1.

Cervical Cancer
1.1. Description Definition and Overview Cancer that forms in tissues of the cervix (the organ connecting the uterus and vagina). It is usually a slow-growing cancer that may not have symptoms but can be found with regular Pap tests (a procedure in which cells are scraped from the cervix and looked at under a microscope). Cervical cancer is almost always caused by human papillomavirus (HPV) infection. Area of competence 2, of the Doctor Competencies Standart from Indonesian Medical Council To make the diagnosis based on physical examination and additional examination such as simple laboratory tests or x ray. Making appropriate referral to relevant specialist and follow ups. 1. Student have knowledge about anatomy and natural history related to cervical cancer 2. Student understands the principle of cervical cancer screening and precancer treatment 3. Student understands classification and staging of cervical cancer by FIGO 4. Student understands the principle of cervical cancer prevention and management Lectures (Teaching Learning Process) Case Presentation and Discussion Video Session Classroom, Computer, LCD and Screen 3 x 50 minute : module task 3 x 50 minute : discussion 90 minute : expert lecture (teaching session) This module is a part of Module on Reproductive Disorders, integratedly designs for medical student through Teaching Learning Process. This part of Module will facilitate the student to understand the basic of cervical cancer screening, prevention, and management (lecturer or lecturers taken from list of the doctors from Reproductive Block, as scheduled) Post test after teaching session 1. Comprehensive Cervical Cancer Control : A guide to essential practice. WHO. 2006 2. Berek & Novak's Gynecology. 14th Ed. 2007 3. Williams Gynecology.1st ed. 2008 4. Ilmu Kandungan. YBP Sarwono Prawirohardjo. 2007

Competency Area Competency Component Clinical Competence

Learning Methods Equipment Time Lecture Description

Lecturer Evaluation Suggested Refferences

INCIDENCE
Worldwide, cervical cancer is common, and ranks second among all malignancies for women (Parkin, 2005). In 2002, an estimated 493,000 new cases were identified globally and 274,000 deaths were recorded. In general, higher incidences are found in developing countries, and these countries contribute 83 percent of reported cases annually. Economically advantaged countries have significantly lower cervical cancer rates, and add only 3.6 percent of new cancers. This incidence disparity highlights successes achieved by cervical cancer screening programs in which Papanicolaou (Pap) smears are regularly obtained.

RISKS
In addition to demographic risks, behavioral risks have also been linked with cervical malignancy. Most cervical cancers originate from cells infected with the human papillomavirus (HPV), which is sexually transmitted. Early coitarche, multiple sexual partners, and increased parity are associated with a substantially greater incidence of cervical cancer. In addition, smokers are at greater risk, although the mechanism underlying this risk in not known.

ANATOMY OF THE FEMALE PELVIS AND NATURAL HISTORY OF CERVICAL CANCER

KEY POINTSy points Basic knowledge of the anatomy of the female pelvis and the natural history of cervical cancer is essential for understanding the disease and communicating messages about prevention, screening, treatment and care. The cervix undergoes normal changes from birth until after the menopause. The cervical transformation zone is the area where the great majority of precancers and cancers arise. The transformation zone is larger during puberty and pregnancy and in women who have used oral contraceptives (OCs) for a long time, which may increase exposure to HPV. This may explain why early sexual activity, multiple pregnancies and, to a lesser extent, longterm use of OCs, are cofactors for the later development of cervical cancer. After the menopause, the transformation zone may extend into the inner cervical canal, requiring the use of an endocervical speculum to see it completely. From the time that mild dysplasia is identified, it usually takes 10 to 20 years for invasive cancer to develop; this means that cervical cancer control is possible through screening and treatment. HPV infection is a necessary, but not a sufficient, cause of cervical cancer; host factors, as well as behavioural and environmental factors, may facilitate cancer development. Female External Genitalia The external genitalia include the major and minor labia, the clitoris, the urinary

opening (urethra), and the vaginal opening or introitus. The area between the vulva and the anus is called the perineum. artholin glands are two small bodies on either side of the introitus.

Female Internal Genitalia the vagina and uterus lie behind and above the pubic bone in the pelvis. The urinary bladder and urethra are in front of the vagina and uterus, and the rectum is behind them. The ureters (small tubes that deliver urine from the kidney to the bladder) lie close to the cervix on each side.

The cervical epithelia The surface of the cervix is lined by two types of epithelium: squamous epithelium and columnar epithelium. The stratified squamous epithelium is a multilayered epithelium of increasingly flatter cells. It normally covers most of the ectocervix and vagina and, in premenopausal women, appears pale pink and opaque. Its lowest (basal) layer, composed of rounded cells, is attached to the basement membrane, which separates the epithelium from the underlying fibromuscular stroma. In postmenopausal women, the squamous epithelium has fewer layers of cells, appears whitish-pink, and is prone to trauma, which is often visible as small haemorrhages or petechiae. The columnar epithelium lines the cervical canal and extends outwards to a variable portion of the ectocervix. It consists of a single layer of tall cells sitting on the basement membrane. This layer is much thinner than the squamous lining of the ectocervix. When seen with an endocervical speculum, it appears shiny red. The original squamocolumnar junction (SCJ) appears as a sharp line, with a step produced by the different thicknesses of the columnar and squamous epithelia. The location of the original SCJ varies with the womans age, hormonal status, history of birth trauma, pregnancy status, and use of oral contraceptives

Squamous metaplasia and the transformation zone When exposed to the acidic environment of the vagina, the columnar epithelium is gradually replaced by stratified squamous epithelium, with a basal layer of polygonalshaped cells derived from the original columnar cells. This normal replacement process is termed squamous metaplasia and gives rise to a new SCJ. When mature, the new squamous epithelium closely resembles the original squamous epithelium. However, the newly formed SCJ and the original SCJ are distinct on examination. The transformation zone is the area between the original and the new SCJ, where the columnar epithelium is being or has been replaced by squamous epithelium . Development of precancer and cancer The stratified squamous epithelium covering the cervix provides protection from toxic substances and infection. Under normal circumstances, the top layers are continually dying and sloughing off, and the integrity of the lining is maintained by the constant, orderly formation of new cells in the basal layer. However, in the presence of persistent HPV infection and other cofactors, the metaplastic squamous cells of the transformation zone take on an abnormal appearance, cervical squamous precancer (dysplasia). These cells later multiply in a disorderly manner typical of cancerous change to produce squamous cell carcinoma. During puberty and pregnancy, and in women using oral contraceptives, the transformation zone on the ectocervix is enlarged. Exposure to HPV at such times may facilitate infection, which may explain the association between squamous cell cervical cancer and early sexual activity, multiple pregnancies and, to a lesser extent, long-term use of oral contraceptives. Ninety per cent of cervical cancer cases are squamous cell carcinomas arising from the metaplastic squamous epithelium of the transformation zone; the other 10% are cervical adenocarcinomas arising from the columnar epithelium of the endocervix

The development of cervical cancer The primary cause of squamous cervical cancer is persistent or chronic infection with one or more of the so-called high-risk or oncogenic types of human papillomavirus. The most common cancer-causing types are 16 and 18, which are found in 70% of all cervical cancers reported. Other oncogenic types (e.g. 31, 33, 45, and 58) are found less commonly and may have different prevalence in different geographical areas. Low-risk HPV types 6 and 11 are not associated with cancer, but cause genital warts. The key determinants of HPV infection for both men and women are related to sexual behaviour, and include young age at sexual initiation, a high number of sexual partners, and having partners with multiple partners. High-risk HPV infection is most common in young women, with a peak prevalence as high as 2530% in women under 25 years of age. In most sites, prevalence decreases sharply with age. While infection with a high-risk HPV is the underlying cause of cervical cancer, most women infected with high-risk HPV do not develop cancer. Most cervical HPV infections, regardless of type, are short-lived, with only a small number persisting and even fewer progressing to precancerous lesions or invasive cancer. The conditions or cofactors that lead HPV infection to persist and progress to cancer are not well understood, but the following probably play a role. HPV-related cofactors: viral type; simultaneous infection with several oncogenic types; high amount of virus (high virus load). Host-related cofactors : immune status: people with immunodeficiency (such as that caused by HIV infection) have more persistent HPV infections and a more rapid progression to precancer and cancer; parity: the risk of cervical cancer increases with higher parity. Exogenous cofactors: tobacco smoking; coinfection with HIV or other sexually transmitted agents such as herpes simplex virus 2 (HSV-2), Chlamydia trachomatis and Neisseria gonorrhoeae; long-term (> 5 years) use of oral contraceptives. This last cofactor is of particular concern since limiting the use of oral contraceptives could have farreaching effects on womens choice of contraceptive and hence on the rates of unwanted pregnancy, unsafe abortion and maternal mortality. A WHO expert group, convened to examine the evidence and formulate recommendations, concluded that all methods of contraception, including OCs, carry risks and benefits. With respect to cervical cancer, the benefits of OCs outweigh the risks, because the number of cervical cancers that result from their use is likely to be very small; therefore, women who choose to use OCs should not be prevented or discouraged from doing so.

Progress from normal epithelium to invasive cancer

Cervical precancer: different terminologies used for cytological and histological reporting

Natural history of invasive cervical cancer Invasive cervical cancer is defined by the invasion of abnormal cells into the thick fibrous connective tissue underlying the basement membrane. It starts with a microinvasive stage, which is not visible with the naked eye on speculum examination and has to be diagnosed histologically, using a tissue sample from a cone biopsy or hysterectomy. It then evolves into larger lesions, which may extend to the vagina, pelvic walls, bladder, rectum and distant organs. If left untreated, cervical cancer progresses in a predictable manner and will almost always lead to death. The International Federation of Gynecology and Obstetrics (FIGO) system is often used to describe the extent of cancer invasion and to select treatment options. There are four, usually sequential, routes through which invasive cancer progresses. The disease is generally confined to the pelvis for a long period, where it is accessible to treatment. 1. Within the cervix. Spread from a tiny focus of microinvasive cancer, eventually involving the entire cervix which can enlarge to 8 cm or more in diameter. The cancer can be ulcerating, exophytic (growing outwards) or infiltrating (invading inwards). 2. To adjacent structures. Direct spread in all directions is possible: downwards to the vagina, upwards into the uterus, sideways into the parametrium (the tissues supporting the uterus in the pelvis) and the ureters, backwards to the rectum, and forwards to the bladder. 3. Lymphatic. Spread to pelvic lymph nodes occurs in 15% of cases when the cancer is still confined to the cervix, and increases as the cancer spreads. Lymph node metastases are at first confined to the pelvis and are later found in the chain of nodes along the aorta, eventually reaching the supraclavicular fossa (the space above the collar bone). If the cancer has advanced into the lower third of the vagina, the groin nodes may become involved and will be palpably enlarged. 4. Distant metastases through the bloodstream and lymph channels. Cervical cancer cells may spread through the blood stream and lymphatic system to develop distant metastases in the liver, bone, lung and brain.

SCREENING FOR CERVICAL CANCER

Key points Screening is testing of all women at risk of cervical cancer, most of whom will be without symptoms. Screening aims to detect precancerous changes, which, if not treated, may lead to cancer. Screening is only effective if there is a well organized system for follow-up and treatment. Women who are found to have abnormalities on screening need follow-up, diagnosis and possibly treatment, in order to prevent the development of

cancer or to treat cancer at an early stage. Regardless of the test used, the key to an effective programme is to reach the largest proportion of women at risk with quality screening and treatment. Organized screening programmes designed and managed at the central level to reach most women at risk are preferable to opportunistic screening.

SCREENING TESTS A good screening test should be: accurate; reproducible; inexpensive; easy to perform and easy to follow up; acceptable; safe. The following tests meet the above criteria to a greater or lesser extent: cytology: conventional (Pap smear) and liquid-based; HPV DNA test; visual inspection: with acetic acid (VIA)

DIAGNOSIS AND MANAGEMENT OF PRECANCER

Keypoints Further investigations are needed in all women with a positive or abnormal screening test, in order to make a definitive diagnosis. The standard method for diagnosis of cervical precancerous lesions is histopathological examination of tissue obtained through biopsy guided by colposcopy. The screen-and-treat approach involves providing treatment on the basis of a positive screen test, without further diagnostic testing. This is a new approach and the long-term impact on cancer incidence has yet to be evaluated. It is essential that precancerous lesions graded CIN 2 or 3 are treated. CIN 1 lesions are more likely to resolve spontaneously, but should be treated if it is likely that the woman will not return for follow-up, and in other special circumstances. Outpatient treatments, such as cryotherapy and loop electrosurgical excision procedure (LEEP), are preferable to more invasive treatments (such as cold knife conization), which require anaesthesia and often hospitalization, and have more complications. Cold knife conization is appropriate when the eligibility criteria for cryotherapy and LEEP are not met. Hysterectomy should not be used to treat precancer, unless there are other compelling reasons to remove the uterus. A desire for surgical sterilization is not an acceptable reason.

Comparison of cryotherapy, LEEP and cold knife conisation

MANAGEMENT OF INVASIVE CANCER

Keypoints Health care providers at all levels should know the common symptoms and signs of cervical cancer. If a woman presents with such symptoms, her cervix should be examined visually to determine whether further testing is needed. The stage of the cancer is a measure of how far it has advanced. This determines how it can be treated, and the likely outcome. Invasive cervical cancer should be treated by specialists at central-level facilities. Treatment is by surgery or radiation therapy, with or without chemotherapy. Access to treatment greatly improves prognosis and survival rates. Curative treatment is possible for all except the most advanced disease.

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The availability of a basic radiotherapy unit (teletherapy and brachytherapy) can permit effective treatment and palliation in all cases of invasive cancer. Specialists who diagnose or treat women with cervical cancer should write clear referral letters back to the provider closest to the home of the patient. Patients should be made aware that they will need long-term follow-up and contact with the cancer unit where they have received treatment. Providers should facilitate this.

Symptoms of invasive cervical cancer

Investigations for staging and treatment for cervical cancer according to FIGO

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Overview of FIGO stages related to management and prognosis

Stage 0: Carcinoma in situ, cervical intraepithelial neoplasia Grade III. This is not considered invasive cancer, since the lesion has not gone beyond the basement membrane. Stage I: Carcinoma confined to the cervix. Extension to the uterus is disregarded. IA: Microinvasive carcinoma, strictly confined to the cervix. Can only be diagnosed by microscopy; it is not clinically visible. Stage IA1: Stromal invasion no greater than 3.0 mm in depth and not more than 7.0 mm in horizontal spread. 5-year survival with optimal treatment: ~98%. Stage IA2: Stromal invasion of more than 3.0 mm but not more than 5.0 mm in depth and with horizontal spread of 7.0 mm or less. 5-year survival with optimal treatment: ~95%. IB: Carcinoma strictly confined to the cervix and clinically visible; or a microscopic lesion greater than IA2. IB1: Clinically visible lesion 4.0 cm or less in greatest dimension. 5-year survival with optimal treatment: ~85%. IB2: Clinically visible lesion more than 4.0 cm in greatest dimension. 5-year survival with optimal treatment: ~75%. Cervical cancer stage IB Stage II: Carcinoma confined to the cervix. Extension to the uterus is disregarded. IIA: Spread beyond the cervix, including upper two-thirds of the vagina, but not to tissues around the uterus (parametria). 5-year survival with optimal treatment: ~75%. Cervical cancer stage IIA

IIB: Spread beyond the cervix, with parametrial invasion, but not as far as the pelvic wall or the lower third of the vagina. 5-year survival with optimal treatment: ~65%. Cervical cancer stage IIB

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Stage III: Tumour extends to pelvic wall or involves lower third of the vagina, or causes hydronephrosis or nonfunctioning kidney. IIIA: Invasion of the lower third of the vagina, with no extension to the pelvic wall 5-year survival with optimal treatment: ~30%. Cervical cancer stage IIIA IIIB: Extension to the pelvic wall, or hydronephrosis or nonfunctioning kidney. 5year survival with optimal treatment: ~30%. Cervical cancer stage IIIB

Stage IV: Tumour has spread IVA: Spread to involve the mucosa of the bladder or rectum. 5-year survival with optimal treatment: ~10%.

IVB: Spread to distant organs, such as extrapelvic lymph nodes, kidneys, bones, lungs, liver and brain. 5-year survival with optimal treatment: <5%.

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Treatment by stage Of all cervical cancer patients presenting at multidisciplinary gynaecological assessment clinics in tertiary hospitals in developing countries, only about 5% have microinvasive or early invasive cancer (tumours up to stage IB1/IIA <4 cm in diameter). These cases are preferably treated with surgery because: The surgical procedure and recovery in hospital takes less than 2 weeks. The extension of the tumour and completeness of removal can be assessed immediately. Ovarian function is retained, which is particularly important for premenopausal patients. The patient keeps a functional, elastic, and lubricated vagina. Most complications are seen within a few days of the procedure. Surgery should also be favoured for patients with pelvic inflammatory disease, especially when there is an abscess in or near the uterus (pyometra). Radiotherapy, while having the same high 5year survival rates as surgery, takes about 6 weeks to administer, and the total extent of the tumour cannot be evaluated. Sequelae, such as loss of vaginal elasticity (fibrosis), shortening and narrowing (stenosis) and dryness of the vagina, may occur months to years after radiation and may make intercourse painful. About 80% of all cases are in stage IB2 to stage IIIB, with cervical tumours and parametrial involvement extending towards or up to the pelvic side walls, with or without obstruction of the ureters. These bulky tumours, which may measure 10 cm across, have a cure rate ranging from 30% to 75% when treated with radical radiotherapy. Large stage IIA tumours ( 4 cm or more in diameter) are treated as stage IB2 tumours. Stage IVA, with rectal or, less commonly, bladder invasion, accounts for about 10% of cases. Only about 10% of these can be cured, and fistulae between the involved organs and the vagina are frequent. Stage IVB (5% of cases), with distant haematogenous metastases, is incurable by any currently known means. However, effective palliative care can be given in these cases. If the cancer recurs, it is usually in the two years following treatment. The treatment of recurrent cancer is determined by the extent of disease at recurrence, the disease-free interval, the general condition of the patient, and the primary treatment given.

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2. DYSTOCIA
1.1. Description Definition and Overview Dystocia literally means difficult labor and is characterized by abnormally slow labor progress. It arises from four distinct abnormalities that may exist singly or in combination: a) Abnormalities of the expulsive forces; b)Abnormalities of presentation, position, or development of the fetus c)Abnormalities of the maternal bony pelvis; d) Abnormalities of soft tissues of the reproductive tract Area of competence 2, of the Doctor Competencies Standart from Indonesian Medical Council To make the diagnosis based on physical examination and additional examination such as simple laboratory tests or x ray. Making appropriate referral to relevant specialist and follow ups. 1. Student have knowledge about mechanism of dystocia and can identify the cause of dystocia : power, passage, passenger 2. Student will be able to identify abnormality of labor progress related to dystocia and making adequate referral Lectures (Teaching Learning Process) Case Presentation and Discussion Video Session Classroom, Computer, LCD and Screen 3 x 50 minute : module task 3 x 50 minute : discussion 90 minute : expert lecture (teaching session) This module is a part of Module on Reproductive Disorders, integratedly designs for medical student through Teaching Learning Process. This part of Module will facilitate the student to understand the basic mechanism of dystocia and identify the abnormal labour. (lecturer or lecturers taken from list of the doctors from Reproductive Block, as scheduled) Post test after teaching session 1. William obstetrics 23rd.ed.2010 2. Current Diagnosis & Treatment Obstetrics & Gynecology, Tenth Edition.2007

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Learning Methods Equipment Time Lecture Description

Lecturer Evaluation Suggested Refferences

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DEFINITION
Dystocia literally means difficult labor and is characterized by abnormally slow labor progress.

INCIDENCE
In 2007, the cesarean delivery rate was 31.8 percentthe highest level ever reported for the United States. According to the American College of Obstetricians and Gynecologists (2003), approximately 60 percent of primary cesarean deliveries in the United States are attributable to the diagnosis of dystocia. In nulliparous patients the incidence of labor disorders is approximately 25%. The clinical diagnosis of dystocia often is retrospective. If the outcome is uneventful and spontaneous vaginal delivery occurs, dystocia may go unreported. Failure to progress and cephalopelvic disproportion are most often diagnosed after clinical identification of abnormal labor patterns. Dystocia is currently. the most common indication for primary cesarean section, approximately 3 times more common than either nonreassuring fetal status or malpresentation.

ETIOLOGY
Dystocia arises from four distinct abnormalities that may exist singly or in combination: 1. Abnormalities of the expulsive forces. Uterine contractions may be insufficiently strong or inappropriately coordinated to efface and dilate the cervixuterine dysfunction. Also, there may be inadequate voluntary maternal muscle effort during second-stage labor. 2. Abnormalities of presentation, position, or development of the fetus. 3. Abnormalities of the maternal bony pelvisthat is, pelvic contraction. 4. Abnormalities of soft tissues of the reproductive tract that form an obstacle to fetal descent (see Chap. 40, Reproductive Tract Abnormalities). More simply, these abnormalities can be mechanistically simplified into three categories that include abnormalities of: the powersuterine contractility and maternal expulsive effort; the passengerthe fetus; and the passagethe pelvis. Common Clinical Findings in Women with Ineffective Labor Inadequate cervical dilation or fetal descent: Protracted laborslow progress Arrested laborno progress Inadequate expulsive effortineffective pushing Fetopelvic disproportion: Excessive fetal size Inadequate pelvic capacity Malpresentation or position of the fetus Ruptured membranes without labor

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ABNORMAL LABOR PATTERNS, DIAGNOSTIC CRITERIA, AND METHODS OF TREATMENT

MECHANISMS OF DYSTOCIA
Abnormalities of the Expulsive Forces (POWER)
Cervical dilatation and propulsion and expulsion of the fetus are brought about by contractions of the uterus, reinforced during the second stage by voluntary or involuntary muscular action of the abdominal wall"pushing." From these observations, it is possible to define two types of uterine dysfunction. In the more common hypotonic uterine dysfunction, there is no basal hypertonus and uterine contractions have a normal gradient pattern (synchronous), but pressure during a contraction is insufficient to dilate the cervix. In the second type, hypertonic uterine dysfunction or incoordinate uterine dysfunction, either basal tone is elevated appreciably or the pressure gradient is distorted. Gradient distortion may result from contraction of the uterine midsegment with more force than the fundus or from complete asynchronism of the impulses originating in each cornu or a combination of these two.

Maternal Pushing Efforts

With full cervical dilatation, most women cannot resist the urge to "bear down" or "push" each time the uterus contracts. The combined force created by contractions of the uterus and abdominal musculature propels the fetus downward. At times, force created by abdominal musculature is compromised sufficiently to slow or even prevent spontaneous vaginal delivery. Heavy sedation or regional analgesia may reduce the reflex urge to push and may impair the ability to contract abdominal muscles sufficiently. In other instances, the inherent urge to push is overridden by the intense pain created by bearing down.

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Abnormalities of the Passage

Using roentgenographic studies, Caldwell and Moloy classified the 4 major types of adult pelvic types: gynecoid, android, anthropoid, and platypelloid. Pure forms of these pelvic types are rare; mixed elements are more often present in each type of pelvis. The gynecoid pelvis is considered the most typically "female" type and is the most favorable for uncomplicated vaginal delivery. Found in approximately 50% of all women, the pelvic inlet has an oval configuration with a transverse diameter slightly greater than the anteroposterior diameter. Pelvic side walls are straight, the ischial spines are not prominent, the subpubic arch is wide, and the sacrum is concave. The android, or "male," type of pelvis is found in approximately 33% of white women and approximately 15% of black women. The inlet is wedge-shaped with convergent side walls, the ischial spines are prominent, the subpubic arch is narrowed, and the sacrum is inclined anteriorly in its lower third. The android pelvis is associated with persistent occiput posterior position and deep transverse arrest. The anthropoid pelvis is present in almost half of black women and 20% of white women. The inlet is oval, with an anteroposterior diameter greater than the transverse diameter. Pelvic side walls are divergent, and the sacrum is inclined posteriorly. This pelvic type is most often associated with persistent occiput posterior position. The platypelloid pelvis is present in fewer than 3% of all women. This pelvis is characterized by a transverse diameter that is wide with respect to the anteroposterior diameter. Deep transverse arrest patterns of labor are commonly associated with this pelvic type.

Fetopelvic Disproportion
Fetopelvic disproportion arises from diminished pelvic capacity, excessive fetal size, or more usually, a combination of both.

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Pelvic Capacity
Any contraction of the pelvic diameters that diminishes its capacity can create dystocia during labor. There may be contractions of the pelvic inlet, the midpelvis, or the pelvic outlet, or a generally contracted pelvis may be caused by combinations of these.

Contracted Inlet
The pelvic inlet usually is considered to be contracted if its shortest anteroposterior diameter is less than 10 cm or if the greatest transverse diameter is less than 12 cm. The anteroposterior diameter of the inlet is commonly approximated by manually measuring the diagonal conjugate, which is approximately 1.5 cm greater. Therefore, inlet contraction usually is defined as a diagonal conjugate of less than 11.5 cm. Prior to labor, the fetal biparietal diameter has been shown to average from 9.5 to as much as 9.8 cm. Therefore, it might prove difficult or even impossible for some fetuses to pass through an inlet that has an anteroposterior diameter of less than 10 cm. A contracted inlet plays an important part in the production of abnormal presentations. In normal nulliparas, the presenting part at term commonly descends into the pelvic cavity before the onset of labor. When the inlet is contracted considerably, however, descent usually does not take place until after labor onset, if at all. Cephalic presentations still predominate, but the head floats freely over the pelvic inlet or rests more laterally in one of the iliac fossae. Accordingly, very slight influences may cause the fetus to assume other presentations. In women with contracted pelves, face and shoulder presentations are encountered three times more frequently, and the cord prolapses four to six times more often Contracted Midpelvis This finding is more common than inlet contraction. It frequently causes transverse arrest of the fetal head, which potentially can lead to a difficult midforceps operation or to cesarean delivery. The obstetrical plane of the midpelvis extends from the inferior margin of the symphysis pubis through the ischial spines and touches the sacrum near the junction of the fourth and fifth. A transverse line theoretically connecting the ischial spines divides the midpelvis into anterior and posterior portions. The former is bounded anteriorly by the lower border of the symphysis pubis and laterally by the ischiopubic rami. The posterior portion is bounded dorsally by the sacrum and laterally by the sacrospinous ligaments, forming the lower limits of the sacrosciatic notch. Average midpelvis measurements are as follows: transverse, or interischial spinous, 10.5 cm; anteroposterior, from the lower border of the symphysis pubis to the junction of S4-S5, 11.5 cm; and posterior sagittal, from the midpoint of the interspinous line to the same point on the sacrum, 5 cm. The definition of midpelvic contractions has not been established with the same precision possible for inlet contractions. Even so, the midpelvis is likely contracted when the sum of the interspinous and posterior sagittal diameters of the midpelvisnormal, 10.5 plus 5 cm, or 15.5 cmfalls to 13.5 cm or less. Contracted Outlet This finding usually is defined as an interischial tuberous diameter of 8 cm or less. The pelvic outlet may be roughly likened to two triangles, with the interischial tuberous diameter constituting the base of both. The sides of the anterior triangle are the pubic rami, and its apex is the inferoposterior surface of the symphysis pubis. The posterior triangle has no bony sides but is limited at its apex by the tip of the last

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sacral vertebranot the tip of the coccyx. Diminution of the intertuberous diameter with consequent narrowing of the anterior triangle must inevitably force the fetal head posteriorly. Outlet contraction without concomitant midplane contraction is rare. Although the disproportion between the fetal head and the pelvic outlet is not sufficiently great to give rise to severe dystocia, it may play an important part in the production of perineal tears. With increasing narrowing of the pubic arch, the occiput cannot emerge directly beneath the symphysis pubis but is forced increasingly farther down upon the ischiopubic rami. The perineum, consequently, becomes increasingly distended and thus exposed to greater danger of laceration.

Abnormalities of the Passenger

Dystocia may be caused by abnormalities of the "passenger," or fetus. Common fetal abnormalities leading to dystocia include excessive fetal size, malpositions, congenital anomalies, and multiple gestation. Malposition and Malpresentation Fetal malpresentations are abnormalities of fetal position, presentation, attitude, or lie. They collectively constitute the most common cause of fetal dystocia, occurring in approximately 5% of all labors. Persistent occiput posterior and occiput transverse positions, brow presentation, face presentation, transverse or oblique lies, and breech and compound presentation are included in this category.

Shoulder Dystocia
There is evidence that the incidence of shoulder dystocia has increased in recent decades, likely due to increasing birthweight. Maternal Consequences Postpartum hemorrhage, usually from uterine atony, but also from vaginal and cervical lacerations, is the major maternal risk from shoulder dystocia.

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Fetal Consequences Shoulder dystocia may be associated with significant fetal morbidity and even mortality. Gherman and coworkers (1998) reviewed 285 cases of shoulder dystocia and found that 25 percent were associated with fetal injuries. Transient Erb or Duchenne brachial plexopathy accounted for two thirds of injuries. In this same cohort of 285 infants, 38 percent had a clavicular fracture, and 17 percent sustained a humeral fracture. There was one neonatal death, and four newborns had persistent brachial plexopathy injuries. Mehta and associates (2007) found a similar number of injuries in a study of 205 shoulder dystocia cases in which 36 or 17.5 percent had injuryagain, most involved the brachial plexus. The American College of Obstetricians and Gynecologists (2002) reviewed studies and concluded that: 1. Most cases of shoulder dystocia cannot be accurately predicted or prevented. 2. Elective induction of labor or elective cesarean delivery for all women suspected of having a macrosomic fetus is not appropriate. 3. Planned cesarean delivery may be considered for the nondiabetic woman with a fetus whose estimated fetal weight is > 5000 g or for the diabetic woman whose fetus is estimated to weigh > 4500 g. Hernandez and Wendel (1990) suggested use of a shoulder dystocia drill to better organize emergency management of an impacted shoulder: 1. Call for helpmobilize assistants, an anesthesiologist, and a pediatrician. Initially, a gentle attempt at traction is made. Drain the bladder if it is distended. 2. A generous episiotomyconsider mediolateral or episioproctotomymay afford room posteriorly. 3. Suprapubic pressure is used initially by most practitioners because it has the advantage of simplicity. Only one assistant is needed to provide suprapubic pressure while normal downward traction is applied to the fetal head. 4. The McRoberts maneuver requires two assistants. Each assistant grasps a leg and sharply flexes the maternal thigh against the abdomen. These maneuvers will resolve most cases of shoulder dystocia. If they fail, however, the following steps may be attempted: 1. The Woods screw maneuver. 2. Delivery of the posterior arm is attempted, but with a fully extended arm, this is usually difficult to accomplish. Other techniques generally should be reserved for cases in which all other maneuvers have failed. These include intentional fracture of the anterior clavicle or humerus and the Zavanelli maneuver. The American College of Obstetricians and Gynecologists (2002) has concluded that there is no evidence that any one maneuver is superior to another in releasing an impacted shoulder or reducing the chance of injury. Performance of the McRoberts maneuver, however, was deemed a reasonable initial approach.

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