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Repair of inguinal hernias. Surgery is the only curative procedure for inguinal hernias; there are no lesser therapies that have proved effective. A recent study has reported that the risk of incarceration is low in minimally symptomatic hernias and that observing them is a safe alternative (JAMA. 2006 Jan 18;295(3):285–292).

Repair of indirect inguinal hernia involves

Return of the hernia contents into the peritoneal cavity;

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Division and/or ligation of the base of the hernia sac at the level of the peritoneal cavity—the sac is always anteromedial to the cord at the level of the internal ring;

In adults , tightening of the internal ring and repair of the abdominal wall defect inguinal canal floor to prevent recurrence.

Repair of direct inguinal hernia is based on reinforcement of the inguinal canal floor after invaginating the hernia sac.

Repair of femoral hernia involves approaching the femoral sheath through the floor of the inguinal canal. The space is closed by apposing the posterior reflection of the inguinal ligament to Cooper's ligament (Cooper's ligament repair) or by plugging the space with polypropylene mesh.

Repair of the floor of the inguinal canal can be done with many techniques. Two classic techniques used less commonly now are described first, then two newer techniques are described.

Bassini repair

The transversalis fascia and conjoint tendon above are sutured to the reflection of the inguinal ligament (i.e., the shelving edge of Poupart's ligament) below.

In men, the spermatic cord is returned to its normal anatomic location between the reinforced inguinal canal floor and the external oblique aponeurosis.

In women, the round ligament may be ligated and the internal ring closed (true for all inguinal hernia repairs in women).

Cooper's ligament repair (McVay's method)

This method is similar to the Bassini repair except that the transversalis fascia and conjoint tendon are sutured to Cooper's ligament, which is the periosteum of the pubic ramus.

Because Cooper's ligament is more posterior than the inguinal ligament and subjects the repair to increased tension, a “relaxing” incision is often made in the anterior rectus sheath adjacent to the external oblique aponeurosis. This counterincision allows the conjoint tendon to be sutured to Cooper's ligament with less tension.

Tension is the problem with this technique, causing both postoperative pain and early and late recurrences.

Shouldice repair uses the transversalis fascia, which is divided longitudinally and imbricated upon itself in two layers. The internal oblique muscle and conjoint tendon are then sutured to the reflection of the inguinal ligament in two layers (total four suture lines).

Prosthetic mesh repairs (Lichtenstein repairs) are supplanting older techniques. These involve repairing the inguinal floor by using mesh to close the space, suturing it (as in a Bassini repair) to the transversalis fascia and conjoint tendon above and to the reflection of the inguinal ligament (i.e., the shelving edge of Poupart's ligament) below.

Open and laparoscopic techniques (Chapter 30) are used to place polypropylene mesh to reinforce the weakened transversalis fascia. Open techniques also place mesh into the defect deep to the transversalis fascia.

For indirect hernia repairs, a cone -shaped polypropylene mesh is placed adjacent to (anteromedial to) the spermatic cord.

For direct hernia repairs, the cone -shaped mesh is used to “plug” the transversalis fascia defect.

Recurrence rates after surgical repair vary depending on the type of hernia, but generally, inguinal hernias recur in under 10% of cases. This figure is usually higher for hernias at other sites.

Special situations

When strangulation or necrosis of the incarcerated bowel is suspected but the bowel returns to the peritoneal cavity spontaneously before visual examination by the surgeon, the abdomen should be opened and explored so that any necrotic bowel can be resected.

Recurrent hernias or hernias with large defects may require the insertion of prosthetic material such as polypropylene mesh to repair the abdominal wall defect adequately.

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Simple high ligation of the hernia sac is used for hernias in the pediatric age group. No floor repair is needed.

A truss is a device that exerts external compression over the hernia defect, keeping the space compressed. It is used only when surgery cannot be safely performed or when the patient refuses surgery.

C Other types of abdominal wall hernias

Umbilical hernias occur through the defect where the umbilical structures passed through the abdominal wall.

Umbilical hernias occur 10 times more often in women than in men.

The defect is common in children but usually closes by age 2 years, and fewer than 5% of umbilical hernias persist into later childhood and adult life.

In adults, umbilical hernias are often associated with increased intra -abdominal pressure, as with ascites or pregnancy.

Repair of an umbilical hernia consists of a simple transverse repair of the fascial defect.

Epigastric hernias, also called epiploceles , result from a defect in the linea alba above the umbilicus.

They occur more commonly in men (in a 3:1 ratio).

Some 20% of epigastric hernias are multiple at the time of repair.

Repair (simple suturing) is associated with a recurrence rate as high as 10%.

Ventral hernias occur in the abdominal wall in areas other than the inguinal region.

An incisional hernia , the most common type of ventral hernia, results from poor wound healing in a previous surgical incision and occurs in 5%–10% of abdominal incisions.

Common causes include midline incision, wound infection or hematoma, advanced age, obesity, general debilitation or malnutrition, surgical technique, or a postoperative increase in abdominal pressure, as occurs with paralytic ileus, ascites, or pulmonary complications after surgery.

Incisional hernias are repaired after the patient has recovered from the prior surgery trauma.

Repair requires definition of the adequate fascial edges surrounding the defect, closure with nonabsorbable sutures, and use of prosthetic mesh (polypropylene or ePTFE) when the defect is too large to be closed primarily.

Spigelian hernias protrude through the abdominal wall along the semilunar line (the lateral edge of the rectus muscle) at the semicircular line of Douglas (below the umbilicus where the transversus abdominis and internal oblique aponeuroses change to pass anteriorly to the rectus muscle).

Obturator hernias occur in the pelvis through the obturator foramen. The hernia can cause pain along the obturator nerve (mid -anterior thigh), referred to as Howship -Romberg sign.

Lumbar hernias occur on the flank and are seen in the superior (Grynfeltt's) and inferior (Petit's) triangles.

Perineal hernias occur in the pelvic floor usually after surgical procedures such as an abdominoperineal resection.

Peristomal hernias develop adjacent to an intestinal ostomy.

IV Surgical Oncology

A Overview

Cancer is a group of diseases caused by unregulated growth and spread of neoplastic cells. Neoplasias may be either benign (noninvasive growth, no metastases) or malignant (invasive growth, metastases).

Types

Carcinomas are malignancies that arise from epithelium.

Adenocarcinomas are malignancies that arise from epithelium and have a glandular component.

Sarcomas are malignancies that arise from mesodermal tissues.

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Neoplastic transformation. Neoplastic cells have “escaped” from the normal homeostatic inhibition (or regulation) of cell proliferation. Causes of neoplastic transformation are listed next with illustrative examples of human tumors. Because no single etiology exists for most human cancers, remember that multiple factors lead to neoplastic transformation.

Chemical carcinogens. Soot is associated with cancer of the scrotum of chimney sweeps (described by Pott in 1775); asbestos is associated with mesothelioma of the pleura; and smoking tobacco is associated with squamous cell carcinoma of the lung.

Physical carcinogens. Ultraviolet light is associated with basal cell and squamous cell carcinomas of the skin; ionizing radiation is associated with bone cancer in radium-dial workers, lung cancer in uranium miners, and leukemia in atomic bomb survivors (Hiroshima); and papillary thyroid cancer appears in individuals treated with neck irradiation.

Hereditary factors. A few cancers have direct genetic links, such as retinoblastoma, familial adenomatous polyposis, and multiple endocrine neoplasia syndromes (e.g., pheochromocytoma, medullary carcinoma of the thyroid, and other endocrine tumors) (Chapter 17).

Geographic factors are unexplained epidemiologic phenomena whereby a particular cancer is very common in

certain locations (e.g., gastric cancer is common in Japan and esophageal cancer in southeastern China).

Oncogenic viruses. Epstein -Barr virus is linked to Burkitt's lymphoma and nasopharyngeal carcinoma; human papilloma virus is linked to cervical and anogenital carcinomas; human T -cell leukemia virus type 1 (HTLV-1) is linked to adult T -cell leukemia; and hepatitis B and C are linked to hepatocellular carcinoma.

B Epidemiology

Cancer is the second leading cause of death in the United States (20% of all deaths); approximately 1 million new cases are diagnosed annually. One in four U.S. residents will develop cancer during his or her lifetime, with an overall 5-year survival rate of 40%.

Mortality

Overall, the highest number of deaths is caused by lung cancer (incidence rising), followed by colon and rectal cancer and breast cancer (incidence stable), and pancreatic cancer (incidence rising). Lung cancer is now the most common cause of cancer death for both sexes (having exceeded breast cancer for women).

A decreasing number of deaths are found from gastric cancer and uterine/cervical cancer. For gastric cancer, the incidence is falling for unknown reasons. For uterine/cervical cancer, early diagnosis (Pap smear) and improved treatments are presumably responsible.

Incidence. Overall, the order is the same as for mortality. However, for women, the most common cancer is breast

cancer.

C Molecular physiology of neoplastic cells

Neoplastic cells proliferate more rapidly than normal cells and fail to acknowledge signals to stop dividing.

Cancer is caused by a cascade of inherited and acquired mutations in those genes, which result in unsuppressed cellular proliferation.

Mutations in DNA produce altered or lost genes: point mutations (altered single base pair), deletions (loss of a DNA segment), and translocations (rearrangements).

Recessive mutations must cause loss of both copies of a growth -regulating molecule to contribute to malignant transformation.

There are at least three types of cancer-causing genes.

Oncogenes result from mutations of the normal host proto -oncogenes.

Proto -oncogenes are expressed during cellular proliferation, e.g., during embryonic development or during injury/healing responses.

Examples of oncogenes:

The HER -2/ neu gene is a membrane receptor mimic, and it encodes a protein similar to the epidermal growth factor receptor. This gene is amplified (overproduced) in 30% of breast and ovarian carcinomas and independently adversely effects prognosis.

The ras oncogene encodes a signal transduction protein and is found in 20% of solid tumors and in 50% of colon carcinomas.

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C-myc is a nuclear transcription factor that binds to enhancer and promoter regions of target genes. C-myc expression is increased in many solid tumors. In Burkitt's lymphoma, c-myc is uniformly translocated adjacent to the immunoglobulin (Ig)G or IgM light chain genes.

Tumor suppressor genes function to suppress or regulate cellular proliferation.

Loss of function results from mutation or deletion in both genes.

p53 is a tumor suppressor oncogene. Normally, p53 suppresses DNA replication sites.

Loss of p53 is the single most common genetic change found in malignancy (75% of colon carcinomas, 90% of hepatocellular carcinomas caused by aflatoxin).

Human papilloma virus gene product E6 binds and inhibits p53.

C

DNA repair genes encode for proteins that correct most of the errors that creep into replicated DNA. Diminished or lost function of these genes increases the net mutation rate in other genes.

D Multistep carcinogenesis

Malignancy is the result of the accumulation of critical mutations that produce a cancerous cell.

As a corollary, a single specific oncogene or lost suppressor gene may be necessary but not sufficient by itself to produce the malignant phenotype.

An important point is the diverse functions of the lost or mutated molecules. The multiplicity of genes and their products and the multitude of possible mutations leads to enormous diversity on every level for human cancers.

Hereditary factors are well illustrated by the BRCA -1 and BRCA -2 genes.

BRCA -1 and BRCA -2 are genes, certain mutations of which increase a woman's risks of breast (BRCA -1 only) and ovarian cancers. These mutations are usually inherited and are highly penetrant autosomal dominant traits.

The BRCA -1 gene is a tumor suppressor gene. Mutations are present in 10% of young women (younger than 35 years old) with breast cancer but in 20% of young Jewish women with breast cancer.

For BRCA -1 and BRCA -2, the prevalence of these mutations is 0.0014. The cumulative lifetime risk of breast cancer for carriers is 73.5%, in contrast to a risk of 6.8% for noncarriers.

For ovarian cancer, the equivalent lifetime risks are 28% for carriers and 2% for noncarriers.

In the United States, individuals with BRCA -1 mutations account for 3% of breast cancers and 4.4% of ovarian cancers.

The steps in colon carcinogenesis are relatively well understood.

APC (adenomatous polyposis coli) gene mutations occur early and may be the first event in tumorogenesis of sporadic cases. APC mutations are typically found in benign calonic adenomatous polyposis.

When two copies of this recessive gene are inherited, the individual has Familial Adenomatous Polyposis and develops multitudinous colonic polyposis with early cancers.

The DCC (deleted in colorectal carcinoma) gene is typically lost late in adenomatous polyposis. Loss of the DCC gene also plays a role much later, after tumorigenesis, in propensity of a cancer to metastasize.

K -ras, an oncogene, typically mutates in adenomes, perhaps enabling small adenomatous polyposis to enlarge.

p53 is a tumor suppressor gene, and loss of the second normal allele typically occurs at the initiation of malignancy.

For HNPCC (hereditary nonpolyposis colon cancer), a different etiology of carcinogenesis has been described. These patients are hypermutable because of defects in the DNA repair genes. However, the cascade of mutations seen in sporadic colon cancers (APC, DCC, K -ras, p53) also occurs in HNPCC.

Cancerous cells (i.e., growth unregulated cells) are not necessarily capable of metastasis. Further changes are required to produce the metastatic phenotype. Some of these changes may include the following:

Altered or increased expression of cell adhesion molecules or their receptors, which allows circulating blood - or lymph -borne cancer cells to adhere to endothelial cells.

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Ability to produce extracellular matrix molecules for its own milieu or enzymes to degrade the existing matrix, e.g., type IV collagenase to degrade endothelial basement membrane collagen and to gain access to new tissues.

Ability to produce cytoskeletal proteins for increased cell motility.

Ability to produce angiogenic factors for neovascularization of the new “colony.”

E Diagnostics

A single malignant cell that undergoes 30 doublings results in 1 billion cells, which creates a 1-cm diameter tumor.

With tumor doubling times of clinical cancers ranging from 20–120 days, one can extrapolate that most human tumors have been present for 1–10 years to reach clinical detection.

Flow cytometry is a test done on tumor cells to detect the relative amount of DNA and the growth rate.

Ploidy describes the amount of DNA.

Diploid signifies a normal amount of DNA (i.e., two copies of each chromosome).

Aneuploid signifies abnormal DNA content.

Polyploid signifies increased DNA content at integer multiples of normal.

S -phase measures the proportion of cells in the S -phase of the cell cycle. When elevated, this indicates more rapid tumor growth and presumably a more aggressive tumor.

Tumor markers are tests developed to detect tumor or tumor-specific products.

Classification includes tumor-specific antigens, tumor-specific enzymes, and tumor-specific hormones.

Screening. A marker used for screening should possess a high sensitivity for the detection of early, curable lesions in asymptomatic patients. Prostate-specific antigen (PSA) is an example.

Prognosis and detection of residual disease. Carcinoembryonic antigen (CEA) is used as a measure of colorectal malignancy. A rising level of CEA indicates recurrence as well as prognosis (see Chapter 13, IV B 9 c).

Molecular diagnostics increases the sensitivity of biopsy material.

For more accurate pathology of lymph nodes in breast cancer, immunohistochemistry is used to look for cytokeratin (an epithelial cell marker) in lymph nodes. Approximately 10%–30% of nodes considered negative with standard pathology will be found positive by the above techniques.

Quantitative immunohistochemistry for oncogene c-erbB -2 on frozen sections of breast cancer primary tumors correlates increased expression of c-erbB -2 with poorer survival.

To increase the sensitivity of pancreatic aspiration cytology biopsies, polymerase chain reaction (PCR)

amplification for the K -ras oncogene has a 96% sensitivity for pancreatic cancer cells.

F Clinical manifestations of cancer

Seven classic symptoms of cancer spell out the mnemonic “CAUTION:”

Change in bowel or bladder habits

A sore that does not heal

Unusual bleeding or discharge

T hickening or lump in the breast or elsewhere

I ndigestion or difficulty swallowing

O bvious change in a wart or mole

Nagging cough or hoarseness.

Other manifestations

Growth, causing a mass, obstruction, or neurologic deficit

Growth into neighboring tissues causing pain, paralysis, fixation, or immobility of a palpable mass

Tumor necrosis causing bleeding or fever

Systemic manifestations such as thrombophlebitis, endocrine symptoms due to hormones secreted by the tumor, and cachexia

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Extreme weight loss over a short period of time

Metastatic spread as the first symptom such as enlarged lymph nodes, neurologic symptoms, or pathologic bone fractures.

Screening tests for cancer detection. Asymptomatic cancers detected by screening generally have a better prognosis than symptomatic cancers. Common screening tests and the current American Cancer Society's recommendations for their use include:

Mammography (annually after age 35–40)

Stool for occult blood and digital rectal examination (annually after age 50)

Pap smear of the cervix (every 3 years after two negative tests 1 year apart)

G Staging of cancer

The standard staging of most cancers is based on the tumor, nodes, and metastasis (TNM) system. Various TNM classes are then grouped into stages. The staging of gastric cancer will be used to exemplify this system (Table 2-2).

T describes the primary tumor.

N describes the involvement of lymph nodes with metastatic spread.

M describes distant metastases.

Stage grouping. Staging is necessary to choose the appropriate therapy and to assess the prognosis. It also allows investigators to report their results in a standardized way so that conclusions regarding treatments and their outcomes are interpretable.

H Diagnostic procedures

Biopsy. It is mandatory that tissue be obtained to prove microscopically that a malignancy is present. Therefore, a biopsy is always obtained in diagnosing and treating cancer. There are several types of biopsy.

Aspiration biopsy or aspiration cytology biopsy. A narrow needle (e.g., 22 -gauge needle) is inserted into the lesion, and cells are aspirated into the needle and deposited on slides. The specimen is similar to that obtained by a Pap smear and is read by a cytopathologist.

TABLE 2-2 Tumor, Nodes, and Metastasis (TNM) Classification System and Stage Grouping for Gastric Adenocarcinoma

Tumor (T)

Stage grouping

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Needle biopsy. A large needle (e.g., 18 -gauge) is inserted into the lesion and a core of tissue is removed for histology. Because a needle biopsy removes more tissue than does aspiration, complications (e.g., bleeding) are more common, but the specimen is larger and the diagnosis obtained is more precise.

Incisional biopsy removes a superficial or accessible portion of the lesion for diagnosis.

Excisional biopsy completely removes a discrete tumor without a wide margin of normal tissue and is not curative for malignancy. It is used when local removal will not interfere with the therapy to be used for definitive local control.

Staging laparotomy for Hodgkin's disease establishes the correct stage.

Imaging studies , such as computed tomography (CT) scan, ultrasound, and MRI are useful for assessing the extent of spread when the study is positive. A negative imaging study does not exclude the possibility of microscopic disease spread.

Positron emission tomography (PET) scanning is an imaging modality that measures the radiation emitted by radioactive tracer molecules as they are taken up by specific cells.

The data are translated into an image by CT reconstruction.

Cancer cells exhibit accelerated glucose membrane transport. Administered radio-labeled 2-fluoro -2- deoxy -D-glucose (FDG) is metabolized intracellularly and remains trapped in the cell for essentially all human cancers.

PET -FDG scanning has been demonstrated to be superior to CT scanning in detecting colorectal cancer both for preoperative staging and post-treatment assessment of recurrence, metastases, etc.

Laparoscopy for staging has become standard for upper abdominal tumors (gastric, pancreatic, hepatic) to exclude intra -abdominal spread. This decreases the number of laparotomies at which unresectable (i.e., nonsurgical) disease is found.

I Multimodality cancer therapy

Most cancer patients are treated surgically, with radiation, chemotherapy, and immunotherapy playing increasingly important roles. Choice of therapy is based on disease, stage, histologic grade, patient age, other concomitant diseases, and the intent of therapy (i.e., cure vs. palliation).

Surgery and radiation therapy are both used for the treatment of the primary tumor and the regional lymph nodes. Neither has any effect on areas of distant spread.

Chemotherapy and immunotherapy are systemic therapies with the potential to affect distant areas of spread.