi-agency response is vital to this stage of Disaster Management in order to reduce the impact of a disaster and its long-term results with relief activities including :

  • Rescue
  • Relocation
  • Provision Food and Water
  • Provision Emergency Health Care
  • Prevention of Disease and Disability
  • Repairing Vital Services e.g. Telecommunications, Transport
  • Provision Temporary Shelter

Disaster Recovery-

Vulnerability of communities often continues for long after the initial crisis is over. Disaster Recovery refers to those programmes which go beyond the provision of immediate relief to assist those who have suffered the full impact of a disaster and include the following activities:

  • Rebuilding Infrastructure e.g. Homes, Schools, Hospitals, Roads
  • Health Care and Rehabilitation
  • Development Activities e.g. building human resources for health
  • Development Policies and Practices to avoid or mitigate similar situations in future

How Physiotherapists Can Contribute

The roots of physiotherapy can be traced back to the early 20th century when physiotherapists were involved in the rehabilitation of people affected by war and illness.

Physiotherapists continue to be involved in these situations and are often called on to be part of a humanitarian response. This could include providing support to people in conflict-affected parts of the world, being part of humanitarian response to a natural disaster, or working with people affected by pandemics.

We can advocate to make sure physiotherapists have access to appropriate equipment to work safely and effectively.

Equipment donation

Many World Physiotherapy member organisations and their individual members are involved in programmes as donors or recipients of physiotherapy equipment in different countries.

We have developed an information note, with input from a range of stakeholders (including ADAPT, ICRC, WHO), to help donors and recipients find the best possible solution for the donation of physiotherapy equipment.

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Renal vascular disorders

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Most kidneys work well to clean the blood and keep the body’s fluids and electrolytes in balance. But sometimes, the arteries of the kidneys can get smaller or become blocked. This can seriously damage this important filtering system. It can limit the blood supply going to and from the kidneys.

Renovascular diseases are diseases of the arteries to the kidneys. High blood pressure and/or kidney failure can result from these diseases.

Renal vascular disease affects the blood flow into and out of the kidneys. It may cause kidney damage, kidney failure, and high blood pressure.

Vascular conditions include:

  • Renal artery stenosis (RAS). This is a narrowing or blockage of an artery to the kidneys. It may cause kidney failure and high blood pressure. Smokers have a greater risk of getting RAS. It’s most common in men between the ages of 50 and 70. High cholesterol, diabetes, being overweight, and having a family history of heart disease are also risk factors for RAS. High blood pressure is both a cause and a result of RAS.
  • Renal artery thrombosis. This is a blood clot in an artery that supplies the kidney. It may block blood flow and cause kidney failure.
  • Renal vein thrombosis. This is the formation of a clot in a vein to the kidney.
  • Renal artery aneurysm. This is a bulging, weak area in the wall of an artery to the kidney. Most are small and don’t cause symptoms. Renal artery aneurysms are rare and are often found during tests for other conditions.
  • Atheroembolic renal disease. This happens when a piece of plaque from a larger artery breaks off and travels through the blood. This blocks small renal arteries. This disease is becoming a common cause of kidney problems in the older adults.

Renin is a strong hormone that raises blood pressure. Decreased blood flow to the kidney(s) from renal vascular disease may cause too much renin to be made. This can lead to high blood pressure.

types of renovascular diseases

There are two main diseases of the renal (kidney) arteries:

  • Atherosclerotic renal artery stenosis (AS-RAS), and
  • Fibromuscular dysplasia (FMD)

Atherosclerosis is better known as hardening of the arteries. It is a common disease. Atherosclerosis is the cause of 9 out of 10 renovascular disease cases. It can involve the large and/or small branches of the renal artery. People with diabetes, aortoiliac occlusive disease, coronary artery disease or other forms of high blood pressure are at risk.

The main risk factors for AS-RAS are:

  • High blood pressure
  • High cholesterol
  • Older age
  • Smoking
  • Diabetes
  • Heavy alcohol use or drug abuse

If you have AS-RAS you may have ongoing narrowing of the renal artery. This means that the arteries continue to narrow for many years, even after treatment. Many arteries can become totally blocked. For some people, their kidney shrinks. AS-RAS is seen if you have diabetes or similar problems. This disease can be missed if hypertension or kidney dysfunction doesn’t occur.

Fibromuscular dysplasia (FMD) is a group of vascular diseases that affect the linings of the renal artery. About 10% of AS-RAS cases also have FMD. It is more common in women and people between age 25 and 50. FMD involves the main renal artery and its branches. It looks like beads in the arteries with imaging tests (angiograms). It rarely leads to total artery block, but it is still a problem.

The cause of FMD is not known, though some experts think genetics play a role. Smoking, hormones and disorders of the blood supply to the renal artery may also play a role.

causes

The most common cause of renal artery stenosis is a buildup of fatty deposits called plaque. It can happen in either or both renal arteries. This is often called “hardening of the arteries,” or atherosclerosis. The buildup can narrow the artery and reduce blood flow to the kidneys.

Renal artery stenosis can also be caused by fibromuscular dysplasia. This is a condition in which some of the cells that line the renal arteries grow or don’t develop the right way. This growth can cause the arteries to narrow.

The cause of renal vascular disease will depend on the specific condition involved. The main causes are:

  • Atherosclerosis
  • Injury
  • Infection
  • Inflammatory or other underlying disease
  • Surgery
  • Tumor
  • Aneurysm
  • Pregnancy
  • Certain medicines
  • Birth defect

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symptoms

Symptoms of renal vascular disease vary depending on the type of disease and degree of involvement present.

Renal Artery Stenosis

  • High blood pressure that doesn’t get better with 3 or more medicines.
  • Increased urea (a waste product made by the kidneys) in the blood.
  • Unexplained kidney failure.
  • Sudden kidney failure when first taking an angiotensin-converting enzyme (ACE) inhibitor for blood pressure and/or heart treatment      

Renal Artery Thrombosis

  • Sudden onset of side pain between the ribs and the upper border of the hip bone (flank pain), pain and tenderness
  • Fever
  • Blood in the urine
  • Nausea and vomiting
  • Sudden decrease in kidney function
  • High blood pressure

A gradual or incomplete clot may not cause symptoms and go undetected

Renal Artery Aneurysm

  • There are often no symptoms·     
  • High blood pressure
  • Tear in aneurysms may cause flank pain and blood in the urine

Atheroembolic Renal Disease

  • Skin lesions or red or purple color of the skin.
  • Discolored areas of the toes and feet
  • Kidney failure
  • Belly pain
  • Diarrhea
  • Confusion
  • Weight loss
  • Fever
  • Muscle aches

Renal Vein Thrombosis

Slow Onset

  • Most often causes no symptoms

Sudden Onset

  • On-going severe flank pain with spasms at times
  • Soreness over the kidney, between the ribs and the backbone
  • Decreased kidney function
  • Blood in urine    

diagnosis

Duplex Doppler ultrasound.

This test uses sound waves to show how blood flows through a blood vessel. It can show reduced flow of blood through narrow areas in the renal arteries. Computed tomography (CT) angiogram.

This test uses X-rays to provide pictures of the renal arteries. The test uses a special dye that is put into a vein (IV) to make very detailed pictures of the arteries. It can show if the artery is narrowed or blocked. Magnetic resonance angiogram.

This test uses a magnetic field and pulses of radio wave energy to make pictures of the renal arteries. It can show narrowing in the renal arteries that may be causing reduced blood flow. This test allows the doctor to see both the blood flow and the condition of the artery walls. A catheter angiogram of the kidney.

This is an X-ray test that provides pictures of the blood flow in a blood vessel, such as the renal arteries. During an angiogram, the doctor will put a thin, flexible tube into a blood vessel in your groin or arm. This tube is called a catheter. The doctor guides the tube to the blood vessel that will be studied. Then a dye is injected through the tube to make the area easier to see. X-rays or pictures are taken of the area. An angiogram can also show narrowing or a blockage in a blood vessel that affects blood flow. Sometimes a problem can be treated during this test. For example, a catheter can be used to open a narrowed renal artery.

risk factors

Many of the risk factors for renal artery disease are the same as those for atherosclerosis in other parts of the body, such as coronary artery disease and peripheral arterial disease. Risk factors for renal artery disease include:

  • age over 50
  • diabetes
  • high cholesterol
  • smoking
  • high blood pressure
  • a family history of coronary artery disease
  • a family hisotry of peripheral arterial disease
  • a family history of renal artery disease
  • neurofibromatosis.

treatment choices for renal artery disease

In nearly half of patients, untreated renal artery disease gets progressively worse and can lead to kidney failure. In one large study at Cleveland Clinic, obstruction of the arteries progressed in 44 percent of untreated patients; in 16 percent of those, total occlusion occurred. For unknown reasons, women are at higher risk for disease progression than men.

Like treatment for heart disease, there are many treatments available for renal artery disease. The right treatment for an individual depends on the severity of the disease and the person’s medical history.

Medical Therapy

All patients with renal artery disease require treatment for cardiovascular risk factors (such as high blood pressure, high cholesterol, diabetes) and lifestyle changes such as weight reduction, smoking cessation, exercise and a low-salt and low-fat diet. Medication to lower blood pressure is an important part of treatment, along with careful monitoring of the response to the blood pressure medications to be sure the blood pressure is lowered to the treatment goal. Regular follow-up every 4 to 6 months will be part of the treatment plan so your physician can monitor your condition.

Procedures

For some patients with significant narrowing of the renal arteries, particularly patients with narrowed areas in the renal arteries on both sides of the body, or those with severe symptoms, a procedure may be recommended to open up the blocked arteries to restore circulation. In some cases, opening the blocked arteries may improve kidney function and may improve control of high blood pressure. Not surprisingly, the techniques used to open blocked renal arteries are very similar to those used to treat blocked coronary arteries.

Renal angioplasty: A small catheter – a long, thin tube – carrying a tiny balloon is inserted through a small puncture in the groin and guided by X-ray to the kidney artery. When the catheter is guided to the narrowed part of the artery, the balloon is inflated. As it expands, it compresses the plaque against the artery walls, re-opening the vessel for blood to flow through. Once the artery is open, the physician may insert a stent at the site to keep the artery open and support the arterial wall.

In carefully selected patients, renal angioplasty improves blood pressure and kidney function with minimal risk. It can be done as an outpatient procedure or with only an overnight stay, does not require general anesthesia and has a short recovery time.

Surgical treatment: With the development of new and improved types of stents, angioplasty with stenting is the preferred treatment for renal artery disease. But, in certain cases, surgical treatment may be necessary to restore blood flow to the kidney and preserve kidney function.

Surgical treatments for renal artery disease include:

Endarterectomy, during which a vascular surgeon removes the diseased inner lining of the artery and the plaque deposits.

Bypass procedure, which involves using a segment from another artery or vein to construct a detour around the blocked area of the renal artery. The most commonly used technique creates a bypass from the abdominal aorta (the large artery in the abdomen) to the kidney using a segment from the saphenous vein in the leg or the hypogastric artery from the abdomen.

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Pancreatitis

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Pancreatitis is inflammation in the pancreas. The pancreas is a long, flat gland that sits tucked behind the stomach in the upper abdomen. The pancreas produces enzymes that help digestion and hormones that help regulate the way your body processes sugar (glucose).

Pancreatitis can occur as acute pancreatitis — meaning it appears suddenly and lasts for days. Or pancreatitis can occur as chronic pancreatitis, which is pancreatitis that occurs over many years.

Mild cases of pancreatitis may go away without treatment, but severe cases can cause life-threatening complications.

hronic pancreatitis is a long-term progressive inflammatory disease of the pancreas that leads to permanent breakdown of the structure and function of the pancreas.

The pancreas is a gland organ that is located in the abdomen, behind the stomach and below the ribcage. It specializes in producing important enzymes and hormones that help break down and digest foods. It also makes insulin to moderate the levels of sugar in the blood.

The most common cause is long-term alcohol abuse – it is thought to account for between 70 and 80 percentTrusted Source of all cases.

Chronic pancreatitis results in over 122,000 visits to a doctor and 56,000 hospitalizations annually in the United States.

Significantly more men than women are affected.

Pancreatitis is a disease in which your pancreas becomes inflamed.

The pancreas is a large gland behind your stomach and next to your small intestine. Your pancreas does two main things:

  • It releases powerful digestive enzymes into your small intestine to help you digest food.
  • It releases insulin and glucagon into your bloodstream. These hormones help your body control how it uses food for energy.

Types of Pancreatitis

The two forms of pancreatitis are acute and chronic.

  • Acute pancreatitis is sudden inflammation that lasts a short time. It can range from mild discomfort to a severe, life-threatening illness. Most people with acute pancreatitis recover completely after getting the right treatment. In severe cases, acute pancreatitis can cause bleeding, serious tissue damage, infection, and cysts. Severe pancreatitis can also harm other vital organs such as the heart, lungs, and kidneys.
  • Chronic pancreatitis is long-lasting inflammation. It most often happens after an episode of acute pancreatitis. Another top cause is drinking lots of alcohol for a long period of time. Damage to your pancreas from heavy alcohol use may not cause symptoms for many years, but then you may suddenly have severe pancreatitis symptoms.

Causes

Pancreatitis occurs when digestive enzymes become activated while still in the pancreas, irritating the cells of your pancreas and causing inflammation.

With repeated bouts of acute pancreatitis, damage to the pancreas can occur and lead to chronic pancreatitis. Scar tissue may form in the pancreas, causing loss of function. A poorly functioning pancreas can cause digestion problems and diabetes.

Conditions that can lead to pancreatitis include:

  • Abdominal surgery
  • Alcoholism
  • Certain medications
  • Cystic fibrosis
  • Gallstones
  • High calcium levels in the blood (hypercalcemia), which may be caused by an overactive parathyroid gland (hyperparathyroidism)
  • High triglyceride levels in the blood (hypertriglyceridemia)
  • Infection
  • Injury to the abdomen
  • Obesity
  • Pancreatic cancer

Endoscopic retrograde cholangiopancreatography (ERCP), a procedure used to treat gallstones, also can lead to pancreatitis.

Sometimes, a cause for pancreatitis is never found.

Pancreatitis Symptoms

Symptoms of acute pancreatitis

  • Fever
  • Higher heart rate
  • Nausea and vomiting
  • Swollen and tender belly
  • Pain in the upper part of your belly that goes into your back. Eating may make it worse, especially foods high in fat.

Symptoms of chronic pancreatitis

The symptoms of chronic pancreatitis are similar to those of acute pancreatitis. But you may also have:

  • Constant pain in your upper belly that radiates to your back. This pain may be disabling.
  • Diarrhea and weight loss because your pancreas isn’t releasing enough enzymes to break down food
  • Upset stomach and vomiting

When to see a doctor

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Make an appointment with your doctor if you have persistent abdominal pain. Seek immediate medical help if your abdominal pain is so severe that you can’t sit still or find a position that makes you more comfortable.

Diagnosis

There are no reliable tests to diagnose chronic pancreatitis. A doctor will suspect the disease because of the patient’s symptoms, history of repeated acute pancreatitis flare-ups, or alcohol abuse.

Blood tests may be useful in checking the blood glucose levels, which may be elevated.

Blood tests for elevated levels of amylase and lipase are not reliable at this stage. Amylase and lipase blood levels rise during the first couple of days of pancreatitis, and then settle back to normal after five to seven days. A patient with chronic pancreatitis would have had the disease for much longer.

Doctors need to have a good look at the pancreas in order to diagnose the disease properly. This will most likely involve:

  • An ultrasound scan: High frequency sound waves create an image on a monitor of the pancreas and its surroundings.
  • A CT scan: X-rays are used to take many pictures of the same area from several angles, which are then placed together to produce a 3-D image. The scan will reveal changes of chronic pancreatitis.
  • Magnetic resonance cholangiopancreatography (MRCP) scan: This scan shows the bile and pancreatic ducts more clearly than a CT scan.
  • An endoscopic retrograde cholangio-pancreatography (ERCP) scan: An endoscope is inserted into the digestive system. The doctor uses ultrasound to guide the endoscope through.

Patients with chronic pancreatitis have an elevated risk of developing pancreatic cancer. If symptoms worsen, especially the narrowing of the pancreatic duct, doctors may suspect cancer. If so, they will order a CT scan, MRI scan, or endoscopic study.

Complications-

There are several ways in which chronic pancreatitis can develop and become more harmful to a person’s wellbeing.

Stress, anxiety, and depression

The disease may have an effect on the patient’s psychological and emotional well being. Constant or recurring pain, which is often severe, may cause distress, anxiety, irritability, stress, and depression.

It is important for patients to tell their doctors if they are emotionally or psychologically affected. If there is a support group in your area, being able to talk to people who share the same condition may help you feel less isolated and more able to cope.

Pseudocyst

This is a collection of tissue, fluid, debris, pancreatic enzymes, and blood in the abdomen, caused by leakage of digestive fluids escaping from a faulty pancreatic duct.

Pseudocysts do not usually cause any health problems. However, sometimes they can become infected, cause blockage to part of the intestine, or rupture and cause internal bleeding. If this happens, the cyst will have to be surgically drained.

Pancreatic cancer

Even though pancreatic cancer is more common among patients with chronic pancreatitis, the risk is only 1 in 500.

Risk factors

Factors that increase your risk of pancreatitis include:

  • Excessive alcohol consumption. Research shows that heavy alcohol users (people who consume four to five drinks a day) are at increased risk of pancreatitis.
  • Cigarette smoking. Smokers are on average three times more likely to develop chronic pancreatitis, compared with nonsmokers. The good news is quitting smoking decreases your risk by about half
  • Obesity. You’re more likely to get pancreatitis if you’re obese.
  • Family history of pancreatitis. The role of genetics is becoming increasingly recognized in chronic pancreatitis. If you have family members with the condition, your odds increase — especially when combined with other risk factors.

Prevention

Patients with acute pancreatitis significantly reduce their risk of developing chronic pancreatitis if they give up drinking alcohol. This is especially the case for patients who drink heavily and regularly.

Treatment

The following treatments are commonly recommended for chronic pancreatitis.

Lifestyle changes

People with chronic pancreatitis will need to undergo some lifestyle changes. These will include:

  • Stopping alcohol consumption: Giving up drinking will help prevent further damage to the pancreas. It will also contribute significantly towards relieving the pain. Some people may need professional help to quit alcohol.
  • Stopping tobacco use: Smoking is not a cause of pancreatitis, but it can accelerate the progression of the disease.

Pain management

Treatment should not only focus on helping ease the pain symptoms, but also depression which is a common consequence of long-term pain.

Doctors will usually use a step-by-step approach, in which mild painkillers are prescribed, gradually becoming stronger until pain becomes manageable.

Insulin

The pancreas may stop producing insulin if the damage is extensive. The individual is likely to have developed diabetes type 1.

Regular insulin treatment will become part of the treatment for the rest of the person’s life. Diabetes type 1 caused by chronic pancreatitis involves injections, not tablets, because most likely the digestive system will not be able to break them down.

Surgery

Severe chronic pain sometimes does not respond to painkilling medications. The ducts in the pancreas may have become blocked, causing an accumulation of digestive juices which puts pressure on them, causing intense pain. Another cause of chronic and intense pain could be inflammation of the head of the pancreas.

Several forms of surgery may be recommended to treat more severe cases.

Endoscopic surgery

A narrow, hollow, flexible tube called an endoscope is inserted into the digestive system, guided by ultrasound. A device with a tiny, deflated balloon at the end is threaded through the endoscope. When it reaches the duct, the balloon is inflated, thus widening the duct. A stent is placed to stop the duct from narrowing back.

Pancreas resection

The head of the pancreas is surgically removed. This not only relieves the pain caused by inflammation irritating the nerve endings, but it also reduces pressure on the ducts. Three main techniques are used for pancreas resection:

  • The Beger procedure: This involves resection of the inflamed pancreatic head with careful sparing of the duodenum, the rest of the pancreas is reconnected to the intestines.
  • The Frey procedure: This is used when the doctor believes pain is being caused by both inflammation of the head of the pancreas as well as the blocked ducts. The Frey procedure adds a longitudinal duct decompression to the pancreatic head resection – the head of the pancreas is surgically removed, and the ducts are decompressed by connecting them directly to the intestines.
  • Pylorus-sparing pancreaticoduodenectomy (PPPD): The gallbladder, ducts, and the head of the pancreas are all surgically removed. This is only done in very severe cases of intense chronic pain where the head of the pancreas is inflamed, and the ducts are also blocked. This is the most effective procedure for reducing pain and conserving pancreas function. However, it has the highest risk of infection and internal bleeding.

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Atelectasis and Hyaline Membrane Disease

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Hyaline membrane disease (HMD), also called respiratory distress syndrome (RDS), is a condition that causes babies to need extra oxygen and help breathing.

  • HMD is one of the most common problems seen in premature babies.
  • The more premature the baby, the higher the risk and the more severe the HMD.
  • HMD typically worsens over the first 48 to 72 hours and then improves with treatment.
  • More than 90 percent of babies with HMD survive.

pathophysiology

Hyaline membrane disease: A respiratory disease of the newborn, especially the premature infant, in which a membrane composed of proteins and dead cells lines the alveoli (the tiny air sacs in the lung), making gas exchange difficult or impossible. The word “hyaline” comes from the Greek word “hyalos” meaning “glass or transparent stone such as crystal.” The membrane in hyaline membrane disease looks glassy.

Hyaline membrane disease is now commonly called respiratory distress syndrome (RDS). It is caused by a deficiency of a molecule called surfactant.

RDS almost always occurs in newborns born before 37 weeks of gestation. The more premature the baby is, the greater is the chance of developing RDS. RDS is more likely to occur in newborns of diabetic mothers.

Surfactant, a mixture of phospholipids and lipoproteins, is secreted by lung cells. The air-fluid interface of the film of water lining the alveoli of the lung (where the exchange of oxygen and CO2 occurs) exerts large forces that cause the alveoli to close if surfactant is deficient. Lung compliance is decreased, and the work of inflating the stiff lungs is increased. The preterm newborn is further handicapped because his or her ribs are more easily deformed (compliant). Breathing efforts therefore result in deep sternal (breastbone) retractions but poor air entry if the ribs are compliant compared with the lungs. This results in diffuse atelectasis (collapse of the lungs).

Rapid, labored, grunting respirations usually develop immediately or within a few hours after delivery, with retractions above and below the breastbone and flaring of the nostrils. The extent of atelectasis (lung collapse) and the severity of respiratory failure progressively worsen.

Not all infants with RDS have signs of respiratory distress; extremely low birth weight newborns (i.e., < 1000 g) may be unable to initiate respirations at birth because their lungs are so stiff; they may fail to initiate breathing in the delivery room.

The incidence of RDS can be reduced by assessment of fetal lung maturity to determine the optimal time for delivery. When a fetus must be delivered prematurely, giving betamethasone systemically to the mother for at least 24 hours before delivery induces fetal surfactant production and usually reduces the risk of RDS or decreases its severity.

If untreated, severe RDS can result in multiple organ failure and death. However, if the newborn’s ventilation is adequately supported, surfactant production will begin and RDS will resolve by 4 or 5 days. Recovery is hastened by treatment with pulmonary surfactant.

causes-

HMD occurs when there is not enough of a substance in the lungs called surfactant. Surfactant is made by the cells in the airways and consists of phospholipids and protein. It begins to be produced in the fetus at about 24 to 28 weeks of pregnancy, and is found in amniotic fluid between 28 and 32 weeks. By about 35 weeks gestation, most babies have developed adequate amounts of surfactant.

symptoms

While each baby may experience symptoms differently, some of the most common symptoms of HMD include:

  • difficulty breathing at birth that gets progressively worse
  • cyanosis (blue coloring)
  • flaring of the nostrils
  • tachypnea (rapid breathing)
  • grunting sounds with breathing
  • chest retractions (pulling in at the ribs and sternum during

Symptoms of HMD usually peak by the third day and may resolve quickly when your baby begins to diurese (excrete excess water in urine) and needs less oxygen and mechanical help to breathe.

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complications-

Your baby may develop complications of the disease or problems as side effects of treatment. As with any disease, more severe cases often have greater risks for complications. Some complications associated with HMD include the following:

  • air leaks of the lung tissues such as:
  • pneumomediastinum – air leaks into the mediastinum (the space between the two pleural sacs containing the lungs).
  • pneumothorax – air leaks into the space between the chest wall and the outer tissues of the lungs
  • pneumopericardium – air leaks into the sac surrounding the heart
  • pulmonary interstitial emphysema (PIE) – air leaks and becomes trapped between the alveoli, the tiny air sacs of the lungs
  • chronic lung disease, sometimes called bronchopulmonary dysplasia

Who is affected by HMD?

HMD occurs in about 60 to 80 percent of babies born before 28 weeks gestation, but only in 15 to 30 percent of those born between 32 and 36 weeks. About 25 percent of babies born at 30 weeks develop HMD severe enough to need a mechanical ventilator (breathing machine).

Although most babies with HMD are premature, other factors can influence the chances of developing the disease. These include the following:

  • Caucasian or male babies
  • previous birth of baby with HMD
  • Cesarean delivery
  • perinatal asphyxia (lack of air immediately before, during or after birth)
  • cold stress (a condition that suppresses surfactant production)
  • perinatal infection
  • multiple births (multiple birth babies are often premature)
  • infants of diabetic mothers (too much insulin in a baby’s system due to maternal diabetes can delay surfactant production)
  • babies with patent ductus arteriosus

diagnosis

HMD is usually diagnosed by a combination of assessments, including:

  • appearance, color, and breathing efforts (these signs indicate your baby’s need for oxygen)
  • x-rays of lungs: x-rays are electromagnetic energy used to produce images of bones and internal organs onto film. In HMD, they often show a unique “ground glass” appearance called a reticulogranular pattern.
  • blood gases (tests for oxygen, carbon dioxide, and acid in arterial blood): often show lowered amounts of oxygen and increased carbon dioxide.
  • echocardiography (EKG): may be used to rule out heart problems that could cause symptoms similar to HMD. An electrocardiogram is a test that records the electrical activity of the heart, shows arrhythmias (abnormal rhythms), and detects damage to the heart muscle.

treatments-

Treatment for HMD may include:

  • placing an endotracheal tube (breathing tube, also called an ET) into your baby’s windpipe
  • mechanical breathing machine (to do the work of breathing for your baby)
  • supplemental oxygen (extra amounts of oxygen)
  • continuous positive airway pressure (CPAP): a mechanical breathing machine that pushes a continuous flow of air or oxygen to the airways to help keep tiny air passages in the lungs open
  • surfactant replacement with artificial surfactant: this treatment has been shown to reduce the severity of HMD, and is most effective if started in the first six hours of birth. It may be given as preventive treatment for babies at very high risk for HMD, or used as a “rescue” method. The drug comes as a powder that is mixed with sterile water and given through the ET tube. This treatment is usually administered in several doses.
  • medications (to help sedate and ease your baby’s pain during treatment)

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Infective Endocarditis

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What is infective endocarditis?

Endocarditis is a life-threatening inflammation of the inner lining of your heart’s chambers and valves (endocardium).

Endocarditis is usually caused by an infection. Bacteria, fungi or other germs from another part of your body, such as your mouth, spread through your bloodstream and attach to damaged areas in your heart. If it’s not treated quickly, endocarditis can damage or destroy your heart valves. Treatments for endocarditis include medications and, sometimes, surgery.

People at greatest risk of endocarditis usually have damaged heart valves, artificial heart valves or other heart defects.

Infective endocarditis is an infection in the heart valves or endocardium. The endocardium is the lining of the interior surfaces of the chambers of the heart. This condition is usually caused by bacteria entering the bloodstream and infecting the heart. Bacteria may originate in the:

  • mouth
  • skin
  • intestines
  • respiratory system
  • urinary tract

When this condition is caused by bacteria, it’s also known as bacterial endocarditis. In rare cases, it can also be caused by fungi or other microorganisms.

Infective endocarditis is a serious condition that requires prompt medical treatment. If left untreated, the infection can damage your heart valves. This can lead to problems including:

  • stroke
  • damage to other organs
  • heart failure
  • death

This condition is rare in people with healthy hearts. People who have other heart conditions are at higher risk.

You may need to take antibiotics before certain medical and dental procedures if you’re at high risk for infective endocarditis. Antibiotics help stop bacteria from entering your bloodstream and causing infection. Talk to your surgeon or dentist before any surgical procedure.

Etiology

Endocarditis occurs when germs, usually bacteria, enter your bloodstream, travel to your heart, and attach to abnormal heart valves or damaged heart tissue. Fungi or other germs also may cause endocarditis.

Usually, your immune system destroys any harmful bacteria that enter your bloodstream. However, bacteria that live in your mouth, throat or other parts of your body, such as your skin or your gut, can sometimes cause endocarditis under the right circumstances.

Bacteria, fungi and other germs that cause endocarditis might enter your bloodstream through:

  • Improper dental care. Proper toothbrushing and flossing helps prevent gum disease. If you don’t take good care of your teeth and gums, brushing could cause unhealthy gums to bleed, giving bacteria a chance to enter your bloodstream. Some dental procedures that can cut your gums also may allow bacteria to enter your bloodstream.
  • Catheters. Bacteria can enter your body through a thin tube that doctors sometimes use to inject or remove fluid from the body (catheter). This is more likely to occur if the catheter is in place for a long period of time. For example, you may have a catheter if you need long-term dialysis.
  • Illegal IV drug use. Contaminated needles and syringes are a special concern for people who use illegal IV drugs, such as heroin or cocaine. Often, individuals who use these types of drugs don’t have access to clean, unused needles or syringes

Symptoms-

Endocarditis may develop slowly or suddenly, depending on what germs are causing the infection and whether you have any underlying heart problems. Signs and symptoms of endocarditis can vary from person to person.

Common signs and symptoms of endocarditis include:

  • Aching joints and muscles
  • Chest pain when you breathe
  • Fatigue
  • Flu-like symptoms, such as fever and chills
  • Night sweats
  • Shortness of breath
  • Swelling in your feet, legs or abdomen
  • A new or changed heart murmur, which is the heart sound made by blood rushing through your heart

Less common signs and symptoms of endocarditis can include:

  • Unexplained weight loss
  • Blood in your urine, which you might be able to see or that your doctor might see when he or she views your urine under a microscope
  • Tenderness in your spleen, which is an infection-fighting organ located just below your left rib cage
  • Red spots on the soles of your feet or the palms of your hands (Janeway lesions)
  • Red, tender spots under the skin of your fingers or toes (Osler’s nodes)
  • Tiny purple or red spots, called petechiae (puh-TEE-kee-ee), on the skin, in the whites of your eyes or inside your mouth

Pathophysiology

Infective endocarditis develops most commonly on the mitral valve, closely followed in descending order of frequency by the aortic valve, the combined mitral and aortic valve, the tricuspid valve, and, rarely, the pulmonic valve. Mechanical prosthetic and bioprosthetic valves exhibit equal rates of infection.

All cases of IE develop from a commonly shared process, as follows:

  1. Bacteremia (nosocomial or spontaneous) that delivers the organisms to the surface of the valve
  2. Adherence of the organisms
  3. Eventual invasion of the valvular leaflets

The common denominator for adherence and invasion is nonbacterial thrombotic endocarditis, a sterile fibrin-platelet vegetation. The development of subacute IE depends on a bacterial inoculum sufficient to allow invasion of the preexistent thrombus. This critical mass is the result of bacterial clumping produced by agglutinating antibodies.

In acute IE, the thrombus may be produced by the invading organism (ie, S aureus) or by valvular trauma from intravenous catheters or pacing wires (ie, NIE/HCIE). Staphylococcus aureus can invade the endothelial cells (endotheliosis) and increase the expression of adhesion molecules and of procoagulant activity on the cellular surface. Nonbacterial thrombotic endocarditis may result from stress, renal failure, malnutrition, systemic lupus erythematosus, or neoplasia.

The Venturi effect also contributes to the development and location of nonbacterial thrombotic endocarditis. This principle explains why bacteria and the fibrin-platelet thrombus are deposited on the sides of the low-pressure sink that lies just beyond a narrowing or stenosis.

In patients with mitral insufficiency, bacteria and the fibrin-platelet thrombus are located on the atrial surface of the valve. In patients with aortic insufficiency, they are located on the ventricular side. In these examples, the atria and ventricles are the low-pressure sinks. In the case of a ventricular septal defect, the low-pressure sink is the right ventricle and the thrombus is found on the right side of the defect.

Nonbacterial thrombotic endocarditis may also form on the endocardium of the right ventricle, opposite the orifice that has been damaged by the jet of blood flowing through the defect (ie, the MacCallum patch).

The microorganisms that most commonly produce endocarditis (ie, S aureus; Streptococcus viridans; groups A, C, and G streptococci; enterococci) resist the bactericidal action of complement and possess fibronectin receptors for the surface of the fibrin-platelet thrombus. Among the many other characteristics of IE-producing bacteria demonstrated in vitro and in vivo, some features include the following:

  • Increased adherence to aortic valve leaflet disks by enterococci, S viridans, and S aureus
  • Mucoid-producing strains of S aureus
  • Dextran-producing strains of S viridans
  • Streptococcus viridans and enterococci that possess FimA surface adhesin
  • Platelet aggregation by S aureus and S viridans and resistance of S aureus to platelet microbicidal proteins

The pathogenesis of pacemaker IE is similar. Shortly after implantation, the development of a fibrin-platelet thrombus (similar to the nonbacterial thrombotic endocarditis described above) involves the generator box and conducting leads. After 1 week, the connective tissue proliferates, partially embedding the leads in the wall of the vein and endocardium. This layer may offer partial protection against infection during a bacteremia.

Bacteremia (either spontaneous or resulting from an invasive procedure) infects the sterile fibrin-platelet vegetation described above. Bloodstream infections develop from various extracardiac types of infection, such as pneumonias or pyelonephritis, but most commonly from gingival disease. Of those with high-grade gingivitis, 10% have recurrent transient bacteremias (usually streptococcal species). Most cases of subacute disease are secondary to the bacteremias that develop from the activities of daily living (eg, brushing teeth, bowel movements).

The skin is quite resistant to S aureus infection, largely as a result of its production of antimicrobial peptides. Soong et al discovered that, in vitro, the secretion of alpha toxin by S aureus allows the organism to successfully penetrate the keratinocyte layer. This could explain the presence of staphylococcal bacteremia in the absence of any gross damage to the epithelial layer.

Bacteremia can result from various invasive procedures, ranging from oral surgery to sclerotherapy of esophageal varices to genitourinary surgeries to various abdominal operations. The potential for invasive procedures to produce a bacteremia varies greatly. Procedures, rates, and organisms are as follows:

  • Endoscopy – Rate of 0% to 20%; coagulase-negative staphylococci (CoNS), streptococci, diphtheroids
  • Colonoscopy – Rate of 0% to 20%; Escherichia coli, Bacteroides species
  • Barium enema – Rate of 0% to 20%; enterococci, aerobic and anaerobic gram-negative rods
  • Dental extractions – Rate of 40% to 100%; S viridans
  • Transurethral resection of the prostate – Rate of 20% to 40%; coliforms, enterococci, S aureus
  • Transesophageal echocardiography – Rate of 0% to 20%; S viridans, anaerobic organisms, streptococci

The incidence of nosocomial bacteremias, mostly associated with intravascular lines, has more than doubled in the last few years. Up to 90% of BSIs caused by these devices are secondary to the placement of various types of central venous catheters. Hickman and Broviac catheters are associated with the lowest rates, presumably because of their Dacron cuffs. Peripherally placed central venous catheters are associated with similar rates.

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Intravascular catheters are infected from one of the following 4 sources:

  • Infection of the insertion site
  • Infection of the catheter
  • Bacteremia arising from another site
  • Contamination of the infused solution

Bacterial adherence to intravascular catheters depends on the response of the host to the presence of this foreign body, the properties of the organism itself, and the position of the catheter. Within a few days of insertion, a sleeve of fibrin and fibronectin is deposited on the catheter. Staphylococcus aureus adheres to the fibrin component.

Staphylococcus aureus also produces an infection of the endothelial cells (endotheliosis), which is important in producing the continuous bacteremia of S aureus BSIs. Endotheliosis may explain many cases of persistent methicillin-susceptible S aureus (MSSA) and MRSA catheter-related BSIs without an identifiable cause.

Staphylococcus aureus catheter-related BSIs occur even after an infected catheter is removed, apparently attributable to specific virulence factors of certain strains of S aureus that invade the adjacent endothelial cells. At some point, the staphylococci re-enter the bloodstream, resulting in bacteremia.

Four days after placement, the risk for infection markedly increases. Lines positioned in the internal jugular vein are more prone to infection than those placed in the subclavian vein. Colonization of the intracutaneous tract is the most likely source of short-term catheter-related BSIs. Among lines in place for more than 2 weeks, infection of the hub is the major source of bacteremia. In some cases, the infusion itself may be a reservoir of infection.

Colonization of heart valves by microorganisms is a complex process. Most transient bacteremias are short-lived, are without consequence, and are often unpreventable. Bacteria rarely adhere to an endocardial nidus before the microorganisms are removed from the circulation by various host defenses.

Once microorganisms do establish themselves on the surface of the vegetation, the process of platelet aggregation and fibrin deposition accelerate at the site. As the bacteria multiply, they are covered by ever-thickening layers of platelets and thrombin, which protect them from neutrophils and other host defenses. Organisms deep in the vegetation hibernate because of the paucity of available nutrients and are therefore less susceptible to bactericidal antimicrobials that interfere with bacterial cell wall synthesis.

Complications of subacute endocarditis result from embolization, slowly progressive valvular destruction, and various immunologic mechanisms. The pathologic picture of subacute IE is marked by valvular vegetations in which bacteria colonies are present both on and below the surface.

The cellular reaction in subacute bacterial endocarditis is primarily that of mononuclear cells and lymphocytes, with few polymorphonuclear cells. The surface of the valve beneath the vegetation shows few organisms. Proliferation of capillaries and fibroblasts is marked. Areas of healing are scattered among areas of destruction. Over time, the healing process falls behind, and valvular insufficiency develops secondary to perforation of the cusps and damage to the chordae tendineae. Compared with acute disease, little extension of the infectious process occurs beyond the valvular leaflets.

Levels of agglutinating and complement-fixing bactericidal antibodies and cryoglobulins are markedly increased in patients with subacute endocarditis. Many of the extracardiac manifestations of this form of the disease result from circulating immune complexes. Among these include glomerulonephritis, peripheral manifestations (eg, Osler nodes, Roth spots, subungual hemorrhages), and, possibly, various musculoskeletal abnormalities. Janeway lesions usually arise from infected microemboli.

The microscopic appearance of acute bacterial endocarditis differs markedly from that of subacute disease. Vegetations that contain no fibroblasts develop rapidly, with no evidence of repair. Large amounts of both polymorphonuclear leukocytes and organisms are present in an ever-expanding area of necrosis. This process rapidly produces spontaneous rupture of the leaflets, of the papillary muscles, and of the chordae tendineae.

The complications of acute bacterial endocarditis result from intracardiac disease and metastatic infection produced by suppurative emboli. Because of their shortened course, immunological phenomena are not a part of acute IE.

When to see a doctor

If you have signs or symptoms of endocarditis, see your doctor as soon as possible — especially if you have risk factors for this serious infection, such as a heart defect or history of endocarditis. Although less serious conditions can cause similar signs and symptoms, you won’t know for sure until you’re evaluated by your doctor.

If you’ve been diagnosed with endocarditis, tell your doctor about any signs or symptoms that may mean your infection is getting worse, such as:

  • Chills
  • Fever
  • Headaches
  • Joint pain
  • Shortness of breath

If you’re being treated with antibiotics for endocarditis, tell your doctor if you develop diarrhea, a rash, itching or joint pain. These signs and symptoms may mean you’re having a reaction to your prescribed antibiotic.

diagnosis

When you visit your doctor, you will first be asked to describe your symptoms. Your doctor will then perform a physical examination. They will listen to your heart with a stethoscope and check for sounds of a murmur, which may be present with infective endocarditis. Your doctor may also check for a fever and feel for an enlarged spleen by pressing on your left upper abdomen.

If your doctor suspects infective endocarditis, your blood will be tested for bacteria. A complete blood count (CBC) may also be used to check for anemia. A shortage of red blood cells can occur with infective endocarditis.

Your doctor may order an echocardiogram, or an ultrasound of the heart. This procedure uses sound waves to produce an image. The ultrasound wand may be placed on your chest. Alternatively, a smaller device may be threaded down your throat and into your esophagus. This can offer a more detailed image. The echocardiogram looks for damaged tissue, holes, or other structural changes in your heart valve.

Your doctor may also order an electrocardiogram (EKG). An EKG monitors electrical activity in your heart. This painless test can find an irregular heartbeat caused by endocarditis.

Imaging tests can check if your heart has enlarged. They may also be able to detect signs that infection has spread to other areas of your body. Such tests include:

  • chest X-ray
  • computed tomography (CT) scan
  • magnetic resonance imaging (MRI)

If you’re diagnosed with infective endocarditis, you will be immediately admitted to the hospital for treatment.

Risk factors

You’re more likely to develop endocarditis if you have faulty, diseased or damaged heart valves. However, endocarditis does occasionally occur in previously healthy people.

You have an increased risk of endocarditis if you have:

  • Older age. Endocarditis occurs most often in older adults over age 60.
  • Artificial heart valves. Germs are more likely to attach to an artificial (prosthetic) heart valve than to a normal heart valve.
  • Damaged heart valves. Certain medical conditions, such as rheumatic fever or infection, can damage or scar one or more of your heart valves, increasing the risk of infection.
  • Congenital heart defects. If you were born with certain types of heart defects, such as an irregular heart or abnormal heart valves, your heart may be more susceptible to infection.
  • Implanted heart device. Bacteria can attach to an implanted device, such as a pacemaker, causing an infection of the heart’s lining.
  • A history of endocarditis. Endocarditis can damage heart tissue and valves, increasing the risk of a future heart infection.
  • A history of illegal IV drug use. People who use illegal drugs by injecting them are at a greater risk of endocarditis. The needles used to inject drugs can be contaminated with the bacteria that can cause endocarditis.
  • Poor dental health. A healthy mouth and healthy gums are essential for good health. If you don’t brush and floss regularly, bacteria can grow inside your mouth and may enter your bloodstream through a cut on your gums.
  • Long-term catheter use. Having a catheter in place for a long period of time (indwelling catheter) increases your risk of endocarditis.

If you’re at risk of endocarditis, let all of your doctors know. You may want to request an endocarditis wallet card from the American Heart Association. Check with your local chapter or print the card from the association’s website.

Complications

In endocarditis, clumps made of germs and cell pieces form an abnormal mass in your heart. These clumps, called vegetations, can break loose and travel to your brain, lungs, abdominal organs, kidneys, or arms and legs.

As a result, endocarditis can cause several complications, including:

  • Heart problems, such as heart murmur, heart valve damage and heart failure
  • Stroke
  • Pockets of collected pus (abscesses) that develop in the heart, brain, lungs and other organs
  • Blood clot in a lung artery (pulmonary embolism)
  • Kidney damage
  • Enlarged spleen

Prevention

You can take the following steps to help prevent endocarditis:

  • Know the signs and symptoms of endocarditis. See your doctor immediately if you develop any signs or symptoms, especially a fever that won’t go away, unexplained fatigue, any type of skin infection, or open cuts or sores that don’t heal properly.
  • Take care of your teeth and gums. Brush and floss your teeth and gums often, and have regular dental checkups. Good dental hygiene is an important part of maintaining your overall health.
  • Don’t use illegal IV drugs. Dirty needles can send bacteria into your bloodstream, increasing your risk of endocarditis.

Preventive antibiotics

Certain dental and medical procedures may allow bacteria to enter your bloodstream.

If you’re at high risk of endocarditis, the American Heart Association recommends taking antibiotics an hour before having any dental work done.

You’re at high risk of endocarditis and need antibiotics before dental work if you have:

  • A history of endocarditis
  • A man-made (prosthetic mechanical) heart valve
  • A heart transplant, in some cases
  • Certain types of congenital heart disease
  • Congenital heart disease surgery in the last six months

If you have endocarditis or any type of congenital heart disease, talk to your doctor and dentist about your risks and whether you need preventive antibiotics.

Treating infective endocarditis

Infective endocarditis can cause irreversible damage to the heart. If it’s not caught and treated quickly, it can become life threatening. You will need to be treated in a hospital to prevent the infection from getting worse and causing complications.

Antibiotics and initial treatment

While in the hospital, your vital signs will be monitored. You will be given antibiotics intravenously (IV). Once you go home, you will continue with oral or IV antibiotics for at least four weeks. During this time, you will keep visiting your doctor. Regular blood tests will check that the infection is going away.

Surgery

Surgery may be needed if your heart valves have been damaged. Your surgeon may recommend repairing the heart valve. The valve can also be replaced using a new valve made from either animal tissue or artificial materials.

Surgery may also be necessary if the antibiotics are not working or if the infection is fungal. Antifungal medications are not always effective for infections in the heart.

Recovery and outlook

If left untreated, this condition will be fatal. However, most people are able to recover with antibiotic treatment. The chance of recovery depends on factors including your age and the cause of your infection. In addition, patients who get early treatment have a better chance of making a full recovery.

It may take you longer to recover completely if surgery was necessary.

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ISCHEMIC HEART DISEASE

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INTRODUCTION-

Ischemia is a condition in which the blood flow (and thus oxygen) is restricted or reduced in a part of the body. Cardiac ischemia is the name for decreased blood flow and oxygen to the heart muscle.

Ischemic heart disease is a condition of recurring chest pain or discomfort that occurs when a part of the heart does not receive enough blood. This condition occurs most often during exertion or excitement, when the heart requires greater blood flow. Ischemic heart disease, also called coronary heart disease, is common in the United States and is a leading cause of death worldwide.

Ischemic heart disease develops when cholesterol particles in the blood begin to accumulate on the walls of the arteries that supply blood to the heart. Eventually, deposits called plaques may form. These deposits narrow the arteries and eventually block the flow of blood. This decrease in blood flow reduces the amount of oxygen supplied to the heart muscle.

The signs and symptoms of ischemic heart disease may develop slowly as arteries gradually become blocked, or they may occur quickly if an artery suddenly becomes blocked. Some people with ischemic heart disease have no symptoms at all, while others may have severe chest pain (angina) and shortness of breath that can pose a risk of heart attack.

Fortunately, ischemic heart disease can be treated successfully with lifestyle changes, medicines, and surgical procedures. Even better, you can reduce your risk of ischemic heart disease by following heart-healthy practices, such as eating a low-fat, low-sodium diet, being physically active, not smoking, and maintaining a healthy body weight.

Left untreated, ischemic heart disease may lead to severe heart damage. Heart damage can result in heart attack and shock and may be life threatening. Seek immediate medical care (call 911) for serious symptoms, such as difficulty breathing, which may be accompanied by pale or blue lips, rapid heart rate (tachycardia), and severe chest pain. Seek prompt medical care if you are being treated for angina but have mild symptoms that recur or are persistent.

ETIOLOGY-

Ischemic heart disease is caused by a decrease in blood flow through one or more of the blood vessels that carry oxygen to your heart (coronary arteries). When blood flow is reduced, the heart muscle does not receive the amount of oxygen it needs to function properly.

Ischemic heart disease may develop slowly, as plaque builds up over time, or it may occur quickly if an artery is suddenly blocked. For this reason, ischemic heart disease occurs most frequently in people who have atherosclerosis (buildup of plaque on the walls of the coronary arteries), blood clots, coronary artery spasm, or severe illnesses that increase the heart’s need for oxygen.

SYMPTOM –

If your coronary arteries narrow, they can’t supply enough oxygen-rich blood to your heart — especially when it’s beating hard, such as during exercise. At first, the decreased blood flow may not cause any symptoms. As plaque continues to build up in your coronary arteries, however, you may develop the following coronary artery disease signs and symptoms:

  • Chest pain (angina). You may feel pressure or tightness in your chest, as if someone were standing on your chest. This pain, called angina, usually occurs on the middle or left side of the chest. Angina is generally triggered by physical or emotional stress. The pain usually goes away within minutes after stopping the stressful activity. In some people, especially women, the pain may be brief or sharp and felt in the neck, arm or back.
  • Shortness of breath. If your heart can’t pump enough blood to meet your body’s needs, you may develop shortness of breath or extreme fatigue with activity.
  • Heart attack. A completely blocked coronary artery will cause a heart attack. The classic signs and symptoms of a heart attack include crushing pressure in your chest and pain in your shoulder or arm, sometimes with shortness of breath and sweating. Women are somewhat more likely than men are to have less typical signs and symptoms of a heart attack, such as neck or jaw pain. And they may have other symptoms such as shortness of breath, fatigue and nausea. Sometimes a heart attack occurs without any apparent signs or symptoms.

Ischemic heart disease reduces the flow of blood to the coronary arteries, which carry oxygen to the heart. This reduction in blood flow may result in a number of symptoms, which can vary in intensity among individuals.

Common symptoms of ischemic heart disease

You may experience ischemic heart disease symptoms daily or just occasionally. Common symptoms include chest pain, chest pressure, or shortness of breath that:

  • Is relieved by rest or medicine
  • May feel as if pain starting in the chest spreads to the arms, back, or other areas
  • May feel like gas or indigestion (more common in women)
  • Occurs repeatedly; episodes tend to be alike
  • Occurs when the heart must work harder, usually during physical exertion
  • Usually lasts a short time (five minutes or less)

Serious symptoms that might indicate a life-threatening condition

In some cases, ischemic heart disease can be life threatening. Seek immediate medical care (call 911) if you, or someone you are with, have any of these life-threatening symptoms including:

  • Chest pain, typically on the left side of the body (angina pectoris)
  • Clammy skin
  • Nausea with or without vomiting
  • Pain in the neck or jaw
  • Rapid breathing (tachypnea) or shortness of breath
  • Shoulder or arm pain

When to see a doctor

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If you think you’re having a heart attack, immediately call 911 or your local emergency number. If you don’t have access to emergency medical services, have someone drive you to the nearest hospital. Drive yourself only as a last option.

If you have risk factors for coronary artery disease — such as high blood pressure, high cholesterol, tobacco use, diabetes, obesity a strong family history of heart disease — talk to your doctor. Your doctor may want to test you for coronary artery disease, especially if you have signs or symptoms of narrowed arteries.

RISK FACTOR-

Risk factors include:

  • Age. Getting older increases your risk of damaged and narrowed arteries.
  • Sex. Men are generally at greater risk of coronary artery disease. However, the risk for women increases after menopause.
  • Family history. A family history of heart disease is associated with a higher risk of coronary artery disease, especially if a close relative developed heart disease at an early age. Your risk is highest if your father or a brother was diagnosed with heart disease before age 55 or if your mother or a sister developed it before age 65.
  • Smoking. People who smoke have a significantly increased risk of heart disease. Breathing in secondhand smoke also increases a person’s risk of coronary artery disease.
  • High blood pressure. Uncontrolled high blood pressure can result in hardening and thickening of your arteries, narrowing the channel through which blood can flow.
  • High blood cholesterol levels. High levels of cholesterol in your blood can increase the risk of formation of plaque and atherosclerosis. High cholesterol can be caused by a high level of low-density lipoprotein (LDL) cholesterol, known as the “bad” cholesterol. A low level of high-density lipoprotein (HDL) cholesterol, known as the “good” cholesterol, can also contribute to the development of atherosclerosis.
  • Diabetes. Diabetes is associated with an increased risk of coronary artery disease. Type 2 diabetes and coronary artery disease share similar risk factors, such as obesity and high blood pressure.
  • Overweight or obesity. Excess weight typically worsens other risk factors.
  • Physical inactivity. Lack of exercise also is associated with coronary artery disease and some of its risk factors, as well.
  • High stress. Unrelieved stress in your life may damage your arteries as well as worsen other risk factors for coronary artery disease.
  • Unhealthy diet. Eating too much food that has high amounts of saturated fat, trans fat, salt and sugar can increase your risk of coronary artery disease.

Risk factors often occur together and one may trigger another. For instance, obesity can lead to type 2 diabetes and high blood pressure. When grouped together, certain risk factors make you even more likely to develop coronary artery disease. For example, metabolic syndrome — a cluster of conditions that includes high blood pressure; high triglycerides; low HDL, or “good,” cholesterol; high insulin levels and excess body fat around the waist — increases the risk of coronary artery disease.

Sometimes coronary artery disease develops without any classic risk factors. Researchers are studying other possible risk factors, including:

  • Sleep apnea. This disorder causes you to repeatedly stop and start breathing while you’re sleeping. Sudden drops in blood oxygen levels that occur during sleep apnea increase blood pressure and strain the cardiovascular system, possibly leading to coronary artery disease.
  • High-sensitivity C-reactive protein (hs-CRP). This protein appears in higher-than-normal amounts when there’s inflammation somewhere in your body. High hs-CRP levels may be a risk factor for heart disease. It’s thought that as coronary arteries narrow, you’ll have more hs-CRP in your blood.
  • High triglycerides. This is a type of fat (lipid) in your blood. High levels may raise the risk of coronary artery disease, especially for women.
  • Homocysteine. Homocysteine is an amino acid your body uses to make protein and to build and maintain tissue. But high levels of homocysteine may increase your risk of coronary artery disease.
  • Preeclampsia. This condition that can develop in women during pregnancy causes high blood pressure and a higher amount of protein in urine. It can lead to a higher risk of heart disease later in life.
  • Alcohol use. Heavy alcohol use can lead to heart muscle damage. It can also worsen other risk factors of coronary artery disease.
  • Autoimmune diseases. People who have conditions such as rheumatoid arthritis and lupus (and other inflammatory conditions) have an increased risk of atherosclerosis.

A number of factors increase the risk of developing ischemic heart disease. Not all people with risk factors will get ischemic heart disease. Risk factors for ischemic heart disease include:

  • Diabetes
  • Family history of heart disease
  • High blood cholesterol
  • High blood pressure
  • High blood triglycerides
  • Obesity
  • Physical inactivity
  • Smoking and other tobacco use

Reducing your risk of ischemic heart disease

You may be able to lower your risk of ischemic heart disease by:

  • Carefully managing your diabetes, if applicable
  • Getting regular physical activity
  • Keeping your cholesterol at a healthy level
  • Maintaining normal blood pressure
  • Quitting smoking and other tobacco use
  • Reducing the amount of cholesterol and fat in your diet

COMPLICATION-

Coronary artery disease can lead to:

  • Chest pain (angina). When your coronary arteries narrow, your heart may not receive enough blood when demand is greatest — particularly during physical activity. This can cause chest pain (angina) or shortness of breath.
  • Heart attack. If a cholesterol plaque ruptures and a blood clot forms, complete blockage of your heart artery may trigger a heart attack. The lack of blood flow to your heart may damage your heart muscle. The amount of damage depends in part on how quickly you receive treatment.
  • Heart failure. If some areas of your heart are chronically deprived of oxygen and nutrients because of reduced blood flow, or if your heart has been damaged by a heart attack, your heart may become too weak to pump enough blood to meet your body’s needs. This condition is known as heart failure.
  • Abnormal heart rhythm (arrhythmia). Inadequate blood supply to the heart or damage to heart tissue can interfere with your heart’s electrical impulses, causing abnormal heart rhythms.

EPIDEMIOLOGY

On the basis of data from the National Health and Nutrition Examination Survey (NHANES) for the period 2003 to 2006, an estimated 17.6 million Americans age 20 or older have CHD, with an overall prevalence of 7.9 percent (9.1 percent in men and 7 percent in women). The overall prevalence of MI is 3.6 percent (4.7 percent in men and 2.6 percent in women). The estimated annual incidence of MI is 935,000, which includes 610,000 new and 325,000 recurrent infarctions. The overall prevalence of angina pectoris is 4.6 percent, with age-adjusted prevalence higher in women than men. CHD accounts for more than half of all cardiovascular events in men and women under age 75. The lifetime risk of developing CHD after age 40 is 49 percent for men and 32 percent for women (Lloyd-Jones et al., 2010).

CHD is the leading cause of death in both men and women. It caused one of every six U.S. deaths in 2006; CHD mortality was 425,425, and MI mortality was 141,462. Approximately every 25 seconds, an American will experience a coronary event, and approximately every minute a death will be attributed to a coronary event. Approximately every 34 seconds, an American will have an MI and 15 percent will die of it (Lloyd-Jones et al., 2010).

In addition, in 2006, 1,115,000 inpatient diagnostic cardiac catheterizations were performed as well as 661,000 inpatient percutaneous coronary interventions (PCIs) and 253,000 coronary artery bypass surgery (CABG) procedures. The estimated direct and indirect cost of coronary heart disease for 2010 is $177.1 billion (Lloyd-Jones et al., 2010).

DIAGNOSIS AND METHOD –

Coronary heart disease (CHD) is usually diagnosed after a risk assessment and some further tests.

Risk assessment

If a GP thinks you may be at risk of CHD, they may do a risk assessment for cardiovascular disease, heart attack or stroke. 

The DOCTOR will:

  • ask about your medical and family history
  • check your blood pressure
  • do a blood test to assess your cholesterol level

Before having the cholesterol test, you may be asked not to eat for 12 hours so there’s no food in your body that could affect the result.

The GP or practice nurse can carry out the blood test. A sample will be taken either using a needle and a syringe or by pricking your finger.

The GP will also ask about your lifestyle, how much exercise you do and whether you smoke. All these factors will be considered as part of the diagnosis.

Further tests

You may be referred for further tests to help confirm CHD. A number of different tests are used to diagnose heart-related problems, including:

  • electrocardiogram (ECG)
  • exercise stress tests
  • X-rays
  • echocardiogram
  • blood tests
  • coronary angiography
  • radionuclide tests
  • MRI scans
  • CT scans

PREVENTION-

The same lifestyle habits used to help treat coronary artery disease can also help prevent it. A healthy lifestyle can help keep your arteries strong and clear of plaque. To improve your heart health, follow these tips:

  • Quit smoking.
  • Control conditions such as high blood pressure, high cholesterol and diabetes.
  • Stay physically active.
  • Eat a low-fat, low-salt diet that’s rich in fruits, vegetables and whole grains.
  • Maintain a healthy weight.
  • Reduce and manage stress.

TREATMENT –

Treatment for coronary heart disease (CHD) can help manage the symptoms and reduce the risk of further problems.

CHD can be managed effectively with a combination of lifestyle changes, medicine and, in some cases, surgery.

With the right treatment, the symptoms of CHD can be reduced and the functioning of the heart improved.

Things you can do to help with coronary heart disease (CHD)

If you’ve been diagnosed with CHD, making simple lifestyle changes can reduce your risk of having further episodes.

For example, stopping smoking after a heart attack quickly reduces your risk of having a heart attack in the future to near that of a non-smoker.

Other lifestyle changes, such as eating more healthily and doing regular exercise, will also reduce your future risk of heart disease.

Further information

  • exercise and fitness
  • healthy eating
  • stop smoking

Medicines

Many different medicines are used to treat CHD. Usually they either aim to reduce blood pressure or widen your arteries.

Some heart medicines have side effects, so it may take a while to find one that works for you. A GP or specialist will discuss the various options with you.

Heart medicines should not be stopped suddenly without the advice of a doctor as there’s a risk this may make your symptoms worse.

Blood-thinning medicines

Blood thinners are a type of medicine that can help reduce the risk of a heart attack by thinning your blood and preventing it clotting.

Common blood-thinning medicines include:

  • low-dose aspirin
  • clopidogrel
  • rivaroxaban
  • ticagrelor
  • prasugrel

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Statins

If you have high cholesterol, cholesterol-lowering medicine called statins may be prescribed.

Examples include:

  • atorvastatin
  • simvastatin
  • rosuvastatin
  • pravastatin

Statins work by blocking the formation of cholesterol and increasing the number of low-density lipoprotein (LDL) receptors in the liver.

This helps remove LDL cholesterol from your blood, which makes a heart attack less likely. 

Not all statins are suitable for everyone, so you may need to try several different types until you find one that’s suitable.

Beta blockers

Beta blockers, including atenolol, bisoprolol, metoprolol and nebivolol, are often used to prevent angina and treat high blood pressure.

They work by blocking the effects of a particular hormone in the body, which slows down your heartbeat and improves blood flow.

Nitrates

Nitrates are used to widen your blood vessels. Doctors sometimes refer to nitrates as vasodilators.

They’re available in a variety of forms, including tablets, sprays and skin patches such as glyceryl trinitrate and isosorbide mononitrate.

Nitrates work by relaxing your blood vessels, letting more blood pass through them. This lowers your blood pressure and relieves any heart pain you have.

Nitrates can have some mild side effects, including headaches, dizziness and flushed skin.

Angiotensin-converting enzyme (ACE) inhibitors

ACE inhibitors are commonly used to treat high blood pressure. Examples include ramipril and lisinopril.

They block the activity of a hormone called angiotensin-2, which causes the blood vessels to narrow.

As well as stopping the heart working so hard, ACE inhibitors improve the flow of blood around the body.

Your blood pressure will be monitored while you’re taking ACE inhibitors, and regular blood tests will be needed to check that your kidneys are working properly.

Less than 1 in 100 people have problems with the blood supply to their kidneys (renal stenosis) as a result of taking ACE inhibitors.

Side effects of ACE inhibitors can include a dry cough and dizziness.

Angiotensin-2 receptor blockers (ARBs)

Angiotensin-2 receptor blockers (ARBs) work in a similar way to ACE inhibitors.

They’re used to lower your blood pressure by blocking angiotensin-2.

Mild dizziness is usually the only side effect. They’re often prescribed as an alternative to ACE inhibitors, as they do not cause a dry cough.

Coronavirus advice

If you have coronavirus (COVID-19), or think you might have it, keep taking your blood pressure medicines as usual.

There is no clear evidence that taking angiotensin-converting enzyme (ACE) inhibitors or angiotensin-2 receptor blockers (ARBs) will cause complications.

Calcium channel blockers

Calcium channel blockers also work to decrease blood pressure by relaxing the muscles that make up the walls of your arteries.

This causes the arteries to become wider, reducing your blood pressure.

Examples include amlodipine, verapamil and diltiazem.

Side effects include headaches and facial flushing, but these are mild and usually decrease over time.

Diuretics

Sometimes known as water pills, diuretics work by flushing excess water and salt from the body through urine.

Procedures and surgery

If your blood vessels are narrow as the result of a build-up of atheroma (fatty deposits) or if your symptoms cannot be controlled using medicines, interventional procedures or surgery may be needed to open up or bypass blocked arteries.

Here are some of the main procedures used to treat blocked arteries.

Coronary angioplasty

Coronary angioplasty is also known as percutaneous coronary intervention (PCI), percutaneous transluminal coronary angioplasty (PTCA) or balloon angioplasty.

Angioplasty may be a planned procedure for someone with angina, or an urgent treatment if the symptoms have become unstable.

Having a coronary angiogram (a type of X-ray used to check blood vessels) will determine if you’re suitable for treatment.

Coronary angioplasty is also performed as an emergency treatment during a heart attack.

During the procedure, a small balloon is inserted to push the fatty tissue in the narrowed artery outwards. This allows the blood to flow more easily.

A metal stent (a wire mesh tube) is usually placed in the artery to hold it open. Drug-eluting stents can also be used. These release medicines to stop the artery narrowing again.

Coronary artery bypass graft

Coronary artery bypass grafting (CABG) is also known as bypass surgery, a heart bypass, or coronary artery bypass surgery.

It’s carried out in people whose arteries are narrowed or blocked.

A coronary angiogram will determine if you’re suitable for treatment.

Off-pump coronary artery bypass (OPCAB) is a type of coronary artery bypass surgery. It’s performed while the heart continues to pump blood by itself without the need for a heart-lung machine.

A blood vessel is inserted (grafted) between the main artery leaving the heart (the aorta) and a part of the coronary artery beyond the narrowed or blocked area.

Sometimes, an artery that supplies blood to the chest wall is used and diverted to one of the heart arteries. This allows the blood to bypass (get around) the narrowed sections of coronary arteries.

Heart transplant

Occasionally, when the heart is severely damaged and medicine is not effective, or when the heart becomes unable to adequately pump blood around the body (heart failure), a heart transplant may be needed.

A heart transplant involves replacing a heart that’s damaged or is not working properly with a healthy donor heart.

Side Effects of Treatments

Nitroglycerin and nitrates can cause vasodilation-induced headache, a decrease in blood pressure, and, more rarely, severe hypotension with bradycardia. The vasodilation by nitroglycerin may be markedly exaggerated and prolonged in the presence of the phosphodiesterase inhibitors sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis), so these agents should not be used concurrently with nitrates.

Most of the adverse effects of beta-blockers occur as a consequence of the known properties of these drugs and include cardiac effects (e.g., severe sinus bradycardia, sinus arrest, reduced LV contractility), bronchoconstriction, fatigue, mental depression, nightmares, gastrointestinal upset, sexual dysfunction, intensification of insulin-induced hypoglycemia, and cutaneous reactions. Lethargy, weakness, and fatigue may be caused by reduced cardiac output or may arise from a direct effect on the central nervous system. Bronchoconstriction results from blockade of beta2 receptors in the tracheobronchial tree. As a consequence, reversible obstructive lung disease (e.g., asthma) may be considered as relative contraindications to beta-blockers, even to beta1-selective agents (Egred et al., 2005).

Calcium channel blockers are potent vasodilators, which may lead to dizziness, hypotension, and reflex tachycardia—particularly with some dihydropyridines. Peripheral edema can occur, usually with the dihydropyri dines. Both verapamil and diltiazem can cause bradycardia or conduction disturbances, particularly if coadministered with beta-blockers. Diltiazem and verapamil may exacerbate or precipitate heart failure in patients with reduced LV ejection fraction.

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FILARIA

Synonyms of Filariasis

  • Bancroftian Filariasis
  • Filarial Elephantiasis
  • Filariasis Malayi
  • Malayi Tropical Eosinphilia
  • Wuchereriasis

INTRODUCTION-

Lymphatic filariasis is a disease associated with parasitic infection of one of three different nematodes: Wuchereria bancrofti, Brugia malayi, or Brugia timori. The microscopic worms enter the human body via mosquito transmission- in both children and adults- and can live up to 5-7 years in the lymphatic system. Although most people who are infected are asymptomatic, a small percentage of people will develop extreme lymphedema and multiple secondary infections as a result of years of exposure to the parasites.

Filariasis is an infectious tropical disease caused by any one of several thread-like parasitic round worms. The two species of worms most often associated with this disease are Wuchereria bancrofti and Brugia malayi. The larval form of the parasite transmits the disease to humans by the bite of a mosquito. In the early stages of the infection, the patient characteristically complains of fever, chills, headaches and skin lesions. Any one of several antiparasitic agents may be effective in eliminating the worm. However, if the disease is left untreated, obstruction of the lymph flow will cause particular areas of the body especially the legs and external genitals, to swell profoundly. Symptoms are primarily a response to adult worms that cause inflammation. Chronic inflammation may progress to hardening of the lymphatic vessels (fibrosis) and obstruction of the lymph flow.

ACCORDING TO WHO

Lymphatic filariasis, commonly known as elephantiasis, is a neglected tropical disease. Infection occurs when filarial parasites are transmitted to humans through mosquitoes. Infection is usually acquired in childhood causing hidden damage to the lymphatic system.

The painful and profoundly disfiguring visible manifestations of the disease, lymphoedema, elephantiasis and scrotal swelling occur later in life and can lead to permanent disability. These patients are not only physically disabled, but suffer mental, social and financial losses contributing to stigma and poverty.

In 2018, 893 million people in 49 countries were living in areas that require preventive chemotherapy to stop the spread of infection.

The global baseline estimate of people affected by lymphatic filariasis was 25 million men with hydrocele and over 15 million people with lymphoedema.  At least 36 million people remain with these chronic disease manifestations. Eliminating lymphatic filariasis can prevent unnecessary suffering and contribute to the reduction of poverty.

CAUSES-

Filariasis is a rare infectious tropical disorder caused by the round worm parasites (nematode) Wuchereria bancrofti or Brugia malayi. Symptoms result primarily from inflammatory reactions to the adult worms. Some people may also develop hypersensitivity reactions to the small larval parasites (microfilariae).

Lymphatic filariasis is caused by infection with parasites classified as nematodes (roundworms) of the family Filariodidea. There are 3 types of these thread-like filarial worms:

  • Wuchereria bancrofti, which is responsible for 90% of the cases
  • Brugia malayi, which causes most of the remainder of the cases
  • Brugia timori, which also causes the disease.

Adult worms nest in the lymphatic vessels and disrupt the normal function of the lymphatic system. The worms can live for approximately 6–8 years and, during their life time, produce millions of microfilariae (immature larvae) that circulate in the blood.

Mosquitoes are infected with microfilariae by ingesting blood when biting an infected host. Microfilariae mature into infective larvae within the mosquito. When infected mosquitoes bite people, mature parasite larvae are deposited on the skin from where they can enter the body. The larvae then migrate to the lymphatic vessels where they develop into adult worms, thus continuing a cycle of transmission.

Lymphatic filariasis is transmitted by different types of mosquitoes for example by the Culex mosquito, widespread across urban and semi-urban areas, Anopheles, mainly found in rural areas, and Aedes, mainly in endemic islands in the Pacific.

Prevalence

It is estimated that more than 120 million people in 80 countries worldwide are currently infected with one of the three nematodes. Greater than 90% of those 120 million people are infected with the Wuchereria bancrofti filaria, and the majority of the remaining ~10% are infected with the Brugia malayi filaria. Reports also suggest that more than 40 million people are significantly dibilatated and disfigured by the disease. Worldwide distribution of Lymphatic Filariasis. Image credit: CDC


Lymphatic filariasis is endemic is the tropic and sub-tropics of Southeast Asia, Africa, the India Subcontinent, the Pacific islands, and parts of the Caribbean and Latin America.

Total Global Elimination treatments:

Region# of Countries TreatedTotal # of Treatments (millions)Total Treatments to Children (millions)
Africa175112.8
Americas42.70.8
Eastern Med20.50.1
Mekong Plus515.94.9
Pacific140.30.09
Southeast Asia90.444.6
Total51496.263.5

SIGN AND SYMPTOM-

Some people with filariasis have no symptoms. Other affected individuals may have episodes of acute inflammation of lymphatic vessels (lymphangitis) along with high temperatures, shaking chills, body aches, and swollen lymph nodes. Excessive amounts of fluid may accumulate (edema) in the affected areas (i.e., arms and/or legs), but the accumulation typically resolves after the other symptoms are gone. Attacks may also be accompanied by acute inflammation of the genitalia leading, in males, to inflammation, pain and swelling of the testes (orchitis), sperm track (funiculitis), and/or sperm ducts (epididymitis). The scrotum may become abnormally swollen and painful.

Bancroftian filariasis affects both the legs and the genitals. The Malayan variety affects the legs below the knees.

Some people with filariasis have abnormally high levels of certain white blood cells (eosinophilia) during acute episodes of symptoms. When the inflammation resolves, these levels return to normal.

Filariasis may cause chronic lymph node swelling (lymphadenopathy) even in the absence of other symptoms. Longstanding obstruction of the lymphatic vessels may lead to several other conditions. These include accumulation of fluid in the scrotum (hydrocele), the presence of lymphatic fluid in the urine (chyluria), and/or abnormally enlarged lymphatic vessels (varices). Other symptoms may include progressive edema (elephantiasis) of the female external genitalia (vulva), breasts, and/or arms and legs. Chronic edema may result in skin that is abnormally thick and has a “warty” appearance.

Characteristics/Clinical Presentation

The majority of people who become infected with filariasis do not show any overt clinical signs or symptoms, although they will experience irregularities in their lymphatic drainage. It is estimated that only one-third of those infected by any of the filarial nematodes show obvious clinical features of the condition. Experts have attributed the severity of symptoms as being positively correlated with extended time of exposure and accumulation of worms.

ACUTE Signs & Symptoms

  • Adenolymphangitis
  • Filarial fever
  • Tropical pulmonary eosinophilia

Acute adenolymphangitis: Characteristics include painful lymphadenopathy and retrograde lymphangitis that most often affect the inguinal nodes, genitalia, and lower extremities leading to extreme edema, elephantiasis, and sometimes skin breakdown and secondary infections. Flare-ups can last 4-7 days and occur up to 4 times per year depending on the severity of the lymphedema.


Filarial fever: Often an acute fever that occurs independently of any other signs of lymphadenopathy. Filarial fever is sometimes misdiagnosed as a manifestation of malaria and other tropical diseases because of the lack of associated symptoms.

Tropical pulmonary eosinophilia: Most commonly seen in young males and is caused by microfilariae being trapped in the lungs. The immune system exhibits a respiratory “hyperresponsiveness” to the problem, causing excessive nocturnal wheezing.

CHRONIC Signs & Symptoms:

  • Lymphedema
  • Renal Pathology
  • Secondary infections

Lymphedema: Commonly involves vessels in the inguinal and axillary lymph nodes, affecting all four extremities.  Early stage lymphedema is usually characterized by pitting edema, but more chronic stages exhibit non-pitting edema with hardening of the surrounding tissues, eventually leading to hyperpigmentation and hyperkeratosis. Chronic manifestations can also involve the breasts and male genitalia. Hydroceles (swelling of the scrotum) can be greater than 30cm in diameter, but are usually painless unless bacterial infection is present. 

Renal Pathology: When renal system lymphatic are obstructed, lymph fluid can be passed into the renal pelvis. Chyluria, or lymph fluid in the urine, causes a milky appearance in the excreted urine. Hematuria and proteinuria may also be present and can eventually cause  nutritional deficiencies and anemia.

Secondary infections: Bacterial and fungal infections become problematic in lymphatic filariasis due to edema-causing skin folds and skin tears.

DIAGNOSIS-

Nonspecific test abnormalities:

  • Eosinophilia (>3000/microliter)
  • Microscopic hematuria
  • Microscopic proteinuria

Blood smears:

  • Samples are drawn ideally between 10pm and 2am due to peak biting time of mosquito vectors
  • 20 microliters of blood can detect microfilariae, but a 1 mL blood sample may be required to make a diagnosis
  • >10,000 microfilariae per 1 mL of blood can be found in endemic regions
  • Samples are stained and centrifuged
  • Microfilariae species can be differentiated by morphological characteristics

Antibody tests:

  • Serologic testing for filarial antibodies can detect elevated levels of IgG and IgE
  • Poor specificity
  • Cannot distinguish between filarial types
  • Cannot differentiate between past and present infections
  • Newer tests are being developed that look at specific anti-filarial IgG4 antibodies for showing active infections

Antigen tests:

  • Detect the presence of adult worms
  • Circulating Filarial Antigen (CFA) tests are considered the gold standard for diagnosing Wuchereria bancrofti infections
  • No antigen testing currently available for Brugian malayi filariasis

Radiology:

  • Ultrasound can be used to detect adult worms and vessel destruction
  • Ultrasound can localize worms in epididymal and breast lymphatics
  • “Filarial dance”, or the constant movement of live worms, can be picked up with ultrasound imaging and is sometimes used to monitor effectiveness of certain treatments
  • Lymphoscintigraphy is used for assessment of the extent of lymphatic destruction.

Differential Diagnoses-

Most highly suspected causes of Lymphadenopathy:

  1. Mononucleosis
  2. Epstein-Barr Virus
  3. Toxoplasmosis
  4. Cytomegalovirus
  5. HIV
  6. Cat-scratch disease
  7. Pharyngitis
  8. Tuberculosis
  9. Secondary syphilis
  10. Hepatitis B
  11. Lymphogranuloma venereum
  12. Chancroid
  13. SLE
  14. Rheumatoid Arthritis
  15. Lymphoma
  16. Leukemia
  17. Serum sickness
  18. Sarcoidosis
  19. Kawasaki disease

Travel-related causes of Lymphadenopathy:

  1. Coccidioidomycosis
  2. Bubonic Plague
  3. Histoplasmosis
  4. Scrub typhus
  5. African trypanosomiasis
  6. American trypanosomiasis
  7. Kala-azar
  8. Typhoid fever

Systemic Involvement

1. Lymphatic: Adult filariae can live in the lymphatic system for up to 7 years while continuing to reproduce, leading to obstruction of drainage and destruction of vessels.

2.  Renal: Intestinal lymph fluid can be deposited into the renal pelvis and eventually make its way to the urine to be excreted by the body (chyluria). This can lead to hypoproteinemia, hematuria, and anemia as large amounts of fat and protein are lost through the urine and lymph fluid. 

3. Dermatological: Pitting edema, hyperpigmentation, and hyperkeratosis are present as a result of the associated lymphedema. In severe cases, affected individuals develop elephantiasis. Lymphatic filariasis.

4. Reproductive: In females, involvement of the breast tissue and ovaries (along with upper or lower limb edema) is not uncommon. In males, the genitalia can be severely affected. Unilateral or bilateral hydroceles in the scrotum (especially in the spermatic cord) can lead to disfigurement and loss of sexual function.

5. Immune: Other bacterial or fungal infections often develop as a secondary result of lymphatic filariasis, primarily due to excessive skin folds and skin tears.

Related Disorders

Symptoms of the following disorders can be similar to those of Filariasis. Comparisons may be useful for a differential diagnosis:

Acanthocheilonemiasis is a tropical infectious disease caused by a multicellular parasite (filarial worm [nematode]), called Acanthocheilonema perstans. This parasite is found most commonly in Africa. Initially people with Acanthocheilonemiasis may have no symptoms. Symptoms may include itchy skin (pruritis), abdominal pain, chest pain, muscle pain (myalgias), and/or areas of swelling under the skin. Other symptoms may include an abnormally enlarged liver and spleen (hepatosplenomegaly), and inflammation in the affected organs. (For more information on this disorder, choose “Acanthocheilo” as your search term in the Rare Disease Database.)

Filarial Disease, or the general term “filariasis,” may also refer to a group of parasitic diseases caused by various species of filarial worms (nematodes). These include mumu, loiasis (Calabar swellings), dirofilariasis (human infection by dog heartworm), and onchocerciasis (river blindness). All these except dirofilariasis can be acquired only in the tropics, where they are common, but are extremely rare in temperate climates such as North America. Taken together, filarial diseases of all types affect approximately 100 million people worldwide.

MEDICAL MANAGEMENT –

  • Prescription Drug Therapy
  1. Prevention
  2. Post-infection treatment
  • Clinical Care
  1. Lymphedema management
  2. Wash and dry affected area twice daily
  3. Elevate lower extremities at night
  4. Exercise and move affected limb regularly
  5. Antibiotics/Topical medications for small wounds
  6. Comfortable shoes
  • Surgery
  1. Hydroceles
  • Patient Education
  • Patient Counseling

Prevention for travelers:

Chronic conditions of LF is generally not a concern for those people who wish to visit endemic regions of the world because they do not stay long enough to accumulate a harmful amount of microfilariae, although the following mild, allergic-like symptoms have been reported: lymphangitis/lymphadenitis, urticaria (hives), rash, and peripheral eosinophilia. Recommendations for travelers are as follows: wear long sleeves and long pants, sleep under a mosquito net or in air conditioning, use bug repellent, and stay indoors or away from mosquito breeding grounds between dusk and dawn (they’re preferred biting time).

Physical Therapy Management

Clinical manifestations of filariasis such as lymphedema and elephantiasis are caused by prolonged exposure to filariae and the mosquitos that transmit them in endemic regions. These affected individuals are usually not actively infected; rather, they are suffering from the effects of years of exposure to one of the three nematodes. Medical management is not appropriate for these individuals.

Physical therapy management of the disease primarily consists of treatment from a lymphedema therapist, along with education of proper skin care and hygiene. Appropriate exercise prescription and wound care management are also indicated. There is no physical therapy intervention indicated for hydrocele; those infected usually do not respond well to DEC, and surgery is required in some cases.

WHO response

World Health Assembly resolution WHA50.29 encourages Member States to eliminate lymphatic filariasis as a public health problem. In response, WHO launched its Global Programme to Eliminate Lymphatic Filariasis (GPELF) in 2000. In 2012, the WHO neglected tropical diseases roadmap reconfirmed the target date for achieving elimination by 2020.

WHO’s strategy is based on 2 key components:

  • stopping the spread of infection through large-scale annual treatment of all eligible people in an area or region where infection is present; and
  • alleviating the suffering caused by lymphatic filariasis through provision of the recommended basic package of care.

Large-scale treatment (preventive chemotherapy)

Elimination of lymphatic filariasis is possible by stopping the spread of the infection through preventive chemotherapy. The WHO recommended preventive chemotherapy strategy for lymphatic filariasis elimination is mass drug administration (MDA).  MDA involves administering an annual dose of medicines to the entire at-risk population. The medicines used have a limited effect on adult parasites but effectively reduce the density of microfilariae in the bloodstream and prevent the spread of parasites to mosquitoes.

The MDA regimen recommended depends on the co-endemicity of lymphatic filariasis with other filarial diseases. WHO recommends the following MDA regimens:

  • albendazole (400 mg) alone twice per year for areas co-endemic with loiasis
  • ivermectin (200 mcg/kg) with albendazole (400 mg) in countries with onchocerciasis
  • diethylcarbamazine citrate (DEC) (6 mg/kg) and albendazole (400 mg) in countries without onchocerciasis

Recent evidence indicates that the combination of all three medicines can safely clear almost all microfilariae from the blood of infected people within a few weeks, as opposed to years using the routine two-medicine combination.

WHO now recommends the following MDA regimen in countries without onchocerciasis:

  • ivermectin (200 mcg/kg) together with diethylcarbamazine citrate (DEC) (6 mg/kg) and albendazole (400 mg) in certain settings

The impact of MDA depends on the efficacy of the regimen and the coverage (proportion of total population ingesting the medicines). MDA with the two-medicine regimens have interrupted the transmission cycle when conducted annually for 4–6 years with effective coverage of the total population at risk. Salt fortified with DEC has also been used in a few unique settings to interrupt the transmission cycle.

At the start of GPELF, 81 countries were considered endemic for lymphatic filariasis. Further epidemiological data reviewed since, indicate that preventive chemotherapy was not required in 10 countries. From 2000 to 2018, 7.7 billion treatments were delivered to more than 910 million people at least once in 68 countries, considerably reducing transmission in many places. The population requiring MDA has declined by 42% (597 million) where infection prevalence has been reduced below elimination thresholds.  The overall economic benefit of the programme during 2000-2007 is conservatively estimated at US$ 24 billion. Treatments until 2015 are estimated to have averted at least US$ 100.5 billion of economic loss expected to have occurred over the lifetime of cohorts who have benefited from treatment.

Sixteen countries and territory (Cambodia, The Cook Islands, Egypt, Kiribati, Maldives, Marshall Islands, Niue, Palau, Sri Lanka, Thailand, Togo, Tonga, Vanuatu, Viet Nam, Wallis and Futuna, and Yemen) are now acknowledged as achieving elimination of lymphatic filariasis as a public health problem. Seven additional countries have successfully implemented recommended strategies, stopped large-scale treatment and are under surveillance to demonstrate that elimination has been achieved. Preventive chemotherapy is still required in 49 countries and within 15 of these countries MDA has not yet been delivered to all endemic areas as of the end of 2018.  

Morbidity management

Morbidity management and disability prevention are vital for improving public health and are essential services that should be provided by the health care system to ensure sustainability. Surgery can alleviate most cases of hydrocele. Clinical severity and progression of the disease, including acute inflammatory episodes, can be reduced and prevented with simple measures of hygiene, skin care, exercises, and elevation of affected limbs. People with lymphoedema must have access to continuing care throughout their lives, both to manage the disease and to prevent progression to more advanced stages.

The GPELF aims to provide access to a minimum package of care for every person with associated chronic manifestations of lymphatic filariasis in all areas where the disease is present, thus alleviating suffering and promoting improvement in their quality of life.

Success in 2020 will be achieved if patients have access to the following minimum package of care:

  • treatment for episodes of adenolymphangitis (ADL);
  • guidance in applying simple measures to manage lymphoedema to prevent progression of disease and debilitating, inflammatory episodes of ADL;
  • surgery for hydrocele;
  • treatment of infected people with antifilarial medicines

Vector control

Mosquito control is a supplemental strategy supported by WHO. It is used to reduce transmission of lymphatic filariasis and other mosquito-borne infections. Depending on the parasite-vector species, measures such as insecticide-treated nets, indoor residual spraying or personal protection measures may help protect people from infection. The use of insecticide-treated nets in areas where Anopheles is the primary vector for filariasis enhances the impact on transmission during and after MDA. Historically, vector control has in select settings contributed to the elimination of lymphatic filariasis in the absence of large-scale preventive chemotherapy.

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