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Fibroid period: A Visual Guide to Uterine Fibroids

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Uterine Fibroid Pain Symptom Relief

For most women, a certain degree of menstrual pain is relatively common. In fact, as many as 80 percent of women experience period pain. However, it can also be a sign of something more serious, like uterine fibroids.

What Are Uterine Fibroids?

If you’re experiencing long-lasting period pain, or pain that worsens as you get older, it may be a sign of uterine fibroids.

“Uterine fibroids are benign, smooth muscle growths of the uterus,” says Linda Bradley, MD, director of the Fibroid and Menstrual Disorders Center at Cleveland Clinic in Ohio. These growths are rarely cancerous, and they’re very common — as many as 80 percent of women develop fibroids by age 50, according to the U.S. Department of Health & Human Services.

That said, they’re more common in some populations than others. Although fibroids can develop at any age, uterine fibroids are most common in women ages 30 to 40. Black women are more likely to develop uterine fibroids than white women; fibroids tend to develop at a younger age and grow more quickly in Black women, as well.

Common Symptoms of Uterine Fibroids

Some women who have uterine fibroids may not experience any symptoms. Others, however, may experience a range of symptoms that affect their period and beyond, such as:

  • Abdominal or lower back pain
  • Pelvic pain and cramping
  • Painful sex
  • Heavy menstrual bleeding
  • Long, frequent periods
  • Bleeding between periods
  • Anemia (from blood loss)
  • Bladder or bowel pressure
  • Frequent or urgent urination
  • Bowel movements that are difficult, frequent, or urgent
  • Increased abdominal size
  • Miscarriage
  • Infertility

“Your symptoms generally depend on the location and number of uterine fibroids,” says Dr. Bradley.

Why Uterine Fibroids Cause Painful Periods

Each month, your uterus goes through a cycle: It creates a thickened inner lining in case a pregnancy occurs. If pregnancy does not occur, your body sheds that lining — this is your period.

During a normal period, your body releases hormones called prostaglandins. These hormones can cause pain and inflammation and can increase the intensity of uterine contractions, which may worsen menstrual cramping. And women who have elevated levels of prostaglandins may experience even more severe menstrual pain.

Fibroids can make this pain more intense: First, fibroids put pressure on the uterine lining. Then, if you have fibroids within the uterine wall, or fibroids that protrude into the uterine cavity, more surface area is created, which means more thickened lining for your body to shed during your period — that is, a heavier flow.

“For women who bleed a lot, large clots can form,” says Bradley. “As all of this blood and clotting is trying to come through the narrow cervix and be expelled from the body, the uterus is contracting more, which can cause pain.”

In the days leading up to your period, you might feel more intense cramping as your uterus goes through its motions to force out the lining, and a stronger sensation of pressure when your period starts because of the heavier blood flow.

If the uterine fibroids are large, you also may feel a stronger sensation of pressure at the time of your period due to blood flow to the fibroids.

Treatment Options for Uterine Fibroid Pain

Aside from uterine fibroids, period pain can be caused by other health conditions like endometriosis or ovarian cysts. So if you’re dealing with period pain, it’s important to see your doctor or gynecologist to determine the underlying cause and recommend the proper course of treatment, says Bradley.

If you are diagnosed with uterine fibroids, a variety of treatment options can help you manage symptoms like heavy menstrual bleeding, pelvic pain, and pressure, and certain medications also treat the underlying uterine fibroids.

  • Pain relievers, including nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen or naproxen, can help alleviate period pain and decrease bleeding, but do not shrin the size of the fibroids themselves
  • Hormonal birth control, such as the pill, the ring, injections, and intrauterine devices (IUDs), help decrease bleeding and alleviate menstrual pain and cramping, but do not shrink the size of uterine fibroids
  • Oral medications, including hormonal or nonhormonal options, which treat heavy menstrual periods and in turn can help alleviate uncomfortable symptoms
  • Hormone injections, such as gonadotropin-releasing hormone (GnRH) agonists, can induce a temporary menopause-like state and help shrink the size of uterine fibroids while you’re taking the medication, which in turn can help improve your symptoms — but once you stop taking the drug, the fibroids usually grow back, and these medications cannot be taken long-term
  • Complementary therapies, ranging from using heating pads, to exercising regularly and altering your diet, to trying strategies like acupuncture and massage, may help you manage pain and other symptoms related to uterine fibroids

“If it’s getting to the point where your quality of life is bad — you’re staying home and missing work, activities, and hobbies — your physician needs to look at other therapies, such as surgical procedures,” says Bradley.

In the past, a hysterectomy, which removes the entire uterus, was the hallmark procedure for treating uterine fibroids. However, today there are a wide range of surgical options that are significantly less invasive and have a shorter recovery time.  These procedures, like radiofrequency ablation or embolization, aim to shrink or remove the uterine fibroids.

“The number one cause of hysterectomies in America are due to uterine fibroids with pain, heavy bleeding, or discomfort,” says Bradley. “But it’s 2020, and we have new options — you’re not relegated to a hysterectomy. There are many other procedures that are less aggressive or less invasive.”

Treatment is an individualized decision, and you need to see a physician who really looks at the whole patient, explains Bradley. The type of treatment you opt for should take into consideration your age, fertility plans, and the size and location of the uterine fibroids — and should be as minimally invasive as possible, she adds.

Women’s Healthcare of Princeton: Gynecologists

1.  You’re not alone if you have fibroids.

The National Institutes of Health estimates that 80% of all women will develop uterine fibroids at some point during their lives. Because many women don’t experience any symptoms, it’s possible the incidence of uterine fibroids is even higher. Fibroids are considered benign or noncancerous, but can make life painful.

2.  There’s only one kind of uterine fibroid.

You may hear them referred to as:

  • Leiomyomas
  • Myomas
  • Uterine myomas
  • Fibromas

These terms are all just different names for a uterine fibroid, which is a rubbery mass of tissue that arises out of the muscular portion of your uterus.

3.  Fibroids come in different shapes and sizes.

Fibroids may be tiny and described as “seedlings” or grow large enough to alter the shape and size of your uterus. Those that grow on the outer wall of your uterus, which is called the serosa, can develop on a narrow stem that supports the larger growth. We call these pedunculated fibroids.  

We also classify uterine fibroids according to their location in your uterus. Those that grow within the uterine wall are called intramural fibroids. Submucosal fibroids protrude into the uterine cavity, and subserosal fibroids project outward from the uterus.

4.  Your fibroids may or may not cause symptoms.

Some women have no symptoms with their fibroids and are surprised when they’re discovered during a routine gynecological exam. Depending on the location of the growth, we can sometimes feel a fibroid during a pelvic exam.

Many women, however, seek our care for relief of symptoms that they may not connect to fibroids. These symptoms can include:

  • Heavy bleeding during your menstrual period
  • Periods that last more than a week
  • Pain or pressure in the pelvic region
  • Frequent urination and difficulty emptying your bladder
  • Constipation
  • Back or leg pain

Fibroids can cause such heavy bleeding that you may be at risk for developing anemia. A large fibroid that pushes your uterus out of shape can also make it difficult to maintain a pregnancy. You may have trouble becoming pregnant when a fibroid blocks a fallopian tube or otherwise interferes with your reproductive cycle.

5.  We recommend diagnostic studies to confirm the diagnosis and further evaluate your fibroids.

We may recommend an ultrasound or other advanced imaging studies, including:

  • A hysterosalpingography, during which we use a dye to highlight the uterine cavity and fallopian tubes on X-ray images
  • Magnetic resonance imaging (MRI) which can show the size and location of fibroids and identify different types of tumors
  • Hysterosonography, also called a saline infusion sonogram, during which we expand the uterine cavity with a saline solution to makes it easier to obtain images of submucosal fibroids
  • Hysteroscopy, for which we insert a small telescope (hysteroscope) through your cervix and into your uterus so we can carefully examine the walls of your uterus

6.  Experts still don’t know what causes fibroids.

It’s not clear yet what causes fibroids, but we can point to a few factors that can increase your risk of developing these growths, which may include:

  • Family history of fibroids
  • Early menarche (onset of menstruation)
  • Obesity
  • A diet which includes a high amount of red meat and few green vegetables
  • Alcohol use

While they develop from the muscular tissue of your uterus, fibroids have a very different genetic profile than normal uterine muscle tissue, and they contain more estrogen and progesterone receptors. These two hormones stimulate your uterine lining to prepare for pregnancy during your menstrual cycle each month and seem to promote uterine fibroid growth.

7.  Fibroid growth patterns can vary greatly, or not.

Uterine fibroids can grow very slowly or enlarge quite rapidly. They may remain the same size for years. They can also shrink on their own, and those that are present during pregnancy often disappear afterward. Your risk of developing new fibroids typically decreases with menopause and tumors already present may shrink.

8.  A hysterectomy is not the only option for treating fibroids.

Fibroids were once the leading reason for performing hysterectomies. Advances in medical technology and treatment techniques allow us to choose less drastic measures for treating these benign growths these days.

We may recommend medications that manipulate your hormones enough to control excessive bleeding due to the fibroids. These medications can shrink your fibroids but won’t eliminate them. Birth control pills can also control bleeding but have little effect on the size of your fibroids.

If fibroids are interfering with your ability to become pregnant or maintain a pregnancy, we can consider surgical removal of the fibroids while leaving your uterus and other reproductive organs intact. This type of surgery can often be done laparoscopically, which requires just a few small incisions and offers a faster healing time than traditional, open surgery.

At Women’s Healthcare of Princeton, we care for all aspects of your health, including diagnosis and treatment of uterine fibroids. Call or click to set up an appointment.     

Fibroids – NHS

Fibroids are non-cancerous growths that develop in or around the womb (uterus).

The growths are made up of muscle and fibrous tissue, and vary in size. They’re sometimes known as uterine myomas or leiomyomas.

Many women are unaware they have fibroids because they do not have any symptoms.

Women who do have symptoms (around 1 in 3) may experience:

In rare cases, further complications caused by fibroids can affect pregnancy or cause infertility.

Seeing a GP

As fibroids do not often cause symptoms, they’re sometimes diagnosed by chance during a routine gynaecological examination, test or scan.

See a GP if you have persistent symptoms of fibroids so they can investigate possible causes.

If the GP thinks you may have fibroids, they’ll usually refer you for an ultrasound scan to confirm the diagnosis.

Read more about diagnosing fibroids.

Why fibroids develop

The exact cause of fibroids is unknown, but they have been linked to the hormone oestrogen.

Oestrogen is the female reproductive hormone produced by the ovaries (the female reproductive organs).

Fibroids usually develop during a woman’s reproductive years (from around the age of 16 to 50) when oestrogen levels are at their highest.

They tend to shrink when oestrogen levels are low, such as after the menopause when a woman’s monthly periods stop.

Who gets fibroids?

Fibroids are common, with around 1 in 3 women developing them at some point in their life. They most often occur in women aged 30 to 50.

Fibroids are thought to develop more frequently in women of African-Caribbean origin.

It’s also thought they occur more often in overweight or obese women because being overweight increases the level of oestrogen in the body.

Women who have had children have a lower risk of developing fibroids, and the risk decreases further the more children you have.

Types of fibroids

Fibroids can grow anywhere in the womb and vary in size considerably. Some can be the size of a pea, whereas others can be the size of a melon.

The main types of fibroids are:

  • intramural fibroids – the most common type of fibroid, which develop in the muscle wall of the womb
  • subserosal fibroids – fibroids that develop outside the wall of the womb into the pelvis and can become very large
  • submucosal fibroids – fibroids that develop in the muscle layer beneath the womb’s inner lining and grow into the cavity of the womb

In some cases, subserosal or submucosal fibroids are attached to the womb with a narrow stalk of tissue. These are known as pedunculated fibroids.

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Treating fibroids

Fibroids do not need to be treated if they are not causing symptoms. Over time, they’ll often shrink and disappear without treatment, particularly after the menopause.

If you do have symptoms caused by fibroids, medicine to help relieve the symptoms will usually be recommended first.

There are also medications available to help shrink fibroids. If these prove ineffective, surgery or other, less invasive procedures may be recommended.

Read more about treating fibroids.

Community content from HealthUnlocked

Page last reviewed: 17 September 2018
Next review due: 17 September 2021

Could I Be Bleeding Due to Fibroids?

While it may be scary, abnormal bleeding is a common gynecologic condition. However, if you are bleeding due to fibroids, the inconvenience may be overwhelming.

Vaginal bleeding is considered to be abnormal if it occurs: (i)

  • Between periods (including spotting)
  • After sex
  • During menstruation but is heavier than usual, lasts longer than usual, or lasts more than seven days
  • After menopause

There are many causes of abnormal vaginal bleeding, including: (i)

  • Uterine fibroids
  • Endometrial polyps
  • An infection of the uterus
  • Pregnancy
  • Miscarriage
  • Ectopic pregnancy
  • Cancers of the uterus including endometrial and cervical cancers

Your doctor may perform a physical exam, including a pelvic exam, and other tests to determine the cause of your abnormal bleeding. (i)

Fibroids can usually be detected during a pelvic examination, which allows your doctor to feel for any abnormalities in the shape and size of the uterus. If your uterus is enlarged or irregularly shaped and you have symptoms of uterine fibroids, your doctor may order an ultrasound and additional imaging tests to confirm the presence of fibroids.

What Causes Uterine Fibroids?

Fibroids are growths of muscle and fibrous tissue in or on the wall of the uterus. They often develop in women between the ages of 35 and 50. (ii) Researchers have several theories about uterine fibroid causes, but much is still unknown.

The types of uterine fibroids diagram

Fibroid growth is related to the following: (iii)

  • Estrogen
  • Progesterone
  • Growth hormones
  • Genetic changes
  • Misplaced cells in the body present before birth
  • The number of micronutrients — nutrients that the body needs only small amounts of — in your
  • Major stressors

It’s thought that fibroids are caused by the combination of many of these factors.

Related: 10 Possible Causes of Uterine Fibroids

What Are the Symptoms of Uterine Fibroids?

Most women with uterine fibroids have no symptoms. However, fibroids can cause a number of symptoms depending on their size, location within the uterus, and how close they are to other organs in the pelvic region.

Abnormal bleeding is the most common symptom of a uterine fibroid. If the tumor is located within the uterine cavity or near the uterine lining, it may cause excessive menstrual bleeding. The uterine fibroid may also cause bleeding between periods.

Uterine fibroid symptoms can include: (iv, v)

  • Heavy or prolonged menstrual periods
  • Abnormal bleeding between menstrual periods
  • Pelvic pain
  • Frequent urination
  • A firm mass, often located near the middle of the pelvis
  • A feeling of fullness in the pelvic area (lower abdomen)
  • Enlargement of the lower abdomen
  • Pain during sex
  • Lower back pain
  • Complications during pregnancy and labor, including a six-time greater risk of cesarean section
  • Reproductive problems, such as infertility (very rare)

What Are Some Complications Caused by Uterine Fibroids?

Sometimes uterine fibroids may cause more serious problems. Uterine fibroids can make menstrual bleeding heavy and full of clots. (ii) Heavy menstrual bleeding and fibroids that cause bleeding between periods can make a woman anemic. If you’re feeling fatigued, visit your doctor to have a blood test to measure your level of red blood cells.

Other complications may include:

  • Infertility
  • Blockage of the urinary tract or bowels
  • Deteriorating fibroids, which can cause severe, localized pain
  • Development of cancerous fibroids, which is rare and less than one in 1,000 (ii)

Treatment for Fibroids

The question of how aggressively to treat your fibroids depends on your symptoms and how they are interfering with your quality of life. For example, bleeding, unless it is causing anemia, is not harmful and is rarely an indication of a serious underlying problem.

You could do nothing — often called “watchful waiting” — and just have your gynecologist continue to monitor your health. If you’re not that far from menopause, you may choose to wait and see if the bleeding stops once you no longer get your period. The fibroids may shrink once the estrogen level in your body decreases.

If you have bleeding due to fibroids, treatment will depend on many factors, including your age, the severity of the bleeding, and whether you want to have children. One treatment option, uterine fibroid embolization (UFE), is a minimally invasive and safe alternative to hysterectomy. This nonsurgical procedure effectively shrinks uterine fibroid tumors and offers relief from the unpleasant symptoms that come with them while sparing your uterus. It can be performed in an outpatient setting where you can go home the same day of your procedure for a quicker recovery, as compared to traditional surgery.

When considering the various uterine fibroid treatments, talk with your doctor to weigh the risks and benefits of each procedure.

Download our free information sheet, Understanding Uterine Fibroid Embolization, for more information or call 844-UFE-CARE (833-2273) to schedule an appointment with a vascular specialist.


Sources:
(i) Radiological Society of North America. (2016, March 17). Abnormal Vaginal Bleeding – Evaluation and Treatment. Retrieved July 23, 2018, from https://www.radiologyinfo.org/en/info.cfm?pg=vaginalbleeding
(ii) Richardson, M., MD. (2011, May). Ask the doctor: Heavy bleeding, fibroids, and polyps – Harvard Health. Retrieved June 17, 2018, from https://www.health.harvard.edu/newsletter_article/heavy-bleeding-fibroids-and-polyps
(iii) What causes uterine fibroids? (2016, December 1). Retrieved June 12, 2018, from https://www.nichd.nih.gov/health/topics/uterine/conditioninfo/causes
(iv) Office on Women’s Health. (2018, March 16). _Uterine fibroids. Retrieved June 18, 2018, from https://www.womenshealth.gov/a-z-topics/uterine-fibroids
(v) UCLA Health. (n.d.). _Fibroids. Retrieved June 18, 2018, from http://obgyn.ucla.edu/fibroids

How can fibroids affect your periods?

An introduction to periods and fibroids

Fibroids are benign growths that form from the smooth muscle of the womb. Fibroids are fairly common and often do not give rise to symptoms. There are different types of fibroids, so-called depending on their size and location, and the symptoms they give rise to can vary as a result of this.

Fibroids are more likely to develop in women in their 20s and 30s and tend to disappear as a woman reaches the menopause. This makes sense as the main cause of fibroids is thought to be the result of excess oestrogen and levels of this hormone begin to decrease as a woman’s periods stop.

On this page I discuss some of the causes and symptoms of fibroids, how they can have an effect on your menstrual cycle and how home, herbal and conventional treatments can help to keep them under control.

Causes of fibroids

Fibroids form as the result of an overgrowth of smooth muscle cells in the uterus which form into a mass. A number of factors are thought to contribute to the formation of fibroids:

  • Female hormones – Fibroids are thought to form in most cases as a result of excess oestrogen. The tissue making up these fibrous masses is sensitive to the sex hormones, especially oestrogen, and in the presence of hormone imbalance they can easily proliferate.  Both excess oestrogen and the presence of the fibroids themselves are thought to contribute to heavier, more painful periods
  • Genetics – Although hormones are thought to be the main cause of fibroids, genetics are thought to be somewhat involved too. Women of Afro-Caribbean origin are thought to have an increased risk
  • Environmental factors – Diet and lifestyle factors could be making you more susceptible to fibroids although again, are unlikely to be the primary cause. Many modern-day chemicals (often found in non-organic food and polluted environments) can mimic hormones, and depending on how toxic a lifestyle you lead, this could have an influence
  • Body weight – Again, although your body weight isn’t a direct cause of fibroids, being overweight may increase your risk of developing them. Adipose tissue, or fat cells around your body, act like little reservoirs for hormones and the accumulation of oestrogen can be problematic.

Symptoms of fibroids

The severity of the symptoms of fibroids is variable and the only sure way of diagnosing them is by having an ultrasound scan. Some common symptoms of fibroids are described below. If you think you have fibroids, please pay a visit to your doctor.

  • Heavy periods – Heavy periods are perhaps the most common symptom of uterine fibroids. Fibroids can actually increase the surface area of the womb, meaning there is more lining to be shed which can give rise to a heavier flow. However, as fibroids are often a result of excess oestrogen, and oestrogen is involved in thickening the lining of your womb prior to your period, excess oestrogen is likely to result in a thicker lining to be shed in the first place. Very heavy periods can result in anaemia which can affect your energy levels
  • Painful periods – Fibroids can give rise to pain and discomfort in the abdomen depending on their size and location. Also, painful periods often go hand in hand with heavy periods. Having formed a thicker lining of the womb, this requires more effort to shed! Contractions of the womb are often more forceful and more prostaglandins are released in many cases which can cause further pain and inflammation
  • Other symptoms of hormone imbalance – You may also find you suffer from other symptoms which are a result of the hormone imbalance causing the fibroids in the first place. Some typical symptoms of oestrogen dominance include; heavy, painful periods, sensitive breasts, bloating and water retention and suffering from mood swings which can leave you feeling angry and irritable.

Home remedies for fibroids

There are some simple steps you can take at home that can help to minimise the effects of fibroids:

  • Eat well – Eating well can help to minimise the growth of fibroids. A good diet puts less pressure on your liver. Your liver is responsible for more than just processing the food you eat – it is also in charge of recycling excess hormones, such as oestrogen. If you put your liver under pressure as a result of a poor diet, it is less likely to keep up to speed with breaking down hormones. Excess oestrogen can support the growth of fibroids
  • Manage your weight – Being overweight or obese can also affect the balance of hormones around your body. Excess adipose tissue can result in an accumulation of oestrogen in the body which could be encouraging the growth of uterine fibroids.

How can natural remedies help?

There are some natural remedies available that could help:

  • Agnus castus – Agnus castus works by gently supporting progesterone, the opposing hormone to oestrogen and can help to restore hormonal balance. This herbal remedy can be useful to help treat some of the symptoms of PMS such as painful periods. Please note, if you are taking hormonal contraceptives such as the pill, hormone- balancing herbal remedies may not be suitable for you
  • Milk thistle – Add milk thistle to your regime in order to support the functions of the liver.

When should I see my doctor?

Depending on the type and severity of the fibroids, it might be necessary to pay a visit to your doctor.

Your doctor can examine you and discuss any appropriate treatments. Hormonal contraceptives are often a solution, (for example progesterone-based options such as the pill or the implant) as these can help to sort the imbalance between oestrogen and progesterone.

Anti-inflammatory medication or pain killers may also be offered if you are in pain or discomfort as a result of the fibroids, although you should carefully consider any possible side effects.

In extreme cases, medication may be prescribed to stop or reduce heavy bleeding, such as Tranexamic acid, or surgery might be an option in some cases in order to remove existing fibroids.

Uterine Fibroids | ACOG

Anemia: Abnormally low levels of red blood cells in the bloodstream. Most cases are caused by iron deficiency (lack of iron).

Hysterectomy: Surgery to remove the uterus.

Hysterosalpingography: A special X-ray procedure in which a small amount of fluid is placed in the uterus and fallopian tubes to find abnormal changes or see if the tubes are blocked.

Hysteroscopy: A procedure in which a lighted telescope is inserted into the uterus through the cervix to view the inside of the uterus or perform surgery.

Intrauterine Device (IUD): A small device that is inserted and left inside the uterus to prevent pregnancy.

Laparoscopy: A surgical procedure in which a thin, lighted telescope called a laparoscope is inserted through a small incision (cut) in the abdomen. The laparoscope is used to view the pelvic organs. Other instruments can be used with it to perform surgery.

Menstruation: The monthly shedding of blood and tissue from the uterus that happens when a woman is not pregnant.

Menopause: The time when a woman’s menstrual periods stop permanently. Menopause is confirmed after 1 year of no periods.

Pelvic Exam: A physical examination of a woman’s pelvic organs.

Progestin: A synthetic form of progesterone that is similar to the hormone made naturally by the body.

Resectoscope: A slender telescope with an electrical wire loop or roller-ball tip used to remove or destroy tissue.

Sonohysterography: A procedure in which sterile fluid is injected into the uterus through the cervix while ultrasound images are taken of the inside of the uterus.

Ultrasonography: A test in which sound waves are used to examine inner parts of the body. During pregnancy, ultrasonography can be used to check the fetus.

Uterus: A muscular organ in the female pelvis. During pregnancy this organ holds and nourishes the fetus.

Uterine Fibroids & Abnormal Bleeding | Von Voigtlander Women’s Hospital

Abnormal bleeding is a common gynecologic condition. Vaginal bleeding is considered to be abnormal if it occurs between a woman’s menstrual cycles, in situations where flow is significantly heavier than normal for a particular individual, or when it occurs after menopause. Abnormal vaginal bleeding has many possible causes. By itself, it does not necessarily indicate a serious condition. In some cases, it can be associated with uterine fibroids, endometrial polyps, polycystic ovary syndrome (PCOS), intrauterine device (IUD) or birth control usage.

Uterine Fibroids

Uterine fibroids are noncancerous growths of the uterus. Fibroids can grow on the inside of the uterus, within the muscle wall of the uterus, or on the outer surface of the uterus. Many women who have uterine fibroids do not have symptoms. When symptoms are present, they can include:

  • Abnormal vaginal bleeding, such as heavier, longer periods or bleeding between periods
  • Pelvic pain, including pain during sex
  • Low back pain that does not go away
  • Urinary problems

Sometimes uterine fibroids may cause more serious problems, such as infertility, blockage of the urinary tract or bowels, or anemia.

Resources

Treatment Options for Abnormal Bleeding & Fibroids

Treatment for abnormal bleeding will depend on many factors, including the cause, your age, the severity of the bleeding, and whether you want to have children. Common medical treatment options may include use of birth control pills, hormone injections, or a hormone-releasing IUD (intra-uterine device). Some women with abnormal vaginal bleeding may need to have surgery to control bleeding or to remove growths (such as polyps or fibroids) that are causing the bleeding. Common surgical treatment options include endometrial ablation, endometrial polyp removal, myomectomy, or hysterectomy.

VIDEO: Treatment options for abnormal uterine bleeding and fibroids

Learn more about our surgical treatment options.

Laser correction of fibrinoid syndrome in the postoperative period after cataract extraction | Novoderezhkin V.V.

Laser correction of fibrionoid syndrome in postoperative period after the cataract extraction

Novoderezhkin V.V.
Our cumulated experience of dealing with early postoperative complications and prolonged observations let us get positive result in patients, in which complications manifested in later period. Laser operations started to be carried out more frequently if slowly proceeded inflammation is detected.It allowed to make sure that the reason for such complication is fibrin. And it is often not detected by routine methods. But the test with concussion with YAG – laser let to specify the diagnosis. The following fibrin fragmentation and active anti-inflammatory and fibrinolytic treatment allow to reach the stable clinical effect.

In the postoperative period after cataract extraction, pronounced fibrinous exudation is often observed. It is known that fibrin in the eye cavity stimulates the migration of pigment epithelial cells and causes their transformation into fibroblast-like cells.It is also believed that the fibrin clot is a matrix for the proliferation of pigment epithelial cells and glial cells. This can lead to the formation of epiretinal, transvitreal and cyclical contractile membranes with subsequent detachment of the retina, ciliary body and the development of subatrophy.
Depending on the characteristics of the pathological process, 3 nosological subgroups of patients with fibrinoid syndrome after cataract extraction can be distinguished – patients with pronounced precipitates, fibrin, blood clots, pigment in the lumen of the pupil and on the IOL; patients with pupillary block; patients with developing synechiae.
Fibrin can have various anatomical forms: in the form of a cloud, a canopy, or a sail and filaments. Cloud-like fibrin in the pupil area can be mushroom-shaped, in the area of ​​the incision in the form of a sphere or an elongated “sausage”. The canopy usually extends from the pupillary margin or iris to the incision. The filaments can be in any position, but there is a tendency of tension from the pupil or iris to the incision or junction of the edge of the pupil. A combination of these forms may occur. In the process of accumulation and resorption, there is a transition from one form to another.With the accumulation of fibrin, there is an approach to the cloudy, with involution – to the filmy or filamentous. Fibrin can be absorbed completely (favorable course) or “dry out” with the formation of a film or strand, which has a tremendous traction effect. The color varies from complete transparency to shades of gray and brown, varying in saturation (with pigment dusting on the surface).
By severity, fibrin can be divided into three groups. I – it is not possible to detect fibrin, its presence can be determined only with the help of a YAG laser or suspected by clinical manifestations.II – fibrin is difficult to visualize or is determined only with gonioscopy. III – when fibrin is detected when viewed with a slit lamp without difficulty.
Working with recent cases of fibrinoid syndrome provides good clinical results. Appointment of adequate conservative therapy promotes resorption of the film. In those cases when a large amount of fibrin is observed or there is already a tendency to the organization of a conglomerate, the use of a YAG laser for fragmentation allows avoiding the formation of adhesions and restoring functional usefulness.The inflammation subsides faster, vision is restored, anatomical defects are eliminated.
But often the inflammation is mild. In this case, the postoperative period is outwardly smooth. The patient is discharged from the hospital with a sufficiently high vision, moderate signs of inflammation, which, according to the doctor, should be adequately treated on an outpatient basis. In patients after cataract extraction, the eyes look satisfactory. There is a small injection of the conjunctiva, the cornea is almost calm, the moisture of the anterior chamber is transparent, the iris is moderately edematous, the pupil is rounded.
At the control examination after 1–2 months, a completely different picture is observed in some patients. This is most clearly manifested in the eyes with cataract extraction. The pupil is pulled up and deformed, the iris is soldered to the incision area, secondary cataract is formed, vision is reduced, IOP may be increased. Similar phenomena are regularly observed in the late postoperative period after 6-12 months or more. With a careful collection of anamnesis, it is revealed that the change in the eye was preceded by: hypothermia, exacerbation of a chronic disease (arthritis, sinusitis, etc.)transferred viral infections.
Our extensive experience in dealing with early postoperative complications and long-term observations made it possible to obtain a positive result in patients who developed complications in a later period. Laser interventions have begun to be carried out more widely in cases of suspicion of the presence of a sluggish inflammatory process. This made it possible to make sure that fibrin is the cause of such complications. Moreover, most often it is not visualized by conventional methods.But the test with the YAG-laser concussion made it possible to clarify the diagnosis. Further fragmentation of fibrin and active anti-inflammatory and fibrinolytic therapy make it possible to obtain a stable clinical effect.
Fibrin treatment has several directions – conservative, laser and surgical, the second and third are necessarily supported by the first. Laser treatment is reduced to discision of fibrous masses or their fragmentation. Sometimes coagulation with argon or other emitter is used, especially if fibrin has blood inclusions or is covered with blood clots.
Technique of the operation of discision of fibrinous masses. Under epibulbar anesthesia, an Abraham lens with a contact medium is placed on the eye. Discision is performed using a YAG laser. The pilot beam is aimed at or in front of the fibrin surface. The energy is selected specifically for each case (from minimal to sufficient). During the operation, the energy usually rises, because the transparency of the media falls due to fragments floating in the moisture of the anterior chamber. This technique is applicable when fibrin is localized in the pupil region or on the iris.
The easiest way is to work without the use of optical instruments. Laser exposure is carried out directly through the cornea. This technique has another advantage: it is not always necessary to carry out epibulbar anesthesia (which is quite important with the growing allergization of the population). In addition, epibulbar anesthesia often causes epitheliopathy and desiccation, which interfere with normal functioning. But the technique does not allow working in the corner of the anterior chamber.
We use laser correction of complications after intraocular lens implantation at:
n secondary membranous cataract;
n deposition of pigment precipitates on the surface of the IOL;
n the formation of an exudative capsule on the surface of the IOL;
n ectopia of the IOL.
Secondary cataract develops after cataract extraction from the subcapsular epithelium, the remaining lens masses, pigment cells that migrated in the capsule during resorption of the masses. Secondary (membranous) cataracts lead to decreased vision, and sometimes nullify the results after extraction.
When examining the eye with lateral illumination, secondary cataract looks like a heterogeneous grayish-white, sometimes pigmented film. With transmitted light, it is possible to see a dull fundus reflex.With biomicroscopy, the anterior and posterior capsules with shapeless lens masses enclosed between the capsule leaves are clearly visible.
No matter how the anterior lens capsule is excised during extracapsular cataract extraction, the equatorial germinal zone of the subcapsular epithelium remains in the eye. Possessing a sufficiently high regenerative capacity, the subcapsular epithelium produces lens fibers. They rarely reach maturity, undergo hydrotic degeneration, turning into ball cells that fill the intercapsular space, first along the periphery, and then in the center.The reborn cells become large. When biomicroscopic examination, they are clearly visible and resemble frog eggs. Despite the apparent transparency, ball cells reduce vision due to incorrect refraction of the rays.
Secondary cataracts require surgical treatment. Modern instrumentation and an operating microscope make it possible to clean the posterior capsule of the lens to its complete transparency through a two-millimeter translimbal incision. With fibrous degeneration of the posterior capsule, its dissection is required – capsulotomy.Lasers have been used with great success to dissect the capsule.
Laser phacodestruction is performed using a Q-switched YAG laser in the presence of lenticular masses after extracapsular cataract extraction. Lumps up to 1 mm in diameter are crushed, for which the laser beam is focused on the surface of lens particles, gradually breaking them into smaller dust-like fragments. After that, their complete resorption is observed in more than 90% of patients. The pulse energy is selected individually within the range of 1–4 mJ.Laser intervention is performed under the guise of intensive anti-inflammatory therapy.
Posterior capsulotomy in eyes with pseudophakia has a fundamental difference in the case of contact of the posterior capsule with the posterior surface of the optical part of the lens. In these cases, the posterior capsulotomy must be performed through the Abraham lens in the region of the optic periphery. Focusing the YAG laser on the border of the IOL and the posterior capsule, they achieve the formation of a gas bubble in this zone, which, as it increases, peels the capsule from the IOL.Then the focus of the laser is shifted to the posterior capsule and dissected. After that, peeling off the capsule with defocused radiation using hydrodynamic action, it is gradually destroyed. Damage to the lens optics occurs only at its periphery and does not affect the optical results of the operation. The pulse energy is 2–4 mJ.
To eliminate pigment overlays and precipitates from the optical surface of the IOL, the safest technology is to remove them using defocused YAG laser radiation.For this, the laser beam is focused to a point located at a distance of 0.5–0.7 mm from the lens surface at a convergence angle of at least 12 °. When 1.0–2.0 mJ energy is used, the overlays are washed off the lens surface due to the action of the shock wave.
In severe postoperative iridocyclitis, the IOL may be embedded in an exudative capsule. In this case, a phased anterior and posterior capsulotomy technique is used. First, within 1–3 sessions, an anterior capsulotomy is performed along the pupil circumference, gradually exposing the optical part of the lens.Then, against the background of anti-inflammatory therapy, after 1-14 days, a posterior capsulotomy is performed in 1-2 sessions.
In case of IOL ectopia caused by anterior synechiae or vitreous cords, we perform anterior synechiotomy or anterior vitreolysis under the guise of anti-inflammatory therapy.
Thus, laser correction of fibrinoid syndrome and associated complications arising in the postoperative period improves the visual results of the operation.

.

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90,000 Rheumatic diseases

This group includes 8 diseases.

1 \ Rheumatism

2 \ Rheumatoid arthritis

3 \ Systemic lupus erythematosus

4 \ Systemic scleroderma

5 \ Periarteritis nodosa

6 \ Dermatomyositis

7 \ Rheumatoid spondylitis \ ankylosing spondylitis \

8 \ Dry Sjogren’s syndrome.

They are united by 3 groups of common factors:

1 \ The clinic is characterized by a chronic recurrent course.

2 \ Pathomorphology- 1 \ localization – systemic damage to connective tissue

2 \ nature of the process – immune inflammation

3 \ staging – all diseases in their development go through 4 stages:

(mucoid swelling, fibrinoid swelling, granulomatosis, sclerosis).

3 \ Features of etiopathogenesis. Lack of a clear etiological beginning. Immune factors \ immune complexes, antigens, antibodies, T lymphocytes \ act as a damaging agent. All of them reflect a violation of humoral and cellular immunity.

But there are also differences between each disease. They are manifested in the nature of the etiology and localization of the process, according to the primary etiological principle, which plays the role of a trigger. All rheumatic diseases are divided into 2 groups.The former are characterized by streptococcal infection \ rheumatism, systemic scleroderma, periarteritis nodosa \. For the second group, the triggering factor is viruses \ rheumatoid arthritis, systemic lupus erythematosus, dermatomyositis, dry Sjogren’s syndrome, rheumatoid spondyloarthritis \ ankylosing spondylitis \.

Features of the localization of the pathological process. Despite the fact that all rheumatic diseases are systemic diseases of the connective tissue, each of them is characterized by a special localization, where damage manifests itself with special force.

Rheumatism – mainly affects the heart.

Rheumatoid arthritis – joints.

Systemic lupus erythematosus – kidney and skin.

Systemic scleroderma – skin.

Periarteritis nodosa – arteries.

Dermatomyositis – skeletal muscles.

Ankylosing spondylitis – joints of the spine.

Dry Sjogren’s syndrome – exocrine glands.

Clinical and pathomorphological characteristics of rheumatic diseases.

1 \ Rheumatism

It was isolated as an independent systemic pathology of connective tissue in 1836-1853 thanks to the works of Sokolsky and Buyo. Subsequently, Ashof \ 1904 \, Talalaev-1929, Skvortsov and other researchers made a great contribution to the study of the clinical and pathomorphology of the disease.

The clinical and morphological core of the disease is a rheumatic attack, which in the classical version lasts 6 months and fits into 4 stages.

3 \ Stage of granulomatosis – from 1.5 to 3 months.

4 \ Sclerosis stage – from 3 to 6 months.

1 \ Stage of mucoid swelling (first 0.5 months)

It is characterized by an alterative-exudative reaction at the site of deposition of immune complexes in various parts of the connective tissue of the heart, joints and other organs.

Pathogenesis of the process: immune complexes – activation of proteolytic enzymes – shift of pH to the acidic side – accumulation of acidic mucopolysaccharides – increase in vascular permeability – hydration and disorganization of the interstitial substance and collagen fibers.In the focus of pathology, acidic mucopolysaccharides, proteins, cells (lymphocytes, plasma cells, macrophages, histiocytes) accumulate.

Mucoid swelling is a superficial and reversible disorganization of connective tissue. After the termination of the action of the damaging factor, a complete recovery occurs.

2 \ Stage of fibrinoid swelling (period from 0.5 to 1.5 months)

It is characterized by deep and irreversible disorganization of the connective tissue.

Pathomorphology: complete destruction of the interstitial substance and collagen fibers

– picrinophilia

– accumulation of neutral polysaccharides

– Argentophilia

– increase in vascular permeability

– vasculitis

– impregnation with immunoglobulins and fibrin.

The focus of pathology turns into a structureless mass of detritus with the appearance of fibrinoid masses.Pathology is based on three processes 1 \\ plasmorrhage with the release of fibrinogen

2 \ breakdown of collagen and reticular fibers 3 \ denaturation of stromal protein. As a result, fibrinoid necrosis develops, the zone of which is replaced by coarse scar tissue.

3 \ Stage of granulomatosis . It is characterized by the development of productive inflammation in the area of ​​fibrinoid necrosis in the form of granulomas. The structure of the granuloma. The center is necrotic masses. Peripherals – cells: large basophilic cells of the macrophage series, lymphocytes, plasma cells, fibroblasts.

Types of granulomas – 1 \ blooming, 2 \ fading, 3 \ scarring. They reflect the stages in the development of the inflammatory response. Blooming granuloma is an early stage when the processes of cleansing the zone of fibrinoid necrosis are just beginning. A fading granuloma reflects the completion of the cleansing of the pathological focus from necrotic masses. A scarring granuloma indicates the beginning of recovery.

Localization of granulomas –1 \ myocardium, 2 \ heart valves, 3 \ extravalvular endocardium, 4 \ epicardium, 5 \ vessels, 6 \ tonsils, 7 \ joints, 8 \ skeletal muscles, 9 \ and especially often the left atrial appendage.

4 \ Sclerosis stage .

This is the next stage of healing. It begins after the inflammation has performed its cleansing function. In the stage of sclerosis, the dominant role is played by the fibroblast, which produces tropocollagen. As a result, scar tissue forms at the site of the pathological focus. Scar tissue is a weak point in the body, since destructive processes often begin in it with relapses of the disease.

In addition to the granulomatous inflammation characteristic of rheumatism, this disease can cause uncharacteristic reactions in the form:

– exudative-infiltrative inflammation

– vasculitis

– mast cell accumulations with the production of heparin, which promotes healing.

The immunomorphological nature of inflammation in rheumatism reflects the accumulation of immune complexes, antibodies, plasma cells, B lymphocytes in the tonsils, lymph nodes, spleen, and bone marrow.

Organ damage in rheumatism.

Tonsils . Streptococcal infection of the tonsils with the development of chronic tonsillitis is the first impetus in the initiation of rheumatism. Streptococci in the tonsils cause sensitization of the body and the appearance of immune complexes, which include streptococcal antigen.Streptococcal antigen in its properties is close to the antigens of the heart, therefore, immune complexes in rheumatism selectively affect the heart.

Heart . There is a famous catch phrase – rheumatism bites the heart. It reflects the features of heart damage in rheumatism. These are: the severity of the process and its prevalence. In rheumatism, all the membranes of the heart are affected. Pancarditis develops. Moreover, at the time of a rheumatic attack, exudative-alterative processes prevail in the heart, and in the interictal period – granulomas and sclerosis.

Endocarditis . Valvular and nonvalvular endocardium is also affected. There are 4 types of rheumatic valvular endocarditis 1 \ valvulitis, 2 \ fibroplastic endocarditis, 3 \ acute warty endocarditis, 4 \ recurrent warty endocarditis.

1 \ Valvulitis. In this endocarditis, the process is localized in the depth of the valve. The endothelium is intact. This endocarditis occurs with the first rheumatic attack.

2 \ Fibroplastic endocarditis. This endocarditis develops with repeated rheumatic attacks and is characterized by valve thickening due to fibrosis.

3 \ Acute warty endocarditis develops during the first rheumatic attack. The process affects not only the thickness of the valve, but also causes erosion of the atrial surface of the valve. In the foci of erosion, blood clots settle, which look like small warts.

4 \ Recurrent warty endocarditis. This endocarditis develops with repeated rheumatic attacks, when warty thrombi form on the valves disfigured by fibrosis in the foci of erosion. With repeated rheumatic attacks, the valves of the heart, due to cicatricial processes, shrink and grow together.Valvular defects develop. In rheumatism, the leaflets of the mitral valve are always affected. There may be combined lesions of the mitral and aortic valves. Less commonly, the tricuspid valve and pulmonary artery valves are involved.

Types of valve defects on the example of mitral valve lesion:

1 \\ insufficiency of the mitral valve – the leaflets of the mitral valve do not completely cover the mitral opening during systole

2 \ stenosis of the left atrioventricular opening

3 \ combination of mitral valve insufficiency and mitral stenosis.

Myocarditis . More often there is granulomatous myocarditis, less often nonspecific diffuse myocarditis. The latter can lead to heart failure and is commonly found in children. As a result of myocarditis, myocardial dystrophy develops.

Pericarditis . Has the character of productive inflammation, which ends with an adhesive process and obliteration of the pericardial cavity. When lime is deposited into the fibrous tissue, a calcareous shell appears, which complicates the activity of the heart.This phenomenon is called the armored heart.

Vessels.

1 \ Coronary arteries – inflammation, stenosis, ischemia, heart attack.

2 \ Myocardial vessels – capillaritis, impaired trophism, myocardial dystrophy and diffuse cardiosclerosis.

3 \ Aorta – aortitis, erosion of the aortic wall with possible rupture.

4 \ Arteries of the brain, kidneys and other organs: arteritis, stenosis, ischemia, heart attacks.

Kidney . A cardiorenal form of rheumatism is described, in which arteriolosclerosis, focal glomerulonephritis, vasculitis, arteriosclerosis, blood shunting through the medulla, dystrophy and necrosis of the epithelium of the tubules of the cortical layer are noted in the kidneys.

Liver . There are interstitial hepatitis, vasculitis, sclerosis.

Lungs. Interstitial productive inflammation \ rheumatic pneumonia \, vasculitis, pneumosclerosis.

Joints. Rheumatism affects various joints: ankle, knee, wrist, shoulder. Pathomorphology is typical. There is an effusion into the joint cavity, edema of the periarticular tissues, granulomatosis and sclerosis. In the acute period, there is a sharp soreness of the affected joints.But in the end, with the attenuation of the process, a complete recovery occurs without the development of joint deformation. Rheumatism licks the joints.

Skeletal musculature . Dystrophy. Serous-infiltrative inflammation. Granulomas.

Nervous system . Micro-granulomatous encephalitis. Meningitis. Vasculitis.

Endocrine system . Productive inflammation, sclerosis, atrophy in various endocrine organs \ ovary, adrenal gland, thyroid gland \.

Leather . 1 \ Rheumatic nodules, 2 \ Erythema multiforme, 3 \ Rheumatic purpura. Vasculitis. Capillarites. Cellular infiltration of the stroma and fibrosis.

Clinical and morphological forms of rheumatism .

1 \ Cardiovascular: the heart is affected.

2 \ Polyarthritic: the heart and joints are affected.

3 \ Nodose: heart and skin are affected.

4 \ Cerebral: the heart and brain are affected.

RHEUMATOID ARTHRITIS.

Rheumatoid arthritis is a systemic autoimmune chronic recurrent disease of the connective tissue. In this disease, connective tissue is primarily affected, secondarily joints and other organs.

Etiopathogenesis. Stages:

1 \ Infection with X antigen \ presumably Ebstein-Barr virus \.

2 \ Transformation of common immunoglobulins under the influence of a virus into a rheumatoid factor \ autoantigen \.

3 \ Dissociation of the lymphocyte-macrophage system and the formation of toxic immune complexes, which include rheumatoid factor.

4 \ Damage to the fibro-cartilaginous tissues of the joint with the development of immune inflammation, lymphaticization of the synovium and the production of large quantities of autoantigens and autoantibodies.

5 \ General sensitization with subsequent damage to the connective tissue of the whole organism.

Pathomorphology. Stages

1 \ Mucoid swelling,

2 \ fibrinoid swelling,

3 \ cellular response \ productive immune inflammation \

4 \ sclerosis.

Localization – joints and internal organs.

Joints .

Dynamics: the knee joint is initially affected, then the small joints. Less commonly, the disease begins with inflammation of the hip, shoulder, ankle joints.

Stages of polyarthritis.

1 \ Acute polyarthritis . Damage to the tissues of the joints by immune factors causes mucoid, fibrinoid swelling and the development of alterative-essudative inflammation. It is expressed in plethora, infiltration with lymphocytes, plasma cells, macrophages and the accumulation of synovial fluid in the joints. Vasculitis and thickening of the villi of the synovial membranes are noted.

2 \ Subacute polyarthritis . At this stage, the formation of granulation tissue, narrowing of the joint cavity, ankylosis and fibrosis occurs.Fibrous particles appear, which have received a figurative name – rice bodies. Histological examination reveals total fibrosis with foci of necrosis, accumulation of plasma cells and histiocytes. This picture is defined by a special term – pannus. Pannus has aggressive properties in relation to the fibrous, cartilaginous, bone tissues of the joint. In essence, pannus is an abnormal granulation tissue.

3 \ Chronic polyarthritis . At this stage, fibrosis, osteoporosis, hyalinosis, petrification, bone growths, joint deformity and dysfunction are noted.Particularly significant changes are noted in the small joints of the arms and legs. Fibrous nodes, necrosis, inflammatory infiltration, sclerosis, and hyalinosis are noted in the periarticular tissues.

Internal organs.

Heart and blood vessels – focal endocarditis. Vasculitis. Dystrophy of cardiomyocytes. Myocardiosclerosis. Koranariitis with possible ischemic damage to the myocardium.

Lungs . Vasculitis. Interstitial pneumonia. Pneumosclerosis. Bronchitis.Bronchiectasis.

Gastrointestinal tract – mucosal atrophy due to vasculitis and productive inflammation.

Liver . Dystrophy. Interstitial hepatitis. Fibrosis. Amyloidosis.

Kidney . Acute and chronic glomerulonephritis. Amyloidosis.

The nervous and endocrine systems are also affected.

In view of the above, 4 visceral forms of the disease are distinguished:

1 \ articular-cardiac

2 \ articular-renal

3 \ articular-nervous

4 \ articular-pulmonary.

Pathomorphosis is manifested in the following:

– maximum lethality: 30 – 50 years

– more often articular-visceral forms

– causes of death: renal failure, pulmonary heart failure, hepatic failure, alimentary exhaustion on the background of sclerosis and amyloidosis

– increased frequency of amyloidosis.

SYSTEM RED Lupus.

Typical rheumatic disease of viral etiology.

Classification. 2 types:

1 \ Chronic discoid lupus erythematosus without visceral manifestations – 1 \ localized 2 \ common.

2 \ Systemic lupus erythematosus with damage to the visceral organs.

Options 1 \ acute 2 \ subacute 3 \ chronic.

The onset of the disease is similar to an acute infectious disease with fever, rash, swollen lymph nodes, pericarditis, pleurisy, jaundice, splenomegaly.

Pathomorphology.4 features are characteristic:

1 \ skin lesion

2 \ Libman-Sachs endocarditis

3 \ lupus nephritis

4 \ bulbous hyalinosis of the spleen.

Leather . It is often affected, but not always. Localization – face, limbs, trunk.

Dynamics – dark red spots – bubbles – ulceration – scales and crusts – depigmentation – atrophy.Microscopic picture: keratinization, death of the growth layer, ulcers, karyorrhexis with the appearance of hematoxylin bodies, productive and destructive vasculitis, phlegmonous inflammation, destruction of collagen fibers, atrophy, fibrosis.

Muscles – inflammation, degeneration, sclerosis, atrophy.

Joints – polyarthritis, but without serious consequences.

Lungs . Always affected . Some authors even single out the pulmonary form of the disease.Typical: hyperergic vasculitis, fibrinoid necrosis, interstitial pneumonia, chronic bronchitis, metaplasia, in acute form, phlegmonous inflammation.

Heart. Obliterating pericarditis. Abacterial endocarditis of the mitral valve. Diffuse myocarditis with an outcome in cardiosclerosis.

Vessels . Typically – productive inflammation of the splenic artery with the development of splenic infarction. But other arteries can also be affected.

Esophagus often acute or chronic esophagitis with ulceration.Less commonly, gastritis, enteritis, colitis.

Liver – interstitial hepatitis, dystrophy and necrosis of hepatocytes, cirrhosis.

Pancreas Interstitial productive inflammation, sclerosis, islet atrophy.

Kidneys – very often affected. Lupus glomerulonephritis develops.

Dynamics 1 \ infiltration around the glomeruli, 2 \ penetration of the infiltrate deep into the glomeruli, 3 \ circular sclerosis and hyalinosis. Uremia.

Pathomorphosis.It appears as follows:

– mortality more often up to 35 years

– increased frequency of acute and chronic course

– damage to organs: 1 \ kidney – 90% 2 \ lungs – 63%

3 \ heart – 56% 4 \ polyserositis – 44%

– causes of death: 1 \ renal failure

2 \ cardiovascular insufficiency

– decrease in the frequency of characteristic productive inflammation,

increased fibroplastic reaction

SYSTEMIC SCLERODERMIA .

It is characterized by lesions of the skin and internal organs.

Etiopathogenesis is explained from the standpoint of the autoimmune theory.

The primary etiological beginning is streptococcus, and the main damaging factors are immune complexes, antigens, antibodies.

Initially, most often the disease manifests itself as a lesion of the skin of the face and upper extremities. There are 3 stages of the disease.

1 \ Stage of edema.

Duration – up to several weeks.Manifestations – small areas of thickening of the skin of a ribbon-like or plaque-like shape, skin edema, vasculitis, inflammatory infiltration along the ducts of the sweat and sebaceous glands. This corresponds to the morphological picture of serous inflammation.

2 \ Compaction stage.

At this stage, there is a thickening and thickening of plaques to the consistency of cartilage with ulceration of the skin in places of bony protrusions, atrophy of the epidermis and skin appendages, hyperkeratosis, sclerosis and hyalinosis.

3 \ Atrophy stage .

It is expressed in thinning of the dermis, atrophy of muscles, adipose tissue, in fusion of the skin with bone tissue, sclerosis, vascular hyalinosis. The face becomes masked.

Organ damage.

Joints. Large and small joints of the arms and legs are affected, with deformation and dysfunction.

Heart. Cardiosclerosis. Miolysis. Fibrosis and hyalinosis of the fibrous ring, endocardium. Scleroderma heart.

Vessels . In small arteries, arterioles, fibrinoid necrosis of the intima, thrombosis, sclerosis, hyalinosis, circular arteriosclerosis are noted.

Lungs . Lower and middle lobes. Types of processes – 1 \ cystic 2 \ compact. Pathomorphology is a productive inflammation of the interstitial tissue around the bronchi and between the alveoli.

Tongue, esophagus, stomach, intestines . Atrophy. Sclerosis. Hyalinosis. Stenosing.

Liver . Interstitial hepatitis, dystrophy.

Kidneys. 2 types of changes: 1 \ low-symptom 2 \ fast. With oligosymptomatic clinical manifestations are scanty, and pathomorphological processes are expressed very clearly in the form of sclerosis, hyalinosis of individual glomeruli and stroma; necrosis, atrophy and dystrophy of the tubular epithelium. With the rapid type, renal failure is rapidly increasing. The pathological picture is characterized by obliteration of the lumen of the arteries due to sclerosis and hyalinosis with the development of a heart attack.

NODULAR PERIARTERITIS.

Initiated by streptococcal infection, but proceeds as a chronic autoimmune disease. The main thing is the defeat of medium and small arteries of the whole organism.

Clinical and morphological manifestations of the disease depend on localization. These can be arteries of the heart, kidneys, brain, intestines, extremities, etc.

Characterized by the appearance of nodules along the arteries. Variants of arteritis: 1 \ destructive 2 \ productive 3 \ productive-destructive.

Complications: thrombosis, aneurysm, rupture, heart attack.

Frequency of organ damage.

1 \ Kidneys – 90%.

2 \ Heart – 60%.

3 \ Liver – 60%

Less commonly, the lungs, brain, stomach, intestines, skin, muscles, bones, joints, peripheral nerves, spleen are affected.

BEKHTEREV’S DISEASE.

Rheumatoid spondylitis. This is a variant of rheumatoid arthritis.

DERMATOMYOSIT.

The main thing is damage to 1 \ skeletal muscles, 2 \ skin.

But other organs are also affected: heart, gastrointestinal tract, lungs.

Pathomorphology: productive inflammation, degeneration, necrosis, fibrosis, calcification.

Forms – 1 \ primary \ idiopathic \

2 \ secondary \ tumor \.

DRY SHEGREN’S SYNDROME.

The main lesion of exocrine glands: lacrimal glands, salivary glands, bronchial glands, gastrointestinal tract and glands of other localizations. There is a characteristic triad – 1 \ polyarthritis 2 \ xerophthalmia 3 \ xerostomia.

Pathomorphology – immune inflammation, as well as dystrophy, necrosis, atrophy, sclerosis. Currently, many researchers consider dry Sjogren’s syndrome a component of the generalized process in the body caused by the hepatitis virus.

Morphological transformation of intestinal graft after cystectomy with orthotopic bladder plasty

M.E. Sitdykova, A. Yu. Zubkov
FSBEI HE “Kazan State Medical University” of the Ministry of Health of the Russian Federation; Kazan, Russia

Introduction

Radical cystectomy with lymph node dissection and various types of intestinal urine diversion is the gold standard for treatment of patients with muscle-invasive bladder cancer [1]. Despite a fairly large number of clinical observations of patients after cystectomy with the formation of an isolated intestinal graft, the histomorphological state and mechanisms of transformation of the intestinal epithelium of the orthotopic bladder remain insufficiently unexplored [2-5].

The aim of the study is to study morphological adaptive-compensatory changes in the intestinal graft (CT) wall and their relationship with homeostasis at various stages after surgical treatment.

Materials and methods

The morphological state of the CT wall was investigated in 42 patients who underwent cystectomy with the formation of an orthotopic intestinal bladder (ileum 15, sigmoid colon 27) for periods from 1 to 6.5 months.and 1 year or more after surgery. All patients used the original method of “creating a“ U ”-shaped, anti- or isoperistaltic artifactual intestinal bladder from an isolated segment of the small or large intestine according to the method of E.N. Sitdykov. Histological material was collected by endoscopic “cold” pinch biopsy and examined using hematoxylin, van Gieson eosin and mucicarmine staining.

Results

Changes in the CT wall begin from the moment the contents, unusual for the intestine, enter its lumen, i.e.e. urine, which occurs in combination with a change in the stereotypical dynamics of the organ. Pronounced changes are observed in all parts of the wall of the small intestine. The epithelium is practically absent in all visual fields, and single cells of the epithelial cover are found only in the depths of the crypts (Fig. 1)

Figure 1. Small bowel graft (3 months after surgery). Necrosis of the superficial parts of the villi, desquamation of the epithelium, small groups of epithelial cells in the depths of the crypts

In the remaining cells, pycnosis of nuclei with their hyperchromia, swelling or decrease in the size of the cytoplasm, in which the phenomena of vacuolar dystrophy are noted, are observed in places.A significant part of the remaining cells lose contact with the basement membrane, desquamate and are located near it. The number of intestinal villi decreases unevenly, the height of the villi decreases, which is accompanied by the expansion of the base. They are small hilly elevations, and the crypts are not determined by the alignment of the intestinal lamina propria. The submucosal layer and the stroma of the villi are somewhat edematous, which is accompanied by collapse of the lymphatic vessels. The blood vessels, on the other hand, are full-blooded with pronounced perivascular edema.As one approaches the lumen of the intestine, thrombosis of the vessels is observed, expressed in the zones of fibrinoid necrosis of the superficial parts of the mucosa, in some places reaching a total lesion (Fig. 2).

Figure 2. Small bowel graft (3 months after surgery). Thrombosis of the bloodstream of the superficial parts of the intestinal mucosa

The stroma of the villi is diffusely infiltrated with a predominance of plasma cells, lymphocytes and macrophages, with a small number of eosinophils and segmented leukocytes.A small part of the cellular infiltrate is diffusely located in the submucosal layer, but the number of cells near the basement membrane is low, only single lymphoid elements are found in the muscle layer. On the other hand, the most pronounced local lymphoid accumulations are found in the submucosal layer, in places forming foci such as follicles without centers of reproduction.

Changes in the wall of the large intestine in the period from 1 to 6.5 months have a similar character and severity of the manifestations described in the CT scan formed from the small intestine.There is a pronounced desquamation of the epithelium of the mucous membrane mainly in the apical parts of the intestinal villi, accompanied by necrosis of the stroma. At the base of the intestinal villi and crypts, small layers of epithelium are preserved, and some of the cells here are in a state of necrobiosis or necrosis. The cells themselves change their typical oblong shape and turn out to be deformed or rounded. Epithelial cells are located in the form of a monolayer of cylindrical cellular elements, among which dystrophy and necrosis with complete destruction of the mucous membrane are not uncommon (Fig.3).

Figure 3. Colon graft (6 months after surgery). Desquamation of the epithelium of the superficial parts of the mucous membrane of the flattened surface of the intestine

The height of the villi decreases, and their upper sections are flattened. In some areas, the villi take a horizontal position, closely adhering to one another, forming a flat inner surface. In some areas, fibrinoid necrosis is observed, which spread to a great depth and capture superficially located blood vessels, some of which are thrombosed.A large number of blood vessels in the submucous layer are hyperemic, while the lymphatic capillaries are usually collapsed. In the areas of destruction of the superficial parts of the mucous membrane in the zones of necrosis, intense lymphoid infiltration is observed. In other areas, cellular infiltration is predominantly diffuse and is represented by lymphocytes and macrophages. In the stroma of the villi and the submucosal layer, there is a pronounced edema, less noticeable in the muscle layer.

For periods of more than 12 months after the operation, a gradual restoration of the mucous membrane of the small intestine CT is observed. An integral epithelial lining covers almost the entire inner surface of the reservoir, and only the apical sections of single villi are devoid of epithelial cover in the form of areas. The mucous membrane is represented mainly by goblet cells. These cells have hyperchromic nuclei located in the basal region and the cytoplasm expanded in the form of a large drop in the apical region.Cylindrical suction cells with signs of atrophy are located between the mucous cells. In the apical part of individual villi, the number of such atrophic cells increases significantly, and they form a kind of cell covering in the form of a dense layer (“palisade”) of fusiform cell elements (Fig. 4).

Figure 4. Small bowel graft (12 months after surgery). A layer (“palisade”) of fusiform cylindrical cells on the thickened apex of the villi

At the same time, the flattened apical parts of the villi are deprived of the epithelial cover.In these areas, fibrinoid necrosis and thrombosis of the vessels of the superficial zone are often observed. The size of the villi, especially their height, is markedly reduced, which is accompanied by a decrease in their transverse size. Accordingly, the number of villi per unit area of ​​CT

also decreases.

The mucous membrane of the colonic orthotopic bladder in 12 months was restored in the greater part, only the laminar parts of the villi sometimes turned out to be devoid of the epithelial lining. The cells lining both the superficial sections and most of them deep in the crypts are identical in morphological structure to the mucous (goblet) cells (Fig.five).

Figure 5. Colon graft (12 months after surgery). Mucous cells that form the lining of the intestinal reservoir

Single lymphocytes, macrophages and lymphoid follicles are diffusely located in the stroma of villi and submucosal layer with a small amount of loose fibrous connective tissue. Lymphatic vessels are not detected, and the number of blood vessels is reduced and some of them are sclerosed and thrombosed in the superficial parts of the CT wall.The muscle layer does not undergo significant morphological changes, except for a slight atrophy of the muscle elements. In some areas, a monolayer of intestinal epithelium with a large number of cylindrical cells grows over the flattened villi and intestinal fossae (Fig. 6).

Figure 6. Colon graft (12 months after surgery). A monolayer of cylindrical cells growing on the mucosal surface.

The detected changes are identical to acute alterative-desquamative enteritis and colitis, which suggests a malabsorption mainly due to the loss of the intestinal epithelial lining.On the other hand, a sharp venous plethora contributes not only to malabsorption, but, on the contrary, can lead to the release of a certain amount of fluid from the wall of the damaged intestine. Consequently, already in the early stages, damage to the mucous membrane of CT is accompanied by blocking of absorption, which makes it physiological for it to perform its functions with certain secondary changes in the walls.

A year later, regeneration and restructuring of the epithelium occurs, expressed in atrophy and a decrease in the number of suction cylindrical cells and an increase in the number of mucus-forming goblet elements.This, combined with a decrease in the number and size of villi and crypts, a reduction in the lymphatic bed and sclerosis of the blood vessels and stroma, blocks absorption. The increase in the number of mucus-forming goblet cells provides the creation of a barrier that protects the CT mucosa from urine exposure.

Conclusion

Morphological changes occurring in the CT wall under the influence of urine contribute to the preservation of homeostasis and are identical in colonic and small intestinal bladder plastics.

Literature

  1. Bladder cancer (classics and innovations). Ed. Kogan M.I. M.: Medforum; 2017.
  2. Tsvetov E.P. Morphological changes in the graft in intestinal plastic of the bladder. New surgeon. Archive. 1961; 1: 48-54.
  3. Shakhov E.V. Histological characteristics of the small bowel graft used for plastic surgery of the urinary bladder in the experiment. Materials of the 2nd All-Union Symposium. Bitter; 1973.
  4. Komyakov B.K., Anichkov N.M., Bodareva N.V. Morphological adaptation of the artifactual bladder. Materials of the ROU Plenum. Krasnodar, 2010.
  5. Reprint V.A. Optimization of the surgical treatment of muscle-invasive and locally advanced bladder cancer. Dissertation. … Doctor of Medical Sciences. Rostov-on-Don. 2016: 420.
  6. Yuan J, Lin H, Li P, Zhang R, Luo A, Berardinelli F, Dai Y, Wang R. Molecular mechanisms of vacuum therapy in penile rehabilitation: a novel animal study.EurUrol. 2010; 58: 773-80. DOI: 10.1016 / j.eururo.2010.07.005
  7. Lin H, Yang W, Zhang J, Dai Y, Wang R. Penile rehabilitation with a vacuum erectile device in an animal model is related to an antihypoxic mechanism: blood gas evidence. Asian J Androl. 2013; 15: 387. DOI: 10.1038 / aja.2013.18
  8. Yuan J, Hoang A, Romero C, Lin H, Dai Y, Wang R. Vacuum therapy in erectile dysfunction-science and clinical evidence. Int J Impot Res. 2010; 22: 211-9. DOI: 10.1038 / ijir.2010.4

The article was published in the journal “Bulletin of Urology” No. 2 2018, p.38-43

Fibrinoid swelling

#

At an autopsy of a 32-year-old woman who died of heart failure, the mitral valve was macroscopically deformed. With histological staining with hematoxylin-eosin, it gives a basophilic reaction, with toluidine-blue it turns pink.What changes in connective tissue are characteristic of the phenomenon of metachromasia?

0

Fibrinoid swelling

0

Edema of connective tissue

1

Mucoid swelling

0

Hyalinosis

0

Fibrinoid necrosis

#

Pathohistological examination of the kidneys of a 55-year-old woman who died from renal failure revealed sharply narrowed arterioles with the deposition of homogeneous hyaline-like masses in the subendothelial space.Immunohistochemically, these masses contain immune complexes, fibrin and decaying components of the vascular wall. Indicate which of the listed substances is most likely to be deposited in the subendothelial space?

1

Complex vascular hyaline

0

Simple vascular hyaline

0

Vascular lipogyalin.

0

Fat-protein detritus.

0

Amyloid.

#

The patient suffered from rheumatism for a long time.Death came from chronic heart failure. At the opening of the mitral valve leaflets are thickened, adhered, translucent, cartilaginous density, whitish in color. Name the type of mitral valve pathology.

0

Mucoid swelling

0

Fibrinoid swelling

0

Fibrinoid necrosis

1

Hyalinosis

0

Edema

#

Microscopic examination of the skin area of ​​a patient with allergic vasculitis revealed: the walls of the vessels are thickened, homogeneous, painted yellow with picrofuchsin, sharply SHIK-positive.The phenomenon of metachromasia is not pronounced. Name the type of mesenchymal pathology.

0

Mucoid swelling

0

Sclerosis

0

Edema

0

Slime

1

Fibrinoid swelling

#

An autopsy of a 55-year-old patient, who suffered from adhesive intestinal obstruction, revealed a spleen with a dense, thickened, whitish capsule resembling hyaline cartilage (“glazed spleen”).Name the pathological process in the spleen capsule.

0

Mucoid swelling

0

Fibrinoid swelling

1

Local hyalinosis

0

Amyloidosis

0

Generalized hyalinosis

#

An overview light microscopy of the tissues of a deceased patient suffering from diabetes mellitus revealed: the walls of the arterioles are thickened, homogeneous, pink in color, the lumen is sharply narrowed.When stained with Sudan, they give an orange coloration. Name the substance found in the vessel wall.

0

Simple vascular hyaline

1

Vascular lipogyalin

0

Amyloid

0

Complex vascular hyaline

0

Albumin

#

An autopsy of a 64-year-old woman who was overweight revealed an enlarged heart with excess fat deposition under the epicardium in the form of a sheath and adipose tissue invasion into the myocardium.Name the pathological process in the heart.

0

Tiger Heart

0

Glycogenosis

0

Dysproteinosis

0

Amyloidosis

1

Heart obesity

#

A 35-year-old patient suffering from rheumatism died of heart failure. A histological examination of the heart valves in collagen fibers that retain the bundle structure reveals swelling and fibrillary dissociation.The phenomenon of metachromasia is determined. What process are these changes typical for?

0

Hyalinosis

0

Fibrinoid swelling

0

Fibrinoid necrosis

1

Mucoid swelling

0

Sclerosis

#

The patient’s body weight exceeds the norm by 60%, while adipose tissue is deposited evenly in all parts of the body. Diagnosis:

0

Upper type obesity, II st.

0

Obesity of the average type, III st.

0

Lower type obesity, II st.

0

Symmetrical type of obesity, II st.

1

Symmetrical type of obesity, stage III.

#

When examining the brain of a deceased patient suffering from arterial hypertension, it was found that the vessels of the circle of Willis are sharply narrowed, have a dense whitish wall and resemble glass tubes.Name the pathological process in the vessels.

0

Mucoid swelling

0

Fibrinoid swelling

1

Generalized vascular hyalinosis

0

Amyloidosis

0

Local vascular hyalinosis

#

Microscopy of the ovarian tissue of a 74-year-old woman who died revealed white bodies of a homogeneous structure, stained pink with hematoxylin and eosin. Name the type of changes in the white bodies of the ovaries.

0

Mucoid swelling

0

Fibrinoid swelling

0

Lipidosis

0

Senile amyloidosis

1

Hyalinosis

#

In the pathological examination of the organs of the corpse of a woman suffering from thyroid insufficiency, it was revealed that the connective tissue itself, the stroma of the organs are swollen, translucent, mucoid, and the tissue cells have a stellate shape.Name the type of pathological changes.

0

Pathological intracellular accumulation of protein substances

0

Pathological intracellular accumulation of lipid substances

0

Amyloidosis

1

Pathological extracellular accumulation of carbohydrate substances

0

Systemic hyalinosis

#

In a 35-year-old woman, a patient with rheumatoid arthritis, microscopic examination of the periarticular tissue revealed bundles of collagen fibers, homogeneous, stained yellow with picrofuchsin.Metachromasia is not expressed. Specify the type of connective tissue changes.

0

Mucoid swelling

1

Fibrinoid swelling

0

Hyalinosis

0

Sclerosis

0

Lipidosis

#

Microscopic examination of the myocardium of a 74-year-old patient who died of heart failure revealed atrophic changes in cardiomyocytes, between which there are massive layers of adipose tissue.In this case, macroscopically under the epicardium, an array of adipose tissue is visible, surrounding the heart in the form of a sheath. Specify the type of pathology.

0

Tiger Heart

0

Lipomatosis

0

Lipo-hyalinosis

0

Parenchymal fatty degeneration

1

Heart obesity

#

A 54-year-old patient has been diagnosed with a hyperplastic type of obesity. Indicate the morphological signs that are characteristic of this type of obesity.

0

Symmetrical obesity type

0

Fat cells are enlarged and contain a large amount of triglycerides

1

Increased number of adipocytes without changing their functions and metabolism

0

Local increase in the amount of adipose tissue

0

Accumulation of cholesterol in the intima of arteries

#

A 35-year-old woman consulted a nutritionist for being overweight.With the right diet and regular exercise, the weight began to gradually decrease. What is the putative mechanism of the patient’s obesity?

0

Cerebral

0

Metabolic

1

Alimentary

0

Endocrine

0

Pituitary

#

A 57-year-old patient with rheumatoid arthritis underwent biopsy of the knee joint capsule and adjacent soft tissues.Microscopically: foci of swelling of intermuscular tissues, giving metachromasia when stained with toluidine blue. Name the type of connective tissue pathology.

1

Mucoid swelling

0

Fibrinoid changes

0

Hyalinosis

0

Amyloidosis

0

Lipidosis

#

In a patient with rheumatism with signs of heart failure, a histopathological study of atrial biopsy was carried out: foci of complete destruction of connective tissue with a pronounced macrophage reaction were found in the endocardium.What process is found in the endocardium?

0

Mucoid swelling

1

Fibrinoid necrosis

0

Generalized hyalinosis

0

Amyloidosis

0

Local hyalinosis

#

When examining the brain of a 57-year-old patient who died from a hypertensive crisis, it was found that the vessels of the base of the brain are sharply narrowed, have a dense whitish wall, are fragile and resemble glass tubes.Name the pathological process in the vessels.

0

Mucoid swelling

0

Fibrinoid swelling

1

Generalized vascular hyalinosis

0

Amyloidosis

0

Local vascular hyalinosis

#

In a woman who died of heart failure, white bodies were found in the ovarian tissue, when stained with hematoxylin and eosin, they looked like pale pink homogeneous masses.Name the type of mesenchymal pathology.

0

Mucoid swelling

0

Fibrinoid swelling

1

Hyalinosis

0

Senile amyloidosis

0

Lipidosis

#

During an autopsy of the corpse of an obese woman, a tumor-like formation was found in the pituitary gland. What is the type of obesity you suspect?

0

Hereditary

0

Idiopathic

0

Alimentary

1

Pituitary

0

Endocrine

#

Microscopic examination of the organs of a deceased patient, who had suffered from thyroid insufficiency for a long time, revealed that the actual connective tissue, organ stroma, adipose tissue were swollen, swollen, translucent, mucus-like, with foci of colliquation and necrosis.Cells of tissues of a bizarre stellate shape. Name the type of developed pathology of mesenchymal tissues.

0

Lipo-hyalinosis

0

Intracellular accumulation of lipid substances

0

Intracellular accumulation of protein substances

1

Tissue mucus

0

Mucoid swelling

#

An excised skin area with a gross scar defect was delivered for pathohistological examination.Microscopy in the scar tissue revealed the deposition of a homogeneous pale pink substance, from a distance resembling hyaline cartilage. Name the type of connective tissue pathology.

0

Mucoid swelling

0

Generalized hyalinosis

0

Fibrinoid necrosis

0

Amyloidosis

1

Local hyalinosis

#

An autopsy of a 57-year-old patient who suffered from adhesions of the abdominal cavity and polyserositis revealed a “glaze spleen”.Name the pathological process in the spleen capsule.

0

Mucoid swelling

0

Fibrinoid swelling

1

Local hyalinosis

0

Amyloidosis

0

Generalized hyalinosis

#

Microscopic examination of the pancreas of a deceased patient suffering from arterial hypertension and atherosclerosis revealed that the lumen of the arterioles is sharply narrowed, the walls are thickened, homogeneous, pink in color.Name the substance, which in this case is deposited in the subendothelial space of arterioles.

1

Simple hyaline

0

Lipogyalin

0

Amyloid

0

Complex hyaline

0

Albumin

#

A histological examination of the patient’s adipose tissue was diagnosed with a hypertrophic type of obesity. Indicate the morphological signs that are characteristic of this type of obesity.

0

Symmetrical obesity type

1

Fat cells are enlarged and contain a large amount of triglycerides

0

Increased number of adipocytes without changing their functions

0

Local increase in the amount of adipose tissue

0

Accumulation of cholesterol and β-lipoproteins in the intima of arteries

#

Microscopic examination of the spleen tissue of a woman who died of peritonitis revealed that the lumen of the central arterioles was narrowed, the walls were thickened, homogeneous, pink in color.Name the change in the vascular wall in this case.

0

Complex hyaline deposition

0

Lipogyalin deposition

0

Amyloidosis

1

Physiological hyalinosis

0

None of the above

#

Microscopic examination of the myocardium of a patient who died of heart failure revealed the proliferation of adipose tissue displacing the bundles of atrophied cardiomyocytes.Specify the type of heart muscle pathology.

0

Lipo-hyalinosis

0

Lipomatosis

0

None of the above

0

Tiger Heart

1

Heart obesity

#

Microscopic examination of the kidneys of a deceased person suffering from diabetes mellitus revealed that the walls of the renal arterioles are thickened, homogeneous, pink, and when stained with Sudan they turn bright orange.Name the substance found in the walls of blood vessels.

0

Simple hyaline

1

Lipogyalin

0

Amyloid

0

Complex hyaline

0

Albumin

#

Microscopic examination of the kidneys of a patient suffering from glomerulonephritis and who died from renal failure revealed narrowed small arteries and arterioles with deposition of homogeneous, pale pink masses in the subendothelial space.Immunohistochemically, these masses contain immune complexes and fibrin. Indicate the substance found in the subendothelial space:

1

Complex hyaline

0

Simple hyaline

0

Lipogyalin

0

Fat-protein detritus

0

Amyloid

#

Microscopy of a biopsy specimen from the atrial appendage of a patient with rheumatism in the endocardium revealed small cellless homogeneous foci of destruction surrounded by macrophages.What process is found in the patient’s heart?

0

Mucoid swelling

1

Fibrinoid necrosis

0

Generalized hyalinosis

0

Amyloidosis

0

Local hyalinosis

#

In a 58-year-old deceased from typhoid fever, waxy Zenker’s necrosis was found in the rectus abdominis muscles. Indicate which of the listed etiological factors of necrosis is the most probable?

0

Traumatic

0

Trophoneurotic

0

Allergic

1

Toxic

0

Vascular.

#

An autopsy of a patient who died from acute miliary tuberculosis revealed a dense knot with a diameter of 2.5 cm in the hilum of the right lung; on the cut, it was whitish-yellow and dull. Microscopic examination of the lymph node revealed a homogeneous structureless gray-white, easily crumbling mass. Set the process in the lymph node.

0

Fibrinoid necrosis

0

Waxy necrosis

0

Heart attack

0

Colliquation necrosis

1

Caseous necrosis

#

An elderly patient with atherosclerosis developed sharp pains in the left foot, soft tissues that became black, soft, edematous, increased in volume, and the skin was macerated.There is no demarcation zone. Your diagnosis:

1

Wet gangrene

0

Mummification of the foot

0

Coagulative necrosis of the foot

0

Dry gangrene

0

Sequestration of the foot.

#

A patient with phlebothrombosis of the lower extremities developed thromboembolism of segmental pulmonary arteries after physical exertion. Red wedge-shaped foci of necrosis of dense consistency appeared in the lungs.What form of necrosis has developed in the lungs?

1

Hemorrhagic infarction

0

Ischemic infarction

0

Coagulation necrosis

0

Gangrene

0

Colliquation necrosis

#

One day after the injury, a patient developed subcutaneous crepitus and rapidly spreading necrosis and edema of the soft tissues of the limb. The pathogen, bacterium perfringens, was isolated from the tissues.Specify the diagnosis.

1

Gas gangrene

0

Wet gangrene

0

Noma

0

Dry gangrene

0

Decubitus

#

In a patient with stenosing atherosclerosis of the lower extremities, the tissues of the first toe are intolerably painful, swollen, blackened, the epidermis is exfoliated. Total soft tissue necrosis was revealed histologically. What form of necrosis has developed in the patient?

1

Gangrene

0

Sequestration

0

Noma

0

Heart attack

0

Bedsore

#

An autopsy revealed a thrombosis of the left middle cerebral artery and a large focus of gray, moist softening of the tissue of the left hemisphere of the brain.What pathological process has developed in the brain?

0

Bedsore

0

Coagulation necrosis

1

Ischemic infarction

0

Wet gangrene

0

Sequestration.

#

During surgery, a large wedge-shaped focus of dark red, dense tissue was found in the upper lobe of the right lung. Cyto-biopsy revealed necrosis of the walls of the alveoli, the lumens of the alveoli are densely filled with erythrocytes.Your diagnosis:

0

Fibrinoid necrosis

0

Ischemic lung infarction

0

Gangrene of the lung

1

Hemorrhagic lung infarction

0

Lung atelectasis.

#

In a bedridden patient with circulatory insufficiency, immobilized after a stroke, the skin and soft tissues in the sacrum area acquired a black color and increased moisture; after the epidermis had been rejected, ulcers opened in the black tissue.What has developed in the patient?

1

Decubitus

0

Dry gangrene

0

Noma

0

Heart attack

0

Selective necrosis.

#

What organ is characterized by the formation of a well-defined white wedge-shaped infarction?

0

Brain

0

Intestine

0

Hearts

1

Spleen

0

Lung

#

Autopsy on a child who had died of measles had a dirty gray necrotic soft tissue defect on his cheek.What is the name of the identified change?

0

Gangrene

0

Sequestration

0

Heart attack

0

Bedsore

1

Noma

#

The patient was admitted to the clinic with frostbite of the feet. The tissues of the foot are dense, wrinkled, gray-brown in color. What form of necrosis are these changes typical for?

0

Heart attack

1

Dry gangrene

0

Fibrinoid necrosis

0

Wet gangrene

0

Sequestration

#

An autopsy of a 38-year-old deceased man revealed an infarction of the posterior wall of the left ventricle of the myocardium.What are the most probable changes that can be detected microscopically in the heart attack focus?

1

Karyolysis

0

Fatty degeneration

0

Carbohydrate dystrophy

0

Calcification

0

Keratinization

#

An autopsy of a deceased from typhoid fever found that the rectus muscles of the anterior abdominal wall are compacted, whitish in color, reminiscent of a stearic candle. What pathological process do these phenomena indicate?

1

Waxy necrosis

0

Fibrinoid necrosis

0

Colliquation necrosis

0

Caseous necrosis

0

Apoptosis

#

Patient M., 50 years old, diagnosed with fibrosarcoma. Histological examination of the removed tumor revealed karyopycnosis and karyorrhexis in individual malignant cells. When immunohistochemically labeled, these cells react positively with antibodies against the p53 protein. What process are such manifestations typical for?

0

Coagulation necrosis

0

Cariocytolysis

1

Pathogen-induced apoptosis

0

Immunocellular killing

0

Critical alteration of tumor cells

#

Patient B., 75 years old, suffering from atherosclerosis of the arteries of the lower extremities for a long time, went to the hospital with complaints of sharp pain in the right lower extremity and numbness of the right leg. After radiopaque vasography of the arteries of the lower extremities, complete occlusion of the right popliteal artery was diagnosed. The development of which process will be most likely in this patient in the absence of treatment?

1

Gangrene

0

Spontaneous recovery

0

Trophic ulcer of the right leg

0

Heart attack

0

Selective necrosis of striated muscle fibers

#

On autopsy of a patient who died of botulism, the muscles of the anterior abdominal wall are dull, dense, waxy.What process has developed in this case?

0

Gas gangrene

0

Dry gangrene

0

Bedsore

0

Colliquation necrosis

1

Zenker necrosis

#

Patient A., 55 years old, underwent donor kidney transplantation. After some time, a graft rejection developed. Microscopy reveals lymphocytic infiltration in the transplanted kidney.Which lymphocytes in this case take part in the rejection reaction, and by which molecules of the main histocompatibility complex (MHC) do they recognize foreign cells?

0

CD8 + T-killers, MHC class 2

0

CD4 + T-killers, MHC 1st class

0

CD4 + T-helpers, MHC class 2

1

CD8 + T-killers, MHC class 1

0

CD4 + T-killers, MHC class 2

#

Microscopic examination of the brain tissue of a deceased patient with a stroke revealed neurons with hypereosinophilic cytoplasm and pyknotic nucleus.What ultrastructural feature, detected by electron microscopy, will make it possible in this case to distinguish apoptosis of neurons from their coagulation necrosis?

1

Preservation of organelles

0

Expansion of endoplasmic reticulum tanks

0

Destruction of cytoskeleton proteins

0

Karyopyknosis

0

Swelling of mitochondria

#

Which of the following cell structures are the object of critical alteration?

0

Ribosomes and the biosynthetic system of the cell

1

All of the above is true

0

Cell nucleus and genetic apparatus

0

Mitochondria and the bioenergetic system of the cell

0

Plasma membrane and its transport systems

#

What is the name of the long-term process of gradual destruction of tissue, as a result of which, with microscopy, it is possible to simultaneously observe cells in pre-necrotic and necrotic phases, as well as post-necrotic transformations of dead cells.

0

Sequestration

0

Apoptosis

1

Necrobiosis

0

Gangrene

0

Autolysis

#

Patient N., 70 years old, within several hours developed a clinic of acute cerebrovascular accident due to thrombosis of the right middle cerebral artery. What type of organ necrosis developed in this case? If the patient survives, what is the most likely variant of his postnecrotic transformation?

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Dynamics of morphological changes in fibrin in the soft membranes and substance of the brain in acute traumatic brain injury

OO 3 4

As manuscript

KOSHAK Konstantin Vyacheslavovich

DYNAMICS OF MORPHOLOGICAL CHANGES OF FIBRIN IN THE PULS AND SUBSTANCE OF THE BRAIN IN ACUTE CRANIAL INJURY

14.a / fidsh * medical sciences

1 h ……

Novosibirsk, 2008

003459400

GOUVPO

NOVOSIBIRSK STATE MEDICAL UNIVERSITY

As manuscript

KOSHAK Konstantin Vyacheslavovich

DYNAMICS OF MORPHOLOGICAL CHANGES OF FIBRIN IN THE PULS AND SUBSTANCE OF THE BRAIN IN ACUTE CRANIAL INJURY

14.00.15 – pathological anatomy 14.00.24 – forensic medicine

Abstract of dissertation for the degree of candidate of medical sciences

Novosibirsk, 2008

The work was carried out at the Department of General Clinical Pathology of GOU DPO “Novokuznetsk State Institute for Advanced Training of Doctors” and in the Norilsk city branch of the KSUZ “Krasnoyarsk Regional Bureau of Forensic Medicine”.

Scientific advisers:

candidate of medical sciences, professor candidate of medical sciences, associate professor

Official opponents: Doctor of Medical Sciences, Professor Doctor of Medical Sciences, Professor

Rykov Vladimir Alexandrovich Chikun Vladimir Ivanovich

Novoselov Vladimir Pavlovich Ageeva Tatiana Avgustovna

Leading enterprise: GOU VPO Altai State Medical University of Roszdrav (St.Barnaul)

Defense will take place “_” _ 2008 at_hour. at the meeting

Dissertation Council D 208.062.05 at the Novosibirsk State Medical University of Roszdrav (630091, Novosibirsk, Krasny Prospekt, 52).

The thesis is available in the library of the Novosibirsk State Medical University (630091, Novosibirsk, Krasny Prospekt, 52) ..

Abstract sent out “_” _ 2008

Scientific Secretary

Dissertation Council D 208.062.05

Doctor of Medical Sciences, Professor Volkov A.B.

GENERAL OPERATING CHARACTERISTICS

Relevance of the topic. Traumatic brain injury (TBI) is one of the most common injuries and accounts for about 40% of all types of injuries (Konovalov A.N., Likhterman L.B., 1994), is characterized by high mortality and varying severity of harm to health. In addition, TBI is characterized by a varied character depending on the conditions of occurrence and types of traumatic effects, which increases the importance of various scientific and practical methods aimed at studying the prescription of occurrence, nature, volume and predicted consequences of CNS damage.The problem of TBI is one of the leading areas of forensic medicine, since the establishment of the mechanism, lifetime and duration of injury, clarification of thanatogenesis and the immediate cause of death, assessment of the ability of victims to perform active targeted actions and the provision of a well-founded expert opinion allows to resolve many issues arising in the -investigative practice.

In the practice of forensic medical examination, morphological examination of foci of brain damage in the absence of anamnestic, investigative and other data is the main and, at times, the only source of information about the time of occurrence of the injury and the duration of the post-traumatic period.

Currently, the pathological anatomy of CNS injuries, studied by many authors, allows us to judge with great certainty the nature, prevalence and timing of injury, which are based on mechanical damage itself, general and local disorders in the hemostasis system, pathological conditions of the vascular wall.

The pathological anatomy of damage to the brain substance in TBI has been studied quite fully, primarily on the extensive sectional material of a combat head injury during the Great Patriotic War, when fundamental research on the pathological anatomy of TBI was carried out (Snesarev P.E., 1946; Smirnov L.I., 1947, 1949). Later, large-scale works of domestic authors concerned mainly the biomechanics of the formation of damage to the brain substance during various types of traumatic effects (Singur H.A., 1970, Popov V.L., 1988).

However, it is obvious that in the study of the origin, development and organization of lesions in TBI in modern conditions, it is not enough just to describe certain microscopic processes in the lesions. It is necessary to compare them with the data of the clinic, to determine the correspondence of the damage to the nature of systemic disorders that inevitably arise in the body as a result of severe damage to the central nervous system.Therefore, an extremely important and necessary aspect is the study of systemic and local changes in the vascular bed, vascular wall and pathomorphosis of the protein components of the blood (Ricker, 1924; Smirnov AA, 1972; Tikk AA, 1978; Kumura E, 1987; Bouma GJ, 1991; Hulka F., 1996; Churlyaev Yu.A. 2003), first of all, the nature of changes in the blood coagulation system and the assessment of the link “fibrinogen – fibrin – products

fibrin degradation “(Smirnov A.A., 1972; Brueton M.J., 1976; Bajo R., 1980; Dalens B., 1981; Nowak S. 1984; Evseev E.M., 1985; Ueda S. 1985; Gadzhiev M.G., 1991; Lafuente J. V. 1999; Haagh W.A., 2006).

Selective fibrin staining methods were first proposed by Lendrum A.C. (1962) to identify the conditional time of fibrin coagulation. These are the methods of Marcius-Scarlett-Blue (MSB), Picro-Mallory V, Masson 44/41. Of these, the most promising is the MSB method proposed for determining the time of fibrin coagulation in vascular thrombi. In 1984 Zerbino D.D. and Lukasiewicz JI.JI. completely transformed this method, replacing hard-to-obtain imported dyes with domestic counterparts, as well as simplifying some stages by assigning new abbreviations for the first letters of the main dyes – the OCG method (“orange-red-blue”). They identified three “ages” of fibrin – “young”, “mature” and “old”. The spectrum of their coloring by the laser method includes orange, red and violet colors and transitional shades.

Therefore, the use in the work of specific histological and histochemical stains of changes in fibrin, as a kind of marker of the age of traumatic brain injury, is of great theoretical and practical interest.

The aim of the work was to study the dynamics of changes in fibrin in the vascular bed and in the foci of CNS lesions for a new diagnostic approach to the morphological assessment of the duration of traumatic brain injury.

Research objectives:

1. To reveal the sensitivity of specific stains to fibrin of autopsy material for diagnosing the age of brain damage.

2. Determine reliable differential diagnostic morphological signs for determining the duration of brain damage.

3. To study changes in the vascular plexuses of the brain in acute traumatic brain injury using specific stains for fibrin.

4. To develop an accessible practical method for establishing the prescription of brain damage based on the use of specific stains for fibrin.

Scientific novelty of the research. The main advantage of the work is that it was first studied in detail:

1. Characterization of the temporal aspects of fibrin pathomorphosis for objectifying the criteria for diagnosing the timing of trauma based on morphological data.

2. Selective histochemical assessment of vascular and extravascular fibrin in acute TBI, indicating the high specificity and sensitivity of these methods.

3. Systematization of organic changes in the foci of brain damage, identified using specific stains for fibrin (Picro-Mallory V method modified by DD Zerbino).

4. Changes in the choroid plexuses of the brain in acute TBI.

5. From a morphological point of view, an explanation is given to the mechanism of intractable traumatic edema and swelling of the brain substance, even in the absence of areas of destruction of the brain substance and successful evacuation of acute intracranial hematomas.

Scientific novelty of the research. In this work, for the first time, the characteristics of the temporal aspects of fibrin pathomorphosis have been studied in detail to objectify the criteria for diagnosing the timing of trauma based on morphological data.

Selective histochemical evaluation of vascular and extravascular fibrin in acute TBI was carried out, indicating the high specificity and sensitivity of the method of selective staining of Pkro-MaRoV V modified by D.D. Zerbino. It was found that fibrin appears almost simultaneously in the lumen of microvessels, in the vascular wall and outside the vessels in the foci of traumatic hemorrhages, which is associated with blood plasma perfusion

Organic changes in the foci of brain damage, identified using specific stains for fibrin (method) were systematized, which made it possible to establish a clear time dynamics of pathomorphological changes and its dependence on the duration of the injury.

For the first time, changes in the vascular plexuses of the brain in acute TBI were studied using selective staining. The established dynamics of circulatory disorders in the microvasculature of the vascular plexus, which made it possible from a morphological point of view to explain the mechanism of intractable traumatic edema and swelling of the brain matter, even in the absence of areas of destruction of the brain matter and successful evacuation of acute intracranial hematomas.

Systematization of the data obtained allowed the development of a differential diagnostic table of morphological changes in the area of ​​damage to the substance of the brain, vascular plexuses and the nature of fibrin transformations, the use of the data of which will make it possible to objectify the expert’s conclusions and improve the quality of forensic medical examinations.

The practical value of the work lies in the fact that the method of selective staining of fibrin in foci of damage to the brain and meninges according to Ryugo-Ma11or 5 (modified by Zerbino) can be used to objectively establish the prescription of TBI in everyday forensic practice. The nature of changes in the vascular plexuses of the brain in acute TBI allows tracing the mechanism of vasogenic cerebral edema from a morphological point of view.

Approbation of the work: The main provisions of the dissertation were reported at a meeting of the Academic Council of the Medico-Diagnostic Faculty of the Novokuznetsk State Institute of Higher Education on December 18, 2007, and at a meeting of the Dissertation

Council at Novosibirsk State Medical University 07 November 2008.

Publications. On the topic of the dissertation, 5 publications have been published, 1 of which is in the edition recommended by the Higher Attestation Commission of the Russian Federation for the publication of the results of dissertations. 1 methodical manual was developed and proposed for use. 1 rationalization proposal was proposed and approved.

Structure and volume of the thesis. The thesis is presented on 126 pages of computer text, consists of an introduction, 6 chapters, conclusions and a bibliographic index, including 73 works by domestic and 51 works by foreign authors.The thesis is illustrated with 48 micrographs, 14 tables and diagrams.

MATERIAL AND RESEARCH METHODS.

Practical material for the dissertation work was the sectional observations of victims of traumatic brain injury (TBI), whose death occurred directly at the scene, or followed later in medical institutions in Norilsk. The autopsies were carried out on the basis of the Norilsk city branch of the Krasnoyarsk regional bureau of forensic medical examination, the processing of histological material and microscopic examinations were also carried out here.

A total of 127 deaths from TBI were investigated, including 105 men and 22 women.

Table 1

Age distribution of material

V J J J V K o G–

h h h h h h o

o o o o o o C

(H go tG “about cho 9 * h

. — 1 1 a

Men 4 21 28 32 14 6

Women 1 5 6 5 2 2 1

Of these, 43 people died in hospital, including 35 men (81%, or 28% of the total number of deaths) and 8 women (19%, or 6% of the total number of deaths).84 people died outside the hospital, including 70 men (83%, or 55% of the total number of deaths) and 14 women (17%, or 11% of the total number of deaths). At the time of injury, 79 men and 17 women (respectively 75% and 77%, or 76% of the total number of deaths) were in a state of alcoholic intoxication.

Table 2

Distribution of material by kind of death__

Structure of indicators

Men Women

n% n%

murder 26 24.8 7 31.8

suicide 7 6.7 3 13.6

industrial accident 4 3.8

non-production accident 36 34.3 6 27.3

kind of death not established 31 29.5 6 27.3

other 1 0.9

Table 3

Distribution of material by type and nature of head injury

by type of injury by nature of injury

isolated other combined open closed with a fracture of the skull bones without fracture

Men 76 29 25 80 51 54

Women 18 4 1 21 8 14

Table 4

Distribution of material by the mechanism of injury

men women

n% n%

Road traffic accidents: 14 13.5

Work injury: 3 2.8

Damage by blunt objects: 52 49.6 15 68.2

Damage by sharp objects 3 2.8

Falls from a height: including from a height of their own height 25 16 23.8 7 3 31.8

Fire damage: 4 3.8

Combined injuries: including: TBI + mechanical asphyxia TBI + gunshot injuries to the body TBI + carbon monoxide poisoning 3 1 1 1 2.8

Others 1 0.9

Preference in the study was given to autopsy material from persons who died in the first minutes and hours after injury (from several minutes to 3 hours).

Table 5

Life expectancy after injury.

Men Women

The control group consisted of morphological studies of the brain and choroid plexuses in persons who died from stab wounds – mainly with a small number of wounds (1-2) and heart damage, accompanied only by hemorrhage into the bursa and cardiac tamponade. A short period of time before death following such injuries and a relatively small amount of blood loss without pronounced exsanguination of internal organs allowed us to judge the normal histological structure of the central nervous system.

A total of 10 corpses of persons aged 19 to 40 years (9 men and 1 woman) were examined. In 9 cases out of 10, death occurred as a result of a penetrating stab-cut wound of the chest with damage

hearts, in the 1st case – from a gunshot blind bullet wound to the chest, also with damage to the heart. In all cases, the death of the victims occurred within a short period of time (no more than 5-10 minutes) as a result of tamponade of the cardiac shirt with blood poured out, without pronounced anemia of the internal organs.

Research method. At autopsy, the selection and marking of damaged areas of the substance of the brain and pia mater, as well as the choroid plexuses of the cerebral ventricles (in 39 cases) were performed. The material was fixed in formalin, then subjected to standard dehydration in an alcohol battery, followed by the manufacture of paraffin blocks. After the preparation of histological sections, they were stained with hematoxylin and eosin, as well as by the method of Plcro-Ma11oru V, modified by D.D. Zerbino – “orange – red – blue” (OCG), which turned out to be the most indicative and effective in detecting fibrin at different stages of its formation. The fibrin “age” was determined depending on the staining:

• “YOUNG” (0-6 hours) – yellow-orange color

• “MATURE” (6-24 hours) – shades from orange-red (6-12 hours) through bright red (12-18 hours) to red-violet (18-24 hours)

• “OLD” (more than 24 hours) – purple color gradually turning into gray-blue (over 48 hours).

The rest of the tissues were stained as follows – erythrocytes orange, muscle tissue purple, collagen fibers dark blue.

RESULTS AND DISCUSSION

1. Microscopic changes in the soft membrane and substance of the brain during staining by routine and selective methods.

The morphological study of the membranes and matter of the brain in acute TBI with the use of specific stains for fibrin suggests that the severity of TBI, in addition to the direct effect of mechanical energy, is influenced by complex and diverse mechanisms of hemodynamic and hemorheological disorders – both local and generalized.

The trigger for circulatory disorders is a mechanical trauma to the brain, when damage to the membranes and brain matter is accompanied by a natural physiological reaction of vascular spasm. At the same time, the activation of the coagulation and platelet hemostasis systems develops, compensated by the activation of the anticoagulant and fibrinolytic systems. Therefore, in all cases of acute TBI, discirculatory and dyshemic disorders of the central nervous system are accompanied by the development of local, and in the most severe cases, generalized disseminated intravascular coagulation syndrome with the formation of platelet-fibrin microconvulsions in the system.

microcirculation.As a result, secondary ischemic, hemorrhagic and necrotic phenomena develop in vital organs, including the brain, which affects the course and outcome of TBI.

The main morphological substrate in the diagnosis of disseminated intravascular coagulation, including its stages, is the presence of microthrombi in the lumen of the vessels of the microcirculatory bed – with a fibrin framework or entirely consisting of fibrin. The formation of fibrin in the lumen of the vessels occurred both as a result of isolated damage to the vascular wall, and as a result of generalized imbalance in the hemostatic system; and had a number of clearly defined successive stages.At different stages of its development and regression, fibrin is able to perceive very specific (selective) dyes. In this case, the color of fibrin when using special staining methods directly speaks of its age.

This technique was the basis of our study for the development of differential diagnostic criteria when establishing the age of TBI, which allows us to draw the following conclusions when summarizing the material:

– in the first minutes after the infliction of TBI in the zone of damage to the membranes and substance of the brain, only discirculatory changes are noted, characterized mainly by anemia of all structural areas of the bloodstream (arterial, capillary, venous) with symptoms of angiospasm and vascular collapse.There are focal hemorheological disorders in the form of plasma separation, focal plasma impregnation of the vessel walls, focal plasmorrhages; focal edema and loosening of the pia mater. The damaged brain tissue looks like small cavities with an optically empty lumen; intact brain tissue without any changes, only focal dystrophic changes in neurons in the superficial parts of the cortex, which are most sensitive to hypoxia, are noted;

– when death occurs within a period of time up to 1 hour after the infliction of TBI, there are also predominantly discirculatory changes, which, however, have different features in different areas – with persistent angiospasm in the area of ​​traumatic destruction, uneven reactive plethora, dystonia and vascular paresis.Hemorheological disorders develop in the form of stasis and sludge of erythrocytes with plasma separation, plasma impregnation of the vessel walls and plasmorrhages. In the foci of brain damage, free-lying unchanged erythrocytes are visible. In the molecular layer of the cerebral cortex – a fine-mesh rarefaction, in other layers of the cortex – focal swelling of neurocytes with a weak chromatolysis, focal swelling of neuroglial cells with single “honeycomb structures”;

– at the onset of death a few hours after the injury (2-6), uneven blood filling of the vessels, vascular spasm is replaced by a pronounced stagnant venous plethora with pronounced hemorheological disorders (stasis, aggregation, sludge of erythrocytes in

10

microvasculature, phenomena of focal vein thrombosis of large and medium caliber).In the foci of traumatic hemorrhages, the beginning of erythrocyte lysis is noted with the destruction of the cytoplasm and their transformation into a homogeneous, in places granular oxyphilic mass, pronounced plasma separation, the appearance of leukocyte infiltration of varying intensity on the periphery of the hemorrhage sites (which is especially noticeable in the pia mater). In connection with venous congestion, the phenomena of tissue hypoxia are expressed to varying degrees – pronounced perivascular edema with the formation of “muff-like” cavities, hemo- and plasmorrgy, interstitial edema, swelling and dystrophic changes in cellular elements with a weakly expressed tissue reaction in the form of microglial satelliteitis (.Expressed fibrinoid swelling of fibrous structures in the vessel wall and in the meninges with focal fibrinoid necrosis, with uneven lymph-leukocyte infiltration of varying intensity, and initial symptoms of leukodiapedesis. When staining for fibrin by the OCG method, a diffuse protein precipitation of the vascular wall with its bright yellow staining is noted, which is especially clearly in contrast with the swollen crimped blue-blue collagen fibers. In the lumen of the vessels and perivascular, single or numerous lumps of “young” yellow-orange fibrin are found;

– upon the occurrence of death in the period from 6 to 24 hours in the foci of traumatic hemorrhage – leaching and lysis of erythrocytes with uneven plasma separation and abundant uneven leukocyte infiltration; with a prolapse of fibrin on the periphery in the form of threads or soft-mesh masses.The phenomena of congestive venous plethora are even more pronounced, numerous blood clots from erythrocytes, platelets and a few leukocytes, as well as diffuse fibrinoid swelling of the walls with focal necrosis and abundant leukocyte infiltration, are determined in the lumen of vessels of different caliber. In the substance of the brain, severe discirculatory-dystrophic changes caused by tissue hypoxia, necrobiosis and foci of necrosis of neurocytes with microglial satelliteitis and the initial phenomena of neuronophagy.In the cortex and white matter – uneven swelling of neuroglial cells with the formation of “honeycomb structures”. In the white matter – swelling, focal tortuosity and fragmentation of axons, periaxial microglial satelliteitis. The formation of areas of necrosis begins near larger foci of traumatic destruction with secondary hemorrhages from unchanged erythrocytes. When staining for fibrin by the OCG method – uneven thickening and loosening of the walls of blood vessels with diffuse staining in a yellow-orange color.In some places, the thickened walls of blood vessels have a reddish or red tint – fibrinoid necrosis. In the lumen of the vessels, there are masses of aggregated ocher-yellow erythrocytes with the phenomena of focal sludge and homogenization (while destroyed erythrocytes retain a bright ocher-yellow color). Among the erythrocytes – lumps and filaments of orange and reddish fibrin; isolated fibrin aggregates completely obstruct the lumen of the capillaries like blood clots. Perivascular spaces

are significantly expanded, optically empty or filled with unchanged erythrocytes and homogeneous masses with yellow-orange color of varying intensity.In the foci of hemorrhage fibrin is found both on the periphery and in the center of the foci in the form of pale-mesh masses of orange-red, sometimes violet-red color;

– when death occurs within 24-72 hours after TBI, subdural and subarachnoid hemorrhages are represented by the masses of mostly lysed and leached erythrocytes; among which are thick filaments and optically dense lumpy masses of fibrin, most often in the form of reticular or annular conglomerates with abundant leukocyte infiltration.On the periphery of hemorrhages, a few macrophages appear among the leukocyte infiltrate, some of them are loaded with blood pigment. Circulatory disorders are of a diffuse nature, venous congestion with thrombotic-hemorrhagic phenomena persists. In the area of ​​traumatic destruction, the phenomena of necrosis with secondary hemorrhages, as well as diffuse exudative inflammation, are expressed. Sheath and parenchymal hemorrhages are characterized by an extremely “motley” morphological picture – along with the masses of destroyed erythrocytes, there are unchanged or leached erythrocytes, among which optically dense “ring-shaped” masses of fibrin are distinguishable, which, when stained by the OCG method, have a dull violet-red and gray-violet, and also bluish-gray color (“mature”, “aging” and “old” fibrin) with a clear coarse-fibrous reticular structure.There is a diffuse impregnation of loose connective tissue (pia mater, stroma of villi and villi of the choroid plexus) with fibrin, which has the appearance of large-lumpy and coarse-fibrous masses of orange-red and red;

– when death occurs within 4-7 days and later after the infliction of TBI, the processes of reparation, resorption and cleansing of foci of brain damage by tissue macrophages begin to prevail. There is a restoration of blood flow in the microvasculature, blood clots from the “young” fibrin in the lumen of the vessels are no longer detected (normalization of the hemostasis system).Also, “young” fibrin is not detected in the vascular wall and in the foci of traumatic hemorrhage. The masses of “old” fibrin are everywhere subjected to lysis by polymorphonuclear leukocytes; resorption of fibrin by tissue macrophages arises and gradually begins to prevail. However, the previous violations of the permeability of the vascular wall, caused by a prolonged hypoxic state, vascular thrombosis and necrosis of the vascular wall, persist. This is also associated with the preservation of degenerative-dystrophic changes in the cellular structures of the cerebral cortex, local circulatory disorders in the brain due to the functional insufficiency of the newly restored cerebral blood flow.

2. Microscopic changes in the vascular plexuses of the brain in acute traumatic brain injury.

In our study, it was theoretically assumed that the choroid plexuses of the brain (CHP) are a kind of “target” for the localized and then generalized DIC syndrome developing as a result of acute TBI. Microthrombi formed and circulating in the victim’s blood inevitably enter the arterioles and capillaries of the vascular plexus in large quantities, which entails their occlusion and, as a result, a complete or partial block in the tissue and cerebrospinal fluid circulation system.

This, in particular, can serve as an explanation for the mechanism of rapidly developing and intractable traumatic edema and swelling of the brain substance. After all, any tissue damage inevitably entails local hyperemia, which is a natural reaction of the human body to damage. And in the case of TBI with the development of a hemodynamic block at the level of the SSGM, local hyperemia of the central nervous system leads to a progressive increase in the release of the liquid part of blood into the perivascular spaces, then into the interstitial tissue of the brain (neuropil).

The central nervous system (CNS) is a unique entity from both morphological and pathophysiological points of view. Of particular interest is the balance of fluid media in the central nervous system, since, as you know, there are no lymphatic vessels to drain excess tissue fluid (Nash A., Cormack D., 1979, Robertson J.D., 1962).

Most of the tissue cerebrospinal fluid is formed in the SSGM, which are located in the vascular cover of the upper wall of the third ventricle of the brain.The tire has 2 thin sheets formed by a soft shell; along both edges of the tire, these leaves, passing into each other, form a set of villi, richly supplied with blood vessels, which protrude into the cavity of the lateral ventricles (Faivre, 1854; Meek W., 1907; Fridman A.P., 1957). The blood supply to the SSGM is carried out by 2 anterior choroid arteries (branches of the internal carotid arteries) and 2 posterior choroidal arteries (branches of the posterior cerebral arteries). And the central part of the plexus, or the vascular ball – 2 middle choroid arteries (from the superior cerebellar arteries).Arteries pass into arterioles, then into a huge number of capillaries. Blood from the capillaries is collected in venules and veins, which flow into the choroid vein, into the vein of the transparent septum and into the border vein, and then through the internal cerebral veins, the blood flows into the large unpaired vein of Galen (Klosovsky B.N., 1951; Avtandilov G.G. ., 1962).

Microscopically, SSGMs are represented by a large number of leaf-like processes with many small villi on the surface, lined with low cubic epithelium, similar to the epithelium of the ventricular ependyma (Fig.5.7). In the plexuses, a grain-shaped part is distinguished, where, inside the villi and villi, in the loose connective tissue stroma there is a complex, wide-looped system of small arteries and arterioles, passing into capillary plexuses located in the villi directly under

epithelium; and the non-serrate part (loose connective tissue stroma at the base of the plexuses, where there are a large number of bundles of collagen and elastic fibers that form a large-looped network). Depending on age, a different number of psammous bodies is found in the aciniform part, which is associated with a slowdown in the circulation of tissue fluid and metabolic disorders in the SSGM (Avtandilov G.G., 1957).

In the aciniform part of the capillaries through the epithelium and diffusion of fluid from the vascular bed into the lumen of the cerebral ventricles occurs. The choroid plexus, in fact, is one of the components of the blood-brain barrier. The excess cerebrospinal fluid formed in the cerebrospinal fluid is absorbed through the holes in the roof of the IV-ro ventricle into the subarachnoid space, and then through the arachnoid villi of the Pachyon granulations – into the venous sinuses of the dura mater (Friedman A.P., 1957).

Each of the SSGM is an integral organ, the activity of which is determined by the structural and functional relationships between all its main components – the vascular-capillary network, epithelium and connective tissue (Kulikov V.V., 1968).

In case of circulatory disorders in the brain in the choroid plexuses, congestive venous plethora with stromal edema, vacuolization of the epithelium, loosening of the epithelial layer, expressed to varying degrees, are noted.Stagnant plethora of SSGM occurs as a consequence of general venous plethora, the edematous state of the pericapillary stroma is associated with the increasing permeability of the capillary walls (Avtandilov G.G., 1962).

Traumatic brain injury triggers a whole cascade of dangerous, including biochemical, changes that occur against the background of altered vascular wall permeability and the blood-brain barrier (BBB). According to the literature, there are 2 main forms of brain damage: primary – as a result of the direct impact of mechanical energy; and secondary – arising as a result of complex and diverse mechanisms that develop from the moment of injury.Violation of permeability, dysfunction and BBB insufficiency are one of the factors of secondary brain damage (Semchenko V.V., 1999; Nikiforova N.V., 2004; Kan SL., 2006). Secondary brain damage is based on its exceptional sensitivity to metabolic disturbances arising from oxygen starvation. In acute ischemic conditions, the brain’s need for oxygen and oxidation substrates significantly exceeds their intake with the blood (Goman T.F., 1981).

That is, the substrate (primary damage) occurs at the time of injury and is the result of a mechanical factor. And post-traumatic cerebral reaction (secondary damage) is not necessarily associated with a traumatic substrate, since it can develop not only near them, but also at a distance, and in addition, sometimes occurs in the absence of primary brain lesions in response to mechanical stress. Expressiveness and

The consequences of secondary complications associated with brain reactions to trauma are very different in their manifestations, but at the same time, their essence is determined, as a rule, by three main pathogenetic mechanisms that inevitably accompany head trauma: 1) hypoxia; 2) edema and 3) hyperemia (Kvitnitsky-Ryzhov Yu.N., 1988, Romodanovsky P.O., 1991)

Thus, regardless of the TBI mechanism, the entire system of the membranes of the brain and intershell spaces is exposed to the traumatic effect of mechanical energy, which is morphologically manifested by damage to the membranes (hard, arachnoid, vascular), which is often accompanied by hemorrhages (epi- and subdural, subarachnoid). In all cases, the brain is displaced and then returned to its original position.This is inevitably accompanied by a dynamic redistribution of cerebrospinal fluid in the subarachnoid space and the ventricular system of the brain (Pashinyan G.A., 1992). In the studies of a number of authors (Singur H.A., 1970, Potemkin A.M., 1975, Shishkov T.T., 1990, Svadovsky A.I., 1991), it was found that in TBI, the choroid plexus and ependyma of the ventricles undergo certain changes. Since SSGMs themselves are a morphological substrate of the blood-brain barrier, and the ependyma of the ventricles is the cerebrospinal fluid barrier, damage to the first leads to disruption of cerebrospinal fluid production, and the second to disruption of metabolic processes between the cerebrospinal fluid and the brain, which can lead to the development of hydrocephalus and cerebral edema.The severity of pathomorphological changes in the choroid plexus and ependyma of the cerebral ventricles varies depending on the duration of the posttraumatic period of TBI and its severity. Structural changes in SSGM in the form of edema of the stroma of the villi and disruption of the integrity of the lining of the chorionic epithelium can lead to disruption of the functioning of the blood-brain barrier and contribute to the emergence of hydrocephalus, and pathomorphological changes in the ependymal lining (subependymal edema, violation of the integrity of the layer of ependymal cells, formation of “bays”) the functioning of the cerebrospinal fluid barrier and contribute to the development of cerebral edema (Pashinyan G.A., 1992).

In our work, we studied the pathomorphological changes in the SSGM in acute fatal TBI. The sampling of material for the study was carried out in cases of known pre-daily mortality after TBI.

In addition to the routine staining methods (hematoxylin-eosin), the OCG staining method was carried out. The normal histological structure of the SSGM, noted in the control group, corresponds to a specific color scale with this method of staining – yellow-orange erythrocytes, dark blue coloration of collagen fibers of the stroma and vascular walls.The choroidal epithelium is stained in a dark yellow-brown color. During the study, the following results were obtained:

– in the first minutes and tens of minutes after receiving a TBI, edema and loosening of the connective tissue stroma, anemia and collapse, swelling of the walls of small arteries and arterioles were noted in the SSGM. When staining with the OCG method, the specific differentiation of the layers was preserved (blue intima and adventitia, violet-red muscle fibers of the media). Among the loosened collagen and muscle fibers in the wall of the arterioles, focal deposits of homogeneous yellow masses – “young” fibrin, appeared;

– in a few tens of minutes – up to 3-6 hours after the injury, the anemia of the vessels was replaced by reactive uneven plethora, stasis and sludge of erythrocytes were noted; swelling and focal desquamation of the choroidal epithelium.In the lumen of venules and capillaries, when stained by the OCG method, there are spherical and teardrop-shaped blood clots from young yellow fibrin and destroyed erythrocytes. In the 1st case (falling from a great height) – diffuse fibrinoid swelling of the walls of the vessels, the walls of the vessels are diffusely stained in bright yellow, in the lumen of the vessels there are orange-red fibrin thrombi;

– from 3-6 hours to 1 day – the lumen of the vessels of the venous bed in the “cluster-shaped” part was filled with thrombotic masses such as red and, to a lesser extent, mixed thrombi; there was an uneven fibrinoid impregnation of the villi, capillary walls and arterioles, multiple foci of fibrinoid necrosis on the surface of the villi; necrobiosis, necrosis and desquamation of the cubic epithelium of the villi.When staining with the OCG method, numerous orange-red and red fibrin thrombi were seen in the capillaries and arterioles against the background of pronounced plethora;

– a day or more after receiving a severe TBI, a pronounced venous congestion with symptoms of fibrinoid swelling and “sticking” of villi, fibrinoid necrosis both in the stroma of the villi and in the walls of blood vessels with the development of secondary angionecrotic hemorrhages was determined;

– 3-4 days or more after the injury, the phenomena of reparation were noted – regeneration of the choroidal epithelium, focal restoration of blood flow in the microvasculature of the villi, proliferation of fibroblastic elements in the stroma.

It can be assumed that rapidly developing pronounced disorders of hemodynamics and hemorheology in the choroid plexuses of the cerebral ventricles with symptoms of fibrinoid necrosis and diffuse thrombus formation are one of the main causes of rapidly progressive cerebral edema due to complete or partial block of hemolytic dynamics. This can serve as an explanation for intractable traumatic edema and swelling of the brain even in cases of successful evacuation of an intracranial hematoma and hemostasis of damaged meningeal or parenchmatous vessels.

The collection of vascular plexuses at autopsy and their histological examination are not difficult. Developing discir-

Culatory destructive changes in SSGM can serve as a morphological marker of TBI even before the development of gross destructive changes in the brain substance. This makes it possible to judge the role of the CSF circulation system in the pathogenesis of traumatic brain injury as additional expert criteria for the complex mechanism of brain damage.

It should be noted that in the subacute period of TBI (4-7 days and later), changes in the CCM most clearly characterize the state of cerebral circulation, especially at the level of the microvasculature. At this time, traumatic injuries are organized in the damaged areas of the pia mater and the brain substance, exudative, then productive inflammation, proliferation of granulation tissue with symptoms of hemosiderosis and neoplasm of blood vessels are noted, which can visually distort the morphological state of the bloodstream.In the substance of the brain outside the zone of traumatic injury, blood vessels are unevenly located, and falling into the field of view with light microscopy, they cannot always be a source of information about the state of cerebral blood flow.

At the same time, fragments of the SSGM taken for microscopic examination are represented by numerous vessels in different sections of the microvasculature. As a rule, there are no traumatic or gross inflammatory changes here; therefore, the microscopic picture fully characterizes not only the state of cerebral blood flow at the microcirculatory level, but also the state of the cerebrospinal system – changes in the stroma and epithelium of choroid villi and villi (necrosis, desquamation, regeneration, as well as sclerosis and stromal fibrosis).

PRACTICAL RECOMMENDATIONS

Evaluation of the results of the study made it possible to draw up a diagnostic table that enables a forensic expert to determine the prescription of TBI by the nature of fibrin pathomorphosis.

# # p / p Duration of TBI Changes in lesions Pathomorphosis of fibrin in the staining of OCG Changes in SSGM

1. minutes Anemia, angiospasm, hemorrhages from unchanged erythrocytes Fibrin is not determined Bloodlessness, angiospasm, swelling of the villous stroma.Choroidal epithelium is not changed

2. tens of minutes -1 hour Polymorphism of vascular reactions. Stasis and sludge of erythrocytes, plasmorrhage. Fibrin is bright yellow in the form of small lumps in the lumen and in the vessel wall, sometimes perivascular. Reactive hyperemia, swelling of the villous stroma. Swelling, focal desquamation of the epithelium.

3.2-6 hours Reactive venous hyperemia, focal venous thrombosis. Lysis of erythrocytes, migration of leukocytes to the area of ​​injury. Fibrin is yellow-orange, forms blood clots in vessels of various sizes.Large lumps in the foci of hemorrhage. Reactive hyperemia, stasis and sludge. Necrosis and desquamation of the epithelium. Multiple blood clots from young fibrin in the vessels.

4. 6-24 hours Stagnant venous congestion, multiple blood clots in the lumen of the vessels. Lysis of erythrocytes, abundant leukocyte infiltration. Fibrin in the form of thin individual fibers. Fibrin orange-red, then bright red, then violet-red in blood clots and foci of hemorrhage Diffuse thrombosis of the vascular bed of the SSGM.Villous necrosis. Blood clots of red and purple fibrin in the vessels and in the stroma of the villi.

5. 24-72 hours Congestion, thrombosis, secondary hemorrhages. Fibrin in the form of annular and coarse-mesh conglomerates, with leukocyte lysis and the beginning of resorption by macrophages. Fibrin conglomerates of gray-violet and gray-blue color, fragmentation of fibrin conglomerates Widespread necrosis of villi and non-scaphoid part; clumping of villi, secondary hemorrhage.

6.4 and more days Lysis of erythrocytes and fibrin, cleansing of lesions of damage by tissue macrophages.Repair, the beginning of the formation of scar tissue. Fragmentation, lysis and resorption of fibrin. Recanalization of blood clots. Normalization of blood flow. Regeneration of the choroidal epithelium. Restoration of blood flow. Recanalization of blood clots. Fibrin is not detected

CONCLUSIONS:

1. Comprehensive morphological assessment of cerebral hemorrhages in closed blunt traumatic brain injury, based on the study of pathomorphological local changes in the lesions, pathomorphosis of fibrin and the nature of structural transformations of the choroid plexus allows you to determine the duration of the formation of brain damage.

2. In the morphogenesis of the formation of cerebral hemorrhages in closed blunt traumatic brain injury, in addition to direct mechanical action, local and generalized circulatory disorders in combination with changes in the hemostasis system play an important role, which is accompanied by consistently developing phenomena of vascular anemia, followed by reactive plethora. thrombosis, necrosis of the vascular wall, with the formation of secondary hemorrhages and the gradual development of reparative processes.

3. Morphological diagnosis of the age of fibrin formation in the area of ​​cerebral hemorrhage in closed blunt traumatic brain injury is based on the assessment of the stages of development of the DIC, represented by transformations of true and mixed microthrombi.

4. Age-related dynamics of extravascular fibrin and fibrin microthrombi is revealed by a specific selective color “orange-red-blue” and fully corresponds to the stages of development of DIC.

5.Fibrin appears simultaneously in the lumen of blood vessels, in the wall of blood vessels and in foci of hemorrhage, which is associated with the perfusion of blood plasma containing protein structures – precursors of fibrin.

6. With a closed blunt traumatic brain injury in the vascular plexuses of the brain, pronounced hemodynamic and hemorheological disorders develop, accompanied by plethora, thrombosis, desquamation of the choroidal epithelium, villous necrosis and secondary hemorrhages, which should be considered from the brain substance as one of the causes of progressive the brain due to the emerging disorders of hemolikvorodynamics.

7. To solve the problems of pathomorphological diagnostics of the prescription of cerebral hemorrhage formation in closed blunt traumatic brain injury, a differential diagnostic table of morphological changes in the area of ​​damage to the brain substance, choroid plexus and the nature of fibrin transformations is proposed, the use of data of which will make it possible to objectify the expert’s conclusions and increase the quality of forensic medical examinations.

The following works have been published on the topic of the thesis.

1. Using the method of selective fibrin staining to determine the duration of brain damage in acute traumatic brain injury. // Siberian Medical Review, – 2008, № 6.

2. On the role of the vascular plexus of the brain in the pathogenesis of acute vasogenic edema. // Topical issues of theory and practice of forensic medical examination. Issue 6. – Krasnoyarsk, 2008.

3. Pathomorphological changes in the vascular plexuses of the brain in acute traumatic brain injury.// Topical issues of theory and practice of forensic medical examination. Issue 6.-Krasnoyarsk, 2008.

4. Pathomorphological characteristics of changes in the vascular plexuses of the brain in acute traumatic brain injury. // Medicine in Kuzbass. Topical issues of medicine. State-of-the-art care in a multidisciplinary hospital. Special issue No. 3. – Novokuznetsk, 2008 – p. 4243.

5. Changes in the microvasculature of the vascular plexuses of the brain in acute traumatic brain injury.// Topical issues of modern pathology. Collection of scientific papers of the All-Russian jubilee scientific and practical conference of pathologists with international participation to the 100th anniversary of prof. P.G. Podzolkova. -Krasnoyarsk, 2008 – p. 223-225.

KOSHAK Konstantin Vyacheslavovich

DYNAMICS OF MORPHOLOGICAL CHANGES OF FIBRIN IN THE PULS AND SUBSTANCE OF THE BRAIN IN ACUTE CRANIAL INJURY

14.00.15 – pathological anatomy 14.00.24 – forensic medicine

Abstract of dissertation for the degree of candidate of medical sciences

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