Archive for April, 2008.
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How can you cure cervical cancer? Because you have a gross mass present, you only can give 4500 centigrade to 5000 centigrade to the pelvis, how do we give enough radiation to kill a cancer that is on the cervix. That is done by what we call brachy therapy and brachy therapy is giving a high dose of radiation directly to the cancer and these are the implants. Modern day implants are based on what we call the Manchester system. Historically what we used to do in Stockholm, we used to put two radiation sources right against the cervix at tandem and give very high doses of radiation therapy to the tumor over a day and then remove it and were able to cure the cancer. The only problem here was that the complication rate was extremely high. Because of that, the Manchester system was developed in England where we gave an implant where the implant would deliver a low dose of radiation over an extended period of time and with a tandem containing radiation sources in the uterus, thereby killed the cancer yet minimized the complications. Modern day implants are based on what we call the Fletcher Suit system, this is an implant and in the Fletcher Suit system, what we do is we place two ovoids, and a tandem in the uterus. Each of these ovoids have a radiation source in them, the tandem have anywhere from two to three sources in them, but to calculate the dose, what you have to realize is that the radiation dose falls what we call by inverse square, so subsequently what happens is that if you look at 2 cm lateral to the cervix, what we call point A, the dose delivered from an implant is only one-fourth or inverse square of the distance. If you look at point B, point B is 3 cm further than point A or 5 cm from the external os, the dose delivered is 1/25th the dose of the implant. What is significant about point A is point A is the perimetria and that’s where the parametrial nodes are. Those are the most common nodes that are positive with a cervical cancer. Point B is the obturator nodes. Anatomically, what’s important about point A, is that’s where the uterine artery goes over the ureter, and that’s the reason often you can see a ureteral stricture secondary to an implant.
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The radiation sources used for an implant nowadays are cesium, cesium 137 is used and has a half life of 30 years, so it’s not necessary to calculate the dose with regard to the radiation implant every year, because these are long lived isotopes. We used to use radium or radium 226, the problem with radium 226, it has a very long half life of 1620 years, but in addition, in it’s decay, gave off radon gas and when the sources would crack, radon gas would be given off and became a health hazard to the personnel in the hospital, causing lung cancers. This is a Fletcher Suit implant, what you see here, is the ovoids which fit into the fornices and the tandem which contains radiation sources that are placed within the uterine cavity. To determine whether an implant is in it’s right position, x-ray films are taken and here you can see the ovoids as well as the tandem. The problem you have here, is you don’t know if it’s placed correctly. To determine that, a lateral film is taken and as you can see here, here is the tandem and here are the ovoids, what you are concerned about is that tandem is right angle to the ovoids, its not twisted which causes complications, secondly, is that each of these radiation sources in the tandem do not cross the sources in the ovoids because if that does happen, what your doing to the patient, is causing a hot spot and thereby having the possibility of causing either a rectovaginal or vesicovaginal fistula, so if you get called and the radiation oncologist isn’t around and this tandem is twisted or you see it pulled back, the proper thing is to call the radiation oncologist, have the sources taken out and take the implant out. When you have an indentation, what you are basically doing is you have the potential of the cancer recurring. Cheap soma without prescription.
Occasionally, in a morbidly obese patient, who has endometrial cancer, what the radiation oncologist will do is place Hayman capsules. What Hayman capsules are, are small radiation sources that usually contain cesium that are 5 to 10 mg of cesium, they place the sources actually into the uterus to radiate the surface of the uterus. The problem here clinically is that the ability to cure the cancer decreases about 15 to 20%. So when we give radiation therapy, our goal is to give external beam radiation therapy 4000 to 4500 centigrade and implant given to point A, an additional 40 to 45 gray or 4000 to 4500 giving a total dose, when you get the total dose you will add the external beam radiation therapy, the intracavitary implant and you get 80 to 85 gray to point A or 8000 to 8500 centigrade to point A. That is the dose you will would like to achieve to point A. With ovarian cancer occasionally, usually with an early stage ovarian cancer we’ll go ahead and use P32. What P32 is, is an isotope that is a colloidal suspension, or a fine particulate matter that is given into the peritoneal cavity, what P32 does, is it radiates the entire pelvic and abdominal cavity but with very low energy radiation, it delivers what we call a gamma ray as you have with x-ray and implants, it delivers beta energy. The problem with P32, it doesn’t distribute adequately and secondly, it’s depth of penetration, unlike x-ray therapy is very low, it penetrates only 1 to 3 mm in depth and that’s the reason it’s good only for microscopic disease.
When a patient goes to radiation oncology, the treatment plan is always to give the patient, for example in cervical cancer both external beam radiation therapy and intracavitary or brachy therapy. The reason that patient’s receive external beam radiation therapy is to control the pelvis or what we call regional control. What you are treating is the tumor bed as well as the lymphatics in the pelvis. When a patient receives an implant or brachy therapy what you are trying to control is what we call central disease or to control the disease itself for example, the cervix that has the cancer. So when a patient receives external beam radiation therapy, they go down to radiation therapy and they receive their dose with a high energy Lanier machines. These high energy Lanier machines are able to produce different amounts of energy. In the old days we used to use cobalt and then went to 250 Kvs and here is a cobalt machine. Each of these are different types of energy produced by different machines, and now, patient’s can receive 22 MEV Lanier accelerator. The reason we have gone to higher energy, is pretend this is the skin of the patient is what you see at lower energy, for example cobalt 50 or 250 MEV is that 100% of the energy is delivered either at the skin or 1 cm below. So what happens is, these are the patient’s, if you re fortunate enough to see a patient who was treated in the 60s, who have severe radiation fibrosis because the energy was delivered directly to the skin. Buy abilify online at cheap canadian pharmacy. With the higher energy machines we use now, 100% of the dose is not delivered at the surface but 3 to 5 cm below the surface, thereby sparing the skin so the higher energy machines spare the skin and thereby cause less problems to the patient.
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When patient’s go down to radiation, they are simulated, what they do when they simulate the patient is basically develop a treatment plan or go ahead and plan out what region they are treating with regard to the external beam radiation therapy. In gynecologic oncology, we usually treat the pelvis, and when we treat the pelvis, the field is usually 15 x 15 cm and the reason is because you want to incorporate the pelvis and the internal iliac obturator nodes as well as part of the external iliac nodes. Occasionally, with ovarian cancer, what one will see is patient’s will receive whole abdomen radiation therapy. In the 1970s, whole abdomen was quite frequently given to patient’s and what happened was we saw a 30% bowel complication and it has gone out of favor until recently because of the Princess Margaret data for microscopic ovarian cancer, it has become an option again. The problem with whole abdomen radiation therapy is you are not only treating the pelvis, but you are treating the upper abdomen. When we treat the upper abdomen, unlike the pelvis, there are many radiosensitive organs. For example, the kidney, the small bowel are extremely radiation sensitive and one cannot give as high a dose to the upper abdomen as to the pelvis. For example, the kidneys, the radiation sensitivity of it is about 1500 centigrade. Small bowel is about 2500 centigrade where the pelvis can tolerate up to 6000 centigrade so the upper abdomen is extremely sensitive with regard to complications that can be associated with radiation therapy. The patient then goes down to radiation therapy and a treatment plan is made and ports are drawn and this is the port of a patient with a gynecologic malignancy and what encompasses as you can see as I mentioned is the pelvis, the external iliac and internal iliac arteries but the periaortics are usually not included in the port unless there is periaortic involvement with regard to the cancer. External beam radiation therapy can be delivered in numerous ways, half the dose can be delivered from the front and half from the back, that’s called APPA port or method of delivering it, four-field means that a fourth of the dose is given from the front, a fourth from the back, and one-fourth from each side, or it can be delivered in the 360 degree rotation where a small dose is delivered as the radiation is being delivered to the patient.
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It all depends really on what your treatment field and what you are trying to accomplish. For example, here is the tumor as you can see, if you go from front to back, is that there is less of a margin with regard to the amount of radiation that is being delivered to periphery, so what happens is that there is a higher complication rate giving APPA versus 360 degree rotation. For radiation to be effective with regard to cancer, the size of the cancer becomes extremely important, as you can see here, is if there is greater than a 2 cm nodule, 5000 to 6000 centigrade is required to kill the cancer. If there is microscopic disease, only 2500 to 3000 is required. What’s important clinically is that for example, for ovarian cancer, one cannot give tumor doses to the tumor bed to a large cancer mass because usually the cancer is over 2 cm. Yet if microscopic disease is remaining, or you are trying to give therapy for adjuvant setting when there is no evidence of disease remaining, then, whole abdomen radiation may be effective because you can give to the upper abdomen from 2500 to 3000 centigrade. The normal tissue is a problem with regard to why can’t you give enough radiation therapy, and each of the tissues in the pelvis and upper abdomen have their own radiation tolerance. As I mentioned before, the kidney is rather radiation sensitive, it can only tolerate 2000 centigrade, the liver about 3000 centigrade. However, if you look at the structures in the pelvis, they are rather radiation resistant. The colon, rectum, bladder ureter are able to tolerate from 6,000 to 7500 centigrade. Viagra professional.
When we speak about radiation oncology, on the biological level. What we’re trying to do is kill a cancer cell. What one has to realize is radiation is effective only in microscopic disease for the most part, and it’s not effective during the entire time period that the radiation is being given. The reason is, if you look at the biology of cancer, and you think about the dividing cell, the majority of a cancer mass does not divide at any one time, only about 10% of the cancer is dividing, so if you look at the cell cycle, what you see is that the majority of cells are what we call the G0 phase in a tumor mass, 90% of the cells are actually resting. For radiation to be effective, these cells have to be recruited out of their resting phase and have to be actually dividing because radiation will kill a cell when it’s either in the mitotic phase or beginning from the resting phase or the G2 phase.
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The clinical implication of this is that one sees the maximum effect of radiation, not during the time of radiation but within three to four weeks after a patient completed radiation therapy. The reason we give a small dose initially of 180 to 200 rads is that lower doses, the cell has the ability to repair the damage of the radiation and that is called the sublethal effect. That is this little slope you see here. As you get over 200 centigrade, you begin to see the higher the dose, the more likely the cancer cell will be killed. Radiation therapy is based upon what we call the Compton effect, what the Compton effect is, is that when a photon or an x-ray hits a cell, it will go ahead and eject the nucleus from the outer shell of the cell of the atom producing what we call a scatter photon, and what you have to remember is x-rays are like energy or photons. This is the way radiation works. Radiation doesn’t work in large masses because the majority of cancers have a hypoxic out nucleus or have necrosis.
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When angiogenesis takes place, and there is a vascularity, what happens is the vasculature oxygenates the center of the tumor mass and what we have found over the years, is the more oxygenated the cancer mass is, the greater the likelihood the cancer will die and here you have a comparison of what happens when cell are in a toxic background or no oxygen and when there is oxygen present. As you can see, treating cells with radiation what you will see is that there is a greater ability to kill the cancer cell when oxygen is present. This is important clinically because when a patient goes for radiation therapy, we like the patient not to anemic and to be transfused with a hematocrit over 30. This is the basis for it. When you send a patient to radiation oncology, they always give you a dose, 10 years ago what we used to report is dose in rads, and what rads was radiation absorbed dose. A patient would get for example, 4 to 5 thousand rads of external beam radiation therapy. However, the terminology has changed and what we now talk about rather than rads is centigrade and centigrade is if you pick up an older chart, you convert rads to centigrade by remembering that one rad is equivalent to one centigrade, 100 centigrade is equivalent to one grade, so if a patient receives 40 grade, they have received 5,000 centigrade or 5000 rads, they are all equivalent. Herbal xanax.
Sarcomas of the uterus are rare; they comprise only 3-5% of all uterine tumors. These tumors primarily arise from two tissues: endometrial sarcomas from endometrial glands and stroma and leiomyosarcomas from the uterine muscle itself. Other sarcomas arise in supporting tissues and are very rare. Sarcomas have been classified as pure (composed of one cell type only) and mixed (composed of more than one cell type). The site of origin has also been used in the classification of sarcomas, with homologous tumors defined as those that contain tissue elements entirely indigenous to the uterus and heterologous tumors defined as those that contain tissue elements foreign to the uterus. Although several classifications have been suggested and used over the years, a simplified classification is endorsed by the Gynecologic Oncology Group and has been used successfully:
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• Leiomyosarcomas
• Endometrial stromal sarcomas
• Mixed homologous müllerian sarcomas (carcinosarcomas)
• Mixed heterologous müllerian sarcomas (mixed mesodermal sarcoma)
• Other uterine sarcomas
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Particularly with leiomyosarcomas, the diagnosis of this entity is determined almost solely on the basis of mitotic index (the number of mitoses per 10 high-power fields). Cellular atypia has also been used by some investigators.
Sarcomas are usually found in postmenopausal women; leiomyosarcomas are identified about 10 years earlier than mixed mesodermal sarcomas and endometrial stromal sarcoma. Menorrhagia and postmenopausal bleeding are common symptoms. Abdominal pain or mass is a frequent complaint. Particularly in the postmenopausal patient, a rapidly enlarging uterus should suggest sarcoma as a possible etiology. A large friable polypoid mass extending through a dilated cervix into the vagina also should raise suspicion of sarcoma, particularly in the postmenopausal patient. A mixed mesodermal tumor and endometrial stromal sarcoma can usually be diagnosed with a directed or endometrial biopsy, whereas a leiomyosarcoma may or may not be identified preoperatively.
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Total abdominal hysterectomy and bilateral salpingo-oophorectomy are considered the hallmarks of therapy for uterine sarcomas. In many instances, patients with sarcomas tend to have extrauterine disease, which may be present intraperitoneally or in the lymph nodes. This is particularly true for homologous and heterologous mixed müllerian tumors. Although radiation therapy has been used for a long time in patients with uterine sarcoma, it has not been associated with any improvement in survival compared with surgery alone. There does appear to be less local recurrence after radiation therapy, but because most patients that have recurrence have it at distant sites, the overall survival has not been affected. Adjunctive therapy with chemotherapeutic agents has been evaluated; however, none have been shown to improve survival even in patients with limited disease. Unfortunately, many patients with stage I uterine sarcomas will develop a recurrence. The use of adjuvant chemotherapy has to date minimally affected the survival of these patients. Preliminary data regarding the use of ifosfamide, mesna, and cisplatin suggest encouraging response rates, but their impact on survival awaits further evaluation.
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Estrogen Replacement Therapy after Endometrial Cancer
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Estrogen replacement therapy can be used safely in patients who have had endometrial cancer. This suggestion is based on the fact that patients with a disease with a good prognosis, although estrogen-progesterone receptor positive, nevertheless have no remaining cancer cells after their treatment. Those patients with a lesion with a poor prognosis are usually receptor poor; therefore, replacement therapy theoretically would have no impact on development of recurrences. There are now five studies in the literature (none of them prospective and randomized), and all suggest that hormone replacement therapy is not detrimental to these patients. Some investigators will start the patient taking estrogen replacement therapy immediately after primary therapy for her cancer, although others think that waiting a number of months or even years is necessary to be safe. A Committee Opinion of the American College of Obstetricians and Gynecologists stated that in women with a history of endometrial carcinoma, estrogens can be used for the same indications as they are used for any other woman, except that the selection of appropriate candidates should be based on prognostic indicators and the risk that the patient is willing to assume. A prospective, randomized study of estrogen replacement therapy in endometrial cancer patients is anticipated to begin shortly under the auspices of the Gynecology Oncology Group. The experience over the last 10-15 years would suggest that if estrogen replacement therapy is detrimental to patients with endometrial cancer, the risk is extremely small. Because most patients with endometrial cancer are long-term survivors, the risks of cardiovascular disease and osteoporosis appear to be significant and higher than the risk of recurrence of the endometrial cancer. Benefits of estrogen replacement therapy, therefore, appear to greatly outweigh the theoretical risk in patients who have had endometrial cancer.
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Endometrial Hyperplasia
Both the diagnosis and management of endometrial hyperplasia have generated tremendous confusion. The natural history would suggest that some of these lesions revert to normal spontaneously or with medical therapy, some persist, and a few will progress to endometrial adenocarcinoma. Most endometrial hyperplasias are thought to result from persistent or prolonged estrogenic stimulation of the endometrium, either endogenously (anovulatory cycle or hormone-producing tumor) or with unopposed exogenous estrogen. In the mid-1980s, a new classification was developed by the International Society of Gynecologic Pathologists, which eliminated a plethora of terms that carried different connotations.
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The diagnosis of endometrial hyperplasia is made pathologically, usually on an endometrial biopsy that is obtained because of irregular or postmenopausal bleeding. Four categories of hyperplasia are now recognized: simple, simple atypical, complex, and complex atypical. It would appear that only those patients with atypical hyperplasia are at risk of developing endometrial cancer if the hyperplasia is allowed to go untreated for varying periods (up to and more than 10 years). The diagnosis of atypical hyperplasia is based on cytologic atypia. Architectural changes that previously were thought to indicate high risk for developing endometrial cancer no longer carry that implication unless atypia is present. Even when complex atypical hyperplasia is present, data suggest that only one fourth to one third of these patients might develop endometrial adenocarcinoma some years in the future.
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In the patient who has atypical hyperplasia on an endometrial biopsy, a thorough curettage is usually recommended because as many as one third of these patients will have a coexistent adenocarcinoma. In the patient with hyperplasia without atypia, curettage is usually not warranted. Hyperplasias, both with and without atypia, can be treated successfully in most instances with progestins. Various progesterone regimens (ie, use of medroxyprogesterone acetate or its equivalent for a few months) have been effective. The younger patient usually needs a higher dose. The goal is to make the endometrium atrophic, and a rebiopsy is recommended 2-3 months after commencement of the pro-gestin therapy. If hyperplasia persists on biopsy, progestin may be continued for another period. In many patients with atypical hyperplasia, particularly if they are postmenopausal, a simple hysterectomy and bilateral salpingo-oophorectomy have been advocated. These surgical patients may use estrogen replacement therapy postoperatively.
Simple hysterectomy and bilateral salpingo-oophorectomy remain the hallmarks of therapy for corpus cancer. After complete surgical staging, if disease is limited to the uterus, most patients need no further therapy. The one exception is patients with a poorly differentiated, deeply invasive cancer. Nonrandomized studies controlled for prognostic factors suggest that pelvic radiation in this group may prevent both local and distant recurrence. In all other instances, radiation therapy did not appear to be of benefit. In the only prospective, randomized study comparing radiation with no radiation, it appeared that radiation decreased local recurrence but overall survival was the same.
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The role of brachytherapy postoperatively does not appear to be efficacious in most surgical stage I cancers because vaginal vault recurrence appears to be no more than 1-2%, irrespective of whether the patient receives radiation. Fortunately, most adenocarcinomas of the endometrium are surgical stage I, and most of those are adequately treated with surgery only.
When disease is present outside of the uterus, there is no general agreement as to optimal therapy. Unfortunately, prospective, randomized studies have not been done, and the clinician’s experience, both published and unpublished, affects the therapeutic recommendation. The question that has been raised is whether surgical staging is only diagnostic and therefore has no impact on survival. Data are now appearing in the literature suggesting that lymphadenectomy can be therapeutic to a greater degree than simple hysterectomy and bilateral salpingo-oophorectomy patients with true stage II disease has not been investigated in any depth. Again, most oncologists would probably treat these patients with postoperative radiation, although some have suggested that surgery may be definitive, particularly for those with stage IIA cancers. The role of radical hysterectomy in patients with clinical stage II disease has essentially been discarded from our armamentarium. In patients with surgical stage III and IV disease, treatment is usually individualized and combination therapy with surgery and radiation is common. The use of chemotherapy and hormones both in adjuvant and therapeutic modes in patients with advanced disease has not proved to be efficacious. Multiple regimens have been attempted, but response rates remain suboptimal.
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Recurrent disease historically has been treated in many different ways. If a local recurrence appears in the vaginal vault, surgery alone or in combination with radiation therapy has saved many of these patients. If recurrence is in the lower vagina, success has been limited. For metastatic disease, progestins have been primarily used; reports have noted an objective response in about one third of patients. More recent data suggest that the response rate is 15-20%. Original grade of tumor, length of time from primary treatment to recurrence, and hormone receptor status of the original tumor all appear to be indicative of the patient’s response to progestin. Several cytotoxic agents have been used with objective responses noted. The most experience has been with adriamycin and cyclophosphamide, cisplatin with or without adriamycin, and more recently paclitaxel. Unfortunately, when there is a response, it is relatively short lived. The ideal single or combination regimen for recurrent endometrial cancer has not yet been identified.