Ovarian Torsion

Juneil R. Laurente BSN- 4G

Class Instructor : Mrs. Luminarias R.N.

Ovarian Torsion Sex : Ovarian torsion applies strictly to the female sex only. Age : Ovarian torsion can occur at any age, but most cases occur in the early reproductive years. Approximately 17% of cases have been found to occur in premenarchal or postmenopausal women. Background : Ovarian torsion (adnexal torsion) is an infrequent but significant cause of acute lower abdominal pain in women. The clinical presentation is often nonspecific with few distinctive physical findings, commonly resulting in delay in diagnosis and surgical management. Anatomy : The ovary has a dual arterial and venous blood supply. The arterial supply is derived from the ovarian arteries that branch from the abdominal aorta, as well as from the adnexal branches of the uterine artery. The venous system parallels the arterial, with the exceptions that the left ovarian vein empties into the left renal vein and that the right ovarian vein courses into the inferior vena cava. The fallopian tubes are fed and are drained by means of vessels that anastomose with ovarian branches derived from uterine vessels in the mesosalpinx.

Exercise-induced ovarian torsion in the cycle following gonadotrophin therapy: case study article E.D. Littman, J. Rydfors and A.A. Milki The incidence of ovarian torsion has been reported to be increased during controlled ovarian hyperstimulation. In this report we describe exercise-induced ovarian torsion in an ovary with a persistent cyst, following a failed gonadotrophinstimulated intra-uterine insemination cycle. This report suggests that the risk of ovarian torsion persists beyond the treatment cycle and that patients should be instructed to refrain from exercise or strenuous activity if regression to normal ovarian size has not been documented. Ovarian torsion should be high in the differential diagnosis in patients experiencing abdominal pain with a history of recent gonadotrophin stimulation. Key words: exercise/gonadotrophin stimulation/laparoscopy/ovarian torsion

Case study article : The patient is a 38-year-old, gravida 1, para 1 female, with a history of unexplained infertility, who previously was able to conceive and successfully deliver, after her first cycle of gonadotrophin stimulation and intra-uterine insemination (IUI). Approximately 1 year after delivery of her first child, the patient returned to her primary gynaecologist for further therapy to achieve a second pregnancy. She underwent a gonadotrophin/IUI cycle, which resulted in two follicles on the right ovary (20 mm, 16 mm) and two follicles on the left ovary (18 mm, 13 mm). She received an injection of HCG, and underwent IUI 38 h later. The cycle was unsuccessful and the patient was found to have persistent cysts on the left ovary measuring 25 mm and 11 mm, on a baseline ultrasound performed on day 3 of her menstrual cycle. This led to the cancellation of a repeat gonadotrophin cycle. Two weeks later, while the patient was participating in a kick-boxing class, in which no abdominal trauma was sustained, she began experiencing severe pelvic and

abdominal pain. She was seen by an Urgent Care physician who attributed the pain to abdominal wall sprain. Over the next 2 weeks she had intermittent abdominal pain of a colicky nature which radiated to the left groin area. She reported to her gynecologist for another baseline ultrasound after her subsequent menstrual period, in order to begin a new gonadotrophin cycle. Transvaginal ultrasound revealed an enlarged left ovary measuring 7 x 8 x 10 cm. She was diagnosed with chronic left ovarian torsion and was taken to the operating room for further therapy. A laparoscopy was performed and showed an enlarged, mostly necrotic, left ovary. The necrotic portion, which was thought to represent 80% of the ovary, was removed. The patient recovered well from her laparoscopic surgery and since then has undergone two gonadotrophin-injection cycles and one IVF cycle without success. During the IVF cycle one oocyte was retrieved from the left ovary.

- Pathophysiology Ovarian torsion classically occurs unilaterally in a pathologically enlarged ovary. The irregularity of the ovary likely creates a fulcrum around which the oviduct revolves. The process can involve the ovary alone but more commonly affects both the ovary and the oviduct (adnexal torsion). Approximately 60% of torsion occurs on the right side. Multiple factors have been found to be responsible for the development of ovarian torsion. Although torsion may rarely occur in normal adnexa, adnexa refers to the appendages of an organ, it more frequently arises from one of many anatomic changes. Torsion of a normal ovary is most common among young children, in whom developmental abnormalities such as excessively long fallopian tubes or absent mesosalpinx may be responsible. In fact, less than half of torsed ovaries in pediatric patients involve cysts, teratomas, or other masses. During early pregnancy, the presence of an enlarged corpus luteum cyst likely predisposes the ovary to torsion. Women undergoing induction of ovulation for infertility carry an even greater risk, as numerous theca lutein cysts significantly expand the ovarian volume. Ovarian tumors, both benign and malignant, are implicated in 50-60% of cases of torsion. Involved masses are nearly all greater than 4-6 cm, although torsion is possible with smaller masses. In United States of America, studies reveal that ovarian torsion is the fifth most common gynecologic surgical emergency accounting for 2.7% of cases of acute gynecologic complaints in one series.but in other countries ovarian torsion is encountered more often in women who have had ovarian stimulation, which likely accounts for a small increased incidence in developed countries.

Mortality/Morbidity Most patients with ovarian torsion have a delayed diagnosis, often resulting in infarction and necrosis of the ovary. The ovarian salvage rate has been reported below 10% in adults but as high as 27% in a study among pediatric patients. Although it is unlikely that the loss of a single ovary results in significantly reduced fertility and no cases of death have been reported due to ovarian torsion, early diagnosis allows for conservative laparoscopic treatment and reduction in complications.

Clinical Details Confident and early diagnosis of adnexal torsion is imperative. Color Doppler sonography has a vital role in the examination of women with lower abdominal and pelvic pain. The signs and symptoms associated with torsion are variable and nonspecific. Most patients present with severe lower abdominal and pelvic pain, nausea, and vomiting. The differential diagnosis to be considered at clinical examination include appendicitis, gastroenteritis, ectopic pregnancy, pelvic inflammatory disease, and ruptured corpus luteum. Among adolescents, hemorrhagic ovarian cysts must also be considered. Laboratory tests are not helpful, because most signs and symptoms of ovarian torsion can be associated with leukocytosis.

Preferred Examination Diagnostic sonography should be the first examination performed; typically, the affected ovary is enlarged, with multiple immature or small follicles along its periphery. Color Doppler sonography can help in determining whether blood flow is impaired. MRI may demonstrate ovarian enlargement and intraperitoneal fluid. In one case report, MRI demonstrated a twisted pedicle. If hemorrhagic infarction is present, MRI can demonstrate an enlarged ovary with displaced follicles. T2-weighted images show low signal intensity caused by interstitial hemorrhage, and T1weighted images show a thin rim of high signal intensity without contrast enhancement Although a lack of intraovarian arterial and venous flow enables confident diagnosis, torsion may be incomplete; incomplete torsion may be associated with adnexal flow, as depicted with color Doppler sonography. Rarely, the use of improper settings can cause erroneous findings of absent flow. Check that the proper settings are used by looking for flow in the internal iliac vein. In some cases, flow depiction may be difficult to obtain from the affected ovary, as well as the healthy contralateral ovary. In these cases, the characteristic gray-scale morphologic image of ovarian torsion alone may help in making the diagnosis.

Medical Intervention Surgery is done

Reaction : It relates on what we discuss about the different disorders in reproductive system. We discussed also the female reproductive system on our last part of our lesson on Medical Surgical Nursing that was been thoroughly discussed by Mrs. Luminarias B.S.N., R.N. We also tackle the reproductive system of both female and male. We learn that the ovary is the most important part of female that also produces the sex hormones estrogen and progesterone. It is where the egg cell forms that produce baby when sperm cells contact to each others and bears a fetus inside the uterus. With this disorders or abnormalities a female can’t produce a certain egg cell because of its ovary that forms into a torsion. There are no drugs that can treat this kind of abnormality rather than a surgical operation must be done. this abnormality occur during the early age of teen on female sex only due to multiple factors that can affect ovarian torsion one of this is excessively long fallopian tubes or absent mesosalpinx. There is no such case that ovary torsion can be lethal but complication may lead to death. It is said that the ovary is the cleanest and purest part of the body, daily check up to obstetrician may help to prevent or even treat this kind of abnormality.

Jessielou Visto BSN 4-G Article : Polycystic Kidney Disease Patricia D. Wilson, Ph.D. Polycystic kidney diseases are a leading cause of end-stage renal failure and a common indication for dialysis or renal transplantation. Recent advances have led to insights into mechanisms underlying the cause and prognosis of these diseases and suggest new directions for treatment. Polycystic kidney disease may arise sporadically as a developmental abnormality or may be acquired in adult life, but most forms are hereditary. Among the acquired forms, simple cysts can develop in kidneys as a consequence of aging; dialysis, drugs, and hormones can cause multicystic disease; and renal cysts are often secondary manifestations of genetic proliferative syndromes. The inherited polycystic kidney diseases, which are due to germ-line mutations in single genes, inherited as mendelian traits, include autosomal dominant and autosomal recessive polycystic kidney disease, nephronophthisis, and medullary cystic diseases. The age at onset, the severity of symptoms, and the rates of progression to end-stage renal failure or death vary widely in this group of diseases. Definition: Polycystic kidney disease (PKD) is a genetic disorder characterized by the growth of numerous cysts filled with fluid in the kidneys. PKD cysts can reduce kidney function, leading to kidney failure. PKD can also cause cysts in the liver and problems in other organs, such as the heart and blood vessels in the brain. PKD is the fourth leading cause of kidney failure and affects approximately 600,000 people in the US. According to the National Kidney Foundation, about 50 percent of people with autosomal dominant form of PKD progress to kidney failure, or endstage renal disease (ESRD), by age 60 and about 60 percent will have kidney failure by age 70. What causes it? There are two types of inherited PKD. The more common type is autosomal dominant PKD, which usually causes symptoms in midlife, although it may become apparent much sooner. Ninety per cent of cases are autosomal dominant due to an abnormal gene on chromosome 16. It needs only one parent to pass on the abnormal gene, giving a person a one-in-two chance of developing the disease later in life. The childhood form, autosomal recessive PKD, is much rarer. It affects about one in 10,000 babies. In at least some cases, the gene is found on chromosome 6. It needs both parents to pass on an abnormal gene - meaning a child has a one in four chance of developing the disease in childhood. It progresses rapidly. PKD may also occur as a non-inherited, acquired form as a result of long-term kidney problems, dialysis and old age. The gene responsible for causing polycystic kidney disease has been identified. This means those with a family history of the disease can receive genetic counselling to help with family planning.

In PKD, fluid-filled cysts develop in the kidneys, giving them a honeycomb appearance. Gradually these cysts replace the normal kidney tissue, enlarging the kidneys but making them less and less able to function normally. Eventually, the kidneys fail completely. In addition to the kidney damage, the fluid in the cysts may become infected, which can cause pain in the back and abdomen, and trigger fever. Adults may not develop symptoms for many years. When they do arise they may include: • • • • •

Blood in the urine Vague discomfort or aching in the abdomen and/or lower back Attacks of sudden and severe pain in the abdomen and/or lower back Headaches Urinary tract infections

Adults can also develop cysts in the liver and pancreas, abnormal heart valves, kidney stones, brain aneurysms (bulges in the walls of blood vessels) and diverticulosis (small bulges in the wall of the colon). High blood pressure (hypertension) may develop as a result of kidney damage. This may exacerbate the problem by damaging the kidneys further. However, progress of the disease is usually very slow and it may go undetected for years. What's the treatment? At present, it isn't possible to prevent the cysts forming within the kidneys. However, it is possible to slow the damage. Keeping blood pressure at a safe level helps prevent further damage to the kidneys. If infection develops, it needs to be treated promptly and effectively. Eventually, kidney failure occurs. For around seven out of ten people with adult PKD, this happens by the age of 65. At this stage, kidney dialysis or transplant is necessary.

Benjamen R. Villanueva BSN – 4G

Article: Renal cell carcinoma Renal cell carcinoma accounts for approximately 3% of adult malignancies and 90-95% of neoplasms arising from the kidney. It is characterized by a lack of early warning signs, diverse clinical manifestations, resistance to radiation and chemotherapy, and infrequent but reproducible responses to immunotherapy agents such as interferon alpha and interleukin (IL)-2. New agents, such as sorafenib and sunitinib, having antiangiogenic effects through targeting multiple receptor kinases, have activity in patients failing immunotherapy. In the past, these tumors were believed to derive from the adrenal gland; therefore, the term hypernephroma was used often.

Signs and symptoms The classic triad is hematuria (blood in the urine), flank pain and an abdominal mass. This is now known as the 'too late triad' because by the time patients present with symptoms, their disease is often advanced beyond a curative stage. Today, the majority of renal tumors are asymptomatic and are detected incidentally on imaging, usually for an unrelated cause.

Other signs may include: • • • • • • • • • •

Abnormal urine color (dark, rusty, or brown) due to blood in the urine Weight loss, malnourished appearance The presenting symptom may be due to metastatic disease, such as a pathologic fracture of the hip due to a metastasis to the bone Enlargement of one testicle known as varicocele (usually the left, due to blockage of the left gonadal vein by tumor invasion of the left renal vein -- the right gonadal vein drains directly into the inferior vena cava) Vision abnormalities Pallor or plethora Hirsutism - Excessive hair growth (females) Constipation High blood pressure Elevated calcium levels (Hypercalcemia)

Causes Renal cell carcinoma affects about three in 10,000 people, resulting in about 31,000 new cases in the US per year. Every year, about 12,000 people in the US die from renal cell carcinoma. It is more common in men than women, usually affecting men older than 55. Kidney cancer both RCC & TCC currently is diagnosed in some 6,600 people in Britain/UK per annum and some 3,600 people who die are recorded as having died of kidney cancer in a given year. The morbidity rate recorded is thought to underestimate the percentage who die of kidney cancer. Often the cause of death recorded on the death certificate may not mention kidney cancer but the subsequent metastases. It is clear that well over 50% of those diagnosed with kidney cancer in Britain will die of the disease or as a result of the disease. Why the cells become cancerous is not known. A history of smoking greatly increases the risk for developing renal cell carcinoma. Some people may also have inherited an increased risk to develop renal cell carcinoma, and a family history of kidney cancer increases the risk. Increasingly there is a belief that inhalation of a diversity of chemicals may be causal and it is also noted that there is a steady increase in diagnosis in women. That a

disproportionate percentage of those diagnosed with kidney cancer are obese is increasingly believed to be a significant factor. People with von Hippel-Lindau disease, a hereditary disease that also affects the capillaries of the brain, commonly also develop renal cell carcinoma. Kidney disorders that require dialysis for treatment also increase the risk for developing renal cell carcinoma. From Wikipedia

Pathophysiology The tissue of origin for renal cell carcinoma is the proximal renal tubular epithelium. Renal cancer occurs in both a sporadic (nonhereditary) and a hereditary form, and both forms are associated with structural alterations of the short arm of chromosome 3 (3p). Genetic studies of the families at high risk for developing renal cancer led to the cloning of genes whose alteration results in tumor formation. These genes are either tumor suppressors (VHL, TSC) or oncogenes (MET). At least 4 hereditary syndromes associated with renal cell carcinoma are recognized: (1) von Hippel-Lindau (VHL) syndrome, (2) hereditary papillary renal carcinoma (HPRC), (3) familial renal oncocytoma (FRO) associated with Birt-Hogg-Dube syndrome (BHDS), and (4) hereditary renal carcinoma (HRC). von Hippel-Lindau disease is transmitted in an autosomal dominant familial multiplecancer syndrome, which confers predisposition to a variety of neoplasms, including the following: • • • • • • •

Renal cell carcinoma with clear cell histologic features Pheochromocytoma Pancreatic cysts and islet cell tumors Retinal angiomas Central nervous system hemangioblastomas Endolymphatic sac tumors Epididymal cystadenomas

Renal cell carcinoma develops in nearly 40% of patients with von Hippel-Lindau disease and is a major cause of death among these patients. Deletions of 3p occur commonly in renal cell carcinoma associated with VHL disease. The VHL gene is mutated in a high percentage of tumors and cell lines from patients with sporadic (nonhereditary) clear cell renal carcinoma. Several kindreds with familial clear cell carcinoma have a constitutional balanced translocation between 3p and either chromosome 6 or chromosome 8. Mutations of the VHL gene result in the accumulation of hypoxia inducible factors (HIFs) that stimulate angiogenesis through vascular endothelial growth factor and its receptor (VEGF and VEGFR, respectively). VEGF and VEGFR are important new therapeutic targets. Hereditary papillary renal carcinoma is an inherited disorder with an autosomal dominant inheritance pattern; affected individuals develop bilateral, multifocal papillary renal carcinoma. Germline mutations in the tyrosine kinase domain of the MET gene have been identified. Individuals affected with familial renal oncocytoma can develop bilateral, multifocal oncocytoma or oncocytic neoplasms in the kidney. Birt-Hogg-Dube syndrome is a hereditary cutaneous syndrome. Patients with Birt-Hogg-Dube syndrome have a dominantly inherited predisposition to develop benign tumors of the hair follicle (ie, fibrofolliculomas), predominantly on the face, neck, and upper trunk, and are at risk of developing renal tumors, colonic polyps or tumors, and pulmonary cysts.

Mortality/Morbidity Renal cell carcinoma is the eighth or ninth leading cause of cancer death in the United States. The 5-year survival rates initially reported by Robson in 1969 were 66% for stage I renal carcinoma, 64% for stage II, 42% for stage III, and only 11% for stage IV.2 Except for stage I, these survival statistics have remained essentially unchanged for several decades.

Race Renal cell carcinoma is more common in people of Northern European ancestry (Scandinavians) and North Americans than in those of Asian or African descent. In the United States, its incidence has been equivalent among whites and African Americans, but incidence among African Americans is increasing rapidly.

Sex Renal cell carcinoma has a male-to-female preponderance of 1.6:1.

Age This condition occurs most commonly in the fourth to sixth decades of life, but the disease has been reported in younger people who belong to family clusters.

Author: Kush Sachdeva, MD, Private Practice, Southern Oncology and Hematology Associates, South Jersey Hospital System, Fox Chase Cancer Center Reaction: When we talk about cancer, we think of it as an dangerous disease because it affects many of our body parts. This kind of disease makes our life shorten to live. Renal cell carcinoma is the eight to ninth leading cause of death in the united states. This condition most affects to male than females at the age of 50 and above. It is the most common form of kidney cancer arising from the renal tubules. It is resistant to chemotherapy and radiation therapy, and in some cases respond to immunotherapy. To identify these kind of condition it has three common symptoms, they are called as the classic triad which is hematuria (blood in the urine), a feeling of flank pain and an abdominal mass. For our future life we should be careful in taking care of our health.

Lecel Fernandez BSN 4-G

Latest Research for Kidney Cancer: Unlike many other cancers, advanced kidney cancer does not respond well to chemotherapy. Drugs like interferon or interleukin-2 (IL-2), which are given to try and get the body’s immune system to attack the tumor, are also not particularly effective and have a lot of side effects. As a result, there is a lot of interest in finding something new and effective. New medications designed to attack cancers on the molecular level (Nexavar® and Sutent®) have caught the attention of the cancer doctors. Researchers have found that they are more effective than standard care in slowing the progression of kidney cancer with a lot less side effects. Two articles in the January 11 edition of the New England Journal of Medicine report the latest results for Nexavar® and Sutent® in advanced kidney cancer. The findings were somewhat mixed. They found that the disease didn’t progress as fast, but they couldn’t show that it kept patients alive significantly longer. So, although these drugs show a lot of promise in treating a very difficult disease and are less toxic than the standard treatment, patients need to understand that they don't offer a cure. Kidney Cancer Symptoms There are many variations of kidney cancer. The most commonly diagnosed type of kidney cancer is renal cell carcinoma. It accounts for more than 85% of kidney cancer diagnosis'. The most commonly experienced kidney cancer symptoms (renal cell carcinoma) are: •

Chronic fatigue

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Unexplained, rapid weightloss

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Leg and ankle swelling Hypertension (high blood pressure) Fever Presence of blood in urine (seen either by the eye, or microscopically)

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Pain in side or lower back

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Mass or lump in the abdomen