President’s Message

Hello everyone!  I hope that you are having an enjoyable summer.  This is our first online newsletter.  So please let us know what you think.  If you missed our annual meeting in Asheville, you really missed an outstanding opportunity to learn from some of the greatest speakers in our profession.  We had a terrific turnout and the reviews from the meeting were fantastic.  If you were not available to attend the meeting in Asheville, or if you need a one-day CME refresher, please join us at our fall meeting at the Friday Center in Chapel Hill, North Carolina on October 25th.  The fall committee members are lining up some excellent speakers for all specialty areas.  I look forward to seeing you there.

Our annual meetings are all about relaxation, innovation, and of course, education.  Once more, we are returning to Myrtle Beach, South Carolina for the 2009 NCUS Annual Symposium from March 27 through March 29 at the Marriott Grande Dunes .  Myrtle Beach is loaded with restaurants and attractions, including the new Hard Rock Amusement Park, and plenty of nearby shopping. Bring the family along.  They will have plenty to do while you learn more about sonography. 

Don’t forget to encourage your coworkers to join the NCUS.  We need your support to continue to grow and provide North Carolina and surrounding states with high-quality continuing education. 

Respectfully,

Steven M. Penny, B.S., RT(R), RDMS
North Carolina Ultrasound Society President

Polycystic Ovary Syndrome
SON140
Instructor: Alice Bradley
Karen Arney
April 16, 2008

Abstract

Polycystic ovary syndrome is a common endocrine disorder that affects approximately 10 percent of women from menarche to menopause (RDH, 2004). This endocrine disorder can cause women to be infertile (RDH, 2004). Polycystic ovary syndrome (PCOS) causes mild to severe symptoms such as acne, hair loss, irregular periods, obesity, hirsutism, and/or infertility (RDH, 2004). Patients that are diagnosed with PCOS are considered at a higher risk for developing disorders like type 2 diabetes, hypertension, hyperlipidemia, and cardiovascular disease (RDH, 2004). Patients that present with symptoms of hyperandrogenism and anovulation may also have polycystic ovaries (Nursing Standard, 2004). However, not all women with polycystic ovaries are diagnosed with PCOS (Clinical Laboratory Science, 2004). Polycystic ovaries are typically diagnosed with ultrasound depicting the enlarged ovaries with cysts around the periphery (British Journal of Nursing, 2006). Once a diagnosis is given, physicians will determine the best course of treatment (British Journal of Nursing, 2007). Treatment can be in the form of life-style changes, drugs, or surgery (British Journal of Nursing, 2007), but is considered incurable (RDH, 2004).

Introduction

Polycystic ovary syndrome (PCOS) or Stein-Leventhal syndrome is described as the most common endocrine disorder among women of child-bearing years (British Journal of Nursing, 2007), and is considered to be the number one cause for female infertility (RDH, 2004). PCOS is reported to affect approximately 4-10 percent of women (Nursing Standard, 2004), and most are unaware of their condition until fertility issues occur (Pediatric Nursing, 2005). PCOS was first acknowledged as a syndrome in 1935 by Drs. Stein and Leventhal when they recognized similar characteristics among a small group of women with irregular menses (Clinical Laboratory Science, 2004).

Diagnosing PCOS requires the patient to meet certain criteria that can be clinically proven (Drugs, 2006). Hirsutism, obesity, acne, hair loss, infertility, and/or irregular menses are also characteristics that have been used to assist in identifying PCOS (RDH, 2004).

Research has shown that this endocrine disorder has been associated with diabetes, high blood pressure, high cholesterol, heart disease (RDH, 2004), and infertility (Drugs, 2006), and can predispose women to endometrial hyperplasia and cancer (Clinical Laboratory Science, 2004).

Ultrasound is useful in illustrating the presence of multiple follicular cysts within an enlarged ovary (British Journal of Nursing, 2006), and is used in conjunction with clinical symptoms for an accurate diagnosis of PCOS (Clinical Laboratory Science, 2004).

Treatment, whether medical or surgical, is focused on reducing symptoms that may restrict ovulation and/or cycles, and risk factors can be cut primarily with a successful weight loss and exercise regime (British Journal of Nursing, 2007). Polycystic ovary syndrome has no known cure (RDH, 2004).

Causes

Polycystic ovary syndrome is characterized as a complex heterogeneous endocrine disease that can affect as many as 10 percent of menstruating women in the United States (Pediatric Nursing, 2005). Unfortunately, there has not been a clear understanding to the cause(s) of PCOS (Clinical Laboratory Science, 2004). According to Ebtisam Elghblawi (2007), there has been significant research that links PCOS with high insulin levels. The reports show that approximately 30-40 percent of the women diagnosed with PCOS also suffer with glucose metabolism problems and obesity (British Journal of Nursing, 2007). Another unverified cause for Stein-Leventhal could be a disruption between the hypothalamus and the pituitary gland, which controls gonadotropin hormone levels (Clinical Laboratory Science, 2004) and is important in ovary functions (RDH, 2004).

PCOS has been speculated to be caused when the female cycles of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are abnormal (British Journal of Nursing, 2006). In Polycystic ovary syndrome, FSH is decreased and LH is increased which directly causes an increase in secretion of the male sex hormone (hyperandrogenism) by the ovaries (RDH, 2004) and prevents ovum release (British Journal of Nursing, 2006).

Signs and Symptoms

According to The Rotterdam European Society of Human Reproduction/American Society for Reproductive Medicine (ESHRE/ASRM), the definition of Stein-Leventhal syndrome is patients must meet two of the following three criteria: (i) infrequent or no ovulation, (ii) signs or symptoms of hyperandrogenism, and/or (iii) multicystic ovaries (Drugs, 2006). This definition is merely guidelines set in place to assist with diagnosing PCOS, but is not always followed by physicians (www.inciid.org, 2006). The most common symptoms of PCOS are hirsutism (extra body hair), infertility, infrequent or no menses, obesity, acne, and loss of hair (Clinical Laboratory Science, 2004). According to Jeffrey Chang (2007), only 20% of the polycystic ovary syndrome sufferers experience a loss of menstrual cycle, and a tenth of these women ovulate normally. The majority of women that experience irregular menses do so because of an excess of estrogen (Nature Clinical Practice, 2007).

Hirsutism is the increase of hair growth of the face, between breasts, and abdomen (www.inciid.org, 2006). This excessive hair has a distinct pattern that mimics that of males (Nature Clinical Practice, 2007). This condition is caused by the increase of androgen or testosterone (hyperandrogenism) which affects approximately 50 percent of PCOS sufferers (British Journal of Nursing, 2006). In the most extreme cases of PCOS, patients may present with alopecia (baldness), depth of voice, and enlarged clitoris; all signs of virilization (development of male sex characteristics) (Clinical Laboratory Science, 2004). In Figure 1 below, one can see an example of abnormal facial hair growth on a patient diagnosed with hirsutism.

Figure 1. Hirsutism identified on a female face.
Note. Retrieved on April 8, 2008 from library.med.utah.edu/.../mml/hrovt_chin.html.

Risks

Patients that are diagnosed with PCOS are at risk for developing obesity, type 2 diabetes, insulin resistance, Acanthosis nigricans, high cholesterol, hypertension, heart disease (INCIID, 2006) and/or hyperplasia or cancer of the endometrium (Clinical Laboratory Science, 2004). According to Marcin Stankiewicz and Robert Norman (2006), PCOS patients in there thirties or forties are at a 10-20 percent greater risk for developing type 2 diabetes than those who do not present with PCOS symptoms (Nursing Standard, 2004).

Research has shown that more than 50 percent of the women in the United Stated diagnosed with PCOS are overweight (Drugs, 2006). Insulin resistance is commonly seen in half to two-thirds of the patients that present with polycystic ovary syndrome, and statistically 60 percent of the these patients are obese (Nature Clinical Practice, 2007). Research has shown that PCOS patients (typically obese) can be resistant to some of the effects of insulin that can result in an increase of insulin (British Journal of Nursing, 2006). With insulin elevated (hyperinsulinemia), the ovaries will most likely function irregularly or not at all (British Journal of Nursing, 2006). Some women may show signs of insulin resistance with patchy dark skin called Acanthosis nigricans (AN) (Nursing Standard, 2004). This darkened skin can appear in the axillary, neck, and/or breast folds, and is most common in obese or diabetic patients (Clinical Laboratory Science, 2004). In Figure 2 below, one can see an example of Acanthosis nigrican.

Figure 2. Acanthosis nigrican of the neck region.
Note. Retrieved April 8, 2008 from www.visualdxhealth.com/adult/acanthosisNigric...

Risk factors of hypertension and high cholesterol go hand-in-hand with obesity, and can cause a PCOS patient to develop heart complications (Pediatric Nursing, 2005). According to Karri Hoyt and Margaret Schmidt (2004), people with type 2 diabetes are at a 3:1 higher risk for developing heart disease and 2:1 higher risk for high blood pressure. An increase in blood pressure and low-density lipoprotein (LDL) cholesterol can intensify the effects of polycystic ovary syndrome and decrease the quality of life for the patient (Pediatric Nursing, 2005).

An increased risk for developing endometrial hyperplasia can be linked to exposure to excessive estrogen, and can lead to endometrial cancer (Clinical Laboratory Science, 2004). Cancer of the endometrium occurs in approximately 1-8 percent of the PCOS sufferers that are younger than 40 (Dahlgren & Janson, 2000). If symptoms of Stein-Leventhal are not address and treated, the risk of endometrial cancer can be expected to increase (Dahlgren & Janson, 2000).

Lab Values

Laboratory tests are used to help the clinician confirm or rule out PCOS in women (Lab Tests Online, 2007). There is not one specific lab test that can identify PCOS; a variety of tests need to be performed to accurately diagnose a patient (INCIID, 2006). Hormone tests may include luteinizing hormone, follicle-stimulating hormone, testosterone, DHEA-sulfate, 17-hydroxyprogesterone, and prolactin (Clinical Laboratory Science, 2004). Other forms of testing that may steer the doctor in a diagnosis are a negative pregnancy test and abnormal cholesterol and glucose levels (Clinical Laboratory Science, 2004). Physicians may use lab tests to rule out other causes of irregular ovulation, such as hormone imbalance, Cushing’s syndrome, androgen secreting masses, or pregnancy, before diagnosing PCOS (Pediatric Nursing, 2005) and (Drugs, 2006). After a variety of tests are performed, the physician will compile the results and add them to the clinical symptoms such as hirsutism, obesity and/or PCO to determine if the patient meets criteria for PCOS (Drugs, 2006).

Diagnosis

A diagnosis of Stein-Leventhal syndrome is typically based on clinical presentation, laboratory values, and pelvic ultrasound of the ovaries (Callen, 2008). In addition to the signs and symptoms previously mentioned, the diagnosing physician will, in most instances, require a sonographic evaluation of the physical attributes of the ovaries (Callen, 2008). Ultrasound is considered to be the “gold standard” of choice among radiologic modalities for detecting and imaging polycystic ovary syndrome (Callen, 2008). To effectively illustrate the cystic characteristics of the ovaries, an endovaginal method is used (INCIID, 2006) during the third to fifth day of menstruation (Drugs, 2006). According to Sandra Hagen-Ansert (2006), a polycystic ovary will appear normal to enlarged in size with an increase echogenicity of the ovarian tissue. Most often PCOS is demonstrated bilaterally with each ovary containing at least 10 small follicles that are located near the edges of the ovary like a “string of pearls” (Callen, 2008). Approximately 70-100 percent of all sufferers that present with ovulation irregularities and/or signs of androgenic condition have characteristics of polycystic ovaries (British Journal of Nursing, 2007). In Figure 3, one can see the distinct gross anatomy characteristics of multicystic ovaries.

Figure 3. Gross pathology of polycystic ovary.
Note. Retrieved on April 8, 2008 from www.endotext.org/female/female4/female4.htm.

In Figure 4 below, multiple cysts around the periphery of the ovary are demonstrated with ultrasound. This is commonly called “string of pearls” because the cysts seem to form a chain around the outside edges of the ovary tissue (Callen, 2008).

Figure 4. “String of pearls” around the periphery of ovary with echogenic ovarian tissue.
Note. Retrieved April 8, 2008 from test.cvtcollege.org/.../k.troyer.html.

Women can be diagnosed with PCOS even if their ovaries are not symptomatic of enlargement and multiple cysts (INCIID, 2006). If a patient presents with only enlarged multicystic ovaries, but doesn’t have any further symptoms of irregular menses or hirsutism, she may be diagnosed with polycystic ovaries, not polycystic ovary syndrome (INCIID, 2006).

Treatment

The best form of treatment for polycystic ovary syndrome is management of the symptoms to prevent long term effects of the disorder (Drugs, 2006). The first type of treatment that may be utilized is the non-medicinal approach that encompasses lifestyle changes like diet, stress reduction, and weight loss (Nursing Standard, 2004). If that approach is unsuccessful, physicians may suggest a medicinal form of therapy such as birth control pills to regulate menses and control symptoms of acne and hirsutism (Nursing Standard, 2004). According to Dr. Aherne (2004), birth control pills can level out the cycle of estrogen and progesterone, reduce the risk of cancer of the endometrium, as well as prevent pregnancy.

To help with ovulation issues, PCOS patients may be given progesterone to stimulate ovulation (INCIID, 2006). A drug that can increase the follicle-stimulating hormone and increase ovulation of the ovum is Clomifene or clomiphene citrate (Drugs, 2006). The use of FSH medication can lead to multiple pregnancies, but is used primarily because it is less invasive than in vitro fertilization procedures (Drugs, 2006). An effective medication that can help with ovulation stimulation is Metformin (Glucophage) (Drugs, 2006). Metformin is an insulin-sensitizing drug that has helped some PCOS sufferers with anovulatory problems (Drugs, 2006). With the reduction of insulin, patients may see increased ovulation, clearer skin, and less signs of excess hair growth (British Journal of Nursing, 2007).

Surgery is another treatment method for anovulation. One such method is ovarian drilling that puts holes in the ovary (British Journal of Nursing, 2006). According to Maggi Banning (2006), this procedure is performed by endovaginal laser stimulation of the ovary that has been shown to induce ovulation. In Figure 5 below, one can see a post-surgical image of an ovary with ovarian drilling holes.

Figure 5. Post-ovarian drilling.
Note. Retrieved on April 12, 2008 from www.geocities.com/BourbonStreet/3032/ovary.htm.

Ovarian wedge resection (predecessor to ovarian drilling) was one of the first surgical treatments performed for anovulation (Buckett, Benjamin & Tan, 2000). The resection was of the affected cystic area, which hopefully would cause the remaining ovarian tissue to stimulate ovulation (Lab Tests Online, 2007). Unfortunately, most pelvic surgeries can cause complications such as pelvic adhesions that can further restrict pregnancy (Buckett, Benjamin & Tan, 2000). Surgery is considered an effective treatment, not a cure, for polycystic ovary syndrome (Bucket, Benjamin & Tan, 2000).

Treatment is also necessary for the more visible signs of polycystic ovary syndrome. To reduce hair growth of the face and body from hirsutism, patients may see results with oral contraceptives and insulin-sensitizing drugs (INCIID, 2006). Unfortunately, there are patients that may need to wax the extra hair away or go for electrolysis to permanently remove the hair (INCIID, 2006). Not only do women experience physical challenges with hirsutism, but emotional and psychological challenges as well (Dahlgren & Janson, 2000).

Conclusion

Polycystic ovary syndrome is a complex endocrine, metabolic disorder that affects reproductive aged females with a variety of symptoms. PCOS causes confusion for most people because of the illusion that this disorder affects only the ovaries. To help clarify Stein-Leventhal syndrome, Dr. Michael D. Birnbaum (2008) creatively labeled the syndrome as “polycystic ovary, excess androgen production, adrenal hyperplasia, insulin resistant, hyperlipidemic, often overweight, anovulatory, hirsute, and sometimes acne syndrome”. The confusion of the disorder and symptoms has prompted a basic definition be implemented (Clinical Laboratory Science, 2004). Physicians use this definition as a guide to diagnosing PCOS, but in most instances there are too many variables to follow the PCOS standard definition. Patients have many levels of need during their struggle with PCOS and its symptoms. These patients should receive ample concern, understanding, and commitment from their medical providers to fully understand and treat each symptom individually. Continued treatment can facilitate a normal life for most women plagued with polycystic ovary syndrome, but their struggle will continue throughout their lives because no cure has been discovered for PCOS yet.

References

• Aherne, S.A. (2004). Polycystic ovary syndrome. Nursing Standard, 18(26), 40-44.
• Banning, M. (2006). Symptoms and treatments of polycystic ovary syndrome. British Journal of Nursing, 15(12), 635-639.
• Brian, J.N. & Heine, D.N. (2004). PCOS a common endocrine disorder can have a profound effect on the quality of life for women, RDH (January), 52-55.
• Birnbaum, M.D. (2008). Poly-Cystic Ovary Syndrome - "PCOS". Retrieved from www.infertilityphysician.com/androgen/pcos.html.
• Buckett, W.M., Benjamin, A., & Tan, S.L. (2000). Pregnancy outcome for women with polycystic ovary syndrome. In Kovacs, G.T. (Ed.), Polycystic ovary syndrome (pp. 187- 201). Retrieved from www.netlibrary.com.
• Callen, P.W. (2008). Ultrasonography in obstetrics and gynecology (5th ed.). Philadelphia: Saunders Elsevier.
• Chang, R.J. (2007). The reproductive phenotype in polycystic ovary syndrome, Nature Clinical Practice, 3(10), 688-695.
• Dahlgren, E. & Janson, P.O. (2000). Long-term health implications for women with polycystic ovary syndrome. In Kovacs, G.T. (Ed.), Polycystic ovary syndrome (pp. 70-78). Retrieved from www.netlibrary.com.
• Elghblawi, E. (2007). Polycystic ovary syndrome and female reproduction. British Journal of Nursing, 16(18), 1118-1121.
• Hagen-Ansert, S.L. (2006). Textbook of diagnostic ultrasonography (6th ed.). St. Louis: Mosby Elsevier.
• Hoyt, K.L. & Schmidt, M.C. (2004). Polycystic ovary (stein-leventhal) syndrome: etiology, complications, and treatment. Clinical Laboratory Science, 17(3), 155-163.
• Kovacs, G.T. (2000). Introduction: polycystic ovary syndrome is not just a reproductive problem. In Kovacs, G.T. (Ed.), Polycystic ovary syndrome (pp. 1-3). Retrieved from www.netlibrary.com.
  library.med.utah.edu/.../mml/hrovt_chin.html
• Polycystic Ovary Syndrome (PCOS) FAQ. Retrieved April 7, 2008, from
  www.inciid.org/faq.php?cat=infertility101&id=2
• Snyder, B.S. (2005). Polycystic ovary syndrome (PCOS) in the adolescent patient: recommendations for practice. Pediatric Nursing, 31(5), 416-421.
• Stankiewicz, M. & Norman, R. (2006). Diagnosis and management of polycystic ovary syndrome a practice guide. Drugs, 66(7), 903-912.
  test.cvtcollege.org/.../k.troyer.html
  www.endotext.org/female/female4/female4.htm
  www.geocities.com/BourbonStreet/3032/ovary.htm
  www.visualdxhealth.com/adult/acanthosisNigric...
  

Testicular Cancer: A Young Man’s Disease
Chasity Krause
July 6, 2008

Testicular cancer is a rare form of cancer that affects young Caucasian males, mainly in the ages of 15 to 35. The most common tumor type is the seminoma tumor, which accounts for nearly 40% to 50% of all germ cell tumors. Diagnosis typically includes an initial evaluation of the scrotum with ultrasound, followed by computed tomography and chest x-ray. Treatment is some combination of orchidectomy, retroperitoneal lymph node dissection (RPLND), radiation, and chemotherapy. In addition, due to the radiosensitivity of seminomas the prognosis is usually better than in non-seminoma tumors. In fact, the overall cure rate is approximately 99% when the cancer is treated early. One way to improve the chances of finding a tumor early is to perform self-examinations regularly. This may lead to an early treatment and an early cure.

Introduction

The testes are the paired male gonads of reproduction located in the scrotum of the male pelvis. Their functions include producing, storing, and transporting sperm, as well as, producing testosterone. A fibrous layer called the tunica albuginea, which extends into the testis to form the mediastinum testis, surrounds the testis. Within the testis are approximately 250 seminiferous tubules, where the spermatozoa are produced. The spermatozoa are directed into the rete testis within the mediastinum and through the efferent ducts into the epididymis where they are stored and matured into sperm (Kammermeier, 2004). The interstitial cells located between the seminiferous tubules are responsible for producing testosterone (Shier, Butler, & Lewis, 2007). Figure 1 is a drawing of a testis, epididymis, and ductus deferens.

Figure 1: Testis, epididymis, and ductus deferens.

Note: Image from Eilts, B. E., Jones, E., & Huey, E. (2004, November 1). Testis, epididymis, and ductus deferens. Retrieved March 29, 2008, from http://www.vetmed.lsu.edu/eiltslotus/theriogenology-5361/male%20r18.gif

As with all organs of the body, complications may arise. One disorder of the testes is testicular cancer. This term is very broad in that it includes several classifications and subtypes, as follows:

• Germ cell tumors,
• Stromal tumors,
• Mixed germ cell – stromal tumors,
• Metastatic neoplasms, and
• Rare tumors and non-neoplastic tumorous conditions (Mostofi & Sobin, 1977; Rumack, Wilson, & Charboneau, 2005).

According to McCullagh & Lewis (2005), nearly 95% of all testicular cancers are of the germ cell tumor classification. Germ cell tumors are further divided into seminoma and non-seminoma types. Pure seminoma masses come from cells in the seminiferous tubules (McCullagh & Lewis, 2005). Non-seminomas are subdivided into four categories – embryonal carcinoma, teratoma, choriocarcinoma, and yolk sac tumors (McCullagh & Lewis), and arise from multiple sources. For the purposes of this paper, seminoma malignancies will be the focus as these are the most common, and comprise 40% to 50% of all germ cell neoplasms (Rumack, et al).

Etiology

Testicular cancer is a rare cancer, comprising only 1% of malignancies in men. However, it is the most common cancer of males ages 15 to 35 (Owen, 2006), as well as, the fifth leading cause of death in the same age group (Rumack, et al, 2005). Pure seminoma tumors most often occur in males ages 35 to 39 years old (McCullagh & Lewis, 2005). The causes are not well understood; however, a history of unilateral or bilateral cryptorchidism, family history of the disease, previous bout of the disease, and being Caucasian increases the chances of developing testicular cancer (TC) (Rumack, et al; Stevenson & McNeill, 2004). Additionally, Shaw (2008) maintains that a person with a history of smoking increases the chances of developing TC. For instance, one study showed a two-fold increase for patients with a twelve pack per year history. Unfortunately, if patients cease smoking, the risk does not decrease, nor is there a “difference in risk between former and current smokers” (Shaw, 2008, p. 469).

During fetal development, the testes descend from the area of the kidneys to the scrotum. However, in some instances, one or both testes will not descend all the way, which is termed cryptorchidism. Often the misplaced testis is located in the abdomen, inguinal canal, or other ectopic location. Orchiopexy is the surgical treatment used to relocate the testis to the scrotum (Owen, 2006). The risk of disease increases five to ten times if the patient had cryptorchidism (McCullagh & Lewis, 2005), and does not decrease with orchiopexy although palpation of a lump is easier for early diagnosis and treatment (Owen). In addition, 5% to 10% of men that have had cryptorchidism will develop a tumor in a contralateral, normal testis (Poirier & Rawl, 2000; Rumack, et al, 2005; Stevenson & McNeill, 2004). Rumack, et al (2005, p. 854), also state that “seminoma is the most common tumor type in cryptorchidism.” Finally, cancer tends to develop in the right testis more often than the left, which coincides with cryptorchidism occurring on the right side more frequently (Richie, 1998; Stevenson & McNeill, 2004). Figure 2 depicts the descent of the testes into the scrotum.

Figure 2: Descent of testes into scrotum.
Note: Image from Undescended testes. (2005). Retrieved March 29, 2008, from http://www.thirdage.com/ebsco/files/99744.html

Nearly a third of the patients have a genetic link to the disease. Brothers of cancer patients have six to ten times more chance of having the disease as well. The gene associated with TC is testicular germ-cell tumor 1 (TGCT1) mapped to chromosome Xq27. Most incidences of the disease occur in the northern European countries of Scandinavia, Switzerland, and Germany and New Zealand. The fewest cases occur in Asia and Africa. Consequently, white males tend to develop the disease five times more than black males (McCullagh & Lewis, 2005). Furthermore, estrogen stimulation during pregnancy has also been related to an elevated risk of TC, along with “inguinal hernia, testicular torsion, post-puberty mumps orchitis, high socioeconomic status, and an increase in sedentary behaviour” (McCullagh & Lewis, 2005, p. 47).

Symptomology

The most common sign of TC is an intratesticular lump that may be painful or painless (Shaw, 2008). Additional signs include “swelling of the testicle, change in the tissue texture, aching, feeling of heaviness in the scrotum and asymmetry within the testis” (McCullagh & Lewis, 2005, p. 46). According to Rumack, et al (2005) between 65% and 94% of patients has a painless unilateral testicular mass or a diffusely enlarged testis.

If the condition has metastasized, the patient may present with symptoms of hemoptysis, breathlessness, and back pain (McCullagh & Lewis, 2005). Shaw (2008) also includes neck mass, abdominal mass, cough, dyspnea, and gastrointestinal problems as possible signs of metastasis. Furthermore, gynecomastia may be present if the tumor secretes beta human chorionic gonadotropin (Shaw, 2008). Research indicates that as few as 4% and as many as 30% of patients present with metastatic disease (Rumack, et al, 2005; Stevenson & McNeill, 2004).

Stevenson and McNeill (2004) expand on the sites for metastasis to say that the spread is predictable, and that the sites affected are the retroperitoneum, lungs, and mediastinum. Additionally, metastasis occurs through lymphatic routes in all types of testicular cancer. Consequently, the sites for further evaluation are known in advance. Stevenson and McNeill (2004, p. 357) call these “primary landing zones.” For example, a left testicular tumor will spread to the preaortic and para-aortic lymph nodes, and a right testicular tumor will metastasize to the interaortocaval region. Furthermore, if the disease is large-volume then metastasis may be present in the distal iliac and inguinal lymph nodes. Finally, it is more common for the spread to be contralateral in right-side tumors than in left-side tumors (Sheinfeld & Herr, 1998; Stevenson & McNeill, 2004).

Diagnosis

An initial physical examination by a primary care physician may include transillumination of the abnormal structure. If the light does not pass through the mass, then it is solid; however, if the light does pass through, then the mass is most likely fluid-filled, as in a hydrocele. It is important to remember, though, that this is not a defining test and it should be used in conjunction with ultrasound (Shaw, 2008).

Sonography is extremely important in the diagnosis of scrotal masses because distinction can be made between intratesticular and extratesticular masses. Ultrasound is also useful in differentiating between a testicular mass and a varicocele, hernia, or hydrocele (Rumack, et al, 2005; Stevenson & McNeill, 2004). Extratesticular masses are benign, but intratesticular masses are nearly always malignant (Rumack, et al). Once it is determined that the mass is intratesticular, computed tomography (CT) scans are performed to evaluate for metastasis in the abdomen and pelvis. Additionally, chest x-rays are taken to evaluate for spread to the lungs (McCullagh & Lewis, 2005).

Sonographic characteristics of malignant masses include a hypoechoic mass in comparison to normal testis parenchyma. Additionally, if the mass demonstrates hemorrhage, necrosis, calcification, or fatty changes, there may be focal areas of increased echogenicity within the tumor (Rumack, et al, 2005).

According to Owen (2006), most tumors appear as hypoechoic focal masses on ultrasound. Specifically, seminomas are “homogeneous, hypoechoic masses with a smooth border” (Owen, 2006, p. 550). Additionally, the tumors can be lobulated or multinodular, and larger tumors may infiltrate and replace the entire parenchyma (Eble, Sauter, Epstein, & Sesterhenn, 2004). However, differentiating between benign and malignant masses is not possible with sonography, by evaluating color Doppler, or by use of Doppler waveforms (Owen). Figure 3 demonstrates a testis with a large seminoma and a smaller non-seminoma in the left testis.

Figure 3: Left testis images including A) Longitudinal image visualizing seminoma and non-seminoma tumors and B) Transverse image of color Doppler flow to seminoma tumor.
Note: Images from Chaitali, S. (n. d.). Germ cell tumor testis: Seminoma. Retrieved March 28, 2008, from http://www.sonoworld.com/Sonoworld/Cases/Cases.aspx?CaseID=230

Subsequent imaging typically includes computed tomography (CT) scans and a chest x-ray to evaluate for metastasis. The stage and grade of the cancer is assessed, which will be combined with the findings of the orchidectomy for determination of a treatment protocol. Figure 4 is CT scan showing lymph node metastasis, and Figure 5 shows a mass in the lung.

Figure 4: Lymph node metastases.
Note: Image from Testicular cancer aftercare. (n. d.). Retrieved March 29, 2008, from http://www.tc-cancer.com/atreatment.html

Figure 5: Lung cancer mass.
Note: Image from What is radiology? (2005, November 3). Retrieved March 29, 2008, from http://www.lakeridgehealth.on.ca/patient_care/interventional_radiology/presentations/radiology/slide10.htm
After surgery, the tumor cells are evaluated under a microscope to determine the histological type, seminoma or non-seminoma. Microscopically, a seminoma will have “fairly uniform cells, typically with clear or dense glycogen containing cytoplasm, a large regular nucleus, with one or more nucleoli, and well defined cell borders” (Eble, et al, 2004, p. 230). Visually, the tumors are gray, cream, or pale pink in color. Areas of necrosis may appear yellow (Eble, et al). Figure 6 is a picture from a microscopic evaluation of a seminoma tumor.

Figure 6: Microscopic sample of seminoma tumor.
Note: Image from Shireman, P. (1994, March 7). Seminoma in a 43-year old Kansas City man. High power. Retrieved March 29, 2008, from http://www.lmp.ualberta.ca/resources/pathoimages/PC-S.htm

Lab Findings

Blood samples are taken to evaluate for levels of human chorionic gonadotropin (HCG), alpha-fetoprotein (AFP), and lactate dehydrogenase in patients that are suspected of having cancer (Shaw, 2008). HCG is tested because it is not normally found in the serum or urine of males, and its presence indicates a germ cell tumor. HCG is secreted by trophoblastic cells found in germ cell tumors and by normal placental cells. Yolk sac cells secrete AFP, which is another indicator for germ cell tumors (Damjanov, 2006). According to Damjanov (2006), seminomas do not secrete enough HCG to use this as a typical serologic marker. However, the tumors typically contain trophoblastic giant cells that secrete a small amount of HCG. Conversely, McCullagh & Lewis (2005) states that seminomas do secrete HCG but not AFP. Therefore, even a small amount of HCG will be indicative of cancer. Finally, lactate dehydrogenase is also evaluated because it is found to be elevated when metastasis is present (Shaw).

Treatment

According to Shaw (2008) and McCullagh and Lewis (2005) the primary treatment for testicular masses is orchidectomy. Shaw (2008) further explains that both the testis and spermatic cord are removed. In some instances, retroperitoneal lymph node dissection (RPLND) is the primary procedure used for diagnostic and therapeutic purposes. Most RPLNDs are performed as open surgical procedures; however, research is being conducted to improve upon laparoscopic procedures for lower stage conditions in order to reduce the recovery time and ultimately to reduce morbidity rates (Stevenson & McNeill, 2004).

Before surgery, the patient should be questioned about their history of asthma, diabetes, high blood pressure, and heart disease, all of which can create complications during the surgery. Additionally, the patient should be informed about the possible complications that may affect fertility. Patients often elect to bank sperm in the event fertility decreases after the surgery (Stevenson & McNeill, 2004).

Preoperative lab work includes “complete blood count with differential, chemistry profile, liver function tests, prothrombin time/partial thromboplastin time/international normalized ratio, tumor markers, urinalysis, electrocardiogram, and anesthesia evaluation” (Stevenson & McNeill, 2004, p. 357). Additionally, patients will undergo one of several bowel preparation procedures before entering the hospital. Some of the options include a clear liquid diet, laxatives, or enema. It is important the patient stay hydrated and avoid any blood thinning medications as well (Stevenson & McNeill). The surgery itself, in the case of RPLND, may last as long as five to ten hours, and the patient may be in the hospital for four to seven days afterwards (Stevenson & McNeill).

After performing the orchidectomy and/or RPLND, the mass is evaluated for its histological type. The diagnosis of the histological type is combined with the assessment of the stage of the disease, as determined by the prior computed tomography, chest x-ray, and findings from the laparoscopy, and a treatment protocol is formed. Staging of cancer is based upon the American Joint Committee on Cancer’s categories for “TNMS (primary tumor, regional nodes, metastasis, serum tumor markers)” (Shaw, 2008, p. 471). The questions to be answered are (1) How far has the tumor spread into the surrounding tissues?; (2) Has it spread into the regional lymph nodes?; (3) Has it metastasized?; and (4) What are the levels of the serum tumor markers? There are three stages for describing the level of infiltration of the cancer. In Stage I the cancer is only in the testis. Stage II the cancer involves the testis and retroperitoneal or para-aortic lymph nodes near the kidneys. In Stage III, the cancer has spread beyond the retroperitoneal lymph nodes (Stage Information, n. d.).

The type of adjuvant treatment provided is determined based on the findings of the stage of the cancer (Shaw, 2008). The most common options for follow-up treatment include observation, RPLND, radiation, and chemotherapy (Stevenson & McNeill, 2004; Shaw, 2008). Below are the treatment options for seminomas based on the stage of the cancer (Shaw, 2008, p. 472):

Stage	Treatment
I	Usually radiation, although observation and limited chemotherapy are also options
II	IIA: Radiation of the regional lymph nodes IIB or IIC: Three cycles of three-drug chemotherapy
III	Three-drug chemotherapy; if there is no response, consider clinical trials of other chemotherapy drug combinations Brain metastasis is present: Treat with radiation of the brain or surgical removal

For stage I treatment, monthly lab testing may also be included to ensure the tumor marker values have not increased. For treatments including chemotherapy, the drugs used include cisplatin and etoposide for two-drug regimens, with the addition of bleomycin for three-drug regimens (Treatment Options By Stage, 2007; Shaw, 2008). Finally, as time passes and improvements made, decisions for ongoing treatment are assessed and updated.

Prognosis

Fortunately, as diagnosis and treatment improved, the overall death rate decreased 50% from 1980 to 2000 (Shaw, 2008), with an overall cure rate of approximately 80% to 90% (McCullagh & Lewis, 2005). Additionally, patients with early stages of TC and no metastasis have a 95% to 99% cure rate (McCullagh & Lewis, 2005; Shaw, 2008). If the disease is localized to one spot, the patient has an approximate five-year survival rate of 95%. In the case of seminomas, the slow rate of growth and spread (Stevenson & McNeill, 2004) may contribute to the overall improved prognosis. However, if the patient has metastasis to the retroperitoneum the five-year survival rate declines to approximately 90% (McCullagh & Lewis), and in another study the survival rate was 91% to 96% (Shaw). Patients diagnosed with advanced metastasis have a ten-year survival rate of 66% to 94% depending on the extent of the spread (Shaw).

One major improvement is in the surgery itself. Up until the 1980s RPLND would result in a resection of the nerves that are responsible for emission and antegrade ejaculation (Fosså, 2004). This resulted in what Fosså (2004) calls a “dry ejaculation” that was present in 80% of the patients. Newer nerve-sparing techniques result in only 10% of patients experiencing “dry ejaculation” (Fosså).

Additionally, Fosså (2004) reports that the quality of life is similar to the normal population with chemotherapy patients having the least-favorable responses to survey questions, young patients being more anxious, and some patients experiencing chronic fatigue. However, the percentage of patients experiencing chronic fatigue is 16% as compared to 10% in the general population (Fosså, 2004).

Although, the prognosis is positive, some secondary problems may arise. For example, there is an increased risk of TC developing in the contralateral testis within fifteen years (Shaw, 2008). One study resulted in a 12-fold greater risk of developing a new TC, especially within the first five years and gradually decreasing over time (Shaw). Patients with recurrent TC have a 93% survival rate at ten years, although, it is important that patients visit their physician annually (Shaw). Other sequelae include leukemia, which is the most common secondary malignancy to form, solid malignant tumors, fertility issues, gastrointestinal disorders, and neuropathy (Fosså, 2004; McCullagh & Lewis, 2005; Shaw, 2008). Each of the primary adjuvant therapy types, chemotherapy and radiation, have various effects that may be either short- or long-term (Fosså; McCullagh & Lewis).
Effects of Chemotherapy

Some of the more common clinical symptoms of chemotherapy include alopecia, fatigue, nausea and vomiting, neutropenia, and sepsis (McCullagh & Lewis, 2005). It is not proven that chemotherapy increases the risk of secondary solid tumors, whereas, the risk of leukemia is increased three-fold in treatment with cisplatin (Fosså, 2004). However, both cisplatin and etoposide are linked to the risk of developing leukemia. Typically, leukemia is diagnosed within four to seven years of treatment for TC (Fosså).

Approximately 60% of patients with TC have low fertility at the time of diagnosis. After treatment, as many as 30% have decreased fertility, which can be contributed in part to treatment with chemotherapy (Shaw, 2008). The toxic effect of chemotherapy on the germ cells causes the infertility. Increased follicle-stimulating hormone and luteinizing hormone and decreased testosterone is evidence of hypogonadism, hence, testosterone supplements are required (Shaw). Fosså (2004) reports that 27% of patients have hypogonadism in the contralateral testis, and the azospermia or oligospermia may resolve over time. Although, as many as 10% to 15% of patients have long-term persistent azospermia or oligospermia after treatment (Fosså, 2004). The ability for spermatogenesis to improve depends upon the age of the patient, the severity of oligospermia before treatment, and the cumulative doses of cisplatin-based chemotherapy (McCullagh & Lewis, 2005). Before any treatment begins, it is often recommended for the patient to evaluate cryopreservation of their sperm, in the event they do not regain some fertility (Fosså; McCullagh & Lewis; Shaw).

Chemotherapy can also result in damage to auditory and peripheral sensory nerves. Often, this resolves within six to twelve months after treatment (McCullagh & Lewis, 2005). Fosså (2004) further reports those treatment regimens including etoposide often result in decreased peripheral sensory neuropathy. Although, one study found tinnitus persists for more than ten years in 11% of patients. An additional effect is a Raynaud-like phenomenon that is associated with erectile dysfunction (Fosså, 2004). Other chemotherapy related side effects include cerebrovascular accidents, embolism, myocardial infarction, and angina (Fosså, 2004; McCullagh & Lewis, 2005; Shaw, 2008), which are a result of the hypertension and hyperlipidemia related to cisplatin-based therapy (McCullagh & Lewis, 2005; Vaughn, Gignac, & Meadows, 2002).
Effects of Radiation Treatment

Leukemia is the most common secondary malignancy developing after treatment of TC (Shaw, 2008). Radiation induced leukemia often results in acute myelogenous or lymphocytic leukemia. Fortunately, with improved treatment measures that include lower doses, narrower exposure fields, and no longer exposing the mediastinum this risk has decreased (Shaw). However, the risk of developing leukemia persists for up to twenty years after treatment (Fosså, 2004).

Radiation therapy also increases the risk of solid tumors by two to three times (McCullagh & Lewis, 2005). These tumors are most often diagnosed within ten to fifteen years of treatment (Fosså, 2004). The types of tumors found are primarily sarcomas or cancer of the genitourinary or gastrointestinal tract (McCullagh & Lewis). Furthermore, infradiaphragmatic radiotherapy increases the risk of stomach cancer two-fold. Even prophylactically applied radiotherapy increases the risk of lung cancer and secondary thyroid cancer. Consequently, most of the malignancies are found in or near the target field of radiation (Fosså).

Fertility is affected very little as Leydig cell function is not affected by radiation to a great extent. However, azospermia or oligospermia may be present for up to six to twelve months following treatment. Overall, TC survivors treated with radiation still have decreased testosterone levels and an increased risk of hypogonadism when compared to the average population without TC (Fosså, 2004).

Finally, myelopathy is almost non-existent with radiation therapy, whereas, side effects of the gastrointestinal system include peptic ulcers, diarrhea, and pancreatitis. In addition, infradiaphragmatic treatment can result in decreased renal function that is apparent after 11 years (Fosså, 2004).
Effects of Combined Chemotherapy and Radiation Treatment

In all possible outcomes, combined treatment of chemotherapy and radiation increases the risk of developing a secondary condition. For example, the risk of developing leukemia, solid tumors, infertility, and gastrointestinal disease are all significantly increased (Fosså, 2004).

Conclusion

Testicular cancer is one of the more rare forms of cancer. However, it is important to teach young males about the warning signs and possible outcomes if the condition is allowed to persist. One possibility is to train adolescent males how to correctly perform a testicular self-examination. Shaw (2008) states that “treatment is highly effective even when the diagnosis is made incidentally through examination or because of symptoms” (Shaw, 2008, p. 470). The test should be performed at the same time each month and with the patient standing (Shaw).
Oftentimes, males must overcome feelings of machismo and a lack of expressiveness in order to discuss their symptoms and to receive treatment (McCullagh & Lewis, 2005), which might lead to an extended period of time before treatment is received. Additionally, at the age of adolescence, an enlarged scrotum may encourage feelings of masculinity, when in reality there is a potentially life-threatening problem. Therefore, all young males should receive information on the signs and symptoms of testicular cancer, so they know when there is a problem and how to get help. Appendix A provides an explanation for proper self-examination.

References

• Chaitali, S. (n. d.). Germ cell tumor testis: Seminoma. Retrieved March 28, 2008, from http://www.sonoworld.com/Sonoworld/Cases/Cases.aspx?CaseID=23
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• Eilts, B. E., Jones, E., & Huey, E. (2004, November 1). Testis, epididymis, and ductus deferens. Retrieved March 29, 2008, from http://www.vetmed.lsu.edu/eiltslotus/theriogenology-5361/male%20r18.gif
• Fosså, S. (2004). Long-term sequelae after cancer therapy: Survivorship after treatment for testicular cancer. Acta Oncologica, 43(2), 134-141. Retrieved January 22, 2008, from CINAHL with Full Text database.
• Kammermeier, M. J. (2004). Sonography: Introduction to normal structure and function. (2nd ed.). J. Wilke (Ed.), The male pelvis (p.235-237). St. Louis: Elsevier.
• McCullagh, J., & Lewis, G. (2005, March 2). Testicular cancer: epidemiology, assessment and management. Nursing Standard, 19(25), 45. Retrieved January 22, 2008, from CINAHL with Full Text database.
• Mostofi, F. K. & Sobin, L. H. (1977). International histological classification of tumors of the testes. World Health Organization. Geneva.
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• Richie, J. P. (1998). Neoplasm of the testis. P. C. Walsh, A. B. Retik, E. D. Vaughan, & A. J. Wein (Eds.), Campbell’s urology (7th ed., pp. 2411-2452). Philadelphia: W. B. Saunders.
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Jeopardy Bowl

In case you missed it, a grand educational endeavor took place at the symposium.  After a long day of ultrasound physics, everyone just wanted to unwind.  But this was no time for lighthearted sluggishness.   It was time for a meeting of the minds, and the struggle was on for the right to be called "Jeopardy Bowl Champions" and their names permanently engraved on the Golden Probe Award.

The atmosphere was initially relaxed, as all of the teams represented their respective colleges soundly (no pun intended) in the beginning rounds of the second annual North Carolina Ultrasound Society Jeopardy Bowl.  However, as the teams faced off in the later rounds of this single-elimination competition, we came to realize that there was an underlying, obsessive force that was driving the contestants toward the desirable, ever-elusive Golden Probe Award.  Even the though the stress factor was playing a role on everyone involved, the mood remained pleasant and professional with everyone having a great time.

Regrettably, not all teams could be rewarded, for when the night was over, there were only two champions proclaimed.

  

The Echo Quiz Bowl winners from the left to right are Lisa Heale, Kelly Parker, and Allie Carte  “The Heart Attackers” from Pitt Community College.

The General Quiz Bowl winners are Sarah Mizell, Tiffnay Outlaw and Molly Mathias “The Sono Sea Devils from Cape Fear Community College.

The NCUS Jeopardy Bowl Committee greatly appreciates every team member’s hard work and enthusiasm.  We also would like to thank each college that was represented that night and look forward to your continual support of this competition.

Crossword Puzzle

Across

1.     Benign adrenal tumor arising from the medulla that is associated with hypertension
4.     Malignant pediatric liver tumor
5.     Abnormally shaped red blood cell disorder
8.     Facial bone that helps form the base of the nasal septum
11.   Results from hyperplasia of the gallbladder wall and produces a comet tail artifact
12.   Structure that keeps food from passing into the trachea
13.   The outer part of the kidney.
14.   Lower portion of the sternum
17.   Chewing
19.   Type of glands that release their hormones directly into the bloodstream.
20.   Cerebral lobe responsible for our eyesight.

Down

2.     An abnormal increase in the number of normal cells in a tissue.
3.     The AV node transmits electrical impulses to the....
6.     Blood within stool
7.     Also known as cheiloschisis
9.     Hormones secreted by the adrenal cortex that aid in the development of male sex characteristics
10.   Controls the opening between the right atrium and right ventricle
15.   Muscle that seperates the chest from the abdominal cavity
16.   Any vertical plane that divides the body into unequal left and right portions.
18.   Not malignant