If the fertilized egg implants itself in any area other than the Uterus, it cannot survive. This ensures that the fetus will die, and places the pregnant women at great risk of dying, herself, if not immediately attended to. This condition is the leading cause of maternal death in the first trimester of pregnancy, usually from a fallopian tube rupture associated with excessive bleeding into the abdominal cavity. Additionally, an Ectopic pregnancy may damage the fallopian tube, which can impair a women’s ability to become pregnant in the future. It occurs most frequently in women from 35 to 44 yrs. of age. Seven to thirteen percent of those who sustain an Ectopic pregnancy will remain infertile.

Ninety-nine percent of the Ectopic pregnancies occur in one of the fallopian tubes. Only 1 % occur in the abdominal cavity.

Women, who are at risk for having an Ectopic pregnancy include the following:

1.) Having a history of a previous Ectopic pregnancy.

2.) Having a history of Pelvic Inflammatory disease-
Fallopian tube scarring from this disease process may make
It difficult for the fertilized egg to negotiate the passage
down the tube to the Uterus, setting the stage for a Fallopian
Tube Pregnancy.

3.) Endometriosis

4.) Using an IUD (progesterone Intrauterine device).

5.) Cigarette smoking -slightly increases the risk.

6.) Vaginal douching

7.) Being born to a mother, who took DES (diethyl-
stilbestrol during pregnancy.

8.) Sterility surgery or medications.

9.) Fertility medications.

MECHANISM

If the mucosal lining of the Fallopian tube is disrupted by inflammation, infection or trauma, then the resulting scar tissue will impede the fertilized egg from traversing the tube into the Uterus. Tubal diverticula’s may trap the egg. Since the egg is propelled by myo-electric forces, which are governed by hormones, many fertility hormonal manipulations may predispose the egg to traverse the Fallopian tube in a less then expeditious fashion. This could be the etiology in women approaching menopause. Therefore, with either diminished pulsation or impediments in its traverse, the fertilized egg will, perforce, become trapped in the Fallopian tube and attempt to take up residence in this less than favorable environment. It’s will outgrow this domicile and rupture, often involving the blood vessels, and unrestrained hemorrhage will ensue resulting in the individual exsanguinations.

DIAGNOSIS

The “classic ectopic triad” of abdominal or pelvic pain, cessation of the usual menstrual pattern (amenorrhea) and vaginal spotting or bleeding occurs in 50% of the cases. This usually occurs once the Ectopic mass had ruptured. Nowadays, people present to the Emergency Room earlier, and than they may be relatively asymptomatic. They may complain only of abnormal menses pattern, and a perception of a spontaneous pregnancy loss. Or their abdominal pain may be atypical.

Physical examination may elicit exquisite tenderness of the abdomen on abdominal and vaginal examination, especially on motion of the cervix. Before rupture, this tenderness may not be present. There may be a palpable pelvic mass posterior or lateral to the uterus, which may be mildly enlarged. However, the patient may be too tender and in too much pain to perform a thorough exam.

So a healthy suspicion, bolstered by a history of someone, who is at risk of an Ectopic pregnancy is often necessary. There is no pathognomonic (irrefutable) pain for the diagnosis of Ectopic pregnancy. Only 50% will be diagnosed by history and physical alone.

Nowadays, once suspected by the history and physical examination, with the high sensitivity and specificity of radioimmunological assay of beta-HCG (to determine the presence of pregnancy) and the availability of high resolution sonography using vaginal probes, the diagnosis of Ectopic pregnancies has improved considerably.

The major ultrasound signs of it’s presence are Uterine vacuity, peritoneal liquid and latero-uterine masses. The beta-HCG is accurate above 1,500 to 2,000UI/L. The diagnosis can be uncertain below the discriminative zone mentioned above. Other laboratory markers, suggestive of pregnancy, are progesterone, creatine kinas, VEGF and CA 125. With the doubling time of the quantity of bHCG constant for the first 6 to 8 wks. of gestation, it’s possible to differentiate between an Ectopic pregnancy and an Intrauterine pregnancy by several methods.

Uterine curettage may be attempted when a pregnancy has been confirmed, but the location has not been confirmed by ultrasonography. Once tissue is removed from the uterine cavity, it must be tested to confirm the presence of Chorionic villi, from a budding placenta. This can be done in the operating suite by adding the tissue to saline, where it characteristically floats, in contradistinction to decidual tissue (normal uterine lining) will sink. The Chorionic villi are also identifiable by their characteristic lacy frond appearance. A dissecting microscope is often then used for this purpose. Or alternately, a frozen section may be submitted for identification. If the patient can be followed without fear of impending fallopian tube rupture, serial bHCG levels can be followed and will decrease by >15% within 12 to 24 hrs. If not, or the levels plateau or continue to rise–the rush is on to identify the presence of extra uterine trophoblastic tissue.

TREATMENT

The main thrust in diagnosing an Ectopic pregnancy is to achieve Hemostasis (cessation of any bleeding). Then, attention is turned to the fallopian tube, in the hopes of terminating the pregnancy, before there is any rupture or irreparable damage. Such damage could lessen the chances of future Intrauterine pregnancies, while enhancing the possibility of recurrent Ectopic pregnancies. If the patient is hemodynamically unstable, surgery should be done immediately.

Traditionally, it was Surgery, which was the treatment of choice. Surgical excision of a tubular ectopic pregnancy is done by
laparoscope’s, nowadays, in preference to laparotomy, which is reserved for hemoperitoneum (hemorrhage). Laparoscopy is the gold standard for the diagnosis of ectopic pregnancy. Generally, the fallopian tubes are easily recognized and any distortion, as by a gestational mass, identified. Then the lesion can be removed through several small openings in the stomach wall, facilitating early healing.

Recently, medical management of uncomplicated Ectopic Pregnancies has become popular. Methotrexate, an anticancer drug, which will stop the growth of placental cells has been used to cause death of the ectopic growth. This results in a miscarriage. However, it must be monitored with rigorous surveillance.

Because some women spontaneously absorb the Ectopic pregnancy, closely following the patient with ultrasounds and serial bHCG studies may be attempted with occasional success.

References:

Acta Obstet Gynecol Scand 1982;61(2):107-11
J Reprod Med 2002 Dec;47(12):1047-9
West Indian Med J 2002 Dec;51(4):257-9
Emerg Med Clin North Am 2003 Feb;21(1):61-72,vi
Rev Prat 2002 Oct 15;52(16):1758-9;1781-4
Am J Obstet Gynecol 2003 May;188(5):1192-4

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OSTEOPOROSIS

Osteoporosis: A disease characterized by low bone mass and micro architectural deterioration of bone tissue leading to enhanced bone fragility and a con- sequent increase in fracture incidence. Bone srength reflects the integration of bone density and bone quality.

SUMMARY: Osteoporosis is very common, especially in postmenopausal females and in the elderly of both sexes. It is asymptomatic in it’s early stages and when symptomatic, as with the development of bone fractures, it is well advanced. Poor lifestyles, such as inactivity, poor nutrition, little sunlight exposure and smoking may potentiate the genetically predisposed (white and Asian females) to this malady. Testing for those at risk is helpful and principally revolves around measuring and monitoring bone mass density (BMD). Treatment mandates changes in lifestyle and the recent addition of medication has dramatically lessened the prevalence of low trauma fractures.

Osteoporosis has reached epidemic proportions in the United States, affecting approximately 25 million people, principally women. By age 70, more than 30% of women have osteoporosis. But it is rare in blacks. The white and Asian population have the higher incidence.

Bone mass density usually peaks between the ages 25 and 35. It begins to decline after the age of 35, and in women, this decline is accelerated during the postmenopausal years. The bone mass may decline, in women after menopause, by as much as 3 to 7 percent per year for up to 7 years. Then the bone loss slows up to 1 to 2 percent a year as it does with men. The epidemiology of fractures follows similar trends as the loss of bone density. Fractures of the distal radius increase in frequency before age 50 and plateau by age 60, with onlay a modest age-related increase thereafter.

In general, bone loss associated with age is thought to be related to calcium deficiency. This results in subtle secondary hyper-parathyroid. With the associated skin aging and decreased exposure to sunlight, there is less Vitamin D mobilization and Vitamin D levels fall. This culminates in less absorption of Calcium from the intestine. Additionally, most older adults do not ingest adequate amounts of Vitamin D and Calcium in their diet, aggravating this condition.

Women, in addition, undergo increased absorption of bone, in the immediate postmenopausal years. This is thought to result from increased interleukin and cytokine activity caused by the loss of estrogen.

SYMPTOMS

Generally, Osteoporosis is asymptomatic in the early stages, while the bone mass is still generous. But later, as the bone mass declines, individuals begin to present with fractures of the vertebral column, hips, and forearms. This contributes to extensive disability and increased mortality. Elderly ladies
don’t always slip and fall and break their hips, more often they turn their osteoporotic hip joint as cant and it breaks, and then they fall. Perhaps that’s the reason hip fracture frequency doubles every 5 years after 70, while distal radius fractures increase more modestly; the manner in which the hip fracture patient falls is different than that of the, outstretched hand fall, of the younger osteoporotic. The spinal vertebral compression fractures often occurs with minimal trauma, such as bending, lifting or even coughing. Forearm fractures, from minor falls, may be a sign of osteoporosis.

PHYSICAL FINDINGS

Often, the patient will present with back pain and disability, and with a high index of suspicion on the physician’s part, judging from the patient’s sex, age, general health, smoking habits, etc, an X-ray may be ordered which shows the collapsed vertebrae. Not all compression fractures are acutely symptomatic and the patient may not seek medical attention acutely.

Rapid loss of height and the onset of kyphosis over the years (Dowager’s hump) may be a clue to progression of Osteoporosis. Sometimes, serendipitously, the diagnosis is made from X-rays of other parts of the body, such as a chest X-ray, revealing a loss of bone mass (Osteopenia) and Osteoporosis or even a compression fracture, which was unsuspected.

LABORATORY TESTS

It would be most advantageous to identify those individuals who are at greatest risk of developing Osteoporosis as early as possible, since it is asymptomatic until late in the process and it’s usual mode of revealing itself is so devastating (fractures, disability, pain, etc.). Therefore, presently those with identifiable risk factors may be subjected to bone density studies, such as the Bone mass density test (the gold standard) or the dual-energy absorptiometry test (DXA). The National Osteoporosis Foundation Guidelines for BMD measurement include those with Estrogen deficiency, Osteopenia on X-ray, long-term glucocorticoid therapy, asymptomatic primary hyperparathyroid9sm, and low-trauma fractures.

Bone Density: Osteoporosis is defined operationally as a bone density that
Falls 2.5 standard deviations (SD) below the normal. (Known as a T-score
of -2.5. Those who fall at the lower end of the young normal range ( a T-
score of >1 SD below the mean) have low bone density and are
considered to be at increased risk of osteoporosis. This test may be used
to monitor the treatment of Osteoporosis. It is recommended that BMD
Testing be done at least 12 to 18 months apart.

Other studies include; Complete blood count, Urinalysis, Serum calcium,
Phosphorus, Alkaline phosphates, Live function tests, Thyroid panel Serum
Creatinine, BUN, Testosterone, 25-Hydroxyvitamin D level.

MECHANISM OF PATHOPHYSIOLOGY OF OSTEOPOROSIS

Bone loss is due to normal age-related changes in bone remodeling, which is additionally influenced by intrinsic and extrinsic factors. Modeling occurs by apposition of new bone tissue on the outer surfaces of the cortex. Factors that determine the peak skeletal mass and density are many. Genetic factors are the main determinant. Nutrition and lifestyle also play an important role. Increased sex hormone production at puberty is required for maximum skeletal maturation.

Once the peak skeletal mass has been attained, remodeling becomes the principle metabolic activity of the skeleton. Remodeling serves to repair the micro damage within the skeleton, to maintain skeletal strength and to supply Calcium from the skeleton, when asked, to maintain serum Calcium. The end result is that this remodeling process replaces lost bone with an equal amount of new bone and the skeletal mass stays constant. Hormones, Vit. D, nutrition all play a role in regulating this process. This process is in balance until 35 to 40 yr. of age. After that, bone loss exceeds bone formation, although it’s rate and magnitude differs between individuals.

RISK FACTORS FOR OSTEOPOROSIS

Modifiable Nonmodifiable

Alcohol Age
Smoking Gender
Nutrition Early menopause
Exercise Genetics (family history)
Medications Race/ethnic background

DIFFERENTIAL DIAGNOSIS

The most common variety of Osteoporosis is secondary to postmenopause, which becomes clinically evident 15 to 20 years after the menopause in women. Men and women are susceptible to Osteoporosis when they age older than 70 yrs. with the female-to-male ratio of 2 to 3 : 1.

Secondasry Osteoporosis occurs more commonly in Men and may be secondary to hypogonadism, postgastrectomy status, glucocorticoid use, and alcoholism.

TREATMENT

Hopefully the individual at risk can be identified early, before symptoms develop, in an effort to reduce further bone loss and increase bone density to prevent fractures. Then lifestyle changes can be made, such as increasing activity and exercise, and cessation of smoking. The inclusion of adequate Calcium and Vitamin D in the diet are necessary. Current recommendations are for 1500 mg/day of elemental Calcium for postmenopausal women and men over age 65. Vitamin D requirements are between 400 and 800 IU/day.

Medications to treat primary Osteoporosis are directed at both increasing the BMD and the bone quality. They are:

Estrogen and Estrogen/progesterone combinations: This regime in Post-Menapausal females was initially considered the treatment of choice, and it worked fairly well. However, recently, the finding of breast and uterine cancer increase with these regimes, had dampened the enthusiasm for this approach. The unfavorable benefit/risk ratio has encouraged other forms of treatment. Studies are still underway, evaluating these medications.

Calcitonin: This substance derived from salmon, initially, and now produced synthetically has been associated with a decrease in bone resorption. It is approved only for the treatment of postmenopausal osteoporosis, not prevention It’s availability via nasal spray, has greatly increased it’s popularity. Calcimar is available by injection and Miacalcin is the spray variety. This category has shown efficacy in the spine, but not the hip.

SERM:(Selective estrogen receptor modulators): These are substances that produce tissue-specific erstrogen-like effects on bone without influencing the uterus or breast. They are approved for osteoporosisi prevention in women. They prevent bone loss associated with postmenopause. Evista (Raloxifene) is one of the more prominent members of this category.

Biphosphonates: There are substances which inhibit the action of osteoclasts, whose job it is, to break down bone. There Bisphosphonates decrease bone resorption. Foamex (Alendronate) is approved for both prevention and treatment of osteoporosis. It has been reported to be associated with a 48% reduction in vertebral fracture rate. This category has been especially beneficial in Corticoid-caused osteoporosis.

PTH: Parathyroid Hormone acts an an anti resorptive agent and thusly has been found to cause a decrease in bone remodeling and an increase in the BMD as well as the quality of the bone. It is considered anabolic therapy.

References:

1.)Dawson-Hughes B, Harris SS, Krall EA, et al:
N Engl J Med 1997; 337:670-676.

2.)Endocrinology and Metabolism XIII

3.)Eastell RD: Treatment of postmenopausal osteoporosis.
N Engl J Med 338:736, 1998

4.)Prestwood KM, Kenny AM: Osteoporosis: pathogenesis,
Diagnosis, and gtreatment in older adults. Clin Geriatr
Med 1998; 14:577-599

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SAMUEL E. GREENBERG, M.D.

OSTEOPOROSIS

Osteoporosis: A disease characterized by low bone mass and micro architectural deterioration of bone tissue leading to enhanced bone fragility and a con- sequent increase in fracture incidence. Bone srength reflects the integration of bone density and bone quality.

SUMMARY: Osteoporosis is very common, especially in postmenopausal females and in the elderly of both sexes. It is asymptomatic in it’s early stages and when symptomatic, as with the development of bone fractures, it is well advanced. Poor lifestyles, such as inactivity, poor nutrition, little sunlight exposure and smoking may potentiate the genetically predisposed (white and Asian females) to this malady. Testing for those at risk is helpful and principally revolves around measuring and monitoring bone mass density (BMD). Treatment mandates changes in lifestyle and the recent addition of medication has dramatically lessened the prevalence of low trauma fractures.

Osteoporosis has reached epidemic proportions in the United States, affecting approximately 25 million people, principally women. By age 70, more than 30% of women have osteoporosis. But it is rare in blacks. The white and Asian population have the higher incidence.

Bone mass density usually peaks between the ages 25 and 35. It begins to decline after the age of 35, and in women, this decline is accelerated during the postmenopausal years. The bone mass may decline, in women after menopause, by as much as 3 to 7 percent per year for up to 7 years. Then the bone loss slows up to 1 to 2 percent a year as it does with men. The epidemiology of fractures follows similar trends as the loss of bone density. Fractures of the distal radius increase in frequency before age 50 and plateau by age 60, with onlay a modest age-related increase thereafter.

In general, bone loss associated with age is thought to be related to calcium deficiency. This results in subtle secondary hyper-parathyroid. With the associated skin aging and decreased exposure to sunlight, there is less Vitamin D mobilization and Vitamin D levels fall. This culminates in less absorption of Calcium from the intestine. Additionally, most older adults do not ingest adequate amounts of Vitamin D and Calcium in their diet, aggravating this condition.

Women, in addition, undergo increased absorption of bone, in the immediate postmenopausal years. This is thought to result from increased interleukin and cytokine activity caused by the loss of estrogen.

SYMPTOMS

Generally, Osteoporosis is asymptomatic in the early stages, while the bone mass is still generous. But later, as the bone mass declines, individuals begin to present with fractures of the vertebral column, hips, and forearms. This contributes to extensive disability and increased mortality. Elderly ladies
don’t always slip and fall and break their hips, more often they turn their osteoporotic hip joint as cant and it breaks, and then they fall. Perhaps that’s the reason hip fracture frequency doubles every 5 years after 70, while distal radius fractures increase more modestly; the manner in which the hip fracture patient falls is different than that of the, outstretched hand fall, of the younger osteoporotic. The spinal vertebral compression fractures often occurs with minimal trauma, such as bending, lifting or even coughing. Forearm fractures, from minor falls, may be a sign of osteoporosis.

PHYSICAL FINDINGS

Often, the patient will present with back pain and disability, and with a high index of suspicion on the physician’s part, judging from the patient’s sex, age, general health, smoking habits, etc, an X-ray may be ordered which shows the collapsed vertebrae. Not all compression fractures are acutely symptomatic and the patient may not seek medical attention acutely.

Rapid loss of height and the onset of kyphosis over the years (Dowager’s hump) may be a clue to progression of Osteoporosis. Sometimes, serendipitously, the diagnosis is made from X-rays of other parts of the body, such as a chest X-ray, revealing a loss of bone mass (Osteopenia) and Osteoporosis or even a compression fracture, which was unsuspected.

LABORATORY TESTS

It would be most advantageous to identify those individuals who are at greatest risk of developing Osteoporosis as early as possible, since it is asymptomatic until late in the process and it’s usual mode of revealing itself is so devastating (fractures, disability, pain, etc.). Therefore, presently those with identifiable risk factors may be subjected to bone density studies, such as the Bone mass density test (the gold standard) or the dual-energy absorptiometry test (DXA). The National Osteoporosis Foundation Guidelines for BMD measurement include those with Estrogen deficiency, Osteopenia on X-ray, long-term glucocorticoid therapy, asymptomatic primary hyperparathyroid9sm, and low-trauma fractures.

Bone Density: Osteoporosis is defined operationally as a bone density that
Falls 2.5 standard deviations (SD) below the normal. (Known as a T-score
of -2.5. Those who fall at the lower end of the young normal range ( a T-
score of >1 SD below the mean) have low bone density and are
considered to be at increased risk of osteoporosis. This test may be used
to monitor the treatment of Osteoporosis. It is recommended that BMD
Testing be done at least 12 to 18 months apart.

Other studies include; Complete blood count, Urinalysis, Serum calcium,
Phosphorus, Alkaline phosphates, Live function tests, Thyroid panel Serum
Creatinine, BUN, Testosterone, 25-Hydroxyvitamin D level.

MECHANISM OF PATHOPHYSIOLOGY OF OSTEOPOROSIS

Bone loss is due to normal age-related changes in bone remodeling, which is additionally influenced by intrinsic and extrinsic factors. Modeling occurs by apposition of new bone tissue on the outer surfaces of the cortex. Factors that determine the peak skeletal mass and density are many. Genetic factors are the main determinant. Nutrition and lifestyle also play an important role. Increased sex hormone production at puberty is required for maximum skeletal maturation.

Once the peak skeletal mass has been attained, remodeling becomes the principle metabolic activity of the skeleton. Remodeling serves to repair the micro damage within the skeleton, to maintain skeletal strength and to supply Calcium from the skeleton, when asked, to maintain serum Calcium. The end result is that this remodeling process replaces lost bone with an equal amount of new bone and the skeletal mass stays constant. Hormones, Vit. D, nutrition all play a role in regulating this process. This process is in balance until 35 to 40 yr. of age. After that, bone loss exceeds bone formation, although it’s rate and magnitude differs between individuals.

RISK FACTORS FOR OSTEOPOROSIS

Modifiable Nonmodifiable

Alcohol Age
Smoking Gender
Nutrition Early menopause
Exercise Genetics (family history)
Medications Race/ethnic background

DIFFERENTIAL DIAGNOSIS

The most common variety of Osteoporosis is secondary to postmenopause, which becomes clinically evident 15 to 20 years after the menopause in women. Men and women are susceptible to Osteoporosis when they age older than 70 yrs. with the female-to-male ratio of 2 to 3 : 1.

Secondasry Osteoporosis occurs more commonly in Men and may be secondary to hypogonadism, postgastrectomy status, glucocorticoid use, and alcoholism.

TREATMENT

Hopefully the individual at risk can be identified early, before symptoms develop, in an effort to reduce further bone loss and increase bone density to prevent fractures. Then lifestyle changes can be made, such as increasing activity and exercise, and cessation of smoking. The inclusion of adequate Calcium and Vitamin D in the diet are necessary. Current recommendations are for 1500 mg/day of elemental Calcium for postmenopausal women and men over age 65. Vitamin D requirements are between 400 and 800 IU/day.

Medications to treat primary Osteoporosis are directed at both increasing the BMD and the bone quality. They are:

Estrogen and Estrogen/progesterone combinations: This regime in Post-Menapausal females was initially considered the treatment of choice, and it worked fairly well. However, recently, the finding of breast and uterine cancer increase with these regimes, had dampened the enthusiasm for this approach. The unfavorable benefit/risk ratio has encouraged other forms of treatment. Studies are still underway, evaluating these medications.

Calcitonin: This substance derived from salmon, initially, and now produced synthetically has been associated with a decrease in bone resorption. It is approved only for the treatment of postmenopausal osteoporosis, not prevention It’s availability via nasal spray, has greatly increased it’s popularity. Calcimar is available by injection and Miacalcin is the spray variety. This category has shown efficacy in the spine, but not the hip.

SERM Selective estrogen receptor modulators): These are substances that produce tissue-specific erstrogen-like effects on bone without influencing the uterus or breast. They are approved for osteoporosisi prevention in women. They prevent bone loss associated with postmenopause. Evista (Raloxifene) is one of the more prominent members of this category.

Biphosphonates: There are substances which inhibit the action of osteoclasts, whose job it is, to break down bone. There Bisphosphonates decrease bone resorption. Foamex (Alendronate) is approved for both prevention and treatment of osteoporosis. It has been reported to be associated with a 48% reduction in vertebral fracture rate. This category has been especially beneficial in Corticoid-caused osteoporosis.

PTH: Parathyroid Hormone acts an an anti resorptive agent and thusly has been found to cause a decrease in bone remodeling and an increase in the BMD as well as the quality of the bone. It is considered anabolic therapy.

References:

1.)Dawson-Hughes B, Harris SS, Krall EA, et al:
N Engl J Med 1997; 337:670-676.

2.)Endocrinology and Metabolism XIII

3.)Eastell RD: Treatment of postmenopausal osteoporosis.
N Engl J Med 338:736, 1998

4.)Prestwood KM, Kenny AM: Osteoporosis: pathogenesis,
Diagnosis, and gtreatment in older adults. Clin Geriatr
Med 1998; 14:577-599

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Do you have a topic you would like to see discussed by our doctors in a future article? If so, give us your suggestions below and we will do our best to discuss the most frequently asked topics in future articles.

Despite the great advances in medicine, breast cancer remains for the most part an unpreventable disease, and is the most common cancer in women. The majority of women with breast cancer indeed are cured of their disease; nonetheless, breast cancer is only secondary to lung cancer among the causes of deaths from malignancy in American women. Recent advances, particularly early detection, have improved survival in women with breast cancer.

Breast cancers typically are detected in one or more of three ways: examination by a physician or other person, by breast self-examination, and since the late 1960’s, by mammography – X-ray examination of the breasts. Of these, only mammography has definitively been demonstrated to make an improvement in the cure rate of the disease, presumably because of earlier discovery.

Mammography

Current recommendations for “screening mammography” [performing the examination when there is nothing known to be abnormal in the breast] in women without high risk of breast cancer include a “baseline” mammogram between ages 35 and 40, and annual mammography screening starting at age 40. How long this should continue late into life is somewhat controversial; it is this surgeon’s opinion, and that of many other physicians, that annual screening should continue as long as a woman remains in generally good health. In special high-risk instances, such as when close family members have had breast cancer, the initiation of screening might well start at an earlier age.

It is most important that mammography be performed at a facility that is accredited by the American College of Radiology. Interpreting mammograms requires considerable skill, and should be done by a physician who is board certified or board eligible in radiology (the field of interpreting X-rays and other imaging studies).

Mammograms are relatively inexpensive; modest discomfort at most can be expected during the procedure. Most studies obviously are normal, but a suspicious finding on mammography does not mean breast cancer – it merely is the proper result of the screening examination, indeed the very purpose of doing the study. Of necessity, radiologists must call attention to all potentially significant abnormalities on mammography X-rays; far less than half eventually turn out to be cancer.

Mammography is not perfect. Some 8 to 12 percent of cancers simply are not detectable by X-ray. If an abnormality is found on a mammogram, the radiologist may recommend biopsy, request additional X-ray views, or recommend close follow-up, with a repeat study in perhaps three to six months. An ultrasound study may be requested to see if the lesion is a cyst (fluid filled); if so, it likely is not of concern. When biopsy is recommended, several options are available: the most common method when a breast lesion cannot be felt is to do a needle-directed biopsy, whereby the radiologist marks the lesion with a fine wire, and then subsequently a surgeon takes out the area in question. Other methods of breast biopsy include needle aspiration, and the use of X-ray guided stereotactic methods. These are discussed in the separate article on surgery for breast lumps.

Evaluation of Breast Lumps:

If a woman, or her doctor, husband, or other person finds a lump in her breast, it must be explained – either by its complete disappearance when a needle is placed within it and fluid removed or by its complete surgical removal and subsequent pathological examination (excisional biopsy). When a woman presents with a breast lump the next step often is mammography. The primary purpose of the X-ray in this instance is not the evaluation of the lesion in question, but rather to search for additional undetected lesions. IT IS A GRAVE MISTAKE TO ASSUME THAT A BREAST LUMP IS NOT CANCER BECAUSE THE MAMMOGRAM IS NORMAL.

Many surgeons and other physicians perform an aspiration as the first step in the evaluation of a breast lump, often at the initial office consultation. Using local anesthesia, a needle is placed into the lump. If it is a cyst, it likely will disappear as the fluid is aspirated into the syringe. Unless the fluid is bloody, a woman can be reassured that all is fine. Simple follow-up to be sure that the lump stays resolved is all that is needed.

If the lump proves to be solid on the initial needle aspiration, a sample of the microscopic cells suctioned into the syringe may be sent for microscopic evaluation. This fine needle aspiration cytology can be very helpful; the important thing to remember is that it is definitive only when positive for cancer. If it is negative or indeterminate, it does not mean there is no cancer, although such a negative study can be somewhat reassuring.

The only compete and definitive method of evaluating a breast lump to be sure it is not cancer, other than its disappearance when aspirated, is its complete removal and examination by a pathologist. Anything less is unacceptable, and could result in the potential opportunity to cure cancer being lost.

Common Questions:

What if a lump is found to be a cyst on mammography and/or ultrasound? Cysts are benign – is any further treatment needed? Most authorities agree that if a lump is shown to be a fluid filled cyst by ultrasound study, and it cannot be felt on examination, leaving it alone is safe. If it can be felt, it has to be treated by needle aspiration, or if that fails, by removal.

If a mammogram is consistently normal year after year, do I still need the study every year — after all, Medicare pays for screening only every two years? The reason Medicare reimburses for screening mammography only once every two years is based on financial concerns of the Medicare program, not any scientific study. No one knows the “lead time” necessary to detect cancers before they spread and are less likely to be curable. The one-year standard we have adopted for mammography is somewhat arbitrary. The average breast cancer takes at least three years to grow from a tiny cell division gone awry to the development of invasive cancer. Numerous studies have proven the one-year interval to be safe and cost effective. One has to balance the rate of growth of the cancer versus our ability to detect it, and leave some room to correct the unavoidable errors that occur in any human endeavor.

Treatment of breast cancer is beyond the scope of this short article. With early detection, before a cancer can even be felt, cure is far more likely than when the cancer is not found until it grows large enough to be felt. Further, breast conservation treatment, avoiding the disfigurement of breast removal, is much more likely to be both feasible and successful earlier rather than later, when the lump is larger and treatment options more limited.

Francis C. Evans, MD, FACS

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Cancer is a pervasive part of our society. It affects all ages and each generation has its unique experiences with this menace to our well being. Gastroesophageal cancer is a silent stalker here in the South. More specifically, it is a cancer that develops at the junction between the esophagus, the tube that connects the stomach with the mouth, greater part of their lives and its onset is slow and insidious. Recent statistics and my and the stomach itself. It often preys on patients who use alcohol and tobacco for the own personal experience suggest that this disease may be becoming more ominous and more aggressive that historical controls would indicate.

A typical patient with cancer of the esophagus seeks medical attention because of symptoms of dysphagia or difficulty swallowing and weight loss. The patient maybe unable to swallow solid food but may do OK with liquids. Other patients may find the reverse to be true. Usually the patient feels that he or she is otherwise healthy and has no unusual risk factors or recent illnesses. The duration of symptoms is usually 1 to 6 months and most patients have no history of this type of problem in their family. All are convinced that a pill from their doctor will fix whatever is wrong with them and they will be free to resume their usual activities and bad habits quickly. What are the real facts?

It is well accepted by cancer researchers that cancer of the distal esophagus and proximal stomach (GE junction tumors) are the end result of a multistage process involving an “initiation stage” and a “promotion phase.” The initiation phase begins when a carcinogen (an alkylating agent or chemical irritant) attacks the wall of the esophagus or stomach. This initial damaged area may heal on its own, or if not properly repaired, lead to changes in the underlying cell structure.

The promotion phase occurs as the injured cell structure begins to grow faster than the cells surrounding the damaged area. This early lesion is called an in situ tumor or early tumor localized to a very superficial area of tissue. The following sequence of events seems to follow: Normal tissue leads to hyperplasia or fast growth cell structure and this leads to dysplasia or abnormal cell structure. The next step is in situ or early invasive cancer followed by full blown invasive cancer and then lastly metastasis or spread to other parts of the body. Most cancers in this area historically grow from either the lining of the esophagus (squamous cell) or the lining of the stomach (adenocarcinoma). We are also beginning to see unusual variants of other cell lines all with similar clinical presentations.

Most patients with cancer of the GE junction are in their 60ties. They are usually male and usually have enjoyed tobacco and alcohol for many years. A recent review at Memorial Hospital in New York of 258 patients showed a 27 month overall survival for adenocarcinoma arising from the stomach and a 22 month survival for tumors arising in the esophagus both treated with surgery. Patients treated with radiation or chemotherapy died in 7 months. More malignant types of tumor in this same area called small cell tumors often cause death in 6 months regardless of the type of treatment. If tumors can be discovered in their early phases, the survival rate for all tumor types is much higher with possibility for cures.

On the basis of my experience and published data, if the patient has early signs and symptoms related to swallowing and weight loss problems, the following tests are needed to rule out an early cancer.
A chest x-ray
2.) A CAT scan of the chest and abdomen
3.) An endoscopy in which the surgeon looks down the esophagus with a scope at the area in question and performs a biopsy.
4.) A barium swallow in which the radiologist asks you to swallow barium dye and then takes a series of x-rays to look at the area.
5.) A bronchoscopy which is a test to look at the inside of the airways in the lung with a scope for any evidence of tumor extension into the lung.
6.) An evaluation of the strength of your heart function and breathing capacity.
7.) A bone scan to see if the tumor has spread to your bones.
Assuming that you pass all of the screening tests, then you may be a candidate for surgery and may have an increased hope for cure. Surgery itself is planned to remove all of the known tumor and then to reconnect the lower normal part of the stomach to the mid to upper portion of the remaining esophagus. The surgery sounds ghastly, but actually has worked well, and most patients are able to eat a normal diet and return to their usual activities.

Recommendations

1.) Evaluate all early symptoms of weight loss and difficulty swallowing as soon as you can see your doctor.
2.) The preoperative work-up outlined above can be used as a reference for the tests that you may need during this process.
3.) There is hope for the future with early recognition of the problem and aggressive work-up. Your doctor may ask you to see an Oncologist for recommendations and perhaps a Radiation therapist. If you are a candidate for surgery this remains the gold standard for the best hope for cure. Good luck.

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MYALGIA MYOSITIS RHABDOMYOLYSIS
SUMMARY:
RHABDOMYOLYSIS is a syndrome resulting from destruction of striate(skeletal) muscle cells with leakage of muscle intracellular toxins into the bloodstream, characterized by few symptoms, the most common being myalgia (muscle aches and cramps) and dark urine, and few sentinel laboratory findings, the most specific being a positive dipstick test for blood with few rbcs seen on microscopy, and elevated CK (creatine kinase ) in the blood. It occurs in Trauma situations, such as Crush injuries, where large quantities of muscle are destroyed. More commonly, it develops in situations where moderate to severe exercise occurs, particularly in hot humid climates, in de-conditioned individuals. Renal failure, cardiac arrhythmias, coma and death may develop. Dehydration is especially conducive to serious complication of Rhabdomyolysis. Toxins, illnesses, genetic defects (regarding ATP production) and electrolyte imbalance, are common environments where this syndrome often occurs. First and foremost is the ability to suspect rhabdomyolysis in the appropriate clinical settings. Treatment consists of treatment of the underlying condition, removal of the offending medication or toxin, rest, rehydration, and alkalinazation of the urine. Renal dialysis and treatment of Hyperkalemia may become necessary.)

When skeletal muscle is irritated or inflamed it often becomes sore and tender and the muscles ache. This MYALGIA can occur in a number of conditions. Viral Influenza is one of the more common causes of generalized muscle aches or myalgia. Certain medications, such as Statins, which are used for Hypercholesteremia, are occasionally associated with the onset of myalgia. Myalgia is most often transient, especially in it’s most common form, which is over exercise. It may resolve once the underlying illness has run it’s course, or the offending medication is stopped or simply by rest and hydration.

When myalgia intensifies, it involves the death and destruction of the skeletal muscle cells, called myo-cytes, then MYOSITIS develops. In this instance, substances, which belong within the cytoplasm of the cell, leak out into the blood. Such substances as creatine, myoglobin, aldolase, potassium, and lactate dehydrogenase are extruded into the blood stream. Myoglobin is the form of Hemoglobin found in muscle cells which transfers Oxygen and Carbon Dioxide. Myositis is characterized as exquisite tenderness of the affected muscles and the person may not be able to tolerate even the slightest pressure. The muscles may become swollen and boggy in consistency.

If the myositis is allowed to intensify, then irreversible damage may occur, generally from the muscle swelling, which, in turn, causes compression of vessels and nerves and results in massive dissolution of significant quantities of muscle. Dissolution of the myo-cytes and the subsequent release of large quantities of toxic intracellular components into the systemic circulation and the end organ consequences constitute the syndrome of RHABDOMYOLYSIS.

RHABDOMYOLYSIS may involve many organ systems, but the life threatening consequences are related to electrolyte abnormalities, i.e., acute hyperkalemia, hypocalcemia, and acute renal failure. When muscle is deprived of nutrition and circulation, intracellular-free Calcium is increased to critical levels and this triggers several degradative processes culminating in muscle cell death and in extravasation of intracellular toxins into the systemic circulation. The contraction of the extra cellular fluid volume appears to be the principal determinant of the renal toxicity of myoglobin.

Signs and Symptoms

The symptoms of Rhabdomyolysis are nonspecific and consist of an increase in ventilation, in an effort to blow off acidic CO2, and central nervous system function depression, manifesting itself as headache, lethargy, stupor and even coma, as well as severe
unexplained muscle pain, cramps and weakness. The muscles may be swollen and tender. The most commonly affected muscles are those utilized in exercise. Fever may be present, especially if associated with infections. The extremeties will demonstrate painful decreased range of motion. However, some patients are asymptomatic, necessitating the laboratory workup to suggest the diagnosis. So, it’s important that physician must maintain a high index of suspicion, which generally is tipped off by appropriate history and physical in the clinical situation, reflecting one of the many causes of Rhabdomyolysis.

Laboratory elevation of the CK (Creatine Kinase) is a key to the diagnosis, and is the most sensitive indicator. The CK is usually 5 times or more greater than the normal level and can be greater than 100,000 IU/L. Exercise to near exhaustion, is associated with a CK rise of only about 10,000 IU/L. Still, there is poor correlation between CK elevations and the morphologic degree of muscle damage. Urinalysis, initiated because the urine will darken (often the first clue) with the increased excretion of myoglobin, will demonstrate a positive test for hemoglobin, but the microscopic exam will show only a few red blood cells, suggesting Rhabdomyolysis. Microscopic urine exam may demonstrate “Muddy casts”, which re diagnostic of myoglobin or hemoglobin in the renal tubular fluid.

Once suspected, from the clinical symptoms, the clinical setting, especially the history of the illness, and the initial lab. tests, then measuring the Myoglobin in the urine and serum may confirm the diagnosis. Once the renal threshold for myoglobin is reached, myoglobin is cleared at 75 per cent of the glomerular filtration rate. If there is marked muscle breakdown, the serum myoglobin lever may be elevated.

Abnormal electrolyte findings may trigger off the premonition suggesting Rhabdomyolysis, by he presence of Hypernatremia, Hyperkalemia, Hyperuricemia (secondary to enhanced release of purine precursors), and Lactic acidosis (secondary to glycogen depletion and anaerobic mertabolism).

As the renal status deteriorates, the urine output may fall suggesting oliguric renal failure.

CAUSES OF RHABDOMYOLYSIS

Traumatic damage to large quantities of muscle was recognized during Crush Injuries in the Second World War and the diagnosis of Rhabdomyolysis was anticipated and recognized frequently.

Since then, Non-traumatic causes of Rhabdomyolysis are now recognized as being more frequent than the traumatic causes. It may occur after moderate to severe exercise in otherwise healthy people. This is reported to occur among young unconditioned military recruits, particularly in hot and humid military training. The heat generated during exercises encourages shunting of the blood to the surface for heat dissipation, depriving the kidneys and gastrointestinal tract of blood. This causes deterioration of the gut wall, allowing invasion of intestinal bacteria and bacterial toxins into the blood stream. This transient septicemia in the environment of a contracted body fluid volume can lead to myoglobin-induced renal failure.

Some genetic enzyme deficient conditions are associated with muscle necrosis even after minimal exercise.

Chronic Alcoholics are particularly susceptible to Rhabdomyolysis in certain situations. After binge drinking, there are significant electrolyte concentration changes in he muscle cells causes by direct injury from alcohol. These people often have deficiencies in potassium and phosphorus homeostasis, as well as easy susceptibility to infection, which may intensify the toxic effects of alcohol. In cirrhosis of the liver, phosphorus and potassium are shifted from the blood into the intracellular compartment, rendering the alcoholic more susceptible to rhabdomyolysis.

Recently Rhabdomyolysis has been associated with viral , bacterial and rickettsial Infections. It appears that the these organisms may attack the muscle directly or may lead to muscle-specific toxin generation. It occurs most commonly with influenza virus type A and B. It is seen in HIV patients as a sequelae to acute myositis, especially as part of the febrile illness that precedes seroconversion after infection. Certain bacteria, such as Lenionella species, Streptococcus species, Tularensis and Salmonella species have been incriminated. Several reports confirm the association between Q fever and Rocky Mountain spotted fever, rickettsial infections, to Rhabdomyolysis.

Chronic electrolyte imbalances, such as hypokalemaia and hypophophatemia may precipitate rhabdomyolysis. This has been reported also, in patients who drink excessive quantities of fluid, especially water, lowering their sodium (hyponatremia). Low potassium conditions which may potentiate the possibility of Rhabdomyolysis are seen with chronic administration of long-acting thiazide diuretics, certain antibiotics, and even ingestion of mineral corticoid-like substances, such as licorice. Hypomagnesemia, and even hypernatremia have been incriminated. Diabetic ketoacidosis has been reported to cause Rhabdomyolysis.

Heatstroke has been incriminated, as has hypothermia. This is especially susceptible when the addition of exercise is added. Once again, this appears to be do to shifts in intracellular Calcium and Phosphorus.

Miscellaneous Causes include Cocaine abuse, carbon monoxide poisoning, neuroleptic malignant syndrome, and prolonged coma in a fixed position (Saturday night Palsy).

Another classification of Rhabdomyolysis divides the types into 1.) Pure exertional, 2.) Exertion in those with genetic enzyme deficiencies, and 3.) Exertion in Nonhereditary forms. The first type is the typical heavy exertional type. The second category occurs in those individuals, who have defects in the pathways by which ATP is generated. These defects in the environment of exercise will contribute to Rhabdomyolysis. The third category includes those precipitating factors such as drugs, toxins, or infections, in which, the addition of exercise will cause muscle breakdown. Therefore exercise in patients who are alcoholic or have ingested cocaine (especially if they have an associated potassium and phosphate deficiency) places them at exceptional risk for Rhabdomyolysis.

DIFFERENTIAL DIAGNOSIS

The major physical clue to Rhabdomyolysis is the presence of painful, aching, and tender muscles. But this can also occur in primary muscular disorders, such as: Polymyositis, dermatomyositis, rheumatoid arthritis, fibrositis, polymyalgia rheumaica, tendonitis, localized infection and even with some medications (steroids, diuretics).

The other major clue, i.e., dark brown urine, can be seen in: hemoglobinuria, porphyria, uorbilinogen, medications (nitrofurantoin, priqmaquine, metronidazole, rifampin).

KIDNEY FAILURE

Renal failure appears to occur form the direct toxic effects of the excessive myoglobin. Myoglobin’s toxic effects appear to be enhanced by a diminution in extra cellular fluid volume, which is especially seen in trauma, where large volumes of fluid may extravasate into the lower extremities, resulting in severe ECF volume contraction. Renal failure is one of the most common cause of death in this condition.

Myoglobin, through it’s metabolites, is directly cyto-toxic to the renal cells. The production of oxygen and non-oxygen free radicals, because of the excess of free iron, lead to oxidant stress and injury to the renal cells. There is evidence that the alterations in the intracellular glutathione may contribute to the pathogenesis of pigment-induced renal failure.

Myohemoglobin may form tubular casts in the renal tubules, especially in an acid urine, which, once formed, may cause intra-tubular obstruction and increase in pressure and resultant diminished glomerular filtration rate, aggravating the already ongoing kidney damage.

TREATMENT

Irrespective of the etiology of the breakdown of the muscle cells, Rhabdomyolysis is potentiated if the extra cellular fluid volume is contracted, such that the urine output is diminished. So, the first and most important goal in treatment is to increase the urine output. This is most expeditiously done by giving IV normal saline, from 4 to 6 liters within the first 24 hrs.

Since the nephrotoxic effects of myoglobin are potentiated in an acidic urine setting, giving of Bicarbonate to alkalinize the urine is very beneficial. Maintenance of the urine pH greater than ki6 prevents disassociation of the myoglobin.

Since diuresis of the excessive Myoglobin is one of the goals, the giving of an osmotic diuretic such as Mannitol is very helpful. Lasix also can be given for it, fast diuretic action and it’s acidification of the urine.

Treatment of the underlying condition, such as a Compartment Syndrome, where increased intercompartmental pressure is elevated with deprivation of blood flow and death of tissue, by a fasciotomy is crucial.

Treatment is continued until the urine dipstick is negative for blood, creatinine is normal and the other laboratory tests indicative of Rhabdomyolysis are returned to normal.

COMPLICATIONS

Acute Renal Failure–This is the most serious complication, and may require renal dialysis, hopefully for the short haul, only.

Cardiac Arrhythmias– Because of the electrolyte imbalances commonly encountered, the heart muscle may become irritable and potentially fatal rhythms may ensue. Checking for and treating these imbalances are mandatory.

Disseminated Intravascular Coagulopathy (DIC)–This is a condition combining bleeding and excessive clotting simultaneously, resulting in death of vital organs. It must be anticipated and treated expeditiously and aggressively.

Cardiomyopathy and respiratory failure may ensue.

PREVENTION

Since excessive exercise is the more common culprit in the enviroment of predisposing factors, such as Substance Abuse, genetic enzymatic defects, or de-conditioning, it is wise to recommend gradual increase in exercise activity, particularly in the proper temperature and humidity, and to encourage adequate hydration.

References:

Bobby Adcock;Rhabdomyolysis: XIV Musculoskeletal/Connective Tissue Diseases);

P. Visweswaran M.D., J. Guntupalli, M.D.;Rhabdomyolysis; Critical Care Clinics, Vol 15. No. 2. April 1999, (Pg. 415-427).

Juha P. Kokko:Rhabdomyolysis: IX Critical Care Medicine; Pg. 522-525;

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Transesophageal echocardiography, which physicians call TEE, is a Special form of echocardiography. Echocardiography is the second most commonly ordered test in Cardiology. It utilizes high frequency sound waves which are not audible to the human ear. These sound waves are emitted from a special device called a transducer which is held onto the chest wall next to the heart (transthoracic echocardiography ). Heart tissue reflects these sound waves, and the reflection is recorded onto the screen of an echocardiography machine. With this information, cardiac anatomy, and how this anatomy functions, can bedetected, such as the atrial and ventricular chambers and the cardiacvalves. Blood flow direction and velocity can also be determined from any ofthe valves, and this helps in determining whether or not a valve is abnormal,Sound waves from a transducer held onto the the chest wall are absorbedby skin, fat, bone and lung tissue. Because of this, and In spite of the remarkable advances in the transthoracic method of echocardiography since it was initially developed in the 1950’s, 15% of all echoes do not provide sufficient information for the physician. Consequently, TEE was developed in the 1970’s in order to overcome the limitations of transthoracic echocardiography.

TEE utilizes an especially designed ultrasound transducer that can beswallowed. TEE emits sound waves that reflect off the heart that aregenerated from inside the esophagus, which is next to the heart. None of theimages that are obtained by TEE suffer from the sound interruptions that atransducer on the chest wall shows.

Besides providing echo images where transthoracic echo is notsatisfactory, TEE has been found very useful in locating and determining thefunction of various cardiac structures that cannot be imaged at all with a transthoracic echo.

Some examples of the other information available from TEE include:

1. evaluation of artificial heart valves and valve infection

2. evaluation cardiac anatomy in stroke patients

3. evaluation of tears of the aorta

4. evaluation of congenital heart disease

TEE has been found to be very useful in the emergency department andquickly resolves issues such as the cause of cardiovascular shock whenpatients are too unstable to be sent for tests such as a CT scan or MRI.

Its use in the critical care area is well recognized because it providescardiac images when there are chest bandages present and when patients are on ventilators. Routine echocardiography in the critical care area is frequentlyinadequate for the above reasons. It is used routinely in cardiac surgery to provide monitoring of cardiac function.

TEE for an outpatient is performed with the patient supine and rolled onto his side. Individuals which are usually present include the cardiologist, a nurse and an echo technician who controls the echo machine. The head of thepatient is elevated slightly with a pillow. An intravenous line is started for administration of mild sedation, and the throat is sprayed with an anesthetic. Patients are not put to sleep during this procedure.

During the procedure the EKG is monitored, and blood oxygen is monitored with a finger optical device. A suction tube is available to remove secretions from the throat which usually accumulate. The TEE transducer is a cable about the diameter of an adult’s small finger and is inserted into the esophagus by having the patient swallow when it is placed in the back of the throat. There is usually some initial gagging, but once the transducer is in the correct place to obtain images, the patients become more comfortable.

Breathing is not disturbed; patients can talk; and occasionally watch their own echoes during the procedure. The procedure requires about 10 minutes to perform. If sedation is used patients are observed for one hour after the procedure. Patients are also told not to drink or eat for 2 hours until the throatanesthetic wears off.

Since its inception, TEE has provided a major leap in diagnostice chocardiography, and has become the gold standard of practical ultrasonic cardiac imaging.

** Dr. Frazin holds the proud distinction and honor of inventor of the Transesophegeal Echocargiogram. This incredible accomplishment has literally changed the face of Cardiology and made Dr. Frazin internationally reknown.

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CARDIOMYOPATHY is as the name implies, i.e., pathology of the myocardium, (heart muscle), of the cardia (heart). Initially, it was applied to unknown causes of deteriorating heart muscle function, principally in young, otherwise healthy persons, although, it may also include the old as well. As our knowledge of causes and pathology has improved, there has been a blurring of the distinction between heart muscle malfunction of unknown causes and those of known causes. This classification, exclusively, still focuses on heart muscle abnormalities, in contradistinction to those maladies involving the heart valves, or the covering over the heart (pericardium).

The best classification has revolved around distinct functional or hemodynamic properties. Since most Cardiomyopathies result in Congestive Heart Failure and/or arrhythmias, this classification is of great utility in the treatment of these conditions. Five major forms are recognized: (i) dilated cardiomyopathy, (ii) hypertrophy cardiomyopathy,(iii) restrictive cardiomyopathy, (iv) right ventricular cardiomyopathy and (v) non-classifiable cardiomyopathies with distinct hemodynamic properties. Some of the specific dysfunctions of the heart muscle may overlap in this classification, but the clinical usefulness is still helpful. These functions are expressed as 1.)Dilatation (ventricular enlargement), 2.) Thickness of the heart muscle (Hypertrophy), or 3.) Stiffness of the heart muscle.

Known causes of heart muscle dysfunction, often referred to as Secondary Cardiomyopathies, are also included in categories of Cardiomyopathies. The new World Health Organization’s, World Health Foundation’s (WHO/WHF) definition comprises Inflammatory cardiomyopathy, defined as MYOCARDITIS in association with cardiac muscle dysfunction. Also, Autoimmune, and Infectious forms of cardiomyopathy are recognized. Viral Cardiomyopathy, which may be accompanied by inflammation, has been recognized in some instances. Some cardiomyopathies have a relationship with other organ systems, while still others are hereditary.

The end result of all these different forms of Cardiomyopathies is the worsening of cardiac work. This results, either, from failure of the pump function or from failure of the heart muscle to relax, called ventricular compliance. Hence, the clinical presentation of these Cardiopathies as Congestive Heart Failure. This muscle damage may also interfere with the electrical properties of the heart and result in severe Arrhythmias.

FUNCTIONAL IMPAIRMENT

DILATED CARDIOMYPOATHY

This is a syndrome characterized by a large dilated heart, often accompanied by Congestive Heart Failure. It is frequently referred to as “Congestive Cardiomyopathy”. This is because a dilated heart with stretched cardiac muscle acts like a rubber band, which has been stretched too far and therefore lacks the power to contract. This results in a flabby heart unable to propel the blood forward, i.e., pump failure. The muscle thickness may be normal, increased, or decreased. Most often, the cause of Congested Dilated Cardiomyopathy is elusive and unknown, but it is probably the end result of many forms of heart muscle damage caused by a variety of toxic, metabolic, or infectious agents. Alcohol, pregnancy, hypertension, are a few of the known causes of his syndrome. Once these are ruled out, as well as infection, the syndrome is often referred to as Idiopathic Congestive Cardiomyopathy.

The pathology demonstrates enlargement and dilatation of all four chambers of the heart. The ventricles are more dilated than the atria. Histological examination reveals interstitial and peri- vascular fibrosis in the walls of the ventricles.

The symptoms are those of left ventricular failure, i.e., congestive heart failure. Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and rest dyspnea occur. Fatigue and weakness due to diminished cardiac output are prominent. Physical examination reveals a weak pulse, gallop heart rhythm and in the late stages, swollen feet and a swollen liver, associated with abdominal swelling (Ascites).

Treatment, as the syndrome suggests, is directed in strengthening the heart muscles, diminishing the fluid backup, and relieving the heart muscle of resistance to pump against. So Digitalis, which strengthens the heart muscle; diuretics to promote fluid mobilization, and peripheral vasodilators to decrease peripheral resistance are of great help. Other more recent medications, which facilitate the same goals are being incorporated in the treatment with fair results.

Alcoholic cardiomyopathy is probably the most common cause of congestive dilative cardiomyopathy in the western world.

HYPERTROPHIC CARDIOMYOPATHY

This is a condition where the left ventricular wall is thickened (hypertrophied), and the cavity is perforce small. Hypertension is the most common cause of this form of Cardiomyopathy, but an inheritable form, (IHSS-Idiopathic hypertrophy sub-aortic stenosis) is the originator of this classification. Actually, the wall of the left ventricle may be symmetrically hypertrophied, or the hypertrophy may involve the sub aortic, valvular, or supravalvular areas of the ventricle, or only the septum may be asymmetrically involved (ASH).

The pathological examination reveals a marked increase in myocardial mass, with the ventricular cavities being small. The atria are also often hypertrophied and dilated. Myocardial fiber disarray is seen in the interventricular septum in the IHSS cases.

The clinical symptoms include dyspnea from impaired ventricular filling do to the small cavities and the rapid buildup of pressure do the thickened wall stiffness. Fatigue and syncope, as well as angina pectoris are common. Understandably, exertion tends to exacerbate the symptoms. The physical examination may reveal a prominent chest wall thrust of the thickened heart against the inner chest wall in systole. There is often a systolic heart murmur which may vary in intensity with respiration and can be accentuated by having the patient bear down and strain. This, understandably, increases the peripheral resistance and the heart has to push the blood out harder against this increased pressure, causing the murmur from turbulence of this fast moving blood through the narrow passageway to emit a higher pitched and louder sound.

The EKG and especially, the Echocardiogram have made the diagnosis of all forms of this disorder more easily identifiable. Treatment consists of medication to rest the heart muscle in order to increase the ventricular volume, or the use of medication to decrease peripheral resistance.

RESTRICTIVE CARDIOMYOPATHY

This condition occurs either as an inheritable condition or when a disease state occurs which enables the heart muscle to be infiltrated by the disease pathology. In this condition, the heart muscle becomes stiff and unpliable, such that it cannot relax and therefore the quantity of blood which enters the heart chambers and the force of muscular contractility exerted by the heart muscle are both severely limited, causing poor blood flow. Sarcoidosis and Amyloidosis are examples of disease states which can be associated with this condition.

SUMMARY: Cardiomyopathies refer to diseases or conditions which weaken the heart muscle, either exclusively or in conjunction with other organ involvement. Many of the Cardiomyopathies are from unknown causes. This damage to the heart muscle impairs its function and the blood either backs up into the lungs causing Congestive Heart Failure or is unable to be propelled forward and hypotension ensues. The internal damage to the muscle may interfere with electrical conduction and life threatening arrhythmias may occur. Their prognosis is very grave.

Classifying the Cardiomyopathies into the functional categories of dilatation of the heart muscle, thickening of the muscle, or stiffening of the muscle, is helpful in therapeutic decision making. Medications which rest the heart muscle, allowing it to expand more leisurely and thus, allow the chambers to fill with more blood, and those which strengthen the muscle’s contractile properties, as well as those medications which diminish peripheral resistance are of substantial utility in the treatment of these conditions.

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Congestive Heart Failure (CHF) is a condition, not a disease. It is a constellation of signs and symptoms, caused by a multitude of diseases, not all of which, primarily involve the heart muscle. This explains why most states, Louisiana in particular, preclude the use of heart failure, as well as respiratory and cardiac arrest as a cause of death, on the Death Certificate. These are all modes of dying, not causes of death.

Congestive Heart Failure (CHF) is exactly what it’s name implies-failure of the heart muscle to keep the lung from becoming congested. This congestion occurs when fluid leaks out of the blood vessels into the air sacs and displaces the air. When the pressure in the blood vessels is elevated by the heart muscle’s inability to propel the blood forward, out of the lungs into the rest of the body, fluid leaks out of the blood stream, through micropermeable vessel walls into the air sacs (alveoli). This manifests itself, clinically, as Congestive Heart Failure.

So any inability of the heart muscle to pump the blood out of the lungs, whether from a weakening of the muscle or by an overburdening of the heart muscle can result in CHF.

Weakening of the heart muscle, most commonly, in Western Societies comes from Coronary Artery disease, whereby cholesterol plaques build up in the lining of the blood vessels. This build up of cholesterol plaques results in obstruction of blood flow and death of a portion of the heart muscle. Other causes of heart muscle injury vary from viral infections of the muscle (called myocarditis), to toxins such as alcohol, to disease states, such as hypertension, kidney or liver failure.

Over-burdening of the heart muscle, on the other hand, occurs in hypermetabolic states such as hyperthyroidism, vitamin deficiency (Beri Beri), severe anemias, and cardiac valvular defects, such as Aortic Stenosis or Mitral Regurgitation.

SIGNS AND SYMPTOMS

The signs and symptoms of CHF include, getting tired easily, weakness, confusion, shortness of breath (initially with exercise, but, as the CHF worsens, at rest and associated with the inability to lie or sleep lying flat in bed. This necessitates sleeping with 2 or more pillows called 2 pillow Orthopnea), a persistent cough from congested lungs, swelling of the feet and abdomen, from fluid accumulation as the heart muscle weakens, along with darkening of the finger and toenails (cyanosis), from oxygen poor blood perfusing the extremities at a slower rate of flow.

Physically, fluid in the air sacs can be heard with a stethoscope, as well as the addition of one or two additional heart sounds. Instead of just the lub-dub, lub-dub of the 1st. and 2nd. heart sounds, a 3rd. and 4th. heart sound are added, either da-lub-dub or lub-dub-da (Ken-tuc-ky or Ten-ne-see). The pulse may even vary in intensity on alternate beats (pulsus alternans). There is, of course, a faster pulse at rest and with exercise, as the heart tries to mitigate its weakness, by increasing its rate. The patient will often complain of the heart feeling as if he had run around the block, when all he did is cross the room. Prominent engorged veins, from blood backup, is noticeable as prominent neck and abdominal wall veins and a large palpable swollen liver is detected. Swollen feet and ankles, initially occurring after prolonged sitting or standing and disappearing overnight, but later persisting all the time, becomes evident.

Congestive Heart Failure is divided into many categories:

Acute and Chronic CHF
Compensated and Decompensated CHF
Systolic and Diastolic CHF
Right and Left sided CHF
High and Low output CHF

I.) Acute and Chronic CHF

A.) Acute CHF- As the name implies; when the heart muscle suddenly becomes too weak to propel the blood forward, sudden CHF ensues. This is usually heralded by the abrupt onset of Shortness Of Breath.

The classic example of this occurrence is from the onset of a fairly extensive heart attack (myocardial infarction). This occurs from Coronary Atherosclerotic Artery disease. With so much muscle damage at one time, the remaining muscle cannot compensate and CHF develops. Occasionally, the patient will present to the Emergency Room in acute CHF from a myocardial infarction, but without a history of chest discomfort (Silent myocardial infarction). Therefore it is incumbent upon the physician to suspect and to check for a myocardial infarction in all and any cases of acute CHF, even if there is no antecedent pain. This is the standard of care, since, if detected early enough, possibly something can be done to save the heart muscle and reverse some or all of the damage.

Other causes of Acute CHF are: 1.) Arrhythmias, such as a very fast or very slow heart rate; 2.) Rhythm irregularities between the upper and lower chambers of the heart as in Heart blocks; 3.) Sepsis; 4.) Pulmonary Emboli; 5.) Acute stroke; 6.) Viral infections.

B.) Chronic CHF- This is, most often, an insidious condition, occurring slowly over a period of months or years. In this condition, shortness of breath on exertion is often the only first symptom. Sometimes the feet will swell during the afternoon and go down at night, assisted by frequent nocturnal trips to urinate this excessive fluid. As the weakened heart muscle , which is too weak during the active daytime, is able to mobilize the fluid from the subcutaneous tissues during a horizontal and restful night, the kidneys are presented with more blood and, therefore, more urine is produced. Later, sleeping with 2 pillow Orthopnea becomes necessary.

Causes of Chronic CHF are of a more chronic duration, but can occur from some of the same causes as with Acute CHF. 1.) Repetitive small myocardial infarctions; 2.) hypertension; 3.) valvular defects; 4.) slow renal deterioration 5.) multiple recurrent small pulmonary emboli; 6.) and diseases that infiltrate the heart muscle.

II. Compensated and Decompensated CHF

Compensated CHF simply refers to the chronic form of CHF that is under control with medication. Whereas, if symptoms are frequent, such as nocturnal shortness of breath, which goes away in the morning or when sitting up and moving around, with or without treatment, the condition is referred to as Decompensated.

III. Systolic and Diastolic CHF

If the heart muscle is too weak to push the blood in the ventricular chambers forward, but still fill up with the usual quantity of blood, as they do in the healthy state, and do so without creating a greatly increased pressure in those chambers, then Systolic CHF is present. In other words, even though the muscle is too weak to propel enough blood forward, the muscle can still dilate to comfortably handle the incoming blood without stress on the chamber walls and, therefore, without an increase in the pressure inside those chambers.

If, as in Hypertensive Heart Disease, the chambers hold less blood, in part because the wall is thickened from having to push against increased resistance, i.e., high Blood Pressure, then the chamber wall muscles are not as elastic, do not have the give to dilate as much and the pressure builds up, such that, even less blood can be pushed into that chamber from the upper chambers (Atria). Then Diastolic CHF is present, because less blood can enter the lower chambers (Ventricles) and must, perforce, back up into the lungs, causing CHF.

IV. Right and Left CHF

The heart is divided into 2 lower chambers (Ventricles). The Right Ventricle sends blood to the lung. The Left Ventricle sends blood out of the heart to the rest of the body. Failure of the Right Ventricle, before the blood reaches the lungs, results in the backup of blood in the venous return system of the body, resulting in distended veins, a swollen liver, occasionally with fluid in the abdominal cavity (ascites) and with swollen legs. Failure of the Left Ventricle, after the blood has gone through the lungs results in the classical symptoms of shortness of breath, cyanosis, etc., because of inability to propel the oxygenated blood forward to the distal tissues. If Left sided CHF lasts long enough, it will result in Rt. sided CHF also developing. Because the Kidney puts out hormones which regulate salt and fluid retention, when it does not receive enough blood, as in Lt . sided heart failure, it will hold salt and fluid in the body hoping to increase the fluid volume, since it interprets this lack of blood and oxygen as one of an anemic state. If the liver becomes engorged with backed up blood, as in Rt. sided CHF, it will not destroy these kidney hormones in it’s usual efficient manner and they will accumulate, holding more salt and water in the body.

V.) High and Low Output CHF

Low Output CHF results from a weakened heart muscle and is commensurate with the classical sign and symptoms of CHF. High Output CHF occurs in the overburdening types of CHF, such as Beri Beri, or Hyperthyroidism or severe Anemia, where the heart is in a feverish state of activity, having to move the blood around vigorously, and wearing itself out.

TREATMENT OF CHF

Since CHF occurs from the presence of excessive fluid in the air sacs due to an absolute or relative weakened heart muscle, the solution is directed at these two problems. Of course, once the patient is comfortable, then the underlying disease should be sought for and addressed, such as treating the Hyperthyroidism, or balloon dilating and stenting the Coronary Arteries, or giving blood, etc.

So, first we try and remove the fluid from the lungs so the patient can breath.

Then, we try and increase the strength of the heart muscle if possible, or, at least, relieve the burden on the heart muscle.

1.) Relieve the lungs of fluid – By simply dehydrating the blood stream with the use of Diuretics, leaving less free fluid to be available to infiltrate the tissues, leak into the air sacs or for the heart muscle to have to move around, in it’s weakened state.

2.) Strengthen the heart muscle – Unfortunately, this is our biggest problem. We have very few medications which can be absorbed orally and not be destroyed by the stomach juices, which will strengthen the heart muscle.

A.) Digitalis – This drug has been in use for a century and is still very useful in treating CHF. It has been shown to improve the stamina and life style of CHF patients, but, for some unknown reason, not prolong life. At present, this is the only oral heart muscle strengthening muscle (IONOTROPIC AGENT) available.

B.) Other Ionotropic Agents – Intravenously, we do have some very good agents, but, of course, the route of administration is cumbersome and expensive. Dobutamine and Dopamine are examines of this genre. On the horizon, however, there are plenty of candidates, which should be available shortly, some of which can be taken orally. What about a patch?

3.) Decrease the burden against which the heart muscle must push against. (Peripheral Vascular Dilators).

A.) ACE Inhibitors – Stands for Angiotensin Converting Enzyme Inhibitors. These ACE Inhibitors are the 1st. drugs of choice in early CHF. They have been proven to increase the quality of life and to prolong life. They work by decreasing the work of the heart by decreasing the peripheral resistance against which the heart muscle must work. They also work on the kidney vessels to prevent them from deteriorating and compounding the congestive state. They do so by inhibiting the enzymes which tell the kidney to retain salt and water, a mechanism the body uses when the tissues do not receive enough oxygen and blood nutrients. In this case it is self-destructive. A new improved and more selective class of ACE Inhibitors has come on the market with great promise. (I will update that shortly).

B.) Other types of peripheral vascular vasodilators exist and have been found to be beneficial in difficult CHF cases, which work on either the arteries or veins, such as Alpha Blockers or Nitroglycerine.

4.) Decrease the frenatic activity of the heart muscle so that it can relax, allowing more blood to enter its chambers without elevating the pressure.

A.) Beta Blockers – Unique in that these drugs allow the heart muscle to rest and slow down and thereby become more efficient, even in their weakened state. Of course, we do not want weakened muscles to fall asleep and not work at all, making the CHF worse, so these drugs must be carefully monitored.

SUMMARY

Congestive Heart Failure occurs when the heart muscle is, eitherweakened or overburdened. It occurs because of the inability of the heart to effectively pump blood out into the lungs or to the rest of the body. This blood in the vessels, principally in the lungs, builds up increasing the pressure and causesfluid to leak out into the surrounding tissues, such as the air sacs, in the lungs, or the subcutaneous tissue in the extremities. Symptoms vary from Shortness of Breath to swelling of the lower extremities. Signs include liquid heard in the air sacs (rales), compressionable swelling of the extremities (edema), and purplish fingers and/or toes (cyanosis), among others. Treatment is directed towards mobilization of fluid plus strengthening and reducing the stress on the heart muscle. So, diuretics, Ace Inhibitors, vasodilators, Ionotropic agents and Beta blockers may be employed, separately or together to effect this relief.

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Thoracoscopic surgery of the chest was first described in terms of its original concept in 1922 by Dr. Jacobaeus. He was far ahead of his time in terms of originality of thought and almost 50 years ahead of the technology needed to make this exciting new diagnostic and therapeutic tool available for clinical use. In 1970, Dr. Joe Miller, Jr., at the Emory Clinic, began to match changes in technology with clinical applications and the field of thoracoscopic surgery was born. My first experience did not come until the early 1990 ties when thoracoscopy emerged from lab use and was available for every day practice.

The thoracoscope consists of a slender fiberoptic tube than can be inserted into a 1/2 inch incision in the chest. The image is then combined with a tiny telescopic lens, a powerful light source, and a small video camera and is projected onto a TV screen. The surgeon can literally see into the chest.

Then using graspers, endoscopic scissors, and endostaples, the surgeon can perform a whole host of procedures. The revolutionary changes this technique has brought to thoracic surgery mark a milestone in the evolution of surgical technology. Thoracoscopy offers many patients marked advantages over standard open procedures. First, it gets the patient home from the hospital in 36 to 48 hours after the procedure. Second, recovery time from surgery and the level of pain experienced by the patient is markedly reduced. Lastly, the small incisions used are better tolerated than the old larger open thoracotomy incisions.

The most familiar use of thoracoscopy is to diagnose disease within the chest wall. In this case, small pinch biopsies of the pleura, the membrane surrounding the lung, the chest wall, the lung, and the pericardium surrounding the heart can be obtained. In addition, the mediastinum or, the area between the two lungs, can be readily visualized and lymph nodes biopsied. In patients with fluid collections around the lung called pleural effusions, samples can be obtained for culture studies and cells for cytological examination.

Patients with asbestos exposure who may have concerns about pleural tumors called mesotheliomas are usually good candidates for this technique. Other patients with abnormal chest x-rays and pulmonary nodules within the lung may benefit from small wedge resections made with the help of an endostapling device. Often, the lesions removed can be determined to be a benign tumor such as sarcoid or a malignant cancer of the lung. Using the wedge technique, small to moderate sized masses can be completely removed and sent to pathology for examination under the microscope.

A second common use for thoracoscopy is therapeutic. A number of topics fall into this grouping. Treatment of pleural disease, removal of pus collections call empyemas and lysis of adhesions from entrapped lungs are but a few indications. Other applications of this new technique involve removal of blebs or weak areas on the surface of the lung, staging of lung cancers and resections of metastatic disease from other areas of the body. In terms of the heart and the pericardium, pericardial effusions can be drained and cardiac tamponade relieved.

In my own practice I have operated on a series of patients with excessive sweating called hyperhidrosis, Raynaud’s disease and reflex sympathetic dystrophy. In these cases, the sympathetic chain of nerves passing on the inside of the chest wall can be resected and sweating and pain reduced to symptomatic arms, hands and fingers. Another group of patients with esophageal conditions such as acid reflux disease and benign tumors of the esophageal wall can be helped.

This is but a quick review of a revolutionary new technique available to the thoracic surgeon to diagnose and treat a wide variety of conditions found in the chest. More indications seem to come along each year all to the patient’s benefit.

Recommendations:

1) If you have an abnormal chest x-ray and are told that a mass, nodule, lymph node or fluid collection is present, a test called a CT scan of the chest is usually recommended to better define or isolate the abnormality.

2) A second test called a bronchoscopy may then be indicated. This test involves using a small tube with a light on the end to look down the airways in hopes of seeing the lesion and possibly getting a biopsy.

3) A third test called a CT directed needle biopsy may then aspirate cells from the mass or collect fluid samples.

4) Finally, you may be referred to a thoracic surgeon for the new thoracoscopy procedure. Hopefully, this single test may be used to both make the diagnosis and effect the removal of the abnormal area. If all else fails, the old open thoracotomy can be held in reserve to allow a hands on approach to the problem. Good Luck and I hope you benefit from the new fiberoptic technology.

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When a lump is found in a woman’s breast, and it is not a fluid-filled cyst, it usually requires removal, both for diagnosis to see whether or not it might be a cancer, and for treatment. Surgery to remove or biopsy breast lesions is relative simple, not usually associated with great pain, and almost always done as an out-patient procedure, often under local anesthesia.

If one can feel the lump, the surgery usually involves its complete removal (excisional biopsy). A relatively small incision is made, taking into consideration the location of the scar, not only for reasons of appearance, but also for potential future treatment. When a lump is quite large, and suspicious for cancer, only a small portion may be taken (incisional biopsy) to establish the diagnosis and provide information necessary to start treatment. As with other less invasive methods of the detection, such as fine needle aspiration or core needle biopsy, only a positive study is definitive; if negative, one must remove the lesion in total for complete biopsy.

When a lump cannot be felt, the surgeon has to turn to the radiologist for help in “localizing” the mass – in other words, pointing out where a lump too small to feel, yet one that might be an early cancer, is located. The most common method used is needle localization biopsy: using the mammogram as a guide, the radiologist inserts a special needle and then a wire into the lesion, and “marks the spot” for the surgeon, who subsequently traces the wire in the breast, finds the area in question, and removes it. It then is sent for evaluation by the pathologist, often with additional guidance from the radiologist as to where to look.

Other methods to evaluate mammogram-detected lesions include fine needle aspiration for cytologic analysis of the area in question, and the use of X-ray guided “stereotactic” biopsy devices. Two such instruments are commonly used – the mammotome, which takes a small core needle biopsy, and the Advance Breast Biopsy Instrument (ABBI), which often can totally remove a suspicious area. A more recent development, and still experimental method, is to identify the milk duct supplying the area, and then inserting a very fine catheter (tube) into that duct, introducing some sterile fluid to irrigate the duct, thus obtaining cells from the area to examine microscopically.

There are some uncertainties in the evaluation of breast lumps. First, not all pathologists will diagnose the same lesion identically. While there is some standardization, one must realize than no person can look at each and every cell in a breast biopsy, and there are honest differences of opinion. Recent advances in pathology allow the detection of cancer in minute microscopic quantities, diagnosing lesions we never knew of previously. It now is quite common to find cancers that have not yet gained the ability to metastasize (spread to other areas), or even lesions that have not yet changed sufficiently from normal to be called cancer. These early cancers, called carcinoma in-situ, need treatment, and often serve as a warning for the future development of cancer elsewhere in the same or the other breast. This allows true measures of prevention occasionally to be instituted.

Francis C. Evans, MD, FACS

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