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PROFESSIONAL CERTIFICATE IN ONCOLOGY NURSING

SUBJECT CODE : ONNM 4103 Nursing Management of Cancer


in Adult and Children

PRESENTATION TOPIC TESTICULAR CANCER

LECTURER NAME PUAN NOREDAH BINTI AJIS

STUDENT NAME BRENDA WONG CHIA CHEE

MATRIX NO SD01-201705-002598

SUBMISSON DATE 16TH JUNE 2017


INDEX

1. INDEX---------------------------------------------------------------------------------------2

2. INTRODUCTION-------------------------------------------------------------------------3

3. CLASSIFICATION--------------------------------------------------------------------4-6

4. ETIOLOGY------------------------------------------------------------------------------7-8

5. PATHOPHYSIOLOGY-------------------------------------------------------------9-10

6. MANIFESTATION----------------------------------------------------------------------11

7. ASSESSMENT FINDING--------------------------------------------------------12-16

8. STAGING----------------------------------------------------------------------------17-19

9. TREATMENT-----------------------------------------------------------------------20-23

10. COMPLICATION-----------------------------------------------------------------------24

11. PROGNOSIS----------------------------------------------------------------------------25

12. SCENARIO OF TESTICULAR CANCER------------------------------------26-27

13. NURSING INTERVENTION & MANAGEMENT---------------------------28-32

14. REFERENCE----------------------------------------------------------------------------33

2
INTRODUCTION

The testicles are part of a mans reproductive system. Each man has 2

testicles, and they are located under the penis in a sac like a pouch called the

scrotum. They can also be called testes or gonads. The testicles produce

sperm and testosterone. Testosterone is a hormone that plays a role in the

development of a mans reproductive organs and other characteristics.

About testicular cancer

A malignant tumor that has developed from abnormal cell formation in

the testicles is called testicular cancer. Testicular cancer begins when

healthy cells in a testicle change and grow out of control, forming a mass

called a tumor. A cancerous tumor is malignant, meaning it grow and spread

to other parts of the body.

Testicular cancer is almost always curable if found early, and it is usually

curable even when at a later stage. Another name for testicular cancer is

testis cancer.

3
CLASSIFICATION

There are 2 main categories of germ cell tumors that start in the testicle.

Seminoma.

o Classical - More than 95% of seminomas are classical. These

usually occur in men between 25 and 45.

o Spermatocity - Occur in older men diagnosed with

spermatocytic seminoma is about age 65.

Non-seminoma. A non-seminoma contains any of the following in the

tissue:

o Choriocarcinoma

o Embryonal carcinoma

o Yolk sac tumor

o Teratoma

Generally, non-seminomas tend to grow and spread more quickly than

seminomas, but prompt diagnosis and treatment are important for both

tumors. Many germ cell tumors are a mixture of teratoma and other types of

germ cell tumors. Each of these can occur alone in any combination.

Sometimes, seminoma can be found as part of a non-seminoma at any

percentage level. For example, a tumor that is 99% and 1% yolk sac tumor is

still diagnosed and treated as non-seminoma.

Embryonal carcinoma:

This type of non-seminoma is present to some degree in about 40% of

testicular tumors, but pure embryonal carcinomas occur only 3% to 4% of the

4
time. When seen under a microscope, these tumors can look like tissues of

very early embryos. This type of non-seminoma tends to grow rapidly and

spread outside the testicle. Embryonal carcinoma can increase blood levels

of a tumor marker protein called alpha-fetoprotein (AFP), as well as human

chorionic gonadotropin (HCG).

Yolk sac carcinoma:

These tumors are so named because their cells look like the yolk sac

of an early human embryo. Other names for this cancer include yolk sac

tumor, endodermal sinus tumor, infantile embryonal carcinoma, or

orchidoblastoma.This is the most common form of testicular cancer in

children (especially in infants), but pure yolk sac carcinomas (tumors that do

not have other types of non-seminoma cells) are rare in adults. When they

occur in children, these tumors usually are treated successfully. But they are

of more concern when they occur in adults, especially if they are pure. Yolk

sac carcinomas respond very well to chemotherapy, even if they have spread.

This type of tumor almost always increases blood levels of AFP (alpha-

fetoprotein).

Choriocarcinoma:

This is a very rare and aggressive type of testicular cancer in adults.

Pure choriocarcinoma is likely to spread rapidly to distant organs of the body,

including the lungs, bones, and brain. More often, choriocarcinoma cells are

present with other types of non-seminoma cells in a mixed germ cell tumor.

These mixed tumors tend to have a somewhat better outlook than pure

5
choriocarcinomas, although the presence of choriocarcinoma is always a

worrisome finding.This type of tumor increases blood levels of HCG (human

chorionic gonadotropin).

Teratoma:

Teratomas are germ cell tumors with areas that, under a microscope,

look like each of the 3 layers of a developing embryo: the endoderm

(innermost layer), mesoderm (middle layer), and ectoderm (outer layer).

Less common types of testicular tumors include:

Leydig cell tumor

Sertoli cell tumor

Carcinoma of the rete testes, which is a part of the testicles

6
ETIOLOGY

Healthy cells grow and divide in an orderly way to keep your body

functioning normally. But sometimes some cells develop abnormalities,

causing this growth to get out of control these cancer cells continue

dividing even when new cells aren't needed. The accumulating cells form a

mass in the testicle.

Nearly all testicular cancers begin in the germ cells the cells in the

testicles that produce immature sperm. What causes germ cells to become

abnormal and develop into cancer isn't known.

Factors that may increase your risk of testicular cancer include:

1. An undescended testicle (cryptorchidism). The testes form in the

abdominal area during fetal development and usually descend into the

scrotum before birth. Men who have a testicle that never descended are

at greater risk of testicular cancer than are men whose testicles

descended normally. The risk remains elevated even if the testicle has

been surgically relocated to the scrotum.

2. Abnormal testicle development. Conditions that cause testicles to

develop abnormally, such as Klinefelter syndrome, may increase your

risk of testicular cancer.

3. Family history. If family members have had testicular cancer, you may

have an increased risk.

7
4. Age. Testicular cancer affects teens and younger men, particularly those

between ages 15 and 35. However, it can occur at any age.

5. Race. Testicular cancer is more common in white men than in black men.

8
PATHOPHYSIOLOGY

The cause of testicular cancer is not known. The characteristic genetic

change found is an isochromosome of the short arm of chromosome 12,

which is often seen in sporadic cancers. This suggests that genes in this

region are important in the development of germ cell tumors. A number of

other genes that have a relatively weak effect are also involved in the

development of testicular cancer.

That genetic factors have a role in the development of testicular cancer is

shown by the fact that the risk for the disease is higher in first-degree

relatives of cancer patients than in the general population. About 2% of

testicular cancer patients report having an affected relative. Siblings are at

particularly increased risk, with a relative risk of 810. For sons of affected

men, the relative risk is 46.

Two models of testicular carcinoma in situ have been proposed. The first

posits that fetal gonocytes whose development into spermatogonia is blocked

may undergo abnormal cell division and then invasive growth mediated by

postnatal and pubertal gonadotropin stimulation.

The second model postulates that the most likely target cell for transformation

is the zygotene-pachytene spermatocyte. During this stage of germ cell

development, aberrant chromatid exchange events associated with crossing

over can occur. Normally, these cells are eliminated by apoptosis. On

occasion, this crossing over may lead to increased 12p copy number and

9
overexpression of the cyclin D2 gene (CCND2). The cell carrying this

abnormality is relatively protected against apoptotic death because of the

oncogenic effect of CCND2, leading to re-initiation of the cell cycle and

genomic instability

Malignant transformation of germ cells is the result of a multistep process of

genetic changes. One of the earliest events is the increased copy number of

12p, either as 1 or more copies of i(12p) or as tandem duplications of

chromosome arm 12p. This abnormality is found in occult carcinoma in situ

lesions as well as more advanced disease. Further studies indicate

that CCND2 is present at chromosome band 12p13 and that CCND2 is

overexpressed in most germ cell tumors, including carcinoma in situ.

Amplification of CCND2 activates cdk4/6, allowing the cell to progress

through the G1-S checkpoint.

10
MANIFESTATION

Men with testicular cancer may experience a variety of symptoms or signs.

An enlarged testicle or a small lump or area of hardness are the first signs of

testicular cancer. Any lump, enlargement, hardness, pain, or tenderness

should be evaluated as soon as possible. Other symptoms of testicular

cancer usually do not appear until after the cancer has spread to other parts

of the body.

The following are common manifestations of metastasis testicular cancer:

Neck mass (supraclavicular nodes)

Cough or hemoptysis or dyspnea (pulmonary metastasis)

Gastrointestinal disturbances: anorexia, nausea, vomiting, GI bleed


(retroduodenal metastasis)

Lumbar backpain (bulky retroperitoneal diseases involving psoas


muscle or nerve roots)

Bone pain (skeletal metastasis)

Neurological symptoms (cerebral, spinal cord or peripheral root


involvement)

Unilateral or bilateral lower extremity swelling (iliac or caval venous


obstruction or thrombosis)

11
ASSESSMENT FINDINGS

Physical Examination

The presence of a testicular swelling is the most common presenting

symptom. Dull ache or sensation of heaviness in scrotum or inguinal canal is

often an early symptom. Acute pain may be due to to associated epididymitis,

haemorrhage, torsion or infarction within the tumor. History of lumbar should

raise suspicion about the presence of retroperitoneal lymph node involvement.

Physical examination includes palpation of testis between the thumb

and the finger beginning with the normal testis. The normal testis is of

homogeneous consistency, freely mobile and separable from the epididymis.

Any firm , fixed or hard area within the tunica albugineais suspect. The cord

and scrotum should be examined for tumor involvement. Most often, the

testicular tumor is found as a painless swelling of the testis with or without

hydrocoele. Firm or variegated consistency of the swelling and loss of

testicular sensation should alert about it being a malignant testicular tumor.

Infrequently, tumor may be present without any significant increase in size.

It is important to rule out tumor in undescended testis in young men

presenting with an abdominal mass. Careful abdominal palpation for

retroperitoneal lymph nodes metastases and the left supraclavicular region

for Virchows node is mandatory. The nature, size,growth pattern, etc. Can

give clue to the nature of histology.

12
Laboratory Investigation

Tumor markers

Tumor markers are substances, which are produced by malignant cells

and released in the systemic circulation. These markers are used for

diagnosis, staging, monitoring of treatment response and predicting

prognosis. They are particularly used in the follow-up of patients for early

diagnosis of recurrences. There are two types of germ cell tumor markers:

a. Oncofetal substances associated with embryonic development (AFP and

B-hCG)

b. Cellular enzymes such as lactic acid dehydrogenase (LDH) and placental

alkaline phosphate (PLAP)

Alpha Fetoprotein(AFP)

Alpha fetoprotein (AFP) is major serum protein of the fetus, having a

molecular weight of 70,000. Fetal liver, gastrointestinal tract and the yolk sac

produce it. Elevated AFP levels may occur in association with a number of

malignancies (testes, liver, pancreas, stomach, and lung). AFP may be

produced by pure embryonal carcinoma, teratocarcinoma, yolk sac tumoror

combined tumor nut not by pure choriocarcinomas or pure seminomas. The

metabolic of half-life of AFP in humans is 5-7 days. Elevated AFP levels in a

seminoma suggest the presence of a nonseminomatous element and the

tumor should be reclassified and treated as nonseminomatous tumor.

13
Human Chorionic Gonadotropin (hCG)

Human chorionic gonadotropin (hCG) is a glycoprotein, having a

molecular weight of 38,000, which is normally produced in the placenta. The

specific beta chain of hCG are produced by syncytiotrophoblastic cells in

seminoma, embryonal carcinoma, choriocarcinoma. Increased values for

hCG are seen in about 10% of all seminomas and these patients have a

poorer prognosis than patients negative for B-hCG. In disseminated testicular

non-seminomatous tumor, 40-60% will have raised circulating levels of AFP

and/or hCG, with higher values in the more advanced stages. Spuriously

raised levels of B-hCG have seen in individuals using marijuana or with very

high levels of luteinizing hormone (LH). the biologic half-life of B-hCG is 24

hours.

LDH and Enzymes

LDH is a no-specific tumor marker, the gene for LDH Isoenzyme-1

maps to chromosome 12 and levels have been correlated with the number of

i(12p) copies in tumor, which is a reliable tumor marker for germ cell tumor.

Lactate dehydrogenase (LDH) increase in patients with advanced disease

having large tumor volumes, especially seminomas. Placental alkaline

phosphatase (PLAP) has also been examined as a possible specific tumor

marker for seminomas and teratomas. (PAP) is not commonly used. Gamma-

glutamyl transpeptidase (GGT) is also found to be elevated infews patients

with active seminomas. Simultaneous determinations of PLAP and GGT

revealed elevation in patients with active diseases.

14
Imaging Investigation

Ultrasonographic evaluation of a testicular mass is a sensitive and a

valuable technique that can discriminate between testicular neoplasm and

non-neoplastic lesions (hydrocele, varicocele, epididymitis, etc). Hypoechoic

or heterogenous mass in the testis should prompt further evaluation and if

required a diagnostic orchiectomy may be undertaken. Sonography may

detect a non-palpable testicular neoplasm.

Chest X-ray

Chest X-ray is done to rule out pulmonary metastases. Lesions larger

than 1cm can be seen on chest X-ray, whereas CT of the chest can

demonstrate lesions of 0.5cm and as a general rule is recommended in poor

prognostic testicular tumors. It can also demonstrate presence of mediastinal

lymphadenopathy.

Ultrasonography (USG)

USG is complementary to computerized tomography (CT) scan of the

abdomen and can identify:

a. Retroperitoneal lymph nodes that are closely adjacent to the main

vessels

b. Palpably normal testes and evidence of extragonadal germ cell

malignancy

15
Computerized tomography (CT)

CT is most effective means for staging retroperitoneal disease. Gross

nodal metastases are easily visualised. Lymph nodes less than 2cm in

diameter in the upper para-aortic regions can be identified in addition to soft

tissue structures and regional viscera. The para-aortic retrocrural space

above the crus of the diaphragm can be visualised and is an important site of

metastasis. CT scan or MRI of the chest is indicated in patients with massive

lymphadenopathy. CT or MRI of the brain is indicated in symptomatic patients.

Lymphangiography is no longer performed. Treatment planning and

simulation studies for radiation therapy can be accomplished simultaneously.

Biopsy and Diagnostic Orchiectomy

Testicular biopsy is very rare performed in the preoperative

assessment of a testicular mass and not suggested. Trans-scrotal biopsy is

contraindicated and should never be attempted, if malignancy is suspected.

16
STAGING

All purpose of a clinical staging is to predict the prognosis and to provide a

basis for the treatment protocol. The TNM staging system based on surgical,

pathological and tumor marker assessment, grading is not applied to testicular tumor.

TNM staging system

For testicular cancer, an Serum tumor marker (S) is added to the Tumor (T), Node

(N), Metastasis (M) system. Serum tumor markers are AFP, beta-hCG, and LDH.

There are also 2 different types of staging in testicular cancer:

1. Clinical staging -

The clinical stage is based on a physical examination or x-rays, CT scans, and other

imaging tests.

2. Pathological staging -

The pathological stage is based on evaluating tissue under a microscope after it has

been removed during surgery.

Pathological staging is more accurate than clinical staging, but it is not always

needed.

Primary Tumor (T)

TX Primary tumor cannot be assessed

T0 No evidence of primary tumor (eg:histologic scar in testis)

Tis Intratubular germ cell neoplasm (carcinoma in situ)

T1 Tumor limited to the testis and epididymis without vascular/lymphatic invasion.

Tumor may invade into the tunica albuginea but not the tunica vaginalis

T2 Tumor limited to the testis and epididymis with vascular/lymphatic invasion, or

tumor extending through the tunica albuginea with involvement of the tunica

vaginalis

T3 Tumor invades the spermatic cord with or without vascular/lymphatic invasion

T4 Tumor invades the scrotum with/without vascular/lymphatic invasion

17
Regional Lymph Nodes (N) Clinical

NX Regional nodes cannot be assessed

N0 No regional lymph node metastasis

N1 Metastasis with a lymph node mass 2cm or less in greatest dimension; or

multiple lymph nodes, none more than 2cm in greatest dimension

N2 Metastasis with a lymph node mass, more than 2cm but not more than 5cm in

greatest dimension, or multiple lymph nodes, any one greater than 2cm but not

more than 5cm in greatest dimension

N3 Metastasis with a lymph node mass more than 5cm in greatest dimension

Regional Lymph Nodes (N) Pathological

NX Regional nodes cannot be assessed

N0 No regional lymph node metastasis

N1 Metastasis with a lymph node mass, 2cm or less in greatest dimension and

less than or equal to 5 nodes positive, none more than 2cm in greatest

dimension

N2 Metastasis with a lymph node mass, more than 2cm but not more than 5cmin

greatest dimension, or more than 5 nodes positive; none more than 5cm; or

evidence of extranodal extension of tumor

N3 Metastasis with a lymph node mass more than 5cm in greatest dimension

18
Distant metastasis (M)

MX Distant metastasis cannot be assessed

M0 No distant metastasis

M1 Distant metastasis

M1a Non-regional nodal or pulmonary metastasis

M1b Distant metastasis other than to non-regional lymph nodes and lungs

Serum Markers (S)

SX Markers studies not available or not performed

S0 Marker study levels within normal limits

S1 LDH <1.5 x N and HCG (mIu/ml) <5000 and AFP (ng/ml) <1000

S2 LDH 1.5-10 x N or HCG (mIu/ml) 5,000-50,00 or AFP (ng/ml) 1000-10,000

S3 LDH >10 x N or HCG (mIu/ml) >50,000 or AFP (ng/ml) >10,000

19
TREATMENT

Surgery: Radical Inguinal Orchiectomy

Treatment of testicular cancer usually starts with surgery to remove

the testicle with cancer, called radical inguinal orchiectomy. This operation is

done through an incision in the groin along the beltline. During the surgery,

the entire testicle and most of the spermatic cord are removed. The spermatic

cord contains the blood supply to the testicle as well as the channel through

which sperm travel from the testicle toward the penis. A man may develop

cancer in both testicles either at the same time or at different times. However,

this is rare, occurring in about 2% of men with testicular cancer. Then, both

testicles need to be removed in a procedure called a bilateral orchiectomy.

Chemotherapy

Chemotherapy is the use of drugs to destroy cancer cells, usually by

stopping the cancer cells ability to grow and divide. Chemotherapy is given

by a medical oncologist, a doctor who specializes in treating cancer with

medication.

Chemotherapy for testicular cancer is given directly into a vein so that

it enters the bloodstream and reaches cancer cells throughout the body.

There are also types of chemotherapy that can be taken by mouth but they

are not generally used for testicular cancer.

A chemotherapy regimen (schedule) usually consists of a specific number of

cycles of treatment given over a set period of time. A cycle of chemotherapy

for testicular cancer typically lasts 3 weeks. And, men with testicular cancer

may receive 1 to 4 cycles of treatment, depending on the stage of the cancer.

20
During treatment, a patient may receive 1 drug at a time or combinations of

different drugs at the same time.

Radiation therapy

Radiation therapy is the use of high-energy x-rays or other particles to

destroy cancer cells. A radiation therapy regimen (schedule) usually consists

of a specific number of treatments given over a set period of time. The most

common type of radiation treatment is called external-beam radiation therapy,

which is radiation therapy given from a machine outside the body. For

testicular cancer, the radiation is generally directed at lymph nodes in the

abdomen for men with stage I or II pure seminoma. Sometimes, the radiation

treatment area includes lymph nodes on the same side of the pelvis as the

testicle where the cancer started.

Radiation therapy for stage I seminoma is now used less often than in the

past. Surveillance or, less commonly, carboplatin chemotherapy is usually

used instead of radiation therapy as the preferred treatment of stage I

seminoma at many treatment centers because of the risk that radiation

therapy may cause other cancers and heart disease. However, radiation

therapy remains an option for stage I, IIA, and IIB pure seminomas. It is also

sometimes used to treat brain metastases from either seminoma or non-

seminoma, but testicular cancer rarely spreads to the brain.

21
Seminoma Therapy

Seminomas most present as clinically localized disease confined to

the testis. Pure early-stage seminomas exhibit dramatic radiosensitivity.

Removal of affected testicle, or radical inguinal orchiectomy, is the initial

treatment for all stages of seminomas. This procedure is performed on an

outpatient basis. Following ochiectomy stage 1 seminomas are treated with

25 to 30 Gy of radiationtherapy(RT) to the infradiaphragmatic area including

the para-aortic lymph nodes. Mediastinal prophylaxis is generally not given,

since relapse at this site is rare. Surveillance has been studied as an

alternative to RT and may be a viable option in selected patients who are

committed to vigilant folow-up.

Patient with stages 2 seminomas are also treated with post-

orchiectomy RT 35-40 Gy to the infradiaphragmatic and para-aortic nodes

and the ipsilateral iliac nodes. Patient having a horseshoe kidney (result from

fusion at one pole occurring during embryonic development), RT is not the

treatment of choice; these patient are treated with good-risk chemotherapy.

The recommended regimen consists of four cycles of etoposide plus cisplatin

(EP) or 3 cycles of bleomycin, etoposide and cisplatin (BEP).

Approximately 90% of patients with advanced disease will achieve cure with

platinum-based chemotherapy regimen.

22
Nonseminoma Therapy

The majority of nonseminomas have more than one cell type. Tumors

with mixed cell types are treated as nonseminomas. Two treatment options

exist for stage 1A nonseminomas: nerve-sparing retroperitoneal lymph node

dissection (RPLND) or observation. The cure rate for either approach is

approximately 95%, but is predicted on vigilant follow-up and chemotherapy

for those 30% of patients who relapse. Follow-up for patient selecting

observation includes chest x-rays monthly for a year 1, and every 2 months

for year 2. Pelvic and abdominal CT scan every 2-3 months for the first year

and every 3-4 months during the second year, along with serum marker

studies. For patients with stage 1B tumors, treatment options include nerve-

sparing (RPLND), observation or chemotherapy with RPNLD being the

preferred option. Chemotherapy consists of two cycles of BEP. Patients with

stage 1S disease and no radiographic evidence of disease are treated with

chemotherapy: four cycles of EP or three cycles of BEP. These patients tend

to have disseminated disease, and thus chemotherapy is preferable to

RPLND.

Stage 2 nonseminomas treatment is largely influenced by serum tumor

marker status, with elevated levels indicating a need for aggressive

chemotherapy with either BEP or EP regimens. Chemotherapy for more

advanced disease such as extragonadal primary sites is based on the risk

stratification system of the International Germ Cell Cancer Collaborative

Group, and may include nonpulmonary metastases and high serum tumor

marker concentrations, or mediastinal primary site. These patientts may

choose to investigate clinical trials.

23
COMPLICATION

After the introduction of platinum-based combination chemotherapy

(CT), cure is achievable in the majority of patients with metastatic testicular

cancer. However, long-term complications after cancer treatment are

increasingly recognized as a major burden for cancer survivors and their

communities. Survivorship research is particularly important in testicular

cancer because of the high cure rate and the young median age at diagnosis,

with correspondingly long expected survival. These are the complication:

secondary malignant neoplasms, pulmonary complications, cardiovascular

toxicity, neurotoxicity, ototoxicity, nephrotoxicity, fatigue, hypogonadism and

fertility issues.

24
PROGNOSIS

An estimated 8,850 men in the United States will be diagnosed with

testicular cancer. For men ages 15-44, it is the most commonly diagnosed

cancer. The average age of diagnosis is 33, but 7% of cases are diagnosed

in men 55 or older and 7% of cases are diagnosed in boys and adolescents.

The 5-year survival rate tells you what percent of men live at least 5

years after the cancer is found. Percent means how many out of 100. The 5-

year survival rate for men with testicular cancer is 95%.

25
CASE STUDY

Mr XXX, male, 33 years old. A educator (teacher). Smoker, non-alcohol

drinker. Married with 1 child. No past medical history. No family history of

cancer. Ecg: sinus rhythm. No known drug allergies. Body weight: 54kg.

Height: 163cm. Patient felt a small lump at Right testicular in January.

Enlarged quickly in February. Diagnose: Large Right testicular mass ?

seminoma.

Done blood investigation shown:

Anaplastic lymphoma kinase (ALK) 402,

Gamma-glutanyl transferase (GGT) 83,

Creatinine 130,

AFP 3.9,

B-hCG 20.8,

Testosterone 12.4nmol/L.

Done CT scan chest, abdomen, pelvis confirmed:

Large >5cm para-aortic (PA) nodal mass compressing the Right ureter

and causing some Right hydronephrosis.

Large mass in scrotum.

No distant metastasis seen.

Done Right Inguinal Orchidectomy:

Uncomplicated and post-operative recovery.

26
HPE confirmed:

120mm classical seminoma extending to involve the epididymis and

spermatic cord.

Lymphovascular invasion seen.

Resection margin of the spermatic cord - not involve by tumor.

Immuno-histo chemistry for confirmation done - seminoma.

Pathological staging (TNM): pT3, pNX, pMX.

Treatment:

Adjuvant therapy - EP regime chemotherapy with pre-medication +

hydration fluid.

m2
IV cisplatin 20mg/

m2
IV etoposide 100mg/

For 4 cycles, 5days/cycle, 3 weekly.

27
NURSING DIAGNOSIS, INTERVENTION & RATIONALE

1. Risk of infection : low WBC related to chemotherapy.

Intervention: Rationale:

assess for local or systemic signs opportunistic infections can easily

of infection, such as fever, chills, develop, especially in

malaise, swelling and pain. immunosuppressed patients.

Stress the importance of through Hand washing is a priority in both

and washing by the patient, hospital or home setting to

caregiver and visitors. prevent transmission of pathogen.

Reinforce the need for daily These to measure prevent skin

hygiene, mouth care and perineal breakdown and reduce the risk

care. for infection.

Instruct the patient to avoid These are sources of infection for

contact with persons with colds or the compromised patient.

infections. Children 12 years of age or

younger put the patient at risk

because they can be carriers of

infection, especially URTI.

Instruct the patient to report signs Get treatment. Antibiotics may be

and symptoms of infection indicated.

immediately.

28
2. Imbalanced nutrition : less than body requirement related to fatigue, loss

of appetite, nausea and vomiting.

Intervention: Rationale:

Consult dietitian for further Dietitian have a greater

assessment and recommendation understanding of nutritional value

regarding food and nutritional of foods and may be helpful in

support. assessing specific ethnic of

culture foods.

Patient with changes in sense of Seasoning may enhance the

taste, encourage use of flavor of food and entice eating.

seasoning.

For hospitalized patients, Patient will like homemade foods

encourage the family to bring than hospital food.

food from home.

Suggest supplemental nutrition Such ensure/ myotein can be

drinks. used to increase nutritional status

without interfering with voluntary

food intake.

Encourage exercise. Metabolism and utilization of

nutrients are enhanced by

activity.

29
3. Disturbed body image related to post-operative orchiectomy.

Intervention: Rationale:

Assess and validate feelings The extent of the response is

about changes in appearance. related more to value or

importance the patient places on

the body part than to the actual

value or importance.

Acknowledge normalcy of Acknowledging the patients

emotional response to actual or emotional response enables the

perceived change in body patient to move through the

structure and function. grieving process.

Teach patient self-care activities These enable adaptation to the

related to body image. changes in body image.

Reinforce any attempts to care for Positive reinforcement allows the

the scrotum. patient to feel good about

accomplishment and gain

confidence.

Provide information about Social services, support groups

institutional, internet-based, and and community agencies can

community resources for coping help the patient cope with this

with testicular cancer. illness and treatments. As more

men are being cured, as growing

body of survivors

30
4. Knowledge deficit related to testicular cancer treatment.

Intervention: Rationale:

Encourage questions about the Allow verification of

diagnosis of testicular cancer and understanding of given

proposed treatment regimen. information and the opportunity to

correct misconception.

Provide information on laboratory Evaluated for potential

& diagnostic test. metastasis, tumor lesion &

response to treatment.

Provide information on follow-up Realize cancer is not a death

therapy: sentence.

Chemotherapy Chemotherapy is indicated for

nonseminomatous tumor or for

metastasis diseases. A proven

effective therapies.

Radiation therapy Radiation beam therapy is

indicated for patients with pure

seminoma, because this tumor is

radiosensitive.

31
5. Ineffective sexual patterns related to testicular cancer.

Intervention: Rationale:

Explore awareness of and Patient and couples may have

comfort with a range of sexual limited knowledge of ways to

expression and activities (not just express their sexuality. The

sexual intercourse). patient may be unaware of

potential options

Discuss the effect of an Removal of only one testicle does

orchiectomy on future fertility not interfere with ejaculation and

fertility.removal of both testes

does cause infertility. Cancer

treatment can also affect sexual

function.

Refer to a are productive If fathering a child is an important

specialist about sperm banking. role for the patient, and if sperm

banking is not an option, discuss

others options such as donor

insemination and adoption.

Encourage discussion of feelings Removing one testicle does not

regarding alternative methods for affect fertility or sexual function.

reproduction. NEW: nerve-sparing surgical

procedures are improving fertility

rates.

32
REFERENCE

1. Mehta, A., & Bansal, S. C. (2004). Diagnosis and management of

cancer. New Delhi: Jaypee Brothers Medical .

2. Langhorne, M., Fulton, J., & Otto, S. E. (2007). Oncology nursing. St.

Louis, MO: Elsevier Mosby.

3. Miaskowski, C. (1997). Oncology nursing: an essential guide for

patient care. Philadelphia: W.B. Saunders.

4. Gates, R. A., & Fink, R. M. (2008). Oncology nursing secrets. St.

Louis, MO: Mosby Elsevier.

5. Wilkes, G. M., & Barton-Burke, M. (2015). 2015 oncology nursing

drug handbook. Burlington, MA: Jones & Bartlett Learning.

6. Gulanick, M., & Myers, J. L. (2011). Nursing care plans: diagnoses,

interventions, and outcomes. St. Louis, MO: Elsevier Mosby.

7. Testicular Cancer. (n.d.). Retrieved June 14, 2017, from

https://www.cancer.org/cancer/testicular-cancer.html

8. Testicular Cancer. (n.d.). Retrieved June 14, 2017, from

https://www.cancer.gov/types/testicular

9. Testicular Cancer. (2014, June 16). Retrieved June 14, 2017, from

http://www.cancer.net/cancer-types/testicular-cancer

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